Clinical Aphasiology

Clinical Aphasiology

This book presents a collection of cutting edge work from leading researchersand clinicians around the world on a range of topics within Clinical Aphasi-ology. However, more than this, the volume is also a tribute to Chris Code,one of the foremost scholars in the field. Professor Code has made a galvani-zing impact on the field: as a savant, a motivator and an impresario of trendswhich have resulted in several significant developments in the field. In the firstchapter of this book the editors outline the considerable contributions ChrisCode has made to the area.

The remaining contents have been divided into three main approaches to thestudy of aphasia, reflecting Professor Code’s own interests. First are the con-tributions that fall under the heading of Conceptual Considerations. These aremainly interdisciplinary in nature, spanning linguistics, phonetics, psychologyand neurology, as well as social aspects of communication disorders. Thesecond section of the book deals with Research Considerations, with chaptersranging from how the study of disrupted communication can inform modelsof normal language processing, through tone production and processing inspeakers with aphasia, to anomia and progressive multifocal leukoencepha-lopathy. Each of these chapters explores different aspects of research method-ology, including quantitative and qualitative research. The final section of thecollection deals with Clinical Considerations; the chapters here cover counsell-ing, computerized training, cultural and linguistic diversity in aphasia, righthemisphere disorders, and communication problems in the dementias.

Clinical Aphasiology will be an invaluable tool for both students and practi-tioners in speech and language pathology, psychology, neurology, and relatedfields.

Martin J. Ball is Hawthorne-Board of Regents’ Support Fund Endowed Pro-fessor, Head of the Department of Communicative Disorders, and Director ofthe Doris B. Hawthorne Center for Special Education and CommunicationDisorders at the University of Louisiana at Lafayette.

Jack S. Damico holds the Doris B. Hawthorne Eminent Scholar Professor-ship in Communicative Disorders at the University of Louisiana at Lafayetteand is a Fellow of the American Speech-Language-Hearing Association.

Clinical AphasiologyFuture directions

Edited by Martin J. Ball andJack S. Damico

A Festschrift for Chris Code

First published 2007 by Psychology Press27 Church Road, Hove, East Sussex BN3 2FA

Simultaneously published in the USA and Canadaby Psychology Press270 Madison Avenue, New York, NY 10016

Psychology Press is an imprint of the Taylor & Francis Group,an Informa business

© 2007 Psychology Press

All rights reserved. No part of this book may be reprinted orreproduced or utilized in any form or by any electronic,mechanical, or other means, now known or hereafterinvented, including photocopying and recording, or in anyinformation storage or retrieval system, without permission inwriting from the publishers.

This publication has been produced with paper manufactured tostrict environmental standards and with pulp derived fromsustainable forests.

British Library Cataloguing in Publication DataA catalogue record for this book is available from the British Library

Library of Congress Cataloging in Publication DataClinical aphasiology : future directions / edited by Martin J. Ball andJack S. Damico.

p.; cm.Includes bibliographical references and index.ISBN-13: 978–1–84169–670–6 (hardcover)ISBN-10: 1–84169–670–6 (hardcover)1. Aphasia. 2. Speech disorders. 3. Language disorders. I. Ball,

Martin J. (Martin John) II. Damico, Jack Samual. III. Code,Christopher, 1942–

[DNLM: 1. Aphasia—Festschrift. WL 340.5 C6386 2007]RC425.C55 2007616.85′52—dc22

2006032956

ISBN: 978–1–84169–670–6

This edition published in the Taylor & Francis e-Library, 2007.

“To purchase your own copy of this or any of Taylor & Francis or Routledge’scollection of thousands of eBooks please go to www.eBookstore.tandf.co.uk.”

ISBN 0-203-96255-9 Master e-book ISBN

Contents

Professor Chris Code’s publications and presentations xTabula gratulatoria xxContributors xxiiiPreface xxvi

1 Chris Code’s contribution to aphasiology 1MARTIN J. BALL AND JACK S. DAMICO

PART IConceptual considerations 15

2 Investigations in speech and language and related disorders:Crossing the boundaries between disciplines—a tribute toChris Code 17MANFRED HERRMANN AND THORSTEN FEHR

3 Independent evidence for the unification of explanatoryparadigms in the neurosciences 28HUGH W. BUCKINGHAM AND SARAH S. CHRISTMAN

4 The social and neuropsychological underpinnings ofcommunication disorders after severe traumatic brain injury 42SKYE McDONALD

5 Social validation of recovery in aphasia 72LEONARD L. LaPOINTE AND KERRY L. LENIUS

6 Interactional aphasia: Principles and practices oriented tosocial intervention 92JACK S. DAMICO, MARTIN J. BALL, NINA N. SIMMONS-MACKIEAND NICOLE MÜLLER

PART IIResearch considerations 105

7 From the study of language dysfunction and handicap to abetter understanding of linguistic processing in normality 107JEAN-LUC NESPOULOUS AND JACQUES VIRBEL

8 Production and perception of word tones in patients withbrain damage 125INGER MOEN

9 Subcortical aphasia: Historical perspective andcontemporary thinking 136BRUCE E. MURDOCH

10 Mechanisms of lexical selection and the anomias 156TOBIAS BORMANN, GERHARD BLANKEN ANDCLAUS-W. WALLESCH

11 Repetitive verbal behaviours in PML: An exploratory study ofconversation 168NICOLE MÜLLER, ALANA KOZLOWSKI AND PATTIE DOODY

12 Multiparty interactions in aphasia 181ALISON FERGUSON

13 Stroke stories: Conveying emotive experiences in aphasia 195ELIZABETH ARMSTRONG AND HANNA K. ULATOWSKA

PART IIIClinical considerations 211

14 Counseling families and adults with speech and languagedisorders: The view from a wellness perspective 213AUDREY L. HOLLAND

15 Cultural dimensions of aphasia: Adding diversity andflexibility to the equation 222CLAIRE PENN

16 Assessment of aphasia in a multi-lingual world 245SUSAN EDWARDS AND ROELIEN BASTIAANSE

vi Contents

17 Computerized aphasia treatment outcomes research:The past and a proposal 259RICHARD C. KATZ AND ROBERT T. WERTZ

18 Traumatic brain injury rehabilitation: Advancedcommunication training perspectives 270LEANNE TOGHER

19 The future of our knowledge about communicationimpairments following a right-hemisphere lesion 284YVES JOANETTE, MAUD CHAMPAGNE-LAVAU,KARIMA KAHLAOUI AND BERNADETTE SKA

20 Progressive language and speech disorders in dementia 299MARIA PACHALSKA

Author index 325Subject index 339

Contents vii

Gabrielle Code

Professor Chris Code’s publicationsand presentations

Books

Müller, D., Munro, S., & Code, C. (1981). Language assessment for remediation.Beckenham, UK: Croom Helm.

Code, C., & Müller, D. (Eds.) (1983). Aphasia therapy. London: Edward Arnold.(Translated and published in Italian as Terapia dell’Afasia. Roma: Marrapese Edi-tore, 1984.)

Code, C., & Ball, M. (Eds.) (1984). Experimental clinical phonetics. London: CroomHelm.

Code, C. (1987). Language, aphasia and the right hemisphere. Chichester, UK: JohnWiley. (Translated and published in Japanese, Central Foreign Books, Tokyo, 1990.)

Code, C. (Ed.) (1989). The characteristics of aphasia.Brain damage, behaviour and cog-nition series. Hove, UK: Lawrence Erlbaum Associates Ltd. (Previously publishedby Taylor & Francis, London.)

Code, C., & Müller, D. (Eds.) (1989). Aphasia therapy (2nd ed). London: Cole &Whurr.

Code, C., & Müller, D. J. (1992). The Code-Müller protocols: Assessing perceptions ofpsychosocial adjustment to brain damage. Kibworth: Far Communications.

Code, C., & Müller, D. J. (Eds.) (1995). The treatment of aphasia: From theory topractice. London: Whurr.

Code, C., & Müller, D. J. (Eds.) (1996). Forums in clinical aphasiology. London: Whurr.Code, C., Wallesch, C.-W., Lecours, A.-R., & Joanette, Y. (Eds.) (1996). Classic cases in

neuropsychology. Hove, UK: Lawrence Erlbaum Associates Ltd.Ball, M. J., & Code, C. (Eds.) (1997). Instrumental clinical phonetics. London: Whurr.McDonald, S., Togher, L., & Code, C. (Eds.) (1999). Traumatic brain injury and

communication disorders. Hove, UK: Psychology Press.Code, C., Wallesch, C.-W., Lecours, A.-R., & Joanette, Y. (Eds.) (2003). Classic cases in

neuropsychology: Volume II. Hove, UK: Lawrence Erlbaum Associates Ltd.O’Halloran, R., Worrall, L., Code, C., Toffolo, D., & Hickson, L. (2004). The inpatient

functional communication interview. Bicester, UK: Speechmark Publications.Code, C. (Ed.) (2006). The representation of language in the brain. Hove, UK:

Psychology Press.Tesak, J., & Code, C. (in press). Milestones in the history of aphasia: Theories and

protagonists. Hove, UK: Psychology Press.

Chapters in books

Code, C. (1983). Hemispheric specialization retraining in aphasia: Possibilities andproblems. In C. Code & D. Müller (Eds.), Aphasia therapy. London: EdwardArnold.

Code, C., & Müller, D. (1983). Perspectives in aphasia therapy. In C. Code & D. Müller(Eds.), Aphasia therapy. London: Edward Arnold.

Müller, D., & Code, C. (1983). Interpersonal perceptions of psychosocial adjustmentin aphasia. In C. Code & D. Müller (Eds.), Aphasia therapy. London: EdwardArnold.

Code, C. (1984). Delayed auditory feedback. In C. Code & M. Ball (Eds.), Experi-mental clinical phonetics. Beckenham, UK: Croom Helm.

Code, C., (1984). Dichotic listening. In C. Code & M. Ball (Eds.), Experimental clinicalphonetics. Beckenham, UK: Croom Helm.

Code, C., & Ball, M. (1988). Apraxia of speech: The case for a cognitive phonetics.In M. Ball (Ed.), Theoretical linguistics and disordered language. Beckenham, UK:Croom Helm.

Code, C. (1989). From symptoms to syndromes to models: The nature of aphasia. InC. Code (Ed.), The characteristics of aphasia. Hove, UK: Lawrence ErlbaumAssociates Ltd.

Code, C. (1989). Speech automatisms and recurring utterances. In C. Code (Ed.),The characteristics of aphasia. Hove, UK: Lawrence Erlbaum Associates Ltd.(Previously published by Taylor & Francis, London.)

Code, C., & Müller, D. J. (1989). The future history of aphasia therapy. In C. Code & D.Müller (Eds.), Aphasia therapy (2nd ed). London: Cole & Whurr.

Code, C. (1994). The role of the right hemisphere in the treatment of aphasia. InR. Chapey (Ed.), Language intervention strategies in adult aphasia. Baltimore,MD: Williams & Wilkins.

Code, C., & Müller, D. (1995). Cognitive and neuropsychological approaches. InC. Code & D. J. Müller (Eds.), The treatment of aphasia: From theory to practice.London: Whurr.

Code, C., & Müller, D. (1995). Efficacy & effectiveness. In C. Code & D. J. Müller(Eds.), The treatment of aphasia: From theory to practice. London: Whurr.

Code, C., & Müller, D. (1995). Pragmatic, linguistic and functional perspectives. InC. Code & D. J. Müller (Eds.), The treatment of aphasia: From theory to practice.London: Whurr.

Code, C., & Müller, D. (1995). Psychosocial perspectives. In C. Code & D. J. Müller(Eds.), The treatment of aphasia: From theory to practice. London: Whurr.

Code, C. (1996). Aphasia therapy. In J. G. Beaumont & J. Sergent (Eds.), Blackwelldictionary of neuropsychology. Oxford, UK: Blackwell.

Code, C. (1996). Auditory techniques. In C. Code & M. Ball (Eds.), Instrumentalclinical phonetics (2nd ed). London: Whurr.

Code, C. (1996). Classic cases: Ancient and modern milestones in the development ofneuropsychological science. In C. Code, C.-W. Wallesch, Y. Joanette, & A.-R.Lecours (Eds.), Classic cases in neuropsychology. Hove, UK: Lawrence ErlbaumAssociates Ltd.

Code, C. (1996). Speech from the isolated right hemisphere? Left hemispherectomycases E.C. and N.F. In C. Code, C.-W. Wallesch, Y. Joanette, & A.-R. Lecours (Eds.),Classic cases in neuropsychology. Hove, UK: Lawrence Erlbaum Associates Ltd.

Chris Code’s publications xi

Code, C., & Müller, D. (1996). Assessing for treatment. In C. Code & D. J. Müller(Eds.), Forums in clinical aphasiology. London: Whurr.

Code, C., & Müller, D. (1996). Computers in clinical aphasiology. In C. Code &D. J. Müller (Eds.), Forums in clinical aphasiology. London: Whurr.

Code, C., & Müller, D. (1996). Issues in clinical aphasiology. In C. Code & D. J. Müller(Eds.), Forums in clinical aphasiology. London: Whurr.

Code, C., & Müller, D. (1996). Psychosocial issues. In C. Code & D. J. Müller (Eds.),Forums in clinical aphasiology. London: Whurr.

Code, C. (1997). A metamodel for recovery from aphasia. In J. Ponsford, P. Snow, &V. Anderson (Eds.), International perspectives in traumatic brain injury. Melbourne:Australian Academic Press.

Code, C. (1997). Aphasia recovery, therapy and psychosocial adjustment. In A. Baum,C. McManus, S. Newman, J. Weinman, & R. West (Eds.), The Cambridge handbookof psychology, health & medicine. Cambridge, UK: Cambridge University Press.

Code, C. (1997). Experimental audioperceptual techniques. In M. J. Ball & C. Code(Eds.), Instrumental clinical phonetics. London: Whurr.

McDonald, S., Togher, L., & Code, C. (1999). The nature of traumatic brain injury: Anoverview. In S. McDonald, L. Togher, & C. Code (Eds.), Traumatic brain injury andcommunication disorders. Hove, UK: Psychology Press.

Togher, L., Code, C., & McDonald, S. (1999). Communication problems followingtraumatic brain injury. In S. McDonald, L. Togher, & C. Code (Eds.), Traumaticbrain injury and communication disorders. Hove, UK: Psychology Press.

Togher, L., Hand, L., & Code, C. (1999). Exchange of information in the talk ofpeople with traumatic brain injury. In S. McDonald, L. Togher, & C. Code (Eds.),Traumatic brain injury and communication disorders. Hove, UK: Psychology Press.

Herrmann, M., Müller, D. J., Ebert, A. D., & Code, C. (2000). Erwartungshaltungenan psychosoziale Anpassung nach Hirnschadigungen. In W. Fries & C. Wendel(Eds.), Ambulante Komplex-Behandlung von Hirnverletzten Patienten. München:W. Zuckschwerdt Verlag.

McCooey, R., Toffolo, D., & Code, C. (2000). Assessing and treating functional com-munication in the acute hospital. In L. Worrall & C. Fratalli (Eds.), Functionalcommunication. New York: Thieme Science.

Code, C., & Hogan, A. (2001). Engaging the client in a helping relationship. InA. Hogan (Ed.), Hearing rehabilitation for deafened adults. London: Whurr.

Code, C., Eales, C., Pearl, G., Conan, M., Cowin, K., & Hickin, J. (2003). Supporteds-help groups for aphasic people: Development and research. In I. Papathanasiou &R. de Bleser (Eds.), The science of aphasia: From therapy to theory. London:Elsevier.

Code, C., & Herrmann, M. (2003). The relevance of emotional and psychosocialfactors in aphasia to rehabilitation. In W. H. Williams & J. J. Evans (Eds.), Bio-psychosocial approaches to neurorehabilitation: Assessment and management ofneuropsychiatric mood and behavioural disorders. Hove, UK: Psychology Press.

Code, C., & Joanette, Y., (2003). Neural plasticity in the control of language in theadult brain: The role of the separated right hemispheres in cases PS, VP and JW.In C. Code, C.-W. Wallesch, Y. Joanette, & A.-R. Lecours (Eds.), Classic cases inneuropsychology: Volume II. Hove, UK: Lawrence Erlbaum Associates Ltd.

Code, C., & Müller, D. (2003). Psychosocial and quality of life issues in treatment. InR. Kent (Ed.), The MIT encyclopaedia of communication disorders. Cambridge,MA: MIT Press.

xii Chris Code’s publications

Kaczmarek, B., Code, C., & Wallesch, C.-W. (2003). ‘Z’. In C. Code, C.-W. Wallesch,Y. Joanette, & A.-R. Lecours (Eds.), Classic cases in neuropsychology: Volume II.Hove, UK: Lawrence Erlbaum Associates Ltd.

Code, C. (2004). Syllables in the brain. In R. Hartsuiker, R. Bastiaanse, & A. Postma(Eds.), Phonological processing and monitoring. Hove, UK: Psychology Press.

Code, C., Müller, N., Tree, J. T., & Ball, M. J. (2006). Syntactic impairments canemerge later: Progressive agrammatic agraphia and syntactic comprehensionimpairment. In C. Code (Ed.), The representation of language in the brain. Hove,UK: Psychology Press.

Code, C., & Wallesch, C.-W. (2006). The form of representation of language in thebrain and the influence of John C. Marshall. In C. Code (Ed.), The representation oflanguage in the brain. Hove, UK: Psychology Press.

Code, C. (in press). Aphasia recovery, therapy and psychosocial adjustment. InA. Baum, C. McManus, S. Newman, J. Weinman, & R. West (Eds.), TheCambridge handbook of psychology, health & medicine (2nd ed). Cambridge, UK:Cambridge University Press.

Code, C. (in press). The operculum syndrome: Foix-Chavany-Marie Syndrome.In M. McNeil (Ed.), Clinical management of sensorimotor speech disorders(2nd ed). New York: Thieme Publishers.

Papers in peer-reviewed journals

Code, C. (1979). Genuine and artificial stammering: An EMG comparison. BritishJournal of Communication Disorders, 14, 5–16.

Code, C. (1980). Delayed auditory feedback and auditory-feedback masking withstammerers and normal speakers. Australian Journal of Human CommunicationDisorders, 8, 40–48.

Code, C., & Müller, D. (1980). Is the Edinburgh Masker really successful? BritishJournal of Disorders of Communication, 15, 141–142.

Code, C. (1981). Dichotic listening with the communicatively impaired: Resultsfrom trials with a short British-English dichotic word test. Journal of Phonetics, 9,375–383.

Code, C. (1982). Neurolinguistic analysis of recurrent utterances in aphasia. Cortex,18, 141–152.

Code, C. (1982). On the origins of recurrent utterances in aphasia. Cortex, 18,161–164.

Code, C., & Ball, M. (1982). Fricative production in Broca’s aphasia. Journal of Phon-etics, 10, 325–331.

Müller, D., Code, C., & Mugford, J. (1982). Predicting psychosocial adjustment inaphasia. British Journal of Disorders of Communication, 17, 23–29.

Code, C. (1983). On “Neurolinguistic analysis of recurrent utterances in aphasia”:Reply to De Bleser & Poeck. Cortex, 19, 261–264.

Code, C. (1986). Catastrophic reaction and anosognosia in anterior–posterior andleft–right models of the cerebral control of emotion. Psychological Research, 48,53–55.

Code, C., & Gaunt, C. (1986). Treating aphasia and apraxia with a combinedspeech and gesture approach: A single case study. British Journal of Disorders ofCommunication, 21, 11–20.

Chris Code’s publications xiii

Code, C., & Brown, J. W. (1987). Aphasia from the wrong (right) hemisphere:Questions for crossed aphasia. Aphasiology, 1, 401–402.

Code, C., & Lodge, B. (1987). Language in dementia of recent referral. Age andAgeing, 16, 366–372.

Code, C., & Rowley, D. (1987). Age, sex, handedness and aphasia type. Aphasiology, 1,339–345.

Code, C. (1991). The computerized Boston: Aphasia assessment database with diag-nostic features. Computer Users in Speech and Hearing, 7, 314–322.

Code, C. (1994). Speech automatism production in aphasia. Journal of Neuro-linguistics, 8, 135–148.

Code, C., Rowley, D. T., & Kertesz, A. (1994). Predicting recovery from aphasia withconnectionist networks: Preliminary comparisons with multiple regression. Cortex,30, 527–532.

Ball, M. J., Code, C., Rahilly, J., & Hazlett, D. (1994). Non-segmental aspectsof disordered speech: Developments in transcription. Clinical Linguistics andPhonetics, 8, 67–83.

Code, C. (1995). Asymmetries in ear movements and eyebrow raising in menand women and right and left handers. Perceptual and Motor Skills, 80, 1147–1154.

Code, C., & Ball, M. J. (1995). Syllabification in aphasic recurring utterances:Contributions of sonority theory. Journal of Neurolinguistics, 8, 257–265.

Code, C. (1996). Aphasia therapy. British Journal of Clinical Psychology, 35,157–159.

Code, C., Khanbha, F., Isman, K., & Mattiazzo, V. (1996). Perceptions of emotionaland psychosocial state in laryngectomised patients, their significant others and cli-nicians at three months post-surgery. Asia Pacific Journal of Speech, Language andHearing, 1, 91–104.

Harasty, J., Halliday, G., Code, C., & Brooks, W. (1996). Anatomical evidence for avisual and auditory semantic network in a case of focal dementia. Brain, 119,181–190.

Hemsley, G., & Code, C. (1996). Interactions between recovery in aphasia, emotionaland psychosocial factors in subjects with aphasia, their significant others andspeech pathologists. Disability and Rehabilitation, 18, 567–584.

Herrmann, M., Code, C. (1996). Weighting of items on the Code-Müller protocols:The effects of clinical experience of aphasia therapy. Disability and Rehabilitation,18, 509–514.

Code, C. (1997). Can the right hemisphere speak? Brain and Language, 57, 38–59.Herrmann, M., Hogan, A., Müller, D., & Code, C. (1997). Psychosoziale Anpas-

sungsleistungen und Therapieziele bei Sprach- und Kommunikationsstorungen– Untersuchungen mit den Code-Müller Protokollen. Neurolinguistik, 11, 1–21.

Togher, L., Hand, L., & Code, C. (1997). Analyzing discourse in the traumatic braininjury population: Telephone interactions with different communication partners.Brain Injury, 11, 169–189.

Togher, L., Hand, L., & Code, C. (1997). Disability following head injury: Anew perspective on the relationship between communication impairment anddisempowerment. Disability and Rehabilitation, 18, 559–566.

Togher, L., Hand, L., & Code, C. (1997). Measuring service encounters with thetraumatically brain injured population. Aphasiology, 11, 491–504.

Code, C. (1998). Models, theories and heuristics in apraxia of speech. ClinicalLinguistics and Phonetics, 12, 47–66.

xiv Chris Code’s publications

Cowell, S. F., & Code, C. (1998). Thinking nuclear medicine: PET activation. Journal ofNuclear Medicine Technology, 26, 17–22.

Nespoulous, J.-L., Code, C., Virbel, J., & Lecours, A.-R. (1998). Hypotheses on thedissociation between “referential” and “modalizing” verbal behaviour in aphasia.Applied Psycholinguistics, 19, 311–331.

Code, C. (1999). Re-assembling the brain: Are cell assemblies the brain’s language forrecovery of function? (Commentary) Behavioural and Brain Sciences, 22, 282.

Code, C., Hemsley, G., & Herrmann, M. (1999). Emotional reactions to aphasia.(Special Issue on Psychosocial Issues in Aphasia) Seminars in Speech and Language,20, 19–31.

Code, C., Müller, D. J., & Herrmann, M. (1999). Perceptions of psychosocial adjust-ment to aphasia: Studies with the CMP. (Special Issue on Psychosocial Issues inAphasia) Seminars in Speech and Language, 20, 51–63.

Code, C., Müller, D., Herrmann, M., & Hogan, A. (1999). Perceptions of psychosocialadjustment to acquired communication disorders: Studies with the Code-Müllerprotocols. International Journal of Communication Disorders, 34, 193–207.

Harasty, J., Halliday, G. M., Kril, J. J., & Code, C. (1999). Specific temperoparietalgyral atrophy reflects the pattern of language dissolution in Alzheimer’s disease.Brain, 122, 675–686.

Hogan, A., Code, C., Taylor, A., & Wilson, D. (1999). Employment and economicoutcomes for deafened adults with cochlear implants. Australian Journal ofRehabilitation Counselling, 5, 1–8.

McCabe, P., Sheard, S., & Code, C. (1999). What do speech pathologists know aboutHIV? Advances in Speech Language Pathology, 1, 9–18.

Code, C. (2000). Not fractionating, converging. Brain and Language: Millennium Issue,71, 44–45.

Cowell, S. F., Egan, G. F., Code, C., Harasty, J., & Watson, J. D. G. (2000). Thefunctional neuroanatomy of simple calculation and number repetition: A para-metric PET activation study. NeuroImage, 12, 565–573.

Katz, R., Hallowell, B., Code, C., Armstrong, E., Roberts, P., Pound, C., et al.(2000). A multi-national comparison of aphasia management practices. Inter-national Journal of Language and Communication Disorders, 35, 303–314.

Roger, P., Code, C., & Sheard, C. (2000). Assessment and management of aphasia in alinguistically diverse society. Asia-Pacific Journal of Speech and Language, 5, 21–34.

Code, C. (2001). Multifactorial processes in recovery from aphasia: Developing thefoundations for a multilevelled framework. Brain and Language, 77, 25–44.

McCabe, P., Sheard, C., & Code, C. (2002). Acquired communication impairment inpeople with HIV. Journal of Medical Speech-Language Pathology, 10, 183–199.

Simmons-Mackie, N., Code, C., Armstrong, E., Stiegler, L., & Elman, R. (2002). Whatis aphasia? Results of an international survey. Aphasiology, 16, 837–848.

Code, C. (2003). The quantity of life for people with chronic aphasia. Neuro-psychological Rehabilitation, 13, 365–378.

Code, C. (2003). Vocalisation and the development of hand preference (Commentary).Behavioural and Brain Sciences, 26 (2), 215–216.

Code, C., & Heron, C. (2003). Services for aphasia, other acquired adult neurogeniccommunication and swallowing disorders in the United Kingdom, 2000. Disabilityand Rehabilitation, 21, 1231–1237.

Code, C., & Herrmann, M. (2003). The relevance of emotional and psychosocialfactors in aphasia to rehabilitation. Neuropsychological Rehabilitation, 13, 109–132.

Chris Code’s publications xv

Roberts, P., Code, C., & McNeil, M. (2003). Describing participants in aphasiaresearch. Part 1: Audit of current practice. Aphasiology, 17, 911–932.

Ball, M. J., Code, C., Tree, J., Dawe, K., & Kay, J. (2004). Phonetic and phonologicalanalysis of progressive speech degeneration: A case study. Clinical Linguistics andPhonetics, 18, 447–462.

Chung, K. K. H., Code, C., & Ball, M. J. (2004). Speech automatisms and recurringutterances from aphasic Cantonese speakers. Multilingual Communication Disorders,2, 32–42.

Togher, L., McDonald, S., Code, C., & Grant, S. (2004). Training communicationpartners of people with TBI: A randomised controlled trial. Aphasiology, 18,313–335.

Code, C. (2005). First in, last out: The evolution of lexical aphasic speech automatismsto agrammatism and the evolution of language. Interaction Studies, 6 (2), 311–334.

Code, C., Lincoln, M., & Dredge, R. (2005). Asymmetries in mouth opening duringword generation in male stuttering and non-stuttering participants. Laterality, 10(5), 471–486.

Code, C., Müller, N., Tree, J. T., & Ball, M. J. (2006). Syntactic impairments canemerge later: Progressive agrammatic agraphia and syntactic comprehensionimpairment. Aphasiology, 20, 1035–1058.

Code, C., & Wallesch, C-W. (2006). The form of representation of language in thebrain and the influence of John C. Marshall. Aphasiology, 20, 819–822.

Power, E., & Code, C. (2006). Waving not drowning: Utilising gesture in the treatmentof aphasia (Commentary). Advances in Speech-Language Pathology, 8, 115–119.

McCooey-O’Halloran, R., Worrall, L., Code, C., & Hickson, L. (in press). Develop-ment of a measure of communication activity for the acute hospital setting Part II:Item analysis, selection and reliability. Journal of Medical Speech-LanguagePathology.

McCabe, P., Sheard, C., & Code, C. (submitted). Longitudinal communicationimpairment in the AIDS dementia complex (ADC): A case report. Journal ofCommunication Disorders.

McCabe, P., Sheard, C., & Code, C. (submitted). Pragmatic skills in people with HIV/AIDS. Disability and Rehabilitation.

Packman, A., Code, C., & Onslow, M. (submitted). On the cause of stuttering: Inte-grating brain and behavioral research. Journal of Neurolinguistics.

Invited presentations

Code, C. (1990). Modelling lexical speech automatisms. Invited Paper for Symposiumon Repetitive Verbal Behaviour, European Cognitive Neuropsychology Workshop,Bressanone, Italy (January).

Code, C. (1990). The right hemisphere and interhemispheric inhibition in aphasia.Invited Paper for the Third National Aphasiology Symposium, Gdansk University,Poland, October.

Code, C. (October–November 1990). The role of the right hemisphere in the recoveryand treatment of aphasia: A critical appraisal. ‘Lecture tour’ of the USA: Universityof Texas at Dallas; VA Center Dallas; Arizona State University at Tempe; Universityof Northern Arizona; VA Center Martinez, California.

Code, C. (1990). The role of the right hemisphere in the recovery and treatment of

xvi Chris Code’s publications

aphasia: A critical appraisal. Invited Guest Speaker at Annual Congress of theAmerican Speech and Hearing Associated, Seattle (November).

Code, C. (1991). Developments in the Code-Müller protocols: The British studies.Invited Guest Speaker to the Linguistics Society, University of Freiburg, Germany(July).

Code, C. (1991). Problems in predicting clinical recovery from aphasia. Invited paperpresented at the British Aphasiology Society Conference, University of Sheffield(September).

Code, C., & Müller, D. J. (1992). Measuring perceptions to psychosocial adjustment inaphasia. Workshop presented to British Aphasiology Society Meeting, University ofSheffield (June).

Code, C. (1992). Psychosocial and emotional reactions to brain damage. InvitedSeminar, School of Behavioural Studies, Macquarie University, Sydney (August).

Code, C. (1992). Emotional and psychosocial reactions to aphasia. Invited Workshop,Lotte Stewart Hospital, Sydney (September).

Code, C. (1993). Examining perceptions to psychosocial adjustment in aphasia. InvitedSeminar, University of Queensland (May).

Code, C. (1993). Recovery from aphasia. Invited Workshop, University of Queensland(May).

Code, C. (1993). Linguistic aspects of speech automatisms in aphasia. Invited SeminarDepartment of Linguistics, University of Sydney (August).

Code, C. (1993). Speech automatisms in aphasia. Invited Seminar, Speech PathologyDepartment, Prince Alfred’s Hospital Sydney (September).

Code, C. (1993). Psychosocial adjustment and emotional reaction to aphasia. InvitedKeynote Presentation. First Aphasiology Symposium of Australia, Sydney(October).

Code, (1994). The role of the right hemisphere in recovery and treatment of aphasia.Invited Workshop, Flinders University, Adelaide (April).

Code, C. (1994). Emotional and psychosocial reactions to aphasia. Invited Workshop,University of Melbourne (September).

Code, C. (1994). The linguistics of aphasic speech automatisms. Invited KeynotePresentation at the Fourth Annual Symposium of the International ClinicalLinguistics & Phonetics Association, New Orleans (November).

Code, C. (1994). Invited discussant. 1st Australian Symposium on the Neuro-psychology of Asian Language Processing. University of New South Wales, Sydney(December).

Code, C. (1995). Sprache und Gehirn. Invited Workshops. Summer School, Universityof Freiburg, Germany (August).

Code, C. (1995). Aphasic speech automatisms. Invited presentation in the JacquesLordat Laboratory, University of Toulouse (October).

Code, C. (1995). The role of the right hemisphere in recovery and treatment. Invited4 Hour Workshop: German Neuropsychological Society Conference, Würtzburg,Germany (October).

Code, C. (1995). A metamodel of recovery from aphasia. Invited Keynote Paper,German Aphasiology Society Annual Conference, Magdeburg (November).

Code, C. (1997). The lateral shift hypothesis: The role of the right hemisphere in therecovery and treatment of aphasia. Invited Workshop, Annual Conference of theAustralian Society for the Study of Brain Impairment, Brisbane (November).

Code, C. (1997). Speech production from the right hemisphere. Invited Plenary

Chris Code’s publications xvii

Presentation, Annual Conference of the Australian Society for the Study of BrainImpairment, Brisbane (November).

Code, C. (1998). Psychosocial adjustment to aphasia. Invited Workshop to College ofSt Mark and St John, Plymouth.

Code, C. (1998). Psychosocial adjustment to aphasia. Invited Presentation to Universityof Southwestern Louisiana, Lafayette.

Code, C. (1998). Recovery from aphasia. Invited presentation at Louisiana StateUniversity, Baton Rouge.

Code, C. (1998). The role of the right hemisphere in speech production. Invited Seminar,School of Psychology, University of Cardiff.

Code, C. (1999). The neural and cognitive representation of syllables and apraxia ofspeech. Invited Workshop Presentation, Max Planck Institute, University ofNijmegen, Holland.

Code, C. (1999). What’s right about speech? Invited Keynote Presentation, AnnualConference of the German Neuropsychological Society, Köln, Germany.

Code, C. (2000). Self help for aphasia. Invited presentation, Aphasia, a day oftalks, discussions and workshops in memory of Felicity Osborne, July 14, BirkbeckCollege, London.

Code, C. (2000). Calculation and number repetition: PET evidence. Invited Seminar,Cognitive Neuroscience, Birkbeck College, London (July).

Code, C. (2000). Brain plasticity and speech control by the right hemisphere: Convergingevidence from aphasia, brain imaging, split-brain and hemispherectomy. KeynoteAddress to the Spanish Neurological Society Conference, Marbella, Spain,October 28.

Code, C. (2001). Invited discussant for recovery symposium. European CognitiveNeuropsychology Workshop, Bressanone, Italy (January).

Code, C. (2001). Calculation and the brain: PET studies. Invited presentation, ExeterNeuroscience Network (November).

Code, C. (2002). Calculation and the brain: Past and prospective PET studies. Invitedpresentation, University of Bremen.

Code, C. (2002). The psychosocial impact of aphasia. Invited presentation, Departmentof Neuroscience, University of Bremen.

Code, C. (2003). Numbers in the brain. Hanse Institute for Advanced Study, InvitedFellowship Lecture, Delmenhorst, Germany (December).

Code, C., Ball, M., Tree, J., Dawe, K., Kay, J., & Edwards, M. (2003). Progressivecortical anarthria with apraxias. Invited Visiting Professorship Lecture, Universityof Louisiana at Lafayette (March).

Code, C., Tree, J., Dawe, K., Kay, J., Ball, M., & Edwards, M. (2003). Progressivecortical anarthria with apraxias. Invited Presentation, ‘Vocalise to Localise’Symposium, University of Grenoble (January).

Code, C. (2004). The psychosocial impact of aphasia. Invited Keynote PresentationInternational Aphasia Rehabilitation Conference, Milos, Greece (August).

Code, C. (2004). Disordered communicative interaction: Current and future approaches toanalysis and treatment. Invited Discussant, Stirling University Management Centre,Stirling, October 26.

Code, C. (2004). Mechanisms of aphasic speech automatism production. Invited Key-note Presentation, Argentinian Aphasia Symposium, November 21–24, BuenosAires (funded by British Council).

Code, C. (2004). Psychosocial life and aphasia. Invited Keynote Presentation,

xviii Chris Code’s publications

Argentinian Aphasia Symposium, November 21–24, Buenos Aires (funded byBritish Council).

Code, C. (2004). Speech production from the left and right hemispheres followingbrain damage. Invited Keynote Presentation, Argentinian Aphasia Symposium,November 21–24, Buenos Aires (funded by British Council).

Code, C. (2005). The recovery of aphasia. Invited Keynote Presentation, ThirdCongress of Croatian Speech and Language Pathologists, September 28–October 1,Dubrovnik, Croatia.

Code, C. (2005). The evolution of aphasic speech automatisms to agrammatism and theevolution of human language. Invited Presentation, Macquarie University, Sydney,October 31.

Code, C. (2005). Big writing. Invited Presentation, School of Communication Sciencesand Disorders, November 6.

Code, C. (2006). Presenting the past and passing the future of clinical aphasia. InvitedKeynote Presentation, International Aphasia Rehabilitation Conference, Sheffield,(June).

Code, C. (2006). Unfolding the past of aphasia rehabilitation. Invited KeynotePresentation, Nordic Conference on Aphasia: New Knowledge – New Directions,September 14–16, Oslo, Norway.

Code, C. (2007). Invited Keynote Speaker, 7th International Scientific Meeting ofFaculty of Logopedics, Zagreb, Croatia, July 14–16.

Other public output

Unrefereed articles/software

Code, C. (1980). The shifting brain. Therapy, 6.Code, C. (1985). Investigating the efficacy of treatment for aphasia with a simple ABA

single-case design. Bulletin of the College of Speech Therapists, 394, February.Code, C. (1986). Hearing therapy and the training of speech therapists. Hearing

Therapy, 8, October.Code, C., Purser, H., & Rowley, D. (1986). Developing an aphasiology archive. Speech

Therapy in Practice, 2.Code, C., Heer, M., & Schofield, M. (1989). The computerized Boston. Far Communi-

cations Ltd. (Software Program)Code, C. (1990). Secrets of the brain’s right hemisphere. Therapy Weekly, 16, April 26.Code, C. (1990). An expert prognosis. Therapy Weekly, 16, June 7.Code, C. (1990). Aphasia assessment: The computer meets the Boston. Speech Therapy

In Practice.Code, C. (1994). Towards a post-graduate profession. Bulletin of the College of Speech

and Language Therapists, January.Code, C. (1999). Meeting expectations. Speech and Language Therapy and Communica-

tion in Practice.Code, C. (1999). Profiles of ADA self-help groups. Speaking Up, December. London:

ADA.Code, C., & Heron, C. (2001). Aphasia services in the United Kingdom. Therapy

Weekly.

Chris Code’s publications xix

Tabula gratulatoria

Apart from the contributors, the following requested to have their nameslisted as well-wishers.

Evelyn Abberton University College London, EnglandElise Baker University of Sydney, AustraliaSusan Balandin University of Sydney, AustraliaKirrie Ballard University of Sydney, AustraliaMarcelo Berthier Hospital Universario Malaga, SpainMaria Black University College London, EnglandBronagh Blaney University of Ulster, Northern IrelandRichard Body University of Sheffield, EnglandMarian Brady Glasgow Caledonian University, ScotlandJason Brown New York University School of Medicine, USAShelagh Brumfitt University of Sheffield, EnglandSally Byng Connect UKStefano Cappa Clinica Neurologica dell’Università di Brescia,

ItalyShula Chiat City University London, EnglandKevin Chung University of Hong Kong, PR ChinaCarl Coelho University of Connecticut, Storrs, USAFrancesca Cooper University of Wales Institute, Cardiff, WalesPatrick Coppens Plattsburgh State University of New York, USAAlison Crutchley University of Huddersfield, EnglandLucy Dipper City University London, EnglandGerry Docherty University of Newcastle, EnglandPatrick Doyle VA Pittsburgh and University of Pittsburgh, USAJoe Duffy Mayo Clinic, Rochester, MN, USAMartin Edwards University of Birmingham, EnglandPam Enderby University of Sheffield, EnglandPaul Fletcher University College Cork, IrelandElaine Funnell Royal Holloway College London, EnglandJack Gandour Purdue University, USAHilary Gardner University of Sheffield, England

Mike Garman University of Reading, EnglandFiona Gibbon Queen Margaret University College, Edinburgh,

ScotlandJackie Guendouzi University of South Alabama, USAJennifer Gurd Oxford University, EnglandBrooke Hallowell Ohio University, Athens, USALinda Hand University of Sydney, AustraliaJenny Harasty University of New South Wales, AustraliaBill Hardcastle Queen Margaret University College, Edinburgh,

ScotlandDiane Hazlett University of Ulster, Northern IrelandRuth Herbert University of Sheffield, EnglandAnne Hesketh University of Manchester, EnglandNigel Hewlett Queen Margaret University College, Edinburgh,

ScotlandArgye Hillis Johns Hopkins University, Baltimore, USAJohn Hodges University of Cambridge, Addenbrooke’s Hospital,

UKAnthony Hogan University of Sydney, AustraliaJennifer Horner Medical University of South Carolina, Charleston,

USADavid Howard University of Newcastle, EnglandSara Howard University of Sheffield, EnglandWalter Huber University of Aachen, GermanyDebbie James Flinders University, Adelaide, AustraliaJanice Kay University of Exeter, EnglandKevin Kearns MGH Institute of Health Professions, Boston,

USABelinda Kenny University of Sydney, AustraliaThomas Klee University of Newcastle, EnglandAnnu Klippi University of Helsinki, FinlandHerman J. Kolk Nijmegen University, The NetherlandsMatti Laine Åbo Akademi University, FinlandMargaret Leahy Trinity College Dublin, IrelandGuylaine Le Dorze Université de Montréal, CanadaKerrie Lee University of Sydney, AustraliaEeva Leinonen University of Hertfordshire, England; Oulu

University, FinlandCarolyn Letts University of Newcastle, EnglandMichelle Lincoln University of Sydney, AustraliaMarjorie Lorch University College London, EnglandFelice Loverso Casa Colina Centers for Rehabilitation, Pomona,

CA, USAJane Maxim University College London, EnglandLise Menn University of Colorado at Boulder, USA

Tabula gratulatoria xxi

Jane Marshall City University London, EnglandJohn Marshall University of Oxford, EnglandRobert Marshall University of Kentucky, USANadine Martin Temple University, USATricia McCabe University of Sydney, AustraliaSharynne McLeod Charles Sturt University, AustraliaMalcolm McNeill University of Pittsburgh, USAMike McTear University of Ulster, Northern IrelandKate Morton University of Essex, EnglandDave Müller Suffolk University College, EnglandSiân Munro University of Wales Institute Cardiff, WalesPenelope Myers Mayo Clinic, Rochester, MN, USAMarilyn Newhoff San Diego State University, San Diego, USALyndsey Nickels Macquarie University, AustraliaMark Onslow University of Sydney, AustraliaAileen Patterson University of Ulster, Northern IrelandMick Perkins University of Sheffield, EnglandLisa Perkins Jersey Health Authority, Channel Islands, UKBrian Petheram Frenchay Hospital, Bristol, EnglandEmma Power University of Sydney, AustraliaFriedmann Pulvermüller University of Konstanz, GermanyAlison Purcell University of Sydney, AustraliaVicki Reed James Madison University, Virginia, USAKatherine Ross Carl T. Hayden VA Medical Center, Phoenix, and

Arizona State University, Tempe, USADave Rowley De Montfort University, EnglandAvraham Schweiger Academic College of Tel Aviv-Yaffo, IsraelLewis Shapiro San Diego State University, San Diego, USAChristine Sheard University of Sydney, AustraliaMark Tatham University of Essex, EnglandJeremy Tree University of Exeter, EnglandDavid Trembath University of Sydney, AustraliaHeather Van der Lely University College London, EnglandJan Van Doorn Umeå University, Sweden; University of Sydney,

AustraliaBrendan Weekes University of Sussex, EnglandBill Wells University of Sheffield, EnglandKlaus Willmes University of Aachen, GermanyRichard Wise Imperial College, London, EnglandLinda Worrall University of Queensland, AustraliaWolfram Ziegler Städtisches Klinikum München, Germany

xxii Tabula gratulatoria

Contributors

Elizabeth Armstrong Department of Linguistics, Macquarie University,Sydney.

Martin J. Ball Department of Communicative Disorders, University ofLouisiana at Lafayette, USA.

Roelien Bastiaanse Center for Language and Cognition, University ofGroningen, The Netherlands.

Gerhard Blanken Department of Psycholinguistics, University of Erfurt,Germany.

Tobias Bormann Department of Psycholinguistics, University of Erfurt,Germany.

Hugh W. Buckingham Louisiana State University, Baton Rouge, USA.

Maud Champagne-Lavau Faculté de médecine, Université de Montréal andCentre de recherche, Hôpital Sacré-Coeur de Montréal, Canada.

Sarah S. Christman The University of Oklahoma, Health Sciences Center,Oklahoma City, USA.

Jack S. Damico Department of Communicative Disorders, University ofLouisiana at Lafayette, USA.

Pattie Doody Department of Communicative Disorders, University ofLouisiana at Lafayette, USA.

Susan Edwards School of Psychology and Clinical Language Sciences,University of Reading, UK.

Thorsten Fehr Institute for Cognitive Neuroscience and Center for AdvancedImaging (CAI), Bremen University, Germany.

Alison Ferguson Speech Pathology Program, University of Newcastle,Australia.

Manfred Herrmann Institute for Cognitive Neuroscience and Center forAdvanced Imaging (CAI), Bremen University, Germany.

Audrey L. Holland Regents’ Professor Emerita, University of Arizona,Tucson, USA.

Yves Joanette Centre de recherche, Institut universitaire de gériatrie deMontréal and Faculté de médecine, Université de Montréal, Canada.

Karima Kahlaoui Centre de recherche, Institut universitaire de gériatrie deMontréal, Canada.

Richard C. Katz Veterans Affairs Medical Center, Phoenix, Arizona andArizona State University, Tempe, USA.

Alana Kozlowski Department of Communicative Disorders, Universityof Louisiana at Lafayette, and Communication Disorders and DeafEducation, Lamar University, Texas, USA.

Leonard L. LaPointe Regional Rehabilitation Center, Florida StateUniversity, Tallahassee, USA.

Kerry L. Lenius Regional Rehabilitation Center, Florida State University,Tallahassee, USA.

Skye McDonald School of Psychology, University of New South Wales,Sydney, Australia.

Inger Moen Department of Linguistics and Scandinavian Studies,University of Oslo, Norway.

Nicole Müller Department of Communicative Disorders, University ofLouisiana at Lafayette, USA.

Bruce E. Murdoch School of Health and Rehabilitation Sciences, TheUniversity of Queensland, Australia.

Jean-Luc Nespoulous Laboratoire Jacques-Lordat, University of Toulouse-Le Mirail, France.

Maria Pachalska Department of Developmental Psychology and Neuro-linguistics, Institute of Psychology, Marie Curie-Sklodowska University,Lublin, Poland.

Claire Penn School of Human and Community Development, Universityof the Witwatersrand, Johannesburg, South Africa.

Nina N. Simmons-Mackie Department of Communication Sciences andDisorders, Southeastern Louisiana University, Hammond, USA.

Bernadette Ska Centre de recherche, Institut universitaire de gériatrie deMontréal and Faculté de médecine, Université de Montréal, Canada.

xxiv Contributors

Leanne Togher School of Communication Sciences and Disorders,University of Sydney, Australia.

Hanna K. Ulatowska School of Behavioral and Brain Sciences, Universityof Texas, Dallas, USA.

Jacques Virbel Institut de Recherche en Informatique de Toulouse,University Paul Sabatier, Toulouse, France.

Claus-W. Wallesch Department of Neurology, Otto-von-Guericke-University Magdeburg, Germany.

Robert T. Wertz Formerly Veterans’ Administration Medical Center,Nashville, USA.

Contributors xxv

Preface

This book is a collection of the cutting edge work of many leadingresearchers and clinicians exploring topics within clinical aphasiology. How-ever, it is more than this; it is also a tribute to our friend and colleague, ChrisCode. Chris has been a prime mover in many areas of aphasiology over theyears, and we discuss his contribution to the field in some detail in the firstchapter of this book. The remaining contents we have divided into three mainapproaches to the study of aphasia, reflecting Chris’s own interests.

First, we have five contributions that fall under the heading of Conceptualconsiderations. These are mainly interdisciplinary in nature, thus reflectingChris’s expertise and interests that span linguistics, phonetics, psychologyand neurology, as well as social aspects of communication disorders.

The second section of the book deals with Research considerations, withseven chapters ranging from how the study of disrupted communication caninform models of normal language processing, through tone production andprocessing in speakers with aphasia, to anomia and progressive multifocalleukoencephalopathy. Each of these chapters explores different aspects ofresearch methodology, reflecting Chris’s interests in quantitative research(e.g., his work on perceptual psychoacoustics), and qualitative research(e.g., discourse analysis).

The final section of the collection deals with Clinical considerations, andthe seven chapters here cover counselling, computerized training, culturaland linguistic diversity in aphasia, right hemisphere disorders, and communi-cation problems in the dementias. Again, this part of the collection reflectsChris’s long-term interests in the clinical aspects of aphasiology, as well asthe research aspects.

The authorship of the chapters in this volume reflects Chris’s strong inter-national ties. We have contributions from the United Kingdom, the UnitedStates, Australia, Germany, France, Norway, South Africa, The Netherlands,Canada and Poland. The names in the Tabula Gratulatoria reflect an evenwider range of countries. We would like to thank Ben Rutter for compilingthe indexes.

This collection honours Chris’s contribution to the field, and marks his65th birthday. However, this is not to suggest that he is about to give up his

research into neurological disorders – arguably one of the most fascinatingareas within communication disorders. Indeed, we look forward to manymore years of interesting and important work emerging from the depths ofthe Devonshire countryside, with the support of his ‘partner in greatness’Christine.

Martin J. BallJack S. Damico

Lafayette, Louisiana, August 2006

Preface xxvii

1 Chris Code’s contributionto aphasiology

Martin J. Ball and Jack S. Damico

Introduction

Chris Code is one of the foremost scholars in aphasiology today, and hasadvanced the field in many ways. Over a professional career that has spannednearly 30 years, he has authored or co-authored more than 120 publica-tions and has served as a faculty member or research Fellow in eight institu-tions of higher learning in the United Kingdom, Australia, and Europe.Importantly, he was the Founding Editor of Aphasiology: An Internationaland Interdisciplinary Journal in 1987 and he has continued to serve as Editorin Chief of that journal. When looking back over the career of a colleaguelike Chris, there are many achievements that may be highlighted. For example,he has effectively trained scores of students around the world, and he hasemployed his considerable talents as an editor, editorial board memberand reviewer for no less than 16 journals and book series. The measureof Chris Code as a professional, however, must encompass several otherareas as well. First, he has produced an impressive list of research andclinical publications that have influenced several fields, but especially clin-ical aphasiology. His enthusiasm for his work comes through in these pub-lications as he has advanced our understanding of the areas of aphasia,phonetics, the role of the right hemisphere in speech and language, psycho-social adjustments to brain damage, patient rights issues, and traumaticbrain injury. Indeed, a survey of his publications shows contributions in atleast 18 distinct research areas in the human communication sciences anddisorders. Second, he has been an enthusiastic collaborator with a networkof colleagues that spans the United Kingdom, North American, Europe,and Australia. Starting with his earliest collaborations with Müller andBall in the early 1980s until his most recent articles and book projects,Chris Code has worked closely with no fewer than 60 professionals in hisresearch activities. In these collaborations, he has functioned both as acolleague of equal standing and as a mentor for younger colleagues. Finally,Chris Code has had a galvanizing impact on the field of clinical aphasiologyas a savant, a motivator, and an impresario of trends that have resulted inseveral rather significant developments in the discipline. Despite all his other

accomplishments, this last area may be his most important contributionof all.

In this chapter we briefly discuss several areas of achievement that markChris Code’s career. We survey the areas within aphasiology that havebeen his special concern as indicated by his publications, and we discuss hisrather considerable influence as an instigator and/or supporter of variousdevelopments in clinical aphasiology. Regarding his research and clinicalpublications, we approach his work under the following broad headings:psychosocial and emotional reaction to brain damage and communicationimpairment; linguistics and phonetics of aphasia and related disorders; righthemisphere language and speech; and international aspects of aphasiology.The focus on his influence will encompass his role as Editor in Chief ofAphasiology: An International and Interdisciplinary Journal and how he hasemployed this journal to advance the discipline.

Research accomplishments

Psychosocial adjustment to brain damage

Beginning with some of his earliest research, Chris Code has been interestedin documenting and describing the social and emotional changes that oftenaccompany aphasia (Müller & Code, 1983; Müller, Code, & Mugford, 1982)and this focus has been an enduring theme in his published work (e.g., Code,1997a; Code, Hemsley, & Herrmann, 1999; Code & Herrmann, 2003; Code &Müller, 1989, 1995a, 1996). Taking a more expanded view than was commonat the time, Code and colleagues stressed an effective hybrid model of affect-ive issues in aphasia by advocating that emotional issues and experiencemust always be viewed on an individual basis and within social contexts(e.g., Code, 1986, 1997b; Code & Müller, 1995a; Hemsley & Code, 1996;Müller & Code, 1983). In a series of research studies, he and colleagues havebeen able to show how the emotional state can have a significant impacton motivation, physical functioning, and cognitive and linguistic processingand that these changes may significantly impact recovery from aphasia (e.g.,Code, 1997b, 2001; Code & Herrmann, 2003; Code & Müller, 1992; Code,Müller, & Herrmann, 1999; Hemsley & Code, 1996).

Perhaps his most significant achievement regarding psychosocial adjust-ment has been the development and application of the Code-Müller Protocols.These protocols have developed over time (Code & Müller, 1992; Herrmann& Code, 1996; Müller & Code, 1983; Müller, Code, & Mugford, 1982) and areintended to examine perceptions of psychosocial well-being. By employingthese protocols, Code and others have been able to study depression, motiv-ation, and other emotional responses to both the impact of aphasia and howrecovery may proceed (e.g., Code, 1986, 1997b; Code & Herrmann, 2003;Code & Müller, 1989). This work has also helped determine how various levelsof optimism about recovery across the various players in the rehabilitative

2 Ball and Damico

context (i.e., individual with aphasia, significant others linked to these indi-viduals, therapist) may contribute to the complex interaction between per-ception of potential, psychosocial factors, and recovery in aphasia (e.g.,Code, Müller, & Herrmann, 1999; Hemsley & Code, 1996). With additionalapplications of the protocols using a multiple-attribute utility technique toassign weightings that effectively rank individual priorities of psychosocialadjustment (Herrmann & Code, 1996), it has been shown that different indi-viduals perceive very different priorities during recovery and these may havean important impact on expectations and treatment variables (e.g., Hemsley& Code, 1996; Müller, Code, & Mugford, 1982).

In addition to his own work with the Code-Müller Protocols, this pro-cedure has been widely employed in other research and clinical venues (seeCode, Müller, & Herrmann, 1999; Code, Müller, Herrmann, & Hogan, 1999),and has been influential in the movement toward consideration of quality oflife issues (Code, 2003; Code & Müller, 2003; Worrall & Holland, 2003), theLife Participation Approach to Aphasia (Chapey et al., 2001), and varioussocial models of aphasia (Lyon & Shadden, 2001; Shadden, 2005; Simmons-Mackie, 2001).

Linguistic investigations: Speech automatisms

Another of Chris Code’s main interests has been the study of lexical andnonlexical speech automatisms, also known as real-word and non-meaningful recurrent utterances (Chung, Code, & Ball, 2004; Code, 1982a,1982b, 1987, 1989a, 1994a; Code & Ball, 1994). Chris’s work in the 1980sincluded the first important studies of this area since Alajouanine (1956) and,with colleagues, he has assembled a database of both lexical and nonlexicalspeech automatisms in English, German, and Cantonese. However, his workin this area is not restricted to simply “butterfly collecting” (important as itis to acquire ample exemplars of a phenomenon, it is also important toinvestigate it). The main thrust of this analysis has been first, in the areaof linguistic analyses of the speech automatisms he and colleagues havecollected, and second, on the origins of speech automatisms.

One of the first analyses Code conducted on the English data (Code, 1982a)was a phoneme frequency analysis. This was applied to both the real-wordand non-meaningful recurrent utterances with interestingly different results.With the real-word tokens, there was a high correlation between the soundsused and the sounds of normal conversational English. Looked at more closely(in terms of place and manner of articulation, and voicing) some differencesemerged. These were in respect of manner of articulation with plosives occur-ring more often in the real-word recurrent utterances than in normal speech(up from 29% to 40%; Code, 1982a, 1989a). Explanations for these findingsmay be found in terms of sonority theory and we return to this below.

Significantly fewer English sounds occurred in the non-meaningful recur-rent utterances collected from the English subjects as compared to the

Chris Code’s contribution to aphasiology 3

real-word examples (21 of 44 phonemes as opposed to 40 from 44). There wasalso a greater consonant to vowel ratio (47% to 53% compared to normalEnglish 62.5% to 37.5%, and in the real-word recurrent utterances 56% to46%). A place, manner, and voicing analysis again showed that the mannercategory was the one that deviated most from normal speech, with plosivesaccounting for 62% of the consonants.

In a later study (Code & Ball, 1994, 1995), the authors looked for explan-ations for the phonotactic patterns and inventory constraints in both theEnglish non-meaningful recurrent utterances, and German data collectedby Blanken, Wallesch, and Papagno (1990). The high proportion of plosivespartly reflects motorically easier sounds to produce; but also fits into therequirements of the perceptually driven sonority sequencing principle (SSP;Ball, Müller, & Rutter, forthcoming), where (in syllable initial position atleast) plosive–vowel sequences are preferred. Interestingly, the SSP alsopredicts that in syllable final position (where a coda consonant occurs) theconsonant will be ranked higher on the sonority hierarchy than are plosives.In the data reported in Code and Ball (1994) we do indeed find in finalposition a preference for fricatives and nasals over plosives, although opensyllables were the dominant pattern (as predicted by universals of syllablestructure). The authors use these results to speculate on the nature of sonor-ity, and whether it is a hard-wired feature of phonological processing orsimply an artefact of the speech production process.

Code (1982a) also undertook a linguistic analysis of the real-word recur-rent utterances. As an initial step he examined frequency of occurrence ofthe words used in the English data. He determined that the majority of theseparate words used (proper names and expletives were excluded as not beingrepresented in the normative data) were in the common category: 86% werewords occurring 50 times per million or more in normal conversationalEnglish. Code then presents a syntactic analysis of the data. The majority ofthe real-word recurrent utterances were of the form pronoun + verb (oftenI + modal, e.g., I want to, I can’t, I can try). Expletives were the next mostcommon form, followed by proper names, yes/no, and numbers. Repeatedforms were also common, and a range of other syntactic patterns were seen.Chung, Code, and Ball (2004) extended the analysis to Cantonese speechautomatisms (both real-word and non-meaningful). Results showed verysimilar patterns to those found with the English and German examples.

As we noted earlier, Chris Code is also interested in the origin of speechautomatisms, and Code (1982b) addresses this area. Various attempts toaccount for real-word forms have been proposed: for example, that the utter-ance is one the patient intended to produce at the very moment of the stroke,or that it was the last utterance actually produced before the stroke occurred.Alajouanine (1956) felt these two approaches could be combined into thenotion that the utterance is the last thought being organized into an utterancebefore the stroke. However, Code argues convincingly that the origin of real-word speech automatisms has more to do with post-onset factors than with

4 Ball and Damico

pre-onset ones. For example, the use of family names, frustration expressedthrough expletives and pronoun + verb forms can all be accounted for asbeing the patient’s first attempted utterances on regaining consciousness aftera stroke. Code points out that the non-word examples are clearly not prop-ositional speech, but even the real-word ones cannot be so described, as theyare invariant and so stereotypical. He notes the view that there is right-hemisphere involvement in the production of non-propositional speech, andconcludes “that the right hemisphere is subserving the initial and continuingproduction of RUs [recurrent utterances], perhaps to different degrees in thetwo linguistically distinct types” (Code, 1982b, p. 163).

Phonetic investigations

Chris Code has been especially interested in the application of instrumentalphonetic techniques to the study of a variety of speech disorders, and hissurvey of psychoacoustic techniques with stuttering and aphasia can befound in his 1984a, 1984b, and 1997a work. In this section, however, weconcentrate on two areas of his research: apraxia of speech and progressivespeech deterioration.

Apraxia of speech

Chris Code’s interest in apraxia of speech was sparked by an early study withMartin Ball (Code & Ball, 1982; see also Code & Ball, 1988). In this study, thesubject investigated was able to use voicing appropriately in English sonorantsounds (where contrastive voicing does not play a part), but produced targetvoiced obstruents mainly without vocal fold vibration. Interestingly, however,the subject was able to distinguish final fortis and lenis obstruents throughmaintaining the pre-consonantal vowel length difference found in English;indeed, she compensated for the loss of voicing by enhancing the vowellength differences considerably. These findings led to a consideration of howtraditional binary divisions of speech (phonetics versus phonology) mightaccount for the apraxia of speech, and discussion of alternative models.

Chris Code returned to apraxia of speech in a major review (Code, 1998).In this paper, Code examines a range of multilevel accounts of speech pro-duction and discusses where in these models aphasia, apraxia of speech, anddysarthria might fit. Code concludes that as apraxia of speech is a disorderthat has both phonetic and phonological implications, work in this area “hascontributed significantly to the rethinking of the relationship between phon-ology and phonetics . . . and highlighted the need for a phonetically derivedphonology” (Code, 1998, p. 62). This last point is seen in recent models thatposit some kind of phonetic planning component between the phonologicalorganization, and the articulatory implementation levels. It also chimeswell with recent approaches to theoretical phonology (such as Govern-ment Phonology, Gestural Phonology, and Usage-based Phonology: see


Ball et al., forthcoming) that emphasize phonetic and cognitive aspects ofspeech organization.

Progressive speech deterioration

Recently Chris Code has undertaken investigations of a rare case of pro-gressive speech deterioration (Ball, Code, Tree, Dawe, & Kay, 2004; Code,Müller, Tree, & Ball, 2006). The authors present a range of instrumentalanalyses of the segmental and suprasegmental characteristics of the client,and it is interesting to note that whereas some of these showed simplifications(e.g., epenthetic vowels in consonant clusters), others showed complicatingchanges (such as adding /l/ after /u/ in open syllables, and /p/ or /b/ to /r/initial words). A variety of phonological accounts were discussed that couldthrow light on the client’s speech patterns and their progressive deteriorationover time.

The authors conclude that the client’s speech patterns show that his rela-tively rare progressive speech degeneration “can be captured in terms of acognitive model of representation, together with a gestural formalism thatcan show the loss of integration between the various motor systems of speech(and on occasion, total deletion of a gesture)” (Ball et al., 2004, p. 460). Theeventual complete loss of intelligibility of the client some months after thedata reported were collected shows that the gestural uncoupling and deletionhad continued to devastating effect. The important aspect of this study wasthat Code and his colleagues demonstrated that unusual cases such as the onereported here are amenable to investigation through phonetic description andphonological analysis, and that such studies may throw light on both the caseand on theory building itself.

The role of the right hemisphere

As a result of his commitment to aphasia rehabilitation, Dr Code also hasa longstanding interest in the contribution of the right hemisphere of thebrain to language and speech processing. There are two likely reasons for thisinterest. First, as a trained neuropsychologist, Chris Code has not limited histheorizing or his research to the left hemisphere when discussing speech andlanguage processing. His academic and clinical training enabled him to con-sider the rather substantial contributions that the right hemisphere has tovarious types of perceptual and cognitive processing and how it may alsoimpact other meaning-making systems (Code, 1989b, 1996, 1997c). Second,because of his belief in the rehabilitative process and the need for defensiblemodels, principles, and approaches to effective rehabilitation (e.g., Code,1994b, 1999, 2000, 2001; Code & Brown, 1987; Code & Müller, 1989, 1995b,1995c), he and his colleagues have considered various viable rehabilitationmodels. In his 1987 text, Language, aphasia, and the right hemisphere, Dr Codeeffectively discusses the arguments and the data for a fair consideration of

6 Ball and Damico

the role of the right hemisphere in speech and language processing and inaphasia rehabilitation. For example, he presents detailed data from variousdisciplines that substantiate the role of the right hemisphere in cognitiveprocessing, in some aspects of linguistic comprehension, in the more auto-matic, non-propositional aspects of speech production, and in some of theextra-linguistic aspects of communication. This text provided timely sum-maries of the research and served as an effective review on the right hemi-sphere for a generation of students and professionals in speech-languagepathology.

This 1987 text also dealt extensively with the “lateral shift hypothesis” as itrelates to recovery from aphasia. Taking its simplest variant (“following leftbrain damage there is a shift to the undamaged right hemisphere for languageprocessing”, p. 110) and several other formulations, Chris discussed severalways that this hypothesis may be applied as a potential recovery mechanismfor aphasia and how it relates to other mechanisms of recovery. He thenpresented a wide range of data from lesion case studies, cerebral bloodflow studies, experiments using sodium amytal, electroencephalography, anddichotic listening, and evidence from behavioural studies to assess the evi-dence for the lateral shift hypothesis. While there was some indication that theright hemisphere does play a role in recovery from aphasia, his findings didnot strongly support this hypothesis. Instead, he found that the impact of theright hemisphere on recovery from aphasia was not uniformly demonstrated.While there appeared to be some variation depending on the individual withaphasia, the severity of aphasia, and time post-onset, the right hemispheredoes not appear to be a fully equivalent backup system to the left hemisphere,and its impact does not produce effective change in either the quality orquantity of recovery of function. While some aphasic syndromes may bemore involved with right hemisphere functioning than previously believed,“right hemisphere involvement in language processing following left hemi-sphere damage is probably dependent upon a complex interplay of a range ofvariables” (1987, p. 148).

Since the publication of his 1987 book, Code has continued to contributeto the data regarding right hemisphere processing of speech and language.While still uncertain about the contribution of the right hemisphere to lan-guage rehabilitation (Code, 1994b; Code & Joanette, 2003), he has presenteddata suggesting that some preserved utterances (formulaic expressions) notedin severely impaired individuals with aphasia may be processed in the righthemisphere (Code, 1996, 1997c) and that the right hemisphere does play arole in the creation and functioning of some discourse elements (Code, 1996)and in other forms of symbolic processing in individuals with aphasia(Cowell, Egan, Code, Harasty, & Watson, 2000). As he continues to inves-tigate hypotheses regarding language processing and aphasia (e.g., Code,1997d, 1999, 2001; Code & Joanette, 2003; Harasty, Halliday, Kril, & Code,1999; Nespoulous, Code, Virbel, & LeCours, 1998), it is expected that thisright hemisphere focus will continue.


International issues

As a professional who has worked at universities across the world, Chris Codehas also emphasized an international perspective in his work and collabor-ations. This is evident in his focus on service delivery and research acrosslinguistically diverse populations (e.g., Chung, Code, & Ball, 2004; Roger,Code, & Sheard, 2000) and his work compiling classic cases in neuro-psychology across a number of languages and cultures (Code, Wallesch,Lecours, & Joanette, 1996, 2003). He has also collaborated with variouscolleagues across the world to compare knowledge of aphasia in the publicdomain (Simmons-Mackie, Code, Armstrong, Steigler, & Elman, 2002), andto investigate and compare aphasia management practices across nationalboundaries (Katz et al., 2000). In each of these studies there has been anopportunity to demonstrate that although there are some differences regard-ing institutional and cultural variables, there is also a foundational similarityamong those professionals who work in clinical aphasiology throughout theworld. To some extent these studies are beneficial in that they emphasize thesimilarities rather than the differences in our discipline despite ethnocentricbeliefs and practices.

Influence as accomplishment

In this initial chapter we have attempted to provide a sampling of the manyresearch contributions that Chris Code has made over his 30 years to thearea of clinical aphasiology. We have cited studies and provided numbers asobjective evidence of his achievements. However, his impressive publicationrecord represents only a fraction of his accomplishment in the field. For evenif Chris Code had not published extensively himself, his influence would stillbe profound.

Influence is an interesting phenomenon. One cannot always anticipatehow much influence an individual might have in any given field. Often, thosewith large numbers of publications or other quantifiable indices may havelittle or no impact on a given field, while an individual with one powerfulidea or a galvanizing personality may act as a catalyst for significant change.That is because influence is not so much an indication of one’s productivitybut, rather, a measure of one’s impact on others. When viewed from thisperspective, Chris Code has had an exceptional career. When he proposedand then served as the instigator and prime motivator for the journalAphasiology: An International and Interdisciplinary Journal, he provided thefirst real opportunity to create an international forum for clinical aphasiologyand this forum may be his most enduring accomplishment.

In the mid-1980s there were venues for the publication of papers in aphasiaand the powerful clinical forum created by Bruce Porch, Clinical AphasiologyConference, was already in its 15th year. However, the published articles inclinical aphasiology were spread across numerous journals and were often

8 Ball and Damico

hard to locate and the Proceedings of the Clinical Aphasiology Conferencewere privately published with a limited circulation. Within this context,Chris Code saw an opportunity to establish a journal specifically directedtoward aphasiology and its treatment. Importantly, he did not squanderthis opportunity. Rather, he tirelessly worked and networked, travelled andcorresponded, encouraged and cajoled professionals in the field – both estab-lished researchers and neophytes – to extend their ideas, marshal their data,and prepare manuscripts for his journal. Due to his efforts, Aphasiology:An International and Interdisciplinary Journal has developed from a twice-yearly publication to a monthly publication, and is currently recognized asthe leading journal in the field of clinical aphasiology. Over its 20 yearsof publication, Aphasiology has published 184 issues containing more than1050 papers and articles. In a recent keynote at the International AphasiaRehabilitation Conference in Sheffield England, Code provided some inter-esting data on the content of Aphasiology over its 19 year history (Code,2006). According to his figures, the journal has published 821 articles thatwere of direct clinical relevance and 270 of those were reports of treatmentstudies. These figures do indicate that Aphasiology is the primary venue foraphasia research – especially as it relates to clinical issues. Indeed, even theannual Proceedings of the Clinical Aphasiology Conference is now publishedin this journal. Impressive as the journal as been in capturing the majority ofclinical research in aphasia and in providing a powerful centralized venue forthe discipline, it was the way Chris Code has used the journal that has beenmost influential.

With an eye toward a more international perspective, he has used his pos-ition as Editor in Chief to encourage more interaction and communicationbetween professionals around the world. He has sought out and encouragedclinical aphasiologists on six continents to publish in the journal, and throughthe invited Forums section that highlights particular themes discussed byinvited participants, he has fostered collaborative interactions across thesedifferent countries and across related professional disciplines. This has resultedin greater awareness of the researchers and the theoretical, research, and clini-cal issues that are of particular concern in various locales. Due to his effortsin Aphasiology and the progressive development of Internet technologies,clinical aphasiology is truly a shared international discipline.

Perhaps Chris Code’s greatest accomplishment as Editor in Chief, however,relates to his encouragement and support of various topics, themes, or typesof research. Using the Forum format, he has encouraged important research,discussion, and advocacy regarding a number of important clinically relatedareas. Service delivery issues in aphasia, psychosocial and social issues likesense of self after aphasia, quality of life issues, family therapy, and a focus ontypes of therapies are areas that Dr Code has effectively influenced throughthe journal. Additionally, Aphasiology has been the journal most supportiveof qualitative research studies. Through his encouragement and care whenadvocating for this non-experimental research paradigm, Aphasiology is the


leading journal in the human communication sciences in disorders regardingthis powerful research tradition. Consequently, the discipline is richer andhas greater understanding of the complexity of language, aphasia, and socialaction as a result. When Dr Code’s influence on the discipline of aphasia ismeasured with Aphasiology as one of his instruments of support, advocacy,and change, Chris Code is accomplished indeed.

In his book Crowds and Power (1984), the author Elias Canetti discussedthe importance of social, political, and intellectual movements and how theywere created. He stated that for such movements to occur, there is the needto have effective “crowd crystals”. That is, individuals or small groups ofindividuals that serve as a seed crystal does in chemistry, to precipitatecrowds into action and belief. When looking over Chris Code’s research car-eer and his great influence on the field of clinical aphasiology through hisencouragement and advocacy as the Editor in Chief of Aphasiology, wemust see him as a “crowd crystal”, a precipitator of the highest order. It is forhis efforts and his extensive accomplishments that we dedicate this volumeto him.

References

Alajouanine, T. (1956). Verbal realization in aphasia. Brain, 79, 1–28.Ball, M. J., Code, C., Tree, J., Dawe, K., & Kay, J. (2004). Phonetic and phonological

analysis of progressive speech degeneration: A case study. Clinical Linguistics andPhonetics, 18, 447–462.

Ball, M. J., Müller, N., & Rutter, B. (forthcoming). Phonology for communicationdisorders. Mahwah, NJ: Lawrence Erlbaum Associates, Inc.

Blanken, G., Wallesch, C. W., & Papagno, C. (1990). Dissociations of languagefunctions in aphasics with speech automatisms (recurring utterances). Cortex, 26,41–63.

Canetti, E. (1984). Crowds and power. New York: Farrar, Straus & Giroux.Chapey, R., Duchan, J., Elman, R., Garcia, L., Kagan, A., Lyon, J., et al. (1994).

Life participation approach to aphasia: A statement of values for the future. InR. Chapey (Ed.), Language intervention strategies in aphasia and related neurogeniccommunication disorders (4th ed., pp. 235–246). Philadelphia: Lippincott, Williams& Wilkins.

Chung, K., Code, C., & Ball, M. J. (2004). Speech automatisms and recurring utter-ances from aphasic Cantonese speakers. Journal of Multilingual CommunicationDisorders, 2, 32–42.

Code, C. (1982a). Neurolinguistic analysis of recurrent utterances in aphasia. Cortex,18, 141–152.

Code, C. (1982b). On the origins of recurrent utterances in aphasia. Cortex, 18,161–164.

Code, C. (1984a). Delayed auditory feedback. In C. Code & M. J. Ball (Eds.),Experimental clinical phonetics. London: Croom Helm.

Code, C. (1984b). Dichotic listening. In C. Code & M. J. Ball (Eds.), Experimentalclinical phonetics. London: Croom Helm.

Code, C. (1986). Catastrophic reaction and anosognosia in anterior–posterior and

10 Ball and Damico

left–right models of the cerebral control of emotion. Psychological Research, 48,53–55.

Code, C. (1987). Language, aphasia and the right hemisphere. Chichester, UK: JohnWiley.

Code, C. (1989a). The characteristics of aphasia. Hove, UK: Lawrence ErlbaumAssociates Ltd.

Code, C. (1989b). Speech automatisms and recurring utterances. In C. Code (Ed.), Thecharacteristics of aphasia. Hove, UK: Lawrence Erlbaum Associates Ltd. (Previouslypublished by Taylor & Francis, London.)

Code, C. (1994a). Speech automatism production in aphasia. Journal of Neuro-linguistics, 8, 135–148.

Code, C. (1994b). The role of the right hemisphere in the treatment of aphasia. InR. Chapey (Ed.), Language intervention strategies in adult aphasia. Baltimore, MD:Williams & Wilkins.

Code, C. (1996). Speech from the isolated right hemisphere? Left hemispherectomycases E.C. and N.F. In C. Code, C.-W. Wallesch, Y. Joanette, & A.-R. Lecours (Eds.),Classic cases in neuropsychology. Hove, UK: Lawrence Erlbaum Associates Ltd.

Code, C. (1997a). Experimental audioperceptual techniques. In M. J. Ball & C. Code(Eds.), Instrumental clinical phonetics (pp. 228–261). London: Whurr.

Code, C. (1997b). Aphasia recovery, therapy and psychosocial adjustment. In A. Baum,C. McManus, S. Newman, J. Weinman, & R. West (Eds.), The Cambridgehandbook of psychology, health & medicine. Cambridge, UK: Cambridge UniversityPress.

Code, C. (1997c). Can the right hemisphere speak? Brain and Language, 57, 38–59.Code, C. (1997d). A metamodel for recovery from aphasia. In J. Ponsford, P. Snow, &

V. Anderson (Eds.), International perspectives in traumatic brain injury. Melbourne:Australian Academic Press.

Code, C. (1998). Models, theories and heuristics in apraxia of speech. ClinicalLinguistics and Phonetics, 12, 47–66.

Code, C. (1999). Re-assembling the brain: Are cell assemblies the brain’s language forrecovery of function? (Commentary) Behavioural and Brain Sciences, 22, 282.

Code, C. (2000). Converging not fractionating. Brain and Language: Millennium Issue,71, 44–45.

Code, C. (2001). Multifactorial processes in recovery from aphasia: Developing thefoundations for a multilevelled framework. Brain and Language, 77, 25–44.

Code, C. (2003). The quantity of life for people with chronic aphasia. Neuro-psychological Rehabilitation, 13, 365–378.

Code, C. (2006). Back to the future: A recent history of aphasia rehabilitation. Akeynote speech at the 12th International Aphasia Rehabilitation Conference, Shef-field, UK, June.

Code, C., & Ball, M. J. (1982). Fricative production in Broca’s aphasia: A spectrographicanalysis. Journal of Phonetics, 10, 325–331.

Code, C., & Ball, M. J. (1988). Apraxia of speech: The case for a cognitive phonetics.In M. J. Ball (Ed.), Theoretical linguistics and disordered language (pp. 152–167).London: Croom Helm.

Code, C., & Ball, M. J. (1994). Syllabification in aphasic recurring utterances:Contributions of sonority theory. Journal of Neurolinguistics, 8, 257–265.

Code, C., & Ball, M. J. (1995). The status of sonority theory: Evidence from syl-labification in aphasic recurring utterances. In K. Elenius & P. Branderud (Eds.),


Proceedings ICPhS 95 Stockholm (Vol. 4, pp. 480–483). Stockholm: KTH &Stockholm University.

Code, C., & Brown, J. W. (1987). Aphasia from the wrong (right) hemisphere: Questionsfor crossed aphasia. Aphasiology, 1, 401–402.

Code, C., Hemsley, G., & Herrmann, M. (1999). Emotional reactions to aphasia.Seminars in Speech and Language, 20, 19–31.


Code, C., & Joanette, Y. (2003). Neural plasticity in the control of language in theadult brain: The role of the separated right hemispheres in cases PS, VP and JW.In C. Code, C.-W. Wallesch, Y. Joanette, & A.-R. Lecours (Eds.), Classic cases inneuropsychology: Volume II. Hove, UK: Lawrence Erlbaum Associates Ltd.

Code, C., & Müller, D. (Eds.) (1989). Aphasia therapy (2nd ed.). London: Cole &Whurr.

Code, C., & Müller, D. J. (1992). The Code-Müller protocols: Assessing perceptions ofpsychosocial adjustment to brain damage. Kibworth: Far Communications.

Code, C., & Müller, D. (1995a). Psychosocial perspectives. In C. Code & D. J. Müller(Eds.), The treatment of aphasia: From theory to practice. London: Whurr.

Code, C., & Müller, D. (1995b). Cognitive and neuropsychological approaches. InC. Code & D. J. Müller (Eds.), The treatment of aphasia: From theory to practice.London: Whurr.

Code, C., & Müller, D. (1995c). Efficacy and effectiveness. In C. Code & D. J. Muller(Eds.), The treatment of aphasia: From theory to practice. London: Whurr.

Code, C., & Müller, D. (1996). Psychosocial issues. In C. Code & D. J. Müller (Eds.),Forums in clinical aphasiology. London: Whurr.

Code, C., & Müller, D. (2003). Psychosocial and quality of life issues in treatment.In R. Kent (Ed.), The MIT encyclopaedia of communication disorders. Cambridge,MA: MIT Press.

Code, C., Müller, D. J., & Herrmann, M. (1999). Perceptions of psychosocial adjust-ment to aphasia: Studies with the CMP. Seminars in Speech and Language, 20, 51–63.

Code, C., Müller, D., Herrmann, M., & Hogan, A. (1999). Perceptions of psychosocialadjustment to acquired commnication disorders: Studies with the Code-Müllerprotocols. International Journal of Communication Disorders, 34, 193–207.

Code, C., Müller, N., Tree, J. T., & Ball, M. J. (2006). Syntactic impairments canemerge later: Progressive agrammatic agraphia and syntactic comprehensionimpairment. Aphasiology, 20, 1035–1058.

Code, C., Wallesch, C.-W., Lecours, A.-R., & Joanette, Y. (Eds.) (1996). Classic cases inneuropsychology. Hove, UK: Lawrence Erlbaum Associates Ltd.

Code, C., Wallesch, C.-W., Lecours, A.-R., & Joanette, Y. (Eds.) (2003). Classic cases inneuropsychology: Volume II. Hove, UK: Lawrence Erlbaum Associates Ltd.

Cowell, S. F., Egan, G. F., Code, C., Harasty, J., & Watson, J. D. G. (2000). The func-tional neuroanatomy of simple calculation and number repetition: A parametricPET activation study. NeuroImage, 12, 565–573.

Harasty, J., Halliday, G. M., Kril, J. J., & Code, C. (1999). Specific temporoparietalgyral atrophy reflects the pattern of language dissolution in Alzheimer’s disease.Brain, 122, 675–686.

Hemsley, G., & Code, C. (1996). Interactions between recovery in aphasia, emotionaland psychosocial factors in subjects with aphasia, their significant others andspeech pathologists. Disability and Rehabilitation, 18, 567–584.

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Herrmann, M., & Code, C. (1996). Weighting of items on the Code-Müller protocols:The effects of clinical experience of aphasia therapy. Disability and Rehabilitation,18, 509–514.

Katz, R., Hallowell, B., Code, C., Armstrong, E., Roberts, P. M., Pound, C., et al.(2000). A multi-national comparison of aphasia management practices. Inter-national Journal of Language and Communication Disorders, 35, 303–314.

Lyon, J. G., & Shadden, B. (2001). Treating life consequences of aphasia’s chronicity.In R. Chapey (Ed.), Language intervention strategies in aphasia and related neuro-genic communication disorders (4th ed., pp. 297–314). Baltimore, MD: Williams &Wilkins.

Müller, D., & Code, C. (1983). Interpersonal perceptions of psychosocial adjustmentin aphasia. In C. Code & D. Müller (Eds.), Aphasia therapy. London: EdwardArnold.


Nespoulous, J.-L., Code, C., Virbel, J., & Lecours, A.-R. (1998). Hypotheses on thedissociation between “referential” and “modalizing” verbal behaviour in aphasia.Applied Psycholinguistics, 19, 311–331.

Roger, P., Code, C., & Sheard, C. (2000). Assessment and management of aphasia in alinguistically diverse society. Asia-Pacific Journal of Speech and Language, 5, 21–34.

Shadden, B. B. (2005). Aphasia as identity theft: Theory and practice. Aphasiology,19, 211–223.

Simmons-Mackie, N. (2001). Social approaches to aphasia intervention. In R. Chapey(Ed.), Language intervention strategies in aphasia and related neurogenic communica-tion disorders (4th ed., pp. 246–268). Baltimore, MD: Williams & Wilkins.


Worrall, L. E., & Holland, A. (2003). Editorial: Quality of life in aphasia. Aphasiology,17, 329–332.


Part I

Conceptual considerations

2 Investigations in speechand language andrelated disordersCrossing the boundaries betweendisciplines—a tribute to Chris Code

Manfred Herrmann and Thorsten Fehr

Introduction

Our research in speech and language started in the early 1980s and focusedprimarily on topics in the field of aphasia rehabilitation. Nonverbal com-munication as a compensatory means of communication in severe aphasia,psychosocial alterations following aphasia and psychosocial adjustment toaphasia, the neuronal basis of depressive disorders in aphasic patients, andthe investigation of specific goals of aphasia rehabilitation are just some ofthe topics that were originally influenced by Chris Code. Chris not only initi-ated part of our research but he also participated in several investigations.Even when we expanded the scope of our investigations into basic research(such as molecular neurobiology or the spatiotemporal analysis of neuronalcorrelates of number processing) Chris was with us – not only in a theoreticalsense but also in person (i.e., spending sabbaticals in our labs or as a scientificfellow invited by the Hanse Institute for Advanced Studies). In this chapter,we try to delineate part of this cooperation between Chris and ourselves,which up to now has not only survived more than two decades but alsobridged research on different continents.

Sydney University, 1997

Nonverbal communication in severe nonfluent aphasia

About 25 years ago, our research group, formerly located at FreiburgUniversity, started investigations in the field of aphasia and related disorders.Our first studies focused on the issue of communication and communicationstrategies in people with severe and chronic aphasia. We tried to analyzenonverbal communication as a compensatory behavioral strategy in severelynonfluent aphasia. Based on videotaped conversation sequences we investi-gated the use of nonverbal communication between aphasic patients and theircommunication partners. The data derived from that study show that aphasicpatients used nonverbal channels of communication significantly more often,and for a significantly longer period of time, than their healthy partners.We concluded that severe aphasic patients use nonverbal communicationstrategies in natural conversation settings as a means of compensation forverbal deficits, and that these spontaneously used communication strategiesshould extend the scope of speech therapy towards communication therapy(Herrmann, Reichle, Lucius-Hoene, Wallesch, & Johannsen-Horbach,1988). In a follow-up study with 20 chronically nonfluent aphasic patientswith moderate or severe language deficits we could demonstrate that com-municative and neurolinguistic deficits did not correlate and that non- andparalinguistic communication accounted for the communicative efficiencyin nonfluent aphasia (Herrmann, Koch, Johannsen-Horbach, & Wallesch,1989).

These preliminary data also gave a first indication of communicative effi-ciency in nonfluent aphasia being strongly affected by both the psychosocialstatus of the patient and his family and emotional disorders resulting fromstroke. At that time (the early 1980s), there were only few aphasia therapistsand speech pathologists who were engaged in investigating psychosocialchanges and emotional disorders following stroke and aphasia. We, by chance,became acquainted with a young lecturer from the Leicester Polytechnic,UK, who presented a research instrument and some data on expectationsconcerning psychosocial adaptation in chronic aphasia. Chris Code was oneof the authors of the Code-Müller Scale of Psychosocial Adjustment (SPA;Müller, Code, & Mugford, 1983; Müller & Code, 1983) nowadays known asthe Code-Müller Protocols (CMP; Code & Müller, 1992). Since then, we haveestablished a long-lasting friendship and fruitful scientific cooperation bridg-ing continents and covering a variety of research topics in the field of speechand language and related disorders.

Psychosocial alterations following aphasia

In 1985 we started with a number of studies investigating psychosocialchanges resulting from communicative impairment in chronic aphasic patientsand their relatives. We found that aphasic patients and relatives suffer from aconsiderable amount of professional, social, familial, and psychological stress

18 Herrmann and Fehr

(Herrmann, Bartels, & Wallesch, 1993a; Herrmann, Johannsen-Horbach, &Wallesch, 1992; Herrmann & Wallesch, 1989; Johannsen-Horbach, Wenz,Fünfgeld, Herrmann, & Wallesch, 1993), which in turn seems to be a limitingfactor in patients’ rehabilitation (Herrmann, 1997; Herrmann, Johannsen-Horbach, & Wallesch, 1993b). In a longitudinal study with 58 stroke patientsand their relatives we were able to demonstrate that aphasic patients and rela-tives experience significantly more severe professional and social changes thansubjects without aphasia and their families. Aphasia itself, however, seems tohave no substantial effect on adaptive or maladaptive coping strategies oractivities of daily living (Herrmann, Bartels, Britz, & Wallesch, 1995b). In asmall pilot study we investigated ten chronically aphasic patients and theirrelatives with respect to the emotional experience of psychosocial changes andthe individually perceived stresses and burdens posed by different stroke symp-toms (Wenz & Herrmann, 1990). The most striking result from that study wasthat the respective speech therapists expected the patients to be most severelystressed by speech and language disorders, while the patients’ relatives thoughtthat both aphasia and hemiparesis contribute equally to the patient’s stresses.The patients themselves, however, reported to be most severely affected bymotor symptoms (see Figure 2.1).

Based on these findings we decided to dedicate part of our research oninterpersonal perceptions of psychosocial adjustment to aphasia.

Figure 2.1 Stresses and burdens in chronic aphasic patients as perceived by thepatients, their respective relatives and speech therapists (modified fromWenz & Herrmann, 1990).

Investigations in speech and language and related disorders 19

Psychosocial adjustment to aphasia: Applications of theCode-Müller protocols (CMP)

The CMP (formerly known as the Scale of Psychosocial Adjustment, SPA)were introduced by Chris Code and colleagues in 1983 (Code & Müller, 1992;Müller & Code, 1983; Müller et al., 1983) and originally aimed to compareperceptions of psychosocial adjustment to aphasia from the separate perspec-tives of patients, relatives, and speech therapists. The CMP consisted of tenitems on psychosocial expectations derived from an expert rating, whichcovered the following topics: (1) the ability to work, (2) receiving speechtherapy, (3) independence of others, (4) meeting friends socially, (5) copingwith depression, (6) following interests and hobbies, (7) speaking to strangers,(8) coping with frustration, (9) making new personal relationships, and (10)coping with embarrassment. In a first study (Herrmann & Wallesch, 1989),we found that aphasic patients and relatives significantly overestimatedthe patient’s ability to cope with psychosocial stresses when compared to theassessment of their respective speech therapists. This study replicated theoriginal findings by Chris Code and colleagues, and the findings of our firststudy were also corroborated by a series of future studies. In our view, thesedata showed that a considerable number of patients and relatives expected –even after years of limited progress – that the premorbid status might eventu-ally be restored. This “unhealthy attitude” (Helmick, Watamori, & Palmer,1976), on the other hand, could lead to significant emotional and psycho-social crises on the part of the relatives and of the patients.

Apart from the above described use of the CMP as an instrument thattargeted the expectations of psychosocial adjustment to aphasia, we alsointroduced the CMP items as a scale reflecting particular objectives of aphasiarehabilitation (Herrmann & Wallesch, 1990). By means of the multi-attributeutility technique (MAUT; Edwards & Newman, 1982), we investigatedthe therapeutic staff of a Neurological Rehabilitation Center (occupationaltherapists, physiotherapists, neuropsychologists, neurologists, and speechtherapists) with respect to the relative importance of CMP items / topics asspecific goals of aphasia rehabilitation. The data of this study indicated thatthe specific demands of different therapeutic methods and approaches clearlyinfluence the appraisal of abilities for psychosocial adaptation and aphasiarehabilitation.

In 1995, when Chris came over from Sydney to Germany to spend part ofhis sabbatical in our lab at Freiburg University, we conducted a bigger studywith 122 professionals engaged in aphasia therapy (Herrmann & Code, 1996).These aphasia therapists participated in a summer academy on “Languageand Brain” that was held at Freiburg University and was organizedby Gerhard Blanken. The participants were asked to rank and weight therelevance of the items of the CMP for assessing the expectations of psycho-social adjustment to aphasia as a general target of aphasia rehabilitation. Thedata show two major results: (1) for professionals working in aphasia


rehabilitation independence from others and emotional adaptation emerge asthe most important domains on the CMP (see Figure 2.2), and (2), the rele-vance of CMP items as potential targets in aphasia therapy changes withduration of clinical experience. In 1997, when the first author of the presentchapter spent part of his sabbatical at Sydney University, we worked upour studies on the CMP in two review papers (Code, Müller, Hogan, &Herrmann, 1999b; Code, Müller, & Herrmann, 1999c).

During the last couple of years we have also started to use the CMPas teaching material in courses on neurological and neuropsychologicalrehabilitation. Within a special education program in clinical neuroscience,fourth year psychology students are expected to participate as visiting stu-dents in speech and language therapy, occupational therapy, physiotherapy,and neuropsychological therapy. Before starting the practical courses wealways introduce the CMP (and the respective results derived from the rank-ing and weighting procedure) as a common starting point for discussing therelative importance of different goals of aphasia rehabilitation. Interestingly,the relative weightings of the CMP items in naïve or untrained students donot differ significantly from the weightings given by experienced aphasiatherapists (see Figure 2.2). Disagreement in the assessment of the relative

Figure 2.2 Distribution of relative item weightings of the Code-Müller Protocols(CMP; mean scores). Weightings are standardized to a mean weightof .10. Dark bars show the weightings of experienced aphasia therapists(N = 60) and bright bars indicate the weightings of 4th year psychologystudents (N = 78). Error bars represent ± 1 SEM, p values refer to t-tests(two-sided).


importance of rehabilitation goals was only found with respect to the abilityto work, following interests and hobbies, and coping with frustration. Andonly the ability to work (again) was judged a significantly more importantrehabilitation goal by untrained psychology students.

Emotional disorders in aphasia: Post-stroke depression andneuropathological correlates

As already mentioned above, our experience with the use of nonverbalbehavior as a compensatory means of communication in severe aphasiaseemed to be highly influenced by both the psychosocial and the emotionalstatus of the patients and relatives. We, therefore, also started to investigatedepressive mood changes following brain lesions in aphasic and non-aphasicstroke patients. In a first study conducted from 1987 to 1991 we investigateddepressive alterations in acute and chronic aphasic patients with first-eversingle left-sided stroke lesions (Herrmann et al., 1993a). Patients with majordepression were only found in the acute group, and only among those withnonfluent aphasias. Brain imaging data showed that it was not the volume ofthe lesion but only the lesion location that had a major impact on the typeand severity of depressive symptoms. Superimposition of brain lesions ofaphasic patients with major depressive disorders demonstrated a commonsubcortical lesion area involving putaminal and external pallidal structures,which we interpreted to account for the pathogenesis of post-stroke depres-sion. We were able to replicate these findings in two broader studies (Herr-mann, Bartels, Schumacher, & Wallesch, 1995a, and Beblo, Wallesch, &Herrmann, 1999), both of which supported the hypotheses that (1) brainlesions of the left hemisphere basal ganglia and surrounding white mattertend to play a decisive role in the development of major depression in theearly stage after stroke, and (2) (functional) disruption of frontostriatal cir-cuits seems to contribute to the underlying pathophysiology of post-strokedepression.

These data, however, only account for the development of severe depressivedisorder (major depression) in aphasic patients during the post-acute stageafter stroke onset, but obviously do not contribute to the pathophysiologyof depressive disorders emerging in the later course of stroke and aphasia.Based on data from our own studies (Herrmann et al., 1995b; Herrmann etal., 1992; as well as studies from other colleagues) we argued that during thecourse of aphasia rehabilitation there are different stages during which thepatients exhibit a specific vulnerability to developing depressive disorders.In a first approach we classified these stages as “primary,” “secondary,”and “tertiary” (Herrmann & Wallesch, 1993). These terms, however, mainlyreflect the time of occurrence of depression in aphasia rehabilitation and donot specify the underlying pathophysiology of different types of depression.

At that point of our studies in speech and language and related disorders,Chris again joined our group and helped us to characterize and differentiate the


distinct sub-types of depressive disorders during long-term aphasia rehabilita-tion (Code, Hemsley, & Herrmann, 1999a; Code & Herrmann, 2003).

The neuronal basis of number representation andmental calculation

During the sabbatical stay of the first author of the present chapter at SydneyUniversity in 1997, Chris Code was heavily engaged in disentangling themystery of number processing and mental calculation by the use of positronemission tomography (Cowell & Code, 1998; Cowell, Egan, Code, Harasty, &Watson, 2000). While these very first investigations on number processingwere based on simple calculation tasks, we decided to use a more complexparadigm and advanced methods of spatiotemporal analysis of brain activityin future studies. From 2002 to 2004, Chris was invited to Bremen Universityfor several research stays as a fellow of the Hanse Institute for AdvancedStudies, and we decided to resume investigations on the neuronal basis ofmental calculation. During the last couple of years, a huge volume of studieshave been published, which investigated “mental calculation” or “numberprocessing” by using different study designs including different operators,different stimulation modalities, and different complexities of mental calcula-tion tasks. Our combined UK (Exeter)–Germany (Bremen) approach aimedat spatiotemporal analysis of neuronal correlates of different stimulationmodalities (auditory versus visual), task complexities (e.g., “simple tasks”with results in the number domain below 10 or “complex tasks” with resultsin the number domain between 10 and 100), and basic operations (+, −, ×, /)during mental calculation. Prior to fMRI and MEG examinations we startedwith a German pilot study on a behavioral data level (reaction times (RTs),error rates) followed by a parallel study with British students at ExeterUniversity. Surprisingly, students from Bremen University presented fasterRTs than the age-matched British group (see Figure 2.3), while error ratesdid not differ significantly between groups. So far, we do not have a strongexplanation for how these differences originate, and how Chris might havecontributed to this result. In both groups, participants showed longer RTs forcomplex tasks in comparison to simple tasks. The auditory presentationmode produced longer RTs than the visual presentation mode.

In a further study combining functional magnetic resonance imaging(fMRI) and magnetencephalography (MEG), 11 German subjects werescanned with both methods while they performed the same tasks evaluatedin the pilot study. Data derived from event-related fMRI showed a net-work of activated areas for complex tasks in contrast to simple tasks inprominently right frontal, parietal and central regions. A preliminary findingdemonstrated different task-related and task modality specific spatiotempo-ral characteristics of source space activity as revealed by seeded dipoles basedon the fMRI regions of interest (ROI) and minimum-norm (L2) estimates(see Figure 2.4).


At the present point of analysis our data show that different arithmeticoperations should be analyzed independently of each other. Furthermore, thepresent data indicate that there is no empirical basis for the comparison ofstudies using different presentation modalities.

Conclusions

Most of the studies presented in this chapter were initiated or motivated bythe research or research interests of Chris Code. These areas reflect a verybroad range of scientific interest, with respect to both research topics andresearch methods. The bracket, however, that encloses these diversified activ-ities is always the issue of speech and language and related disorders.Although our studies in the periphery of “aphasiology proper” alwaysremained low-budget research, a great number of PhD students and post-docs participated in the series of investigations as described before. Further-more, part of the research methods originally developed by Chris andcolleagues were also taken into teaching modules in universities and furthereducation in neurological and neuropsychological rehabilitation. So we arequite sure that our cooperation with Chris Code will continue for the nextdecades and that Chris will also accompany our next projects on the molecu-lar basics of brain disorders (Herrmann & Ehrenreich, 2003) and neuro-protection (Ehrenreich et al., 2004).

Figure 2.3 Reaction times for complex mental calculation tasks (/: division; −: sub-traction; ×: multiplication; +: addition) with auditory (left) and visual(right) stimulation modes for two age-matched groups of German (BremenUniversity; dark bars) and British (Exeter University; bright bars) students.Error bars represent ± 1 SEM, p values refer to t-tests (two-sided).


References

Beblo, Th., Wallesch, C. W., & Herrmann, M. (1999). The crucial role of frontostriatalcircuits for depressive disorders in the post-acute stage after stroke. Neuropsychiatry,Neuropsychology, and Behavioral Neurology, 12, 234–246.

Code, C., Hemsley, G., & Herrmann, M. (1999a). The emotional impact of aphasia.Seminars in Speech & Language, 20, 19–31.

Figure 2.4 Left: data from mental calculation processes after auditory stimulation;right: data from mental calculation processes after visual task presenta-tion (both columns represent the contrast “complex” vs. “simple” tasks).The upper row shows MEG signal space averaged responses and thecorresponding global field power (GFP) time courses with the respectivemaxima. The middle row shows minimum-norm (L2) estimates accordingto marked GFP maxima. The lower row shows fMRI contrasts and illus-trates corresponding dipole positions seeded into a standard brain volume(Talairach Space).


Code, C., & Herrmann, M. (2003). The relevance of emotional and psychosocialfactors in aphasia to rehabilitation. Neuropsychological Rehabilitation, 13,109–132.

Code, C., & Müller, D. J. (1992). The Code-Muller protocols: Assessing perceptions ofpsychosocial adjustment to brain damage. Kibworth: Far Communications.

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Cowell, S. F., & Code, C. (1998). Thinking nuclear medicine – PET activation. Journalof Nuclear Medicine Technology, 26, 17–22.

Cowell, S. F., Egan, G. F., Code, C., Harasty, J., & Watson, J. D. (2000). The functionalneuroanatomy of simple calculation and number repetition: A parametric PETactivation study. NeuroImage, 12, 565–573.

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Ehrenreich, H., Aust, C., Krampe, H., Jahn, H., Jacob, S., Herrmann, M., et al. (2004).Erythropoietin: Novel approaches to neuroprotection in human brain disease.Metabolic Brain Disease, 19, 195–206.

Helmick, J. W., Watamori, T. S., & Palmer, J. M. (1976). Spouses’ understanding ofthe communication disabilities of aphasic patients. Journal of Speech and HearingDisorders, 41, 238–243.

Herrmann, M. (1997). Studying psychosocial problems in aphasia: Some conceptualand methodological considerations, Aphasiology, 11, 717–726.

Herrmann, M., Bartels, C., Britz, A., & Wallesch, C. W. (1995b). The impact ofaphasia on the patient and family in the first year post-stroke. Topics in StrokeRehabilitation, 2, 5–19.

Herrmann, M., Bartels, C., Schumacher, M., & Wallesch, C. W. (1995a). Poststrokedepression: Is there a patho-anatomical correlate for depression following thepost-acute stage of stroke? Stroke, 26, 850–856.

Herrmann, M., Bartels, C., & Wallesch, C. W. (1993a). Depression in acuteand chronic aphasia: Symptoms, pathoanatomical–clinical correlations, and func-tional implications. Journal of Neurology, Neurosurgery, and Psychiatry, 56,672–678.

Herrmann, M., & Code, C. (1996). Weightings of items on the Code-Müller protocols:The effects of clinical experience on aphasia therapy. Disability and Rehabilitation,18, 509–514.

Herrmann, M., & Ehrenreich, H. (2003). Brain derived proteins as markers of acutestroke: Their relation to pathophysiology, outcome prediction and neuroprotectivedrug monitoring. Restorative Neurology and Neuroscience, 21, 177–190.

Herrmann, M., Johannsen-Horbach, H., & Wallesch, C. W. (1992). Psychosocialaspects of aphasia. In D. Lafond, Y. Joanette, J. Ponzio, R. Degiovani, &M. Taylor-Sarno (Eds.), Living with aphasia: Psychosocial issues (pp. 187–206). SanDiego, CA: Singular.

Herrmann, M., Johannsen-Horbach, H., & Wallesch, C. W. (1993b). Empathy andaphasia rehabilitation: Are there contradictory requirements of treatment andpsychological support? Aphasiology, 7, 575–579


Herrmann, M., Koch, U., Johannsen-Horbach, H., & Wallesch, C. W. (1989). Com-municative skills in chronic and severe nonfluent aphasia. Brain and Language, 37,339–352.

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Herrmann, M., & Wallesch, C. W. (1989). Psychosocial changes and psychosocialadjustment with chronic and severe nonfluent aphasia. Aphasiology, 3, 513–526.

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3 Independent evidence for theunification of explanatoryparadigms in the neurosciences

Hugh W. Buckingham andSarah S. Christman

Introduction

In this chapter we propose to trace the recent history of a counterintuitiveobservation in the neurosciences that comprises descriptions of active pro-cessing whereby strong stimulus forces evoke weak or insignificant associ-ations, and where weak forces evoke stronger associates. This phenomenonhas been labeled “paradoxical,” since it is opposed to the normal situationwhereby strong elements in a network associate with their most frequentassociates, and weak elements in a network associate with less frequentassociates. We chart the trajectory of the notion as it weaves its way from thePavlovian physiology of conditioned reflexes and stimulus–response motor-sensory reflexes of vegetative and alimentary levels to the neuropsychology ofSigmund Freud, Alexander Luria, and the connectionist modeling of latetwentieth-century neuropsychological science. Our purpose is to highlight thefact that the threads of this paradoxical phase of stimulus–response balance, orrather imbalance, have been cast at three distinct levels of explanation in theneurosciences: Pavlovian physiology; Luria’s concomitant neuropsychologyof language; and Trevor Harley’s connectionist modeling. We emphasize thatthe situation is one that argues for a unification or alignment rather than anyreduction of Luria’s neurolinguistics or Harley’s connectionism to Pavlov’sphysiology.

Independent findings of similar phenomena from distinct scientific meth-odologies in the neuropsychology of language serve to strengthen eachparadigm, and rather than fractionating the neurosciences, there is a growingconvergence, alignment, or unification of information (Code, 2000). Scientificinvestigation is often driven by: (1) the (frequently unstated null hypothesis)search for evidence for one or another hypothesis or model previouslyproposed in the literature, (2) a straightforward and unbiased search for pos-sible evidence for a deductive prediction, and (3) the search for further occur-rence of inductively predicted correlations between events. Often, differentexplanatory methodologies and paradigms will uncover a similar set ofobservations in nature, all of which are in “alignment” (Gotts & Plaut,2004, p. 332) in some way or another. Compatible findings from distinct

methodological inquiries are extremely important in accessing the contribu-tions of the respective explanatory accounts.

The position we adopt in this preliminary study is that the “unification” ofthe sciences avoids the metaphysical trappings of a “reductionist” stand,which would have us believe that ultimately our understanding of the physicaluniverse will itself reduce to the physical – whence the word “physics” isderived. That is, all sciences will eventually come to be explained in the termsof that science. Once we abandon the fear or lingering doubts that mentalobjects can be understood as objects in nature nevertheless (see Chomsky,2000, 2002, on language as a natural object) and therefore studied as such, theeschewing of reductionism and the embracing of a unification view of thesciences is a great deal easier to tolerate. Buckingham and Christman (2004a,p. 292) adopted this view in unifying the heterogeneous methodologies on theissue of perseveration written for a special journal volume collection ofpapers: neuropharmacological, connectionist, neuropsychological, linguisticand rehabilitative. We carefully resisted the ancient tendency to imply thatultimately all will reduce to the biochemistry of the synapse, only to waitaround for physics to explain that.

The topic for our chapter is an outgrowth of an essay by one of us(Buckingham, forthcoming) on Alexander Luria, which made reference to aspecial issue project of Chris Code in the journal Aphasiology, edited by thePolish neuropsychologist Bozydar Kaczmarek in 1995. Chris’s contributionsas a scientist as well as an editor of books and journals have influenced usall in one or another way. The present chapter draws from connectionistmodeling in a historical framework. Here, again, we note Chris’s researchcontributions in stochastic predictions of recovery from aphasia with con-nectionist networks (Code, Rowley, & Kertesz, 1994) and yet another specialeditorial project with Harley’s (1993) detailed overview and assessment forAphasiology on connectionism. Chris, the scholar-researcher, has contributedboth as principal editor of two recent volumes of classical cases in neuro-psychology (Code, Lecours, Joanette, & Wallesch, 1996; Code, Wallesch,Joanette, & Lecours, 2003) for Psychology Press, and has chapters in thesevolumes as well. The marks of Chris’s editorial scholarship and scientificresearch are accordingly implicit through our contribution to his Festschrift.

Ivan Pavlov – physiology

Ivan Pavlov (1962) originally worked out physical principles that he labeled as“laws of strength” or “rules of force.” He was a physiologist, and his explana-tory idiom was the development of conditioned reflexes of sensory-motornerve physiology. Most undergraduates in psychology have studied at leastthe rudiments of Pavlov’s investigations “of the dog, this friend of man sincepre-historic times” (Pavlov, 1962, p. 87). His commitment to physiology wasstraightforward from the beginning. He wrote that he was trying to compre-hend the totality of the dog’s nervous system, “purely physiologically without

Unification of explanatory paradigms in the neurosciences 29

using any psychological ideas or terms” (Pavlov, 1962, p. 87). He conditionedthe alimentary functions of the dog through the “coupling,” as he writes, ofvarious kinds of outside stimuli (whistles, metronomes, lights, bells, and thelike) with presentations of food. As we all recall, he therefore could elicitmany gustatory motor secretions of saliva with one or another of these sens-ory stimuli. Reflecting on his work in a paper delivered at the Sorbonne, Paris,in December 1925, he claimed in French that, “At the present time we havefacts which warrant the assumption that the act of coupling is even an elem-entary physiological process” (Pavlov, 1962, p. 88). Unfortunately, there isno evidence at all that Pavlov was aware of the early suggestions of DavidHartley (1746, 1749; Buckingham & Finger, 1997) to the same effect.

In his study of canine physiology, Pavlov found that the repeated adminis-tration of coupled sensory stimuli led simultaneously to the easy activation ofspecific (conditioned) motor responses and the thorough inhibition of com-peting responses. He believed that this natural phenomenon also character-ized the activity underlying many of the aspects of consciousness that hestudied, such as narcolepsy, hypnotic states, severe psychotic and neuroticstates, the “oneiroid” phases of pre-sleep, and the deeper phases of slumber.For Pavlov, the continuum from wakefulness to complete sleep mirrored in animportant sense a continuum from total consciousness to unconsciousness.He conceived of a multitude of difference “phases” along this continuum,each characterized by different admixtures of activation and inhibition levelsof associated conditioned couplings between elements. All phases were tiedto the interplay, or stasis, of activation and inhibition, inhibition becomingstronger and stronger in phases that approached sleep. Phases were differen-tiated by Pavlov in terms of the behavioral consequences of the many shifts inthe balance of strong and weak stimuli, their activations and inhibitions. Theconditioned reflex was the sine qua non of Pavlovian physiology. For Pavlov,“The idea of reflex in physiology, the gift of Descartes’ genius, is, of course, apurely natural-science idea” (Pavlov, 1962, p. 87).

Pavlov’s paradoxical state

Pavlov’s experiments indicated that not all states of full physiological (ormental) conditioning were instantly achieved; rather the course of the con-ditioning process moved behavioral responses through a series of behavioralphases. Of interest is the phase that Pavlov labeled “paradoxical.” For anillustration, we look at the work in Pavlov’s laboratory by one of his col-laborators, Dr. Razenkov. The experimental paradigm provided a subject(e.g., a dog) with coupled presentations of whistles, metronome beats, andrhythmic mechanical stimulations of the skin, the flashing of an electric bulband the delivery of food. Razenkov brought about “the normal effect of thepositive conditioned stimuli” (Pavlov, 1962, p. 132) when the stimulusstrength yielded 30 drops of salivation. At first presentation, it turned outthat the whistle evoked 5 drops of saliva, the metronome 3.5 drops, the tactile

30 Buckingham and Christman

stimulations 3 drops, and the bulb flashes 2 drops. Pavlov writes that “thestimuli ranged in strength, from the strong to the weak, thus: whistle, metro-nome beats, mechanical stimulation of the skin and flashing of the bulb”(Pavlov, 1962, p. 133). Clearly, not all stimuli appeared equally strong, forceful,or efficient at eliciting a desired response.

This observation led to a crucial follow-up investigation with the sameexperimental subject. We first note that in the above original set of stimuli,the tactile mechanical stimuli included 24 contacts within the 30 secondintroduction of the stimulus, and again it elicited 3 drops of saliva. Thesecond experiment was one in which, along with the other positive stimuli ofthe first experiment, a differentiated tactile stimulus of 12 per minute wasapplied during 30 seconds and followed without any interval by the positivelyconditioned tactile stimulus of 24 per minute, which was also continued for30 seconds and then reinforced in the typical fashion.

The next day the dog was subjected to another experiment where he wastested with the original set of stimuli from experiment 1. One English transla-tion of this paper has Pavlov claiming that the small factor of introducing the12 per minute tactile stimulus “produced an extraordinary effect” (Green,2006, p. 4). Pavlov, in another translation of this paper, writes, “The day afterthis experiment [the second one, HB/SC] and during the subsequent nine daysall the conditioned reflexes disappeared and were manifested only very rarelyand to a minimal extent. This period was followed by a very special period”(Pavlov, 1962, p. 133). Experiments in this special period, which lasted14 days showed “extremely peculiar changes” (Green, 2006, p. 4). The pecu-liar and extraordinary effects were that the mechanical stimulation nowelicited 5.5 drops of salivation, the bulb flashing 3 drops, the metronomebeats 1 drop, and the whistle 0 to 0.3 drops. Crucial for our chapter is thefollowing statement by Pavlov (1962, p. 133):

The result, as you see, is quite the reverse of what formerly occurrednormally: strong stimuli either failed to act or barely acted, while theweak stimuli produced an effect even greater than normal. Followingthe example of N. Vvedensky, we named this state of the hemispheres theparadoxical phase.

The 14-day paradoxical phase slowly shifted to a phase where all previousstimuli seemed to have returned to their original strength or force, since thewhistle (4 drops) and the metronome (4.5 drops) again elicited strongresponses. This phase of response strength overlap came to be called thephase of “equalization,” where strong and weak stimuli had an equal likeli-hood of eliciting the same response. We do not consider this phase in thepresent chapter, although it, too, comprises an intriguing alternative to nor-mal stasis where strong evokes strong and weak evokes weak. The effect ofthe second experiment was an inhibitory one, and it was this inhibition thatbrought about the counterintuitive switch in the rule of force. In any event,


for Pavlov, its outcome pointed to a physiology that eschewed all psychology.Our goal now is to show how the explanatory account of this paradoxicalphase was lifted from the neuronal level to the neuropsychological level andfrom there, through Hebbian learning, to modern connectionist modeling.

Alexander Luria – neuropsychology

Luria (e.g., 1962/1980, 1973) borrowed the so-called laws of strength/rulesof force from Pavlov in his explanations of paraphasia within his neuro-psychological model of language and its related accounts of linguistic break-down secondary to neurological damage. Luria accounted for the normal andabnormal evocation of different linguistic constituents such as phonemesand words within the physiological idiom of Pavlov’s nervous laws. Phonemicand lexical access were captured by the same laws. Luria’s neuropsychology atthe very least pointed to a certain compatibility of the explanatory accountsof physiology and the burgeoning field of the neuropsychology of language– often referred to as “neurolinguistics” by Luria.

Luria, however, was not a reductionist and resisted at all costs a com-plete reduction of his explanatory paradigm to the domain of physiology.Homskaya (2001) charts Luria’s initial attraction to Sigmund Freud’s workat the psychological level, and his psychophysical accounts of human lan-guage and its breakdown in aphasia. Freud’s “software” approach to thefunctionality of language and cognition influenced Lev Vygotsky as well,and both Vygotsky and Luria developed theories of how society and culturewere tightly interwoven with the complexities of human cognition. Later, asa medical student of neurology and subsequently a physician who workedwith all aspects of the neuropsychology of brain and behavior, Luria consist-ently kept the physical and the psychological apart. His take on the mind–brain issue was that of Freud, and as a consequence, he was indebted toJohn Hughlings-Jackson, whose influence on Freud was marked throughoutFreud’s (1891) book on aphasia. Luria’s philosophy, accordingly, took theform of a “psychophysical parallelism,” a kind of dualist “identity theory,”not unlike Hughlings-Jackson’s theory of “concomitance,” defined as atogetherness of mind and brain running concurrently and bringing about a“coin-like” single effect, where both are considered as the respective sides ofthat coin. Nevertheless, when it came to accounting for paraphasias, Luriacontinually gave credit to Pavlov for notions such as the paradoxical phase(e.g., Luria, 1973, pp. 44, 157, 317; and 1962/1980, pp. 513–518).

Luria’s (1973, 1962/1980) neurolinguistic descriptions of lexical or phon-emic paraphasias were couched in terms of selection errors, wherein targetwords or sounds were thought to be erroneously chosen from among their(inappropriately) highly activated competitors. In the normal case, highlyactivated competitors would naturally be those with strong associations (asper Pavlov’s law of strength) to intended targets. For example, if a speakerwere trying to access the word “college,” he would have a statistically greater


likelihood of activating (and then inhibiting) strong associates, such as“school” or “university,” than weakly related associates such as “kinder-garten,” “hospital,” or “gymnasium.” The same principles were thought toapply to phonological as well as lexico-semantic processing.

Luria believed that a certain amount of cortical tone and mobility werenecessary for efficient linguistic processing, and he suggested that theserequisites became impaired as a consequence of neurological pathology. ForLuria, physiological paradoxical and equalization states induced by braindamage were completely compatible with concomitant linguistic outcomes,such as semantic paraphasias, given his predisposition toward psychophysicalparallelism. In his view, a system driven to the paradoxical activation ofweak rather than strong associates for a stimulus would be statistically morelikely to produce weakly related semantic paraphasias such as “kinder-garten,” “hospital,” or “gymnasium” than strongly related associates (suchas “school” or “university”) when attempting the target word “college” dur-ing a naming task. In an equalization state of processing, Luria predicted thatstrong and weak associates for a target would have a statistically equal chanceof being activated, since a reduction of cortical tone would cause normalmechanisms of competitor inhibition to fail. This was thought to be the mostlikely neurolinguistic (and, indeed, connectionistic) characterization of severeanomia, where a likely outcome of the equalization phase would be no out-put at all. The paradoxical stage, on the other hand, would reveal statisticallygreater probabilities of weaker associates – a greater likelihood for error.

D. O. Hebbian learning

The link between a neural associationism and modern connectionismrevolves around the ideas of D. O. Hebb (1949). The notion that couplingsare strengthened between neurons that act in synchrony is most often referredto as “Hebbian learning.” A large number of theoretical rules that mediatethis learning in domains referred to as “neural” networks have been proposedin the last several decades. The notions go back to William James (1890) andto the summation idea that brain activity is governed by the sum of concur-rent inputs to a given single neuron as long as there are (1) a high frequencyof simultaneous synaptic connections, (2) intense firings, and (3) no otherleaks of the firings into other neurons. All must converge on a single neuronunit. At this point, the Aristotelian notions of strength of associative forcecan be quantified into mathematical summation. Also needed are the math-ematical transformations of inhibition and the formulae of change so thatactivated forces can return to their original values “at rest” (resting levels).

These “neural” networks typically support three levels of linguistic pro-cessing: semantic/conceptual, lexical, and phonological. Others have beenadded, but for our purposes a three-level system will be all that is needed.In language, frequency of usage often determines the physiological restingvalues of neurolinguistic units in many models. Furthermore, just as the


setting of initial “weight” values may vary, the nature of the spread of neuralactivation through the system may also vary. Some view the spread of acti-vation as going from level to level more or less instantaneously, while othersincorporate a cascading spread, where subsequent levels may start their acti-vation before all activations at the earlier levels are finished. Most systemshave feedback between and among levels, and some are set up so that elem-ents at their tactic levels may send inhibitory volleys to others at that level.Many models that are organized in the ways indicated above and that havecascading spread are referred to as models of interactive activation (Dell,1986). The connectionist model we are drawing from, which unwittinglysimulated the paradoxical phase, is one proposed by Trevor Harley and hiscolleague, Siobhan MacAndrew (1992).

Harley’s connectionist model of lexicalization

This model was created to account for substitution errors among whole words.It can handle phonemic substitutions as well, but Harley and MacAndrew(1992) concentrated on lexical retrieval processes. Theirs was an interactiveactivation model, closely related to those constructed by Gary Dell (1986)and more recently by Dell, Schwartz, Martin, Saffran, and Gagnon (1997).There is a three-layer architecture containing 26 nodes at the semantic level,70 nodes at the lexical level, and 21 nodes at the phoneme level. That is, thereare 26 conceptual categories, 70 words, and 21 phonemes. As is the case withmost of the connectionist models that have been constructed to date, thelinguistic nodes have limited domains at each level. There are feedback con-nections between the phonological and lexical levels. Unlike many othermodels of this type, the authors built in semantic representations that wouldallow for a “richness” component to concepts with a high degree of image-ability. At the lexical and phonological strata, inhibitory links were estab-lished, which highlight the effects of intra-level “competition,” but whichwhen operating normally serve to speed up processing by inhibiting inappro-priate competitors – phonemes competing with phonemes and words com-peting with words. Inhibitory intra-level connections, when working, provideaccounts of lexical priming in naming, while when inhibition falters, effectssuch as the “phonological blocking” of tip-of-the-tongue (TOT) effects arenicely illustrated. Clusters of plan-external competing phonologically relatedword forms can severely interfere with lexical access.

Harley and MacAndrew (1992) tested four hypotheses with this model:that (1) altered decay rates would interfere with word finding; (2) loss ofintra-level inhibition would interfere with word finding; (3) increased random“noise” would interfere with word finding; and (4) reduction in connectionweights between the semantic level and the lexical level (i.e., reduced flow ofactivation from the semantic to the lexical level) would interfere with wordfinding. As with many models of its type, this system can account for aspectsof recovery in aphasia as well as the influence of frequency of usage and


imageability effects in paraphasic errors. The model computes the inputsummation formulae for activation spreading through the system, and itcomputes formulae for return rates for each cycle (“processing epoch”) toresting levels. Whether returning from higher activation levels or from lowerlevels due to inhibition, processing nodes must reset to their resting stages innormal fashion for the system to work normally for each cycle. Needless tosay, slowed decay rates from recent activation and weakened weight connec-tions between levels would lead to perseveration of words as well as of phon-emes (Buckingham & Christman, 2004b). This model has parameters aswell for processing lateral inhibition among nodes at the same level. Here, theauthors manipulate intra-tactic inhibition at the lexical level only. As men-tioned earlier, the focus of the Harley and MacAndrew (1992) study was onlexical access and substitution. Suffice it to say that the lexical level sendsoutputs to the phonological level and, for production, five-slot seriallyordered phonological templates serving as output frames must be filled. Theproduction level is left in a rather primitive form, allowing for no phonotacticconstraints, and specification of all input features is characterized simply as“on–off” binary units. Harley and MacAndrew motivate many of theseshortcomings with arguments for simplicity.

The simulations of connectionist models for pathology come from differ-ent arrays of alterations of weights, decays, and the addition of inhibition by“noise” at different locations in the system. Harley and MacAndrew (1992)“lesion” their system in varying ways in order to evaluate their impact (re: theabove four hypotheses) on lexical access failure. All other parameters distinctfrom weight values are considered to be “control parameters.” These includepost-activation decay, amounts of random “noise,” the effect of lexical fre-quency, and the time the external semantic input is received by the semanticunits. The investigators search for any errors the model may produce inresponse to some external semantic input. They are specifically testing forinductively based predictions from the aphasia literature on the origin ofparaphasias – words in English, and words that could be but are not inEnglish. Some of the non-words produced by the model bear a form trans-parency to the external semantic input (called the “target”), whereas othersdo not. Some call all non-word productions “neologisms” (e.g., Butterworth,1979), while others reserve the term “neologism” for non-words whoseform is opaque to any likely target word in the context of the utterance(Buckingham & Kertesz, 1976).

An example of this model’s activity may be illustrative at this point.Suppose that an external semantic input (the so-called “jolt”) to the process-ing model is the word “cow.” In a normal cycle, that word would send a joltof activation to, say, five semantic categories: animal, dairy related, four-legged, adult, female. Those categories would converge onto the lexical item<cow>, which would in turn send activation to the phonemes /k/ and /aw/ (adiphthong counts as one phonemic unit). The normal output would be theCV word /kaw/. In Harley and MacAndrew’s study, the word “cow” is the


input target for each hypothesis-testing. For comparison, they plotted notonly the activations of the target against the processing cycle time, but alsothose parameters for “calf” (semantically and phonologically related associ-ate), for “dart” (unrelated), for the onset /k/ phoneme (of “cow” and of“calf”) and for the onset phoneme /d/ of “dart.”

The test of hypothesis 1 did not show much effect in the Harley andMacAndrew (1992) study. With increases in the rate of decay alone, theresponse “cow” was significantly favored. They then combined decay ratewith a time delay of the external semantic input to the semantic level. Theyobserved that doing this reduces the target activation to near zero, but itreduces all possible word competitors as well. In effect, little if anything isproduced – somewhat akin to the “equalization” phase of Pavlov, but we arenot charting that phase abnormality in this chapter. This simulation is notwithout interest, however. The authors rather doubt that decay rate alterationalone is likely to be a good explanatory account of paraphasia. In any event,as they point out, connectionist theory would actually predict that decay ratelesions should only give rise to “smart” errors, whereby inter-level connectiv-ity is still apparent. This would not be the case at least for jargon or complexneologisms, or for the error: “cow” → “dart.”

Harley and MacAndrew next tested for loss of intra-level inhibitory con-nections, leaving vertical connections and decay rates unaltered mathematic-ally (e.g., “unlesioned”). Even though logic seemed to predict that loweredlevels of inhibition at the word level would serve to promote many similarcompetitors with the target, in this study, the target word was still signifi-cantly more likely to be produced over all other possible candidates. Evenwhen the authors added random noise under this condition, there was nonoticeable increase in errors – and certainly no production of jargon neolo-gisms. Research is still ongoing to try to find accounts for lexical priming andTOT errors, but Harley and MacAndrew found no help in these domainswhen altering intra-level word inhibition, even with added noise to the sys-tem. Hypothesis 3 was then tested. Random initial noise was added to thesystem but it failed to evoke much effect for severe paraphasia.

Hypothesis 4 was tested last, with a method involving the weakeningof the connection strengths between concept nodes and lexical nodes, result-ing in weaker lexical activations from the semantic level. Previous studies(e.g., Miller & Ellis, 1987) had indicated that interferences in the normalconnectivity between the semantic and lexical level set the stage for neologis-tic production, where underlying targets would be accordingly blocked in theproduction line, but where other processes would come to bear on the pro-duction of surrogate forms that would in turn effectively mask the accessblock. Those “abstruse” neologisms (Lecours, 1982) would appear bizarreand opaque as to some underlying target. This account of neology was firstlabeled “the anomia theory” by Brian Butterworth (1979). Harley andMacAndrew, however, observed that weakened weights alone between thesemantic and the lexical level did not have much of a dilatory effect on word


finding. Continually weakening the connections over time still showed thatthe target was more likely to be activated, but eventually other semanticcompetitors would decrease even more rapidly, still being distinguished fromthe target, but waning in appearance so that semantic paraphasias fadeaway from the picture, leaving other types of lexical substitutions to beoccasionally produced. These are then likely to be only form related and notsemantically related.

Also, since frequency and imageability result in higher resting levels ofactivation, they may play a role in word selection such that their potency maycounterbalance the overall weakening of the semantic to lexical connections.

With respect to the outcome of the test for hypothesis 4, Harley andMacAndrew (1992, p. 382) state that, “Although this gives a more satisfyingdistribution of lexical activations than the other accounts, it still fails tosatisfy the criterion that, on some occasions, the activation of competitorsshould be above that of the target.” They then introduced some randomvariation into the weakening of the semantic–lexical connections. Accord-ingly, they could increase the severity of lesioning “by adding an amount ofnormally distributed random noise to each connection and increasing thestandard deviation of that noise distribution” (Harley & MacAndrew,1992, p. 382). In this way, without being aware of the long history of the“paradoxical phase,” they ended up simulating the extraordinary, very spe-cial, and counterintuitive phenomenon of Pavlov’s famous inhibitory phase.The other astounding outcome was that Harley and MacAndrew actuallyhad to add increased inhibition with the random noise to the already weak-ened connections. Recall that Pavlov’s abnormal phases were largely due toincreased inhibition in one way or another. Harley and MacAndrew (1992,p. 382) wrote:

Random lesioning of alphasl [“alpha semantic lexical” – the name oftheir parameter that governed the rate of spread of activation betweenthe semantic and lexical levels – HB/SC] affects the target lexical unitsuch that the greater the severity of the lesioning, the lower the prob-ability of the target unit being highly activated. Further, the greater thelesioning, the higher the probability of other lexical units being highlyactivated.

In other words, the greater the severity of the lesioning, the more likely it isthat weak associates will be activated where strong ones should be produced.Harley and MacAndrew (1992) thus describe precisely the paradoxical effectcaptured by the different scientific paradigms of Pavlov and Luria beforethem. Figure 3.1 (Harley & MacAndrew’s Figure 9, 1992, p. 382) shows thatfor input target “cow,” the weaker associate “calf” is more highly activatedthroughout increasing time in cycles, although activation levels begin todecrease after 10 time in cycles. The paradox continues nevertheless to the40 time in cycles, where “cow” almost approaches “dart,” which is practically


off the map for all processing epochs. Note that /k/ has a much greater set ofactivation levels than /d/, for the obvious reason that both “cow” and “calf ”share that onset phoneme. The /d/ is actually more highly activated through-out the cyclings than is the word “dart.” This is most likely to be because asmall number of occasionally activated unrelated words with /d/ onset wereproduced as well as “dart.”

Concluding remarks

Here, we witness the final link in the Pavlov to Luria to Harley/MacAndrewphenomenon of an inhibitory phase in pathology whereby normal laws ofstrength are reversed and strong and weak activation levels operate counter-intuitively. The paradox has been shown to exist at distinct levels of “neural”

Figure 3.1 The effects of introducing some random variation (noise) into theweakened weight connections of the semantic to lexical levels. Nor-mally distributed random noise was added to each connection. Theseverity of lesioning is mimicked by increasing the standard deviationof the noise distribution. Only moderate damage (standard deviation= 0.05) was applied for the effects shown in this figure, which wasFigure 9 in Harley and MacAndrew (1992, p. 382). The randomlesioning into the weakening was such that the more severe the noise,the lower the probability of producing the target input (“cow” in thesecases). Further, the more severe the noise, the higher the probability ofproducing other lexical items. This is the essence of the paradoxicalphase suggested by Pavlov and Luria, although admittedly, theweaker element was “calf,” and not “dart.” The paradoxical nature ofthe phenomenon still holds. (Reproduced from Harley & Mac-Andrew, 1992, with permission to use the figure given by T. Harley,June 13, 2006).


description. Pavlov’s descriptions of the paradox were cast in the vocabularyof his physiological paradigm. This notion then was transferred to wordsand phonemes in the neuropsychological descriptive idiom of AlexanderLuria, an idiom firmly implanted in the psychology of Hughlings-Jacksonand Sigmund Freud (1891) and rather incongruous with the materialismof the Russian revolution and the Union of Soviet Socialist Republics(Homskaya, 2001).

We now have witnessed how the phenomenon of the paradoxical state hasunwittingly been simulated in a modern connectionist model, and thereforehas been aligned with yet another level of neuroscientific description. Modernconnectionism has provided the field of neuropsychology with numerouscomputational simulations of both normal and abnormal human cognitivebehavior. Before the advent of modern connectionism, Luria had borrowedmuch of the cortical neurodynamics of Pavlovian physiology. Luria, however,was incorporating the Pavlovian paradigm at a substantial remove fromPavlov, since Luria’s units were phonemes and words. Luria’s scientificdescriptors drew heavily not only from Pavlov, but also from associationpsychology. By weakening connection strengths between the conceptual(semantic) level and the lexical level, and adding some random noise to thesystem, Harley and MacAndrew independently simulated a phase intriguinglysimilar to the paradoxical states of Pavlov and Luria. The independence ofthis simulation is all the more powerful, since at best they only tweaked thenetwork so as to have it produce paraphasias. The paradox, as illustrated intheir Figure 9, shows that the input target word “cow” strangely enoughevoked “calf” and rarely if ever evoked “cow.” We note, however, that “dart”(totally unrelated) was almost never produced. But, there is neverthelesssomething puzzling about the surfeit of productions of “calf” for the target“cow.” One might suggest that “calf” was perseverated, in which case theargument for a paradoxical phase as it is described would be weakened.Harley and MacAndrew’s paradox-producing lesions did not involve slowingdecay rates, or hampering with any cleanup units in the spirit of Plaut’soriginal suggestion for simulating perseveration (see Gotts & Plaut, 2004). Infact, the only alteration to decay rates they tested was speeding them up – notslowing them down. Harley and MacAndrew’s paradox lesions importantlyinvolved weakening connections between the conceptual and the lexical levelsplus the addition of random noise. More recent connectionist thinking hassuggested that in fact decay rates need not be damaged to simulate persevera-tive production. Gotts and Plaut (2004) and Basso (2004) have suggested thatweakened weight levels in one modality may indeed lead to perseveration,where the onus is on the weakened connectivity. Local weakened connectionsin a certain modality may be such that normal decay rates would in a sensenot operate fast enough to avoid normal post-activation rebound, resulting inperseveration. Harley and MacAndrew did not have architectures such thatthey could set up simulations specifically for reading aloud, repeating, ornaming, although these networks tend to extend more easily to the naming


situation, where the spreading activation begins at the semantic level. Manyquestions, however, remain in the interpretation of simulation correlationsbetween normal and abnormal linguistic processing (e.g., Ruml, Caramazza,Capaso, & Miceli, 2005). Nevertheless, we have presented what we feel aresome extremely interesting descriptions of inverted stimulus–response con-tingencies across three different investigative paradigms in the neural sciences.

Our view is again that we should resist any tendency to claim that theneuropsychological or the modern connectionistic theories should in any wayreduce to Pavlov’s physiology. Rather we suggest that each explanatoryaccount unifies or comes more closely into alignment with the others in obvi-ous ways, but each with its separate scientific methodologies and distinctvocabularies, cast as they are at different levels of human cognition.

References

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Buckingham, H. W. (forthcoming). Alexander Romanovich Luria: The man and hisscience. In N. Koertge (Ed.), New dictionary of scientific biography. FarmingtonHills, MI: Charles Scribner’s Sons.

Buckingham, H. W., & Christman, S. (2004a). Preface. Seminars in Speech andLanguage, 25, 291–293.

Buckingham, H. W., & Christman, S. (2004b). Phonemic carryover perseveration:Word blends. Seminars in Speech and Language, 25, 363–373.

Buckingham, H. W., & Finger, S. (1997). David Hartley’s psychobiologicalassociationism and the legacy of Aristotle. Journal of the History of the Neuro-sciences, 6, 21–37.

Buckingham, H. W., & Kertesz, A. (1976). Neologistic jargon aphasia. Amsterdam:Swets & Zeitlinger.

Butterworth, B. (1979). Hesitation and the production of verbal paraphasias andneologisms in jargon aphasia. Brain and Language, 18, 133–161.

Chomsky, A. N. (1994/2000). Language as a natural object. In A. N. Chomsky, Newhorizons in the study of language and mind (pp. 106–133). Cambridge, UK:Cambridge University Press.

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Code, C., Lecours, A. R., Joanette, Y., & Wallesch, C.-W. (Eds.) (1996). Classical casesin neuropsychology (Vol. 1). Hove, UK: Psychology Press.

Code, C., Rowley, D., & Kertesz, A. (1994). Predicting recovery from aphasia withconnectionist networks: Preliminary comparisons with multiple regression. Cortex,30, 527–532.

Code, C., Wallesch, C.-W., Joanette, Y., & Lecours, A. R. (Eds.) (2003). Classical casesin neuropsychology (Vol. 2). Hove, UK: Psychology Press.

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Dell, G. S., Schwartz, M. F., Martin, N., Saffran, E. M., & Gagnon, D. A. (1997).Lexical access in aphasic and non-aphasic speakers. Psychological Review, 104,801–838.

Freud, S. (1891/1953). On aphasia: A critical study (Trans. and introduction byE. Stengel). London: Image.

Gotts, S. J., & Plaut, D. C. (2004). Connectionist approaches to understanding aphasicperseveration. Seminars in Speech and Language, 25, 323–334.

Green, C. D. (2006). Classics in the history of psychology: “Conditioned reflexes: Aninvestigation of the physiological activity of the cerebral cortex – Lecture XVI:Transition stages between the alert state and complete sleep: hypnotic stages.”Internet resource developed by Christopher D. Green, York University, Toronto,Ontario, Canada.

Harley, T. A. (1993). Connectionist approaches to language disorders. Aphasiology, 7,221–249.

Harley, T. A., & MacAndrew, S. B. G. (1992). Modelling paraphasias in normaland aphasic speech. In Proceedings of the 14th Annual Conference of the CognitiveScience Society (pp. 378–383). Bloomington, Indiana.

Hartley, D. (1746/1959). Various conjectures on the perception, motion, and generationof ideas (Trans. from the Latin by R. E. A. Palmer, and introduction with notesby M. Kallich). Los Angeles, CA: The Augustan Reprint Society, Publication No.77–78. William A. Clark Memorial Library, University of California.

Hartley, D. (1749). Observations on man, his frame, his duties and his expectations.London: S. Richardson.

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from the Russian by Daria Krotova. Ed., with a foreword, by D. E. Tupper).New York: Kluwer Academic/Plenum Publishers.

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ogy, 9 (Mar–Apr).Lecours, A. R. (1982). On neologisms. In J. Mehler, E. Walker, & M. Garrett

(Eds.), Perspectives on mental representations. Hillsdale, NJ: Lawrence ErlbaumAssociates, Inc.

Luria, A. R. (1962/1980). Higher cortical functions in man. New York: Basic Books.Luria, A. R. (1973). The working brain: An introduction to neuropsychology. New York:

Basic Books.Miller, D., & Ellis, A. (1987). Speech and writing errors in “neologistic jargonapha-

sia”: A lexical activation hypothesis. In M. Coltheart, G. Sartori, & R. Job (Eds.),The cognitive neuropsychology of language. Hove, UK: Lawrence Erlbaum Associ-ates Ltd.

Pavlov, I. (1962). I. P. Pavlov: Psychopathology and psychiatry – Selected works (Trans.from the Russian by D. Myshne & S. Belsky. Compiled by Y. Popov & L. Rokhlin).Moscow: Foreign Languages Publishing House.

Ruml, W., Caramazza, A., Capaso, R., & Miceli, G. (2005). Interactivity and continu-ity in normal and aphasic language production. Cognitive Neuropsychology, 22,131–168.


4 The social andneuropsychologicalunderpinnings ofcommunication disorders aftersevere traumatic brain injury

Skye McDonald

Preamble

Chris Code has had a wide and varied research career. While well known forhis research publications, Chis’s role as a mentor is possibly less acknow-ledged. With his innate curiosity, generosity and enthusiasm, Chris hasa remarkable capacity to motivate his colleagues into the pursuit of col-laborative projects. In my case these have led to significant inroads intocommunication research, ongoing collaborations and enduring friendships.Furthermore, although Chris may be best known for his aphasia work, hisinterests have been more wide-ranging than this, delving into other kindsof communication disorders that are characterized less by problems of lan-guage, and more by problems of language use. When Chris Code first arrivedin Australia to take up the inaugural Chair of Communication Sciencesand Disorders at the University of Sydney, he encouraged me to submit areview to Aphasiology, outlining the similarities and differences betweencommunication disorders arising from damage to the frontal lobes of thebrain as opposed to the right hemisphere (McDonald, 1993a). Not longafter, he embarked on a collaboration with Leanne Togher examining com-munication patterns after traumatic brain injury, the result of which hasbeen many innovative and influential published studies. In 1995 Chris initi-ated a meeting in which he proposed that the three of us join forces to pro-duce an edited book entailing a comprehensive overview of the nature ofcommunication disorders after traumatic brain injury from neuropsycho-logical, linguistic, and social orientations. The book (McDonald, Togher,& Code, 1999) had contributions from many of the leading authorities ofthe time, all good friends of Chris’s. It is now a standard text in Psychologyand Speech Pathology departments in over 20 universities across the USA,the UK and Australia. Research has moved on since that time and somefascinating new directions are emerging. It is timely, therefore, that in thistribute to Chris, the following chapter continues on from the themes ofthat text, to review some of the earlier work and to overview more recentinnovations.

Introduction

The notion of communication disorders in people with severe traumaticbrain injury (TBI) has developed significantly over the past few decadesand has been the impetus for a variety of innovative approaches to theway in which such disorders have been conceptualized and subsequentlyassessed. Such approaches were originally stimulated by important obser-vational studies (Levin, Grossman, Rose, & Teasdale, 1979; Thomsen, 1975)that alerted the research community to the unique difficulties that people withTBI experienced when communicating. While aphasic disorders were found,these were clearly apparent in only the minority of cases (estimated between2% and 30%; Heilman, Safran, & Geschwind, 1971; Sarno, 1980; Sarno &Levita, 1986). Far more prevalent were difficulties with communication,including problems of slowness, hesitancy, lack of initiative, reliance on setexpressions, tangentiality, inappropriateness and over-talkativeness (Levinet al., 1979; Thomsen, 1975). These characteristics could not be clearlydefined as aphasia, although some were considered to represent a sub-clinicalaphasic language disorder (e.g., Sarno, 1980; Sarno & Levita, 1986). In theensuing decades, evidence has gradually accrued to suggest that such com-munication disturbances reflect underlying cognitive impairment rather thanlanguage per se. As such, they have represented an unparalleled opportunityto examine the intertwining of language and cognition that is inherent inany act of communication. More recently, the potential role of affect incommunication has begun to be addressed.

Broadly speaking, problems in communication that emerge after traumaticbrain injury have been conceptualized using three theoretical orientations:pragmatics and specifically speech act theory (Searle, 1975); discourse analy-ses, especially systemic functional linguistics (Halliday, 1985); and modelsof social skills (e.g., McFall, 1982). This chapter reviews advances in each ofthese and where possible, considers the neuropsychological underpinnings ofcommunication difficulties as exposed by these approaches, as well as socialand cultural implications.

Conceptualizing communicative ability using pragmatic theory

Pragmatic theory addresses the role that contextual factors play in establish-ing the meanings associated with any given utterance. For example, it isargued that any utterance represents behaviour; that is, a speech act that ismotivated by the desire to have some impact on the listener. Speech acts maybe direct, in that the speaker states what is on his or her mind directly, as in“Please open the window”, or indirect although clearly transparent, as in “Canyou please open the window”, whereby the speaker asks about the listener’sability rather than making a direct request. The motivation to use indirectrather than direct speech acts is often the desire to be polite or to be otherwisethought well of by the listener (Brown & Levinson, 1978). Different forms of

Underpinnings of communication disorders after TBI 43

politeness may be appropriate depending on the familiarity and status of theco-conversant as well as the import of the message. When high degrees ofdiplomacy are required, speech acts may be so indirect as to be opaque intheir meaning (“It is hot in here!”). The idea that the speaker’s attitudetowards the listener motivates their choice of utterance (e.g., the level ofindirectness) suggests that, conversely, their attitude is revealed to the listenerby that choice. Indeed, normal speakers have been shown to be sensitive tothe relative politeness of various surface forms of the same underlyingrequest (“Do you know where Jordan Hall is?” “Could you tell me where Imight find Jordon Hall?”, etc.) which varied systematically with the degree ofindirectness and hesitancy they signalled (Clark & Schunk, 1980).

Several issues arise from this conceptualization of speech acts. First, itsuggests that, in order to be adept at understanding the social nuances oflanguage, listeners must be able to comprehend and use politeness signalssuch as hesitancy. Second, it suggests that there must be some means bywhich opaque indirect speech acts (“It is hot in here!”) are decoded for thespeaker’s intended meaning. Conversely, speakers must have the means toproduce speech acts that convey their intended meanings via inference. Thereis clearly scope to examine pragmatic language competence in people withsevere TBI, as they have often been described as both blunt and insensitivein their language use and concrete and literal in their general responsesand understanding of information (Crosson, 1987; Milton & Wertz, 1986;Prigatano, 1986).

Pragmatic understanding

The comprehension of indirect language after TBI has been the focus of anumber of studies in recent years, with a particular interest in sarcasm andirony. When being sarcastic, the speaker commonly says something that isliterally the reverse, or at least different from, what they mean, such as “Whata great haircut” spoken to suggest the reverse. It is now well established that,in the absence of language deficits, many adults and children with severetraumatic brain injury have great difficulty comprehending irony and sarcasm(Bara, Tirassa, & Zettin, 1997; Channon, Pellijeff, & Rule, 2005; Channon &Watts, 2003; Dennis, Purvis, Barnes, Wilkinson, & Winner, 2001b; McDonald,1992; McDonald & Flanagan, 2004; McDonald, Flanagan, Rollins, & Kinch,2003; McDonald & Pearce, 1996; Turkstra, McDonald, & Kaufmann, 1996).This raises the question as to what deficit is responsible for this difficulty.In 1975 Grice explained the conveyance of sarcasm within his broader con-ceptualization of the communication of conversational inference. Accordingto Grice, conversational inferences are possible due to implicit agreementsbetween speakers regarding the rules of conversation. It is assumed that, first,speakers will cooperate with each other in the act of communication and,second, they will observe certain conventions (maxims) in speech by sayingonly as much as is required, saying this as clearly as possible, and saying only

44 McDonald

what is true and relevant to the context. These commonly shared assumptionscan be exploited to vary the manner in which communication occurs. Ablatant disregard of a conversational maxim will be noticed by the listenerand will cause him or her to reconsider the utterance to make sense of why itwas said in this manner. In doing so, he or she will inevitably take intoaccount other contextual information, and the final interpretation of theconversational meaning will be an inference drawn from both the utteranceand the context in which it was said. By transgressing conversational maxims,speakers can thus communicate indirectly in the service of politeness or othersocial and cultural requirements (Brown & Levinson, 1978). Sarcastic state-ments transgress the maxim of quality (truthfulness). The listener, recogniz-ing from the context that the literal truth of the remark contrasts with knownfacts, but assuming that the speaker said this for a reason (i.e., is attemptingto communicate), reinterprets the statement to make it consistent with thecontext and thus derives the implied meaning, which is frequently opposite tothat asserted.

The process by which the listener comprehends the intended meaning wasconsidered by Grice (1975, 1978) to be similar to that proposed for the inter-pretation of other indirect speech acts (Gordon & Lakoff, 1975; Searle, 1975):(1) the literal meaning is comprehended; (2) some cue indicates this is notsufficient (e.g., the literal meaning is contradicted by the context); (3) inferen-tial rules are implemented in order to derive the intended meaning from theliteral meaning and from the context in which it occurred. Given that themajority of people with TBI do not suffer from basic language impairment,failure to understand sarcasm is unlikely to reflect an inability to compre-hend the literal meaning, hence step 1 is unlikely to be problematic. Con-sequently deficits must reside in other processes, either step 2 or step 3. Inorder to understand how these stages might be affected it is necessary toconsider the nature of neuropsychological disorders following traumaticbrain injury.

Neuropsychological underpinnings of pragmatic understanding

1. Common cognitive deficits arising from traumatic brain injury

While extremely variable, severe traumatic brain injuries typically producelesions concentrated in the frontal and temporal lobes of the brain (Adamset al., 1985; Levin et al., 1987) with attendant diffuse axonal damage (Adams,Doyle, Ford, Gennarelli, Graham, & McLellan, 1989). Consistent with this,disorders of executive functioning (reflecting frontal system dysfunction),disorders of new learning (reflecting temporal and frontal dysfunction), andslowed information processing (reflecting diffuse axonal injury) are welldocumented sequelae of TBI (e.g., Tate, Fenelon, Manning, & Hunter, 1991).

Executive functions are those that mediate and regulate other cognitiveactivities and behaviour in a purposeful and goal directed fashion, and are


often conceptualized as representing either a loss of drive or a loss of control,although both may co-exist in the single individual with frontal systemimpairment (Tate et al., 1991). Disorders of drive will result in apathy andinertia, rigidity, inflexibility and perseveration. Disorders of control lead toimpulsivity, disinhibition and distractiblity. In general, executive dysfunctionsignificantly impairs problem-solving capacity. Individuals may experiencereduced attention and working memory capacity, fail to reason at an abstractlevel (draw inferences) and to develop effective plans, and fail to monitorproblem-solving behaviour effectively or learn from mistakes (Darby &Walsh, 2005). Slowed information processing speed exacerbates these difficul-ties. Executive dysfunction is clearly implicated in the process of decodingindirect speech acts, as outlined by Gordon and Lakoff and others. Theintegration of (verbal) information with the context (step 2) and the applica-tion of inferential rules (step 3) are processes that demand both workingmemory and abstract reasoning.

INFERENTIAL REASONING

The extent to which individuals with TBI experience executive dysfunctionvaries enormously in both severity and kind. Nevertheless, there is a stronglink between frontal injury after TBI and poor inferential reasoning (Dennis,Guger, Roncadin, Barnes, & Schachar, 2001a; Ferstl, Guthke, & von Cramon,2002; MacDonald & Johnson, 2005) and also frontal injury and sarcasmcomprehension (Shamay-Tsoory, Tomer, & Aharon-Peretz, 2005). It is pos-sible, therefore, that pragmatic inferential reasoning represents a particularapplication of generic inferential reasoning skills. In support of this, measuresof general inference making have been linked to poor pragmatic understand-ing in people with TBI (Martin & McDonald, 2005; McDonald, Bornhofen,Shum, Long, Saunders, & Neulinger, 2006).

WORKING MEMORY

At a more refined level, it is interesting to question what particular aspects ofexecutive dysfunction contribute to poor inferential reasoning. Barnes andDennis (2001) have argued that the problem with inferential reasoning may lieless in the computational aspects of inferencing (step 3 above) than in theworking memory demands of integrating discourse meaning and world know-ledge in real time (step 2). By a careful reduction of working memory demands,they demonstrated that deficits in inferential reasoning could be correspond-ingly reduced in children with TBI. Independent studies have also reportedcorrelations between poor working memory capacity and poor inferential rea-soning (Dennis & Barnes, 1990) including the ability to understand sarcasm(Martin & McDonald, 2005; McDonald et al., 2006). Slowed informationprocessing is linked to working memory deficits and has, similarly, beenassociated with poor pragmatic understanding (McDonald et al., 2006).

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FLEXIBILITY

Inferential reasoning deficits are not, however, likely to be completelyexplained by a disorder of working memory. Other executive deficits may alsoplay a role. For example, inflexible, perseverative thinking will impact on theability to resolve pragmatic inference because rigid fixation on the literalmeaning will impede the capacity to understand the implied meaning, evenif working memory demands are low. Empirical evidence for a link betweenpragmatic understanding and measures of flexibility on standard neuro-psychological measures is mixed. A relationship between the ability to under-stand sarcasm and performance on specific concept formation/shift taskshas been found in one study (McDonald & Pearce, 1996) but not in others(Martin & McDonald, 2005; McDonald et al., 2006; Turkstra et al., 1996).A specific measure of rigidity (i.e., perseverative errors) was found to beshare a small amount of variance with scores on a sarcasm task (Martin &McDonald, 2005).

IMPULSIVITY

Impulsivity (poor control) is also likely to impact on inferential reasoningbecause the participant reacts to initial meanings of conversational com-ments. There is even less research regarding this relationship, although acorrelation between sarcasm and impulsivity has been found in the one studyto examine this to date (Channon & Watts, 2003).

NEW LEARNING

The capacity to learn is also likely to affect pragmatic understanding as con-textual information that is relevant to the conversational exchange may haveoccurred some time earlier. There is surprisingly little research that has beenconducted into the effects of poor new learning on pragmatic understandingfollowing TBI (or indeed any clinical population). However, in one studyit has been found that standard measures of new learning (taken from theWechsler Memory Scale III) were correlated with poor understanding ofsarcastic inference (McDonald et al., 2006).

In sum, common cognitive sequelae of severe traumatic brain injury, includ-ing slowed information speed and working memory, rigidity and impulsivity,and poor new learning may each undermine the ability to understandpragmatic inferences. The impact of these executive abilities on inferentialreasoning is consistent with the psycholinguistic account of how indirectspeech acts are processed, suggesting that failure to recognize the conver-sational implicature occurs as a result of a failure to process and integratelanguage and the context in which it occurs in order to reject the literalmeaning for another, inferred, meaning.

Despite this, the three-stage model as advocated by Grice and others has


been criticized as an inadequate explanation for how indirect speech acts aredecoded. For example, some sarcastic comments can be both literally trueand ironic. The mother who states “I love children who keep their roomsclean!” (Gibbs & O’Brien, 1991) may believe this to be true, but may also bespeaking ironically (depending on the state of the bedroom). Sarcasm mayalso be manifested in the excessive politeness of the utterance “Oh I do begyour pardon most exalted one!” As a means to reconcile these issues it hasbeen argued that sarcasm and irony may be better understood in terms of the(in)sincerity of the utterance rather than its truth value (Haverkate, 1990).This suggests that, in order to interpret such utterances, the hearer does notreject the literal meaning at all, but understands it in the context of thespeaker’s attitude. Other kinds of pragmatic inference (e.g., hints) may alsoallude to issues that are on the speaker’s mind rather than in the patentcontext. These considerations suggest a different kind of inference is requiredon the part of the listener; that is, an inference needs to be formed regardingthe speaker’s intentions.

2. Theory of Mind

The capacity to attribute mental states, such as thoughts, beliefs, desires andintentions, is considered pivotal to the ability to make sense of communica-tion. This type of ability is known as having “Theory of Mind” (ToM) andhas been thought to cause the communicative disorders seen in autism. Manyindividuals with high functioning autism or Asperger’s syndrome and normalIQ have fluent and articulate speech but are, nonetheless, pedantic and over-literal (Happé & Frith, 1996), fail to interact normally in conversation, oftentalk at length on obscure or inappropriate topics (Ozonoff & Miller, 1996),have inappropriate non-verbal communication and poor adherence to socialrules (Bowler, 1992). They also fail to appreciate how utterances are usedto convey information in a socially appropriate manner (Surian, Baron-Cohen, & Van der Lely, 1996) and misinterpret both metaphor and irony(Happé, 1993).

Similar deficits in social reasoning and social communication as seen inautism have also been reported in adults with TBI who have been reported asegocentric, self-focused, lacking interest in other people, displaying inappro-priate humour, frequent interruptions, a blunt manner, overly familiar anddisinhibited remarks or advances, and inappropriate levels of self-disclosure(Crosson, 1987; Flanagan et al., 1995; Levin et al., 1979; McDonald,Flanagan, Martin, & Saunders, 2004; McDonald & Pearce, 1998; McDonald& van Sommers, 1992). More particular reasoning deficits that implicateToM have also been found in people with TBI. For example, adults with TBIhave difficulty filling in a questionnaire as though they were somebody else(Spiers, Pouk, & Santoro, 1994), find it difficult to identify the source ofinterpersonal conflict (Kendall, Shum, Halson, Bunning, & Teh, 1997) orotherwise interpret non-verbal interpersonal interactions (Bara, Cutica, &

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Tirassa, 2001; Cicerone & Tanenbaum, 1997). Deficits on explicit ToM taskshave also been found in people with TBI, both adult and child (Bibby &McDonald, 2004; Dennis et al., 2001b; Milders, Fuchs, & Crawford, 2003;Santoro & Spiers, 1994; Stone, Baron-Cohen, & Knight, 1998). Furthermore,ToM performance has been linked to sarcasm comprehension. Specifically,those who experience difficulties understanding second order ToM inferences(i.e., what one person wants another person to believe) are also those mostlikely to experience problems understanding the meaning of sarcasticexchanges (Channon et al., 2005; McDonald & Flanagan, 2004).

It is possible that problems with general inference-making secondary toexecutive deficits in TBI affect both non-social inferences and ToM. Studiesthat have examined this have reported a relationship between the two (Bibby& McDonald, 2004; Martin & McDonald, 2005). Working memory mayalso play a role. For example, a number of studies have shown that youngchildren’s performances on false belief tasks are influenced by workingmemory capacity (Davis & Pratt, 1995; Gordon & Olson, 1998; Hughes,1998; Keenan, 1998), although the evidence suggests that it is not the solecontributing factor (Tager-Flusberg, Sullivan, & Boshart, 1997). In acquiredbrain injury, working memory deficits have been found to contribute topoor ToM performance (Bibby & McDonald, 2004; Stone et al., 1998)although it does not totally explain the difficulties seen (Bibby & McDonald,2004).

Performances on laboratory-based sarcasm tasks and conventional execu-tive tests probably do have some underlying processes in common, but thisdoes not exclude the possibility that inference-making such as ToM alsocalls on specialized systems for processing social information. Indeed, thereis growing speculation (e.g., Adolphs, 2001, 2003; Bechara, 2002) that socialproblem solving may engage distinct neural systems. Social, interpersonalproblems focus on quite different information from the lists of words, numbersand simple figures that so often represent neuropsychological problem-solving tasks. For example, social information emphasizes individual ratherthan categorical differences and is dynamic, changing in response to theobserver (Corrigan & Toomey, 1995). When relationships between executivemeasures and communication tasks requiring ToM are reported, these donot appear to represent exclusive relations. Correlations between pragmaticcomprehension and indices of working memory, information processingspeed, abstract reasoning and inhibition are modest at best (Channon &Watts, 2003; McDonald et al., 2006). Consequently, while there may becommon processes required for social and non-social tasks, depending onthe medium and response requirements (spoken, written, etc.), there mayalso be unique requirements called into play when solving social inferentialtasks such as understanding sarcasm. Whether ToM represents a modularfunction that is differentially impaired in TBI, or a higher order abilityreliant on generic executive skills, it is clearly related to impaired pragmaticunderstanding.


3. Emotion

A potential source of information when interpreting pragmatic inference isthe emotional stance of the speaker. This is especially salient in the recogni-tion of sarcasm, which is almost universally associated with a particularattitude of derision or scorn. Indeed a major criticism of the serial stagemodel of speech act comprehension as advocated by Grice is that such amodel fails to account for the integral role that speaker attitude plays inthe sarcastic retort. Nor does it specify how one inferential meaning isdetermined rather than another (Sperber & Wilson, 1986). As an alternative,Sperber and Wilson postulated a theory of irony within their larger thesisregarding the role of relevance in communication. They argued that everyutterance has at most a single interpretation, which is a product of the listen-er’s search for the relevance the utterance has to the context, and therefore,unlike Grice’s proposition, Sperber and Wilson argued that there are nosuccessive stages of interpretation. According to this position it is the recog-nition of the affective stance of the speaker that alerts the listener to thesarcastic meaning of the comment.

The potential role played by emotion recognition in pragmatic understand-ing in people with TBI needs to be considered. Over the past two decadesthere has been a surge of interest in emotion recognition. There is now aconsiderable body of evidence to suggest that emotion processing deficitsare prevelant in a substantial proportion of adults suffering from severeTBI. People with severe TBI have been found to have difficulties with emo-tion recognition across a range of media including photographs (Croker &McDonald, 2005; Green, Turner, & Thompson, 2004; Jackson & Moffat,1987; Milders et al., 2003; Prigatano & Pribram, 1982; Spell & Frank, 2000),audiotaped remarks (Marquardt, Rios-Brown, Richburg, Seibert, & Cannito,2001; McDonald & Pearce, 1996; Milders et al., 2003; Spell & Frank, 2000)and audiovisual displays (McDonald & Flanagan, 2004; McDonald et al.,2003). Interestingly, there appears to be relatively little association betweenthe ability to recognize emotions and the ability to understand sarcasm(McDonald & Flanagan, 2004; McDonald & Pearce, 1996). Thus, despite thefact that sarcasm is usually associated with affective states, the problemsthat people with TBI have in understanding sarcasm predominantly arisefrom their inability to make inferences, whether these are specifically aboutthe non-literal meanings of the comment or the beliefs and attitudes of thespeaker (McDonald & Flanagan, 2004). This is not to say that emotion def-icits have no role in communication difficulties after TBI. Sarcasm, after all, isonly one example of the rich repertoire of subtle meanings and innuendosavailable to speakers. Emotional cues may well play an important, possiblypivotal, role in many other communication contexts. But there is virtually noresearch in this area to date.

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Pragmatic language production: Politeness theory

Disorders in the production of effective communication have also been exam-ined from a pragmatic theoretical perspective. First, the notion of politenesshas proven useful to elucidate difficulties that arise following TBI in the useof diplomatic language to negotiate social situations. While adults with TBIappear to have an intact repertoire of strategies to moderate the politeness oftheir utterances (McDonald, 1993b) they are less flexible than matched con-trol speakers in their ability to use these across different contexts (Togher &Hand, 1998). When faced with diplomatically challenging communicationtasks such as hinting, or making requests to overcome a perceived reluctanceon the part of the listener, adults with TBI have been found to have difficultyrefraining from stating their desires directly (McDonald, 1993b) and makingcomments that were counter-productive to their desired outcome (McDonald& Pearce, 1998). These studies of politeness suggest that adults with TBI havedifficulties producing language that utilizes pragmatic inference as a means ofcommunication. A study of children with TBI suggests that younger speakersalso have difficulties producing appropriate speech acts to meet contextualconstraints (Dennis & Barnes, 2000).

Neuropsychological underpinnings of politeness useage

According to the pragmatic approaches outlined, certain predictions may bemade concerning the contributions of co-existing cognitive impairments.Specifically, according to politeness theory, speakers need to appraise theirconversational partners in order to determine their social and cultural stand-ing (in relation to the speaker) as well as their particular attitude and sensitiv-ities. Speakers need to have a repertoire of different devices for moderatingthe politeness of their remarks, and they need to choose flexibly betweenthese in order to adapt to different situational and inter-personal contexts.Finally, they need to be able to refrain from making their intentions explicitin the service of diplomacy and saving face. Deficits in flexibility, inhibition,theory of mind judgements and emotion perception are, therefore, likely toimpact on the use of appropriately moderated, polite communication. Failureof restraint, or disinhibition, has already been discussed as a common sequelof frontal lobe injury secondary to TBI. Further, poor performance in theproduction of effective requests has been found to be correlated with indicesof disinhibition on formal neuropsychological tests (McDonald & Pearce,1998) suggesting that more general disorders of control will impact on theability to use language diplomatically. Although inflexibility with politenesshas been documented (Togher & Hand, 1998) there has been no independentresearch linking politeness in discourse to other measures of rigidity inpeople with TBI. Similarly, there has been no research to date that links ToMand emotion recognition deficits to failure to moderate politeness appropri-ately in either the TBI or other clinical populations. So, despite the potential


contribution these deficits make to the ability to use socially appropriatelanguage, we await empirical confirmation of this.

Social knowledge

An additional consideration is the role of social knowledge in communication.The notion that people with TBI have reduced access to social knowledgehas been barely considered to date. Indeed, it is widely believed that peoplewith circumscribed deficits in either memory (learning) or executive functionhave relatively preserved access to knowledge and skills that were acquiredpremorbidly (Darby & Walsh, 2005). However, recent research challengesthis belief in the area of social knowledge. Functional imaging of normalindividuals suggests that ventromedial portions of the frontal lobes, in con-junction with the amygdalae, are involved in judgements concerning “trust-worthiness” based on facial characteristics (Winston, Strange, O’Doherty, &Dolan, 2002). Patients with amygdala damage lose this ability (Adolphs,Tranel, & Damasio, 1998). Other social attributes also appear to be mediatedby frontal–amygdala circuits. For example, personality judgements of extra-version, warmth, neuroticism, reliability and adventurousness that are basedon the movements of light points on a walking figure are impaired in peoplewith focal brain lesions (not TBI), with the relevant cortical region local-ized to the left frontal opercular cortices (Heberlein, Adolphs, Tranel, &Damasio, 2004). Similarly, adults with medial frontal damage appear to beless regulated by implicit gender stereotypes on a reaction time task thanare people with dorsolateral frontal lesions and non-brain-injured controls(Milne & Grafman, 2001). Adults with focal ventromedial frontal lesionsalso appear to be less sensitive to dominance cues (based on gender, age,friendly facial expression and clothing) than adults with brain damage out-side this region or without brain damage at all (Karafin, Tranel, & Adolphs,2004). Finally, preference judgements related to the visual attractiveness offaces activate the ventral striatum (Kampe, Frith, Dolan, & Frith, 2001) andthe orbitofrontal cortex (O’Doherty, Winston, Critchley, Perrett, Burt, &Dolan, 2003), once again suggesting that the frontal, especially medialfrontal, systems of the brain are involved in such social judgements. Theorbitofrontal and medial temporal lobes are specifically vulnerable to theacceleration–deceleration forces of high impact TBI because of their proxim-ity to the bony shelves of the anterior and middle fossa (Darby & Walsh,2005). Consequently, disorders in social appraisal may accompany TBI. Therelationship between such disorders and poor modulation of politeness isunknown.

Pragmatic language production: Grice’s maxims

As another means of utilizing pragmatic theory, the expressive communica-tion of people with TBI has been characterized according to Grice’s maxims.

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Thus, in principle, language production should adhere to the maxims ofquantity, quality, manner and relevance; that is, speakers should be precise,accurate, organized and relevant in their language production. Planneddeviations from these maxims may be effective in order to be diplomatic ordramatic in the right circumstances (as discussed with regard to politeness).Conversely, haphazard failures to adhere to these maxims will result inchaotic, socially unacceptable or ineffective language.

Descriptions of discourse problems following TBI include lack of initia-tive, reliance on set expressions and general impoverishment in the amountand variety of language produced (Chapman et al., 1992; Erlich, 1988;Hartley & Jensen, 1991, 1992) or else over-talkativeness (Hagan, 1984;Milton, Prutting, & Binder, 1984), tangentiality and inappropriateness (e.g.,Prigatano, Roueche, & Fordyce, 1986). These suggest that people with TBIdo have problems adhering to implicit conversational maxims as outlined byGrice.

A number of measures of communication have been developed usingGrice’s maxims as a guide. In a study of two adults with TBI, “blind” ratersevaluated how well two adults with severe TBI were able to explain how toplay a game to a naive listener (i.e., a procedural narrative). Their produc-tions were rated on scales that equated to the maxim of quantity (specifically“repetitiveness” and “amount of detail”) and manner (“clarity, “organization”and “effectiveness”) and compared to those of demographically matchedcontrols (McDonald, 1993b). The blind raters were able to clearly distinguishthe productions of the participants with TBI from the control participants onthese dimensions. A second study of a larger group of adults with TBI con-firmed problems with the demands of the procedural narrative. Typically,they failed to mention essential information, included irrelevant and there-fore misleading information, repeated information and failed to sequenceimportant steps in their correct chronological sequence (McDonald & Pearce,1995). Similar problems with the orderly transfer of information have beenreported when adults with TBI have been presented with different proceduraltasks (Galski, Tompkins, & Johnston, 1998; Prince, Haynes, & Haak, 2002;Snow, Douglas, & Ponsford, 1999). Other discourse genres have also beenanalyzed for characteristics that equate to the maxims of quantity and man-ner. Thus conversational topics have been reported as repetitive (Body &Parker, 2005), and as narratives insufficient or inaccurate with respect to com-municating essential content (Body & Perkins, 1998; Brookshire, Chapman,Song, & Levin, 2000; Snow et al., 1999).

Grice’s maxims have also guided the development of checklists and ques-tionnaires regarding communicative ability for people with TBI (Prutting &Kirchner, 1987). The Latrobe Communication Questionnaire (LCQ; Douglas,O’Flaherty, & Snow, 2000), for example, consists of 30 questions basedon Grice’s maxims, as well as some additional questions tapping partic-ular communication problems arising from cognitive deficits (such as wordretrieval, distractibility and impulsivity). The questionnaire has been found


to be sensitive to discourse difficulties in people with TBI (Douglas, Bracy, &Snow, in press).

Neuropsychological underpinnings of maxim violation

Similar deficits to those that are surmised to underpin pragmatic understand-ing may play a role in disrupting effective expressive communication thatmeets Grice’s maxims. An individual with slow information processing, poorworking memory, rigidity with associated loss of conceptual thought and/ordisinhibition, as well as memory problems is likely to have difficulty planningan effective communication strategy that enables information to be transferredin an orderly and efficient manner.

Interestingly, a factor analytic examination of the LCQ revealed that, whileoriginally conceptualized along the lines of Grice’s maxims, the self-reportquestionaire appeared to cluster somewhat differently (Douglas et al.,in press). Thus two factors seemed to represent “quantity”. On the onehand there appeared to be a constellation reflecting “too much”, suggestingthe impact of disinhibition. On the other there was too little; that is, dysfluen-cies such as word-finding problems, hesitancies and failure to providesufficient information, so suggesting a role for loss of drive and initiative.Another factor that emerged reflected attentional difficulties; that is, losingtrack when conversing and getting sidetracked. Yet another reflected theproblem-solving, planning and monitoring aspect of executive function; thatis, the ability to manage the task of communication, by selecting accurateinformation to meet the listener’s needs, keeping track of main details, puttingideas together logically, self-monitoring, adapting conversational style to dif-ferent situations and knowing when to talk and when to listen. These resultssuggest that Grice’s maxims, while useful for highlighting the role of speakerexpectations in communication, do not map directly onto psychological pro-cesses involved in effective discourse. On the other hand, discourse difficultiesdo appear to correspond to common neuropsychological deficits after TBI.Empirical evidence for a link between discourse errors and independentneuropsychological indices will be discussed in the following sections.

Aspects of social cognition are also likely to have an impact on the abilityto produce effective communication that meets the listener’s needs. The abil-ity to see the situation from the other’s perspective (ToM) is clearly importantin order to formulate utterances that are meaningful for them. So, too, beingable to read the emotional demeanour of others will be important in order to“pitch” one’s utterance at the right level. There has been no research, to date,examining these relationships.

Conceptualizing communication using discourse analysis

Sophisticated linguistic frameworks have been applied in the field of TBI toreveal discourse regularities by close examination of text (either written by

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the participant or transcribed from their speech) produced in response tospecific communication tasks. A number of overviews of discourse analyticapproaches in TBI have been written in recent years (e.g., Coelho, 1999;McDonald, 1998; Togher, Hand, & Code, 1999), which the interested readershould pursue.

In general, discourse analyses are concerned with the discourse as awhole, its continuity, organization and the relation between structure andfunction. Thus discourse analytic methods provide the means to analysemeanings inherent in text across the conventional boundaries of sentencesand clauses. Monologues such as telling a story or relating a procedurehave been useful vehicles for analysing discourse. Two attributes of dis-course that have been a major focus of investigation are efficiency andcoherence.

Efficiency

Efficiency of discourse can be conceptualized as the rate of speech, or other-wise the amount of information imparted in the words produced. Earlyobservational accounts of the communicative characteristics of people withTBI emphasized slow, hesitant, or conversely, over-talkative communicationpatterns. Analyses along the lines of Grice’s notion of “quantity” have simi-lar revealed inefficient information delivery. Analysis of the rate and natureof language produced has confirmed these impressions. Adult and adoles-cent TBI patients have been found to speak more slowly (Hartley & Jensen,1991; Stout, Yorkston, & Pimentel, 2000), produce fewer meaningful words(Brookshire et al., 2000; Chapman et al., 1992; Chapman, Levin, Matejka,Harward, & Kufera, 1995; Hartley & Jensen, 1991), more incomplete,ambiguous or uninterpretable utterances (Body & Perkins, 2004; Hartley &Jensen, 1991; Stout et al., 2000), as well as shorter information units (C-units)(Hartley & Jensen, 1991) and less information overall (Biddle, McCabe, &Bliss, 1996), per minute (Erlich, 1988; Stout et al., 2000) or, alternatively, perinformational unit, expressed as either C-units (Wilson & Proctor, 2002) orT-units; that is, each independent clause plus associated subordinate clauses(Coelho, 2002; Coelho, Grela, Corso, Gamble, & Feinn, 2005) across bothnarrative and procedural discourse tasks.

Coherence

The coherence of discourse relies on the semantic continuity of the text(Patry & Nespoulous, 1990) and may reflect local or global coherence. At a“local” level there must be appropriate relations between adjacent proposi-tions for coherence to occur. At a “global” or macrostructure level there isdevelopment and maintenance of an underlying discourse plan (Coelho,Liles, & Duffy, 1991b; Patry & Nespoulous, 1990). Both notions of coherencehave been investigated in TBI subjects.


1. Local coherence

One measure of local coherence is provided by an estimate of textual cohe-sion created by the interdependence of linguistic items occurring in separateclauses in a text. A cohesive tie occurs wherever one linguistic item relies onanother for its interpretation, via reiteration of semantically linked items “hebrought the bag of apples in, placing the fruit in front of her”, or grammaticallinks such as that formed via pronominal reference “he had an apple but wouldnot share it” (Halliday, 1985; Halliday & Hasan, 1985; Hasan, 1984, 1985).As noted in the earlier section, adults with TBI are frequently insufficientlyinformative, or else overtalkative, as well tangential and disorganized. Thequestion arises, therefore, as to whether they have difficulties developing andmaintaining textual cohesion.

Despite the sophistication in (local) cohesion analyses that has developedin the past 10–15 years, results have produced a somewhat mixed picture. Ingeneral, adults with TBI remain sensitive to the demands of different dis-course requirements, such as procedural versus narrative discourse, varyingthe amount and type of lexicogrammatical cohesion accordingly (Coelho,2002; Davis & Coelho, 2004; Hartley & Jensen, 1991; Liles, Coelho, Duffy, &Zalagens, 1989; Mentis & Prutting, 1987). However, whether the quality ofcohesion is affected is disputed. In some studies TBI speakers have beenfound to use less cohesive ties than non-brain-damaged control subjects(Davis & Coelho, 2004; Hartley & Jensen, 1991; Mentis & Prutting, 1987),but other studies have not found this (e.g., Coelho, 2002; Galski et al., 1998;Hough, 1990; Jordan, Murdoch, & Buttsworth, 1991; Leer & Turkstra, 1999;Wilson & Proctor, 2002). Similarly, there is disagreement as to whether ornot TBI speakers produce more incomplete references where the source forinterpretation of a given linguistic unit is missing or ambiguous (Hartley &Jensen, 1991; Hough & Barrow, 2003; Leer & Turkstra, 1999; Liles et al.,1989; McDonald, 1993b; Mentis & Prutting, 1987).

This variability in study results may reflect the heterogeneity of the popula-tion under examination. After all, not all adults or children with TBI areexpected to have deficits in communication. There may also be differencesin the way in which local coherence is calculated from one study to thenext (see Davis & Coelho, 2004, for further discussion). An importantadditional issue is the need to carefully select the comparison group withrespect to both socioeconomic status (see Snow & Douglas, 2000; Snow,Douglas, & Ponsford, 1997b, for discussion) and premorbid verbal abilitiesfor any kind of discourse examination. Verbal ability and socioeconomicstatus have been clearly shown to influence the ability to produce coherenttext (Brookshire et al., 2000; Coelho, 2002). But, in addition, it is not entirelyclear that linguistic cohesion, thus measured, corresponds to subjectiveimpressions concerning the coherence of the discourse (Glosser & Deser,1991; McDonald, 1993b).

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2. Global coherence

Global coherence has been gauged by identifying the nature and sequenceof the propositional content, propositions being roughly equivalent to apredicate (i.e., verbs, modifiers and connectors) with one or more arguments(Kintsch & van Dijk, 1978; van Dijk & Kintsch, 1983). In story-telling tasksthe propositional structure of TBI discourse has been characterized accord-ing to its organization into episodes defined as sequences of events withspecific beginnings, middles and ends (Brookshire et al., 2000; Chapmanet al., 1992; Jordan et al., 1991; Liles et al., 1989; Mortensen, 2005). Inprocedural narratives, propositions are identified as to whether they representessential, non-essential, ambiguous or irrelevant information, and whetherthey are positioned appropriately according to the sequence of the procedure(Galski et al., 1998; McDonald, 1993b; McDonald & Pearce, 1995; Snow,Douglas, & Ponsford, 1995, 1997b; Turkstra et al., 1996).

Measures of global cohesion have also produced a rather mixed picture.Some studies suggest that, when relating a story, TBI speakers (child andadult) produce as many complete episodes and essential propositions ascontrol speakers (Jordan et al., 1991; Liles et al., 1989; Snow et al., 1997b)while others suggest that they provide fewer episodes, less complex epi-sodes and generally less essential information (Brookshire et al., 2000;Chapman et al., 1992; Coelho, 2002; Coelho, Liles, & Duffy, 1995; Lileset al., 1989).

Arguably, propositional analyses of procedural narratives have been a bitmore consistent. People with TBI, both adult and adolescent, have beenreported to omit essential information, provide a disrupted sequence ofexplanation and include irrelevant and ambiguous material when explaininghow to play a simple game (McDonald, 1993b; McDonald & Pearce, 1995;Turkstra et al., 1996) (although see Snow et al., 1997b). Raters’ impres-sions of procedural texts produced by TBI speakers support notions ofdisrupted global coherence by suggesting they are confused and disorganized(McDonald, 1993b).

Neuropsychological contributions to failed efficiency and coherenceafter TBI

Discourse analytic approaches arise from linguistic rather than psychologicalaccounts of communication. As such, like Grice’s maxims, they would notnecessarily directly address the role of cognitive or neuropsychological abilitiesin discourse production. Even so, the detailed characterization of languagethat such discourse analyses yield suggests a role for several important cogni-tive abilities, some of which have been examined empirically. Clearly wordfinding and word retrieval problems will impede the efficient production ofeffective discourse, and a link between the two has been reported within thechild TBI literature (Brookshire et al., 2000). Second, coherent discourse


requires continuous monitoring of verbal output in order to, for example,ensure that each pronominal reference used has an unambiguous source, andthat ideas are inserted logically and effectively into the language flow. This isan on-line processing task that depends on good working memory capacity.Consistent with this there is empirical evidence for a relationship betweenimpaired working memory and estimates of low efficiency and cohesion(Hartley & Jensen, 1991) and complexity of clauses within T-units (Youse &Coelho, 2005).

The global coherence of text is likely to be affected by executive disordersthat impair the ability to plan and sequence behaviour to meet specifiedgoals. In studies of adults and children with TBI (including mild and severeinjuries) (Brookshire et al., 2000) the amount of essential information pro-vided was associated with measures of conceptual thought, generativityand problem solving (Brookshire et al., 2000; McDonald & Pearce, 1995).Likewise, inability to transform the gist of written text was correlated withpoor problem solving (Chapman et al., 2004). These results strongly suggestthat deficits in the ability to reason flexibly and readily interfere with theorderly transmission of information. Furthermore, certain kinds of tasksmay be more taxing of executive abilities than others. Story generationtasks, for example, wherein the speaker has no template for the structureand flow of information, are likely to be more challenging for those withexecutive disorders than story recall based on prior exposure to an oralor pictorial story. In general, it appears that story generation tasks aremore demanding for adult speakers, be they normal or suffering from TBI(Coelho, 2002).

The ability to relate a narrative in a sensible sequence will also depend onthe ability to recall the events to be narrated, as well as the events of thenarration that have already unfolded. Thus, while story generation tasks maybe more taxing of executive abilities, story recall tasks may rely more onintact memory capacity. Indeed, it appears that various indices of linguisticcohesion and coherence are more affected by poor new learning capacitywhen the task requires someone retelling a previously heard story rather thangenerating one on the basis of a stimulus that remains in front of them(Brookshire et al., 2000; Youse & Coelho, 2005).

Although it is less clear how social cognition (e.g., theory of mind andsocial knowledge) might be relevant to these particular dimensions of dis-course production, emotion may represent a different case. The finding ofLeer and Turkstra (1999) that emotionally salient experiences are related byadolescents with and without TBI (and probably adults although this has notbeen examined) with better informational structure and coherence than lessengaging tasks, raises the question as to whether emotional engagementfacilitates coherent discourse and, if so, how. This is another fascinatingavenue of exploration that awaits empirical research.

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Conversation

The vast bulk of communication occurs as part of an interaction with one ormore other speakers. Furthermore, it is in the social milieu that the problemsexperienced by speakers with TBI become most apparent. Consequently,methodologies are required that can characterize how verbal interactionbetween two or more participants is managed during spontaneous conversa-tion. Broadly speaking, useful approaches for examining conversational skillsfollowing TBI have emerged from either linguistic (conversational) analyses(Patry & Nespoulous, 1990) or behavioural classification based on models ofsocial skills (McFall, 1982).

1. Linguistic approaches to analysing conversation

Using a variety of linguistic approaches it has been found that TBI speakerselicit greater numbers of questions and prompts from their partners (Coelho,Liles, & Duffy, 1991a; Godfrey, Knight, Marsh, Monory, & Bishara, 1989).They have been rated as having poor topic maintenance (Drummond & Boss,2004; Erlich, 1988; Milton et al., 1984), poor initiation (Drummond & Boss,2004; Ehrlich & Barry, 1989) and providing information in an inefficient anddisorganized manner (Mentis & Prutting, 1987; Snow, Douglas, & Ponsford,1997a, 1998).

A particular theoretical approach that has been applied to interactivediscourse in TBI has been Systemic Functional Linguistics (SFL). SFL is atheoretical approach developed by Halliday (1985) that addresses the relation-ship between the purpose and context of communication and its structure.According to this approach there are several levels of meanings within anydiscourse. Ideational meanings reflect the nature of the social interaction(shopping enquiry, social chit-chat, etc.) and are apparent in the vocabularyof the interaction. Interpersonal meanings reflect the nature of the socialrelationship between the speakers such as familiarity, power, and so on, andare realized in the choice of speech act. Thus speakers who have higher statusmay hold (and impart) more information, be in a position to make requestsof their conversational partner and be able to be more direct in their com-munication (i.e., be less reliant on indirect politeness strategies). Finally, thereare textual characteristics, that is, the connectedness of the discourse thatreflects the mode of the language (e.g., spoken versus written). Cohesionanalyses, for example, are based on Halliday and Hasan’s notion of textualcoherence (Hasan, 1985). SFL, particularly as it pertains to interpersonalmeanings, has been useful for examining conversation because it takes intoaccount the discourse of the speaker with TBI in relation to their interlocutoras well as how that interlocutor behaves towards the speaker with TBI.

Using this approach some similar patterns of discourse production to thatalready described have been revealed. For example, people with TBI tendto provide more information, including inappropriate information, to their


conversational partner (Togher, Hand, & Code, 1997a, 1997b). But of poten-tially greater import, analyses have emphasized the role that conversationalpartners have in influencing the opportunities and choices that TBI speakershave when conversing. In general, it has been revealed that conversationalpartners often converse with speakers identified as having a TBI in a mannerthat has the effect of disempowering them. Thus, compared to carefullymatched control speakers, people with TBI were asked more questions forwhich the speaker already knew the answer, were subjected to repeated check-ing of the veracity of their responses, were given more information and wereasked for less. (Togher et al., 1997a, 1997b). Togher and colleagues alsodemonstrated that, placed in an empowering situation, such as educatingschool children on the circumstances of their injury, speakers with TBI con-versed in a manner that was indistinguishable from control speakers (withspinal injuries) (Togher, 2000; Togher & Hand, 1999).

2. Behavioural approaches to conversation

Finally, communication disorders following TBI have been addressed fromwithin the rubric of social skills (McFall, 1982). Notions of social skills haveemerged primarily from a behavioural rather than a linguistic analysis.Checklists and rating scales based on this framework have ranged in focusfrom global measures of verbal and non-verbal behaviour such as “socialperformance” (Newton & Johnson, 1985; Spence, Godfrey, Knight, &Bishara, 1993) to intermediary measures such as “partner-directed behaviour”(Flanagan, McDonald, & Togher, 1995; McDonald et al., 2004) and “turn-taking” (Drummond & Boss, 2004), to measures of specific and discreteattributes of communication such as “frequency of questions” (Godfreyet al., 1989). Using this behavioural approach, severe TBI speakers have beenfound to be generally less interesting, less rewarding and more effortful tointeract with than control speakers (Bond & Godfrey, 1997; Godfrey, Knight,& Bishara, 1991). They are reported to elicit higher rates of verbal facilitationfrom their conversational partner (Godfrey et al., 1989) and to be generallyunskilled in their response to their partner’s questions (Spence et al., 1993).They have also been noted to be egocentric in their discussion and fail toactively involve their conversational partner, such as by asking questions orsupporting them with the use of verbal reinforcers (Flanagan et al., 1995;Marsh & Knight, 1991; McDonald et al., 2004).

Neuropsychological underpinnings of social skills

Theoretical frameworks of social skills typically encompass three basic cat-egories of social skills: (1) Encoding; that is, execution of behaviour includingspeech content, paralinguistic elements (e.g., voice volume), and non-verbalbehaviour (e.g., facial expression), (2) decoding components such as attention,perception and interpretation of social cues, and “social intelligence”; that is,

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the identification of problems and/or goals, and (3) decision making; that is,the generation of alternative plans of action and decisions concerning these(McFall, 1982). These relate very clearly to neuropsychological deficits thathave already been discussed in relation to communication disturbancesafter TBI as evaluated using other models. Thus executive dyscontrol andimpulsivity will impact on the ability to formulate appropriate behavioural(including verbal) responses, and to monitor and regulate behavioural out-put. Attention to, processing and interpretation of social signals will beaffected by deficits in emotion recognition, theory of mind, social knowledgeand ability to think at a conceptual level and plan. Finally, executive dys-function will also impede the ability to generate alternate plans and decisions.Once again, there has been little research to empirically test these hypotheticalrelationships.

Conclusions

In conclusion, research into communication disorders after traumatic braininjury has advanced significantly since the early observational studies of the1970s. The use of linguistic theoretical approaches, such as pragmatics andsystemic functional linguistics, as well as behavioural approaches emanatingfrom a social skills perspective, has provided a sensitive means to elucidatedisorders of communication. Although primary disorders of language arerelatively infrequent after brain injury, it is apparent that for many peoplewith severe TBI the task of communicating with others in a way that is clearand effective, and sensitive to their conversational partner’s needs, is oftencompromised.

The analytic approaches discussed in this chapter emphasize the socialnature of communication. As such they represent an important advance overthe “context-free” assessments of standard language batteries of the past.Social theories of communication expand notions of communicative com-petence to encompass the ability to use language in context and all that thisentails. In doing so they have been shown to be sensitive to subtle but per-vasive disorders of communication wherein basic language abilities remainintact but the ability to apply these sensitively and adaptively is impaired.

Socially orientated theoretical approaches have also heightened awarenessof cultural differences and refined our notions of normality. For example,research by Togher, Snow, Body and colleagues (e.g., Body & Perkins, 1998;Snow et al., 1995; Snow & Douglas, 2000; Togher, 2000; Togher & Hand,1999) highlights the importance of cohort effects in what is considered normaland effective conversational style. Studies such as these seriously challengethe assumption that professionally trained therapists can judge the com-petence of their clients’ communication skills by their own interactions(Ylvisaker, 2000). Socially oriented theories of language have provided themeans to evaluate regularities in language use that may transcend con-ventional notions of “proper” talk and may vary from one context to the


next, from one cohort to the next. They also reveal how important conversa-tional partners are in terms of providing the speaker with TBI with adequateand/or normal opportunities to demonstrate communicative competence.

Importantly, socially oriented theories of communication have also pro-vided the means to consider how cognitive and emotional abilities interactwith the language system to produce normal communicative ability. In thecase of speech act theory (pragmatics), a psychologically based account ofhow indirect speech acts are understood emerged in the 1970s. This providedthe impetus for a number of studies aimed at evaluating the model’s veracityin explaining disorders in the comprehension of irony relative to other com-peting notions (e.g., relevance theory, Sperber & Wilson, 1986). It has alsopointed to a variety of potential mechanisms that align with our growingunderstanding of neuropsychological impairments commonly seen after trau-matic brain injury. Other linguistic approaches have been less concerned withthe psychological mechanisms underlying discourse ability but have, nonethe-less, characterized communication disturbances in sufficient detail to enableclear speculation as to the underlying neuropsychological cause.

As a result of these different approaches it is possible to hypothesize aboutsystematic relationships between a variety of neuropsychological impairmentsand communicative ability and to test these empirically. Thus deficits in atten-tion, working memory, information processing speed and learning have eachbeen found to contribute to communication disorders as operationalized bythese different theoretical frameworks. So too, problems in conceptual rea-soning and problem solving as well as the ability to monitor and regulatebehavioural responses have been clearly implicated in both the ability tounderstand subtle communicative meanings and the ability to produce socialskilled discourse.

Despite this, not all studies have been able to demonstrate significant asso-ciations between aspects of discourse and performance on standard neuro-psychological tests, even when the constructs are clearly relevant (Brookshireet al., 2000; McDonald & Pearce, 1995; Turkstra et al., 1996). It is quitepossible that discourse tasks represent ecologically valid tasks that are com-plex and unstructured relative to standard neuropsychological measures. Theecological validity of standard tests has often been criticized (Silver, 2000). Itis also possible that discourse falls into the domain of social informationprocessing and is therefore more relevantly compared to performance on othersocial problem-solving tasks. There are, however, few standard instruments inthis domain – an issue that is increasingly recognized. But, in addition, recentadvances in our understanding of social cognition identify entirely differentneuropsychological constructs that may be highly relevant to communica-tion. The possibility that emotion recognition, theory of mind judgementsand social attitudes are uniquely represented in the frontal systems of thebrain and processed differently from non-social information opens a wholenew avenue of research. The prevalence of psychosocial dysfunction follow-ing severe TBI is well known. It is becoming increasingly apparent that many

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people with TBI experience various deficits in social information processing.New advances in our understanding of social cognition and how this becomesdisordered following TBI, combined with sophisticated developments incharacterizing discourse and communication as detailed in this chapter, thusprovide us with exciting new directions for characterizing the neuropsychologyof communication difficulties seen following brain injury.

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5 Social validation of recoveryin aphasia

Leonard L. LaPointe andKerry L. Lenius

Introduction

Social validation of an outcome is achieved by assessing the social signifi-cance of the goals, the social appropriateness of the procedures, and thesocial importance of the behavioral change (Kazdin, 1977; Wolf, 1978). Thisis essential if we are to generate meaningful conclusions regarding rehabilita-tion therapy. This chapter provides insights into the origins of social valid-ation of change in the literature, and the application of this concept inaphasia therapy today. An excerpt from Talking about aphasia (Parr, Byng,Gilpin, & Ireland, 1997, p. 82) illustrates the frustration experienced by aperson with aphasia while working on treatment goals. It aptly speaks to theneed for social validation of therapeutic targets and strategies:

Weekly group therapy involved quizzes and language games. At the timehe [Vincent, the person with aphasia] was consumed with a desire toreturn to work and was extremely anxious about his financial and homesituation. While not being at all critical, Vincent points out that theweekly activities in speech and language therapy did not touch on theseissues: “I personally had got a bit bored – I learned a lot of things that Ididn’t know when I had the stroke, like the history of the Royals – Thespeech therapy didn’t give me information about help. The help they giveme is to try and get better.” Vincent eventually left the group, but stays intouch with some of the people he met there.

In this example, the consumer was less than satisfied with the services hereceived. If Vincent’s therapist had simply asked him, “What would you liketo work toward in therapy? What is important to you?” Vincent’s statementmight have gone something like this:

Working in group therapy really helped me learn to socialize withothers in a new way. I learned communication skills that I really neededto try to return to work. Despite the aphasia, I was able to use words,gestures, and drawings to make myself understood. This prepared me

for the communicative interactions I would be facing when I returnedhome.

Social validation of the goals and outcomes of treatment can provide theframework for planning and implementing intervention that is salient andrelevant to each of the individuals with whom we work.

Emergence of social validity in the literature

As early as the 1950s social validation was present in a meager number ofarticles in medicine, psychotherapy, and business. It wasn’t until the 1970sthat the term was more clearly defined by behavioral therapists (Kazdin,1977; Wolf, 1978). Wolf, the first editor of the Journal of Applied BehaviorAnalysis (JABA), provided an entertaining description of the process and theperceived reluctance of the journal in coming to terms with the need toincorporate social importance with subjective assessments of social validity.He provided a delicate example of the need for this type of assessmentby describing a manuscript submitted by Jones and Azrin (1969), whoresearched synchronized speech to reduce stuttering. Despite the reduction ofthe stuttering behavior, the speech sounded artificial. Jones and Azrin dealtwith this problem by having judges rate the speech on the dimension ofnaturalness. Thus the researchers used social validation by having ratersassess the social appropriateness of speech. If social validation was ignoredand clients who stuttered were all instructed to use a regular beat pattern forspeech, the stuttering might be extinguished; but the stigma of “abnormal”speech would remain.

So what? This is the basis for testing social validity. If the changes wemake in therapy are not impacting our clients at home and in the com-munity, did we provide adequate service? If scores on standardized testsincrease one standard deviation but consumers are unable to perceive achange, did we make a difference? When does a difference make a differenceis an important question about any attempt to intervene and facilitate achange in behavior.

Who cares? If we as professionals only use our own expertise and experi-ence in setting up criteria for success, thereby neglecting the values and opin-ions of the other experts involved (the clients), we are implying that consumeropinions do not matter. This can be a serious flaw in the successful realizationof treatment goals. Wolf (1978, p. 210) states that “Behavioral treatmentprograms are designed to help someone with a problem. Whether or not theprogram is helpful can be evaluated only by the consumer.” This may be alittle overstated, as the opinions of professionals and others in the com-munity might indeed contribute to the determination of adequate outcomes,but certainly the opinion of the consumer should be paramount. Wolf alsoposes questions that might well be retained by every clinician during thephases and stages of treatment.

Social validation of recovery in aphasia 73

1 Are the specific behavioral goals that have been generated really whatsociety wants?

2 Does the end justify the means? That is, do the participants, caregiversand other consumers consider the treatment procedure acceptable?

3 Are the consumers satisfied with the results? This includes all results,even unpredicted ones.

Despite this growl by Wolf, trends in the use of social validity in behavioralmodification research remained flat and low. Kennedy (1992) reviewedarticles for inclusion of social validity in JABA from 1968 to 1990 and thejournal Behavior Modification from 1977 to 1990. His graphs show a sluggishtrend toward increased use of social validity. Despite improvement, by 1990social validation procedures were reported in only about 20 percent of thearticles surveyed.

Implementing socially valid treatment

Three main targets exist for the appropriate integration of social validationprocedures in aphasia treatment. These are:

• developing socially valid goals• using valid methods, and• validating the outcomes.

Each of these areas needs to be addressed in order to achieve the result ofproviding treatment that is appropriate, meaningful, and effective in enablingsuccessful communication.

Socially valid goals

Traditionally a clinician may use a standardized test such as the WesternAphasia Battery (WAB) (Kertesz, 1982) to determine areas of impairment,select therapy goals, and possibly to document change. This focus on impair-ment is consistent with traditional approaches to disease characteristic ofthe medical model, but may not be the most efficient way to determinesocially relevant goals. The seemingly ever-changing terminology of theWorld Health Organization is being integrated into models of aphasia treat-ment (Rogers, Alarcon, & Olswang, 1999; Threats, 2002), but the conceptsinvolved are important. Changes in social activities and participation areemerging as more relevant goals of treatment and are eroding the stone faceof impairment-based approaches to intervention. The Life ParticipationApproach to Aphasia is having an impact on approaches to aphasia interven-tion and shaping the very core of the aphasia treatment model (LPAA ProjectGroup, 2000). Most standardized tests of aphasia are predominantlyimpairment-based. Recently, some efforts have been made to incorporate the

74 LaPointe and Lenius

social model of aphasia into assessment procedures. The latest edition ofEisenson’s classic Examining for aphasia (LaPointe, 2006) incorporates prin-ciples of the social model of aphasia into the assessment in an effort to guideclinicians in the quest to develop relevant participation-based treatmentgoals. This approach does not suggest that we discard the baby with thebathwater, as impairments and cognitive-linguistic processes also may need tobe targeted for treatment; but for far too long it has been impairment ornothing, with little emphasis on reintegration of the person into an active,participating milieu.

The traditional biographic standardized test interview needs to be sup-plemented or indeed replaced with specific information gathering as to thegoals, values, hobbies, likes, dislikes, hopes, fears, anticipations, and motiv-ations of each unique individual for whom we are planning treatment. Thiswill assist the informed clinician with planning, delivering, and evaluatingservices (Pound, Parr, & Duchan, 2001). Lubinski (2001), Elman (2005),Simmons-Mackie (2001), Lyon and Shadden (2001), LaPointe (2002), andWorrall and her associates (Cruice, Worrall, Hickson, & Murison, 2005)all provide social model flesh and humanity to the skeleton of treatmentplanning in aphasia. This entire movement, of course, harkens back to thebirth and upbringing of language in context and person-centered conceptsof aphasia intervention nurtured and influenced so thoroughly by AudreyHolland (Holland, 1982a, 1982b).

Interview questions appropriate to determining and creating socially rele-vant and valid treatment goals can be gleaned, inferred, or directly createdfrom all of the above sources and particularly from Lubinski (2001) andSimmons-Mackie (2001), and Elman (2005). The interview allows the clientand any others present to express what life was like before the onset of apha-sia, how life is impacted now, and what areas of communication breakdowngenerate the most stress on relationships.

In an effort to define socially valid aphasia therapy goals Ross and Wertz(2003) set out to determine the difference in quality of life as rated by peoplewith and without aphasia. Two groups (people with aphasia for at leastsix months and non-brain-damaged individuals) completed quality of lifemeasures. The greatest difference between the groups was evident in areas ofactivities of daily living, opportunities to acquire new information and skills,social support, mobility, and sexual activity. Of course it is imperative tocustomize treatment planning and weave specific treatment goals around theidiosyncracies of each person, but this study shows support for languagetherapy focusing on enhancing communication for specific functional situ-ations and expanding participation in society. Sometimes we tend to err onthe side of overzealous treatment planning and implementation. One of theauthors of this chapter (LLL) remembers well an early treatment planningfaux pas when a full court press of intervention (twice per day; intensivereading comprehension strategies integrated into the treatment schedule)was probably not in keeping with the personal goals of the person with


aphasia. After two weeks of rather intensive treatment, I remember hiswords well:

Doc, I thank you for all you’re trying to do here, but, you know, I neverhave completely read through a whole book. I don’t really care if I everdo. I just want to go up on the St. Johns River and live with my brother inthe trailer there, and maybe sit out on the dock and fish a little. I knowyou’re trying real hard Doc, and I appreciate it, but I really don’t care if Ican’t read very good.

If the treatment goals of the person with aphasia are not built into thetreatment plan, misguided expenditures of time, effort, and money can be theresult. This clinical lesson made it abundantly clear that precise activity andparticipation therapy must be harmonious with the expectations and needs ofthe person in therapy. Sometimes the people with whom we work are contentto fish or plant cumquats.

Socially valid methods

In addition to determining goals that are vital to clients’ lives it is imperativeto ensure the methods used to achieve the outcome are acceptable. Sociallyvalid procedures can be facilitated by verifying that the materials being usedare consistent with the patient’s expectations. An example of this is reportedby Lustig and Tompkins (2002, p. 510), They state: “LG was presented with alist of possible conversation topics prior to the study and her preferences weretaken into account when the final stimulus sets were created.”

By allowing the person with aphasia to aid in the selection of stimuli thatare most relevant to him or her, we facilitate participation and ownership inthe therapy. Validating the importance of the materials to each person canonly help motivation and participation in rehabilitation. A fly fishermanprobably would not respond as well to retelling the story of Cinderella as tocreating instructions on how to match the insect hatch. A cake decorator maybe more motivated to work on divorce cake designs than on conjugating theverb “to be.” Materials need to be not only age appropriate but personappropriate.

Treatment procedures are another important consideration in generatingsocially valid intervention. Are the selected treatment procedures within thesocial or cultural norms or expectations of the person with aphasia? Workingon paralinguistic nuances such as improving conversational eye contact maynot be within the cultural norms of a young adult stroke victim who happensto be a Navajo American Indian. In the Navajo culture direct eye contact,particularly with an authority figure or older person, is considered bad man-ners. Naming the edible cuts of meat from a pig may not be a palatableactivity for a Muslim or Orthodox Jew. Writing the stanzas of “What a friendwe have in Jesus,” may be less appropriate for a Sri Lankan Buddhist than a


retired Baptist preacher from Dothan, Alabama. Reading statistics on com-parative handgun violence in America and Australia may not sit well with aformer officer of the National Rifle Association.

Acceptable interventions that are socially appropriate also may take lesstime, are less unsettling, have fewer adverse or apathetic reactions, and arecost efficient according to some research (Reimers, Wacker, Cooper, &DeRaad, 1992). Consumers of aphasia therapy have voiced dissatisfactionwith treatment procedures that are not client centered or age appropriate.Clowns, balloons, circus animals, fluffy puppies and kittens should be ban-ished to the pediatric wards, unless of course one is working with a formerclown or fluffy puppy lover.

We also need to explain why we are doing certain assessments or workingon certain communication tasks. Explaining that we are evaluating coordin-ation and control of the speech articulators (lips, front of the tongue, back ofthe tongue) fosters understanding; as opposed to the unexplained request tosay “pa-ta-ka” over and over. Sometimes we assume too much and our clientswonder what we could possibly learn from the requests “smile; stick out yourtongue; wiggle it from side to side; point to these pictures.” Possible clientreactions are illustrated in the following observation:

When asked about what speech and language therapy entails, peoplewho have aphasia describe a number of different activities . . . therapistsseem to be poor at conveying information about what is being done intherapy, and why. As a result, to some aphasic people the rituals oftherapy seem demeaning and made them feel stupid. Many people pointout that therapy can feel like returning to the classroom. The associ-ation with school can sometimes be reinforced by the manner of thetherapist.

(Parr et al., 1997, p. 78)

A prime example of the need to assure the selection and use of sociallyvalid procedures is clearly demonstrated by consumers of augmentativealternative communication (AAC). Lasker and Beukelman (1999) measuredpeers’ perceptions of storytelling by an adult with aphasia to investigate ifpeers accepted an augmentative alternative communication device. In thisstudy peers ranked the AAC digitized speech to be preferred over naturalspeech. However, this finding is not always the case. Shadden (2005) under-scores this point when describing a stroke survivor with limited verbal output(only able to say “yes” and “no”) who was opposed to augmentative forms ofcommunication. Through a support group he was encouraged to use a totalcommunication approach (gestures, drawings, writing). Eventually he beganusing a DynaVox® and was successfully communicating with everyone excepthis wife. Despite the potential this man had for communicating with thedevice, no gains were made in communicating with his spouse. This high-lights the importance of therapeutic relevance to all the principals in the


constellation of treatment. If one of the principals is not buying into theprocedures, the potential for improvement may be compromised.

Socially valid outcome measures

When measuring treatment effect, one of the pioneers of socially relevantintervention, Kazdin (1977), advocated two criteria by which to determine iftreatment gains are socially valid: social comparison and consumer evaluation.Social comparison occurs when treatment is considered to be improved onlywhen the target behavior is considered to be within “normal” functioning.This is considered one form of social validation since the rest of societyperforms in the same manner as the person with the now “normally” func-tioning behavior, therefore it is presumed that society would find this behavioracceptable.

The drawbacks to using social comparison as a criterion of social validityare fairly apparent. It is, expensive, time consuming, and intuitively ludicrousto be required to gather social norms for every specific treatment target.However, once norms have been established, clear criteria can be set withoutthe obstacles posed by subjective measures. Goldstein (1990) makes a ger-mane point by arguing that social comparison neglects to account for pro-found differences among clients prior to treatment, and that many clients andsignificant others may be satisfied with smaller gains that still fall short of“normal.” Wells (1999, p. 912) asks, “What is the value of such an objectiveassessment when it is so unconfirmed by the perceptions of patients andcarers?” Another problem is that social comparison only measures thechange in level of impairment without considering changes in the ability tocope or compensate for problems. These issues may be why social comparisonis not used as often as consumer evaluations. Kennedy (1992) reported that91 percent of the JABA articles in 1983 that reported on social validityused subjective measures (i.e., consumer evaluation) and only 9 percent usednormative comparison.

Consumer evaluations

These are the most common form of social validity used in determiningtreatment outcomes (Kennedy, 1992). Consumer evaluations typically takethe form of rating scales of the person in treatment and/or caregiver. Thesemay include quality of life (QOL) ratings, informal interviewing (which mayinclude any of the principals involved), or specific judgments when compar-ing pre- to post-treatment abilities (i.e., comparing videotaped behaviors orwriting samples). Sometimes, however, “anecdotal reports of client or familyopinions are often not valued as ‘measures’ because they are considered sub-jective, unreliable, or unprofessional” (Simmons-Mackie & Damico, 2001,p. 22). In determining the social validation of treatment outcomes, manyclinicians, however, value the opinions of the principals involved as much as


they value behavioral measures. Many researchers and clinicians use objectivebehavioral measures as primary dependent measures, and social validation assecondary measures of treatment outcomes (Schwartz & Baer, 1991). A clin-ical fact of life is that some significant changes in behavioral measures maynot signal a corresponding change as to the value of that change. When doesa difference make a difference? That nagging outcome question needs to beaddressed; and that is at the heart of social validation.

Schlosser (1999) separates consumer reported outcomes into four groups:proximal, instrumental, intermediate, and distal. Proximal outcomes are dir-ectly related to the intervention, instrumental outcomes measure generaliza-tion, intermediate outcomes rate change in QOL, and distal outcomes ratechanges on a larger level (i.e., national outcomes). Thus, when working on theability to communicate information in conversation and measuring proximaloutcomes, one could ask consumers, “How successful was Mr. R. at gettinghis message across?” If you choose to measure intermediate outcomes youcould give a general QOL or well-being questionnaire to determine if thetreatment improved psychosocial wellness. Outcomes also can be separatedby activity limitation (previously referred to as disability in earlier WHOmodels) and participation restriction (previously termed handicap). Forinstance, if you plan to improve a person’s communicative interactions with awide range of people, you would be attempting to reduce the participationrestriction; and one option for a satisfaction measure would be to use theCommunication Readiness and Use Index (CRUI) (Lyon et al., 1997) withany of the relevant principals involved.

Multiple approaches may be used to measure consumer opinions. Oneoption is forced choice (improved/not improved); another would be to pro-vide a Likert scale (5 or 7 point), or use of a visual analogue scale (i.e.,Communicative Effectiveness Index, CETI) (Lomas, Pickard, Bester, Elbard,Finlayson, & Zoghaib, 1989). Additionally, consumer opinions could bemeasured by having raters view video clips of the targeted behavior beforeand after treatment, and rate the behavior that is more effective.

In humor, fruit-picking, and romance, timing is everything. Add successfultherapy to the list. Perceptive clinicians begin with the end in mind. We needto plan ahead by determining the type of social validation measure that maybe appropriate for the person enrolled in treatment. If a clinician plans toobtain ratings of pre/post ability one may want to videotape baseline abilitybefore initiating treatment. Post-therapy ratings may be of limited value ifpre-therapy behaviors are lost in the fog of history. Even if one does notintend to use video comparisons, it may be useful to have the person withaphasia and important others complete ratings of QOL or communicationabilities (i.e., CETI) when treatment begins. Simmons-Mackie (2001) pro-vides a comprehensive list of socially valid assessment tools to obtainstakeholder perspectives.


The good, the bad, and the ugly

Although consumer evaluations are extremely useful to gain insight into con-sumers’ perspectives, this is not a perfect science and not without its prob-lems. Many of the subjective rating scales are inconsistent across studies.Validity and reliability of the scales are often unreported, and without thebasics of adherence to psychometric principles, one runs the risk of pro-ducing measurements that have no real meaning. Schwartz and Baer (1991)provide advice on how to administer questionnaires to maximize validity andreliability. One common concern with subjective ratings is the risk of falsepositives. This occurs when people expect treatment to work, so they rate postmeasures more favorably. The placebo effect can intrude when expectationsof improvement are presumed. This may not always be a bad thing, but itmakes it difficult to attribute change to treatment procedures. One way toattempt to minimize this false positive bias is to counterbalance or “blind”the presentation of pre- and post-treatment samples when possible. Also,beware of potential social invalidity. Social invalidity occurs when consumersdisapprove of some component of the program and are not direct or honestwith their evaluations. Truthful opinions and responses that are unbiased bythe desire to please or meet perceived expectations of an authority figuremust be the goal as we gather data via our consumer opinion measures. Weare not the first to draw attention to these dilemmas; others have voicedsimilar apprehensions (Goldstein, 1990; Tompkins, 1994).

Another issue that is specific to communication impairments in aphasia isthe concern that persons with aphasia may experience difficulty comprehend-ing questions or communicating their perceptions. It is acceptable, and evenrecommended, to provide any needed assistance to help people with aphasiacomplete perception ratings. This is a far superior tactic compared to pushingtheir opinions aside, and so overlooking the values of the person at the centerof the illness. Worrall and Holland (2003) suggest several accommodationssuch as changing the format (interview instead of self-completed question-naire); simplifying questions and responses (use simple language and allowthe person with aphasia to answer in yes/no format); adding visual cues (pic-tographs); and prompting and personalizing questions. We can benefit fromthe work of our colleagues in Canada, Australia, and the United Kingdom ingenerating and promoting “aphasia friendly” materials, and these can be usedin harvesting valid opinions of treatment outcomes as well. An example of apictorial QOL rating scale for people with aphasia is described by Engell,Hütter, Willmes, and Huber (2003).

Maintenance of social validation

Documenting maintenance has been an ongoing struggle in rehabilitationefforts and it should not be overlooked in social validation measures. If con-sumers report treatment has improved aspects of QOL at termination of the


study, yet two months later QOL has trickled back to the original level, wastreatment effective? This is a concern voiced by Kennedy (2002) as he arguesto incorporate maintenance as part of social validation before considering atreatment to be effective.

Stakeholders

Indeed, it appears that social validity may be measured only if directconsumers (persons receiving services), indirect consumers (such as thegeneral public who may benefit indirectly from the service), and serviceproviders share in the evaluation of services.

(Kozleski & Sands, 1992, p. 120)

The stakeholders are the principals involved in aphasia treatment, and theprincipals can be defined narrowly or as broadly as the community or society.These include the person with aphasia; spouses and caregivers; immediateand extended family members; acquaintances; friends and enemies; referringand co-working healthcare professionals; and third party payers. Maybe evenpets. If a tail wags when a dog’s name is successfully emitted, that may be aform of cross-species social validation. Nearly everyone is affected somehow,either directly or indirectly, by the services we provide. It is difficult to deter-mine the consequences of aphasia if we do not have a full appreciation ofhow the stakeholders perceive the consequences (Simmons-Mackie, 2001).Schwartz and Baer (1991) divide these consumers into four categories:direct, indirect, members of the immediate community, and members of theextended community.

• Direct consumers are the primary stakeholders, the recipients of theintervention (i.e., the person with aphasia; or, when conducting caregivertraining, the caregiver). This is a crucial target for social validity sinceunderstanding our clients’ perspectives of their own improvement ontasks or improved quality of life is crucial to determining the effective-ness and efficacy of our interventions. Direct consumers are the truefocus of social validation of our services. They provide insight anddirect information into their values; impressions of their well-being; andthe impact of aphasia on their lives, expectations, hopes, and dreams(Worrall & Holland, 2003).

• Indirect consumers are strongly affected by the intervention but are notthe direct consumers. Indirect consumers include spouse or spouses (ifpolygamous), life partners, children, or close friends or relatives of thedirect consumer.

• Members of the immediate community interact with the direct andindirect consumers on a regular basis (teacher, boss, co-worker, neighbor,grocery store clerk, massage therapist, bartender).

• Members of the extended community who do not interact with direct or


indirect consumers but may be affected by the status of the direct con-sumer (other interventionists or professionals; third party payers; journalreviewers; taxpayers; newspaper writers; bass guitar players from Exeter;hillbillys; savants; the average man or woman on the street; and so on).

Different consumers have different viewpoints, expectations, and internalcriteria for acceptability of outcomes. The measurement of quality of life isone area where this has been apparent. QOL is defined by the World HealthOrganization (WHO) as “an individual’s perceptions of their position in lifein the context of the culture and value systems in which they live and inrelation to their goals, expectations, standards and concerns” (World HealthOrganization, 1996, p. 5). QOL is an elusive measure of life satisfaction, andit may not be totally accurate or valid for a healthcare professional (nurse,doctor, or clinician) to judge another person’s quality of life. To do so may befraught with measurement pitfalls (LaPointe, 1999). This was reinforced in arecent study comparing quality of life ratings between self-ratings of peoplewith aphasia and ratings from family members or healthcare providers whoserved as proxies for the people with aphasia (Cruice et al., 2005). TheseAntipodean researchers found that proxy respondents showed a significantnegative bias when rating QOL for the person with aphasia. According tothese findings, we must be cautious in interpreting the evaluations of familymembers and healthcare providers’ ratings of treatment outcomes, especiallywhen comparing these ratings with those of the direct consumer.

Although QOL measures are best garnered directly from the patient, it isimportant to seek additional input from other stakeholders. Communicationis not an isolated act except when sleep talking or mumbling in the bathroom.Procreation and communication are usually dependent on at least a socialdyad. If we as clinicians ignore other consumers, the person with aphasia mayexperience continued isolation from the community and lose the chance forpossible reintegration into the workforce.

Changing priorities in rehabilitation medicine

While traditional health indicators are based on mortality (i.e. death)rates of populations, the ICF [International Classification of Function-ing, Disability, and Health] shifts focus to “life”, i.e., how people live withtheir health conditions and how these can be improved to achieve aproductive, fulfilling life.

(WHO press release, November, 2001)

As is evident from earlier sections of this chapter, the traditional medicalmodel of aphasia intervention and healthcare in general has been evolvingtoward a social model over the past few years. Traditional rehabilitationmainly focused on impairment measures (i.e., range of motion exercise,muscle strength, words per minute, etc.), with less consideration of the direct


consumer, family, and community perceptions. The neurolinguistic model ofaphasia treatment included traditional stimulation and relearning techniquesused in an attempt to improve language behaviors while perhaps recruiting orreorganizing new neuronal networks. More contemporary treatment prin-ciples attempt to generate increased attention on psychological and physicalwellness (Lyon & Shadden, 2001). An example of this intervention emphasisis provided in the Life Participation Approach to Aphasia (LPAA; Chapeyet al., 2001).

In 2001 the WHO published the International Classification of Function-ing, Disability, and Health (ICF). This is a coding scheme model to identifyinteractions between health conditions, body functions and structures, activ-ities and participation, environmental, and personal factors. The WHO insti-tuted a shift from focusing on impairment to social perspectives and this wasa natural opening for an increasing emphasis on social validation of treat-ment outcomes. The ICF has gained attention in our discipline because itconnects communication and life skills. The American Speech-LanguageHearing Association (ASHA) has incorporated the WHO model into itscode of ethics (ASHA, 2001). Individual speech-language pathologists arealso incorporating health classification schemes (i.e., ICF) since they relateto the acquisition of funding, how we communicate to stakeholders, andhow we converse within the profession (Threats & Worrall, 2004). TheICF framework is also appropriate to the application of clinical research,and can facilitate a bridge between clinical practice and current research(Threats, 2002).

Patient-based measures in medicine

With the tide of change in medicine and healthcare in general, and the evolu-tion to patient-based outcomes, numerous health-related quality of life(HRQOL) rating scales are emerging. HRQOL measures typically includeperceptions of social health, role functions, and general well-being. Interest-ingly, the new net of life features that are embraced by HRQOL measuresmay also incorporate spirituality, sexual function, life satisfaction, andaspects of the environment. These outcome measures may be generic for useacross a broad range of medical conditions or specific to a select population.A few of the more common generic scales include the Sickness Impact Pro-file, Quality of Well-Being scale, and the WHOQOL-100. Some examplesof specific scales include the ALS (Amyoptrophic Lateral Sclerosis) Func-tional Rating Scale and the Parkinson’s Disease Questionnaire (Andresen &Meyers, 2000).

Each type of scale (generic or specific) may have different strengths andweaknesses (Guyatt, Feeny, & Patrick, 1993). Several of the popular scalesused in the stroke population have been reviewed fairly extensively inthe literature, with comparisons of the appropriateness, reliability, validity,responsiveness to change, and use in proxy assessments (Salter, Jutai, Teasell,


Foley, Bitensky, & Bayley, 2005). However, there is no consensus on whichscales are the gold standard for measuring societal perspectives of participa-tion. Research and clinical validation of QOL scales continues at a feverishpace and no doubt the next five years will see some improvements and per-haps consensus on QOL scales that meet consumer, societal, and psychometriccriteria.

Social validation in aphasia

So far in this chapter we have reviewed the history, implementation, stake-holders, and health policy related to social validation. We now explore theunderlying basis of social validation in aphasia therapy. If ever there was amiddle earth in clinical aphasiology, this is it. Although some might concludethat the incorporation of social validation models to treatment outcomes inaphasia have been largely characterized by ignorance and apathy, over the pastdecade there have been stirrings that allow some optimism. The rising tide isapparently affecting our small area of healthcare as well. Aphasiologistshave introduced social validation measures in treatments for syntax, dis-course, group therapy, caregiver training, and augmentative and alternativecommunication.

In pioneering work, Doyle, Goldstein, and Bourgeois (1987) were amongthe first to utilize social validation measures in aphasia. These investigatorsconducted a single subject design study to examine generalization and socialvalidation of syntax training using the Helm Elicited Language Program forSyntax Stimulation (HELPSS). Five professional-level Veterans Administra-tion employees who were naïve to the purposes of the study and the subjectsserved as judges. Pre- and post-treatment recordings were presented in acounterbalanced fashion, and raters judged if each response was adequateor inadequate. These rater judgments revealed that the syntax trainingimproved trained grammatical constructs; however, there was no significantgeneralization to new sentence structures. More recently, other studies alsohave utilized pre- and post-treatment comparisons with “naïve” raters todetermine the social validity of a written communication strategy (Lustig &Tompkins, 2002), Linguistic Specific Treatment (LST) (Jacobs, 2001), conver-sational coaching (Hopper, Holland, & Rewega, 2002), volunteer training(Hickey, Bourgeois, & Olswang, 2004), and writing ability (LaPointe, Katz, &Braden, 1999).

LaPointe et al. (1999) recruited a varied assembly of people from the com-munity to rate perceived changes in writing. Unlike most other studies, thesenaïve raters were not restricted to healthcare workers or students but adiverse cross-section of community members in respect to occupation, age,and education. Among the large sample (n = 141) of raters were teachers,blue-collar workers, professionals, students, a preacher, IT experts, and amodel. Raters were shown counterbalanced pairs of writing samples (onefrom baseline and one approximately six months later) and asked to judge


whether the first item or the second item was “better,” or whether there wasno difference between the two items. These judges were able to discern changein writing ability after six months that correlated with the improvementfollowing therapy in multidimensional scoring of writing samples. A cross-section of people in the community from a sample that was diverse in educa-tion, occupation, age, and gender were able to discern and judge as “better”samples of writing taken from six months post-therapy. People could see adifference. Of course it remains for us to determine whether or not this per-ceived change makes a difference. And that is what the social validationprocess is all about.

Who should be the direct or indirect consumers who validate treatmentoutcomes? Careful selection should be employed when determining whichconsumers to target. The work has only started. We need to know the opin-ions of physicians, nurses, rehabilitation specialists, insurance providers, aswell as the direct and indirect segments of society. Hickey and Rondeau(2005) compared ratings from groups with different knowledge of aphasia;one group was relatively unfamiliar with aphasia, and the other group con-sisted of second year speech-language pathology graduate students. Judgeswho were naïve to aphasia were more sensitive to change in pre- and post-treatment ratings, suggesting that members of the general public may providemore robust ratings. The most appropriate consumer groups to target shouldbe carefully selected based on the treatment objectives. Raters who are naïveto the individual with aphasia cannot rate quality of life or broader changein daily communication abilities. Hinckley (2002) sought to describe theemployment status and perceived life satisfaction of adults with chronicaphasia so she directly targeted persons with aphasia.

In a unique alliance that included as a co-author the person with aphasiawho was the focus of the study, Lasker, LaPointe, and Kodras (2005)described the progress of a professor with aphasia whose goal in therapy wasto improve her teaching ability. She was an accomplished researcher andteacher in geography who specialized in geographic aspects of world hunger.Her over-riding objective was to return to the classroom to teach, and tocontinue her contributions to the university and her academic profession.The profundity of aphasia, particularly in verbal sentence formulationand production, in this professor was significant. Treatment modalities andcommunication options included computer-based AAC to supplement herlaborious attempts at verbal production. These strategies and other com-munication options that featured key word prompts were arrived at byconsensus with powerful input from the person with aphasia. After somegratifying improvement and adaptation to using the AAC device to augmentand supplement her lectures, we attempted some social validation of hercommunication changes. We selected a unique segment of indirect consumersby targeting this professor’s students as persons who would provide ratingsof social validity. By selecting students who were expected to understandand learn from her lectures, we were able to target stakeholders who were


significantly impacted by the aphasia treatment outcome. The expectations ofthe students who needed to learn the class material would no doubt differfrom expectations of an outsider viewing brief video clips with no investmentin the class. Changes in teaching and communication effectiveness werereported by class members throughout the duration of a semester. This pro-fessor with aphasia continues to be reintegrated into the academic com-munity and, despite persisting significant verbal production difficulty, hasbeen able to achieve her primary objective of returning to the classroom. Wethink she has improved, adapted, accommodated, and persisted in a way thatis measurable and has clinical significance to her and to us. A significantsegment of stakeholders, her students, agree.

Researchers also have compared social validity ratings to changes onobjective behavioral measures and standardized test scores. Doyle, Tsironas,Goda, and Kalinyak (1996) investigated the relationship between unfamiliarlisteners’ judgments of connected discourse in people with aphasia andthe correct information units (CIU) of the samples. In this study thetwo measures were strongly and positively correlated. Lyon and colleagues(1997) compared consumer ratings to standardized aphasia tests and foundthat, despite the lack of significant improvement on the Boston DiagnosticAphasia Examination (BDAE) and Communication Abilities in Daily Living(CADL) following communication training, caregivers and communicationpartners reported significant gains in communication on the CommunicationReadiness and Use Index (CRUI) and Psychosocial Well-Being Index (PWI).Ross and Wertz (1999) studied the relationship between change in listenerperceptions and standardized impairment and disability measures. They didnot find a significant relationship when comparing scores on aphasia batteriesand disability measures to listeners’ perceptions of change in overall com-munication ability. These findings reinforce the notion that both social valid-ity measures and standardized test measures can be valuable indicators ofclinical significance and meaningful treatment outcomes.

Psychosocial impact of aphasia: More than just language

Aphasia does not affect a person in isolation. This is a condition that affectsthe entire constellation of those who orbit around the person with aphasia.With aphasia the affected person and family members experience devastatingand life-altering changes that alter their expectations and needs in therapy.Many of these changes have been described by those who have experiencedthe process first hand (Hale, 2003; Montgomery-West, 1995). Concepts thatare inherent in adapting to chronicity and the stages and phases of psycho-social effects of the illness experience have been elucidated in some of theliterature on aphasia. Adaptation, adjustment, accommodation, and the con-cept of Aristos (making the best of a given situation) are treated in depth in arecent book on aphasia (LaPointe, 2005). All these factors impact the personwith aphasia and complicate the establishment and verification of treatment


outcomes. Personal roles for an individual with aphasia may be drasticallyaltered by the aphasia. The traditional breadwinner role may be transformedinto a position of starkly increased dependence. Other long-held roles can bemetamorphosed into those that are unfamiliar and frightening. Aphasiacan shiver the soul. Specifically, it can dramatically alter the sense of selfand torque identity. Shadden (2005) poignantly highlights some issues ofre-establishing identity in aphasia. She writes from the expertise of bothprofessional and caregiver, and provides insights that are illuminating to eventhe most experienced clinician. Lubinski (2001) provides a detailed inventoryof potential effects on the family, as well as family needs at different patientstages (severe illness or crisis, recuperation, rehabilitation, post-rehabilitation,and institutionalization). Familiarity with this process is essential to a holisticappreciation of the psychosocial needs of the family with aphasia.

Emotional and psychosocial changes can engulf aphasia recovery. No onehas studied this and contributed more to it than Chris Code. His career ismarked by significant contributions to the science of aphasiology; and one ofhis most precious gifts may be that he has given us a richer understanding andappreciation of the psychosocial realm that accompanies the shock of apha-sia. Code’s professional persona is a strange and wonderful amalgamation ofFreud, Head, Schuell, Pogo, Ringo Starr, and Blind Lemon Jefferson. Hiscontinuing contribution is evident in recent collaborations on the influence ofpsychosocial elements on aphasia recovery (Code & Herrmann, 2003).

In addition to renegotiating identity roles, people with aphasia often areisolated from society. This leads to limited opportunities to participate inverbal communication. Socially valid treatment demands consideration ofpsychosocial elements. Unfortunately “emotional experience and personalperspectives, social roles and psychosocial perceptions are neither objectivenor easy to measure and are not traditionally seen as well suited to experi-mental investigation. Consequently, issues of personal experience are oftenneglected in rehabilitation” (Code & Herrmann, 2003, p. 122). That shouldnot deter us from studying this complex area of inter-related variables. Wehave a responsibility to all who have or will have aphasia to attempt tounderstand these influences and how they may affect our interventions.

Reimbursement

This is a good time to reframe our thinking and restructure our treatmentsto create cost-effective and beneficial programs that are meaningful topatients, their families, and those paying the bills.

(Carol M. Frattali, 1998, p. 242)

Our late colleague and friend, Carol Frattali, captured our charge succinctly.Healthcare reimbursers have taken note of the need to provide therapythat influences life participation abilities. The new ICF health classificationscheme may be used to establish reimbursement decisions. Reporting progress


using social validation outcomes demonstrates the utility of our service tothird party payers (Threats & Worrall, 2004). In addition, direct consumersare becoming more involved in selecting healthcare plans and providers toseek an option that suits their needs (Frattali, 1998). Healthcare services forpeople with chronic conditions, especially in the United States, are still woe-fully inadequate. The reduction in services and reimbursement for rehabilita-tion that we have witnessed in the past two decades is shortsighted and somewould say corrosive. Priorities seem to have elevated insurance, pharma-ceutical, and other profit-driven corporate interests above that of assuringa broad range of human services that are allowed and paid for as longas they are needed. We need social validation of rehabilitation efforts forchronic conditions such as aphasia. We also need societal accountability thataddresses the question of why these services are not readily available to thosewho need them. A civilized society may be judged by the way that it cares forits needy. When geopolitical agendas are financed at the expense of humanservices in healthcare and education, the role of governments in serving pub-lic interests may indeed be questioned. History may not be kind. We can onlyhope that societal values become rebalanced, so that optimal regard can bepaid to people in need of long-term healthcare; particularly those whostruggle daily with the dreadfulness of aphasia.

Conclusion

Social validation of treatment outcomes in aphasia has been relatively neg-lected, and we advocate that it should be an essential component of aphasiatherapy. The principles of social validation can be incorporated duringgoal selection, establishment of priorities of treatment targets, selection ofmaterials and procedures, determination of the context of treatment, and themeasurement of socially relevant outcomes. Consumers represent a numberof stakeholders, all of whom may hold different perceptions of the success orfailure of therapy. In this chapter we have advocated continued research andimplementation of social validation strategies as a means for determining theclinical significance of our services. Our ultimate objective is to enhance thequality of life and daily interactions of the people we serve. As has beennoted before, this will advance the relevance of our interventions. Also it willfacilitate socially relevant management by the clinicians who treat peoplewith aphasia, as well as the future clinicians who are destined to treat us.

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6 Interactional aphasiaPrinciples and practices orientedto social intervention

Jack S. Damico, Martin J. Ball,Nina N. Simmons-Mackie andNicole Müller

One of the real accomplishments during Chris Code’s tenure as Editor inChief of Aphasiology: An International and Interdisciplinary Journal has beenhis consistent advocacy of psychosocial issues and social models of aphasiatreatment. This chapter is intended to advance his efforts and those of numer-ous other social scientists in clinical aphasiology by advocating a more directfocus on interactional aphasiology as a sub-discipline of clinical aphasiology.

In the nineteenth century there was a flourishing of research and clinicalexperience that gave way to the first major focus on the human brain and itsdisabilities (Eling, 1994). Led by physicians and researchers who are now therecognized founders of medical and clinical aphasiology (e.g., Gall, Broca,Wernicke, Freud, Jackson), there occurred a great accumulation of knowledgeregarding the brain and the consequences of brain damage. It took some time,however, before these data were placed within acceptable frameworks forvarious medical and clinical applications. John Hughlings Jackson, one of thefounders of modern neurology, once discussed this problem of data overload.He suggested that although we have multitudes of facts, we require, as theyaccumulate, organizations of them into higher knowledge. He felt that weneeded some better generalizations and working hypotheses (1882).

Over the 125 years since this assertion, we can recognize both the problemthat Jackson stated and several solutions that were eventually employed.With the formulation of neuropsychological approaches of brain functioningand damage pioneered by Lashley (1929) and Luria (1947), the focus onmedical aphasiology led by Geschwind (1965), and the development of clin-ical aphasiology according to Schuell (1953), Darley (1975), and Porch (1967),the accumulated data over the last hundred years have been (somewhat)successfully applied to clinical populations.

Despite these successes, however, there are problems with the ways in whichthe accumulating data are organized and employed within clinical popula-tions. To an even greater extent than occurred in the nineteenth century, weare accumulating data and research findings that require additional general-izations and working hypotheses that are somewhat different from those thathave preceded us. As suggested by Jackson, we have to organize our data into

higher levels of knowledge to create effective working hypotheses of howthese data fit within the framework of individuals who are trying to negotiatethe impact of aphasia.

This chapter proposes one way to better organize some of the data thatcurrently confront us, an orientation that will assist our understanding andfocus on language, interaction, and aphasia. In this chapter, we propose thatwe move toward a more formal, explicit, and high profile focus within ourdiscipline of clinical aphasiology. A focus on authentic interactions in apha-sia utilizing the research methodologies appropriate to these phenomenaand the applications and practices drawn directly from theories and investiga-tions directed to face-to-face interactions. We propose the creation of asub-discipline of Interactional Aphasiology.

Given the recent advances in clinical aphasiology toward a greater accep-tance of qualitative research methods (e.g., Damico, Simmons-Mackie,Oelschlaeger, Elman, & Armstrong, 1999; Goodwin, 1995; Klippi, 1991;Wilkinson, 1999), and a growing focus on the functional and social consider-ations of aphasia (e.g., Ferguson, 1996; Holland, 1991; LeDorze & Brassard,1995; Penn, 1987; Worrall, 1992), this proposal may not seem unusual orbold. Indeed, there have been a number of efforts over the past few yearstoward a focus on aphasia as a clinical and practical impairment that resultsin extensive interactional consequences.

Despite these recent advances within the history of aphasiology, atten-tion to authentic interactional data and how they impact on social con-sequences has only minimally been advanced. It certainly has not been amajor focus within the organized efforts oriented toward clinical aphasiology.For example, in the loosely structured organization that holds the ClinicalAphasiology Conference every year, the vast majority of research papers pre-sented have not focused on authentic interactional data or social con-sequences. Further, a reading of the current trends within the United Statesand within Europe shows they are far more oriented toward linguistic andprocessing approaches to intervention and to modular cognitive models,both to explain aphasia and to provide interventions. Those researchers whofocus on authentic interaction in aphasia are certainly in the minority in theprofessions oriented to clinical aphasiology.

This lack of orientation to interactional issues is surprising when thepervasiveness of the social and interactional consequences of aphasia is con-sidered. One reason for this neglect appears to be that the issues of inter-action in aphasia and of the social impact of aphasia are complex and involvenumerous variables and considerations. When viewing this complexity, it isnot surprising that the discipline of aphasiology with its medical and experi-mental orientations has not focused extensively on these issues. There aremany areas of significance still to be investigated within the realm of aphasia.Aphasia, however, is a large field, capable of entertaining diverse orientations.The time is right for an explicit orientation embracing the complexity ofauthentic interaction and social action rather than ignoring it.

Interactional aphasia 93

To continue developing this line of research and its clinical implications,and more importantly, to get clinicians and researchers, professors and stu-dents to employ the work based on strong research and the principles andpractices that result from this research, it is necessary to extend the awarenessthat the long-term consequences of aphasia are generally linked to the inter-actional realm. For, as Garfinkel (1967) and Goffman (1974) have stated, thegenesis of society and social action is in the face-to-face interactions betweenindividuals.

An operational framework

To create the needed orientation, an operational framework is required.There are several reasons for such a framework. First, it will enable the devel-opment of an effective set of principles or guidelines to direct future workand application within this proposed sub-discipline. To establish a disciplin-ary study, one must have a set of principles or constraints within whichto operate. Second, once the framework is proposed and the principlesdeveloped, researchers oriented to this area can become more improvisa-tional in their approaches to research and clinical application, and still bedirected by the framework. This should enhance the creativity and originalityof the research and clinical initiatives. Finally, an operational framework thatrepresents an enhanced orientation will serve as an impetus to professionalsinterested in this area, so that they can adjust to the needs and opportunitiesof interactional aphasiology. Frankly, to incorporate people into a move-ment, you need a direction, people to advance and implement the movement,and, in effect, a flag or banner that others outside the vanguard will follow.The sub-disciplinary structure and its operational framework will supplysuch a “banner.”

A sub-discipline of interactional aphasiology should consist of a set ofprinciples and practices not just oriented to the social components or con-sequences of aphasia per se, but primarily to the interactional aspects thatinvolve a focus on authentic face-to-face activities and the abilities andvariables of interest within such authentic activities. The need to focuson face-to-face interaction can be accomplished in many ways; directlyvia methodologies like conversation analysis and other products of ethno-methodology, and indirectly as when we investigate the motivations, impact,and affective issues involved with authentic interaction and when we setabout creating applications generated by the data collected.

Further, this framework – even as a working endeavor – should beadvanced in ways that will enhance the objectives, data, implications, andapplications of research regarding authentic interaction to other aphasiolo-gists and to those interested in clinical aphasia. To formulate this framework,we can draw from a large knowledge base. Other realms of social science havetargeted interaction as social action in all its authenticity and complexity, andhave focused on how social action is effectively established, negotiated, and

94 Damico et al.

sustained. Consequently, we can adopt some of this cross-disciplinary workinto a study of social action that can enrich our appreciation of interaction inaphasia. This chapter discusses some of the social science research that maybe outside the clinician’s typical experience, but is relevant to the establish-ment of interactional aphasiology. As a starting point, the following tenprinciples are suggested as the guiding values for the sub-discipline ofinteractional aphasiology.

Principles for interactional aphasiology

Given the complexity of authentic interaction in all its various manifest-ations, it is important to have a set of principles available when engaging indata collection, analysis, and interpretation. These principles can guide howdata are treated and what importance the data or patterns of data mighthold. Further, a set of principles can inform the framework from which weoperate to construct values, strategies, and techniques that can assist inincreasing our knowledge and the applications of this knowledge in inter-actional aphasiology. Based on our research and a survey of the literature,there appear to be a number of interactional principles of social action thatshould be considered. Here is a list of those considered most important atpresent:

Principle one: Authentic face-to-face interaction

For the initial purposes of a framework in interactional aphasiology, theremust be a clearly distinguished focus for our research and clinical endeavors.This focus should consist of a continual orientation of activity towardauthentic face-to-face interaction in its various forms. That is, within thissub-discipline, the topic and context of interest should revolve aroundface-to-face interaction in terms of how it is systematically accomplished,what variables impact on face-to-face interaction, and the implications ofneurological damage to this social dyad.

In their classic sociology text, The Social Construction of Reality, Bergerand Luckmann wrote, “The most important experience of others takes placein the face-to-face situation, which is the prototypical case of social inter-action. All other cases are derivatives of it” (1967, p. 28). This principlesuggests that people construct the meanings of objects and situations throughtheir interactions with one another. That is, through their face-to-face inter-actions, individuals socially construct their behaviors, expectations, andbeliefs (Gergen & Davis, 1985; Goffman, 1974; Rogers, 1980; Scheff, 1990).This belief and its applications provide an effective guide to determining whatshould be investigated, and what should become the object of descriptiveassessment and compensatory intervention. The focus on face-to-face inter-action is the basis for interactional sociology and it can serve us as a firstprinciple as well in interactional aphasiology.


Principle two: The constructive nature of interaction

Within the social sciences there is a pervasive idea that both orients ourattention to the social world and, consequently, must serve as the actualrationale for our endeavors within the sub-discipline of interactional aphasi-ology. This is the principle of social constructivism. It suggests that the majorwork and accomplishment of face-to-face interaction is the construction ofthe meanings of objects and situations based on our interactions with oneanother. That is, through face-to-face interactions, individuals socially con-struct their behaviors, expectations, and beliefs. Based on this principle, manyof the human behavioral traits and psychological processes like self-identity,competence, and the capacity and reactions to intimacy are viewed less asstable internal constructs and more as the products of external interactionswith others (Berger & Luckmann, 1967; Kemper, 1991; Shotter, 1984).

The significance of this principle for interactional aphasiology lies in thefact that it provides one with a theoretical framework relating to the creationand preservation of both social and psychological behaviors. Rather thanassuming that a particular trait or a specific behavior is due solely to a psy-chological construct or neurological module outside the social realm, thisprinciple places the genesis of any trait, belief, or behavior squarely withinthe social sphere. Who we are and how we react is partially and importantlybased on our previous and concurrent social interactions.

In effect, this principle provides us with the rationale for why we shouldstudy face-to-face interaction. There is a social component to all humanbehaviors and traits, and to understand this phenomenon in aphasic patients,to understand how this phenomenon is modified and re-constructed, we muststudy where the social construction occurs – within face-to-face interaction.

Principle three: Local negotiation of social action

Consistent with the first two principles, a third interactional principle alsoplaces the emphasis on the actual activities that occur during face-to-faceinteraction. This principle is based on the widely documented finding withinethnomethodology that successful social action is accomplished at the locallevel (Duranti & Goodwin, 1992; Garfinkel, 1967; Heritage, 1984). Thismeans that any social phenomenon as it unfolds is locally and immediatelyconstituted through the observable activities of the participants. This prin-ciple is consistent with the expectation that an individual’s “common-sense”knowledge during interaction is employed on an instance-by-instance basis toconstruct social action. In this sense, what participants in a social interactionwill do in their next interactive turn is related to what their partners have donein the immediate prior turn.

This reliance on the immediate and local actions and context such that oneaction helps determine the next creates a conditional relevance, so that a firstaction helps determine what may occur as a second action, and the second

96 Damico et al.

actually depends on what occurred as the first action (Goodwin & Heritage,1990; Wilkinson, 1999). In any social action the importance of this localnegotiation can be generally stated as a condition where actions project nextactions. Said another way, the presence and impact of participants in aninteraction impinge on each other as the face-to-face situation continues. Ineffect, authentic interaction is constructed through a continuous reciprocityof expressive acts. Consequently, when researchers and clinicians orient toface-to-face interaction, they can focus on the actual behaviors and possibleinterpretations as revealed in the actual data before them. This provides amechanism for understanding social action without having to delve too faroutside the actual interactional dyad. For our part in interactional aphasiol-ogy, we should orient the aspects of the local management of interaction todiscover how and when this occurs.

Principle four: The complexity of face-to-face interaction

The fourth guiding principle provides us with a realistic set of assumptionsregarding our task of trying to study, account for, and understand the impactof aphasia on face-to-face interaction. We should expect, recognize, andembrace the complexity of the authentic interaction as a human phenom-enon. In authentic contexts, the reactions and interactions, the personalitiesand beliefs, the objective behaviors and subjective interpretations areemphatically close and local. During face-to-face activities, the skills, traits,and behaviors of each participant are continually interacting, and we mustattempt to describe and account for them as best we can. Indeed, that is theobjective of a research agenda focusing on interaction in aphasia. Withoutattention to the complexity, our efforts, our implications and our applicationswill fall short of the needs of our patients and clients. Damico et al. (1999)have discussed this issue, and the fact that one of the problems with much ofthe current experimental research in clinical aphasiology is that it doesn’taccount for the complexity of the neurological and social phenomenonknown as aphasia. The experimental research in the field is effective – as faras it goes – but it is simply not sufficient to account for authentic socialinteraction. In the sub-discipline of clinical aphasiology, the complexity mustbe recognized and various ways to account for the impact of aphasia in all itscomplexity must be a priority when designing and carrying out any researchagenda.

Principle five: The multiplicity of manifestations

Keeping with the complexity theme, the fifth principle strives to emphasizeand then guide the investigation of all the potential manifestations of semi-otic, cognitive, social, and psychological activity that make up the tapestry offace-to-face communication. Within authentic interaction, we should expectthat there are a number of potential manifestations needed to create the


social action. That is, there might be linguistic resources, various types ofcognitive skills and traits, social strategies and knowledge resources, verbaland non-verbal behaviors, neurological traits, and other potential semioticsystems that might be employed to create the emergent phenomena that weknow as social action within face-to-face interaction. As an individualattempts to negotiate within face-to-face interaction, he or she employs anumber of these manifestations to accomplish the desired objectives andthe resultant interactional behavior – one that creates comprehensibility, pre-dictability, and successful expectations – is most likely to be the emergentproperty of interactions between some of this multiplicity of manifestations(Perkins, 1998, 2001, 2002). To use a metaphor employed by Janet Emig(1983), the individual uses these manifestations to “weave a web of meaning.”For our purposes, then, we must be prepared to engage in an objectiveand detailed analysis of our data to determine what variables or mani-festations produce the observed social actions (e.g., Simmons-Mackie &Damico, 1997).

Principle six: Orient to the functional goal

In order to best address the complexity and to keep a handle on the plenti-tude of symptoms and manifestations in face-to-face interaction, it is best tomaintain that the catalyst for interaction is to accomplish social action. Weshould orient our first question to “how was an interaction (or an aspect ofit) accomplished?” If we adopt this functional and strategic approach, thenwe can better handle the complexity of the phenomenon and its potentialemergence via the resources available to the interactants in the dyad or socialgroup.

This focus on the functional aspects of face-to-face interaction is consist-ent with a emerging emphasis in clinical aphasiology over the past 15 years.Work by clinical researchers like Holland (1991, 1998; Holland & Thompson,1998), Lyon (1996) and Elman (Elman & Bernstein-Ellis, 1995) have advo-cated a more functional approach to the description, assessment, and inter-vention in aphasia and these initiatives have greatly influenced the field. Withinthe sub-discipline of interactional aphasiology, a practical and functionalorientation to face-to-face interaction and how it impacts on effectivenessshould serve as the medium within which the data are interpreted.

Principle seven: Social action as collaborative

Another interactional principle necessary in interactional aphasiology is areasonable consequence of most of the principles discussed thus far – socialaction is always a collaborative enterprise. In effect, face-to-face social actionis always collaborative and so we should always remember to incorporate thischaracteristic. Indeed, it should be our watchword. If social construction isaccomplished at the local level, then all social actions are active and dynamic

98 Damico et al.

enterprises wherein (at least) two participants are involved in a process of co-construction. Social actions of all sorts (e.g., conversation, arguments, fights,nonverbal posturing) are not a series of discrete behaviors or messages thatpass from an active individual to a passive one. Rather, all face-to-face inter-action is a process of participants actively constructing and negotiatingmeaning in a coordinated and joint manner as the social action proceeds. Inpractice, we can focus on the aphasic or the non-aphasic interactant, the dyador the group, but eventually any analysis or its interpretation should orientto the collaborative impact needed to construct an interaction (Goodwin& Heritage, 1990; Oelschlaeger & Damico, 1998; Perkins, 1995).

Principle eight: The dynamic character of interaction

Building on the previous point, the construction of our relations with others– especially due to the local management of the interaction – is highly flexible.Whatever patterns and strategies are introduced during an interaction, theywill always be dependent on the interactions and reactions of the other par-ticipant. Consequently, the behaviors and goals, interactions and reactionswill be continually modified through the exceedingly variegated and subtleinterchange that goes on when accomplishing social action. We must alwaysbe aware of this fact. It is possible that this characteristic will eventually limitthe wholesale applications of some of our research. But it is equally possiblethat we may find that, although individual manifestations change across con-texts, individuals, and over time, general and underlying principles will bediscerned. For the moment, however, the dynamic character of face-to-faceinteraction should serve as the caveat of the sub-discipline.

Principle nine: Contextual impact

Although some social researchers have tried to focus exclusively on conversa-tion as the prime face-to-face interaction, there are other equally valid andauthentic social dyads and groupings that may also require investigationdepending on various contextual issues. Harvey Sacks (1992) and others (e.g.,Goodwin & Heritage, 1990; Scheff, 1990; Schegloff, 1968), focusing on con-versation, acknowledged this in their writings and their research foci. Todetermine which social dyads should be the focus of attention, one mustrecognize the contextual relevance of social action. Not only do the variousmanifestations of social action change depending on the local context, but, aswith all aspects of human semiotic systems, context determines the primesocial dyads and groups from one interactional opportunity to another.Therefore, we should employ an awareness of contextual relevance whendetermining what kind of face-to-face interaction should be the focus of ourattention in various settings.


Principle ten: Adopting methods suitable to the phenomena we study

The last principle I want to discuss as necessary for the sub-discipline ofinteractional aphasiology involves the tools and methods that we should useto investigate authentic face-to-face interaction. That is, what kinds ofresearch methodologies are adequate for conducting research on complexand authentic social action like this? For a host of reasons, the answer is thatwe should adopt qualitative research methodologies.

Over the last few decades, there has been a trend in the philosophy ofscience to recognize that research and systematic investigation becomes scien-tific by adopting the methods of study appropriate to its subject matter. Thisstance is called “scientific realism” and is currently a dominant philosophicalposition rather than the formerly dominant neo-positivistic approach(Okasha, 2002; Papineau, 1996). Among other things, scientific realism sug-gests that science is defined by the results and findings not the methodology.Within this focus, qualitative research – by definition – appears to be the mostappropriate research paradigm for interactional aphasiology.

Basically, qualitative research refers to a variety of analytic proceduresdesigned to systematically collect and describe authentic, contextualizedsocial phenomena with the goal of interpretive adequacy (Damico et al.,1999). The idea of interpretive adequacy – what Graham Button has describedas explication of social action – should be the goal of interactional aphasia,and so qualitative research methodologies are best employed within this sub-discipline. Of course, this qualitative research paradigm involves a number oftraditions of inquiry. While we may be most familiar and even prefer – withinthis context – to employ the most analytic of the qualitative methodologies –conversation analysis, it is not the only tradition of inquiry we should employ.In fact, to completely investigate and understand authentic interactionaldata, its variables, complexity, and implications, conversation analysis is notsufficient by itself. Other qualitative traditions of inquiry are more appropri-ate in some instances. Other traditions of inquiry include biographical study,case study research, ethnography and ethnographic methodologies, groundedtheory, historical methodology, and other types of naturalistic data collectionstrategies like participant observation, ethnographic interviewing, discourseanalysis, artifactual analysis, focus groups, and lamination research andphenomenology (Damico & Simmons-Mackie, 2003; Damico el al., 1999).

Within a sub-discipline of interactional aphasiology, this paradigm andthese traditions of inquiry and the various naturalistic data collection strat-egies can assist us in achieving the other nine principles within the previouslydescribed operational framework.

Conclusion

These ten principles should help orient us to an understanding of how socialaction is achieved in face-to-face interaction, and how it impacts on the social

100 Damico et al.

accomplishments and consequences of individuals with aphasia. Of course,we still have to develop the implications and applications that might arisefrom the sub-discipline of interactional aphasiology. For example, we mustask: “How do we get others to understand and focus on the interactionalcomplexity of face-to-face interaction?” and “How can the practices resultingfrom this research be applied in clinical settings?”

It is certainly possible that the principles proposed in this chapter arepreliminary and naïve. In the final analysis, however, whether we adopt anapproach consisting of these or other principles, whether we strive to createa sub-discipline or not, there is a need to embrace the complexity of apha-sia and its implications within a social action framework. For, whenaddressing the issues and concepts in clinical aphasia, regardless of what wetheorize and discuss about language and processing, grammar and modularcognitive systems, the real significance of all of these areas means nothingunless we see these abstract conceptions played out in the arena of authen-tic face-to-face interaction. After all, that is where the human creatureexists.

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Part II

Research considerations

7 From the study of languagedysfunction and handicap to abetter understanding oflinguistic processingin normality

Jean-Luc Nespoulous and Jacques Virbel

Introduction

There are certainly several ways of paying tribute to a scholar and a friendsuch as Chris Code. Rather than referring explicitly to specific contributionshe has made to aphasiology, we have chosen to offer him a chapter dealingwith a somewhat new definition of the notion of “handicap” which, wethought, he might like, knowing how attached he has been throughout hiscareer to a clinical approach such as the one we adopt here. Doing so, wehope Chris will react to our proposals, thus pursuing an interaction whichbegan during a sabbatical year he partly spent in our laboratory, in Toulouse,a decade ago.

Deficits, normality, cognitive flexibility and adaptive and/orpalliative strategies

Probably for etymological reasons, the first definition given by dictionaries ofthe word handicap is related to horse-races and the equalization of thechances of success between riders by the imposition on the best horses ofheavier weights to carry or of longer distances to run. According to thisearliest definition, the word handicap has a proper “positive” sense since itrefers to a horse, and more generally, to a sportsman or a player whosesuperiority is recognized and whose advantage is being attenuated in order toproduce a more equitable competition with those less powerful than him.

According to these same dictionaries, it is only in second place that, ina figurative sense, the word handicap has come to indicate all “deficiency,physical or mental”, likely to affect somebody in any activity whatsoever.

With regard to the word handicapped – adjective, past participle, turnedsubstantive – these same dictionaries frequently reverse the order of themeanings, so giving priority to the latter, with its “negative” semanticattributes.

In the field of language, as in a good many other fields which will notbe the subject of this article, the handicap – in the last acceptation of the

term – usually evokes a certain type of deficit or dysfunction, lasting ormomentary, compared to a state known as stable, or “normal”. The origin ofsuch a dysfunction, as indicated above, is classically regarded as resultingfrom intrinsic physical and/or mental deficiencies (see above) but no one hasyet extended the scope to the social sphere, thus agreeing to take into accountvarious extrinsic or environmental parameters in the characterization of thehandicap and those who suffer from it (Bernstein, 1975; Besse, de Gaulmyn,Ginet, & Lahire, 1992; Nespoulous, 1978).

It is within this latter framework, non-restrictive and open, that we shall bepositioning this article, convinced that at one time or another, to a greater orlesser extent, temporarily or permanently, all human beings – speaker and/orinterlocutor – might find themselves in a situation of linguistic (or other)handicap.

In this context, the observation and the fine characterization of such adysfunction is not only able to provide invaluable information about thenature of the disturbances highlighted, but also to make it possible to betterapprehend, through after-effect, (a) the full details of the functioning oflanguage in a subject considered “normal” as well as (b) the strategies –“spontaneous” or induced, “natural” or technologically relayed – broughtabout to (try to) “adapt” to the dysfunction and to compensate as well aspossible for the deficiencies affecting a speaking subject (Nespoulous, 1996).

Our argumentation will be based primarily on data obtained from aphasicpatients with whom one of us has been working for about 30 years, butwe will frequently widen the range of our remarks to other populations(of handicapped persons) and to other (“handicapping”) situations so asto characterize the handicap in as general and as large a way as possible andto extract a maximum of information, particularly as regards cognitive flexi-bility, of the observation of degradations of communication, whatever theorigins might be: pathological or not, occasional or durable, and so on.

Some “central” dysfunctions of language in aphasia and theirpalliative strategies

The cerebral lesion that causes aphasia creates at the same time a deficit and acommunication handicap, making any verbal interaction difficult. Generally,the components of the language as a whole are not affected by the lesion andthere are even cases where only one component proves to be dysfunctional.Comparisons of different patients presenting different selective deficits andshowing evidence of “double dissociations” allow for the identification ofvarious specific, and relatively autonomous, functional components, in thefunctional architecture of language in the human brain-mind, even withso-called “normal” subjects. It is on such bases, particularly over the past40 years, that the traditional neuropsychological approach to language, alsocalled cognitive neuropsycholinguistics, has developed (Nespoulous, 2004).

Parallel to the generation of a deficit and a communication handicap,

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the cerebral lesion in handicapped subjects develops, often unconsciously,various palliative strategies that, in the best cases, allow subjects to circum-vent the deficit and to overcome their handicap, at least partially. It isthis tendency that makes Audrey Holland (1977, p. 173) state: “aphasicscommunicate better than they speak”.

However, from the start, aphasiology has been much more concerned withthe characterization of the underlying deficit (see above) than with the stra-tegic and adaptive potential of the patient confronted with this deficit. It iscertainly not a question of radically opposing the two approaches, insofar asthey seem to be complementary: the first makes it possible to identify (a) thedirect “negative” manifestations of the deficit (“linguistic symptoms”), aswell as (b) the “positive” manifestations relating to the aspects of the lin-guistic function that have remained intact; and the second makes it possibleto apprehend (c) the palliative strategies built up by the patient in spite of thisdeficit and thus his or her cognitive flexibility in the processing of linguisticinformation (Nespoulous, 1994).

If one agrees to adopt such a double, or even triple, approach, with regardto aphasiology, one is ineluctably led to reject all characterization of verbalbehaviour in (binary) terms of respect or violation by an individual of thecanonical properties of his or her language, in favour of an adaptive vision ofthis behaviour. Speaking and understanding – just like acting and perceiving –become adapting to (or attempting to adapt to) the constraints of the situ-ation in which one finds oneself, albeit more or less successfully, depending onwhether one is aphasic or a so-called normal speaker (see the diagram below).

We will now give some examples to help illustrate our argument.

Temporal adverbs to the rescue of deficient verbal inflections

There are certain people with aphasia – called agrammatic – who are charac-terized by major difficulties in the management of grammatical morphemes

From language dysfunction and handicap to normal linguistic processing 109

and/or syntactic structuring of verbal messages. Among other symptoms,these patients present a reduction of inflexional morphology that leads them,in languages like French or English, to produce infinitives, in the first case,and gerunds (sleeping, walking . . .) in the second, instead of conjugatedforms of the verbs. Such a reduction, likely to particularly disturb the tem-poral marking of utterances is, however, frequently compensated for byresorting to adverbs of time (yesterday, tomorrow . . .) or by employingphrases carrying temporal information (next week, last summer . . .). Thistype of strategy makes it possible for the patient to circumvent the deficitmentioned above and the communication can then continue effectively, atleast on this point, all the more since there is more semantic precision in theselexical markers of time than in temporal inflections of the present, past orfuture (Nespoulous, 1973).

Circumlocutions and gestures to the rescue of the missing word

Inability to recall a word, or problems of access to the mental lexicon(or anomia) is a particularly frequent symptom of aphasia, whatever theclinical category may be. Although it is possible to observe a patient abso-lutely unable to find and/or to produce an adequate word – in a naming task(from pictures) or in spontaneous language – it is extremely rare that thislexical deficiency results in total mutism and an absolute absence of speechproduction. Usually, indeed, the patient will resort – just like a normal subjectwho has a transitory lexical difficulty – either to periphrastic strategies (i.e., heor she tries to formulate a definition of the word he or she is not able torecall), or to mimo-gestural strategies (i.e., the patient tries to mime the use ofthe object referred to by the word he or she is not able to find in his or hermental lexicon: Nespoulous, 1979). In so doing, these patients provide, more-over, the proof of the integrity of underlying semantic representations: theyknow what they want to say but cannot say it (see below).

Phonemic paraphasias and “repair strategies”

In nearly all the work relating to phonetic and/or phonemic disturbances inaphasia, as in preceding domains, clinicians and researchers have generallycharacterized the patients’ deficiencies negatively in terms of “performanceerrors”.

More recently, however, and on the basis of new theoretical frameworks inphonology, the approach to such pathological phenomena has been greatlyrenewed (Béland, 1985; Moreau, 1993; Nespoulous, 1998; Nespoulous &Moreau, 1997; Paradis, 1988). Therefore, instead of resorting to a strictlydescriptive taxonomy of the phonetic and/or phonemic “errors” (i.e., in termsof omissions, additions, substitutions and displacements of segments), itbecame possible (a) to predict the nature of the disturbances according to thecanonical structure of the words the patient had to produce in a particular


task, and (b) to apprehend them as the consequence of the use of “repairstrategies” applied to a word of which the phonological structure wasinaccessible to the patient, certainly because it was too complex. Thus, inthe presence of a word like “brouette” (/bwεt/, which is “wheelbarrow”,in English), – certainly difficult to produce for an aphasic person just as for achild in the learning period because of the presence of the consonantal clus-ter /b/ – clinicians and researchers often simply spoke about (a) errors ofomission, when the subject said /bwεt/, or (b) errors of addition, when he said/bewεt/. Considering such phenomena, the “theory of constraints andrepair strategies” (Paradis, 1988) aims at considering that, faced with a con-sonant cluster like /b/, the patient who has difficulty in producing such agroup makes use of at least two universal strategies of “repair”, which he canapply to simplify the syllabic structure of a word like “brouette”: the syncope,which leads the patient to delete the liquid consonant //, and the epenthesis,which leads him to insert a vowel between the two consonants. Certainpatients thus showed that they resorted preferentially to one or the other ofthese two strategies, while others sometimes used one and sometimes theother of these two strategies, even on the same words (Nespoulous, 1998).

Towards a new distribution of roles in dialogue . . .

Since Bally (1942), it has been agreed to regard any speech act as the combin-ation of “referential” elements (Bally’s dictum) and of “modalizing” elements(the same linguist’s modus).

Thanks to the former, speakers set up the elements of the information theywish to communicate; they encode a “proposition”, according to the logi-cians’ definition of this term (i.e., the explicit relation of a predicate and itsarguments); and they refer to people, objects, ideas, and so on that are part ofthe socio-cultural context of the community to which they belong.

Thanks to the latter, the same speakers this time formulate the positionthey wish to adopt in relation to the above referential content; giving theirspeech their own particular “signature”. They thus express a doubt or acertainty; make comments; accept or refuse the propositional content thatthey themselves have set up or that has been set up by their interlocutors.

However, several studies in aphasiology have clearly shown that cerebrallesions affect these two types of elements in unequal ways (Nespoulous, 1980,1981; Nespoulous, Code, Virbel, & Lecours, 1998). So, while the wording ofthe referential elements of speech poses a major problem to aphasic patients,the great majority of them remain able to manage the modalizing elements.Thus an aphasic patient can say: “I cannot say it” (see above), but at the sametime cannot say: “she cannot sing it”, to take two sentences that have, apartfrom anything else, the same lexical and syntactic characteristics (Nespoulous& Lecours, 1989).

In “strategic” terms, it appears possible to exploit this kind of dissociationin order to consider recourse to a particular type of verbal interaction likely


to improve the transmission of information between the patient and thoseclose to him or her, in particular in a dialogue situation. Thus if the therapistor a member of the patient’s family addresses – in the context of a questionrequesting an opinion – the essential part, or even the totality, of the neces-sary referential elements, the patient should, in most cases, be able to producethe adequate modalizing elements in his or her answer, thus guaranteeing thesuccess of the verbal exchange.

This procedure is certainly not ideal. It has its limitations; but it mustallow, at least initially, the freeing up of many communication situations thatwould be doomed to failure without the use of such strategies. Adapting likethis to the constraints of the situation – here pathological – is by no meansoriginal: what do we do when we address somebody who does not have agood understanding of our language? What do we do when we speak to achild who is not yet proficient in the use of his or her mother tongue? Whatdo we do if not to give a maximum of informative elements in our question sothat our “non-expert” interlocutor can answer us, parsimoniously, but no lesseffectively?

In the four illustrations above, the range of the concept of strategy differs,certainly. Thus, for example, the first three types appear to emerge spon-taneously from the patient, because they would seem to be part of the generalsemiotic potential anchored (without their knowledge) in any human being;the fourth requires, at least partially, an inter-individual adjustment, whichcertainly will not escape the protagonist’s awareness. In all these cases, how-ever, the verbal behaviour does not appear (or no longer appears) as a stereo-typed human response but rather as a highly adaptive and flexible cognitiveactivity. We shall return to this later.

Some “peripheral” dysfunctions of language and theirpalliative strategies

In what precedes, we endeavoured to illustrate our introductory remarks bydrawing our examples from a “central” pathology such as aphasia; a path-ology that affects some of the components at the heart of human linguisticactivity (phonological, lexical, morpho-syntactic processing, and so on).

There are, however, other linguistic dysfunctions that, although only affect-ing the more “peripheral” components of the functional architecture oflanguage, are still of interest for our purposes. These dysfunctions, sensoryand/or motor, can be highlighted in certain aphasic patients, different fromthose considered up to now, as a result of cerebral lesions, which, too, aredifferent. They can however also be observed among patients whose centralnervous system is intact but who suffer from certain attacks that block thefunctioning of afferent (e.g., vision, hearing) or efferent (phonation, manualdexterity) systems.

Contrary to the palliative strategies previously evoked in the context of“central” pathologies – strategies whose range, although real, remains limited


– the “peripheral” dysfunctions sometimes lead the patients to develop wholesystems of substitution: for example, the replacement of the audio-phonatoryloop by a visuo-gestural system, sign language for the profoundly deaf; thereplacement of visual information intake by tactile means, via Braille, forthe blind (e.g., O’Regan & Noe, 2001).

In such a context, resorting to external palliatives, produced by recenttechnological advances, proves to be crucial and not only because such pallia-tives are likely to facilitate the adaptation of certain patients to their deficitbut because they raise, in return, important questions (a) as to the “determin-istic” hardwiring of the human nervous system, and/or (b) as to its adaptiveflexibility (Lenay & Pfaender, 2004).

Technological palliatives

Data processing and linguistic handicaps

The relationship between data processing and linguistic handicaps is circum-scribed by that which relates, on the one hand, to the treatment of statements(in “natural” language), and on the other hand, by the consideration ofusers of computerized devices. To simplify, it is possible to determine twosituations, or classes of cases, that in fact are very closely related, are eveninterlinked, in reality.

The first situation is that of the design and development of specific devicesproviding computerized assistance. The principle mainly at work here isthat, as previously indicated, of semiological substitution: substitution of themodality of existence of information simultaneous with the sensory substitu-tion of access to this new form of information. Thus text to speech synthesissystems and computerized Braille come to the assistance of the partiallysighted or blind; conversely, vocal dictation that transforms (oral) speech intotext compensates for the handicap of the hard of hearing or deaf; vocalcommands or special keyboards compensate for difficulty in or impossibility ofwriting or typing resulting from certain motor handicaps of the upper limbs.

The principal problems encountered in this class of application are partly‘classic’, related to language: the objective of automation imposes a level ofextent and detail of the linguistic data and of formalization of the modelsoften over and above what the descriptions and the linguistic or psycho-linguistics models propose, at all levels of language. For example (Maurel,Lemarié, Vigouroux, Virbel, Mojahid, & Nespoulous, 2004) on the onehand, the apparently very modest question of oral interpretation (or “trans-lation”) of certain visual structures of the texts is much more complex thanone might think (especially if one views writing as a non-pertinent “code”from a significant point of view), and, on the other hand, not manydata have been gathered yet on this phenomenon (Virbel, 1989). But inaddition, such data, as extended as necessary, must also be pertinent on thecognitive level. The procedure then aims at developing interdisciplinary


research where the researchers of the disciplines concerned inter-react, andamong them, as a recent new element, are researchers who are themselveshandicapped.

But it is the very notion of substitution that covers the greatest complexity,because in the end, it mobilizes that of identity or equivalence of contents. Itcan be noted that intra-modal substitution is already attested on differentlevels in the case of translations, summaries, transliterations and lists of con-tents. In addition, objects like logigrammes, used for example in the field oftechnical instructions, combine discursive and figurative aspects (in particu-lar diagrammatic), and thus undoubtedly generate representations of differ-ent natures: propositional and analogical. Thus the question of knowingwhether two messages of identical or different modality really are equivalent(questions which are the basis of the transpositions evoked here) constitutes aformidable problem of nature, both logical and cognitive, if one aims at leastat introducing a form of guarantee of this equivalence reminiscent of a the-orematic demonstration. This type of question is central in semantics, logicand philosophy of language, where major theoretical divergence exists, bring-ing into play the very design of language and of its relationships with theworld and the mind. This is a crucial but rather speculative question, butwhich here leads to experimental possibilities relating to multimodal com-munication, not much studied until recently, but central in the context of thecommunication of handicapped people.

“Information for all” and handicaps

Another situation is that where, like anyone else, handicapped people needaccess to, and use of computerized devices: word processing, the Internet,databases, on-line services, computerized physical environments (domesticapparatus, cars, houses, etc.), be it for professional or private reasons (training,purchases, amusement, administrative procedures, reservations, etc.).

Research in this area encounters questions of appreciably the same order,with an emphasis on the fundamental problem posed here, that of accessibil-ity to information and to physical objects related to various cognitive orphysiological deficits. Some of the problems experienced by handicappedpeople in the access to these devices are caused by the modes of interface used(screens, keyboards, the mouse) and of interactivity (for example: double-click on highlighted zones), which are not convenient, or even simply notpracticable for the blind or partially sighted, or for those who have insuffi-cient mobility in their hands. And, for example, on the first point, many newtechniques are being developed as access interfaces (special keyboards, scan-ning, voice recognition, piloting by ocular movements, monitoring of facialexpressions, interpretation of biological electric signals, laser stimulation ofthe retina, voice synthesis, multidimensional sound, tactile stimulation,return of effort, etc.).

It may seem at first that this is a specific case of what has already been


discussed, in the following sense: data processing, contributing to aid theexercise of the faculty of variously handicapped language, also does so whenthis faculty is exercised in relation to and through computerized devices. Butin fact it goes far beyond a simple specific case. Indeed, what deeply charac-terizes the situation evoked is that it aims at constituting a particular casecalled “information for all”, by which is meant all users, all uses andall types of information. This point is very important because it appearsas of now that it is the source of deep conceptual and methodologicalreformulations.

For computing, this is indeed a challenge without precedent, which is atthe origin of the recent foundation of the (in French) STIC: Sciences etTechnologies de l’Information et de la Communication (Science and Technologyof Information and Communication) for the structuring of research. In thismovement, the consideration of the characteristics of users no longer comesat the end, but at the beginning and is situated at the centre of the design ofcooperative, interactive systems, provided with certain dialogical aptitudes.Concepts such as those just mentioned, and others like utilizability, accessibil-ity, adaptivity and adaptability are given new simultaneously operational def-initions, for the conceptions of applications, and based on knowledge formedwith the disciplines of human and social sciences or of the life concerned(and concernable). The work of J. Carrol (Carrol, 2002) is very representativeof such developing knowledge in connection with “utilizability”. Anotherexample is the case of the notion of assistance, which is not unrelated to oursubject. The conceptual, logical and philosophical growth of knowledgebrought to the concept of handicap, by J. Perry (and colleagues), one of thefounders of the “semantic of situations” can also be appreciated (Perry,Macken, & Israel, 2004). According to him, handicap should not beconsidered in a static way, solely in opposition to performances considerednormal, but in relation to a complex function of capacities and aptitudes,targeted tasks, and circumstances, by which is meant environment (infra-structural, artefactual): disability, inability and handicap thus receive relativedefinitions that bring into play a “circumstantial” conception, making itpossible to conceptualize the background of the normal–pathologicalopposition, and to relativize this kind of opposition.

With regard to linguistic handicaps in particular, a very great number ofsituations necessitate the reconsideration of the notions of deficit or variationcompared to a supposed “normality” or an equally problematic “average”:the diminutions of performances due to ageing, fatigability, cognitive over-load, professional crisis situations, incidents or accidents, ineptitudes relatingto the learning capacities of the users, cannot merely be viewed as simplelimits or suspensions of the success of conduct and performance, but must bestudied in the light of more subtle theories of error and failure.

Models of direct or mediated inter-human communication, like models ofaction and decision, must incorporate this kind of design of potential failureor error; all the more since, as we have already seen, the users in situations of


failure develop palliative activities that may succeed only partially, or evennot at all, but that must in no way be confused with other forms of failure.Here the central factor, in a normal, pathological or handicapped situation, isadaptation (of which learning is a part).

Communication, information and handicap

Faced with this new situation, the STIC has resorted to two types of pro-cedure, which are ideally inter-articulated, the limits of one calling on theother. One, which could also be called, as it is in psychology, “domain spe-cific”, generalizes the classic conception of user “profiles”, and includes boththe domains in the strict sense, as well as the processes concerned and themechanisms of adaptation (of the users and the systems). The other, and thisis what we shall concentrate on, aims to exploit and/or develop cognitivetheories of information and communication, making it possible to highlightall the necessary conceptualizations in all cases.

These theories, we emphasize, do not pretend to offer ready-made solu-tions to the problems that concern us here, but they can make it possible tosituate the handicapped use of data processing and/or communication, bothin an enlightening manner on the theoretical level and in an exploitable wayon a more practical level. One of these, the speech acts theory (SAT), inaddition to this first prerequisite, satisfies two others that are very important.For one thing, the SAT can stand up to formalization efforts of a logicalnature essential to any automated treatment (Grice: Logic and Conversation,1975 in Grice, 1989; Searle & Vanderveken, 1985). This remark leads usto the second prerequisite: research relating to SAT is being developed inan extremely wide interdisciplinary context (Champagne, Herzig, Longin,Nespoulous, & Virbel, 2002; Tsohatzidis, 1994; Vanderveken & Kubo, 2002):not only logic, as indicated (of mental states and action), but also linguistics,psycholinguistics and neurosciences of language, the philosophy of the mindand language, and several sub-specialities of computer science (design ofcooperative systems, interactive systems, etc.), a set of domains tending toconstitute contemporary pragmatism.

The handicap “situated” in speech acts theory

We had concluded (see above) with the need for an adaptive (in particularwith reference to the constraints of the situation and the nature of the lin-guistic tasks) and non-stereotyped vision of communication, with the relativ-ity of success and failure and with the existence of palliative activities in thehandicapped subject. We would like to show how the reference to SAT caninform the preceding analyses of linguistic handicaps.

First of all the SAT, as its name indicates, considers communication as anactivity. This apparent truism in fact covers deep elements of renewal of thecommunication approach. In this:


• Like any action, communication does not abide by the true/false oppos-ition, as propositions do, but that of success and failure. And as for mostother types of action, this realm is not governed by an all-or-nothingprinciple (discrete), but on the contrary by gradualism, and it is alsomulti-source. The conditions for success and failure of speech acts arenaturally particular in comparison to physical actions, for example (seebelow), nevertheless it may be noted that a general theory of error likethat of J. Reason (Reason, 1993) proposes concepts that are relevanthere: the concept of latent error (introduced surreptitiously right fromconception and not dependent on the quality of subjects’ performances)and that of error caused by an attempt to recover an earlier error. Con-trary to an “algorithmic” (and angelic) vision of action, we thus noticethat communication is inherently and not anecdotally subject to risks,and risks it is only partially possible to anticipate.

• Like many other acts, communication is also an intentional activity(Cohen, Morgan, & Pollock, 1990) and the intentionality is, in this case,reflexive. Since the founding article of P. Grice (Meaning, 1956 in Grice,1989), which associated the problem of intentionality with that of signifi-cance, and the later work of Strawson (Strawson, 1964) and Searle(Searle, 1969; 1981) on this question, it is considered that by an utteranceu, a speaker does not simply aim to have his interlocutor recognize hisintention to communicate the contents of u to her, but he also intends,through the use of adequate linguistic resources, to have her recognizethis intention. It is by this feature of the demonstration of intentionality(which can also be expressed as intention to draw attention to such anintention) that communication marks its particular form of cooperation.

• Finally, like a number of intentional actions, the communicational actiondepends on necessary (but not sufficient) preconditions; and it is decom-posable into sub-actions whose sequence comes back to the action con-cerned. In the technical sense, it is therefore liable to planning, and onecan, for example, represent this planning both in terms of a “cognitivetask analysis” (Salembier & Pavard, 2004) and in terms of a computerplanning system (Pollock, 1990).

We thus note that the few aspects evoked – intention to attract attention,request for cooperation, satisfaction of preconditions, planning of the action– to characterize in-depth communicational activity can be also the cause ofthe characterization of multiple possibilities of failures of relative import-ance. Moreover, SAT can be considered a pioneer in this field: the initial workof J. Austin (Austin, 1962) was founded (inter alia) on a typology of thevarious ways of not succeeding in a speech act, and Searle’s later develop-ments led him to develop the concept of conditions of success of speech acts,as distinct from that of conditions of satisfaction of their propositional con-tent. There, too, proof was found that there are only a limited number ofways of not succeeding in a speech act and in a characteristic manner


(because a speech act constitutes a structure). This was not without con-sequence for the conceptions of adaptation in communication situations, or,moreover, for the conceptions of language acquisition.

Communication is thus successful only in so far as it avoids risks of failurethat it is at least partly possible to anticipate, and one can seek to define anoverall illocutionary structure on the classes of performance of speech acts(direct, indirect and implicit), linked to a structure of the classes of risks offailure of the same acts. One of the possibilities of communication failure liesin the plurality of linguistic resources for the same communicational goal.This phenomenon is well known for lexemes (synonymy) or more extendedexpressions (periphrases, definitions), or between certain syntactical struc-tures (active vs. passive, full verb vs. verb support + nominalization, forexample). SAT shines an interesting light on this question for our purposes,showing that this source of potential failure is also what gives languageits flexibility. One can take the example of the reference (but the demonstra-tion can extend to predicative and illocutory acts). As Frege established,the possibility of referring to an entity by several different expressions isnot a deficiency of the language, but on the contrary a necessary property(Frege, 1952): one cannot not refer to this entity according to a particularexperience we have had. But all the same, the classes of linguistic expressionsof these (classes of) possible experiences are not unlimited, but in factquite restricted: there are generally less than a dozen types, going fromproper name to pronoun, with various kinds of determination in between(Charolles, 2002). Lastly, the cooperative nature of the reference (see Clark &Wilkes-Gibbs, 1990) forces us to take into account what we may know of ourinterlocutor’s experience of the whole. This aspect is fundamental, and, itwould seem, the source of the most serious errors of appreciation; but inaddition, it has been shown that if the manifestation of the intention to referto a certain entity were sufficiently successful, it could overcome possibledeterminative referential improprieties: “the young woman at the end ofthe room who is holding a glass of Martini in her hand is the mayor’s daugh-ter” can carry out a successful act of reference even if she is holding a glassof Coke.

The theory of speech acts provides all the knowledge required, but in factonly within the framework of the untroubled use of language. It thus predictsthe existence of several forms of relationship between the meaning of anutterance and the meaning aimed at by the speaker of this statement (inaddition to the ordinary case where both coincide) such as irony, metaphor,implicature (a particular form of inference), indirect speech acts, and so on.(It acts as a prediction in that the theory provides an organized and exhaust-ive enumeration of all the possible cases with regard to a model.) However,research pertaining to the comprehension of this type of speech act in sub-jects affected with lesions of the right hemisphere showed that these distinc-tions are less clear-cut than envisaged and do not observe as clearly as wasthought the hierarchy of complexity supposed between these types of speech


act (Champagne et al., 2002; Champagne, Virbel, Nespoulous, & Joanette,2003). Moreover, the situation is appreciably the same in normal subjects.One is then led to reconsider the right versus left hemisphere opposition inthe treatment of language by the mind-brain; and at same time, these datasuggest reasons for the choice of a formal model of representation amongother logically equivalent models.

Linguistic information

The exact nature of linguistic information is without doubt important. It iseasy to perceive that such information is structured in a complex fashion, andone might hope to find that linguistic theories offer profound and enlighten-ing insights permitting the enrichment of reflection about hypotheses on thetreatment of information by the mind-brain. One such theory was formulatedby Z. Harris, whose most recent work, entitled A theory of language andinformation, speaks for itself (Harris, 1991).

Harris, among many other contributions, defines four types of syntacticconstraint that contribute to giving its “sentencehood” to a sequence ofwords, over which 11 types of informational constraint operate, which indi-cate “how sentences carry information”. These two classes of constraints areinterdependent, the strongest among them being the relative order of intro-duction (what dependence operates on the products of the effect of whichother?).

Two points seem pertinent here:

• each application of a constraint contributes simultaneously to thestructure of the sequence, and to a type of information carried by thesentence. Through its structured character, the notion of informationdefined within this framework is very distant from that defined in 1949 byC. Shannon and W. Weaver in The mathematical theory of communication(1949);

• the intermediate outputs of the different levels of application of theconstraints are not dissimilar, at first sight, from childish or pidgin state-ments. So the constraint referred to as dependence on dependenciescomprises only the predicative structure of a sentence. The constraint oflinearization fixes the mutual order of the words according to their (typesof) dependencies. Finally “actualizers” (noun determinants, person/tenseof the verb, etc.) apply to this resulting structure, as products of theconstraint of form reductions. Harris regarded these actualizers as tracesof the reduction of metaphrases; that is, of sentences having elements ofthe basic sentence as arguments. Thus an intermediate state of a sentence(i.e., a sentence in a state where all the constraints have not yet beenapplied) such as “Max met Lea” would be, for example: “Max meet Leabefore me say Max meet Lea”, which can be represented as:

before(meet(Max, Lea), say(me, meet(Max, Lea))).


We see that verbal morphology is not the only way of conveying informationrelating to time (see above).

Another attraction of Z. Harris’ informational theory of language isthat it provides a concept of the basic sentence (founded on the dependenceon dependencies introduced above) operational in various contexts. Thefollowing summary of an experiment serves as illustration.

The evaluation of performances of comprehension/memorization of textsof the narrative type relies on tests known as “cued recall”, where the subjectsare invited to answer questions relative to a text read or heard beforehand.With the aim of formalizing this test (which questions to ask subjects, how,which responses to expect, which of those obtained are significant) a newsemantic concept has been introduced, that of the question/answer (Q/A)structure associated with a text, a structure suggested by, but independent of,its exploitation in this test (Virbel, 1997). Such a concept is in fact already theproduct of two independent approaches (which have been shown to be com-patible with other pre-existing semantic models, like the Rhetorical StructureTheory; RST; Mann & Thompson, 1988): Z. Harris’ linguistic theory, andmore precisely its concept of basic sentences entering into the composition oftextual sentences; and the logical theory known as “set of answers”, wherethe meaning of a clause is represented by the set of the clauses making up theresponses to a question supported by the clause considered. Moreover, andperhaps especially, one can predict certain semantic properties of a textaccording to formal properties of the Q/A graph (e.g., the aspects of coher-ence), and it seems that far from being an experimental artefact, this Q/Astructure possesses cognitive reality: textual units more densely attached toothers by virtue of this Q/A relation would be more easily memorized.Thanks to a recent collaboration with researchers of the Institute of Psych-ology of the University of Rio Grande do Sol (De Mattos Pimenta Parente,Holderbaum, Virbel, & Nespoulous, 2003), the questionability of narratives;that is, the fact that the question–answer relationship between sentences is agood predictor of the memorization of an account, has been highlighted: thecontents of the sentences most densely connected to the Q/A graph tend to beretained best. This result can be exploited not only in the development ofexperimental protocols, but also in that of various types of documents wherethe communicational efficiency is of prime importance (instructions in theevent of incidents or accidents, for example). This research appears to be agood illustration of the mutual contributions of work done in “normal” andhandicapped situations, and of the various subjects concerned.

Conclusion: Flexibility and adaptability of humanverbal behaviour

We have already emphasized the non-stereotypical nature of human verbalbehaviour. Speaking and understanding, in this context, clearly require thebest possible use of one’s semiotic potential to communicate with others,


often in new situations. So communication constitutes a real challenge in thatsuccess is never guaranteed. The extent of the challenge varies in directproportion to the “novelty”, and thus to the inherent difficulty of the newsituation with which the protagonists are confronted. It also varies accordingto the momentary or durable nature of the situation.

Thus, a pathological subject, affected with an often durable deficit, mustface this challenge permanently, and with varying degrees of success accord-ing to whether the deficit is central or peripheral (see above).

In the case of so-called ‘normal’ subjects, they will be confronted withmany communicational challenges, more so if their pragmatic interactions aremultiple and varied. They can also have difficulty with “degraded” situations,for example, an impoverishment of perceived signals or ignorance of moderntechnological media: knowing how to read is not a sufficient condition forbeing able to consult Web pages or surf the Internet; and knowing how towrite is not the only skill needed to handle a word processor effectively!

Even subjects said to be experts in certain complex linguistic tasks, likesimultaneous interpretation, are nevertheless constrained – within the frame-work of their profession – to deploy various strategies of adaptation to dealwith the cognitive difficulty relating to the task they have to achieve; andbeing bilingual is not the sole requirement for a good interpreter.

We see from the above that the novelty and/or the difficulty of a situationof the types we have enumerated make the use of adaptive or palliative strat-egies essential in the pathological subjects who have served as initial illustra-tions, as well as in anyone engaged in unusual or complex situations.

Consequently, the linguistic competence of a speaker/listener – pathologicalas well as normal – can no longer merely be reduced to the control of acertain number of rules – as has long been advocated by many linguisticmodels; it must integrate a certain number of pragmatic parameters relatingto the contexts of use with linguistic tasks, all within the framework of whatsome call “situated cognition”.

As a result, the diagram presented at the beginning of the chapter can bereformulated, in more general and inclusive terms, in the following way:

Therefore, the linguistic handicap, whatever its origin, has a somewhatamended status compared to the one it usually has in contemporary society.


Instead of the variation from an increasingly illusive, not to say illusory,norm, it becomes at once (a) the situation experienced, to differing degreescertainly, by someone in certain circumstances, and (b) a crucial elementin the characterization of the outcome of verbal behaviour as well asthe functional architecture of language in human beings. In other words,it teaches us much more about the functional dynamics of this linguisticcapacity that is said to be “Man’s domain” than the too mechanicalcomputational metaphor prevalent at the time of the creation of cognitivescience.

Echoing the preceding diagram, the following could illustrate the roadtravelled:

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8 Production and perception ofword tones in patients withbrain damage

Inger Moen

Chris Code, in his introduction to Classic cases in neuropsychology emphasizesthe importance of the single case study: “Developments in neuropsychologyowe much to the discovery and careful examination of sometimes rare andremarkable individuals” (Code, Wallesch, Joanette, & Lecours, 1996, p. 1).One of the many contributions of Chris Code to the development of neuro-psychology, aphasiology and clinical linguistics is his remarkable ability tobring to light, and as editor of books and journals make available to theresearch community, single case studies that have provided new insight intothe relationship between language, mind and brain (e.g., Code 1991; Codeet al., 1996; Code, Wallesch, Joanette, & Lecours, 2002).

The interest of clinical linguists in the prosodic features of speech goesback to a case study by Monrad-Krohn (1947) of a patient whose “melody oflanguage”, rhythm and pitch variation, was disturbed as a result of left hemi-sphere damage, while her ability to sing was not affected. “The variations ofpitch had by no means disappeared. On the contrary they were rather greaterthan usual in Norwegian, but they were neither adequate nor quite constantin their inadequacy” (Monrad-Krohn, 1947, p. 411). Monrad-Krohn’s patienthad suffered left hemisphere damage, but the clinical-perceptual impressionis that damage to either hemisphere may lead to deviations of sentenceprosody. Acoustic investigations have revealed both normal and abnormalcharacteristics in the intonation of patients with Broca’s and Wernicke’saphasia and right-hemisphere-damaged patients (Cooper & Klouda, 1987;Cooper, Soares, Nicol, Michelow, & Goloskie, 1984; Danly & Shapiro, 1982;Ryalls, 1982; Shapiro & Danly, 1985). It is, however, unclear to what extentthese abnormalities are linguistic in nature and to what extent they are causedby poor control of the physiological mechanisms associated with phonationand fundamental frequency variation, or whether they are the result of adeficiency in the long-range planning of linguistic units (for a review anddiscussion, see Ryalls & Behrens, 1988).

Speech prosody includes the linguistic categories of stress, rhythm, tone,duration, and intonation. In addition to having strictly linguistic functions,prosody can also be used to signal the speaker’s attitudes and emotions. Theauditory correlates of prosody are variations in pitch, loudness, tempo,

and rhythm. These features have a primary relationship with the physicaldimensions of fundamental frequency, intensity, and time.

A key issue in the investigation of prosody in the brain-damaged populationis the search for the neuroanatomical underpinnings of the various prosodicfunctions.

If the physical correlates of prosody – fundamental frequency, intensity,and time – are of primary importance when it comes to determining hemi-spheric specialization, we would expect unilateral brain lesions to result inthe same type of behaviour, regardless of the linguistic functions of the dis-turbed physical features. We would, for instance, expect disturbed ability tomodulate fundamental frequency to be evident as deviant pitch throughouta patient’s speech, regardless of the linguistic functions of fundamentalfrequency in the particular language. If, on the other hand, the linguisticfunctions are crucial when determining hemispheric specialization, we wouldexpect the behavioural effect of unilateral lesions to vary depending onthe linguistic functions of the physical correlates in the patient’s language.We might expect, for instance, that it would be possible for a patient withunilateral lesions to produce differences in pitch to signal intonationalvariation, but not to signal variation in lexical tone. A third possibility wouldbe that both hemispheres are engaged in the processing of prosody, but thatthey process different acoustic features, for instance that one hemisphereprocesses fundamental frequency and the other hemisphere processes time(Gandour, 1998).

During the last decades data have accumulated on prosodic disorders asa result of brain damage, data that have produced several major hypothesesconcerning the neuroanatomical regions active in prosodic processing (for areview, see Baum & Pell, 1999). The most straightforward of these hypothesesassumes that all aspects of prosody are processed in the right hemisphere andintegrated with linguistic information from the left hemisphere via the corpuscallosum (Klouda, Robin, Graff-Radford, & Cooper, 1988). Van Lancker(1980) proposes a hypothesis which posits that affective or emotional prosodyis controlled by the right hemisphere, whereas the left hemisphere is special-ized for linguistic prosody. This is referred to as the functional lateralizationhypothesis. This hypothesis assumes that there is a scale of prosodic featuresfrom the most linguistically structured (e.g., Chinese and Norwegian tones)associated with left-hemisphere specialization to the least linguistically struc-tured (e.g., emotional tone, voice quality) associated with right-hemispherespecialization. A third major hypothesis assumes that the perception andproduction of prosody are mainly subserved by subcortical regions and arenot lateralized to either of the hemispheres (e.g., Cancelliere & Kertesz,1990). Several recent studies have supported the hypothesis that individualacoustic cues to prosody may be independently lateralized (e.g., Van Lancker& Sidtis, 1992).

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Tone languages

Pitch variation is a property of all natural languages. No language is spokenon a monotone. But pitch differences function differently in different lan-guages. In tone languages differences in pitch at syllable or word level areused to distinguish the lexical meaning of words. In these languages pitchvariations are contrastive in the lexicon. In nontone languages pitch may beused to signal intonation at the level of the phrase and the sentence. Tonelanguages also exhibit sentence intonation, but generally with fewer possi-bilities of variation than nontone languages because of the use of pitch at thesyllable and word level. There is general agreement that the primary acousticcorrelates of tone are states and movements of the fundamental frequency ofthe voice (F0), although there may be concomitant changes in time, intensityand phonation.

Tone languages are quite numerous. According to Fromkin and Rodman(1993) there are more than 1000 tone languages in Africa alone. However,when it comes to the investigation of language as a result of brain damage,the data from tone languages come from only a limited number of languages,to be presise, from different dialects of Chinese, from Thai and fromNorwegian (for a review see Gandour, 1998).

Tone languages differ with regard to number and shape of lexical tones.Mandarin Chinese, for instance, has four lexical tones: high level, rising,low level, and falling (Liang & van Heuven, 2004). Cantonese has six tones:high level, high rising, high-mid level, low level, low rising, low-mid level.In many tone languages there are sets of words that differ only in tone. InThai, for instance, a language with five tones: mid, low, falling, high, andrising, a set of five words can be distinguished by variation in tone only:/khaa/, to be stuck; /khàa/, a kind of spice; /khâa/, to kill; /kháa/, to engage intrade; /khàá/, leg (Gandour, 1998).

In Norwegian, a so-called pitch accent language, where the tonal contrastis restricted to one syllable in a word, pitch and stress are closely linked. Theaccented syllable is also stressed. The accented syllable carries one of twophonemically contrastive tones, referred to as Accent1 and Accent2. Thereare a number of minimal pairs differing only in tone: for example, vannet/1vane/ (the water); vanne /2vane/ (to water); skuffen /1skufen/ (the drawer);skuffen /2skufen/ (the showel) (Moen & Sundet, 1996).

The perception of tone after unilateral brain damage

Studies of the perception of tonal contrasts in brain-damaged speakers oftone languages point to a left-hemisphere dominance in tonal perception.Hughes, Chan and Su (1983) in a study of 12 Mandarin Chinese patientswith right-hemisphere lesions found that only five of the patients showeda mild defect in a tonal identification task. The majority of the patientsachieved a perfect score.

Production and perception of word tones after brain damage 127

In another study of Mandarin Chinese Naeser and Chan (1980) foundthat the perception of Mandarin Chinese tones was impaired for their non-fluent mixed aphasic patient, a bilingual speaker of Mandarin Chinese andCantonese. She scored only 55% correct on a listening identification test ofthe four Mandarin Chinese tones, whereas a normal control scored 100%.Her performance was poor across all four tones. A CT scan showed extensivecortical and subcortical damage to the left hemisphere. The right hemispherewas not affected.

Yiu and Fok (1995) reported on the results of a tonal perception test in21 right-handed Cantonese aphasic speakers: 11 anomic, 2 conduction and2 Wernicke’s, 2 Broca’s and 4 transcortical motor aphasic patients. Therewere two control groups, a normal group of eight persons and a non-corticalbrain-damaged non-aphasic group consisting of three dysarthric patients.Except for four of the anomic patients, where no CT scan was available, theother aphasic patients had left-hemisphere damage demonstrated on CTscans. The aphasic group performed significantly worse than the normalcontrol group and the dysarthric patients. The performance of the normalcontrols and the dysarthric group was very similar. The aphasic subjectsdemonstrated errors with all tones, but they had more difficulty with the levelthan with the falling tones. The scores were not significantly different amongthe aphasic groups, and the scores did not correlate significantly with severityof aphasia or post-onset time. The normal performance of the dysarthricsubjects suggests that the aphasic group’s perception problem can be attributedto left-hemisphere lesions and not to a general brain-damage effect.

Gandour and Dardarananda (1983) studied the perception of tonal con-trasts in a group of four Thai aphasic speakers, two Broca aphasic patients,one transcortical motor aphasic patient, and one conduction aphasicpatient. In addition there were two controls, one right-brain-damaged non-aphasic patient and a normal speaker. The results of the perception testindicated that all four aphasic patients performed significantly worse thaneither of the controls. The right-hemisphere-damaged control achieved nearperfect scores. This result is further support for the assumption that the tonalperception deficit in aphasic speakers of tone languages is not due to ageneral brain-damage effect. No difference in performance among theaphasic patients could be attributed to a specific aphasia syndrome. Theaphasic patients’ tonal confusions were similar to those of normals, and theirperception errors indicated that the perception deficit was general to all fivetones rather than selective to individual tones.

Moen and Sundet (1996) investigated the perception of the two tonalcontrasts in East Norwegian in eight brain-damaged speakers, four left-hemisphere-damaged aphasic speakers and four right-hemisphere-damagednonaphasic speakers. The aphasic speakers included two Broca’s and twoanomic aphasic patients. There was a control group of ten normal speakers.The control group identified all the words correctly. The right-hemisphere-damaged group’s performance was comparable to that of the normal controls:

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only one incorrect identification. In the left-hemisphere-damaged group, onthe other hand, only one of the four patients identified all the target wordscorrectly. The other three patients identified from 50% to 92% of the wordscorrectly. The confusion between the two accents was bidirectional: 17%of Accent1 stimuli and 20% of Accent2 stimuli were reported as the otheraccent.

The general unimpaired performance of right-hemisphere-damagedpatients is not unexpected in view of the fact that dichotic listening experi-ments have demonstrated a right ear superiority in the perception of tonalcontrasts (Moen, 1993; Van Lancker & Fromkin, 1973, 1978). Whether thereduced, but not completely disrupted, performance of the left-hemisphere-damaged patients is due to residual mechanisms still operating within thedamaged left hemisphere, to mechanisms in the right hemisphere, or tosubcortical mechanisms is a moot point.

There is little evidence in the studies reported here for a selective deficitin the perception of particular lexical tones. All tones seem to be equallydifficult. The exception is Yiu and Fok’s study (1995). They found thatfalling tones were easier to identify than level ones. Gandour (1998) pointsout that the tones that seem to be most susceptible to confusion, for aphasicpatients as well as for normal subjects, are those that are phoneticallysimilar in height and shape to other tones in the same tonal system. Thecurrent evidence indicates that, on the whole, the aphasic patients make moreof the same kinds of perceptual errors that the normal subjects make. Thereis a quantitative rather than a qualitative difference between the errors madeby the two groups.

The perception of tone after general brain damage

Moen, Simonsen, Oksengaard and Engedal (2004) investigated the abilityof ten elderly patients with dementia of the Alzheimer’s type (AD) and tenage-matched normal control subjects to distinguish perceptually betweenthe two Norwegian word tones. AD patients suffer from a progressive neuro-degenerative disorder affecting both cerebral hemispheres. It is thereforepossible that their perception of tonal distinctions might differ from that ofpatients with unilateral cerebral damage and from normal controls. The teststimuli were a set of drawings illustrating minimal pairs of words differingonly in word tones. The test words were read by the examiner, and the sub-jects were asked to point to the pictures corresponding to the stimulusword. The test scores of half the AD patients matched those of the normalcontrols. The other five patients’ performance was impaired. The AD patientshad all been tested with the Mini Mental State Examination, a test of cogni-tive ability. Low cognitive test scores corresponded on the whole to impairedperformance on the word tone test, with one notable exception. The patientwith the highest cognitive test scores made most mistakes on the word tonetest. A possible contributing factor to his impaired performance might be


linked to the distribution of his cerebral lesions. It is possible that the damageincluded areas implicated in semantic processing. He may have had problemsdistinguishing the meanings of the word pairs presented to him, in additionto a possible accent discrimination problem.

In order to understand a spoken word, the listener has to convert acousticinput into meaning. This involves at least two distinct processes: phonetic andphonemic decoding, and lexical activation. If the ability to distinguish betweentwo different phonological strings is impaired, this may lead to the activationof a wrong word in the mental lexicon. This is presumably the reason whysome patients with aphasia fail to distinguish between minimal pairs ofwords differing only in word tones. If the distinction between different lexicalitems is reduced due to a breakdown in semantic memory, the ability todifferentiate between pairs of words will also be reduced, and a wrong lexicalitem may be activated. Lexical semantic impairment is a well-documentedcharacteristic of many AD patients (Bayles & Kaszniak, 1987), and thebehaviour of the AD patients during the word tone test also indicated asemantic problem. Whereas patients with aphasia, who had been tested withthe same test previously, pointed relatively unhesitatingly to one of the twopictures when the stimulus word had been presented, the AD patients talkedabout the pictures, and commented on similarities and differences in thedrawings before they made their choice. In some cases they repeated thestimulus word, looked at the pictures and said, “There is no difference.” It is,however, not possible on the basis of this test alone to decide whether the ADpatients’ problem was purely semantic or a combination of blurred semanticdistinctions and reduced phonological perception.

The production of tone after unilateral brain damage

Studies of tone production in the speech of aphasic speakers of Mandarin,Cantonese, Thai, and Norwegian indicate that left-hemisphere damage maylead to deviant tone production, whereas the tone production of right-hemisphere-damaged patients is relatively spared. Deficient tone productionalso seems to depend on type and severity of aphasia and time since onsetof brain damage. A production deficit is most evident in the severly aphasicpatients and more evident shortly after onset of brain damage than later.Non-fluent Broca’s aphasic patients have more problems producing cor-rect tonal contrasts than fluent Wernicke’s or conduction aphasic patients(Gandour, 1987; Gandour, Petty, & Dardarananda, 1988; Gandour et al.,1992; Moen & Sundet, 1996; Naeser & Chan, 1980; Packard, 1986; Ryalls& Reinvang, 1986). There is, however, no indication of a particular patternof tonal disruption in any specific type of aphasia.

The evidence for a selective deficit in the production of particular tonesis inconclusive at present. Investigations of Cantonese and Mandarin seemto indicate that static (level) tones may be more resistant to disruptionthan dynamic (contour) tones. Yiu and Fok (1995) found that their aphasic

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subjects made mistakes in the production of all six Cantonese tones, thoughTone 6 (low level) was the easiest to produce. Liang and van Heuven (2004)studied a Mandarin aphasic subject. In their study, out of the four lexicaltones, the least compromised tone was Tone 1 (high level, 88% correct). Thesecond best production was Tone 3 (low dipping, 20% correct). Accordingto Liang and van Heuven, Tone 1 and Tone 3 can both be analysed as statictones: the high level tone and the low level tone, respectively. The dynamictones, Tone 4 (the falling tone, 16% correct) and Tone 2 (the rising tone,9% correct) were the most difficult to produce. On the other hand, evidencefrom Thai seems to indicate that falling tones are easier to produce than leveltones. Gandour et al. (1988, 1992), in a series of acoustic phonetic studieson tonal disruption in brain-damaged subjects in Thai, found that almostall tonal substitutions resulted in mid, low, or falling tones. The mid, low,and falling tones are all characterized by a falling fundamental frequencycontour throughout their duration, whereas the high and rising tones are not(Gandour, 1998). As a result of the reduction of transglottal air pressure,the pitch has a tendency to drop over the course of an utterance. It may be thesame mechanism that makes a rising pitch contour more difficult to producethan a falling one. This mechanism cannot, however, account for the superiorproduction of the level tones in the Chinese aphasic speakers.

East Norwegian differs from the Asian tone languages under review inhaving only two tones, Accent1 and Accent2. Both accents are associatedwith a low pitch level. The difference between them is located in the beginningof the syllable, before the pitch reaches its lowest level. Accent2 has an exten-sive fall in pitch from the beginning of the syllable to its lowest pitch level.Accent1 may either have an initial narrow fall or a constant low level. Thepitch pattern may be described as high-low in Accent2 syllables and as low inAccent1 syllables. Accent1 is the unmarked accent, the pitch pattern usedwhen the opposition between the two accents is neutralized, and it is theaccent given to new loanwords. An investigation of tonal production in EastNorwegian aphasic patients (one Broca and two anomic) tested the ability todifferentiate between minimal pairs of words differing only in tone. The testmaterial was a set of drawings illustrating minimal pairs of this type. Thetarget words were written below each drawing. The three aphasic patients allfailed to produce correct distinctions between the two accents in some of theminimal pairs (Moen & Sundet, 1996). It is noteworthy that most of themistakes involved the substitution of Accent1 for Accent2. There may be twopossible explanations for these unidirectional mistakes, an articulatoryexplanation and a phonological one. From an articulatory point of view,Accent2, with a high fall, may be more difficult to produce than Accent1,with a limited fall or a low level. From a phonological point of view most ofthe accent mistakes involve the replacement of a marked feature by anunmarked one. According to the theory of phonological underspecification(e.g., Kenstowicz, 1994) only the marked accent will be specified in the lexicalphonological representation. The patients’ accent substitutions could then be


accounted for by assuming that Accent2 words occasionally are retrievedfrom the mental lexicon without accent specification. These words will then,by default, be assigned Accent1.

If the substitution of Accent1 for Accent2 reflects an articulatory problemand not a phonological one, it would be expected that Accent1 would notonly replace Accent2 in words that are members of minimal pairs. One of thepatients from the study, the Broca aphasic person, was also tested in a readingtest that did not consist of minimal pairs. In this test he produced a cleardistinction between the two accents. It is therefore unlikely, in the case of thispatient, that the problem was an articulatory one (Moen & Sundet, 1999).The theory of underspecification cannot alone account for this patient’saccent production. If phonological underspecification was the only mechan-ism at work, one would expect some Accent1 contours on Accent2 wordsregardless of whether they were members of minimal pairs or not. In add-ition to a theory of phonological underspecification, a connectionist modelof lexical access might account for the patient’s tonal productions. Thistype of model assumes that when a target word is accessed, the target wordtogether with phonologically similar words will be activated (e.g., Dell, 1988).If the target word is the member of a minimal accent pair, two identicalsegmental phonological structures with different prosodic patterns will beactivated. The patient then has to choose between these two. When the targetword is not a member of a minimal pair, the patient does not have to makea choice between two identical segmental structures with different pitchpatterns. As a result, the correct accent is also produced on Accent2 words.

Studies of intonation in nontone languages have shown a narrowing of thefundamental frequency range in the speech of aphasic patients (Cooper et al.,1984; Ryalls, 1982). Gandour et al. (1992), however, in their investigation oftonal production in brain-damaged Thai speakers, found that the patients’deviant tone production could not be attributed to a compressed tone space.Not only was there no compression of the fundamental frequency range, butthe patients’ tone space was actually wider than the normal range. Liang andvan Heuven (2004), on the other hand, in their study of a Mandarin speaker,found the patient’s F0 range to be less than half that of a normal control. AndMoen (2004), in a study of three Norwegian patients with Broca’s aphasia,arrived at a similar result. There was a phonological distinction between thetwo word tones in the speech of all the patients, but phonetically the F0

variation in the aphasic patients covered a narrower frequency span than inthe speech of the normal controls. Why these studies have arrived at suchdifferent results is unclear.

Conclusions

Investigations of the tonal perception and production in brain-damagedspeakers of tone languages have demonstrated reduced ability in bothtasks in left-hemisphere-damaged patients, whereas tonal production and

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perception is spared in right-hemisphere-damaged nonaphasic patients,indicating that the processing of lexical tones is the property of the lefthemisphere. Whether the reduced, but not disrupted, performance of theleft-hemisphere-damaged patients is due to residual mechanisms in the lefthemisphere, to mechanisms in the right hemisphere, or to subcorticalmechanisms, is unclear.

There is little evidence of a selective deficit, a rank order of difficulty, in theperception of particular types of tones. The exception is Yiu and Fok’s studyof Cantonese tones, which found that falling tones were easier to identifythan level ones. There is no indication of different perceptual deviationsdepending on type and severity of aphasia. In general, aphasic patientsmake the same kind of perceptual errors as normal subjects do, but theymake more errors.

When it comes to the tonal production of brain-damaged patients, theresults of the investigations are in some respects less clear. The ability toproduce, like the ability to perceive, tonal contrasts is normal in the right-hemisphere-damaged subjects and reduced in the aphasic left-hemisphere-damaged subjects. The severity of the tonal production disability seems todepend on type of aphasia and on time post-onset of brain damage. AnteriorBroca’s aphasic patients have more problems than posterior fluent aphasicpatients. And the problems are most severe in the period shortly after braindamage. There is no indication of a particular type of tonal disruptionassociated with a specific type of aphasia.

There is no clear evidence of selective production deficits of particulartones. But there are indications that a falling tone may be easier to producethan a rising or level tone, possibly due to the general tendency to reduce thetransglottal air pressure during an utterance.

Directions for future research

Although the nature of the mechanisms underlying reduced tonal perceptionand production are at present unclear, the current evidence indicates thattonal processing is impaired following left hemisphere damage in tone lan-guages. There are, however, few investigations of tonal processing in patientswith subcortical damage, such as patients with Parkinson’s disease. Furtherinvestigations of this patient group might expand our knowledge of theneuroanatomical bases for the processing of tonal contrasts. Most studiesof tones in the brain-damaged population have focused on single wordsor short utterances in relatively few languages. Future research will, it ishoped, include longer stretches of speech and data from a wider range of thenumerous tone languages of the world.


References

Baum, S. R., & Pell, M. D. (1999). The neural bases of prosody: Insights from lesionstudies and neuroimaging, Aphasiology, 13 (8), 581–608.

Bayles, K. A., & Kaszniak, A. W. (1987). Communication and cognition in normalaging and dementia. London: Taylor & Francis.

Cancelliere, A., & Kertesz, A. (1990). Lesion localisation in acquired deficits ofemotional expression and comprehension, Brain and Cognition, 13, 133–147.

Code, C. (1991). The characteristics of aphasia. Hove, UK: Lawrence ErlbaumAssociates Ltd.

Code, C., Wallesch, C.-W., Joanette, Y., & Lecours, A. R. (1996). Classic cases inneuropsychology. Hove, UK: Psychology Press.

Code, C., Wallesch, C.-W., Joanette, Y., & Lecours, A. R. (2002). Classic cases inneuropsychology: Vol 2. Hove, UK: Psychology Press.

Cooper, W. E., & Klouda, G. V. (1987). Intonation in aphasic and right-hemisphere-damaged patients. In J. H. Ryalls (Ed.), Phonetic approaches to speech productionin aphasia and related disorders (pp. 59–77). Boston/Toronto/San Diego: Little,Brown & Co.

Cooper, W. E., Soares, C., Nicol, J., Michelow, D., & Goloskie, S. (1984). Clausalintonation after unilateral brain damage, Language and Speech, 27, 17–24.

Danly, M., & Shapiro, B. E. (1982). Speech prosody in Broca’s aphasia. Brain andLanguage, 16, 171–190.

Dell, G. S. (1988). The retrieval of phonological forms in production: Tests ofpredictions from a connectionist model. Journal of Memory and Language, 27,124–142.

Fromkin, V., & Rodman, R. (1993). An introduction to language (5th ed.). New York:Harcourt Brace Jovanovich.

Gandour, J. (1987). Tone production in aphasia. In J. H. Ryalls (Ed.), Phoneticapproaches to speech production in aphasia and related disorders (pp. 45–57).Boston/Toronto/San Diego: Little, Brown & Co.

Gandour, J. (1998). Aphasia in tone languages. In P. Coppens, Y. Lebrun, & A. Basso(Eds.), Aphasia in atypical populations (pp. 117–142). Hove, UK: Lawrence ErlbaumAssociates Ltd.

Gandour, J., & Dardarananda, R. (1983). Identification of tonal contrasts in Thaiaphasic patients. Brain and Language, 18 (1), 98–114.

Gandour, J., Petty, S. H., & Dardarananda, R. (1988). Perception and production oftone in aphasia. Brain and Language, 35, 201–240.

Gandour, J., Ponglorpisit, S., Khunadorn, F., Dechongkit, S., Boongird, P., Boonklam,R., et al. (1992). Lexical tones in Thai after unilateral brain damage. Brain andLanguage, 43, 275–307.

Hughes, C. P., Chan, J. L., & Su, M. S. (1983). Aprosodia in Chinese patients withright cerebral hemisphere lesions. Archives of Neurology, 40, 732–736.

Kenstowicz, M. (1994). Phonology in generative grammar. Oxford, UK: BlackwellPublishers.

Klouda, G. V., Robin, D. A., Graff-Radford, N. R., & Cooper, W. E. (1988). The roleof callosal connections in speech prosody. Brain and Language, 35, 154–171.

Liang, J., & van Heuven, V. J. (2004). Evidence for separate tonal and segmental tiersin the lexical specification of words: A case study of a brain-damaged Chinesespeaker. Brain and Language, 91, 282–293.

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Moen, I. (1993). Functional lateralization of the perception of Norwegian wordtones – Evidence from a dichotic listening experiment. Brain and Language, 44,400–413.

Moen, I. (2004). Dysprosody in Broca’s aphasia: A study of Norwegian braindamaged patients. In L. Verbitskaya & T. Chernigovskaya (Eds.), Teoreticheskijeproblemy jazykoznanija. Sbornik statej k 140-letiju kafedry obshchego jazykoznanijafilologicheskogo fakul’teta Sankt-Peterburgskogo gosudarstvennogo universiteta (pp.341–356) [Theoretical problems of linguistics. Papers dedicated to 140 years of theDepartment of General Linguistics of St Petersburg State University]. St Petersburg:Philological Faculty of St Petersburg State University Publishing House.

Moen, I., Simonsen, H. G., Oksengaard, A. R., & Engedal, K. (2004). Perceptionof the Norwegian word tones in patients with Alzheimer’s disease (AD). InB. Murdoch, J. Goozee, B.-M. Whelan, & K. Docking (Eds.), Proceedings ofthe 26th International Association of Logopaedics and Phoniatrics (IALP) 2004Congress. Brisbane: IALP.

Moen, I., & Sundet, K. (1996). Production and perception of word tones (pitchaccents) in patients with left and right hemisphere damage. Brain and Language, 53,267–281.

Moen, I, & Sundet, K. (1999). An acoustic investigation of pitch accent contrasts inthe speech of a Norwegian patient with a left-hemisphere lesion (Broca’s aphasia).In B. Maassen & P. Groenen (Eds.), Pathologies of speech and language: Advances inclinical phonetics and linguistics (pp. 221–228). London: Whurr Publishers.

Monrad-Krohn, G. H. (1947). Dysprosody or altered melody of language, Brain, 70,405–423.

Naeser, M. A., & Chan, S. W.-C. (1980). Case study of a Chinese aphasic with theBoston Diagnostic Aphasia Exam. Neuropsychologia, 18, 389–410.

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Ryalls, J. H. (1982). Intonation in Broca’s aphasia. Neuropsychologia, 20, 355–360.Ryalls, J. H., & Behrens, S. J. (1988). An overview of changes in fundamental

frequency associated with cortical insult, Aphasiology, 2, 107–115.Ryalls, J., & Reinvang, I. (1986). Functional lateralisation of linguistic tones: Acoustic

evidence from Norwegian. Language and Speech, 29, 389–398.Shapiro, B. E., & Danly, M. (1985). The role of the right hemisphere in the control

of speech prosody in propositional and affective contexts, Brain and Language, 25,19–36.

Van Lancker, D. (1980). Cerebral lateralization of pitch cues in the linguistic signal.International Journal of Human Communication, 13, 227–277.

Van Lancker, D., & Fromkin, V. (1973). Hemispheric specialization for pitch and“tone”: Evidence from Thai. Journal of Phonetics, 1, 101–109.

Van Lancker, D., & Fromkin, V. (1978). Cerebral dominance for pitch contrasts intone language speakers and in musically untrained and trained English speakers.Journal of Phonetics, 6, 19–23.

Van Lancker, D., & Sidtis, J. J. (1992). The identification of afffective-prosodic stimuliby left- and right-hemisphere-damaged subjects: All errors are not created equal.Journal of Speech and Hearing Research, 35, 963–970.

Yiu, E. M.-L., & Fok, A. Y.-Y. (1995). Lexical tone disruption in Cantonese aphasicspeakers. Clinical Linguistics and Phonetics, 9 (1), 79–92.


9 Subcortical aphasiaHistorical perspective andcontemporary thinking

Bruce E. Murdoch

Introduction

The concept that structures lying below the level of the cerebral cortex in thesubcortical regions of the brain may be involved in language processing hasbeen the subject of controversy for more than a century. In recent yearsevidence provided primarily through cliniconeuroradiological investigationshas greatly increased awareness and acceptance that subcortical structuressuch as the basal ganglia and thalamus have a role to play in language. Thisevidence to a large extent has come from a relatively small group ofresearchers who have provided theories and mechanisms by which subcorticalstructures may influence language processing, backed up by empirical evi-dence. The work of these researchers would not have come into the publicdomain without the support of journal editors with sufficiently open mindsto accept and publish work that ran counter to contemporary thinking. Onesuch journal editor has been Chris Code. Chris has always kept an open mindon all aspects of brain function relating to the occurrence of aphasic dis-orders and through his editorship of the journal Aphasiology has alwaysprovided a forum where new theories relating to language processes and lan-guage disorders can be espoused and debated. Without Chris Code and hiswillingness to support and publish work relating to new aspects of brain-related function, much of the progress towards furthering our understandingof subcortical language mechanisms would have been greatly retarded. Thepresent chapter discusses subcortical language mechanisms and subcorticalaphasia from a historical perspective, and presents the latest thinking in rela-tion to how subcortical structures may influence language and languagedisorders. The progress made towards greater enlightenment of subcorticallanguage processes can in many ways be linked to encouragement provided byChris Code and other editors of journals prepared to extend the boundariesof contemporary theory and practice.

Historical perspective

Ever since the era of “phrenological science” the cerebral cortex has beenconsidered the neural substrate of higher psychological function, includinglanguage. In keeping with this view, the standard “associationist” anatomo-functional model of language organization was deeply rooted in corticalareas and their fibre connections (Lichtheim, 1885; Wernicke, 1874). Accord-ing to this still influential model, linguistic representations are stored indiscrete cortical areas, and consequently subcortical brain lesions werethought to only produce language deficits if they disrupted the white matterfibres that connect the various cortical language centres (e.g., disruption ofthe arcuate fasciculus in instances of conduction aphasia).

Despite the emphasis on the cerebral cortex, evidence to suggest the occur-rence of aphasia associated with subcortical brain lesions has been availablesince the late nineteenth century. More than a century ago Broadbent (1872)proposed that words were “generated” as motor acts in the basal ganglia.Marie (1906) challenged the traditional view of aphasia and described aclinical syndrome that he called “anartria,” secondary to dysfunction of aspecific subcortical region involving the caudate nucleus, putamen, internalcapsule and thalamus (Marie’s quadrilateral space). Monakow (1914) alsochampioned the participation of the lentiform nucleus in the pathogenesis ofaphasia. Perusal of the monumental anatomoclinical summaries publishedin the early twentieth century, such as those by Moutier (1908), Henschen(1922) and Nielsen (1946) also reveals a number of cases of language disturb-ances associated with lesions apparently limited to subcortical structures.Unfortunately, these empirical data were subjected to radically differentinterpretations by the various authors. Moutier supported the “quadrilatèrè”proposed by his teacher Pierre Marie. In contrast Nielsen explicitly deniedany role of subcortical structures in mental activities, interpreting his obser-vations in strict adherence to the traditional Wernicke–Lichtheim model.Later, Fisher (1959) described aphasia as a clinical feature in a patient withleft thalamic haemorrhage. Penfield and Roberts (1959) suggested that thethalamus had an integrative function in language processing.

Since the late 1970s, the traditional view of language processing in the brainhas been challenged by the findings of an increasing number of cliniconeuro-radiological correlation studies that have documented the occurrence ofadult language disorders in association with apparently subcortical vascularlesions. The introduction in recent decades of new neuroradiological methodsfor lesion localisation in vivo, including computed tomography in the 1970sand more recently magnetic resonance imaging, has led to an increasingnumber of reports in the literature of aphasia following subcortical lesions(for reviews of in vivo correlation studies see Alexander, 1989; Cappa & Vallar,1992; Murdoch, 1996). In particular, these new neuroimaging techniqueshave allowed more precise identification and localization of subcortical lesionparameters (Alexander, Naesar, & Palumbo, 1987; Cappa & Wallesch, 1994),

Subcortical aphasia 137

and hence the ability to evaluate the influence of specific lesions in producingmotor and cognitive anomalies. Therefore, although the concept of subcorticalaphasia remains controversial, recent years have seen a growing acceptanceof a role for subcortical structures in language and the development of arange of models that attempt to explain the nature of that role. Prior to dis-cussing models of subcortical participation in language, however, it is neces-sary to first review the relevant subcortical neuroanatomy and the reportedclinical features of subcortical aphasia.

Neuroanatomy of the subcortical region

The basal ganglia, thalamus and subcortical white matter pathways representthe subcortical structures that have been afforded the most considerationwithin contemporary models of subcortical participation in language. Morerecently, studies based on deep brain stimulation have also suggested a possiblerole for the subthalamic nucleus in language processes (Whelan, Murdoch,Theodoros, 2003; Whelan, Murdoch, Theodoros, Silburn, & Hall, 2004a).Further, a role for the cerebellum in language has also been suggested(Docking, Murdoch, & Ward, 2003; Leiner, Leiner, & Dow, 1993).

Clinically, the basal ganglia represent a functional system of interconnectedcomponents that typically include the corpus striatum (i.e., caudate nucleus,putamen and internal [GPi] and external [GPe] segments of the globus pal-lidus), subthalamic nucleus and substantia nigra (pars compacta [SNPC] andpars reticulata [SNPR]). Anatomically, this system is largely positioned atthe cortico-subcortical boundary, and functionally has been hypothesized tobe composed of a number of neural circuits subserving motor, cognitive andlimbic functions (Alexander & Crutcher, 1990; Alexander, Crutcher, & DeLong, 1990). In general, the basal ganglia can be considered to comprisea group of “input structures” (the caudate nucleus, putamen and ventralstriatum) that receive direct input essentially from all areas of the cerebralcortex and “output” structures (the GPi, the SNPR and the ventral pallidum)that project back to the cerebral cortex via the thalamus. Contemporarythinking is that the striatum acts as a “multi-laned” throughway that formspart of a series of multi-segmented circuits connecting the cerebral cortex,basal ganglia and thalamus (Alexander, De Long, & Strick, 1986; Graybiel &Kimura, 1995; Middleton & Strick, 2000). Thus basal ganglia anatomy ischaracterized by their participation in multiple “loops” with the cerebralcortex, each of which follows the basic route of: cortex → striatum → globuspallidus/substantia nigra → thalamus → cortex in a unidirectional fashion.Within contemporary theories of subcortical participation in language, ithas been suggested that the basal ganglia mediate linguistic processes byway of these cortico-striato-pallido-thalamo-cortical pathways (Crosson,1985; Wallesch & Papagno, 1988). Consequently, these loops constitute theneuroanatomical basis of subcortical participation in language.

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Syndromes of subcortical aphasia

The majority of studies that have attempted to explore the notion of sub-cortical participation in language have investigated the impact of vascularthalamic and striatocapsular lesions on linguistic abilities (Murdoch, 1990),giving rise to syndromes of thalamic and striatocapsular aphasia. Despite thefact that the aphasic symptom complex associated with thalamic lesionsappears to approximate a more uniform syndrome than its striatocapsularcounterpart, heterogeneity within each aphasic category has been documentedwith respect to language profiles and recovery rates (Murdoch, 1996). Thisinconsistency has been partly attributed to methodological limitations includ-ing the wide-ranging scope of assessments utilized and experimental designsemployed. Kennedy and Murdoch (1990) emphasized that general measuresof language function typically utilized in the assessment of subcortical apha-sia, may have lacked the requisite sensitivity to detect more subtle, high-levellinguistic deficits within this population. Furthermore, it has been suggestedthat the complexity of circulatory dynamics and the protean nature ofspontaneous vascular lesions may have also contributed to the inherentvariability of symptoms observed (Graff-Radford, Eslinger, Damasio, &Yamada, 1984).

Thalamic aphasia

Numerous studies have documented aphasia after dominant thalamic lesions,the function of the thalamus in language being described in terms of anintegrative role (Penfield & Roberts, 1959; Schuell, Jenkins, & Jiménez-Pabón,1965), arousal mechanisms (Luria, 1977; McFarling, Rothi, & Heilman, 1982;Riklan & Cooper, 1975), modulation and integration of cortical areas topermit language processing (Ojemann, 1983), semantic verification of formu-lated cortical language segments in verbal production (Cappa & Vignolo,1979; Wallesch & Papagno, 1988), managing of verbal memory (Reynolds,Turner, Harris, Ojemann, & Davis, 1979) or a selective engagement of corticalmechanisms leading to an impairment in the semantic–lexical interface(Nadeau & Crosson, 1997a, 1997b).

Commonly, language disturbances resulting from lesions of the thalamusare of a mixed transcortical sensory aphasia (Crosson, 1992; Murdoch, 1996)and characterized by word finding difficulties, paraphasias, neologistic output,perseveration and reduced spontaneous speech output in the presence ofrelatively preserved repetition and variable, but often good, auditory com-prehension abilities (Crosson, 1984; Jonas, 1982). This profile, however, hasbeen documented to vary (Cappa & Vignolo, 1979; Crosson, 1984), includingreports of normal language abilities in individuals following thalamic haem-orrhage (Cappa, Papagno, Vallar, & Vignolo, 1986). Despite this variability,language disturbances following thalamic lesions do present a more uniformclinical picture than those associated with striatocapsular lesions, and it is


generally accepted that a typical thalamic aphasia can be characterized by theclinical presentation.

Striatocapsular aphasia

Although in vivo correlation studies have documented beyond reasonabledoubt that language impairments may occur in association with lesionsconfined to the striatocapsular region of the dominant hemisphere, mani-festations of language pathology subsequent to lesions of the basal gangliaand internal capsule have failed to establish a homogeneous symptom com-plex with no unitary striatocapsular aphasia being identified (Crosson, 1985;Kennedy & Murdoch, 1993; Nadeau & Crosson, 1997a, 1997b). Further-more, the effects of striatocapsular lesions on language abilities appear, ingeneral, to be more enduring than the impact associated with thalamic lesions(Wallesch, Kornhuber, Brunner, Kunz, Hollerbach, & Suger, 1983). Indeed,reported language profiles extend from normal to severe impairments on theparameters of auditory and reading comprehension, spontaneous speech,repetition, naming and writing (Alexander & LoVerme, 1980; Damasio,Damasio, Rizzo, Varney, & Gersh, 1982; Vallar, Papagno, & Cappa, 1988).Although language disorders are common subsequent to dominant hemi-sphere striatocapsular lesions, it has been suggested that the more overtlanguage symptoms in such cases may be related to concomitant corticaldysfunction (Nadeau & Crosson, 1997a). Mega and Alexander (1994) showedthat the basal ganglia play a more subtle role in the generation of words.More recent evidence indicates that the basal ganglia have a broader role incomplex aspects of language, that is, executive language functions (Copland,Chenery, & Murdoch, 2000b).

Despite the documented variability of language disturbances associatedwith striatocapsular aphasia, some researchers have identified a distinct pat-tern of impairment that conforms to the anterior-nonfluent/posterior-fluentcortical dichotomy (Cappa, Cavallotti, Guidotti, Papagno, & Vignolo, 1983).Other authors have also identified three patterns of language disturbanceassociated with putaminal and internal capsule lesions, including: (1) Broca’stype or transcortical motor aphasia with dysarthria, following lesions of thestriatocapsular region with anterior extension; (2) Wernicke’s type aphasiasubsequent to striatocapsular lesion with posterior extension; and (3) globalaphasia following combined anterior and posterior lesions of the basalganglia and/or internal capsule, plus extension (Murdoch, Thompson, Fraser,& Harrison, 1986; Naeser, Alexander, Helm-Estabrooks, Levine, Laughlin, &Geschwind, 1982). Despite this apparent consensus, several other studieshave questioned the accuracy and utility of the anterior–posterior dichotomyby describing a number of cases in which the patterns of language impair-ment could not be accounted for in terms of this anatomical distinction(Kennedy & Murdoch, 1993; Wallesch, 1985).

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Theoretical models of subcortical participation in language

The possible existence of subcortical aphasia as a clinical entity has catalyzedthe development of contemporary language theories that proffer functionalroles for subcortical nuclei, including the striatum, globus pallidus and thal-amus. These theoretical constructs specifically promote a network model oflanguage organization (Cappa & Vallar, 1992), whereby cortico–subcortical–cortical pathways represent the neural basis of linguistic processing, inpreference to exclusive cortical–cortical connections.

The work of Alexander and colleagues (1986, 1990) provides the basisfor our understanding of the anatomical and functional organization ofcortico–subcortical–cortical circuits. Seminal schemas proposed parallel yetfunctionally segregated basal ganglia–thalamocortical pathways to underlieskeletomotor, occulomotor, cognitive and limbic functions. To date, theskeletomotor circuit has proffered the greatest contribution to the con-ceptualization of basal ganglia–thalamocortical organizational substrates.As such, contemporary models of subcortical participation in language havelargely evolved from theories of motor control, the foundations of whichwere established within studies of basal ganglia dysfunction in primateswith experimentally induced 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP) toxicity (Starr, Vitek, & Bakay, 1998).

Based on clinicoanatomical evidence thus far, three major basal ganglia–thalamocortical circuits have been speculated to participate in the mediationof linguistic processes (Cappa & Vallar, 1992): (1) the anterior “complex”loop (i.e., dorsolateral prefrontal and lateral orbitofrontal circuits (Alexanderet al., 1986): frontal association cortex–caudate nucleus–globus pallidus–ventral anterior thalamus–frontal association cortex; (2) the anterior “motor”loop (i.e., skeletomotor circuit; Alexander et al., 1986): sensory motor cortex–putamen–globus pallidus–ventral lateral thalamus–sensory motor cortex;and (3) the posterior loop (Van Buren & Borke, 1969): temporoparietalcortex–pulvinar–temporoparietal cortex. The anterior “complex” and“motor” pathways were hypothesized to mediate lexical–semantic expressionand articulation respectively, and the posterior loop to facilitate auditorycomprehension (Cappa & Vallar, 1992). Additional subcortical–corticalpathways have also been postulated to participate in the regulation of lan-guage (Cappa & Vallar, 1992), including: temporal auditory cortex–caudatenucleus pathway facilitating auditory comprehension (Damasio et al., 1982;Van Hoesen, Yeterian, & Lavizzo-Mourey, 1981); amygdala–temporal neo-cortex–dorsomedial thalamus (Cappa & Sterzi, 1990) and caudate nucleus–supplementary motor area–anterior (Naeser, Palumbo, Helm-Estabrooks,Stiassny-Eder, & Albert, 1989) regulating speech production. The functionalspecificity of language-dedicated subcortical circuits to date has been largelyrestricted to the elementary linguistic faculties of auditory comprehensionand verbal expression (Alexander et al., 1986). It is anticipated, however, thatcontemporary research may serve to expose functional subdivisions within


nonmotor basal ganglia–thalamocortical circuits, which reflect a similarlevel of organizational complexity to that of the somatotopic channels iden-tified within subcortical motor circuitry (Alexander et al., 1986). Indeed,this disclosure may potentially involve the elucidation of the neural sub-strates underpinning language at both single word and sentential levels ofprocessing.

Several theories have attempted to explicate the subcortical neural mechan-isms underlying receptive and expressive linguistic abilities. These include: thesubcortical white matter pathways (Alexander, Naeser, & Palumbo, 1987),response–release semantic feedback (Crosson, 1985), lexical decision making(Wallesch & Papagno, 1988), and selective engagement (Nadeau & Crosson,1997a) models.

Subcortical white matter pathways model

The subcortical white matter pathways model (Alexander et al., 1987) dis-misses a role for the subcortical nuclei in language and advocates cortico–cortico, corticostriatal, thalamocortical and corticobulbar white matterpathways as critical to the facilitation of auditory comprehension and verbalexpression. The fulcrum of this theoretical schema developed from a series ofrobust clinical-neuroradiological studies that highlighted an array of recep-tive and expressive language deficits in individuals with large striatal lesions,extending into the surrounding white matter pathways (Alexander et al.,1987). This profile was in stark contrast to that observed in patients withrelatively circumscribed lesions of the putamen and caudate nucleus, whichresulted in covert or nominal disturbances to language such as mild wordfinding difficulties and hesitant verbal output. This finding consequentlysupported a minimal function hypothesis for basal ganglia participation inlanguage and directed discussion towards the white matter pathways linkingcortical–cortical and subcortical–cortical regions.

Vascular lesions of the striatum that extended beyond the lateral boundaryof the anterior limb of the internal capsule, incorporating the anterior, extraanterior, anterior superior, superior or posterior periventricular white matter(PVWM), temporal isthmus, insular cortex and/or external capsule, weredocumented to produce a range of expressive and receptive language deficits(Alexander et al., 1987). More specifically, nonthalamic lesions with exten-sions into the anterior superior PVWM were reported to result in transcorti-cal motor aphasia, largely evidenced as sparse verbal output and difficultyinitiating speech. This symptom complex was hypothesized to result fromdamage to the fibre pathways connecting the supplementary motor area andBroca’s area. Anterior superior PVWM pathway disconnection was postu-lated to restrict limbic inputs to cortical language centres, resulting in reducedspeech drive. Repetition deficits were reported to arise from lateral and/orsuperior lesion extensions relative to the putamen, which implicate the externaland extreme capsules and, potentially, the arcuate fasciculus. In relation to

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speech motor control, corticobulbar fibres within the superior PVWM andgenu of the internal capsule, in addition to corticocerebellar and thalamocor-tical fibres within the anterior portion of the superior PVWM and anteriorlimb of the internal capsule, were inculpated. The temporal isthmus, link-ing the medial geniculate nucleus of the thalamus to the primary auditoryassociation cortex, and the auditory association callosal pathway connectingWernicke’s area and the right temporal association cortex were identified asthe subcortical white matter pathways integral to auditory comprehension.Posterior striatal lesion extension incorporating these structures typicallyresulted in comprehension deficits and neologistic output. Furthermore,wide-ranging lesion extension relative to the putamen, including the anteriorlimb of the internal capsule, extra anterior PVWM, anterior PVWM, anteriorsuperior PVWM and temporal isthmus was reported to result in globallanguage impairment. Alexander et al. (1987) avoided attributing a role inlanguage functioning to the thalamus on the basis that language deficitsresulting from thalamic and putaminal lesions are subserved by disparatepathophysiological mechanisms.

Given that white matter pathways provide the means by which componentsof the language system communicate with each other, the importance givento these pathways in the model proposed by Alexander et al. (1987) would,on the surface, appear reasonable. However, the findings of more recentstudies refute the notion that white matter pathway disconnection providesa valid datum for clinical manifestation of subcortical damage (Cappa &Vallar, 1992).

Response-release semantic feedback model

A postulated thalamo-cortical alerting system (Ojemann, 1976) representsthe plinth of the response-release semantic feedback (RRSF) (Crosson,1985) model. The model proposes a role for subcortical structures in regulat-ing the release of preformulated language segments from the cerebral cortex.According to this model, the conceptual, word-finding and syntactic pro-cesses that fall under the rubric of language formulation occur in the anteriorcerebral cortex. The monitoring of anteriorly formulated language segments,as well as the semantic and phonological decoding of incoming language,occurs in the posterior temporoparietal cortex. Language segments areconveyed from the anterior language formulation centre to the posterior lan-guage centre via the thalamus prior to release for motor programming. Thisoperation allows the posterior semantic decoding centres to monitor the lan-guage segment for semantic accuracy. If an inaccuracy is detected, then theinformation required for correction is conveyed via the thalamus back to theanterior cortex. If the language segment is found to be accurate during moni-toring, then it is released from a buffer in the anterior cortex for subsequentmotor programming. In addition to subcortical structures participating inthe preverbal semantic monitoring process, the model also specifies that the


striatocapsular structures are involved in the release of the formulated lan-guage segment for motor programming. Specifically, it is suggested that thisrelease occurs through the cortico-striato-pallido-thalamo-cortical loop inthe following way. Once the language segments have been verified for seman-tic accuracy, the temporoparietal cortex releases the caudate nucleus frominhibition. The caudate nucleus then serves to weaken inhibitory pallidalregulation of thalamic excitatory outputs in the anterior language centre,which in turn arouses the cortex to enable generation of the motor pro-grammes for semantically verified language segments. According to thismodel, Crosson (1985) hypothesized that subcortical lesions within thecortico-striato-pallido-thalamo-cortical loop would produce language deficitsconfined to the lexical–semantic level.

The original conception of the response-release mechanism in Crosson’s(1985) model has since been revised and elaborated in terms of the neuralsubstrates involved (Crosson, 1992). Although the actual response-releasemechanism in the modified version resembles that in the original conception,the route for this release is altered. The formulation of a language segmentcauses frontal excitation of the caudate, which increases inhibition of specificfields within the globus pallidus. However, this level of inhibition alone is notsufficient to alter pallidal output to the thalamus. An increase in posteriorlanguage-cortex excitation to the caudate, which occurs once a language seg-ment has been semantically verified posteriorly, provides a boost to the inhib-ition of the pallidum. The pallidal summation of this anterior and posteriorinhibitory input allows the release of the ventral anterior thalamus frominhibition by the globus pallidus, causing the thalamic excitation of thefrontal language cortex required to trigger the release of the language segmentfor motor programming. Overall, the revised model provides an integratedaccount of how subcortical structures might influence language outputthrough a neuroregulatory mechanism that is consistent with knowledge ofcortical–subcortical neurotransmitter systems and structural features.

Lexical decision making model

In line with the RRSF model, the lexical decision making (LDM) model(Wallesch & Papagno, 1988) also proposes a cortico-striato-pallido-thalamo-cortical loop as the neural platform for linguistic operations, including aspecific thalamocortical arousal mechanism, consistent with Ojemann’s(1976) theorem. Despite evident parallels, however, distinct incongruitiesprevail between these theoretical constructs with respect to functionalcortical organization viewpoints, and the nature of proposed subcorticalmechanisms.

Wallesch and Papagno (1988) postulated that the subcortical componentsof the loop constitute a “frontal lobe system” comprising parallel moduleswith integrative and decision-making capabilities rather than the simpleneuroregulatory function proposed in Crosson’s (1985) model. Specifically,

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the basal ganglia system and thalamus were hypothesized to process situ-ational as well as goal-directed constraints and lexical information from thefrontal cortex and posterior language area, and subsequently to participate inthe process of determining the appropriate lexical item, from a range ofcortically generated lexical alternatives, for verbal production. The mostappropriate lexical alternative is then released by the thalamus for processingby the frontal cortex and programming for speech. Cortical processing ofselected lexical alternatives is made possible by inhibitory influences of theglobus pallidus on a thalamic gating mechanism. This most appropriate lex-ical alternative has an inhibitory effect on the thalamus, promoting closure ofthe thalamic gate, resulting in activation of the cerebral cortex and produc-tion of the desired response. Cortical processing of subordinate alternatives issuppressed as a consequence of pallidal disinhibition of the thalamus, andthe inhibition of cortical activity.

Selective engagement model

Selective engagement (SE) theory represents the most contemporary schemaof subcortical participation in language and principally proposes a frontal–inferior thalamic peduncle (ITP)–nucleus reticularis (NR)–centrum medi-anum (CM) system to subserve the “engagement” of cortical componentsthat mediate attentional and behavioural processes, including language(Nadeau & Crosson, 1997a). This proposed linguistic frontal lobe systemcomplied with the tenets of the LDM model, with the exception of twodistinct anomalies. In particular, selective engagement theory disputes a rolefor the basal ganglia in language and redefines nonspecific thalamic nuclei(i.e., NR, CM and parafascicular nucleus) as critical to the mediation oflinguistic processes. Nadeau and Crosson (1997b) considered ventral anterior(VA) and ventral lateral (VL) thalamic participation in language an insolventhypothesis. This postulate was largely fuelled by two lines of evidence, includ-ing: (1) an observed decline in the incidence of aphasia following surgicallyinduced lesions of the VA and VL thalamus, concomitant with enhancedstereotactic technique accuracy (Fox, Ahlskog, & Kelly, 1991), and (2) thefact that aphasia resulting from tuberothalamic territory infarcts involvingthe VA nucleus typically resembles that following paramedian territorylesions, which spare the VA thalamus. Postulated thalamic engagement of thecortex, however, was in line with Ojemann’s (1976) proposed ventral thalamicfocal altering mechanism in addition to Crosson’s (1985) VA response-release system, relative to the galvanization of verbal output channels. Theexpansion of these postulates to consider the activation of more extensivelanguage-dedicated cortical mosaics (Ojemann, 1983), largely under NR con-trol (Nadeau & Crosson, 1997a), accommodated manifestations of receptiveas well as expressive language deficits observed subsequent to lesions of thethalamus. The RRSF and LDM models previously discussed focused primar-ily on output versus input mechanisms, providing no discernible explanation


for comprehension deficits. In contrast, the structural complexity of theneural system subserving SE mechanisms accommodates the spectrum ofaphasic characteristics observed following lesions of the dominant thalamus(Nadeau & Crosson, 1997b), perhaps approximating a more cogent axiom ofsubcortical participation in language than its antecedents.

An important feature of the selective engagement theory is that it dis-counts a role for the basal ganglia in language. A variable symptom complexwith respect to observed manifestations of language pathology in the pres-ence of classically defined striatocapsular lesions formed the basis of thispostulate. In more detail, Nadeau and Crosson (1997a) analysed the lin-guistic profiles of 50 cases subsequent to relatively uniform striatocapsularinfarctions, including the caudate head, putamen, anterior limb of theinternal capsule and portions of the globus pallidus. Vast heterogeneity rela-tive to the severity and incidence of language deficits including fluency,articulation, comprehension, repetition and naming was reported. Nadeauand Crosson (1997a) hypothesized that an integral role for the basal gangliain language would be fortified by a coherent aphasic syndrome, in the eventof uniform damage. Based on the above evidence, therefore, a minimalfunction hypothesis with respect to the contribution of the basal ganglia tolanguage functions was promoted.

Nadeau and Crosson (1997a) largely attributed language disturbances sub-sequent to lesions of the basal ganglia to cortical hypoperfusion. Thromboticor embolic occlusions primarily of the middle cerebral artery (MCA), or lesscommonly the internal carotid artery, were identified as precursors to striato-capsular infarction (Weiller, Ringelstein, Reiche, Thron, & Buell, 1990). Moreimportantly, circulatory dynamics pertaining to the rate of arterial recanali-zation and the efficiency of anastomotic circulation following basal gangliainfarction, were considered integral factors in determining the presence orabsence of aphasia. Perisylvian cortex ischaemia by way of MCA occlusion-induced cystic infarction, neuronal drop out or generalized tissue dysfunction(Nadeau & Crosson, 1997a), provided a tenable explanation for the variablearray of expressive and receptive language deficits associated with striato-capsular infarcts. Furthermore, haemorrhagic basal ganglia lesions were alsopostulated to disturb cortical circulatory dynamics relevant to language func-tions. Pressure effects inducing cortical ischaemia were held responsible forconsequent manifestations of aphasia.

Evidence is available that disputes Nadeau and Crosson’s (1997a) claimthat lesions of the striatocapsular region fail to establish a homogeneousaphasic syndrome. A coherent aphasic syndrome relative to generativeaspects of language, including verbal fluency, sentence generation andextended discourse, has been reported (Mega & Alexander, 1994). This find-ing suggests a need to revisit the notion of basal ganglia aphasia, payingparticular attention to the scope and sensitivity of linguistic assessments util-ized in addition to circulatory dynamics (Crosson, Zawacki, Brinson, Lu, &Sadek, 1997). Indeed, this evidence supports a potential role for the basal

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ganglia in mediating linguistic processes. In all probability, this role mayentail the regulation of thalamocortical engagement. Proposed mechanismsinclude the switching of engagement between neural nets (Malapani, Pillon,Dubois, & Agid, 1994).

Limitations of theoretical models of subcortical participationin language

Each of the models outlined above has a number of limitations and con-sequently no one model has achieved uniform acceptance. A major limitationof these models is that they fail to fully explain the considerable variability inclinical presentation of subcortical aphasia. According to Cappa (1997), afurther problem is that the models suggest such extensive and widely distrib-uted systems subserving lexical processing that specific predictions appear tobe difficult to disprove on the basis of pathological evidence. In other words,these models do not lend themselves readily to empirical testing. Yet anotherlimitation arises from the nature of the research on which these models arebased. The available models of subcortical participation in language arelargely based on the observation that certain contrasting deficits of languageproduction arise in subjects with particular subcortical vascular lesions whentested on traditional tests of language function. These language measureswere typically designed for taxonomic purposes regarding traditionalcortical-based aphasia syndromes and may be inadequate for developingmodels of brain functioning. It has also been argued that language deficitsassociated with subcortical vascular lesions may actually be related to con-comitant cortical dysfunction via various pathophysiological mechanisms.For instance, due to limitations inherent to currently available neuroimagingtechniques, cortical infarction may not have been detected by neuroimaging.Consequently, inaccurate lesion parameters may have served to contaminateour conceptualization of subcortical aphasia thus far.

In addition to the recognized shortcomings of current neuroimaging tech-niques, a number of physiological mechanisms have also been proposed thatpotentially attribute manifestations of subcortical aphasia to cortical dys-function. Subcortical lesions have been reported to exert distance effects onthe cerebral cortex, including cortical hypoperfusion and hypometabolism(Perani, Valler, Cappa, Messa, & Fazio, 1987). Reduced cerebral blood flowresults in ischaemia-induced neuronal loss (Lassen, Olsen, Hojgaard, &Skriver, 1983) and ischaemic penumbra (i.e., maintenance of tissue viabilityin the presence of neuronal dysfunction), both mechanisms having the poten-tial to disable cortical activity. Also, subcortical lesions may result in dias-chisis or the functional deactivation of distance-related cortical structures(Metter et al., 1983). As yet, however, the relationship between the structuralsite and aetiology of subcortical lesions, the extent of diaschisis, corticalhypometabolism and hypoperfusion, and associated language functionremains to be fully elucidated.


Overall, the validity of the aforementioned operative models of subcorticalparticipation in language remains largely unattested due primarily to a previ-ous incapacity to strictly define the extent of vascular neuropathology. Afurther encumbrance to empirical ratification rests with the inadequacy ofanimal models in providing an appropriate linguistic platform for investiga-tion (Crosson, 1992). The value of model-driven and theoretically foundedstudies of cognition cannot be overestimated in quests to extricate thesubcortical–cortical mechanisms underpinning language (Cappa & Sterzi,1990). The utilization of existing frameworks, however, in the context ofadvancing scientific techniques is considered critical to their ultimate inter-pretation. In line with this proposal, a recent resurgence in functional neuro-surgery to treat the motor symptoms of Parkinson’s disease, involving thegeneration of discrete surgically induced lesions of the subcortical nuclei,would appear to provide an unprecedented opportunity to empirically testcontemporary theories of subcortical participation in language.

Pallidotomy, thalamotomy and deep brain stimulation

Over the course of the past decade or so, primate research has served tocatalyse the development of a sound theoretical framework that hasenhanced our understanding of the pathophysiology underlying movementdisorders, such as those seen in Parkinson’s disease. This, combined withadvances in neuroimaging and neurosurgical techniques and a degree of disil-lusionment with drug treatments for movement disorders, has led to a revivalof stereotactic neurosurgical procedures such as pallidotomy (involvinglesioning of specific components of the globus pallidus) and thalamotomy(involving lesioning of specific nuclei in the thalamus) in the treatment ofParkinson’s disease. In addition to their patent therapeutic value, the discretecircumscribed lesion sites provided by these procedures afford anunprecedented opportunity to empirically test contemporary subcortical lan-guage theories. More recent, as an alternative to ablative procedures such aspallidotomy and thalamotomy that overtly destroy neural tissue, deep brainstimulation (DBS) involving implantation of electrodes within a range ofsubcortical targets such as the subthalamic nucleus (STN), has gainedincreasing support as the preferred method of treatment for Parkinson’s dis-ease. In that DBS has been documented to simulate the effects of ablativelesions (i.e., block neuronal activity at the target site), this technique alsoprovides an opportunity to test models that implicate structures such as theSTN and thalamus in language.

The majority of studies reported to date pertaining to the impact ofpallidotomy (Lombardi, Gross, Trepanier, Lang, Lozano, & Saint-Cyr,2000; Scott et al., 2002; Trepanier, Saint-Cyr, Lozano, & Lang, 1998), andthalamotomy (Fukuda, Kameyama, Yoshino, Tanaka, & Narabayashi, 2000)on cognitive function have been largely neuropsychologically based.Assessment batteries have typically included measures of attention, memory,

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concentration, visuospatial abilities and executive functioning. In regard tolanguage, the domains of confrontation naming, verbal learning, semanticand phonemic fluency have been afforded considerable scrutiny, however, in-depth linguistic analyses were not included. Recently, a series of studies byWhelan, Murdoch and colleagues have addressed this problem by utilizing abattery of high-level language tests to examine the effects of pallidotomy(Murdoch, Whelan, & Theodoros, 2003; Whelan, Murdoch, Theodoros,Silburn, & Hall, 2004b; Whelan, Murdoch, Theodoros, Silburn, & Harding-Clark, 2000), thalamotomy (Whelan, Murdoch, Theodoros, Silburn, & Hall,2002) and DBS of the STN (Whelan et al., 2003, 2004a) on linguistic func-tion. Overall these studies provided evidence to suggest that the concaten-ation of subcortical nuclei comprising basal ganglia–thalamocortical circuitsplays a fundamental role in high-level linguistic processes potentially under-pinning the recruitment and directed interplay of frontal and temporo-parietal cortical regions. With regard to the STN, the findings of Whelanet al. (2003, 2004a) highlighted the need to modify contemporary theoriesof subcortical participation in language to incorporate the STN. Morespecifically, the outcomes of their research challenged unilateral models offunctional basal ganglia organization with the proposal of a potential inter-hemispheric regulatory function for the STN in the mediation of high-levellinguistic processes. Indeed, the STN may contribute to the mediationof linguistic processes by indirectly regulating thalamocortical outputs withinthe cortico–subcortical–cortical language circuits.

Functional neuroimaging

Further clarification of the role of subcortical structures in language is likelyto come through the use of functional neuroimaging techniques and neuro-physiological methods such as electrical and magnetic evoked responses.Functional neuroimaging techniques such as functional magnetic resonance(fMRI) and positron emission tomography (PET) enable brain images to becollected while the subject is performing various language production tasks(e.g., picture naming, generating nouns) or during language comprehension(e.g., listening to stories). These techniques therefore enable visualization ofthe brain regions involved in a language task, with a spatial resolution as lowas a few millimetres. Although functional neuroimaging does therefore offer atool to unravel the role of subcortical structures in language, results fromfunctional neuroimaging studies to date have proven less than definitive(Cabeza & Nyberg, 2000). These studies have, however, revealed a number ofcortical and subcortical structures beyond the perisylvian cortex to be activeduring linguistic processing (Crosson et al., 1999; Peterson, Fox, Posner,Mintum, & Raichle, 1989; Warburton et al., 1996), providing support for adistributed network model of language organization (Mesulam, 2000). Inparticular, word generation studies have shown consistent activation of med-ial frontal cortex, usually near the boundary of pre-supplementary motor


area (SMA) and the rostral cingulated zone. Although the pre-SMA is knownto have extensive subcortical connections, including projections to the striatalgrey matter spanning the internal capsule and to the caudate nucleus andputamen, as well as receiving connections from ventral anterior and dorsalmedial thalamus in the majority of functional neuroimaging studies, thesesubcortical components have not shown consistent activity in functional neu-roimaging studies of word generation. This reported inconsistency in acti-vation of the basal ganglia and thalamus may be the product of limitations innumbers of subjects studied, number of trials during functional neuroimag-ing and experimental design. Recently Crosson et al. (2003), using fMRI,observed significant activity in the subcortical structures during lexical gen-eration tasks but not during nonsense syllable generation. They inferred theexistence of a left pre-SMA–dorsal caudate–ventral anterior thalamic loopinvolved in lexical retrieval. Further, Crosson et al. (2003) hypothesized “thatactivity in this loop was related to maintaining a bias toward the retrieval ofone lexical item versus competing alternatives for each response during wordgeneration blocks” (p. 1075). Several PET studies have also demonstratedactivation of the thalamus and basal ganglia during completion of languagetasks such as picture naming (Price, Moore, Humphreys, Frackowiak, &Friston, 1996a) and word repetition (Price et al., 1996b).

Conclusion

Speculation has existed since the end of the nineteenth century that sub-cortical brain structures have a role in language. Although it is generallyaccepted that the thalamus has a role in language, little consensus has beenreached regarding the involvement, not to mention the role, of the basalganglia in language. In particular controversy still exists as to whether thestructures of the striatocapsular region participate directly in language pro-cessing or play a role as supporting structures for language. Consequently, theimportant question that remains to be answered is: Do the subcortical struc-tures have an inherent language function that contributes a specific cognitivefunction beyond that of the cortex, or do they simply participate in regulatingand enhancing functioning of the cortical language centres? Contemporarytheories suggest that the role of subcortical structures in language is essen-tially neuroregulatory, relying on quantitative neuronal activity. Recentlyreported findings suggest that subcortical structures may be involved in main-taining response biases across time that are set by the cortical components ofcortical–subcortical–cortical loops (Copland, Chenery, & Murdoch, 2000a).Hypotheses generated by these theories of subcortical participation inlanguage require testing in order to advance our understanding of theimportance of subcortical brain mechanisms to language function.

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Warburton, E., Wise, R. J. S., Price, C. J., Weiller, C., Hadar, U., Ramsey, S., et al.(1996). Noun and verb retrieval by normal subjects: Studies with PET. Brain, 119,159–179.

Weiller, C., Ringelstein, E. B., Reiche, W., Thron, A., & Buell, U. (1990). The largestriatocapsular infarct: A clinical and pathological entity. Archives of Neurology, 47,1085–1091.

Whelan, B.-M., Murdoch, B. E., & Theodoros, D. G. (2003). Defining a role for thesubthalamic nucleus with operative theoretical models of subcortical participationin language. Journal of Neurology, Neurosurgery and Psychiatry, 74, 1543–1550.

Whelan, B.-M., Murdoch, B. E., Theodoros, D. G., Silburn, P. A., & Hall, B. (2002).Role for the thalamus in language? A linguistic comparison of 2 cases subsequent tounilateral thalamotomy procedures in the dominant and non-dominant hemi-spheres. Aphasiology, 16, 1213–1226.

Whelan, B.-M., Murdoch, B. E., Theodoros, D. G., Silburn, P. A., & Hall, B. (2004a).Re-appraising contemporary theories of subcortical participation in language:Proposing an interhemispheric regulatory function for the subthalamic nucleus inthe mediation of high level linguistic processing. Neurocase, 10, 345–352.

Whelan, B.-M., Murdoch, B. E., Theodoros, D. G., Silburn, P. A., & Hall, B. (2004b).Redefining functional models of basal ganglia organization: A role for the poster-oventral pallidum in linguistic processing. Movement Disorders, 19, 1267–1278.

Whelan, B.-M., Murdoch, B. E., Theodoros, D. G., Silburn, P. A., & Harding-Clark, J.(2000). Towards a better understanding of the role of subcortical nuclei participa-tion in language. The study of a case following bilateral pallidotomy. Asia PacificJournal of Speech, Language and Hearing, 5, 93–112.

Wernicke, C. (1874). De aphasische Symtomencomplex. Breslau: Cohn & Weigert.


10 Mechanisms of lexical selectionand the anomias

Tobias Bormann, Gerhard Blankenand Claus-W. Wallesch

Introduction

“Aphasia can be approached from several directions, reflecting the range ofinterdisciplinary interest, and each approach has its own story to tell” (Code,1989, p. ix). Chris Code, to whom this chapter is dedicated, has used a varietyof approaches to aphasia and the aphasic person, including the neuro-linguistic, psychosocial, brain science, historical and therapeutic perspective.Chris’s personality and scope of interest are a major reason for the success ofAphasiology – the journal he edits. GB and CWW came into contact withChris Code through our common interest in recurring utterances (Blanken, deLangen, Dittmann, & Wallesch, 1989; Blanken, Dittmann, Haas, & Wallesch,1988; Blanken, Wallesch, & Papagno, 1990; Code, 1982a, 1982b). As we alsodid related research on the psychosocial impact of aphasia on the person andhis or her family, Chris spent some (at least for us) scientifically fruitful andsocially rewarding months with us in Freiburg in the early 1990s. With regardto recurring utterances, we took different perspectives: Whereas Chris wasmainly interested in their pathophysiological basis, we focused on their mean-ing for neurolinguistic models of word production. Using the “classicapproach” of model-based cognitive neurolinguistics, the group of GB, firstin Freiburg, then in Magdeburg, and now in Erfurt, have broadened theirscope to include other phenomena of deficient word production into theirresearch and modelling. This chapter reflects their present state of insight.

Chris Code summarized the strengths and weaknesses of the cognitiveapproach:

Occasionally people find themselves at a loss with cognitive theories,especially when more than one theory or model can be applied to asingle symptom complex (e.g., paraphasia, dyslexia) in a given patient,producing different interpretations and predictions. [. . .] Single caseinvestigations were championed in early cognitive neuropsychology, butthey have fallen out of favour with some in recent years, althoughtheory development is constrained by data from single cases and theirtheory-driven investigation.

(Code & Wallesch, 2006, p. 821)

We would like to encourage further model-driven research into the phenom-enology of aphasia, and present this chapter as an example of the use of thecognitive approach.

For virtually every aphasic patient, speech production is a difficult task.Deficits of single word production affect, to varying degrees, patients with allaphasic syndromes, and have been studied extensively. Frequently, patientsshow phonological errors by substituting, adding, deleting or exchangingtarget sounds. It is assumed that, in these cases, the patient has usually beensuccessful in accessing the intended word form, but is, however, unable toappropriately prepare this abstract phonological form for output (e.g.,Butterworth, 1992). Other patients already have difficulties retrievingthe correct phonological word form from the mental lexicon. The mentallexicon is a long-term store containing entries of a speaker’s words. Forwritten language, an independent orthographic lexicon is assumed, whichmay be accessed independently of phonological lexical access (e.g., Rapp,Benzing, & Caramazza, 1997). In some models, the word’s syntactic features(so-called lemma information, e.g., syntactic category or gender) are part ofthe speaker’s lexical knowledge as well (see Levelt, Roelofs, & Meyer, 1999).It is widely agreed that lexical access in speech production is controlledby semantics, a memory system, which has either been fractionated intoverbal and other modality-specific parts (e.g., Shallice, 1988) or which maybe a single modality-neutral unitary system (e.g., Hillis, Rapp, Romani,& Caramazza, 1990).

Evidence for the independent access to semantic and phonological infor-mation can be observed in aphasic patients. Often, they indicate that theyknow an object and can give details on how and in which contexts it isencountered. This suggests that the patient has successfully processed, forexample, the picture and that the semantic system is working adequately toallow access to semantic knowledge about the object. Often, these patientscan be cued to correctly name the object by giving them the word’s firstphoneme or onset (e.g., “ti” for “tiger”).

Patients with difficulties accessing the correct word form in their mentallexicon are usually called “anomic” (Goodglass & Baker, 1976). The respec-tive anomia has also been termed “phonological anomia”, or “classical ano-mia” (Geschwind, 1967). In contrast, difficulties at the semantic level give riseto a condition termed “semantic anomia” (Howard & Orchard-Lisle, 1984;see Nickels, 1997, for a review). The underlying difficulty is assumed to affectthe semantic system, either as a consequence of progressive degeneration ofbrain structures thought to support semantic memory, or as the consequenceof a stroke (Hillis et al., 1990). These two conditions may be identified byconfronting the patient with other tasks that are supposed to involve thesemantic system (e.g., word–picture matching).

This “cognitive” approach in neurolinguistics is guided by a set of assump-tions, namely that a brain lesion can selectively affect some processingcomponents of the cognitive apparatus while sparing others, and that a

Mechanisms of lexical selection and the anomias 157

patient’s performance is based on the formerly intact and now (oftenselectively) lesioned cognitive structure (e.g., Caramazza, 1984, 1986). The“cognitive” approach has proven most fruitful in revealing the cognitivearchitecture of language processing. In a careful analysis, a patient’s per-formance is related to a model of normal word processing, and the functionallesion within this model is inferred from performance in different tasks aswell as from variables affecting this performance (e.g., Rapp, 2001; Shallice,1988). In addition, patients may display dissociations among tasks thatare not observed in normal subjects. If such performance cannot be recon-ciled with existing models of word processing, these models need revision.A patient’s performance may thus, for example, contribute to models oflexical processing (Caramazza, 1997; Dell, Schwartz, Martin, Saffran,& Gagnon, 1997).

Models of word production

Most psycholinguistic models of word production have been based on nor-mal individuals’ slips of the tongue (Dell, 1986; Fromkin, 1971; Garrett,1975) and on reaction time studies with healthy subjects (Levelt et al., 1999).All models distinguish between semantic, syntactic, and phonological infor-mation, and most authors conceive of the lexicon as some sort of network.Lexical entries are thought to be nodes in the network that receive activationfrom other nodes, usually those representing semantic information. In mostmodels, selection occurs when a lexical node receives activation above acertain threshold.

However, models differ considerably with regard to the way the respectiveinformation is represented and how information at the different levels mayinteract. Modular models assume discrete, non-overlapping processing andvery limited interaction. A successful model of this type has been advocatedby Levelt and co-workers (Levelt, 1989; Levelt et al., 1999; Roelofs, 1992,1997). It conceives of lexical access as a two-stage process. In the first step,a cohort of meaning-related lemmas is activated based on the availablesemantic information. Lemmas are assumed to be modality-independentrepresentations of a word’s syntactic features. They receive activation fromtheir respective lexical concepts at the semantic level. The lemma that receivesmost activation is selected from this cohort, and activation spreads down tothe next level, the level of word form. Usually, only one lemma is beingselected and subsequently activates its corresponding word form. Thus, whilelemmas may be activated in parallel, word forms are not. Only in the (rare)cases of near-synonyms, which are very similar in meaning (sofa, couch),does the model allow for parallel activation of more than one word form(Jescheniak & Schriefers, 1998; Levelt et al., 1999).

Within this two-stage model, semantic errors are attributed to mis-selectionat the lemma level or substitutions at the level of lexical concepts (Leveltet al., 1999). On the other hand, errors of omission are supposed to result

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from a block at the level of word form. As there is no feedback between theword form level and the lemma level, the phonological word form level is notassumed to influence lexical selection, and the two error types, semanticerrors and errors of omission, are considered independent events.

In contrast with this discrete serial model of lexical access, other modelsallow for parallel activation of word forms and for an influence of phono-logical information on lexical selection. Cascading models have rejected theidea of discrete serial processing and allow for parallel processing at differentlevels of the system, including the word form level (Caramazza, 1997;Humphreys, Riddoch, & Quinlan, 1988). Processing at a later stage mayoperate despite incomplete information from earlier levels and does not haveto wait until processing at these earlier levels is completed. In the model ofCaramazza and co-workers (Caramazza, 1997; Caramazza & Miozzo, 1997)the idea of a lemma level is explicitly rejected. Semantic information activatesa cohort of meaning-related word forms. Syntactic information is assumed tobe represented in an independent network.

Another type of model is the interactive model of Dell and colleagues,which assumes a semantic feature level, a lemma level and a phoneme level(Dell, 1986; Dell et al., 1997). It differs from the previous models in that itassumes feedback connections between adjacent levels of representation.Selection occurs at the lemma level after activation has spread between thelevels for some time, thus allowing both semantic and phonological informa-tion to influence lexical selection. Figure 10.1 provides a sketch of (a) thediscrete serial model (of Levelt and co-workers), (b) the cascading model(of Caramazza and co-workers), and (c) the interactive model (of Dell andco-workers). The “nodes” at the semantic level represent holistic lexical con-cepts in the discrete serial model and semantic features in the cascading andinteractive models.

Figure 10.1 Sketch of three different models of word production (see text).


Variables influencing lexical access

In accordance with the postulated levels of processing, a number of variableshave been identified that influence processing at the different levels within thesystem. These variables are important in inferring the functional lesion ofan individual. For example, Butterworth (1992) suggested that a frequencyeffect points to a lexical deficit, while an influence of word length on phono-logical paraphasias suggests a post-lexical origin. This has been termed the“critical variable approach” (Shallice, 1988, p. 72). It may, however, be ofinterest not only to investigate the influence of different variables on correctresponses but also to investigate the influences of the different variables onthe respective errors.

In most patients, at least those with phonological anomia, lexical entriesare not consistently unavailable. First, providing a cue often helps patientsto overcome temporary difficulties. Second, when item-consistency acrossseveral administrations of a naming test is assessed, there is usually greatvariability. Thus anomia seems to affect access to a lexical entry, but notto indicate permanent loss of lexical entries (however, see the case ofHoward, 1995).

Naming performance has been shown to be affected by a target’s con-creteness as well as its familiarity. These variables are thought to affectsemantic processing. Concrete targets are supposed to have richer and morerobust semantic representations than abstract ones (e.g., “honour”, “faith”).Consequently, patients with semantic impairments are often found to besensitive to abstractness and familiarity.

Furthermore, a word’s syntactic category may determine ease of lexicalaccess. It has often been reported that patients have more difficulties pro-ducing verbs compared to nouns (e.g., Miceli, Silveri, Villa, & Caramazza,1984). On the other hand, patients have been reported who demonstrateselective sparing of verbs or nouns, even in only one modality. For example,Caramazza and Hillis (1991) presented two aphasic patients who seemed tohave selective difficulties producing verbs only in the oral or written modality,respectively. Most impressively, these patients also exhibited difficulties pro-ducing a homophone when it referred to actions (“to watch”), but not whenit referred to an object (“the watch”). Other patients revealed intact accessto function words but impaired access to content words in speaking, and thereverse dissociation in writing (Rapp & Caramazza, 1997).

One of the most important factors influencing processing at the lexicallevel is word frequency. It has been reported to affect access to a word’sphonological form. Healthy subjects are faster at producing words of higherfrequency (Jescheniak & Levelt, 1994), and aphasic patients are better atnaming words of higher frequency than words of lower frequency. This“frequency effect” in aphasia has been taken as a strong clue to a lexicaldeficit (e.g., Butterworth, 1992). In cognitive models, the advantage for fre-quent words may be simulated by a lower threshold, which means, the more

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often a word is encountered during everyday life, the lower its threshold andthe easier its selection.

Some authors have suggested that age of acquisition (i.e., the age atwhich a word was first learned) is a stronger predictor of ease of lexicalaccess. Age of acquisition is highly correlated with word frequency, butstudies carefully controlling for this correlation reported an independentinfluence of age of acquisition for healthy subjects (e.g., Barry, Hirsh,Johnston, & Williams, 2001) as well as for aphasic speakers (Hirsh & Ellis,1994).

Aphasia may result in temporarily or permanently raised thresholds of thelexical entries. In many cases, then, no entry may receive activation abovethe threshold level and thus no entry will be selected. In this case, the patientwould give no response (see Dell, Lawler, Harris, & Gordon, 2004). It hasindeed been demonstrated that patients produce more errors of omission inresponse to pictures of low frequency words (Kremin et al., 2003). In contrast,semantic errors have been shown to be relatively independent of word fre-quency. For example, Nickels and Howard (1994) did not find an influence offrequency on semantic errors. They did, however, report an effect of image-ability on naming for some of their patients. On the other hand, Caramazzaand Hillis (1990) observed that in one patient, RGB, semantic errors weremore numerous for low frequency target words.

Semantic neighbourhood

Recently, Blanken, Dittmann, and Wallesch (2002) have identified another,relatively neglected, variable that influences lexical access. Semantic conceptsdiffer with respect to the size of the semantic category they belong to. Forexample, a lemon is part of the relatively large semantic category of “fruits”.In contrast, other items may come from a small or no specific semanticcategory, such as “cage” or “anchor”. The size of the semantic neighbour-hood should influence the chance of semantic errors as, for items from largesemantic categories, semantic competition is higher and mis-selections aremore likely.

Blanken et al. (2002) presented the case of MW, a German globally aphasicsubject with relatively preserved oral naming skills. MW’s responses revealeda clear dependency on semantic neighbourhood: With items from largesemantic categories, he produced many semantic errors and fewer omissions.In contrast, when a target word was a “low competition” item, the patientshowed few semantic errors and more omissions. Under both conditions,the sum of both error types was comparable, indicating that the items didnot differ in their overall difficulty. The results were proposed to be incompa-tible with Levelt’s discrete two-stage model of lexicalization. In this model,both error types are assumed to be independent of each other. Particularly,the number of omissions should not be related to the previous occurrence ofa semantic error.


We tested six further patients with aphasia following a stroke to replicateMW’s pattern of performance. These six patients were part of a larger group(Bormann, Kulke, Wallesch, & Blanken, 2006). Three patients were diag-nosed as suffering from Wernicke’s aphasia and three were diagnosed withamnesic aphasia, according to the Aachen Aphasia Test (AAT; Huber, Poeck,Weniger, & Willmes, 1983). They were shown 33 pictures of objects withmany and clear semantic competitors and 33 object pictures having few orweak semantic rivals. Both target groups were matched for frequency, ageof acquisition, length and normed picture name agreement. The 66 pictureswere presented in a pseudorandomized order. Their first response within5 seconds was scored as correct, omission, semantic error, or other. Theaverage frequencies of semantic errors and errors of omission for both typesof items were submitted to an analysis of variance with repeated measures.For the analysis by subjects, error type and item type were within-subjectvariables. For the analysis by items, item type was a between-item factor,while error type was a within-item factor. Both analyses resulted in a signifi-cant main effect for error type, with omissions being more frequent thansemantic errors, F1(1, 5) = 10.74, p < .05; F2(1, 64) = 20.76, p < .01. The othermain effect, item type, did not reach significance (both F < 0). The interactionof both variables was significant, F1(1, 5) = 9.68, p <.05; F2(1, 64) = 11.55,p < .01. Planned comparisons revealed that semantic errors were more fre-quent for target words with many competitors, while omissions dropped infrequency for low competitive target words. For every patient, the sums ofboth error types under both conditions did not differ significantly as assessedby chi square tests. We discuss the implications below.

Semantic dementia: Progressive semantic impairment

Another population that encounters frequent difficulties in naming singleobjects is patients with a progressive loss of semantic knowledge. A progres-sive loss of conceptual knowledge has been reported for a large numberof patients suffering from probable Alzheimer’s disease (e.g., Hodges &Patterson, 1995). Difficulties in naming everyday objects are among the firstsymptoms, and Hodges, Salmon, and Butters (1991) demonstrated that mostnaming errors in patients with Alzheimer’s disease are semantic in nature.

In most cases of probable Alzheimer’s disease, other cognitive functionsare affected as well. In contrast, there now exist a considerable number ofcase reports of patients showing a rather selective decline in conceptualknowledge with few accompanying cognitive deficits. Progressive fluent apha-sia, or semantic dementia (SD), is a variant of the fronto-temporal lobaratrophies (Salmon & Hodges, 2001; Snowden, Goulding, & Neary, 1989).The cognitive difficulties are associated with atrophy of the temporal lobes,most often the temporal poles and the inferior-lateral temporal areas. Insemantic dementia, atrophy usually affects the left temporal lobe or the tem-poral lobes of both hemispheres. Clinically, patients exhibit poor single word

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comprehension and poor naming, while other components of language, suchas syntax and phonology, are well preserved. Naming errors of patients withsemantic dementia have been reported to be semantic or errors of omission(Hodges, Patterson, Oxbury, & Funnell, 1992) with some patients showing atendency towards more general semantic responses during the course of theillness (Hodges, Graham, & Patterson, 1995).

Hirsh and Funnell (1995) reported naming performance in a patient withSD to be affected by concept familiarity. On the other hand, for a patient withprobable Alzheimer’s disease, only age of acquisition was a significant pre-dictor of naming success. Hirsh and Funnell took this as evidence for amodular architecture of semantic processing and lexical access. While seman-tic dementia was assumed to affect semantic processing, the patient withAlzheimer’s disease was supposed to have impaired access to the lexicon.Lambon Ralph, Graham, Ellis, and Hodges (1998), in contrast, reported thenaming ability of nine patients with semantic dementia to be influenced byfamiliarity, word frequency and age of acquisition. Within an interactivemodel, they claimed, semantic and lexical variables all influence lexicalaccess: Familiarity may reflect a concept’s robustness to impairment, whilefrequency and age of acquisition correlated with ease of access to a lexicalentry. More robust concepts should be better able to activate their respectivelexical entries. More easily accessible entries, on the other hand, may requireless input from the semantic system to reach their selection threshold.

We tested a patient, ZC, with progressive word finding difficulties in theface of relatively spared general cognitive functioning. ZC complained aboutword finding difficulties lasting for more than 2 years. In line with this, CTscans showed atrophy of left frontal and left temporal areas. ZC was fullyorientated for time and space and could give an adequate account of herrecent past. Her forward and backward digit spans were normal or evenabove average.

ZC was confronted with the same 66 pictures as the aphasic group and wasasked to name the respective object using a single word. Responses were ratedas correct, semantic errors, errors of omissions, and circumlocutions. In aregression analysis, we found rated familiarity and age of acquisition to besignificant predictors of her naming success. These results replicate theobservations of Lambon Ralph et al. (1998). The patient’s difficulties werenot restricted to the semantic system and, instead, seemed to affect semanticprocessing and access to the lexicon. Lambon Ralph et al. had taken theirresults as evidence for an interactive type of architecture.

The results from the high–low competition naming test point in the samedirection: For low competitive items, ZC showed one semantic error and14 errors of omission. In contrast, for targets with many lexical competitors,we observed 12 semantic errors and 6 omissions. For semantic errors, thedifference between high and low competitive items was significant (p < .01)while the difference between these item categories for omissions was in theright direction and approached significance (p < .12). In contrast, there was


no difference in the overall number of correct responses for the two groupsof items.

Discussion

The results of the two studies replicate Blanken et al.’s (2002) findings with aglobally aphasic patient, MW. When items have many semantic competitors,more semantic errors occur, while for target items with few competitors, moreerrors of omission are being observed. As the items from both conditionswere comparable in their overall difficulty, a common source of both errortypes is suggested.

The results speak against the proposal of Levelt and co-workers that lexicalselection is carried out at the lemma level and independently of the wordform level. Thus, semantic errors and errors of omission are not independentevents. Instead, the comparable amounts of overall errors implicate a func-tional locus that is relevant for both types of errors to occur. The data arethus easier to reconcile with cascading or interactive models of lexical access.

Within a cascading type of model, the results may be explained by assum-ing that in aphasia and progressive semantic disorders a larger set of lexicalcandidates is activated. Activation then cascades from the semantic levelthrough the lemma level down to the word form level. It is here that theerrors, semantic or omission, arise. However, meaning-related errors are pre-ceded by broad semantic activation and thus may be the result of an inabilityto restrict the number of candidates. A similar account has been proposed byNickels and Howard (1994) and Gerhand and Barry (2000).

Further evidence for an involvement of modality-specific representationsin lexical selection comes from a number of single-case studies comparingoral and written naming. One of the most suggestive observations was thecase PW of Rapp et al. (1997). PW was asked to react to pictures by saying,then writing, then again saying their name (called the “triple naming task”).He gave different responses in his oral and written response but, within amodality, his responses were the same. If lexical selection had been carriedout at the modality-independent lemma level, he should have given the sameresponse across different modalities. If, on the other hand, he had started thewhole selection process anew, he should have exhibited a tendency to produceyet another response in the third naming trial, again in the oral modality.Thus his consistent responses within one modality speak against this alterna-tive explanation. Together with other reports of patients showing semanticerrors in only one modality (Caramazza & Hillis, 1990, 1991), this suggeststhat the idea of lexical selection as occuring exclusively at the lemma level istoo narrow.

In contrast, modality-specific word forms seem to be involved in lexicalselection. On the other hand, this does not necessarily imply that this isalways the case. Our argument applies to aphasic speakers, and it is notclear whether it holds for lexical access of non-aphasic speakers. For these,

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activation of more than one phonological form has been demonstrated fornear-synonyms; that is, words with extreme semantic similarity. These havealso been shown to be involved in a specific type of speech error, blends(e.g., Garrett, 1993). Thus Levelt’s model allows for parallel activation ofphonological forms in some narrowly circumscribed situations of lexicalprocessing.

In general, the distribution of the patterns of semantic substitutionsand omissions within aphasic naming errors can fairly be predicted by prop-erties of the semantic environment of a given target. Our results thereforepoint to the necessity to control test items for the potential impact of afurther variable affecting aphasic naming performance: the targets’ semanticneighbourhood.

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Evidence from the case of a global aphasic. Cognitive Neuropsychology, 1 (2),163–190.

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Humphreys, G. W., Riddoch, M. J., & Quinlan, P. T. (1988). Cascade processes inpicture identification. Cognitive Neuropsychology, 5 (1), 67–103.

Jescheniak, J., & Levelt, W. (1994). Word frequency effects in speech-production:Retrieval of syntactic information and of phonological form. Journal ofExperimental Psychology: Learning, Memory, and Cognition, 20, 824–843.

Jescheniak, J. D., & Schriefers, H. (1998). Discrete serial versus cascaded processingin lexical access in speech production: Further evidence from the co-activationof near-synonyms. Journal of Experimental Psychology: Learning, Memory, andCognition, 24, 1256–1274.

Kremin, H., Lorenz, A., de Wilde, M., Perrier, D., Arabia, C., Labonde, E., et al.(2003). The relative effects of imageability and age-of-acquisition on aphasicmisnaming. Brain and Language, 87, 33–34.

Lambon Ralph, M. A., Graham, K. S., Ellis, A. W., & Hodges, J. R. (1998). Namingin semantic dementia – what matters? Neuropsychologia, 36 (8), 775–784.

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Levelt, W. J. M., Roelofs, A., & Meyer, A. S. (1999). A theory of lexical access inspeech production. Behavioral and Brain Sciences, 22, 1–75.

Miceli, G., Silveri, M. C., Villa, G., & Caramazza, C. (1984). On the basis foragrammatics’ difficulty in producing main verbs. Cortex, 20, 207–220.

Nickels, L. (1997). Spoken word production and its breakdown in aphasia. Hove, UK:Psychology Press.

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Rapp, B., & Caramazza, A. (1997). The modality-specific organization of gramma-tical categories: Evidence from impaired spoken and written sentence production.Brain and Language, 56, 248–286.

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11 Repetitive verbal behavioursin PMLAn exploratory studyof conversation

Nicole Müller, Alana Kozlowski andPattie Doody

Introduction

The science of repetitive verbal behaviours is only one of numerous areasto which Chris Code has made contributions that are impossible to ignore(see e.g., Code, 1982a, 1982b, 1989; Code & Ball, 1994). Repetitive verbalbehaviours (RVBs) occur in the presence of a variety of neurological dysfunc-tions. There is, moreover, a multitude of taxonomies and characterizationsthat incorporate various parameters of description. Table 11.1 (adapted fromWallesch, 1990, p. 134; see also Guendouzi & Müller, 2006, pp. 169–170) givesan indication of the variety of terminologies and definitions encountered inthe available literature.

Literature on RVBs in progressive neurological conditions, including vari-ous types of dementia, shows that RVBs such as echolalia and perseverationstend to be more common in the more advanced stages of the disease inquestion (e.g., dementia of the Alzheimer’s type), and relatively uncommon inearlier stages (see e.g., Cummings, Benson, Hill, & Read, 1985; Shindler,Caplan, & Hier, 1984; Sjogren, Sjogren, & Lindgren, 1952; Wallesch, 1990,pp. 143, 149).

Whereas the studies cited so far classify RVBs mainly on the basis of formand structure, there is also a body of literature that focuses more on therepetition and redundancy of ideas, information and topics (see e.g., thestudies described in Ulatowska & Chapman, 1995). The dominant perspec-tive on RVBs in the available literature can be described as taxonomic andsymptomatic. In other words, the impetus for research is the search for motorand neurological correlates of different types of RVBs, and the researchparadigms are, of necessity, experimental and quantitative, leading to a distil-lation of generalizable characteristics and classifications of RVBs acrossdistinguishable neurological impairments. To date, there is less work thatinvestigates the communicative context of RVBs, their contributions (detri-mental or facilitating) to how conversations are maintained and managed,and their emergence as conversations unfold (see e.g., Body & Parker, 2005;Guendouzi & Müller, 2006; Müller & Guendouzi, 2005; Perkins, Body, &Parker, 1995; Perkins, Whitworth, & Lesser, 1998). Continuing efforts in this

Table 11.1 Types and definitions of RVBs, with sources

Type and definition Sources

Echolalia“the automatic and compulsive repetition of words by the patient in theabsence of the understanding of their meaning”

Brain (1965,p. 105)

“a reflex automatism of verbal response, providing an empty, stereotypedquality to speech”

Hecaen andAlbert (1978,pp. 74–75)

“repetition of the investigator’s utterances with or without mild changes inposition and choice of words”

Huber et al.(1982, p. 80)

Iterationrepetition of parts of words (sounds or syllables), included in Ludlowet al.’s definition of palilalia

Machetanz et al.(1988)

Palilalia“the involuntary repetition two or more times of a terminal word, phrase orsentence”

Critchley (1970,p. 201)

“a disorder of speech characterized by compulsive repetition of a phrase orword that the patient reiterates with increasing rapidity and with adecrescendo of voice volume”

Boller et al.(1973, p. 1117)

“the reiteration of single or partial syllables or combinations of syllablesmany times with increasing rate”

Ludlow et al.(1982, p. 353)

Perseveration“the recurrence, out of context and in the absence of the original stimulus,of some behavioral act”

Buckingham etal. (1979, p. 329)

Recurring/recurrent utterances“a subgroup of speech automatisms which consist exclusively of syllables orsequence of syllables which are linked up in their production”


“an utterance made up of either real words or a non-meaningful string ofspeech sounds which some aphasic patients produce either every time theyproduce speech or just sometimes”

Code (1982a,p. 141)

“The term recurrent utterance is most usually reserved to describe repeatedand unchanging utterances made up of recognizable words which someaphasic individuals produce either every time they attempt speech, oralmost every time they attempt speech”

Code (1989)

Stereotypy“a permanent stereotyped verbal expression with or without linguisticmeaning unconsciously and involuntarily uttered”

Alajouanine(1956, p. 6)

“set phrases that are used recurrently but usually communicativelyadequate”


Speech automatism“a constantly recurring utterance which is formally rigid, consists ofneologistic sequences of syllables, interchangeable words or phrases, doesnot fit into the linguistic context either lexically or syntactically, and whichthe patient produces in contrast to the intention expected by hisinterlocutors”


Speech tics:(a) coprolalia: “all unprovoked swearing using single words or phrases” Ludlow et al.

(1982, p. 353)(b) word tics: “any meaningful word interjected into speech and not part ofcommunicative speech or hesitation phenomena”

Ludlow et al.(1982, p. 353)

Repetitive verbal behaviours in PML 169

direction are necessary, since any impairment of communicative functioninghas an immediate impact on quality of life.

This chapter investigates the occurrence of RVBs in the spoken language ofa person with progressive multifocal leukoencephalopathy (PML) in the con-text of AIDS (see below for more detail). According to McCabe, Sheard andCode (2002), there are numerous studies that cite impaired communicationskills in the context of HIV/AIDS. However, few studies have investigatedlanguage or speech impairment in a comprehensive, contextually embeddedand function-oriented manner. McCabe et al.’s study demonstrates that awide-ranging array of acquired communicative difficulties arise out of HIV/AIDS, and calls for “[f]urther investigation to explore the functional use oflanguage by people with HIV and their pragmatic skills”. This chapter isintended as a small contribution to this area of inquiry.

RVBs in PML: A case study

Method

Participants

This study involves the analysis of conversational behaviours between twoparticipants (see below for details concerning data collection and analysis), Aand D. A is the second author of this chapter, a speech-language pathologistand clinical instructor, and currently a doctoral student. D is a male aged38 years, diagnosed with progressive multifocal leukoencephalopathyconsequent to Acquired Immune Deficiency Syndrome (AIDS). PML is ademyelinating disease of the central nervous system, caused by the JCvirus (named after the initials of the person in whom it was found) (Wyen,Lehmann, Fatkenheuer, & Hoffmann, 2005). It is estimated that in excess of70% of adults harbour the virus; however it remains harmless in persons withhealthy immune systems, but in persons with immune systems compromisedby the Human Immunodeficiency Virus (HIV) or AIDS, the JC virus causesPML. The lesions associated with PML typically occur in the hemisphericwhite matter, but have also been documented in the basal ganglia, the brainstem, the cerebellum (Berger, 2004) and, exceptionally, in the spinal cord(Wyen et al., 2005). The multiple, somewhat unpredictable lesion sites cause awide variety of cognitive and behavioural symptoms, many of which impactcommunication.

D’s speech communication is severely impaired, owing to hypokinetic dys-arthria and frequent RVBs. His speech is characterized by decreased vocalintensity, harsh and breathy voice quality, reduced prosodic contours (both inamplitude and variety), and short, rapid rushes of speech with imprecisearticulation. Conversational speech ranges from a whisper, to a quiet strainedvoice with obvious pitch breaks, to falsetto productions. Reduced intensity isa primary contributor to communication breakdown. Overall, there is lack of

170 Müller et al.

control over pitch contours, and little variability. D does not repair a com-munication breakdown by adjusting stress on a misunderstood phrase orword. RVBs include the repetition of the pitch contour, as well as the lin-guistic content. Overall, speech is perceptually fast, with some parts of utter-ances (including RVBs, but not restricted to them) having an accelerated rateof production. These “rushes” are accompanied by decreased articulatoryprecision. The range of movement of visible articulators is reduced duringspeaking tasks (compared to non-speech tasks). No adjustment of speakingrate or articulatory amplitude or precision is noted when D is aware ofcommunication breakdown. Micrographia affects D’s writing to the extentthat he is no longer willing to use writing as a communicative tool. Herarely produces gestures to aid communication, and those that occur onlyinfrequently aid in clarifying the intended message. Facial affect varies, is flatat times, but at other times unremarkable.

D has been participating, inconsistently, in speech therapy for approxi-mately 18 months. The intelligibility of his speech has progressively worsenedto the point that he was found 0% unintelligible on the single word portion ofthe Assessment of Intelligibility of Dysarthric Speech (Yorkston & Beukel-man, 1981). It was noted during therapy that D could produce loud vocaliza-tions, and often intelligible speech when the task was non-communicative(such as producing a long [�] vowel, which he can sustain for 4.5 s, at 80 dB)and/or involves rote (such as counting, or producing other over-learnedphrases).

Data

The conversation between A and D that forms the basis of analysis for thischapter took place in the speech and hearing clinic D has been attending. Itwas recorded approximately 2 years after D’s diagnosis with PML. A and Dhave known each other for approximately 18 months, during which time Ahas been D’s speech therapist.

While there are some elements of “therapy” in the conversation (such as Aprompting D to monitor and attempt to raise his vocal intensity, or scaffold-ing D’s turn by prompting him to produce “big key words”), there is nofocused therapy activity, much less any therapeutic “drill”. In all, approxi-mately 27 minutes of conversation were recorded and transcribed ortho-graphically. This conversation was closely analysed, and the patterns arisingfrom this micro-analysis were compared with two other recorded conversa-tions between the same interlocutors, and were found to be confirmed. Thefocus of analysis is the linguistic interactional aspects of the conversation,rather than the quality of the speech signal, the prosodic or gestural charac-teristics. While it is of course understood that those characteristics are inte-gral parts of conversational interaction, limitations of space prohibit adetailed holistic analysis of all component systems of the conversation andtheir interaction.


Descriptive and analytic framework

The descriptive framework for the linguistic and interactional characteristicsof D’s RVBs is provided by systemic functional linguistics (SFL). In recentyears, SFL has become an increasingly popular tool with which to approachdisordered speech and language in a variety of social contexts. Among thecharacteristics that make SFL relevant to clinical contexts, Halliday (2005,p. 134) suggests that:

[it] presents language as a semogenic (meaning-making) resource, onegoverned by tendencies not rules, and whose categories (as is typical ofsemiotic systems) are “fuzzy” rather than determinate. It is formulated interms of strengths, rather than of deficits or constraints: what thespeaker can do (and what the language “can do”).

Thus SFL has a social, context-embedded orientation, its focus is thelinguistic choices an individual makes to construct meaning in social inter-actions (Halliday & Matthiessen, 2004; Martin, Matthiessen, & Painter,1997). This social-functional orientation is particularly relevant if one wishesto do justice to persons whose oral or written language is impaired, and who,consequently, suffer significant disempowerment in cultures that highly valuethese skills (Armstrong, 2005). In the course of this chapter, we present astructural characterization of D’s RVBs, and analyse how they function inconversation. To this end, we use the categories of Theme/Rheme, and Given/New information.

Patterns

Structural characteristics of D’s RVBs

D produces 69 verbal utterances that are at least partially intelligible andthus lend themselves to analysis. In these utterances, 99 RVBs of varioustypes occur (mean: 1.43 per utterance). Table 11.2 lists the types of RVBsencountered in this sample.

Single word repetitions clearly dominate, and also have the highest rangeof repetition (with a maximum of five, encountered once; the highest propor-tion being a single repetition of a single word, encountered 28 times).

Table 11.2 Types of RVBs, and range of repetitions

Type

Singleword

Ellipticalclause

Expan-sion

Partword

Noungroup

Falsestart

Clause Prepositionalphrase

Synonym

N 55 14 12 6 4 4 2 1 1% 55.5 14.14 12.12 6.06 4.04 4.04 2.02 1.01 1.01Range 1–5 1–3 1 1–4 1–2 1 1 1 1

172 Müller et al.

The most common single word repetitions are “yes” and “no” (22 timesaltogether), followed by nouns (N = 16) and adjectives (N = 12). Verbs are farless frequent (N = 4), and there is a single instance of “where”. Thus singleword RVBs in D’s speech are content words, rather than reiterations of func-tion words.1 Different types of RVBs often occur in the same utterance, asillustrated in the examples described later.

As discussed in detail by Wallesch (1990), classifying RVBs is not altogetherstraightforward. The closest category of those quoted in Table 11.1 is that ofpalilalia (or iteration, included under palilalia, see above). However, many ofD’s RVBs are not terminal, or utterance-final (as specified in Critchley, 1970).The definitions of palilalia make no reference to the contextual embedding,or linguistic contribution, of RVBs. To this end, an examination of RVBs intheir linguistic context is necessary, which is undertaken in the followingsections.

Theme and Rheme, and Given versus New information

Theme and Rheme are categories in the analysis of a clause as message.According to Halliday and Matthiessen (2004, p. 58), a “clause has meaningas a message; the Theme is the point of departure for the message. It is theelement that the speaker selects for ‘grounding’ what he is going to say.” InEnglish, as in many other languages, Theme and Rheme are signalled byposition: the Theme occupies the initial position in the clause; the Rhemeconsists of the rest of the clause (see Halliday & Matthiessen, 2004, p. 64;Martin et al., 1997, pp. 23–24). The boundary between Theme and Rhemeis drawn such that the Theme of a clause “ends with the first constituent [ofa clause] that is either participant, circumstance, or process” (Halliday &Matthiessen, 2004, p. 79).2 This participant, circumstance, or process in the-matic position is referred to as the topical Theme, and this is what our analysisfocuses on.

SFL treats information structure as a system that is separate from thematicstructure; however, in terms of language use, the two systems are closelylinked. Whereas Theme and Rheme are constituents of the clause, Given andNew information are constituents of what in SFL is referred to as the infor-mation unit, which may be coextensive with a clause, but may also extendbeyond a single clause. The typical, unmarked state of affairs is in fact thatthe information unit maps onto a single clause, and that Given informationcorresponds to the topical Theme, and New information to the Rheme. Thusthe unmarked sequence of information is Given before New (Halliday &Matthiessen, 2004, pp. 87–89).

While acknowledging that Theme/Rheme and Given/New information aretwo separate systems and conceptually different categories, we present theiranalyses together, since the patterns in our data support this step. Having saidthat information structure and thematic structure map closely onto eachother, we also have to keep in mind that it is characteristic of conversational


language that many utterances do not consist of complete clauses. The pro-ductions in our data are no exception to this tendency. Of D’s 69 at leastpartially intelligible utterances, 21 consist of minor clauses (“yes”, “no”, or“right”, typically repeated at least once). From the rest of his utterances,some interesting patterns emerge.

Many of D’s utterances consist of clause fragments that lack a Theme, andconsist of New information only. The ellipsed, “understood” Theme is typi-cally represented by the Rheme of a clause in A’s preceding utterance, orby information that is easily recoverable in the context of the conversation(such as a reference to either D himself, or to another person known to bothinterlocutors). Example 1 illustrates this pattern:

Example 11 A: how was your weekend?2 D: boring steroid shot got a steroid shot steroi- steroid shot st- steroid

shot3 A: I think you just told me it was boring and you got a steroid shot4 D: yes yes

The Rheme of A’s initial clause represents new information; the “weekend”has not been mentioned previously. This becomes the “understood”, ellipsedTheme, now Given information, of D’s first clause fragment, with a quasi-Rheme representing New information: “boring”. The repetitive sequence thatbegins with “steroid shot” contains a clause fragment consisting of Process +Goal (“got a steroid shot”), with the Actor ellipsed (“I”). The ellipsed element,structurally the Actor-subject of the clause fragment, is easily recoverablefrom the situational context, hence can be treated as Given information, andcan therefore justifiably be ellipsed. D’s repetition only encompasses the focusof New information, the most salient part of the quasi-Rheme of his clausefragment (“got” as a Process is semantically “light” in the sense that it doesnot contribute information that cannot be treated as recoverable from theGoal; the default relationship between ellipsed subject and Goal-complementis one of “getting”, or “receiving”). In turn 3, A expands on D’s utterance,and by means of projection (“I think you just told me”) recasts the informa-tion received from D into two clauses with complete Theme–Rheme struc-tures, which are confirmed as an accurate representation of a state of affairsby D in turn 4. Thus the two interlocutors collaborate at arriving at thedefault, unmarked Theme–Rheme, Given–New sequence.

D’s utterance in Example 2 shows the same pattern of Theme-less clausefragments, and expansion of clause fragments:3

Example 27 A: what does what do the steroid shots do?8 D: P pump me up p^ p^ p^ pump (unintelligible) me strong strong dick

hard dick hard make your dick hard dick hard make your dick hard

174 Müller et al.

D’s utterance begins with what we have classified as a false start, which turnsinto a clause fragment representing a New Rheme to an ellipsed GivenTheme (“steroid shots”, or “they”). The second clause fragment (“me strongstrong”) contains neither Actor-Subject nor Process-Verb group. Again, theActor is easily recoverable as Given information (“they” / “steroid shots”).Both the process and the participant roles of “me” and “strong” are inferable,because of the default semantic relationship between “steroid shots”, “me”and “strong”, which is one of causing (“make” or the like) an effect of being“strong” (hence the participant role of Attribute) on a person, “me” (hencethe participant role of Goal). What is reiterated in this clause fragment isagain the focus of New information; “me” is Given. The repetitive sequencethat starts with “dick hard” shows a similar internal structure. The partici-pant roles are the same as with “me” and “strong”; that is, Goal and Attri-bute, and both represent the focus of New information in an incompleteRheme to an ellipsed, Given Theme. The Rheme is completed by the additionof the Process (“make”), and the sequence of partial and completed Rheme isrepeated.

Example 3 represents a similar pattern of expansion and RVBs in relationto thematic and information structure:

Example 3142 A: you’re telling me the kids down the street pushed you and you

ended up with this bruise on your knee143 D: yes yes bad bruise purple purple144 A: yeah it’s awful145 D: purple purple it’s pur pur purple146 A: give me a nice= ((low pitch, moderately loud))147 A: =pur pur pur purple it’s purple and green green

In turn 143, D confirms A’s summary of previous turns by reiterating part ofthe shared information, “bad bruise”, and then proceeds to expand with arepeated New element of information, which again can be construed as theNew Rheme to a Given Theme (“it”, or “the bruise”). D appears to treat A’sturn 144 as an indication that she has not understood him (and correctly so).This is probably due to A’s prevailing strategy of providing expanded, com-pleted clause structures based on D’s utterances, for D to confirm (illustratedin Examples 2 and 3). Therefore, while “purple” in turn 145 is strictly speak-ing not New information as regards the text as a whole (in hindsight, as itwere), it can be treated thus for the purposes of reconstructing the unfoldingtext, the achievement of meaning creation between the interactants. Thus Dtreats “purple” as New, and completes the Given Theme + New Rhemestructure after a repetition of the themeless Rheme. In fact, as indicated byA’s therapy cue in turn 146, there is still no mutual understanding, and Dproduces another turn with the by now familiar sequence of repetition andexpansion: This time, part-word repetitions of “purple” are followed by a


completed and, here, expanded Given Theme + New Rheme sequence, where“purple” is expanded on by the addition of a further adjective, which is inturn repeated.

In most of his turns, D only attempts to introduce one or two New elem-ents of information. Example 4 shows a different structure: All the informa-tion is new, and is not “latched onto” contextually inferable or Giveninformation:

Example 444 D: (unintelligible) sex sex sex T T T-cells ((holding up 3, then 4 fingers))

three eleven Cooper Cooper Cooper tol my mom Cooper CooperCooper Dr Cooper tol my mom (unintelligible) ((shakes 4 fingers))Cooper Cooper Cooper

45 A: I know who we are talking about, Dr Cooper46 D: Cooper ((very high pitched voice; close to crying?)) you’re doing

great

D is unable to integrate the first four New items into any kind of meaningsequence, and changes tack, beginning again with “Cooper”, which he is ableafter two reiterations to expand into a Theme + Rheme sequence (containingNew information only). However, this is still not successful, since the infor-mation necessary to complete the verbal Process “told” (in SFL terms, the“verbiage”) is not forthcoming. After another attempt, starting again withthree productions of “Cooper”, D gives up and A takes over, confirmingunderstanding of “Dr Cooper”, which in turn is re-confirmed by D in turn 46by a single production of “Cooper”.

Of the 99 RVBs in this conversation, only 9 contain Given information asregards the text (in other words, information that has been previously intro-duced). However, of these, three contain information that cannot be treatedas Given, or shared for the purposes of the exchange, since in each case,A’s preceding utterance signals that she still requires confirmation, as inExample 5. Further, three examples represent a rephrasing of a Theme–Rhemesequence offered by A (using pronouns and ellipsis of the Predicator); theseserve as final confirmation of shared information; see Example 6:

Example 5104 A: are we talking about Fran or your dad?105 D: Fran Fran Fran Fran

Example 6128 A: kids pushed you. I just heard you D129 D: you did you did ((smiles))

The tendency for RVBs to associate with New information is also confirmedby the fact that there are only five instances in the text where D introducing

176 Müller et al.

New information does not co-occur with either an identifiable RVB, or thedeterioration of his speech to such an extent that it becomes unintelligible(and may therefore have contained RVBs; there are two such instances). Oneinstance of non-repeated New information is represented by “you’re doinggreat” in Example 4 above, and we may speculate whether it is significant thatthis example represents a direct quotation from another speaker, and that theclause “you’re doing great” is highly formulaic; both factors may assist in itsfluent production. However, these questions await further investigation.

Discussion

The severe dysarthria, as well as the high proportion of RVBs in D’s speechpose a considerable challenge to communicative success. In order to under-stand how these challenges are met and dealt with, it makes sense to analysethese speech patterns in the context of a real communicative event.

The detailed analysis of a conversation between D and A has shown apattern of D consistently violating the unmarked Given Theme + NewRheme structure that is the default for English clause structure. The ellipsisof Given Themes is not an uncommon feature of English conversationalspeech. In fact, the consistent reiteration of Given Themes where they areclearly and unambiguously recoverable would make for very strange con-versations indeed. However, D’s utterances show a pattern where a singleNew item is introduced, and then expanded into a “virtual” complete Rhemeto an ellipsed topical Theme. Further, we found that RVBs pattern with Newinformation. In addition, we noted a strategy on the part of A to expand andintegrate the New information provided by D into unmarked Given Theme +New Rheme sequences for D to confirm. Examples 3 and 5 above illustratethat D actively uses this collaborative pattern to advance the conversation. Ittherefore appears that D’s presentation of New information utterances ini-tially is a strategy that emerged out of his severe communication impairment.

D’s ability to sustain phonation and maintain articulatory precision islimited, as is his ability to vary pitch. The association of RVBs with Newinformation introduces a further complication, because RVBs take up someof the available phonation resources in an utterance, thus further limiting D’smeaning output. In this light, starting utterances with the most salient item,the focus of New information, and relying on an interlocutor to “fill in thegaps” either mentally or out loud, makes a lot of sense. The dialogue can beadvanced collaboratively, while D avoids expending voice on information thatis already Given, or inferable from the situational context. In this context, thepositional constraints for palilalia described in some sources are interesting.Critchley (1970) and Singh and Kent (2000) state in their definitions that thereiterations of words and phrases typically occur towards the middle andend of utterances. A re-examination of the data that gave rise to thesedefinitions might well confirm the pattern we found with D, namely thatthere is a strong association with New information and repetitiveness, if the


speakers’ productions largely followed the unmarked Given Theme + NewRheme sequence of English clauses. D’s RVBs are not restricted to utteranceinternal or utterance final position, but as we have seen, they do not follow“canonical” clause structure.

Garratt, Bryan, and Maxim (1999) noted that palilalia in their participantswas more evident in utterances with increased propositional load. In otherwords, more “meaningful” speech contained more instances of palilalia,while automatic speech tasks had none, which led the authors to concludethat processing demands relate to the emergence of palilalia, and to hypoth-esize that additional processing demands “stress” the damaged motor speechsystem. In contrast, Boller et al. (1973) characterized palilalia as a disturb-ance of speech, rather than language, with no defect in the abilty to handlethe linguistic and symbolic aspects of communication. D’s RVBs, whichappear to structurally fall under the category of palilalia as defined above(Table 11.1), make us inclined to prefer Garratt et al.’s view over Boller et al.’s.

Whether utterance patterns in a person with compromised speech abilityare the result of deliberate choices to structure his or her output to maximumeffect, or whether they are an emergent product of multiple interacting fac-tors, an awareness of the patterns (and how they may further or hinder com-munication) on the part of interlocutors is crucial in order to maximizecommunicative success, and the ability of the individual with impaired speechto participate in society. Eggins (1994) points out that it is through sustaineddialogue that individuals are able to establish and maintain social roles andidentities. It is particularly important to give individuals with progressivelyworsening conditions, such as D, the wherewithal to maintain the ability to“speak for themselves”, and as themselves (if with the help of others) for aslong as possible. The linguistic behaviours documented here on the basis of asingle conversation were confirmed in other interactions. It became clear thatD constructed the client–clinician relationship as essentially one of equalpower and control, and in fact he is able to “turn the tables” on the clinicianand teases her for her lack of understanding, in effect reconstructing andrepositioning the communicative impairment from a problem of productionto one of reception.

Notes

1 We include “yes”, “no” and “where” in the category of content words (althoughthey also clearly have grammatical functions), on the grounds that they can standalone in conversational speech, and thus carry the content of a message, unlikefunction words (such as determiners).

2 A full discussion of different types of themes (topical, interpersonal, and metafunc-tional) is beyond the scope of this chapter. For further detail, see Halliday andMatthiessen (2004, chapter 3).

3 We in no way intend to shock any of our readers by the choice of examples. Thedata are what the data are. Those accustomed to working with neurologicallyimpaired populations frequently encounter language that may be considered

178 Müller et al.

offensive by some, or not suitable for persons below a certain age. In fact, Dtakes great delight in A’s misunderstanding of the potentially offensive item(A interprets it as “dig”; “I was picturing gardening”, turn 42) and having to rely onD’s mother to clarify. Thus D is not only able but willing to use the breakdown ofcommunication to humorous effect.

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Boller, F., Boller, M., Denes, G., Timberlake W. H., Zieper, I., & Albert, M. (1973).Familial palilalia. Neurology, 23, 1117–1125.

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Code, C. F. S. (1982a). Neurolinguistic analysis of recurrent utterance in aphasia.Cortex, 18, 141–152.

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Code, C. F. S. (1989). Speech automatisms and recurring utterances. In C. F. S. Code(Ed.), The characteristics of aphasia (pp. 155–177). London: Taylor & Francis.

Code, C. F. S., & Ball, M. J. (1994). Syllabification in aphasic recurring utterances:Contributions of sonority theory. Journal of Neurolinguistics, 8, 257–265.

Critchley, M. (1970). Aphasiology and other aspects of language. London: Arnold.Cummings, J. L., Benson, D. F., Hill, M. A., & Read, S. (1985). Aphasia in dementia

of the Alzheimer’s type. Neurology, 35, 394–397.Eggins, S. (1994). An introduction to systemic functional linguistics. London: Pinter.Garratt, H., Bryan, K, & Maxim, J. (1999). Palilalia in progressive supranuclear

palsy: Failure of the articulatory buffer and subcortical inhibitory systems. InB. Maassen & P. Groenen (Eds.), Pathologies of speech and language: Advances inclinical phonetics and linguistics (pp. 245–252). London: Whurr.

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Halliday, M. A. K. (2005). Guest contribution. A note on systemic functionallinguistics and the study of language disorders. Clinical Linguistics and Phonetics,19, 133–135.

Halliday, M. A. K., & Matthiessen, C. M. I. M. (2004). An introduction to functionalgrammar (3rd ed.). London: Arnold.

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neuropsychologie. Stuttgart: Thieme.Ludlow, C. L., Polinsky, R. J., Caine, E. D., Bassich, C. J., & Ebert, M. H. (1982).


Language and speech abnormalities in Tourette syndrome. Advances in Neurology,35, 351–361.

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Müller, N., & Guendouzi, J. A. (2005). Order and disorder in conversation:Encounters with dementia of the Alzheimer’s type. Clinical Linguistics and Phonet-ics, 19, 393–404.

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Perkins, M., Body, R., & Parker, M. (1995). Closed head injury: Assessment andremediation of topic bias and repetitiveness. In M. Perkins & S. Howard (Eds.),Case studies in clinical linguistics (pp. 293–320). London: Whurr.

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12 Multiparty interactionsin aphasia

Alison Ferguson

This chapter describes a line of future enquiry in relation to understandinghow people with aphasia communicate in groups, and is inspired by two ofthe major foci of Chris Code’s work in aphasiology, namely his long-standingconcern that services provided for people with aphasia be directed to theindividual needs of the person (Code & Müller, 1995, pp.1–2), and thatemotional response and support is integral to recovery in aphasia (Code,Hemsley, & Herrmann, 1999). Code has played an important role in drawingtogether the diverse range of approaches to the assessment and treatment ofaphasia, which have included group therapy, both in his edited books (Code& Müller, 1995) and through his role as journal editor for Aphasiology, andmore recently for the International Journal of Language and CommunicationDisorders. He has been a strong advocate for the need for an eclectic approachto aphasia therapy, for example, he states, “The major ability of the therapistinvolved in the treatment of aphasia is to be able to carefully select the mostappropriate approach to help support those individuals with aphasia inachieving their goals.” (Code & Müller, 1995, p. 46). In his own researchhe continues to underscore the surprisingly low proportion of services thatprovide this efficacious and efficient method of service delivery (Katz et al.,2000). Group processes work to re-establish the sense of identity and self-esteem of participants, and Chris has always had considerable commitmentto the role of self-help groups in this regard both at a personal level,1 andprofessionally (Code, Eales, Pearl, Conan, Cowin, & Hickin, 2001), withthe development of a simple tool through which counseling support couldbe offered (Code & Müller, 1992; Code, Müller, Hogan, & Herrmann,1999). This chapter takes these two notions (that group therapy is animportant way to provide services and that group interactions provideemotional support for recovery) as foundational “givens,” and seeks to pushour understanding one step further through attempting to identify thosekey elements within the myriad of interactional processes that make groupswork. Understanding these processes allows us to develop our skills in run-ning groups, to educate others to run groups, and to facilitate the interactionsof others who may be involved in group interactions with people withaphasia.

Sampling interaction through monologue?

Previous research on interaction involving people with aphasia has focusedon one-to-one interactions, and these interactions have often been moremonologic than dialogic, involving, for example, clinicians facilitating story-telling by the person with aphasia. However, there are questions regardingthe representativeness of monologue. In a study that involved a monologicstory-telling task (about a frightening experience), Ulatowska and colleagues(2001) looked at a range of discourse measures, quantitatively looking at thenumber of propositions, and qualitatively rating global structure, temporalsequence, reference, suspense, coherence, and clarity on a set of ratingscales. They found no significant relationship between discourse perfor-mance on these measures and measures of impairment (Western AphasiaBattery Aphasia Quotient and Cortical Quotient, and Token Test) or onfunctional measures (ASHA Functional Assessment of Communication Skillsfor Adults) (Ulatowska et al., 2001). This finding raises a number of ques-tions. If we relate these findings to the World Health Organisation (WHO)ICF model of impairment, limitations on communication activity, andrestrictions on social participation (WHO, 2001), then it would appear thatmonologic discourse performance is not related to impairment level measuresor functional participation level measures. It might be argued that monologicperformance describes communication at the level of activity solely, but find-ings such as these suggest that for the study of aphasia in the future, it isimportant that we move beyond monologic discourse sampling and considermore valid discourse tasks (Armstrong, 2000).

From monologue to dialogue

Research on conversation has investigated more interactive exchanges, andwith more usual communication partners, such as spouses, or volunteers.This type of research into interaction allows us to look at what might beregarded as the outstanding feature of conversations involving people withaphasia, which is trouble due to word-finding difficulty, and the repair workthat is undertaken by the interactants to deal with the trouble and keep theconversation going (Booth & Perkins, 1999; Ferguson, 1994, 1998; Hengst,2003; Lindsay & Wilkinson, 1999; Perkins, Crisp, & Walshaw, 1999).

The adjustment that occurs between speakers in dyadic communicationchallenges our notions as to what constitutes the nature of aphasic impair-ment (Heeschen & Schegloff, 1999; Helasvuo, Klippi, & Laakso, 2001).Beeke, Wilkinson, and Maxim (2001) present a brief description of twoexcerpts from interactions between moderate-severely aphasic speakers (onewith a therapist, the other with a partner). Their analysis illustrates howthe speakers combine co-occurring gesture with talk built on the previousutterances in order to convey meaning, despite substantial language impair-ment, and they suggest that the observed language performance demonstrates

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adaptation rather than the impairment of aphasia itself (Beeke et al., 2001).Similar adaptation is discussed by Oelschlaeger and Damico (2003), whopresent a detailed conversation analysis of a series of eight conversationsrecorded at home between a man with aphasia and his wife over a 2-monthperiod, illustrating the systematic use of conversational resources for col-laboration. Their findings highlight adaptation by both partners in theexchange. The partner is shown to adapt her responses and repair work tothe nature of the difficulties the person with aphasia is experiencing, andthe person with aphasia is also suggested to be using repetition of hiswife’s guesses of the word he is searching for as both an interactive strategy(e.g., as confirmation, or disconfirmation, or as turn place-holder in theabsence of being able to make an alternative contribution), as well as possiblya reauditorization strategy to assist his language processing (Oelschlaeger& Damico, 2003).

As soon as we start to look at dyadic communication we begin to recognizethe importance of the other partner and their way of communicating as afactor affecting the aphasic language use. While this presents problems withcontrol for reliability purposes, it reflects the fundamental nature of conver-sational exchange, and so presents a challenge that needs to be exploredrather than minimized (such as occurs through elicitation strategies thatminimize the partner’s contribution, such as monologic discourse elicitation).What we want to know is which partner communicative behaviors are moreor less helpful, and to investigate this we need to try to observe and system-atically describe these communicative behaviors rather than eliminate themfrom assessment.

Group interactions involving aphasic speakers

Social participation typically involves conversational exchanges amonggroups of speakers rather than one-to-one dyadic talk. There is relativelylittle previous research that has looked closely at the communication of apha-sic speakers and others within group settings. Early work by Wilcox andDavis (1977) compared the use of speech acts by people with aphasia inindividual and group therapy, and found that aphasic speakers used morequestions in the group situation than in individual sessions. They suggestedthat group therapy is more facilitative of the use of a greater variety ofpragmatic behaviors (Wilcox & Davis, 1977). Klippi’s work in the area pres-ents the most detailed account currently available of naturally occurringinteractions in groups involving aphasic speakers, using conversation analysismethodology, identifying the multi-modal resources used by people withaphasia in group interactions, and their systematic use of the turn-taking andrepair resources available (Klippi, 1996, 2003; Laakso & Klippi, 1999).

Just as dialogue shows us a different set of communicative behaviors fromthose we can observe in monologic discourse, group interaction will similarlyprovide an opportunity to observe how the person with aphasia manages

Multiparty interactions in aphasia 183

a distinctly different set of communication challenges. However, an issue thatarises in looking at the previous research on aphasia group interactions ishow different the group situations are – some involve chat, some involvemore structured activities, and so on (Aten, Caligiuri, & Holland, 1982;Avent, 1997; Bollinger, Musson, & Holland, 1993; S. Brumfitt, 1995; S. M.Brumfitt & Sheeran, 1997; Drummond & Simmons, 1995; Glindemann &Springer, 1995; McCarney & Johnson, 2001; Wilcox & Davis, 1977; Worrall,1995). What we have to recognize is that “group therapy” is likely to bediverse, both externally, in the sense that different groups will be set up fordifferent purposes and different mixes of participants, and also internally,in the sense that because there are multiple participants there will alwaysbe multiple agendas during the period in which groups of people meet. It canbe useful to think of group therapy as an “activity type” in the sense thatLevinson describes as: “any culturally recognized activity . . . a fuzzy cat-egory whose focal members are goal-defined, socially constituted, bounded,events with constraints on participants, setting, and so on, but above all onthe kinds of allowable contributions” (Levinson, 1992, p. 69). From thisperspective, we can start looking at relevant aspects of setting, participants,goals, speech acts/sequences, how language is used (what is “allowable”),and the genres that occur within this activity.

Multiparty interaction

The term “multiparty” interaction is being used increasingly to describeinteractions involving multiple participants. The term is neutral as to whetherthe participants are in fact a “group”, for example a conversation amongpeople waiting for a bus is a multiparty interaction, but not necessarily agroup interaction in the sense that the people are not affiliated in any way.Nor does the interaction necessarily have a shared focus, for example studentsconversing among themselves in a classroom before a lecture starts may allbe talking at once, but in many different combinations and sub-groupings.The advantage of making the multiparty nature of the interaction the start-ing point is that it allows the analysis to explore potential issues such as theextent of group membership and shared focus, for example. On the otherhand, if only two people within a larger group are talking, is this “multi-party,” or is it essentially no different from a dialogue, and hence is there noneed to invoke other analytic frameworks? One answer is that a multipartyinteraction is occurring when there is at least one other listener to anexchange between at least two participants at any moment; that is, an activelyengaged third-party is required to consider an interaction as “multiparty.”An example comes from Osvaldsson (2004) who analyzed laughter in twoconferences involving clients, family, and staff from youth detention homes.Osvaldsson noted that while in a two-party exchange laughter fits into theturn-taking structure (Sacks, Schegloff, & Jefferson, 1974) in the sense thatone party initiates and the other follows, in the multiparty interaction the

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non-speaking participants use laughter as their contribution – they can uselaughter to initiate, to join in unison, or to indicate disagreement by with-holding laughter, that is, “The initiation of laughter by the other participantsprovides for the multiparty aspects of these exchanges” (Osvaldsson, 2004,p. 542, italics as per original). Multi-modal resources such as eye-gaze, facialand other movement, and other vocal behaviors that regulate turn-taking andprovide information about emotional/attitudinal states, including laughter,provide an important resource for people with aphasia participating ingroups (Klippi, 2003). Just as interactants can use these non-verbal resourcesadaptively, so too can they make verbal adaptations in multiparty inter-actions (as previously discussed with regard to dialogue). Goodwin, forexample, discusses the analysis of how a speaker adjusts one sentence in anunfolding turn as he shifts his attention to each of three hearers successively(Goodwin, 1981).

When we recognize group therapy interactions as a particular activity typewithin a wider frame of multiparty interactions, then we can see that withinany group interaction there is going to be monologue, dialogue, and whatEggins and Slade describe as “multilogue” (Eggins & Slade, 2004/1997, p. 20).In analyzing the multiparty interactions that occur in aphasia group therapywe can focus our attention on each particular type of interaction. For example,while some group activities use rotating turns for monologue elicitation,others can be structured for dialogic exchange, and other group activitiesallow for the multilogue facilitators that are neatly summed up in Elman’sdescription of this type of interaction as “jazz music” (i.e., dynamic, impro-vised; Elman, 2004). The many different types of discourse may occur notjust over the period of the group session but also over the “life” of the group.While attention to the different types of interaction is useful, it is importantnot to compartmentalize the different interactions. As an example, cautionneeds to be taken when abstracting, for instance, a short monologue fromwithin a group interaction. Wilkinson talks about how we often removesuch previously occurring co-text from our analysis of what is going on,and miss how both the speaker and the hearer are using what has gonebefore to provide important context for what they are meaning/interpreting(Wilkinson, 1999).

Mediation in multiparty interaction

People with aphasia by the very nature of their communication disability findthat often they are accompanied by another person (e.g., carer, family mem-ber) into social situations that may involve a group of people. Previousresearch in aphasia has focused on the types of strategies and training neededto support the communication of volunteers and carers when talking directlywith people with aphasia, for example “supported communication” (Kagan,1998, 1999; Kagan, Black, Duchan, Simmons-Mackie, & Square, 2001), butthe role that such communication partners take in “mediating” interaction


between the person with aphasia and third parties has received little atten-tion. The term “mediating” is used here in the sense of acting as a “medium”for the communication, and a focus on multiparty interactions highlights theimportance of this role in this particular type of “multilogue.” Also, as theaccess to both social and therapy groups for people with aphasia increases,people with aphasia are increasingly in situations where they themselvesmediate the interactions between other group participants. This mediationrole is familiar to us all; for example when you take someone with you into aninteraction (particularly one who knows you better than do the people in thegroup), then that person may end up at times “mediating” the interaction,such as by explaining what you meant, or taking over the telling of a often-told story. “Mediation” is distinctively associated with multiparty interaction– in the sense that it requires a third party, and so cannot be observed inmonologue or dialogue – and its facilitative power makes it of key interest tospeech-language pathologists. The notion of mediation provides an alternativeway to view the role of the clinician in facilitating group therapy interactions,and I explore this further in the following section.

So, what communication resources might someone in a mediator roleuse? Candlin and Maley (1994) talk about the discoursal strategies used inmediating legal disputes. These strategies involve the more “textual” aspectsof providing the “gist” of what has just been said, or providing the “upshot”(Heritage & Watson, 1979), but they suggest that what is achieved beyond thisis a cognitive reframing (Goffman, 1974). The “frame” essentially alignsor reinforces the current thinking, while “reframing” involves widening ornarrowing, or changing, the current thinking – that is, reframing is trying tochange people’s view of the situation. They note the similarities of thismediation process with the therapy process, and note how mediation drawson therapy practices, but they also note the differences in which therapyaims to explore the personal aspects, whereas mediation of conflict aims todepersonalize, to objectify the situation for the participants. What is relevantfor the purposes of this chapter is the intermediary’s discoursal role andstrategies, in the sense that the role of group leader, for example, or the roleof carer in group interactions with people who have aphasia, involves thiscognitive process of working out what the person with aphasia is meaning,then working out what others might have understood or misunderstood (i.e.,the frame), and judging when to add any additional provision of gists orupshots (i.e., reframing) through textual processes. For the speech-languagepathologist working as a group leader there is also the therapeutic counselingrole in the reframing process to serve the psychosocial or interpersonal goalsof the group. For the carer in a social interaction this aspect also exists, asthere is a goal for interpersonal harmony, for communication to be success-ful, to facilitate the person with aphasia’s sense of contribution/being valuedin the interaction. Ideally, the person in this mediation role manages to assistwhen necessary, and to draw back when the person with aphasia is able tocommunicate independently. However, this can be a fine line to judge, and the

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intermediary runs the risk of potentially disempowering the person withaphasia in the interaction.

The example that follows is drawn from an aphasia group therapy session,in which A5 (a 59-year-old man with moderate fluent aphasia) is taking onthe “mediation” role, through the telling of another group member’s story(A4), who had fallen while she and A5 were on a train trip. As well as A5’smediation role, we can also see three points where the speech-language path-ologist (SP1) mediates the story for the other group members through provid-ing the gist of the story (asterisked). Note that at these points A5 himself isnot seeking assistance, but rather the speech-language pathologist appears tohave judged that other members of the group may not have the same sharedknowledge regarding the extent of the trip (“coming back from Melbourne”),and may have needed a précis or gist of A5’s fairly lengthy circumlocutionabout the numbers of onlookers (“everyone suddenly came”), and might nothave caught A5’s implicit meaning in his description of the railway officialsbeing “scared” (“worried about getting sued”).

Example: The story of A4’s fall (3.5 minute excerpt, from aphasia group therapysession)The interaction involves 12 people seated around a large rectangular table, with twovideo cameras recording from each end of the room. There are eight people withaphasia (from left cerebrovascular accidents), two female speech-languagepathologists aged between 40 and 50 years, and two speech pathology students (onemale ST1, and one female ST2) aged between 20 and 25 years. The details of theparticipants with aphasia are provided in Appendix 12.1

A5 We w w when we went to aphasia, when we went to come back here, we gotto Central

*SP1 When you were coming back from MelbourneA5 Yeah, we got off at Central, so I got the bags, and A4 wanted to go to the

toiletA4 Yes, I know, embarrass {GENERAL LAUGHTER}SP1 No secrets!A5 What happened there was one part to the street, when she touched, er the leg

er twisted, she went down. There was people everywhere, weren’t there!Security guards!

A4 {SIMULTANEOUS} Oh yesA5 And then there was about six, and they come around and say how are you.

And they try to say how are you, can’t hear you. And A4 couldn’t talkproperly. And there I am, you know when I start to talk, I can’t talksometimes, and I said hang on, we both had stroke, we don’t quiteunderstand, slow down, and get away, give us a bit of room, and weunderstand. Oh gee we got a lot of work! {GENERAL LAUGHTER}

*SP1 Everyone suddenly came.A5 And all we wanted to doSP1 You didn’t have to make them cups of tea? {JOKING}A5 They wanted to send us off in an ambulance, to hospital.A4 Embarrassed, embarrass, embarrass.A5 All we wanted to do was get on the Newcastle train.A7 I suppose, but it’s nice when people are kind, it was really kindness.


Such mediation will be very familiar to speech-language pathologists, andI suggest that we can usefully describe this interactive work on a continuum,from interpreting (e.g., other language interpreting, or within same language“interpreting”) through collaborative production (e.g., saying the word forsomeone), to facilitation (e.g., cues, prompts).

The notion of “interpreting” for someone with aphasia is problematic inthat it raises important ethical questions regarding gray areas of advocacyand the extent to which supporting communication fits within our scope ofpractice (Ferguson, Worrall, McPhee, Buskell, Armstrong, & Togher, 2004).These ethical issues are well known to interpreters of other languages, whencultural “interpretation” is also required. Friedland and Penn’s researchprovides a number of insights into the issues that arise when interpreting isless about linguistic translation and more about mediation (Friedland &Penn, 2003). They used conversation analysis to analyze in detail a 45-minuteinterview with Zulu-speaking parents of an 8-year-old child who had beeninjured in a motor vehicle accident. Their identification of facilitators andinhibitors in this setting would apply to other “mediated” interactions, andthese chiefly revolved around role issues. Facilitators were observed to includethat the mediator was an active participant (initiates, questions) and flexiblyswitched between interpreting and information gathering, and that therewas shared knowledge between the mediator and the other participants.Inhibitors were observed to include different agendas held by participants,interruptions, complicated repair trajectories, and misinterpretation.

Speaking for another person, supplying words for them, and finishing theirsentences are all everyday occurrences, and are used frequently when interact-ing with people with aphasia in two-way interactions as well as multipartyinteractions (Ferguson, 1993; Oelschlaeger & Damico, 2003). The sharedknowledge of familiar communication partners plays an important role in

A5 They were scared, because they had to, they put us on to the train, make surewe were safe. When the train stopped at Wyong, we had to go on a bus fromthere to Cardiff, so the railway bloke come, how are you, all right? Took usout, carry our bags. {GENERAL LAUGHTER}

A7 I don’t think they were scared, I think they were kind.A5 No, have a listen, the whole story was, we got to Cardiff, they sent out the

driver looked out and checked us, the railway bloke ended up there too. (turnsto A4) They were ready to meet your son. And then she ended up getting aletter, didn’t you, from the railway.

A4 Oh yesA5 Saying, they said, how are you, you all right, did you need anything.*SP1 Do you think they were worried about getting sued?A5 Yes. I don’t mind, but other people wereA7 (to A3) Ah the cynicism!A3 TrueA5 But some people wouldA7 No, you’re probably rightA5 It was good that it was helped.SP1 It was probably a combination.

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successful collaborative production, and is probably essential for those takingon the role of mediating communication between a person with aphasia anda third party to be able to assist with word searches. However, such sharedknowledge need not be built on personal familiarity, as shared world know-ledge can be created by speech-language pathologists building up a groupactivity based on particular topics, for example. In real-world situations,the particular knowledge of the context for communication will providecommunication partners with a constrained and hence predictable set ofresources that will assist the necessary guesswork, for example for a solicitortaking instructions for a will (Ferguson, Worrall, McPhee, Buskell, Armstrong,& Togher, 2003). Klippi provides a good example of collaborative team workbetween two people with aphasia in a group interaction, where the speakercannot find the word and writes it down (Klippi, 2003). The speaker cannotread, and so is unsure as to whether what he has written is the word he islooking for, but one of the other members of the group with aphasia canread, and she reads the word aloud for him, which allows him to confirm theword (p. 125).

Most of the available literature that addresses facilitation in group inter-actions focuses on the speech-language pathologist’s role. Bernstein-Ellis andElman present a clear summary of ways a clinician can increase conver-sational initiation (e.g., through directing questions to particular groupmembers, explicitly seeking participation or the help of other membersto assist participation), and ways a clinician can increase exchange of infor-mation (e.g., through supported conversation methods, including pictures,gestures) (Bernstein-Ellis & Elman, 1999, pp. 52–53). Garrett’s approach togroup therapy provides for extensive use of facilitation, through a topic/activity-centered role-play of interactions, in which the clinician providesscaffolding and “language mediation” to assist in the rehearsal stages(Garrett & Ellis, 1999).

However, the work by people with aphasia in facilitating group interactionhas also been recognized. McCarney and Johnson (2001) include the descrip-tion of facilitative contributions in their rating system. Their description ofa rating of 0, 1, or 2 mentions that the contributions were not facilitating(of discussion); but for a rating of 3 the “content of utterance(s) likely facili-tates discussion” (p. 1028), a rating of 4 is described as “facilitating,” and arating of 5 “shows some creative ability to further expand the conversation”(p. 1028). However, they discuss that identifying this aspect of facilitationappeared to cause problems for raters, and affected reliability (which howeverthey report to be satisfactory).

Describing the work of mediation is an analytic challenge, as much of whatis going on is conducted covertly by participants, and to a large extentunconsciously. Mediation makes use of the resources typically used for deal-ing with communication breakdown retrospectively (e.g., repair), in orderto act prospectively and preventively to avoid trouble in communication.The research on repair in aphasic interactions suggests that clinicians may


conduct overt repair less frequently than spouses (Lubinski, Duchan, &Weitzner-Lin, 1980), and spouses may conduct overt repair less frequentlythan less familiar communication partners (Ferguson, 1994). Possibly, spousesare prepared to risk endangering the onward flow of conversation more thanless familiar partners, preferring to get the message straight even though theconversation may be halted. Less familiar partners, through provision ofovert correction (including collaborative production), provide quick repairwork that poses less threat to the onward flow of conversation. Cliniciansin conversation with people with aphasia appear to be very focused on main-taining the flow of conversation, and it is this forward-looking work thatappears to be at the heart of mediation in multiparty interactions.

Conclusion

The challenge for the future is in the frameworks and methods of analysisto capture the complex and dynamic nature of multiparty interactionsinvolving people with aphasia, and there are a number of well-developedsociolinguistic methodologies that will assist in this (Gumperz, 1999; Halliday& Matthiessen, 2004; Norris & Jones, 2005; Prevignano & Thibault, 2003).In this chapter I have suggested that multiparty interactions warrant ourattention as part of increasing the validity of assessment, and have drawnattention to the mediation of communication as a particular feature ofmultiparty interaction. Further research into the nature and factorsinfluencing the success of mediation will contribute to the future develop-ment of assessments that capture the impact of aphasia on people’s lives,and the future development of therapy that aims to facilitate their socialinteraction.

Acknowledgements

The contributions of Megan Alston, Sue Sherratt, Judy Vajak, and JulieHengst to the thoughts that have been developed in this chapter are gratefullyacknowledged. Many thanks are also owed to the members of the AphasiaGroup Therapy program for sharing their experiences.

Note1 A favorite personal reminiscence of mine is seeing Chris carefully balancing the

cheese platter he had prepared for his local aphasia group among the pile ofresearch papers on the back seat of his car – a rather precarious positioning giventhe narrow winding roads of the English countryside!

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Avent, J. R. (1997). Group treatment in aphasia using cooperative learning methods.Journal of Medical Speech-Language Pathology, 5 (1), 9–26.

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Appendix 12.1: Description of group participants with aphasia

Client Gender Age TPO(mths)

Nature ofaphasia

BDAE 1

severityCETI 2 VASES 3

A1 F 93 10 Non-fluent 1 12.90 33A2 M 78 46 Non-fluent 2 23.59 22A3 M 57 26 Non-fluent 2 63.25 22A4 F 58 38 Non-fluent 3 61.18 31A5 M 59 >72 Fluent 3 73.0 37A6 F 53 >72 Non-fluent 3 59.50 30A7 F 60 13 Fluent 5 85.68 36A8 F 73 12 Fluent 5 94.87 40

1 Goodglass, H., & Kaplan, E. (1983). Assessment of aphasia and related disorders (BostonDiagnostic Examination for Aphasia). Philadelphia: Lea & Febiger.

2 Lomas, J., Pickard, L., Bester, S., Elbard, H., Finlayson, A., & Zoghaib, C. (1989). TheCommunicative Effectiveness Index: Development and psychometric evaluation of a func-tional communication measure for adult aphasia. Journal of Speech & Hearing Disorders, 54,113–124.

3 Brumfitt, S., & Sheeran, P. (1999). VASES: Visual Analogue Self-Esteem Scale. Bicester, UK:Winslow.

194 Ferguson

13 Stroke storiesConveying emotive experiencesin aphasia

Elizabeth Armstrong andHanna K. Ulatowska

When patients suffer a loss of language, must they also lose their senseof self ?

(Oliver Sacks, 2005)

Introduction

For many years, Professor Chris Code has worked in both clinical andacademic capacities highlighting the impact of aphasia on the individualsinvolved and their family/carers, and has investigated reactions and “adjust-ment” to aphasia. He has also mentored many research students andacademics, and facilitated the description of aphasia from numerous angles,including linguistic approaches. The current chapter encapsulates both ofthese areas that he has influenced significantly, addressing the ways inwhich people with aphasia describe emotional experiences, using a variety oflinguistic tools to achieve expression of attitudes, opinions, and feelings.

Language as a system of meaning serves many functions, including theconveying of information and the obtaining of goods and services, as well associal bonding and the construction and expression of identity. As one ofour most powerful social tools, language enables us to engage other people inour lives and to participate in theirs. In order to do this, we employ a varietyof linguistic resources that not only relate our experiences in a factual man-ner, but also convey our particular stance on those experiences, so that ouropinions, feelings, judgements and values are apparent and ultimately negoti-able, that is, can lead to dialogue in which these aspects are discussed. We alsoaim to make our conversation interesting to others, but perhaps most import-antly, we also use our language to organize and make sense of our reality(Hydén, 1997).

Individuals with aphasia are potentially disadvantaged in all of theseendeavours because of their language impairment. To date, studies of aphasiclanguage have predominantly focused on the information-giving function oflanguage, that is, the imparting of relatively concrete information in terms ofnaming objects or descriptions of pictures. It is the purpose of this chapter toraise issues related to evaluative language and associated linguistic resources,

and to discuss ways in which they are relatively impaired or preservedin aphasia. We present discourse samples of aphasic speakers analysed fromthe perspectives of both the nature of evaluative language in aphasia, and itsvital role in the expression and construction of identity. We also discussimplications of such discourse analysis that would include taking cliniciansand their aphasic clients beyond the realm of factual language in the therapysituation.

Evaluative language

The role of evaluative language in social interaction has been of interest tolinguists concerned with the role of language in social life for a number ofyears. In a summary of this work, Hunston and Thompson (2003) suggestthree functions of evaluative language:

1 to express the speaker’s or writer’s opinion, and in doing so to reflect thevalue system of that person and their community;

2 to construct and maintain relations between the speaker or writer andhearer or reader;

3 to organize the discourse.

In order to achieve these functions, a variety of linguistic and nonlinguisticdevices are employed that enable individuals to express their attitudes, feel-ings and judgements. Labov (1972) cites various methods of evaluation usedto “signal salience” of information that is separate from the specific ongoingaction involved in the recount. Such information could involve the speaker’sreflection on the action in question, providing direct speech for illustrativepurposes, or use of forceful language such as heavily emotive words, intensi-fiers, superlatives, and comparatives. Prosodic patterns related to evaluativelanguage, including marked changes in volume, speech rate and pitch havealso been investigated (Peterson & McCabe, 1983).

The importance of evaluative language has been acknowledged in manyapplied linguistic fields already, including media studies, education, secondlanguage learning, and sociolinguistic studies of culturally diverse groups(Biber & Finegan, 1989; Carter & Nash, 1990; Labov, 1972; Martin,1995; Stubbs, 1986). Its centrality to meaning is highlighted by Cortazziand Jin (2003), who discuss its role in narratives, noting that “Evaluationis held to be the key to narrative: through evaluation, speakers show howthey intend the narrative to be understood and what the point is” (p. 103)and that “the evaluation makes the narrated events reportable, repeatable,and relevant” (p. 105). Labov and Waletsky (1967) similarly point outthat it is the evaluative function of a narrative that communicates the mean-ing of the narrative by establishing some point of personal involvement.Throughout many different genres, speakers articulate who they are throughthe use of evaluative language. In effect, they are expressing their identity

196 Armstrong and Ulatowska

through providing the listener with an insight into how they view theirworld.

The role of evaluation in narrative and identity

One of the main contexts in which evaluative language has been explored isthe narrative. For several years now, there has been significant interest in thefield of social science in the function of narratives. This has occurred inrelation to the individual’s construction of his or her reality and identity, asshared with others in life stories, as that individual attempts to reflect and“makes sense” of his or her life experiences. Hydén (1997, p. 49) writes:

The narrative’s importance lies in its being one of the main formsthrough which we perceive, experience, and judge our actions and thecourse and value of our lives.

Ochberg (1988, p. 174) also suggests that the stories can actively impact onindividuals’ futures:

They shape how we conduct our lives, how we come to terms with pain,what we are able to appropriate of our own experience, and what wedisown – at the familiar price of neurosis.

The role of narratives as a coping mechanism has also been acknowledgedthrough the way we put our emotions into words (Smyth & Pennebaker, 1999).

In recent years, medical sociologists and anthropologists have focused onillness narratives in the exploration of how individuals experience and “dealwith” disruptive life changes as the result of a variety of chronic illnesses(e.g., Becker & Kaufman, 1995; Faircloth, Boylstein, Rittman, Young, &Gubrium, 2005; Jordens, Little, Paul, & Sayers, 2001; McKevitt, 2000).Re-construction of identity following the onset of chronic illness and in theensuing years has been of particular interest, and is said to be revealed,among other ways, through the organization of, and the language used inillness narratives (Bury, 1982; Hydén, 1997). Much of the literature on illnessnarratives to date, however, has focused on illnesses where the personinvolved has resultant physical changes/impairments/disabilities. Because ofthe very nature of their impairment (i.e., impaired communication), thestories of people with aphasia or other cognitive impairments have rarelybeen explored.

Evaluative language and aphasia

To date, as noted above, studies of language use in aphasic speakershave largely concerned themselves with factual language. Such language hasinvolved the speaker naming concrete objects and actions, or producing

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discourse dealing with descriptions of pictures, retelling stories or specificpractical activities, such as catching a bus, or paying bills. And yet, as men-tioned, individuals with aphasia are especially vulnerable to issues of identitychange and related psychosocial issues (Code, Hemsley, & Herrmann, 1999;Hemsley & Code, 1996; LaPointe, 2001; Shadden, 2005; Shadden & Agen,2004) which are often worked through, in other conditions, via language.While clinicians attempt to address such issues with their clients throughdifferent forms of counselling, the role of language is often underplayed inthis context. Little is known up to this point about how individuals withaphasia talk about their feelings, how their language impairment may com-promise this expression, or what resources they employ to work through andassert their “new” identity post stroke. How does their language reflect theirpsychological state? And how can the clinician access such communication?

While studies have reported on attitudes, feelings, and identity issues ofpeople with aphasia (e.g., Kagan & Duchan, 2004; LaPointe, 2001; Moss,Parr, Byng, & Petheram, 2004; Parr, Byng, Gilpin, & Ireland, 1997), the focusof these studies was to elucidate the aphasic experience, rather than toexplore the linguistic style or devices employed by the aphasic speakers toconvey evaluation. Of the few studies that have specifically used emotivetopics to explore the narratives of aphasic speakers, the primary purposeshave involved investigation of such cognitive and linguistic abilities of apha-sic speakers as their ability to organize and maintain coherence acrosstheir discourse (Ulatowska & Olness, 2001), or their ability to convey emo-tionality as determined by listeners (Borod et al., 1996; 2000). The focus ofthese studies again, however, has not been on examining the lexical or gram-matical resources used to convey the specific emotive content of the narra-tives or on evaluative language specifically. Nonetheless, it is of interestthat speakers with left hemisphere damage have been reported to produce“better” discourse (in terms of overall coherence) when discussing emotionalrather than non-emotional topics (Borod et al., 2000), suggesting that theelement of emotion may well be a facilitating and hence significant factor forspeakers with aphasia. Individuals with aphasia have also been noted to useevaluative language as part of overall text organizing devices (Ulatowska &Olness, 2001).

Results from one study to date (Armstrong, 2005) that has undertakena specific lexicogrammatical analysis of evaluative language in personalaccounts of aphasic speakers, suggests that the aphasic speakers involvedused fewer evaluative resources than non-brain-damaged speakers. However,this study focused on verb usage in particular, which is only one of numerousresources involved in evaluation.

Aphasic narratives

Due to the multi-faceted processes involved in conveying attitudes, feelings,and opinions, including non-verbal and prosodic means, the description


involved in this chapter is obviously not comprehensive or all-encompassing.Rather, the purpose of the discussion is to begin to explore the evaluativelanguage resources available to aphasic speakers, and to suggest potentialtaxonomies both for describing these resources and for using them in a clin-ical context. For clinical purposes, such descriptors can provide informationon the speaker’s linguistic abilities, supplementing formal test results andother analyses of more structured discourse samples. They can also providea window into the individual’s psychological state with regard to their per-ceptions of identity, and ways of viewing the world – vital insights whenplanning and monitoring therapy goals and treatments.

The discourse samples on which the present discussion is based wereobtained from corpora collected in Australia by Armstrong and in the US byUlatowska, Olness, and colleagues, and consisted of people with aphasiadiscussing what happened when they had their strokes. They varied in timepost onset (a factor that will be discussed), and their aphasias ranged frommild to moderate degrees of severity.

Amount and intensity of evaluation

What is immediately obvious when scanning different narratives is the vary-ing amounts of evaluative language used in each – specific evaluative devicesto be described below. People vary in their motivation to evaluate and providepersonal and/or emotional aspects of accounts, as noted by previousresearchers (e.g., McKevitt, 2000; Moss et al., 2004). Potential factors influ-encing evaluation include cultural background, personality, gender (althoughstill a controversial issue), as well as, of course, motivation to participate inthe study at hand (see McKevitt, 2000, for an overview of these issues). In thecase of aphasic individuals, severity of aphasia as well as the amount of timethat has elapsed since the onset of the language disorder (potentially affectingmemory of the event, or perhaps their cognitive ability to reflect on pastevents) may influence the kinds of language the speakers are able to use, aswell as want to use.

It appears that such language occurs on a continuum within speakers’discourse. At the more emotive end of the continuum is the discourse of a55-year-old African American woman, SL, who had suffered a stroke 5 yearspreviously. SL provided a narrative rich in evaluation, as she explored herfeelings at the time of her stroke. She drew on numerous images throughout,using much metaphoric language to convey her feelings. In the setting stageof her narrative, she recounted the following:

Example 1At that time, in my mind, I could see the picture of the old lady. When Isay old, I mean a hundred, a hundred and two or a hundred and fiveand she was sitting in a wheelchair and she was leaning forward like(speaker leans forward). She was leaning forward and she had nothing

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in her arms, nothing in her arms. And she was dressed and she had arobe on and she was turned to the side or something like this (speakertwists her body). And there was a nurse prancing prancing around infront of her and made a a attempt to feed this lady in her mouth and Ipictured that as being me. And I said no no God this can’t be me . . .

Such depiction of SL’s mental state at the time provides a detailed exampleof what Labov would note as external evaluation, where the narrator quotesher feelings at the time, and also her talking to God. There is a suspension ofthe actual chain of events in the physical realm, while the narrator elaborateson particular feelings occurring to her at the time. Accompanying each such“section” of the record of events, however, is emotive language conveyed withthe immediacy of the present tense and said as if the narrator was still in thesituation.

A different type of evaluation is evident in the discourse of the followingspeaker, CP (aged 68, 3 months post onset of her aphasia), who providesmore detail of actual action related to the onset of the stroke, but who alsoprovides evaluation as the narrative progresses, yet less floridly than theprevious example. Interestingly it is embedded in the action in the form ofconversational dialogue:

Example 2Well I was scared when I had my surgery and when I had my stroke.I was scared because I didn’t know what had happened to me. And ah, Igot up, I tried to get up. But I fell back down and then my daughterem said what’s wrong with you momma. I said, I don’t know what’swrong. And they said sit down before you fall again. I said, shootit’s something wrong with me. And they looked at me and said itsho’ is.

In contrast to the above, an example of a text containing little evaluation atall is the following from a 70-year-old male, FP, in which he recounts gettingto hospital and what happened on arrival. At this point, it was only 1 monthsince FP had suffered his stroke:

Example 3On the day it happened I got on the Friday morning and just collapsedon a belt at the uh hospital . . . swell . . . (–) – the one . . .

Clinician: Westmead?Westmead . . . Westmead. And just waited there until oh well 4 o’clock

in the afternoon. And said oh you’ll have just have to wait. And so theywaited there and waited. They put it on the bed and keep me there forSaturday, the Friday, the Saturday, the Sunday, Monday and didn’tfood me anything. They just more or less . . . give me . . . (–) food nofood and that was it.


In this account, there is minimal evaluation. While it must be noted thatmales in the samples examined tended to use less evaluative language overallthan females, similar to other reports (e.g., Holmes, 1998; Page, 2003), furtherdiscussion below reveals how FP’s discourse changed over time, although wasnever as emotive as the females’ discourse. However, a more detailed examin-ation over a larger number of samples would obviously have to be undertakenbefore any statements regarding the effect of gender could be made.

Functions of evaluation

Speaker’s attitudes and maintaining social relations between speakerand listener

As Hunston and Thompson (2003) note, it is difficult to separate out thedifferent functions of evaluative language, and for the purposes of this dis-cussion and the data being presented, the first two functions as described bythese two authors will be discussed concurrently. As noted particularly in thefirst two examples above, the speaker fulfils the two functions of conveyingstance and engaging the listener simultaneously. Other examples expressingthe commonly cited fear and the feeling of not knowing what was happening,experienced in the early stages post stroke, also convey the narrator’s feelings,while capturing the listener’s interest by highlighting that this incident wassomething out of the ordinary, emotional, and significant (“that was a scari-ery moment; I was terrified; that was the most frightening thing; I didn’tknow what had happened to me; what’s the matter?”).

In terms of the language conveying the speaker’s psychological state at thetime, Frank’s (1995) major stages of illness provide a framework withinwhich to view such examples. Frank suggests that there is a chaos stage inwhich the individual is in a state of confusion, with things happening aroundhim or her over which he or she has no control; a restitution stage, where theperson aspires to return to “wellness” and a previous state of normality; anda quest stage, in which individuals see purpose in their illness and their strug-gle through the barriers encountered along the way, and see a way forwardbased on their experience. The above examples of fear and confusion fitappropriately with the chaos stage, while an example of a restitution theme isthe following, although it must be noted that the prior text for this speakerinvolved chaos narrative as well:

Example 4I said I’m handicapped but I will not be but at that moment I saw thatpicture “I said no.” If it was the devil showing me the way that I wasgoing to be he is a LIAR. HE IS A LIAR. HE’S A LIAR. Because I’mnot down yet. But girl that was a scariery moment. I had to make sure Icould talk. I was lying in a position flat on the floor. Thankyou JesusThankyou Jesus.

Stroke stories 201

In this part of her narrative, SL resolves not to be handicapped, and shows afighting spirit, using the religious imagery, as well as imagery of herself notbeing down yet as if in a fighting context. Another speaker, JB (68 years old,15 years post onset) said, “Only thing I was thinking about was gettingmyself together so I could do for myself.” It is of interest, that JB laterbecame a volunteer at the local hospital, working with people with aphasia.Her “narrative” at that time hence became that of quest, as she saw a rolefor herself in assisting others through the experience and seeing meaning/purpose in her own experience.

Another common theme to aphasic narratives also involved thinking ofpremorbid status as an independent capable person who is now unable to dothe simplest things, and also of the fear of becoming dependent on others:

Example 5I’ve got a college degree . . . two years in the running I was on the dean’shonours list and now I’m back learning first grad math, second grademath. And it’s like my life is just like a wiped off blackboard. (PC, aged57, 2 years 3 months post onset)

Example 6When I went to hospital I went by myself ah ah I was very independentcause after twenty years you have to be inde you know in ah a displacedhousewife you have to be independent and strong and I went to hospitalby myself . . . and now I was scare because I was the mother I’m thechild and I have you know there’s no one else and my kids and I wastheir mother like my father was my father you know . . . you were thestrong figure . . . and I and I was get caught I would be somebodydaughter again I didn’t want to be somebody’s kid because I was soscared. (AS, aged 55, 4 years 7 months post onset)

In these examples, again strong feelings are expressed in such a way as toengage the listener beyond the factual account. The juxtaposition of thecollege degree and learning first grade maths is potent in Example 5, as is thediscussion of independence and strength related to being a child again inExample 6.

Organization of the text

The third function of evaluation, as noted above, is to organize the text in acoherent manner. While numerous other organizing forces exist within dis-course, such as cohesive devices, logical connections, and chronologicalcontinuity, evaluation is important in maintaining the “point” of the story,and linking relevant points together. The positioning of the evaluationwithin the narratives is thus of significance in understanding both thenature and the degree of resources retained by the aphasic speaker. For the


non-brain-damaged speaker, evaluation can occur at almost any point inthe narrative. For example, Labov (1972) suggests that it can occur towardsthe end of the narrative, as the speaker provides a summary of the “point”of the story. However, it can also actually interrupt the “action” itself inorder for the speaker to talk to the listener more directly, or even for thenarrator to engage in reported self-talk (external evaluation). Longacre(1996) notes that evaluation is also effective when associated with the climaxof the story. As noted above, the evaluation can also be embedded through-out the narrative via lexical choices that convey certain emotive/attitudinalmeanings and/or by propositions that form part of the narrative itself. Organ-ization of these types can depend on linguistic skills (although little has beenwritten on cognitive/syntactic capacity required of each type).

The aphasic data discussed here revealed evaluation at various pointsthroughout the speakers’ narratives. Evaluation was noted in some as beingpart of all aspects of the narrative; that is, the setting, complicating action,resolution, coda, all in the external evaluation mode discussed by Labov,where the speaker temporarily postpones the sequence of events to reflect insome way. Consider the following example involved in the setting (evaluationin italics):

Example 7Um um when I went to the hospital I went by myself ah ah I was veryindependent cause after twenty years you have to be inde you know in ah adisplaced housewife you have to be independent and strong and I went tothe hospital by myself and I wanted to find out what I had first . . . (AS)

For other speakers, the evaluation was embedded throughout the sequence ofevents:

Example 8I tried to get up. But I fell back down and then my daughter em saidwhat’s wrong with you momma. I said “I don’t know what’s wrong.” Andthey said sit down before you fall again. I said shoot it’s somethingwrong with me. And they looked at me and said it sho’ is. And I tried towrite and I couldn’t write and that scared me. (CP)

Linguistic devices

As can be seen in the examples above, a variety of linguistic devices areemployed by speakers to realize evaluative meanings. As complexity can varywithin the use of any of the realms of devices described below, it is difficult todefend a sequencing of them in this regard. For this reason, the reader shouldbe aware that the following order of description has no particular signifi-cance, and that each of the devices is capable of being used in both simpleand complex forms.

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Evaluative words/phrases

Explicit evaluative meanings are conveyed in a number of ways in the lexico-grammar, examples of which are found in many of the above quotations.Mental clauses involving mental verbs such as “felt”, “worried”, were usedin the aphasic texts, realizing the speaker’s perspective on a particular pro-position, person or thing, while descriptive clauses (e.g., “I was scared, some-thing was wrong”) (described further in Armstrong, 2005) also providedevaluation. Word level evaluative meanings were also conveyed throughevaluative verbs (e.g., “saddled with”, “flopping”), evaluative nouns (e.g. “aburden”), adjectives (e.g., “funny”, “scared”, “numb”), and adverbs (e.g.,“naturally”). In addition, intensifiers (e.g., “most frightening”, “really wanted”)and modal adjuncts (e.g., “unfortunately”) were further resources (for a fullaccount of potential lexical resources, the reader is directed to Martin, 2003).

Hence, it is clear that at least at the mild to moderate level of severity,aphasic speakers do retain the evaluative function at the lexicogrammaticallevel. Even in the presence of clauses that are not syntactically or semantic-ally “correct”, evaluation is obviously present. Consider the following extractfrom the narrative of a man, MD, aged 60, with a moderate degree ofaphasia:

Example 9I know I was gonna be sick some day. I know it. Maybe it was fordreams I did have . . . Anyway I did do cripple. Yeah I did sick it was myhead. Ha. I guess I had it for sixty years but I had some fun . . . It is tolaugh. I have I am still for fun . . . It is to laugh. I have I am still for funbecause I am still alive . . .

In this example, lexicogrammatical breakdown is obvious, however the evalu-ative meanings are clear through both the use of individual words such assick, cripple, fun, as well as the whole process involved, for example it was fordreams, I did do cripple, I am still for fun.

It is obvious, however, that range of wording, when compared with non-brain-damaged speakers is potentially restricted in the narratives of aphasicspeakers (as found by Armstrong, 2001, 2005), depending on both severityand type of aphasia. While aphasic speakers may retain emotive words, theymay be of a general/high frequency nature rather than as broad an array asnon-aphasic speakers might use. In addition, the more sophisticated devicessuch as modal adjuncts, adverbs, and intensifiers may indeed be less availableto aphasic speakers, as evidenced in the data examined.

Repetition

Repetition is a frequent and important evaluative device in discourse, per-forming an emphasizing function. It can occur along a continuum from


the simplest form, where a word or complete proposition is repeated, to themost sophisticated form, in which a proposition is re-phrased either in aliteral or metaphorical form throughout the discourse. Repetition is wellrecognized as a feature of aphasic discourse (Armstrong, 1997; Ulatowska &Olness, 2001). While it can be pathological in the form of perseveration, itmay also be a strategic evaluative resource used by an aphasic speaker forthe purpose of emphasis. Consider the following example of repetition at theword level:

Example 10In my right hand it really tried to scare me because I couldn’t write.And that was one time I was really scared. And I was scared then to firstwhen they told me I had to have my heart surgery and that really scaredme. (CP)

The following provides an example of repetition at the phrase and clauselevel, emphasizing the deep emotion felt by the speaker:

Example 11I thought about killing myself. That was the most frightening thing thatever happened to me. Because I told my supervisor about killing myself.I really wanted to kill myself. (PC)

Direct speech

As mentioned, one of the devices used by several of the speakers was directquotes during the narrative, involving dialogue between the narrator andothers in the story, and other participants’ dialogues, as well as the narrator’sself-talk. Labov (1972) considered direct speech as being one of the highestforms of evaluation in that it “translates our personal narrative into dramaticform” (p. 396). Ulatowska, Streit-Olness, Samson, Keebler, and Goins (2004)found large amounts of direct speech in personal narratives of good story-tellers in African American adults. Interestingly, Ulatowska and Olness(2001) also reported on its use in African American aphasic narratives, whereit was used effectively as a means of engaging the listener in a highly emotiveand immediate way.

While in the examples above, direct speech was used by relatively mildlyaphasic speakers, the following example from a more severely affectedspeaker, GB (aged 47, and 4 years 2 months post stroke) indicates that it isstill possible to use this sophisticated device even in the presence of relativelysevere aphasia. GB’s language was affected in terms of lack of grammaticalcomplexity and lexical variety (Broca’s type aphasia), with the use of directspeech achieved without completeness of clauses or projection:

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Example 12“Help me, help me,” I don’t speak. I I am rushed to Memorial, only toMemorial. Um um six o’clock. Tests won’t though. Um thought I wasgetting better, but no speak. “Help me, help me” no, no I don’t havewords. Noon. “Help me please,” I don’t see, I don’t mmmm no sounds.Five o’clock, um, my little brother and, um, Pat, my lifelong friends,okay. And “it’s okay, we’ll we’ll, we’ll get out of your way” and um,“take me home please.”

This evocative section reveals restricted lexicogrammatical form, and yetmuch emotion. The primary way in which this speaker engages the listenerhere is through the juxtaposition of time elements and direct speech. Thedirect speech was not projected by a clause stating who said what and yetthe meaning is clear.

Metaphoric language

Metaphoric language is used in a number of contexts (e.g., literature, casualconversation) to engage the listener/reader through imagery. Some but not allof the aphasic narratives included such language. One might hypothesize thatindividuals whose language was more severely impaired would have greaterdifficulty with metaphoric language, as it is considered “inherently complex”from both semantic and syntactic perspectives (Halliday, 1994). And indeed,the narratives produced by some of the milder aphasic speakers containedrich imagery. Consider the following examples:

Example 13It was this wrestler or it was like something was pushing down on me. . . and finally I got up enough strength and I gained on him. (SL)

Example 14It’s like my life is just like a wiped off blackboard. (PC)

A more severely impaired speaker in our corpus also used a degree ofimagery, although the following excerpt is obviously less explicit than the firstexamples due to word-finding difficulties:

Example 15And a little bandage of brain or something or other went sss and wentup in the air. And went down there and went out . . . for keeps. That’swhat’s been building back ever since. That’s building up this brain uh. . . up. (FP)

Further studies would have to explore the degree to which metaphoric lan-guage is impaired in severely aphasic individuals, and whether or not it is


possible to produce at a phrase or even single word level (e.g., using the aboveexample, wrestler . . . pushing down).

Change in evaluation over time

While it is noted that identity reconstruction is an ongoing process and thatnarratives can change over time, in the case of the aphasic speaker, time alsoprovides potential recovery of language function and cognitive function, aswell as the time to reflect on what has happened. On the other hand, thefarther we are from an event, our memory for factual details may deterioratesomewhat. From our corpora, the narrative of one aphasic individual, FP,was examined over a 12-month period at 3-month intervals, in order explorethe potential effects of time on aphasic narratives. At the first interview,the speaker FP provided the factual account given above in Example 3. At3 months post onset, a similar narrative was elicited. In the following months,however, more detail emerged, as well as reflections on his impairments,followed by his progress:

Example 16And uh I just lay there and said very little to anybody. Didn’t say a wordand didn’t want to say anything cos I had . . . I couldn’t even speak toanybody.

Example 17I can almost write now . . . normally . . . and speak and I can speakproperly. And uh while I’m writing I I get a bit tired in the arms . . . andthe hand writing. But uh . . . allright otherwise OK.

It must be noted that this speaker’s linguistic resources improved over time inall respects, as well as evaluation. Hence, in this regard, it would appear thatFP’s aphasia certainly inhibited his expression of evaluation in the earlystages post onset.

Implications

From this preliminary exploration, it is clear that while individual variationexists, mildly to moderately aphasic speakers are able to make use of evalu-ative language to convey their attitudes and feelings, and to use evaluativelanguage in a way that helps to organize their discourse coherently. In thisway, they are capable of bonding with, and engaging the listener, as well asusing language to express their identity, and to some extent, construct andconfirm their own view of reality in their post-stroke context. Severity, as wellas factors related to premorbid style, may affect type of evaluation used,although both external and embedded evaluation were evidenced, as well asevaluation as dialogue – all seen in non-brain-damaged discourse. The fact

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that evaluation could be ascertained from incomplete utterances through useof evaluative words and phrases supports the notion that aphasic speakers donot have to be syntactically correct or even semantically accurate in order toconvey meaning. However, the samples used for discussion here were limitedto mildly and moderately aphasic speakers. Aphasia obviously has the poten-tial to impact on evaluative language use in terms of quality and also the kindsof devices used. The extent to which different severities of aphasia affect/restrict expression of evaluation will form the basis of future investigations.

In terms of the experience of suffering a stroke and being aphasic, itappears that the aphasic speakers in the samples examined conveyed thechaos and, to a lesser extent, the restitutive stages of their illness, as reportedin narratives of other populations suffering from chronic illness. The fear,uncertainty and disruption caused by the stroke was obvious in all theaccounts, related to both the initial life-threatening situation and potentialchanges to future independence, as well as ongoing chaos. The importance ofverbalizing such emotions has been reiterated throughout the narrative litera-ture, including the significance to the individual in terms of managing lifeexperiences and relationships. Hence, given the strengths noted above, it maywell be that the illness narrative, as well as other potentially emotive narra-tives, may be powerful contexts to be used in clinical and external situationsfor providing aphasic individuals with the opportunity to express importantissues of identity changes experienced post stroke. The narrative may wellprovide an opportunity for clinicians to engage with the aphasic person indealing with these ongoing emotions. Concurrently, the emotive narrativeprovides a meaningful communication experience for aphasic speakers topractise their verbal expression in the clinical situation. In so doing, they gainstimulation for language other than factual expressions involved in typicaltherapy activities such as naming, or discourse tasks focused on picturedescription.

While the effects of severity and type of aphasia on amount and type ofevaluative language used may constitute further studies, non-verbal means ofconveying evaluation could also be explored. Longitudinal studies document-ing recovery of language function could address some of the issues thatcomplicate the picture in aphasia, such as the impact of the speaker’s psycho-logical state in the early stages post stroke, as well as level of cognitiveimpairment, affecting such aspects as memory, and ability to reflect. In add-ition, co-construction of evaluation in dialogue would be an important areato explore in order to further address the social nature of stance and attitude.Such explorations should further elucidate the issues involved in evaluationand its significance for aphasic individuals.

Acknowledgments

This project was supported by grants from the following: Departmentof Veterans Affairs Rehabilitation Research and Development Program,


National Institute on Deafness and Other Communication Disorders, CallierCenter for Communication Disorders at the University of Texas at Dallas,Community Partners Program (a collaborative program of the University ofTexas at Dallas and Baylor Institute for Rehabilitation). Our thanks to boththe institutions and participants involved

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Part III

Clinical considerations

14 Counseling families andadults with speech andlanguage disordersThe view from awellness perspective

Audrey L. Holland

Introduction

The scope of Chris Code’s contributions to neurolinguistics, and especiallyaphasiology, has been vast. Both as a scientist and as an enabler, through thejournal Aphasiology, he has enhanced what we know about both right andleft hemisphere language processing, and how to influence it through treat-ment. He has also been very open to the importance of the so called “softersides,” that is our understanding of discourse and pragmatics and, finally, thepsychosocial issues that surround negative changes in normal language func-tioning. This chapter has been written to honor that part of his enormousinfluence on the field.

According to the American Speech-Language-Hearing Association(ASHA) Scope of practice (2001) counseling families of children with speech,language, and hearing disorders, as well as adults who have such disorders, isan integral part of clinical responsibility. Counseling is perhaps the mostimportant way we have to help our clients, yet it is likely to be that aspect ofpractice that most Speech-Language Pathologists and Audiologists feel mostuncomfortable about, and are most likely to avoid.

There are probably many reasons for this. Our reluctance might beexplained by a lack of explicit training. Although we are given a wealth ofinformation concerning potential counseling problems faced by individualsand families with communication disorders, we are not instructed in how tomanage them. Counseling is often just tagged on to the end of disorder-specific courses, rather than having a focus as a special art, and a skill that canbe learned in a general way, and then burnished by the specific problemsevidenced by say, an adult and his family who face the realities of living withaphasia following a stroke.

But I suspect there is an additional, probably bigger, reason. Why are weexperts in communication so nervous about assuming our counseling role?Most counseling approaches used with communication disorders have beenborrowed from a clinical psychology that emphasizes psychopathology andits effects on behavior. This, despite the fact that the counseling problems faced

by experts in communication disorders do not stem from psychopathologyper se, but from some form of catastrophe imposed on individuals who forthe most part (even those most likely to be victims of traumatic brain injury)were at least coping with life in a fairly normal way. To my knowledge, ourdiscipline’s reliance on abnormal psychology has seldom been examined,although it might explain why many practitioners feel uneasy with their coun-seling roles. Most families and individuals who experience communicationdisorders don’t fit easily into a psychopathological model.

Much of what follows stems from my conviction that a more appropriatemodel for our counseling lies elsewhere; not in what we know about illnessand psychopathology, but rather in models that are grounded in wellness. Therecent explosion of information and interest in Positive Psychology providesthe best example, particularly as it is illuminated by the work of Seligman andhis colleagues (e.g., Seligman, 1991, 2002; see also Reivich & Shatté, 2002).In fact, although I have used the word “counseling” in this chapter, I believethe notion of “coaching” as is reflected in the growth of contemporary inter-est in the phenomenon of Life Coaching, is probably a more appropriatedescription of our counseling activities.

From the vantage point of Speech-Language Pathology (hereafter simplyreferred to as SLP), it seems to me one of the most appealing aspects of afocus on wellness and positive psychology as a model for counseling is that itfits squarely and comfortably with that aspect of counseling with which weare most comfortable, namely our educational role. In my understanding ofSeligman and his colleagues’ work, positive psychology attempts to teachindividuals a number of exercises and very specific approaches that they canlearn to use daily (or thereabouts) to increase their resilience and optimism(among other things) and that can contribute meaningfully to their leadinghappier and more fulfilling lives.

Our discipline produces good teachers – from helping children to movelateral lisping into more acceptable /s/ production, to re-establishing semanticskills in aphasic adults. To the extent that our counseling can capitalize onour teaching skills, we should be more comfortable with our counseling roles.

What is counseling in SLP?

These remarks are limited to working with adults who have communicationdisorders resulting from catastrophic events and their families; nevertheless,almost all of the ideas I will be discussing also have a place in work with thechildren and families who seek our help. In what follows, I first define coun-seling, then I enumerate the disorders that I believe would fall under therubric of “catastrophic” and provide a very cursory glance at the generalproblems each presents. I then outline a tentative model for counseling inadult catastrophic disorders. Next, I provide information concerning somebasic characteristics of good clinicians, and then briefly digress into a discus-sion of group versus individual counseling. Then, I finally get back to the initial

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question I raised concerning our professional anxieties about the counselingrole.

What is counseling?

Briefly, counseling is a listening process that is geared to understanding howthe world looks to the person being counseled. Once careful listening hasincreased the clinician’s understanding, counseling moves on to guide thecounseled person to express feelings, concerns, anxieties, and so forth. Thethird aspect of the counseling process involves advising, that is, providingthe information people need to hear to help them understand what is happen-ing to them, how to get on with their lives, and to live in a realistic, yetoptimistic and resilient fashion. Then comes the most difficult step; helpingindividuals to translate the information into action that is helpful, satisfyingand successful. That is, the goal of counseling is to help individuals andfamilies to live as successfully as they possibly can, despite the intrusion ofthe unexpected stroke, the unanticipated dementia, the communication-compromising disorder such as laryngeal cancer, or the sudden and dramatictraumatic brain injury. The major aspects of communication counseling havebeen well summarized by Webster (1977) as follows:

1 To receive information that the individual and his or her family wish toshare with you.

2 To give information.3 To help individuals clarify their ideas, attitudes, emotions and beliefs.4 To provide options for changing behaviors.

The intent of counseling in situations such as those encountered withcommunicatively impaired individuals and their families is to help them:

1 to grieve for what has been lost2 to understand it as fully as possible3 to develop coping strategies and increase resilience4 to make peace with the disorder5 to make sensible adaptations to it6 to capitalize on strengths to minimize weaknesses, and7 to live as fully as possible, despite impairment.

We need to be reminded that, for those of us in this profession, counselingis seldom the general focus. Rather, counseling occurs “around the edges” ofmore direct treatment. This in no way denigrates its importance. Far from it,it accentuates the responsibility of clinicians to be on their counseling toes atall times.

Counseling families and adults with speech and language disorders 215

Who has these catastrophic conditions?

Although individuals who stutter (or their families), or families and indi-viduals who as adults are continuing to cope with autism-spectrum disordersor other developmental disabilities, may have significant counseling needs,this is too big a topic for a brief chapter. It seems sensible, therefore, to focushere on those who have previously been coping somewhat successfully, andwhose problems come without warning, creating a crisis. The point here isthat before the onset of these conditions, most individuals have been living inrelative wellness (even a majority of individuals with TBI). Their problemsalso have unique, significant, and reverberating effects on families, who are, inthe main, largely as unprepared for their unwelcome intrusion as are thosewho incur the problems in the first place.

The most important way to differentiate these disorders and their distinct-ive needs is based largely on their typical progression and time course. That is,there are different counseling agendas for those who will improve and thosewho will deteriorate. Make no mistake; all of these disorders are to somedegree chronic. However, in large measure, (although not without exception)these two types of catastrophic problems have different implications for thenature of the counseling challenges they provide.

The first type of disorder involves chronic conditions that tend to improve,to experience some recovery spontaneously over time, or that change in apositive direction substantially with clinical intervention. These includeconditions such as aphasia and right hemisphere cognitive disorders follow-ing stroke, laryngeal cancer, operable and non-metastatic brain tumors, someforms of encephalitis, traumatic brain injury and the like. For such disorders,after the initial listening and the information-providing is done, the counsel-ing focus should be on measured and graceful acceptance, on building real-istic optimism and resilience, and on coping in a balanced positive way towardliving successfully with the disorder.

The second type of disorders includes conditions such as dementia, primaryprogressive aphasia, Parkinsonism, multiple sclerosis, and the particularlychallenging disorders of amyotrophic lateral sclerosis and brain tumors suchas glioblastoma multiformae, which have an unrelentingly grim prognosis.For these disorders, listening and providing information of course must hap-pen, but the truly challenging counseling responsibility is mutually to worktoward acceptance, learning to live the best of what is left of one’s life, andeven possibly to deal with some end-of-life issues such as making peace.

It is important to add a few words about depression and learned helpless-ness. Without exception, the problems mentioned above all have the potentialfor resulting in reactive depression. For disorders that involve brain damage,there is the additional possibility that a concomitant depression, broughtabout by faulty or disturbed patterns of normal neural transmission, mayalso occur. Finally, individuals may have come to their present disorderalready carrying a suitcase full of depression. Counselors in communication

216 Holland

disorders lack the technical skills to treat depression, both behaviorally andpharmacologically. But because depression is so likely to co-occur in someform with the catastrophic problems we deal with, it is extremely importantfor us to be highly sensitive to the problems that forecast it. According toDSM-IV, depression includes mood disorders, lack of zest, unexplained weightloss, sleeping problems, psychomotor problems, excessive fatigue, feelings ofworthlessness, statements of futility, and such. When these problems persist,our ethical responsibility is to state our concerns directly and to makeappropriate referrals.

A useful model

Although it has significant shortcomings, a crisis model, particularly asWebster and Newhoff adapted it (1981), can be useful for understanding theprocess whereby individuals can learn to deal with catastrophic events. Firstdeveloped by Elisabeth Kubler-Ross for dealing with grief, death and dying(1969) it has been useful with many chronic health issues as well. Webster andNewhoff discuss the relevance of crisis to families and individuals followingstroke. Specifically, four stages are postulated to occur as individuals progresstoward healthy resolution. They are, in order, Shock, Realization, Retreat,and Acknowledgment. Not all individuals go through all stages, and not allindividuals actually reach satisfactory acknowledgment (more on this below).Nevertheless these stages set the tone for what are the important counselingparameters for SLPs to keep in mind as they conduct counseling related tocommunication. Following are some examples.

Soon after an aphasia-producing stroke, neither families nor aphasicindividuals are in a particularly good position to take advantage of theinformation we might have to offer them concerning aphasia and its after-math. I am aware that good clinicians almost without exception provide suchinformation. Nevertheless, someone like me (who is unlikely to see aphasicindividuals until they complete their course of formal rehabilitation) almostalways hears that things weren’t explained, that individuals and their familieshad no idea what to expect, and so forth. This happens because early shockpretty much precludes the ability to absorb new information. This does NOTmean that we should stop providing it in the most acute stages, probably inwriting and for placement on fridge magnets and the like, to be consultedlater. But it DOES mean that the first of Webster’s (1977) counseling func-tions probably should be primary. Listening to what people wish to share, totheir fears about the future and such, and simply holding hands and beingthere is what matters then. And only after some realization about what thisproblem might actually be, can information be productively used. (For adetailed look at an approach to aphasia management in the acute stage,readers are referred to Holland & Fridriksson, 2001.)

Although retreat seems to me to be the least universal of these crisis stages,we must be aware of the delicate nature of denial, and the need to deal with it


clinically should it occur in the individuals we work with. A common findingin our clinic for individuals with chronic aphasia is that when families ofthose who are newly discharged from rehabilitation complete the requiredCommunication Effectiveness Index (CETI) (Lomas, Pickard, Bester, Elbard,Findlayson, & Zoghabib, 1989), their scores are substantially better than theywill be the next time they do the CETI, after they have lived with the disorderfor a longer period of time. This is an issue for gentle and careful familycounseling.

Acknowledgment is not a synonym for “giving up.” It is recognizing whereone is, making room for one’s changed condition, and ideally moving onwith life. Ram Dass, who finished his book Still here, after a stroke resulted inaphasia and hemiplegia, eloquently described his experiences, and the goodthat resulted from them. He notes (2000, p. 185):

The stroke was like a samurai sword, cutting apart the two halves of mylife. It was a demarcation between the two stages. In a way, it’s been likehaving two incarnations in one; this is me that was “him.” Seeing it thatway saves me from the suffering of making comparisons, of thinkingabout the things I used to do but can’t do any more because of theparalysis in my hand. In the “past incarnation” I had an MG with a stickshift, I had golf clubs, I had a cello. Now I don’t have any use for thosethings! New incarnation!

Mezirow (1991) has written extensively about the role of transformativelearning in adults, producing evidence that many individuals go through whathe terms “disorienting dilemmas” that cause them to re-evaluate, reflect crit-ically, find out that they are not alone, and for many, restructure the meaningof our lives. This is the sense of acknowledgment that counseling shouldstrive toward, if not always achieve.

What are the characteristics of a good SLP counselor?

Robert Crum, a child psychologist with extensive experience in working withchildren and families with communication disorders remarked to me recently(personal communication, October 2004) that in his view, SLPs were mastersat presenting relevant information, but that their other counseling skills werenot nearly as highly developed. I agree. In our training curricula, counselingand interviewing often are approached together. This makes it almost a giventhat we should see their respective roles as more overlapping than theyactually are.

In addition, we learn early on that we must communicate as much of ourexpertise as possible to our clients. Along the way, we forget that we are onlyone of the “experts.” Along with the individual whose expertise is livinginside the problem, and those whose expertise is living beside the problem(i.e., the family), we bring the expertise of “the one who has seen many such.”

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But we have not lived it. Exquisite awareness of the three sources of expertiseis one characteristic of the successful counselor.

There are others, of course. I believe that the next most important clinicalskill is the ability to be a good listener. (Luckily, listening well is a learnableskill.) Good listening comes in many forms, including affirmative and sup-portive listening, reflective listening, and critical listening. It involves sensi-tivity to both a message’s manifest (surface) content and its latent (deeperemotional) content, and whether or not these two message levels are in agree-ment. Often, insights result from our ability to listen, not only with our ears,but with our eyes as well to non-verbal features of communication includingprosody, intonation and body language.

Counseling skills also include our own words and body language. Sometechnical skills consist of a variety of learnable techniques, such as how toreflect what someone is saying, knowing how to ask appropriate questions,communicating support and affirmation verbally. Because I am an active andinvolved counselor, as opposed to a neutral and passive one, I also comedown on the side of providing advice, but giving it tentatively and from myoutsider position, as noted above.

And we also must capitalize on our information giving skills. As Crum(personal communication, October 2004) suggests, we need to know what isrelevant and what is acceptable to a given client about issues ranging fromwhat can be expected over the next few years concerning a disorder, to how toget the most from services available in the community. As a counselor, I tryvery hard to communicate in every way that I am consistently “being there,”as a helper, an advocate, and as, simply, a listener.

Next, I believe that competent SLP counselors know who they are.1 Theyknow their strengths, and what things are not within their basic competencies.This puts them in a position to work with clients from their own strengthsand capabilities. I firmly believe that a major reason for my being a goodcounselor is that I know pretty well who I am, and how to capitalize on itwhen I counsel. Finally, in an overarching way, good counselors must beoptimists who like people, enjoy challenges, know and accept themselves, andcommunicate their positivity.

Group vs. individual counseling

A few words about the manner in which counseling is conducted seem to bein order. Whether to choose a group or an individual format seems to me tolargely be a matter of mutual choice, agreed on by the counseling clinicianand those being counseled. I personally gravitate toward group work for anumber of reasons. First, given my earlier comments about who are experts,it seems likely that when there is more than one of those other expertsaround, there should be a lot to share, thereby greatly increasing the extent ofexpertise in the room. Second, as Mezirow (1991) points out, social inter-action greatly enhances the likelihood of transformative learning. Third it is


cheaper and more practical, often bringing the group within the reach ofindividuals who otherwise would not be able to afford counseling. But shouldindividual counseling be the order of the day, then I think the clinician hasincreased responsibility for sharing what has been learned from working withothers and being a surrogate expert. And, it must be added, frequently ourcounseling of individual clients occurs “around the edges” of more directtherapy.

I also prefer family groups and groups for individuals who have the dis-orders to meet separately. I have learned the value of this over the years,mostly from the people I have worked with. The focus of combined groupsalmost invariably settles on the individual with the problem, with familyneeds going by the wayside. And this seems to occur despite the fact thatfamily members dominate the talking time.

Concluding comments

This has been a cursory review of counseling issues for clinicians dealingwith adults and families who have neurogenic communication disorders. It isnot a clinical roadmap; rather it attempts to point out the major counselingissues for these people, and to provide a rationale for treating them. The mostimportant underlying message (the latent one) is that professionals in thisfield must take their counseling responsibilities seriously, and that counselingindividuals with neurogenic communication disorders is among the mostimportant things we do to influence individuals in their return to theireveryday lives.

Acknowledgment

A version of this chapter appeared in the newsletter of the CaliforniaSpeech and Hearing Association in Autumn, 2005. I am grateful for CSHA’spermission to expand on and modify it here in honor of Chris Code.

Note

1 A number of self-inventories are useful to clinicians. These include the Myers-Briggs and the Values in Action (VIA). A form of the Myers Briggs can be takenon the Internet at www.Humanmetrics.com and the VIA can be taken atwww.Authentichappiness.org

References

American Speech-Language-Hearing Association (2001). Scope of practice in speech-language pathology. Available as pdf file at www.asha.org

Holland, A., & Fridriksson, J. (2001). Management for aphasia in the acute phasespost stroke. American Journal of Speech-Language Pathology, 10 (1), 19–28.

Kubler-Ross, E. (1969). On death and dying. New York: Macmillan.

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Lomas, J., Pickard, L., Bester, S., Elbard, H. Findlayson, A., & Zoghabib, C. (1989).The Communicative Effectiveness Index: Development and psychometric evalu-ation of functional communication measure for adult aphasia. Journal of Speechand Hearing Disorders, 54, 113–124.

Mezirow, J. (1991). Transformative dimensions of adult learning. New York: Wiley.Ram Dass (2000). Still here. New York: Riverhead.Reivich, K., & Shatté, A. (2002). The resilience factor. New York: Broadway Books.Seligman, M. (1991). Learned optimism. New York: Knopf.Seligman, M. (2002). Authentic happiness. New York: Free Press.Webster, E. (1977). Counseling with parents of handicapped children: Guidelines for

improving communication. New York: Grune & Stratton.Webster, E., & Newhoff, M. (1981). Intervention with families of communicatively

impaired adults. In D. S. Beasley & G. A. Davis (Eds.), Aging: Communicationprocesses and disorders. Orlando, FL: Grune & Stratton.


15 Cultural dimensions of aphasiaAdding diversity and flexibilityto the equation

Claire Penn

The cultural context in which assessment and therapy take place providesprobably the most powerful explanation for many of the features of aphasiathe clinician encounters and is the key to most aspects of therapy and long-term outcome. Certain sociocultural contexts provide a unique opportunityto examine recovery in aphasia. This chapter presents some evidence andsome insights regarding the cultural dimension of aphasia, and proposessome implications for assessment and intervention.

Though the evidence I draw on is based on my experience in South Africa,I believe that in the context of globalization and with increasing diversityin every clinician’s caseload, there are some clear universal principles thatemerge.

I argue that:

1 Multilingual persons with aphasia use the tools in their linguisticrepertoire differently and respond to aphasia in different ways.

2 There tends to be a very fine, often indiscernible, line to be drawnbetween pathological and normal language in the context of naturallanguage use.

3 Narrative discourse provides at the same time a culturally relevantassessment tool and an opportunity to explore the complexity of languageand its use, a window onto cognitive and pragmatic processes and angenre for meaningful intervention.

The context of practice that I draw from is South Africa, in which 11 officiallanguages are acknowledged but in which many more languages and regionalvariations exist, where practically every inhabitant is bi- or multilingual,where there is daily interface of languages, and where language use is coupledstrongly with sociopolitical identity.

This situation has necessitated the development of methods of assessmentand intervention for individuals with speech language pathology that are notbased on the western model. It is not appropriate for example to approach arural illiterate Zulu-speaking aphasic patient with an item from one of thewell-known aphasia tests: “Roses are red and violets are. . .”. Neither is it

appropriate to assume that a traditional one-to-one model of aphasia therapywill work in a situation characterized for the most part by lack of resources,lack of access, and poverty.

However I argue that being aphasic in a multilingual context such as SouthAfrica may not be altogether bad. In fact the nature of language use in thatsociety may well provide a scaffolding framework for compensatory strengthsto emerge in the presence of language pathology. It would seem that certaintasks and certain analysis frameworks allow highly significant cultural fea-tures to emerge, which have strong implications for the clinician and shedlight on language processing in general.

This chapter proposes that a number of the stylistic and syntactic aspectsto be seen in the discourse of such aphasic persons reflect the compensatoryefforts of a group whose sociolinguistic status (marked by diverse dailyinterface/contact) provides well-rehearsed shift strategies. Those individualswith aphasia therefore have a particularly well-stocked armamentarium ofstrategies for deployment during conversational interchange.

Underlying much of my work is the basic premise that aphasic language isabout compensation. It has long been recognized that many of the behaviourswe see in aphasia are not necessarily aphasic symptoms, but the adaptation ofthe organism to the primary deficit. Goldstein for example in 1948 said: “Theaphasic patient has to achieve a condition which allows him to react as well aspossible to the tasks arising from the environment” (p. 21). Such compensatoryexplanations of aphasia are frequent in explaining aphasic symptoms, and inbilingual patients and in specified sociocultural contexts these compensatorybehaviours may play out in a very specific and interesting way.

The prime evidence that I will draw from in this chapter is Afrikaans. Thisis one of the languages unique to South Africa that has a relatively shorthistory, yet ironically is one of the most studied and documented. It existedmuch in today’s form from about 1850, and was given legal recognition in1925 when it became the language of the church and government. It is alanguage that is diverse in terms of region, dialect and social class, originat-ing not only from the Dutch used by the seventeenth-century settlers in SouthAfrica, but also having features of Malay, Portuguese, Khoin, French andGerman as well as English (Combrink, 1978; Roberge, 1995). This is the homelanguage of a large number of people in South Africa (7 million) and untilrecently was the medium of education for a number of non-first-languagespeakers (Kroes, 1978). Viewed as the language of the oppressor for manyyears, it has been the topic of extensive debate among politicians and edu-cationalists and in the formulation of the language policy of the new SouthAfrican government.

There is distinct dialectal version of Afrikaans that has developed in agroup of mixed racial heritage, largely resident in the Cape Province. Thiscommunity developed through events of Dutch colonization in the seven-teenth century and the interaction between the settlers and the indigenouspeople of the Cape. There are estimated to be more than 3 million users of

Cultural dimensions of aphasia 223

Cape Afrikaans, which differs from the language of standard Afrikaansspeakers in a number of different ways. These have been highlighted by vanRensburg (1997), McCormick (1989, 1995) and others, and include differ-ences in phonology, lexicon, syntax and stylistic variables. The code-switching and code-mixing1 that have been documented extensively in thisdialect reflect important sociocultural factors. The strong oral tradition ofthis group, as well as its unique dynamic position in society, account for someof these aspects, including “intensive linguistic exchange” (McCormick,1995, p. 204) and language contact factors with a very strong effect of Eng-lish, often spoken to children in the home and at school by second languagespeakers.

Little work has been done on aphasia in Afrikaans, but given what weknow about the structure of Afrikaans and its origins, areas particularlysusceptible to aphasic breakdown for agrammatic patients at least are theverb and operations surrounding the verb movement. Extrapolating fromthe extensive and explicit work of Kolk, Heling, and Keyser (1990) andBatsiaanse and colleagues on Dutch aphasia, verb movement and retrievaldifficulties as well as problems with prepositions and articles and sentenceembedding would be anticipated (e.g., Bastiaanse & Jonkers, 1998; Bastiaanse& van Zonneveld, 1998; Edwards & Bastiaanse, 1998; Vermeulen, Bastiaanse,& van Wageningen, 1989). Much of the cross-linguistic work that has beendone has been based on tasks that are sentence or clause based, includingpicture and sentence matching, sentence completion and anagrams. Howeverthe impact of the task strongly influences the accuracy and nature of thelanguage obtained, and there remains a scarcity of studies at a discourselevel, especially for the person with mild aphasia. This genre is a particularlyfruitful one in any group (such as those in South Africa) where literacy islimited, especially in older members of society for whom oral narrative is astrong tradition.

This chapter thus focuses on some specific linguistic structures that areparticularly prevalent in the discourse genre. Selecting these aspects serves toillustrate the close connection between linguistic and pragmatic factors inaphasic breakdown. Studying them in the two languages of bilingual subjectsand in aphasic and control subjects provides the opportunity to separate outnormal from compromised processes, and to examine compensatory strategiesoperating that are independent of or dependent on specific linguistic factors indiscourse. Some pragmatic and syntactic findings provide interesting insightsnot just for the bilingual patient, but for, I hope, aphasia in general.

The evidence

A series of studies have been undertaken on the narrative discourse ofbilingual persons with aphasia in South Africa and matched controls (Archer,2006; Kalmek, 2001; Nabeemeah, 2002; Venter, 2000; von Bentheim, 2001).The goal of the research has been to examine the connected language of

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bilingual persons living in a multilingual context in order to better under-stand the cultural influences on aphasia, and to determine ecologically validassessment and therapy approaches.

Participants

We now have data from 62 bilingual participants, 31 people with aphasiaand 31 matched controls. All aphasic participants were right handed anddeveloped aphasia as a result of a single CVA. They had to be a least3 months post onset of stroke and were rated as having a mild to moderatedegree of aphasia on the Western Aphasia Battery (WAB) (Kertesz, 1982;adapted for language and culture).

Participants with severe aphasia were excluded from the study, as thetask involved connected language. Participants were also required to beunder the age of 69 years with at least 7 years education. Control participantswho had no history of neurological or psychiatric problems were matched forage, gender, language, cultural group, education and occupation.

An adapted version of Paradis’ bilingualism questionnaire was adminis-tered to each participant (Paradis, 1987) to ensure the language status ofthis group and to document patterns of language exposure, current contextsof language use, patterns of acquisition, family and educational languagepatterns, and differential recovery patterns.

The participants were tested in both their languages on the same tasks bylinguistically and culturally matched individuals on separate days.

Tasks and analysis framework

A range of narrative tasks were employed, following the protocol ofUlatowska and her colleagues (1993, 1998; Olness, Ulatowska, Carpenter,Williams-Hubbard, & Dykes, 2005). We used picture description, picturesequence, the narrative of personal experience and a fable task. In linewith the framework of Ulatowska et al., our analysis included a rangeof measurements. Productivity measures included calculation of narrativelength, proposition analysis, T-units, words per T-unit, and error analyses.A number of lexical and syntactic aspects were also examined, includingverb and word order aspects which will be considered here.

Quality of narrative was measured using a 5-point rating scale. This wasbased on the work of Labov (1972, 1984) and included the dimensions ofRelevance, Character, Supporting description and Ending. The ratings wereconducted by culturally matched speech-language pathologists from the Capecommunity. Three raters reached acceptable agreement on these measures.The analysis also examined specifically the presence of “ethnic discoursemarkers” described as features particular to a certain cultural group, aswell as a range of stylistic and pragmatic devices including code-switching,repetition and evaluation.


Results

The findings of some of this research have been published in detail elsewhere(Ogilvy, von Bentheim, Venter, Ulatowska, & Penn, 2000; Penn, Venter, &Ogilvy, 2001). In this chapter I focus primarily on the narratives of personalexperience from the bilingual Cape Afrikaans group (with 14 participants), asthe particular nature of their data seems to highlight particularly well theessential challenge of differentiating normal features of discourse, culturalmarkers and stylistic markers from frank aphasic errors.

A summary of the main findings appears in Table 15.1.

Productivity measures

The productivity measures for the aphasic participants and the controls fortheir narratives of personal experience in Cape Afrikaans are summarized inTable 15.2. These results reflect group means but exclude, where relevant, A2whose very lengthy sample (1288 words) rendered him an outlier.

In general the control subjects produced longer narratives with a greaternumber of T-units. The mean length of the narrative for the aphasic samplewas 167 words (range 83–285), indicating generally a shorter and morediverse sample size for the aphasic group than for the controls, whose rangewas 226 to 512 words. This difference was found to be statistically significant(Mann Whitney U test, U = 5.0, p = .22).

The numbers of T-units and propositions were comparable when thesample of A2 was included in the tally of the means, but were significantlyfewer for aphasic subjects when S2’s sample was excluded. This is similarto the findings of Olness, Ulatowska, Wertz, Thompson, and Auther (2002)who found a lower number of propositions in their aphasic African Americangroup.

Table 15.1 Summary of narrative findings in a group of bilingual Cape Afrikaansspeakers with and without aphasia

• Control samples longer than the aphasic samples in both languages tested• Fewer complex or non-canonical sentence forms in aphasic samples in both

languages• Evidence of wider verb variety and complexity in control than aphasic samples• More evidence of verb errors (aux omission) in aphasic samples, and incomplete

sentences• Some tense shift patterns distinctive in aphasia• Equivalent evidence of dialectic features and ethnic markers in aphasic and in

normal samples (in both English and Afrikaans)• Some marked qualitative/coherence rating differences between aphasic and control

samples in temporal sequencing• Qualitative differences in evaluative elements• More language alternation in aphasic than control narratives• Less language alternation in English than in Afrikaans narratives

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Because of the wide variation in sample size, direct comparisons of otherproductivity measures were possible only through ratios expressed in relationto the T-unit. The mean length of the T-units was 9.16 words for the aphasicsubjects (range 7.5–12) and 10.23 for the control subjects (range 8.3–14). Thiswas not statistically significant.

The mean number of verbs per T-unit was also found not to differentiategroups. However, the total number of verbs, the number of verb types andtokens, and the number of subordinations per T-unit were significantlyhigher in the control sample and this is discussed in more detail in thefollowing section.

Table 15.2 Group data for productivity measures in Cape Afrikaans (means)

Variable Aphasic participants (n = 7) Controls (n = 7)

Number of words* 167SD = 122.31

316.57SD = 111.98

Number of propositions* 28SD = 14.81

38.26SD = 12.57

Words per T-unit 9.16 10.23Number of T-units* 25.3

SD = 11.731.7SD = 11.6

Verbs per T-unit 2.0SD = 0.37

2.24SD = 0.28

Auxiliaries per T-unit 0.52SD = 0.27

0.47SD = 0.27

Tense shift per T-unit 0.44SD = 0.17

0.4SD = 0.14

Copulas per T-unit 0.3SD = 0.11

0.2SD = 0.11

Tokens* 27.5SD = 10.58

50.86SD = 21.42

Types* 16.7SD = 5.82

26.6SD = 8.66

TTR 0.53SD = 0.22

0.54SD = 0.13

Tokens/T-unit 0.86SD = 0.23

0.88SD = 0.19

Subordinates/T-unit* 0.12SD = 0.076

0.18SD = 0.09

Verbs–verb tokens 24.71SD = 37.69

18.57SD = 6.425

Number of verbs* 38.33SD = 17.9295

69.42SD = 25.178

Note: * indicates significance without outlier.


Syntactic features

In general there were more frank errors and a higher presence of incompleteand minor utterances in the aphasic samples. There were fewer complex ornon-canonical sentence forms in aphasic samples in both languages, andthere was evidence of wider verb variety and complexity in control than inaphasic samples. There was lower diversity of verbs and more evidence ofverb errors (auxiliary, shown as “Aux” omission) in aphasic samples, as wellas of incomplete sentences.

Disrupted auxiliaries were found in aphasic samples only and took variouspatterns.

Auxiliary doubling was found as in the following instance:

Maar ek het nog altyd gebid hetBut I always prayed

Other examples show Aux omission, for example:

Ek veld loopI walk field

Ek op die plaas geblyI lived on the farm

Ek gele in die bedI lie on the bed

The sample of one participant with a moderate (rather than mild aphasia)was interesting as she had more frank syntactic problems. Interestinglyher difficulties with the auxiliary are manifested in each attempt at use. Inher narrative of personal experience, for instance she produced 12 T-units,9 of which were complete and 3 of which were inaccurate or abandonedattempts. All these false starts related to the management of the past tenseauxiliary:

Aux omission: Ek ge- gedink hy gaat my klap (omission of het)I thought he would hit me

Incomplete Aux: Ek het ged gedink (incomplete) . . . Ek was baie bangI thought . . . I was very scared (arguably changed fromAux to copula form)

Abandoned Aux: Ek het die man wat vir my geslaat het so —I (past tense Aux) the man who hit me so —(abandoned, presumably because of processingdemands induced by syntactic complexity/embedding)

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The rest of her verb use consists of copulas and the use of historical presenttense.

Other errors noted in the aphasic sample included (1) omission of aux “het”and marker “ge” but maintenance of the past tense word order:

A2 Ek veld loop (Target Ek het in die veld geloop)I walk in the veld

Ek op die plaas gebly (Target Ek het op die plaas gebly)I lived on the farm

Ek het hospital twee jaar agt maande (Target Ek het ?in die hospitaltwee jaar agt maande gewees)I was in hospital for 2 years and 8 months

(2) Using the past tense marker ge- (rather than the auxiliary plus -ge) todenote past:

Ek gelê in die bed (Target Ek het in die bed gelê)I lay in the bed

Other syntactic aspects were common to both aphasic and control samplesin Afrikaans. Those common to both have been described as “syntacticconvergence features” and are a documented feature of Cape Afrikaans(McCormick, 1995).

Word order changes/verb movement

Afrikaans samples were examined for the presence of English word order.This optional change to subject–verb–object (SVO) from subject–object–verb(SOV) in Afrikaans is often triggered by a specific main clause verb type(I know, I think, I see) and by the use of the copula in the subordi-nate clause. Also, following the verb complementizer wat (what/which)in Standard Afrikaans will require verb to be in clause final position. InCape Afrikaans an optional rule allows the verb to precede the object; forexample:

A2 En ek sien hier staan ’n ry trokkeAnd I see here stands a row of trucks

Dink ek iets is darem nie reg hier nie isI think something is really not right here

Versus the following examples where verb final position is kept:

Ek dink ek gaan darem nie so na aan hom draai nieI think I will really not turn so close to him


Ek het gedink ek gaan nou nooit weer uit die hospitaal uit kom nieI thought I would never again get out of hospital

Ek dink toe en ek wil gaat na haar toe met ’n bos blommeI then thought and I wanted to go to her with a bunch of flowers

A6 Miskien my spraak gaan wegPerhaps my speech would go away

Such examples were found in both aphasic and control subjects, and variationwas found within subjects, so reinforcing the dialectal nature of this shift.

The presence of English word order in the Afrikaans sample, while notexclusive to the aphasic samples, seemed more prominent among these, andhas some important clinical implications.

A large body of literature has demonstrated that aphasic patients haveproblems processing sentences in which the order deviates from the canonicalone (Thompson, Lange, Schneider, & Shapiro, 1997). There are interestingtherapeutic implications arising from this, suggesting that SVO therapy maybe more effective than SOV therapy, or that when there are optional contexts(seen in normal production), these should be identified and reinforced intherapy (using for a starter, I know, I think, I see verbs). Post-verbal expan-sion frames should also be supported. There are some very promising resultsfrom therapy programmes that are verb focused and are sensitive to theprocessing demands imposed by certain syntactic operations (Mitchum &Berndt, 1994).

An examination of tense-shifting in the samples proved this to be an inter-esting and related phenomenon. Tense-shift occurred regularly in the narrativesamples in both aphasic and control samples. The aphasic samples showederrors in the verb specifically at these junctures, suggesting that this is a“danger point”, and possibly a focus of therapy. None of these errors wereobserved in the narratives of the control participants.

Shifting to the present tense in Afrikaans reduces verb complexity, andavoids word order and morphological changes. It is associated in narrativewith the use of the historical present as well as direct speech. The conver-sational historical present is a stylistic device that adds a theatrical com-ponent to a narrative (Wolfson, 1978). It also conveniently obviates thenecessity for past tense which, as the above examples demonstrate, hasprocessing costs particularly in Afrikaans. The fact that it was found morefrequently in the aphasic than the control subjects suggests that verb varietyand complexity was a choice for the controls but not always a possibility forthe aphasic speakers.

One of the participants showed a unique effect: use of present tense for theentire narrative in Afrikaans and the past tense for the same story in English.This is perhaps a reflection of complexity of past tense in Afrikaans. Whilethis device occurred in the English samples it was less frequent.

An example of both of these aspects is provided from an English narrative:

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C1 And on my way back, well I was on foot, I have to walk home. Andsuddenly I hear something behind me and I know things is notgood for me because we live in crime, we live in lots of things. AndI said to myself “Wow terrible things is going to happen!” Then Istart walking faster but my heart was start doing this and I wasfeeling real ice. I was real scared and I said to myself “If home canjust be very near me now.”

Quality aspects of discourse

Coherence

A coherence rating was undertaken for all the transcripts using a 5-pointrating scale for Temporal organization, Relevance, Character, Supportingdescription and Ending.

As Figure 15.1 suggests, a marked difference was found between thecoherence of the narratives of the aphasic subjects and that of the controlsin clarity and temporal sequencing.

The clear difference between the coherence of the aphasic and the controlnarratives is markedly in contrast to some of the productivity and complexitymeasures utilized in which often no marked differences could be found. Thisfinding has important implications both for assessment and for therapy andseems to reflect the sensitivity of narrative discourse not solely to linguisticfactors but to cognitive and social aspects as well.

Ethnic markers

In the transcripts there were some examples of lexical items typifyingthis dialect and the retention of some old forms of Afrikaans (probablyreflecting the age group). These included words such as Kooi (bed), daai (thedemonstrative “that”), gaat (for gaan (go)) and Slaat (for slaan (hit)).

Figure 15.1 Coherence ratings for narratives of aphasic and control participants.


There are many examples of loan words in the samples, mostly fromEnglish, reflecting the high contact patterns between languages in theWestern Cape region of South Africa. Examples of loan words were foundin most word classes including nouns, conjunctions, adjectives, verbs andadverbials (see Appendix 15.1) (Branford & Claughton, 1995).

Dialectal aspects were also features in both aphasic and control samples,which included, in Afrikaans, regularizing of irregular past tense, shift fromSOV to SVO triggered by specific verbs, topicalization, and reduplication.

In the English transcripts, ethnic markers included deletion of contractibleforms of “be” and “have”, changes in number concord, deletion of past tensemarker “-ed”, deletion of adverbial suffix and preposition substitution, con-firming features of the dialect documented by McCormick (1995) and others.

Stylistic and pragmatic factors

Certain stylistic features have been identified as enhancing the properties ofnarrative, and the narrative genre has been found to yield a high number ofsuch elements (known as evaluative elements) that help to dramatize a storyand provide it with a speaker’s particular structure and “flair”. Also knownas “intensifier elements” of the narrative, they convey the narrator’s feelingsabout characters and events and include ritual utterances, phonologicalintensifiers, lexical items, repetition and gesture, comparatives, syntacticdevices such as ellipsis and topicalization, as well as direct quotations, asidesand sound effects (Chafe, 1982; Dorian, 1997; McCormick, 1995; Wolfson,1978). Labov (1984) suggests that evaluative devices are used to directdiscourse to the intended audience. Those with well-developed discoursecompetence will be able to select a level of detail within which to cast ideas,highlight certain aspects to make the story understandable or exciting, andalter sequences and shift perspectives to portray feelings of other partici-pants. They are closely linked to the ethnic markers identified and it isprobably not appropriate or feasible to differentiate them, especially in CapeAfrikaans. Though evaluative features were present in both aphasic and con-trol samples, there were differences between the control and aphasic groupsin this regard, with more frequency and diversity of such narrative elementsoccurring in the control group.

In the data we found rich examples of such devices including ellipsis andtopicalization, the use of ritual utterances, comment clauses, expressivephonology, direct speech, repetition and enactment. Examples of these areprovided in Appendix 15.1.

Direct reported speech is a fascinating feature of narrative that occurred fre-quently in the samples. It has a strong pragmatic function serving as a stylisticdevice that enriches a narrative but can also be regarded as a well-documentedsimplification strategy mechanism to avoid tense shift and embedding,exploited fairly frequently by aphasic persons (Hengst, Frame, Neuman-Stritzel, & Gannaway, 2005; Penn, 1987). Further it has been considered as a

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powerful measure of the degree of bilingualism and is often foregrounded bya language switch (Dorian, 1997). Many examples of reported speech werefound in both aphasic and control samples, and in both of the languagestested. One of the most delightful is the following, which also illustrates therelationship between direct speech and code-switching:

En ek se vir hom “Ek wil Kaap toe gaan” Hy se. “Eish but you’ve justmissed the train”. “Ah uh”. Hy se vir my “But you are not alone”. Maarek is alone. Ek se vir hom “Of course I’m alone. Daar’s niemand by mynie. I’m not alone!”

Wilkinson, Beeke, and Maxim (2003) and Goodwin (2003) comment onthe pragmatic function of enactment, which is used to describe and reportevents: a demonstration of what participants did or said rather than adescription of the event. This typically involves using direct reported speechas an index of change of voice/footing shift as in the example above. Theseauthors demonstrate the evidence from aphasic conversational samples ofhow persons with aphasia use such enactment in a distinctive way to dealwith the contextual demands of conversation – to describe events andactions and enabling the presentation of the past and future in the hereand now.

Direct speech used in combination with intensifiers (as discussed above)including expressive phonology, repetition, gestures, quantifiers and proforms(which only derive meaning in context), enables such enactment to occur.Given the strong cultural correlations of such enactment, this suggests apowerful medium of therapy especially for more moderate to severe casesof aphasia.

Repetition

Repetition has been identified as an ethnic stylistic feature (e.g., in the dis-courses of African American individuals) but also as an aphasic strategy(Ulatowska, Streit-Olness, Hill, Roberts, & Keebler, 2000). One might predictthat repetition/reduplication might appear more frequently in Afrikaansaphasic samples, first because reduplication is a feature of the dialect,and second, because it is well documented as a compensatory and stylisticdevice

Repetition was found in all samples (English and Afrikaans) and as theexamples illustrate, has an obvious stylistic function. However repetitionseemed to occur more frequently in the aphasic groups and is probablyserving the role of emphasis in the face of restricted linguistic competence.

Language alternation patterns were interesting and correlated closelywithin individual language history profiles. Not unexpectedly such languagealternation/code-switching occurred more in aphasic than in control samples.

An impoverished linguistic system may well account for the presence of


such code-switching in aphasic samples, but the fact that language alternationoccurred more in Afrikaans than in English samples and was used by thecontrol group only in Afrikaans points to more subtle contextual influencesreflecting changing patterns of language use in South Africa and politicalvariables.

Discussion

The findings presented above suggest that while some aspects of the analysisdifferentiated aphasic from non-aphasic bilingual persons, there are a numberof apparently non-standard features of language common to the two groups.Some may be a function of the genre of elicitation and some a function ofthe specific language and the context in which the data were collected. Thepoint made by Ulatowska and Olness (2001, p. 107) that “the key questionin any attempt to look at the interaction between dialect and aphasia isdiscerning which differences are attributable to the dialect and which areattributable to the pathological processes” needs to addressed.

In the sample of fluent bilingual aphasic participants studied, we found arange of linguistic and stylistic features in their narratives, reflecting aspectsthat can be hypothesized to be aphasic in origin, but also unique aspects ofthe languages in their regional form. It is argued that the “default mode” ofnatural language in this context, which includes patterns of code-switching,flexible word order and stylistic intensification, provides a robust compensa-tory and scaffolding structure for some of the primary aphasic deficits andthat the genre of narrative provides a strong basis for such pragmaticstrengths to emerge.

Aspects such as enactment and language alternation may in fact reflectattempts to compensate for a reduction in processing capacity in the on-linetask of narrative. There are some aspects of the data that seem to be featuresof the narrative genre (across cultures and languages); there are some aspectsthat have features that are specific to Afrikaans (and the non-standard varietyin particular); finally there are features that have been identified as possibleaphasic compensatory features which reflect preserved pragmatic competencein the face of linguistic erosion.

This study suggests that, at least in this population, it may be impossible/unrealistic to attempt to single out explanations for the appearance in thesamples of each of the above three aspects. Indeed this would probably be anoversimplification of dynamic and complex data. What might be possiblehowever is to suggest that some of the features are common to all threedimensions, whereas some are more likely to emerge in certain genres, incertain ethnic groups, or in the presence of aphasia. Figure 15.2 presents thisinteraction.

Many of the dimensions examined (e.g., repetition, word order changes,historic present tense, repetition and code-switching) have been commentedon in the literature relating to all three.

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For example, spontaneous verbal repetition in aphasia has been identifiedas a compensatory strategy (Leiwo & Klippi, 2000; Oelschager & Damico,1998; Penn, 1987) but also as an ethnic marker (Labov, 1972; Ulatowskaet al., 2000).

Word order changes similarly may be viewed as a compensation device inaphasia (Menn, Reilly, Hayashi, Kamio, Fujita, & Sasanuma, 1998; Saffran,1980; Schnitzer, 1974), a reflection of syntactic convergence (McCormick,1995) or as having a stylistic purpose (Labov, 1972). Examples of all threeappeared in the narratives of the aphasic and control subjects.

Code-switching (or language alternation) is a particularly challenging andparadoxical behaviour. This is a highly complex phenomenon depending onfactors such as age, internal state and experience in bilingual speakers. It maybe used to emphasize a point, to replace an unknown word, for clarification,to express group identity, to cross social and ethnic boundaries, or for conver-sational purposes (Auer, 1999). Factors that influence type and amount ofcode-switching include the genre, the purpose, the topic, the interlocutors andtheir relationship, their relative level of bilingualism and the structure of thelanguages (including the phonetic structure).

There are apparent examples in the data at all points along a continuum.Some language alternation is conversational, some is participant related,some seems linked to linguistic difficulty, and some is obviously dialectaland probably more linked to the notion of fused lect which McCormick(1995) suggests characterizes Western Cape dialect. In traditional formula-tions of code-switching in bilingual aphasia, it has been suggested thatthis feature may be a pathological phenomenon and a reflection of anunstable language system. Research suggests that bilingual individuals withneurogenic communication disorders may not exhibit normal linguistic flexi-bility (Fabbro, Skrap, & Agliotti, 2000), ranging from rare documented casesof pathological code-switching to more subtle difficulties. For example, ina comparative study on Spanish-English bilingual speakers with aphasiaand neurologically normal speakers, Munoz, Marquardt, and Copeland(1999) found that aphasic speakers demonstrated greater frequency of

Figure 15.2 Discourse model indicating interaction between variables.


code-switching patterns and concluded that their subjects demonstrated anincreased dependence on both languages for communication. These authorsviewed this greater frequency of code-switching patterns as an inability toseparately access languages.

Fabbro et al. (2000) suggest that any lesion in the brain may affect flexi-bility of language use in bilingual speakers, and that frontal lobe lesions inparticular (where the primary deficit is a difficulty in shifting set) may leadto reduced flexibility. Other explanations of code-switching in normal andchild language studies similarly point to the possible processing costs ofcode-switching.

However, contextual aspects seem to play as important a role. In an elec-trophysiological study of code-switching by Moreno, Federmeier, and Kutas(2002) who used event-related potentials to compare switches between twolanguages in bilingual speakers, it was found that for some speakers in somecontexts the processing of a code switch was less costly than the processingof an unexpected within-language item. This finding suggests that the easeof switch is determined by context and task, and that the process of code-switching per se does not necessarily use up additional resources. In factit suggests that language switching may provide the bilingual person withaphasia additional options to those of the monolingual aphasic speaker, andthat at least under conditions of conscious control, code-switching may pro-vide an extra mechanism for the bilingual person to cope with the challengesof aphasia.

Thus, paradoxically, while language alternation may reflect disruptionin access to either language in aphasia, it may also reflect an attuned andsophisticated appreciation of contextual factors and it is therefore likely thatthe natural context may “prime” such strategies in the bilingual speaker.Explanatory paradigms for code-switching in aphasia thus should go furtherthan pathological explanations and should incorporate both socioculturaland pragmatic factors.

Conclusions

The data described above suggest that any explanations of pathological lan-guage must be context-bound and that certain sociocultural contexts providea unique opportunity to examine recovery in aphasia. It should be remem-bered that each participant in the study showed a unique profile, masked bygroup results, but providing a fascinating explanatory basis for the languageprofile and compensatory choices.

Persons living in a society with diverse cultures and languages may wellhave linguistic and cognitive flexibility that will serve them well in the eventof aphasia. Further the realities of the natural context may serve as a primefor the emergence of positive strategies in recovery. The challenge for theclinician is to have an understanding of these aspects and to harness themmeaningfully in therapy.

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Working with the multilingual patient implies some modification of assess-ment procedures to include the examination of interaction with varyinginterlocutors, making a detailed sociocultural analysis of a speaker’s lan-guage history, language context, attitudes towards language use and insitu observation of the effectiveness of mechanisms such as code-switchingand its processing demands on both the speaker and the listener. These areprobably more useful than structured or adapted language tests.

In short our evaluation should be geared at unearthing the well-practisedadaptation patterns that the individual has already developed and thatmay be drawn on in the presence of aphasia. Perhaps, as the literaturesuggests, bilingual people are more adept at reading the interlocutor’s homelanguage, communication style and modality preferences and applying meta-linguistic strategies. How well that capacity is retained may depend both onthe neurological limitations of the individual and on premorbid sociolinguisticstrategies.

Similarly, the results suggest that we may have to be less precise aboutwhich language to remediate. Indeed if the context is one in which lan-guages are mixed and the strategies adopted result in ease of communica-tion, perhaps this could work, particularly if a partner-based approach totherapy is adopted. Finally, some of the implicit features of multilingual-ism may be harnessed effectively in therapy. I would suggest too that thecognitive demands of translation and their potential as a therapy toolshould be explored. In line with other therapy techniques that are thoughtrather than language centred, the operation of translation, accessing as itdoes possibly shared and discrete memories, may well facilitate languagerecovery.

Given the increased diversity of clinical caseloads, monocultural modelsof service delivery are no longer appropriate. I predict that cultural speech-language pathology is an emerging necessity of the twenty-first centuryand clinicians should be expanding their understanding of the influenceof cultural variables on language behaviours as well as the repertoire ofassessment and therapy activities (Penn, 2002). Taking culture into accountundoubtedly makes things more complex, but may lead to explanationsfor some unresolved phenomena. This dimension builds strongly on thework of aphasiologists like Chris Code, who even when it was unfashionable,has always placed emphasis on the critical psychosocial dimensions ofaphasia. Indeed, diversity and flexibility are the essence of the human condi-tion and are probably nowhere better expressed than in the phenomenon ofaphasia.

Acknowledgments

Earlier sections of this chapter were presented at the 10th Congress ofthe International Association of Clinical Linguistics and Phonetics held inLouisiana, USA, in 2004 and in a presentation entitled Cultural influences in


bilingual ageing presented at the American Speech and Hearing Conventionin Philadelphia in the same year.

I am deeply indebted to Brent Archer for his help with analysis of thismaterial; and to Dale Ogilvy, Analou Venter, Ingrid von Bentheim, KautharNabeemeah and Lisa Kalmek who were involved in various phases of thelarger project.

Note

1 The terminology surrounding language alternation is confusing. For the purposesof this chapter I will use code-switching to reflect alternating of units from twolanguage across sentence boundaries; alternation of elements longer than one wordwithin a sentence as code-mixing; and lexical borrowing to describe inclusion ofsingle foreign words into a language.

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Appendix 15.1: Sample examples of evaluative devices used inthe narratives of bilingual aphasic and control participants(translations in italics)

(Extracts from the samples are identified as A for aphasic samples, C forcontrol samples, and Afr and Eng for Afrikaans and English.)

Ellipsis and topicalization

A3 Eng: All of a sudden from nowhere . . . There it wasA4 Eng: Bearing in mind that I was eighteen . . . I decided to argue

C1 Afr: Hoe hy die een aan die arm gryp . . . weet ek nieHow he grabbed one by the arm, I don’t know

C3 Eng: The size of the snake . . . I was mesmerized

A9 Afr: Maar ongelukking is ek daai dag.But unlucky I was that day

A9 Afr: Hoe het ek deur die drade gaan, weet ek nieHow I got through the wires, I don’t know

Ritual utterances

A4 Afr: Het ek vir hom gesê “wo!”I said “hey” what is happening to me now

C1 Afr: Dis net soos in die movies sienIt’s just as (you) see in the movies

C1 Eng: You can’t see your hand in front of youAnd I’m thinking “maybe there’s absolutely nothing”

C4 Eng: I was really showing off

C5 Afr: Maar ek gaan iets probeer hierBut I will try something hereOngelukkig is ek daai dagUnlucky I was that day

C5 Eng: I don’t even want to listen to thisDo you know what that cost us eventually?So we couldn’t argue


Comment clauses

A1

U sal seker nie weet vam n tiekie nieYou probably don’t know about a ticky

Dis nou n ware storie, ne?It’s a true story now, okay?

Expressive phonology

A1 Afr: Oooo ek was bangA4 Eng: It happened maaany years ago

C1 Afr: Ons is veeeer van alle plekke afC3 Afr: ’n Groooot boom

Quantifiers

A3 Eng: All of a suddenThat was the worst experience of my life

A4 Afr: Hy het alle reg die pad te gebruikHe had every right to use the path

C2 Afr: ’n Hele klomp menseDaar was baie van hulle

C3 Eng: It was the biggest snake I have ever seenC4 Eng: I took all my clothes offC5 Eng: We were just married

And I’m thinking “maybe there’s absolutely nothing”C4 Eng: I was really showing off

Repetition

A1: Ek is bang. Ek is baie bangI am scared. I am very scared

A2 Afr: Hy kom kom die slang grypHe comes comes to grip the snake

A3: That was the worst experience of my life . . . It was the mostterrible experience of my life

A5: Ek het gelê en gelêI lay and lay

A4: Maar ex sal nooit vergeet nie. Ek is nou . . . Ek sal dit nooitvergeet nieBut I shall never forget it. I am now I shall never forget it.

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C3: I can actually, I can actually see itC5: Most beautiful beautiful paw paws

All we see is farms and farms and farmsC7: En ons wag en wag en wag

And we wait and wait and wait

Direct reported speech

A1: “Die water is; Oe Vader jy moet my nou help”The water is . . . “Oh Father you must help me”

A3: Maar die doktor . . . sê die Doktor “Nee man”But the doctor . . . the doctor said “no man”

S8: “and she just walked past and said “Kom sluit die deur toe”(Come close the door)

Language alternation (code mixing and lexical borrowing)

From English into Afrikaans:

Aphasic

We went to hand out those eh um dinges

And sy s grapes is the treasure and sy moet verstaan

Hy het ’n groot, ’n groot a big crop gekry

He got a big crop

I just gave him one tramp to the head (Eng: thump)

Sitting with a whole klomp newspapers (Eng: clump)

Why must I sukkel (Eng: struggle)

Those big ouens came and arrested us (fellows)


From Afrikaans into English:

Aphasic

Dit was die grootest in my leweThis was the biggest in my life

Iemand het hom geld gegiveSomeone gave him money

Ek het nie gepanic nieI did not panic

(Note the adoption of English morphological endings in some cases, as wellas retention of Afrikaans morphology on loanwords.)

Dit was nie ’n nice ondervinding nieThat was not a nice experience

Ek was bang dat n stray bullet deur die venster sou komI was scared a stray bullet would come through the window

En die kerels, ons is groot palsAnd the fellows, we are big pals

(Note the noun characteristically has retained the English number marking.)

One two three is hy dood1 2 3 he’s dead

As jy werk sal jy geld vat, as jy sit by die huis op jou bum sal jy niks vat.If you work you will get money if you sit on your bum at home you’ll getnothing.

(Note this example of the dropping of the second negative is a commonfeature reflecting instability of this structure in modern Afrikaans.)

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16 Assessment of aphasia in amulti-lingual world

Susan Edwards andRoelien Bastiaanse

Introduction

Many disciplines engage in the assessment of aphasia, which is conducted invarious languages, in various forms, across many countries and for differentpurposes. In this chapter we consider the use of assessments, briefly reviewthe development of aphasia assessments and describe some types of assess-ments. The need for procedures and materials for testing bi-lingual speakerswith aphasia has been recognized for some time (Paradis, 1987), and there area growing number of tests that are used across different languages. Some ofthese are translations and some are specially adapted for each new language.In this chapter, we consider why it is necessary to make adaptations ratherthan translate tests to use in different languages. By way of illustration, abrief description is given of the development of two tests that are used acrosstwo languages: the PALPA (originally written in English and then adaptedfor Dutch) and the Verb and Sentence Test (VAST: originally written inDutch and then adapted for English). However, it is sometimes necessary toassess people in a language other than their primary language, a contemporaryproblem we discuss.

Background

The assessment of aphasia has developed over the past hundred years frommeticulous, if idiosyncratic, clinical examinations, through the developmentof batteries based on psychometric testing, batteries influenced by cognitiveneuropsychology, and those motivated by linguistic investigation of aphasia.No assessment is theory free, although the underlying theoretical motivationbehind the development of an aphasia assessment may not be explicit or mayhave got lost over time. In the early stages of assessment, neurologists such asHughlings Jackson (1932), Freud (1891) and Henry Head (1926) carefullyrecorded symptoms that they observed in their clinics and related these symp-toms to presumed sites of cerebral lesions. Jackson (1932) developed clinicaltests comprising tasks that are still used today by some neurologists in theirclinical examinations, such as naming the doctor’s pen and watch, and

counting. The neurologists searched for evidence of the major clinical signsof aphasia; problems with word retrieval, sentence construction and under-standing commands. Highly learnt serial speech such as counting or recitingthe days of the week was tested to establish if non-propositional speech hadbeen retained (Jackson, 1932). Many similar tasks are found today both inclinical examinations and in some published aphasia tests, although themotivation for inclusion is far from clear.

The early aphasiologists were spurred on with their work because ofthe number of young men they encountered who had language problems.These were young men returning from the “great” war who, through war-induced brain injury, faced years ahead with aphasia. The purpose of theseearly aphasiologists was to document symptoms and there was no attempt,at least no systematic attempt, to suggest treatment. Following the SecondWorld War, a new impetus arose in the UK, the USA and the USSR toformulate a means of documenting aphasic symptoms, but now there werealso some parallel efforts to think about treatment following assessment(Wepman, 1951). During the war, psychometric testing had been developedand the new tests of aphasia used these developments, mimicking therubric of the psychiatric assessment by using an array of tasks for thispurpose, probing skills in reading, writing, speaking and comprehension ofspoken language. The familiar tasks (used by the early twentieth-centuryneurologists) of serial speech and repetition of language were included byclinicians and survive today. These tests were based on the classical viewof aphasia, which was that the condition affects primarily expression orunderstanding of language, and is termed expressive or receptive aphasia(Eisenson, 1973). This view seriously under-rates the complexity of aphasiaand was overtaken by a more detailed and sophisticated understanding ofthe nature of aphasia during the latter half of the twentieth century andbeyond.

A very different view of aphasia was held by Wepman (1951), developed bySchuell and published as The Minnesota Test of Aphasia (Schuell, 1965).Hildred Schuell’s view of aphasia was based on Pierre Marie’s (1926) ideathat aphasia was a unitary syndrome. This diverged from what had been themainstream view since the classic descriptions of Broca (1865), Wernicke(1874), and Lichtheim (1885). Marie abandoned the idea that there weredifferent aphasia symptoms and conceived aphasia as a unitary phenomenon.This view held that aphasia is a condition in which language is affected, andwhich differed from person to person not by syndrome but by severity and bythe presence or absence of deficits involving written language and articula-tion. Schuell was one of the last followers of this theory. It may surprise somereaders to learn that her assessment (and presumably the theory behind it)was used extensively not only in regular clinical assessments but also inresearch in the latter half of the twentieth century (David, Enderby, &Bainton, 1982; Edwards, Ellams, & Thompson, 1976). The early death ofSchuell curtailed the development of this idea and the publication of the

246 Edwards and Bastiaanse

Boston Diagnostic Aphasia Examination (BDAE) by Goodglass and Kaplanin 1972 re-established the neo-classic view of aphasia.

Another important assessment tool, inspired by and similar to the BDAEwas published in 1982: the Western Aphasia Battery (WAB; Kertesz, 1982).These two assessments of aphasia set out to categorize participants/patientsby classical aphasic syndromes, and despite the low proportion of the clinicalpopulation that can be successfully categorized (Goodglass & Kaplan,1972; Kertesz, 1982) the BDAE and the WAB are the most widely usedassessment tools in North America and Western Europe. The BDAE hasproved to be very robust, with the third edition published in 2000 (Goodglass,Kaplan, & Baresi, 2000), almost 30 years since the first edition, and versionsof this test have appeared in a number of languages other than English.

Slightly earlier than the publication of these two tests, AlexanderRomanovich Luria (1966, 1970) was developing similar ideas on clinicalassessment in the USSR, although his work took some time to reach WesternEurope in translation. His concept of clinical aphasia types was slightly dif-ferent from those in Western Europe and has been, and remains, very influen-tial in Russia and the Nordic countries. Another test that aims for diagnosisof type of aphasia is the Aachen Aphasia Test (Huber, Poeck, Weniger, &Willmes, 1983). This has been widely used in Western Europe and has beenadapted from the original German to Dutch, Italian and English and isconsidered the principal test in Germany, Switzerland, Austria, The Nether-lands, Italy and Belgium. In summary, since 1970, four main aphasia assess-ment tools have been developed that are still widely used around the world.The main goals of these tools were:

• to assess the severity of aphasia in the four language modalities (com-prehension and production of spoken language, reading and writing)

• to classify the patients in one of the classical aphasia types.

Before moving on to discuss more recent assessments that focus on featuresof aphasia, it is interesting to note the relatively new publication of anassessment that has followed a classical design in terms of modalities, pro-duction and understanding of written and spoken language, and in test items.This test, the Comprehensive Aphasia Test (CAT; Swinburn, Porter, &Howard, 2004) includes many classic items such as naming, word fluency andrepetition, but has additional tests for cognitive functions that may impact onaphasia, and a means of exploring the “disability and emotional sequelae ofacquiring aphasia” (p. 5). The CAT is a collection of tests developed fordiagnosis of impairment; to provide guidance for further assessment andmotivation for treatment. It can be used for predicting and tracking changesin language behaviour over time. It is comprehensive in the areas covered but,as it is designed to be administered within two sessions, exploration is brief.Extensive guidance is given on administration, including assessing “grammat-ical well-formedness” (although some of the analysis is debatable), and on

Assessment of aphasia in a multi-lingual world 247

the development of the test. Test data collected from aphasic and non-aphasic subjects are given for each section, providing a really useful clinicalreference. The structure of this test while closely resembling the classic testsdiscussed above, has additional features that reflect research in the field aswell as the “broad church” approach current in clinical practice. Further, anexplicit aim of the test is to provide guidance for intervention. It is currentlyonly available in English.

Single words and grammar: Tests and connected speech data

Although the classic assessments have been successfully used in clinical prac-tice in many countries, their contribution to planning treatment and settinggoals for aphasia therapy has been limited. There are two reasons for this.First, changes in aphasic language behaviour are often slow and/or limited andmay be restricted to part of the language system. These tests are not sensitiveenough to measure such changes. Second, they focus on the severity of apha-sia across different modalities and not on the nature of the underlying lan-guage deficits. They are therefore limited in providing guidance for treatment.

Areas of relative weakness can be identified from the results and generalgoals set, but the results do not readily lead to detailed planning for eitherdeficit based or so-called “functional” aphasia therapy. While the relativeimpairments in different modalities can be identified, these tests do not setout to identify the assumed underlying nature of language deficits. Towardsthe end of the twentieth century, a different type of assessment was developedthat sought to address this matter. In seeking to reveal something about thenature of the aphasic deficits, authors of these tests were obliged to make atleast something about their theoretical assumptions explicit. As a result, wefind a divergence in the type of tests that started to be published. We nowbriefly review some of these.

Single word battery

Towards the end of the twentieth century, a new and different way of assess-ing aphasia was developed, based on neuropsychological and neurolinguistictheories. In many laboratories people were working on experimental taskswithin modular, word processing models (e.g., Ellis & Young, 1988). Amajor development was the publication of an extensive clinical test battery,the Psycholinguistic Assessment of Language Processing in Aphasia (PALPA),a battery of tests for the assessment of production and processing/compre-hension of spoken and written words and sentences (Kay, Lesser, & Coltheart,1992).

This battery of tests was based on ideas from neuropsychology and espe-cially from work with developmental and acquired dyslexia. Rather thantesting for an array of aphasic symptoms, as tests up to that date had done,the new way of assessing aphasia was based on notions of modules and


connections between modules. Tasks were developed to test the functioningof the assumed modules (and inter-modular connections) such as the audi-tory analyser, and phonological assembly. This concept eschewed the pursuitof a relationship between lesion site and symptoms that had been paramountin the neo-classical view. In this test, performance is interpreted within adefined modular, serial model of single word processing, which the authorshave conceded was “under-developed”. Instead of sites of lesion, languagedeficits are located within modules or in the connections between modules. Inaddition to locating the source of the difficulties within this box and arrowplan, some control of certain psycholinguistic variables was built into mostof the tests. The selection of these variables was based on experimental evi-dence that they influenced spoken or written word processing. Referencesto this evidence are given throughout the battery. The variables includedword frequency, imageability, length, and regularity of spelling. The PALPA,although largely concerned with investigating single word processing andproduction, also included two tests of sentence comprehension in the Englishversion. Both tests investigate the same array of syntactic variables; one hasspoken stimuli and the other written. A further test investigates “locativerelations” using eight locatives within 24 NP + PP constructions. Versions ofthe PALPA are available in a number of languages (e.g., Spanish, Dutch,German and, recently, Russian).

The PALPA is strong on investigating noun production and understand-ing, but verbs are largely ignored. However, from the late 1980s on, it becameclear, that word class is an influential factor in word and sentence processingin aphasia. Several studies found that aphasic patients treat verbs and nounsdifferently (e.g., Jonkers & Bastiaanse, 1998; Kohn, Lorch, & Pearson, 1989;Miceli, Silveri, Villa, & Caramazza, 1984). Further, within the class of verbs,various factors seem to play a role: instrumentality (Jonkers, 1998; Jonkers& Bastiaanse, 2006), argument structure (Kiss, 2000; Thompson, Lange,Schneider, & Shapiro, 1997), morphology (Bastiaanse & van Zonneveld,1998; Friedmann, 2000). It would seem that the variables that influence nounand verb processing are different. For example, the effect of frequency mayplay a role in noun retrieval, although there is much individual variation (Kay& Ellis, 1987; Zingeser & Berndt, 1988), but has not been found in verbproduction (e.g., Kemmerer & Tranel, 2000, McCann, 2005). Some experi-mental materials used to investigate aphasia have been adapted for clinicalpractice, for example An Object and Action Naming Battery (Druks &Masterson, 2000), the Thematic Roles in Production (TRIP; Whitworth,1996) and parts of the Verb and Sentence Test (VAST; Bastiaanse, Edwards, &Rispens, 2002).

Batteries focused on grammatical abilities

There is an extensive amount of literature and a relatively large number oftheories on sentence comprehension impairment. Many laboratories have


developed their own tests, suitable for exploring their theories of languagecomprehension, but there has not been a systematic adaptation of these pro-cedures for clinical practice, although many ideas are used in clinical practice,at least in the UK. An exception is a relatively new test, the Verb and SentenceTest (VAST; Bastiaanse et al., 2002), a test that has been motivated by neuro-linguistic theories, but developed for clinical practice as well as for use inresearch laboratories. A unique feature of this assessment is that for all theaphasic features that are tested, there are published treatment protocols orideas. We will come back to this test later.

Spontaneous speech

During the latter half of the twentieth century, the application of linguistictheory to aphasia started to seep into clinical practice and noticeably intoclinical assessment of aphasia. Not only did some linguistically motivatedassessments begin to appear but there was also a move to a completely differ-ent methodology. One major methodological development was the use ofsamples of connected or spontaneous speech data to investigate phonology,lexis and grammar. In these studies, aphasic speech samples were comparedwith non-aphasic samples collected in the same conditions. These studiesprovided insights into how aphasic language sounded when the speaker waspermitted to produce chunks of speech, rather than answering questions ornaming pictures. The picture that emerged was one that supported the sub-traction notion: it was possible to see the extent to which the language systemhad been preserved, and the extent to which it deviated from non-aphasic,normal language. So, for example, for Dutch, Wagenaar, Snow, and Prins(1975) and Vermeulen, Bastiaanse, and van Wageningen (1989) found thatthere were certain linguistic dimensions distinguishable, on which aphasicspeakers could be independently impaired. In English, comparisons of apha-sic and non-aphasic speech were made using matched speech samples(Edwards, 1995; Edwards & Garman, 1992; Edwards & Knott, 1994, Garman& Edwards, 1995). The Dutch and English work was brought together apply-ing the framework developed for the English studies to data from both lan-guages. Edwards and Bastiaanse (1998) examined grammatical and lexicalfeatures in Dutch and English fluent aphasic speakers and found a reductionin the proportion of complex sentences and verb diversity in the Englishaphasic speakers compared with the control data.

The use of connected speech data now plays an important part in evaluat-ing effectiveness of treatment. Researchers are interested in whether improve-ments found in test performances extend to connected speech (Bastiaanse,Hurkmans, & Links, 2006; Edwards & Tucker, 2006; Webster, Morris, &Franklin, 2005). However, the assessment of connected speech data is notstraightforward. There are issues concerning segmentation and reliability,and features to be noted and scored. See Edwards (2005) for a discussion onthe use of connected speech data in assessment. These same issues also impact


on what, on the face of it, looks like an easier task, the investigation of lexiswithin connected speech samples. Given that lexical retrieval is a pervasiveproblem in aphasia, it is not surprising that there are a myriad of studiesinvestigating word retrieval. If one wishes to employ range of vocabulary asa measure of improvement over time, or as a measure to separate types ofaphasia, then there are various methodologies. Wright, Silverman, andNewhoff (2003) have compared the use of three different measures ofvocabulary; type–token ratio (TTR); number of different words (NDW) anda D(iversity) measure developed by Malvern, Richards and colleagues (Mal-vern, Richards, Chipere, & Durán, 2004; Richards & Malvern, 1997). The Dmeasure, a measure of lexical diversity, is obtained via special software. It iscalculated by first randomly sampling words from a transcript to produce aTTR against tokens for the empirical data. The software then finds the best fitbetween this empirical curve and the theoretical curves generated by themodel by adjusting the value of D. Higher values of D represent greaterlexical diversity. The authors claim that this procedure is suitable to use withsmall samples and ensures that all researchers carry out measurement in thesame way (p. 60). In the aphasia study, Wright et al. (2003) found that TTRand NDW correlated when the sample size was held constant, although thisentailed ignoring some of the data. The D measure correlated with the twoother measures only when sample size was held constant, thus illustrating thecomplexity of computing lexical diversity in connected speech.

Other spontaneous speech analysis systems have specifically beendeveloped to analyse the grammatical aspects of Broca’s aphasia (Saffran,Berndt, & Schwartz, 1989; Thompson et al., 1997). The only system thathas been published to date as a clinical tool and is therefore accessible toclinicians is the Quantitative Production Analysis (Berndt, Wayland, Rochon,Saffran, & Schwartz, 2000; Saffran et al., 1989). Of course, some highlymotivated therapists do use procedures that are still experimental. An over-view and critical analysis of spontaneous speech analysis methods can befound in Prins and Bastiaanse (2004). They claim that only a few methods arevalid and reliable and not all are suitable to measure improvement. Neverthe-less we remain committed to the importance of examining samples of spon-taneous speech when trying to measure the effectiveness of treatment. Afterall, as the main goal of treatment of speech production is improving languageuse in daily life, we need to continue to try to monitor and measure relevantfeatures of connected speech very carefully.

Translating tests: Clinical imperatives and empirical pitfalls

There is a reasonably widespread understanding that a straightforward trans-lation of the vocabulary of tests is not sufficient when trying to produce aversion of a test in a language other than the original. Cultural issues need tobe taken into account, such as choice of vocabulary items, illustrations andthe topics utilized, but the issue of translation is broader. There is also a


growing awareness that the psychometric variables that may be controlled forin the original test, such as frequency, age of acquisition and imageability,may only hold for the original language of the test. At a very simple level,clinicians working in the UK know that most of their clients/patients will notbe able to name the bagel or wreath in the Boston Naming Test (Kaplan,Goodglass, & Weintraub 1983). However, the problems are wider than lackof knowledge of certain objects or foods. There is not always a one-to-onetranslation across verbs. For example, Dutch has one word badmintonnen forto play badminton and one word schaken for to play chess so a verb to verbtranslation is not always possible. Further, sentence constituents such asadverbs, that are free morphemes in English and Dutch, may be bound mor-phemes in some languages, Finnish and Hungarian, for example. We cannotbe sure that the verbs take the same argument structure in the language intowhich the test is being translated. Some will but others will not. If the testincludes production and comprehension of sentence structure, then theproblems are even greater as we will see below. There is a large amount oflinguistic data on English and a number of European languages on which todraw conclusions but this is not the case for many other languages. Inaddition, the linguistic tradition differs across the world and the infor-mation available about a language may be incompatible with the theoreticalmotivation of the original test.

Translating tests: Two examples

In this section, two tests that have been translated and adapted to anotherlanguage will be discussed. First the PALPA, which was developed in Englishand has been made available for Dutch. Second, the VAST, a test that wasdeveloped for Dutch and has been adapted to English. Some problems thatwere encountered in the adaptation of these tests are discussed here.

Translation and adaptation of the PALPA to Dutch

The English PALPA is a test battery that consists of more than 50 subtests,divided into four parts: auditory processing, reading and spelling, pictureand word semantics and sentence comprehension. The items in most subtestsare controlled for word frequency, length, regularity of spelling and otherfactors, which make a word-to-word translation into another languageimpossible. Thus only the principles of the PALPA could be preserved inadapting the test for Dutch, although new words that were included in thetest were matched on the same variables and new pictures were necessary.Although many high-frequency English words have high frequency in Dutch,word length is not always the same. In addition, there are problems withtrying to assemble irregularly spelled words as there are fewer irregularlyspelled Dutch words compared to English. Although Dutch has a consider-able number of loanwords that are irregularly spelled, it was not possible to


obtain the same distribution of regularly and irregularly spelled words in theDutch version of the PALPA

Not only did new pictures need to be drawn for words that were notincluded in the English version, but some pictures had to be changed toaccount for cultural difference. For example, the picture of a stamp in theword comprehension subtest in the English version needed to be replaced asit has a picture of Queen Elizabeth II on it. Naturally, the subtests for lowimageability words, synonym judgement and word semantic association, couldnot be translated literally.

All these adaptations were quite easy to implement, but a real problem arosewhen the subtests at the sentence level were considered. The theoreticalmotivation of this part of the PALPA is quite weak compared to that under-lying the tests focused on single word processing. It was decided to omit thispart in the Dutch PALPA and to develop a new, well-motivated test forcomprehension and production of verbs and sentences, which we calledthe Verb and Sentence Test (VAST). This was subsequently translated andadapted to English.

Translation and adaptation of the VAST to English

The Verb and Sentence Test was originally developed for use in Dutch. Whenthe translation and adaptation of the PALPA was finished, the need was feltfor a test that could assess comprehension and production of verbs. Thesubsection of PALPA that tests sentence comprehension was not adapted inthe Dutch version and thus there was a need for a new test of sentencecomprehension and production. The type of sentence structures to be includedfor assessment was carefully considered: sentences that had the basic wordorder for Dutch plus sentences with “moved” NPs and verbs were selected fortesting. One of the principles guiding the development of the VAST was thatonly linguistic variables that have been shown to be affected in aphasia wouldbe included. So verbs were controlled for frequency, name relation with anoun and transitivity. For sentences the main variable was word order, thus intesting Dutch sentences, it was necessary to include sentences that had thebasic word order, so sentences with “moved” NPs (passives, wh-questions)and “moved” (embedded vs. matrix vs. question order) verbs were included.The second principle was that the VAST should be a tool that could be usedwith a broad range of aphasia types. Finally, the VAST should be “treatment-oriented”: for each tested variable a treatment programme or method shouldbe available that shows that this variable can be successfully trained. Thisresulted in 10 subtasks. The VAST has been translated into and adaptedfor a number of languages: English (Bastiaanse et al., 2002), Norwegian(Bastiaanse, Lind, Moen, & Simonsen, 2006), French and German. The testsin the latter two languages are not yet standardized.

When translated into English, a number of problems were encountered.First, a main variable in the Dutch version was “position of the verb”. In


Dutch the verb can take different positions in the sentence, whereas inEnglish it always precedes the object. So “verb movement” could not beincluded in the English version. It was decided to add two extra sentencetypes: subject clefts and object clefts. These structures are not in the Dutchversion because they are ambiguous in Dutch.

In the first version of the Dutch VAST, one test was included whichentailed the selection of the correct wh-word (who, what, when and where).While Dutch non-brain-damaged speakers were able to perform this test,none of the first 10 aphasic patients who were tested with these materialscould to do the task because they did not understand what they were sup-posed to do. It was then decided to remove the task. Because we suspectedthat the task could be valuable, an adapted version was made for the trialEnglish version of the VAST. This proved to be as problematic in English as ithad been in Dutch and so was not included in the final version.

The English VAST is similar to the Dutch version in terms of structure, butmany lexical items as well as the sentences needed to be changed. Somechanges were made because the variables they were controlled for did nottranslate, for example there were different frequency ratings across the twolanguages. The verb “to skate” is much more frequent in Dutch than inBritish English (and has a zero frequency in Australian English). Otheractions are expressed by a verb in Dutch, but by a verb phrase in English: forexample, to play badminton is one word in Dutch, badmintonnen, as men-tioned above. The same problems arose with the verbs that have a namerelation to a noun in Dutch, but not in English, or the other way around.Thus the list of verbs was adapted. The phrasal verbs were removed andthose that did not achieve a high name agreement score were omitted. Anumber of new verbs were added and all variables checked. All items in allsubtests were trialled on non-aphasic English speakers.

Assessment when it is not possible to use standardized tests

We have seen above that there are tests being developed for use in a range oflanguages, yet in many European countries there are now an increasing num-ber of people whose first language is not that of the host country. The increasein demand on speech and language therapy services has arrived before wehave the necessary range of standardized tests for clinical practice despite alongstanding awareness of the need for assessments designed for bilingualspeakers (Paradis, 1987). Unfortunately, some clinicians do try to use directtranslation but, as we have illustrated above, this is far from satisfactory. Asthe new migrants age within their new countries, there are an increasing num-ber of people who have acquired aphasia but do not have native competenceof the language of their adopted country, and clinicians are in the position ofhaving to do the best they can. The development of language assessmentsneeds to be within a context of knowledge of the language of the assessment,and we have endeavoured to demonstrate why straightforward translation of a


test into another language will not provide an assessment tool that can be ofany use. Unfortunately, a detailed knowledge of the languages we need is justnot available. There is some work underway in the UK by Bryan and hercolleagues investigating the comparative influences on test scores of age andhaving English as an additional language, but to date resources are pitifullysmall. This then creates a real practical dilemma for the clinician. In strivingto provide equality of medical provision, the clinician needs some way ofassessing the presenting disorder if only to advise the patient, his or her familyand the other medical staff involved in the care of the patient/client. Practic-ally, a clinician still needs to make some kind of assessment in order to offeradvice, as a minimum of care. The clinician can choose to work through atranslator, selecting parts of tests that can most easily be translated. As wehave argued above, this is less than satisfactory because in changing tests,standardization is lost and so the results can only be used for guidance andmust be interpreted with extreme caution. They can, however, be used todemonstrate to other professionals how aphasia has affected the patient’s/client’s language. The alternative is to offer no help, clearly an unacceptableposition. It may be that there will be sufficient academic interest or politicalpressure to create assessment batteries in a much wider range of languages.Despite more than a hundred years of aphasia investigations by talentedresearchers (such as Chris Code), public awareness of aphasia in mono-lingual contexts is minimal, as Chris and his colleagues have demonstrated(Simmons-Mackie, Code, Armstrong, Stiegler, & Elman, 2002), and ourknowledge of how to assess aphasia in a multi-lingual world is equally limited.We are beginning to explore how to create assessments that are applicable incross-language research and how best to assess people who are aphasic in amulti-lingual world. There is much work still to be done.

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Swinburn, K., Porter, G., & Howard, D. (2004). The comprehensive aphasia test (CAT).Hove, UK: Psychology Press.

Thompson, C. K., Lange, K. L., Schneider, S. L., & Shapiro, L. P. (1997). Agrammaticand non-brain-damaged subjects’ verb and verb argument structure production.Aphasiology, 11, 473–490.

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case of pure anomia: Implications for models of language production. CognitiveNeuropsychology, 5, 473–516.


17 Computerized aphasiatreatment outcomes researchThe past and a proposal

Richard C. Katz and Robert T. Wertz

Almost 20 years ago, we were in the final stages of our 5-year Phase III studytesting the efficacy of our computerized aphasia treatment protocol. At thattime, I was approached by one of the two editors of a new, soon-to-be-released, journal, called Aphasiology. Dr. Code asked if I would write a“lead article for a forum” on the use of computers in aphasia therapy. TheAphasiology forum became not only a staple of that journal, but a model forothers as well, and as the role of computers in rehabilitation grew, the 1986forum articles, and the many subsequent articles on computerized treatmentpublished in Aphasiology, helped to propel this aspect of treatment forwardby offering an international platform to ask questions and discuss and debatefindings. We will always be grateful to Chris for providing, at that criticaltime, the opportunity to discuss with our colleagues from all over the worldour work and the works of others.

Determining the value of aphasia treatment software is complicated by thechanging perspectives of clinicians as to what the primary objective of ther-apy is – to improve language skills, functional communication, or quality oflife. Similarly, continual advances in computer hardware and system softwareprovide new opportunities and just as quickly condemn last year’s programsto obsolescence. The purpose of this chapter is to review selected computer-ized aphasia treatment studies; place them in the five-phase outcome researchmodel (Robey & Schultz, 1998); and suggest additional research necessary totest the efficacy, effectiveness, and efficiency of computerized treatment foraphasia.

Phase I, Phase II, and Phase III studies

Phase I and Phase II studies are brief, employ small samples, and do notrequire external controls. Phase I objectives are to develop the hypothesisabout the treatment that will be tested in later phases in the five-phase model;establish the treatment’s safety; and detect whether the treatment is “active,”essentially, whether aphasic people who receive it improve. Phase II researchbuilds on the results of Phase I studies. The hypothesis is refined, an explan-ation for the outcome is developed, the target population is specified, the

treatment protocol is standardized, the validity and reliability of the outcomemeasures are demonstrated, and the treatment dosage is adjusted to maxi-mize outcome. Phase III efficacy studies are long, complex, and expensive.Large sample size is required to obtain acceptable statistical power, and,usually, the means for obtaining the large sample size requires a multi-centereffort in which several institutions contribute participants to obtain anadequate sample. The required study design is a randomized controlled clin-ical trial in which participants who meet selection criteria are assigned ran-domly to treatment and no-treatment groups. Randomization controls fortreatment selection bias and other potential biases, and the treatment versusno-treatment comparison constitutes a true test of the treatment’s efficacy.Of course, explicit protocols and rigid controls across participating centersare essential to ensure program fidelity and that the trial is truly cooperative –everyone is doing the same thing.

For almost 30 years, researchers have been creating and testing aphasiatreatment software. Early single-subject and small group outcome studies,now designated as Phase I and Phase II computer studies (Wertz & Katz,2004), demonstrated that independent use of the computer in treatment ofaphasia was feasible and that treatment was “active,” but they did not estab-lish whether improvements in outcome measures were of sufficient magnitudeto justify use of the computer, or resulted from the specific intervention pro-vided. Moreover, these Phase I and II studies did not demonstrate whetherthe treatments provided were efficacious, effective, or efficient.

Computerized writing treatment

Seron, Deloche, Moulard, and Rousselle (1980) reported perhaps the firstPhase I study to use a computer (a Digital Equipment model PDP–10 mini-computer, time-shared) to provide a multi-step cognitive intervention forwritten spelling errors of adults with aphasia. Ninety words divided intothree groups (depending on number of syllables and complexity) served asstimuli. An experimenter read aloud the stimulus word and the subjectattempted to type the word on the computer terminal. Intervention consistedof three levels of feedback: the number of letters in the target word (indicatedby square “boxes” displayed on the screen); whether the letter typed was inthe word; and, when the correct letter was typed, whether that letter was inthe correct position. Five subjects completed the program in 7 to 30 sessions.Pre- and post-treatment tests required the subjects to write by hand a general-ization set of single words from dictation. Performance varied among sub-jects, but all decreased significantly (p <. 05); the number of misspelled wordsby an average of 10 words, and the total number of misspelled letters by anaverage of 39 letters, on the post-treatment test. These results suggestedthat typing in response to the computer program improved the subjects’written spelling of words. Four of the five subjects maintained improvedperformance on a second post-treatment test administered 6 weeks later.

260 Katz and Wertz

Building on the Phase I Seron et al. study, Katz and Nagy (1984) reportedusing a computer to provide a different multi-step writing (typing/spelling)intervention for adults with aphasia that was error-specific and linguisticallyrelevant. The program incorporated complex branching algorithms to pres-ent six different levels of cuing, depending on the number of times a stimuluswas incorrectly typed. Single and multiple cues, from a hierarchy of six, wereselected by the program automatically in response to the number of attemptsmade by the patient. Specific cues included anagrams, multiple-choices, copy-ing from a model, and copying from memory. A 7-point scoring system wasused to describe performance and track the effect of each cue. Additionalfeedback included repetition of the successful stimuli and the most recentlysuccessful cues. Additional changes automated every aspect of the programand eliminated the need for a clinician to start the program (a “personalcomputer,” the Apple II Plus, was used instead of a time-shared mini-computer) and present stimuli (line drawings served as stimuli instead ofwords presented verbally). The use of pictures as stimuli also reduced taskrequirements, avoiding complicating the task for patients with auditory com-prehension problems. Finally, copying practice was generated by a printer ashomework to strengthen generalization to writing. Comparison of pre- andpost-writing outcome measures showed significant improvement (p < .01) inspelling of the target words for seven of the eight aphasic subjects, demon-strating that multi-level computerized intervention (in this case, the treatmenthierarchy and copying assignment) was active.

While the Phase I and Phase II studies described above provide the founda-tion for development of a Phase III efficacy study of multi-step writingtreatment, none has been reported. As the treatment in both studies wasdemonstrated to be “active,” either might be used in a Phase III study. Inaddition, the treatment program could combine visual and linguistics cuesfrom both studies. For example, the program might employ an algorithm thatwould select cues (number of letters in the word, position of the letter in theword, anagrams, copying from memory, etc.) in response to errors, randomlyat first and later based on the prior success of an individual cue or a combin-ation of cues. Like Seron et al., a large number of stimulus words would beused, and, like Katz and Nagy, the program would be fully automated andstimuli presented visually to minimize task requirements. Copying homeworkwould not be generated so that outcomes could be attributed to the computerintervention alone. As in all Phase III studies, a sample size of patients thatwas sufficient to attain acceptable statistical power, and random assignmentto treatment and non-treatment groups, would be required.

Computerized auditory comprehension treatment

An early example of a Phase I computerized aphasia treatment study is Mills’(1982) report that used a computer (an Apple II Plus with 48 kilobytes ofRAM) to present an auditory comprehension task to an adult with aphasia.

Computerized aphasia treatment outcomes research 261

Because off-the-shelf “microcomputers” at that time did not have the abilityto time responses or reproduce speech, Mills installed two internal cards inthe fledgling computer: an internal clock and a speech digitizer. He alsoadded a color television monitor to incorporate colored drawings of objectsinto the task. A printer (to display performance) and a graphics tablet (tocreate the color drawings) were also included. The system cost around $4500,a considerable investment in 1982.

Mills’ computerized task was a simple auditory comprehension drill thatconsisted of three levels of difficulty incorporating one, two, or three criticalelements per level. Four color drawings of objects, numbered “1” through“4,” were displayed on the monitor to serve as multiple choice items. Then,depending on the intended level of task difficulty, the speech digitizer pre-sented one-, two-, or three-part verbal “pointing” commands, amplifiedthrough an external speaker. The command consisted of a carrier phrase(“Find the . . .”) and the name or names of the target object or objects.Because a computer mouse was not available as a pointing device in thosedays, the patient responded by pressing the numbered key or keys on thekeyboard that corresponded to the numbered picture or pictures associatedwith the spoken word or words. Intervention was limited to repetitions of theauditory stimulus, elicited when the patient pressed the Return (Enter) key. Ifthe response was correct, the computer responded with a verbal “Good” or“Right” and displayed a flashing square around the correct choice(s). If thefirst response was not correct, a verbal “Wrong, try again” was presented,and the stimulus was repeated. A second error resulted in a flashing squarearound the correct choice(s). Twelve items per level were presented. Resultswere stored on disk. A specially written analysis program was used to showperformance on either the monitor or the printer.

Mills’ patient was a 39-year-old computer programmer who suffered anocclusive stroke 16 months prior to beginning the computerized treatmentprogram. He was described as being “severely involved in all modalities” atthe beginning of the 13-month study. Outcomes were determined by measur-ing accuracy of task performance on the three task levels (gains of 8%, 42%,and 73%, respectively) and periodic administrations of the Porch Index ofCommunicative Ability (PICA; Porch, 1981) auditory comprehension sub-tests VI and X (gains of +4.8 and +1.5 points, respectively) and an unspeci-fied version of the Token Test (gain of 23 percentile points). The influence ofother factors (e.g., placebo effect) cannot be discounted because no with-drawal or multiple baseline single subject research strategies were used.Nevertheless, the study was a first step in adapting auditory comprehensionactivities to the computer and demonstrating that the auditory comprehensionof aphasic patients may improve after using a computer program.

Mills’ (1982) report was not followed by a Phase II investigation. Possiblefollow-up studies might administer more comprehensive auditory and func-tional tests and investigate treatment dosage (intensity and duration). Limitingthe duration of treatment (e.g., 3 months as opposed to 13 months) would be

262 Katz and Wertz

more in line with current clinical practices. In addition, a treatment modelshould be specified. The computerized treatment described by Mills (1982)most closely approximates auditory stimulation treatment. The most widelyused approach for treating aphasia (Duffy & Coelho, 2001) is clinician-provided stimulation treatment, which uses controlled and intensive auditorystimulation to facilitate and maximize the patient’s reorganization andrecovery of language (Schuell, 1974; Schuell, Jenkins, & Jiménez-Pabón,1964). Treatment is designed so that patients respond frequently, to manydifferent stimuli, and at a high rate of accuracy. Phase II research utilizing anauditory stimulation model might increase the number of stimuli from theoriginal dozen and, at the same time, increase the rate of response (number ofresponses per session).

Should outcomes continue to improve in Phase II studies, a Phase IIIauditory comprehension study would be in order. The study could manipu-late stimulus parameters (part of speech, word length, word frequency, etc.)and task parameters (number of multiple choices, auditory/semantic confu-sion among multiple choices, delays, distractions, etc.). A complex branchingalgorithm could advance subjects through a hierarchy of stimulus param-eters, from easy to difficult, with the goal of maximizing rate of presentation(number of stimuli per session) while maintaining high accuracy. Like Mills(1982), the program would be fully automated and designed to minimizeresponse requirements. Again, as in all Phase III studies, adequate samplesize and random assignment to treatment and no-treatment groups would berequired.

Computerized reading comprehension treatment

Phase I studies by Katz and Nagy (1982, 1983, 1985) demonstrated variousfunctions computers could provide for treating reading problems in patientswith aphasia, although like all Phase I studies, interpretation of outcomes islimited due to small sample sizes and research designs. Katz and Nagy (1982)described a program containing five reading tasks designed to provide read-ing stimulation for aphasic patients. (The program also contained a task toimprove simple math, and a testing module.) Five aphasic subjects ran thecomputer programs two to four times per week for 8 to 12 weeks. Onlycorrective feedback was provided. Although several subjects demonstratedimproved accuracy, decreased response latency, and increased number ofattempted items on some computer tasks, changes in pre- and post-treatmenttest performance were minimal. The following year, Katz and Nagy (1983)reported a drill and practice computer program for improving word recogni-tion in chronic aphasic patients. The program simulated tachistoscopicpresentation of 65 words that occur frequently in text (“recognition vocabu-lary”) and incrementally varied the rate of exposure as a function of accuracyof response – stimuli were displayed for shorter durations (down to .01seconds) as words were matched or typed accurately, and displayed for longer


durations as words were matched or typed incorrectly. The goal of the pro-gram was to increase and stabilize the subject’s sight vocabulary; however, nochanges were observed on pre- and post-treatment measures for the fivechronic aphasic subjects.

Katz and Nagy (1985) incorporated concepts from both previous studies ina their Phase II study, where a self-modifying computerized reading programwas administered to severely impaired aphasic adults. The objective of thestudy was to improve functional reading. A program was developed to teachsubjects to read single words without clinician involvement. Line drawings of12 semantically related objects were shown individually on the monitor,under which two to six multiple choices were printed. Multiple choice foilsincluded visually confusing and semantically confusing words. The programalso generated, through a printer, homework (writing activities) that corres-ponded to the subject’s performance. Four of the five subjects demonstratedpre- to post-treatment changes on the treatment items that ranged from 16%to 54%.

Katz and Wertz (1997) conducted the only Phase III study of the efficacyof computerized language treatment and computerized non-language stimu-lation for improving language test performance for chronic aphasic adults.Fifty-five chronic aphasic subjects who were no longer receiving speech-language therapy were assigned randomly to one of three conditions: 78hours of computer reading treatment, 78 hours of computer stimulation(“non-language” activities), or no treatment. The computer reading treat-ment software consisted of 29 activities, each containing eight levels of dif-ficulty, totaling 232 different tasks. Treatment tasks required visual-matchingand reading comprehension skills, displayed only text (no pictures), and useda standard, match-to-sample format with two to five multiple choices. Treat-ment software automatically adjusted task difficulty in response to subjectperformance by incorporating traditional treatment procedures, such as hier-archically arranged tasks and measurement of performance on baseline andgeneralization stimulus sets, in conjunction with complex branching algo-rithms. Software used in the computer stimulation condition was a combin-ation of cognitive rehabilitation software and computer games that usedmovement, shape, and/or color to focus on reaction time, attention span,memory, and other skills that did not overtly require language or other com-munication abilities. Subjects in the two computer conditions worked on thecomputer for 3 hours per week for 26 weeks with minimal clinician inter-action. Subjects from all three conditions were tested using the PICA andWestern Aphasia Battery (WAB; Kertesz, 1982) at baseline, 3 months, and6 months. Statistically significant improvement over the 26 weeks occurredon five language measures for the computer reading treatment group, onone language measure for the computer stimulation group, and on none ofthe language measures for the no-treatment group. The computer readingtreatment group displayed significantly more improvement on the PICAoverall and verbal modality percentiles and on the WAB aphasia quotient

264 Katz and Wertz

and repetition subtest than the other two groups. The results suggest thatcomputerized reading treatment can be administered with minimal assistancefrom a clinician, improvement on the computerized reading treatment tasksgeneralized to non-computer language performance, improvement resultedfrom the language content of the software and not stimulation provided bya computer, and the computerized reading treatment provided to chronicaphasic patients was efficacious.

Potential Phase IV studies

If the treatment is demonstrated to work in Phase III efficacy research, it isjustifiable to continue with Phase IV effectiveness research. The purpose is totest the treatment’s effectiveness under ordinary conditions of clinical prac-tice with typical patients, typically trained clinicians, typical dosage, andtypical compliance. Again, a large sample is required, however external con-trol (e.g., a no-treatment control group) is not. Thus the typical effectivenessstudy design is a large single group where, as in Phase I research, performanceis measured pre-treatment, the treatment is administered under ordinaryconditions, performance is measured post-treatment, and a pre- versus post-treatment comparison is made to determine change. If the group shows sig-nificant improvement from pre- to post-treatment, it can be inferred thatthe treatment is effective; essentially, that it does work under conditions ofeveryday clinical practice.

Additional Phase IV experiments might include examination of variationsin the target population; for example, study participants who do not meet theselection criteria employed in the Phase III efficacy study. In addition, PhaseIV research might examine variation in the dosage, for example, a differentintensity and duration of treatment from that employed in the Phase IIIefficacy research. And one might explore differences in treatment providers,for example, clinicians with less training than those who participated inthe Phase III efficacy research or, perhaps, provision of the treatment bynonprofessional, trained volunteers.

While no Phase IV computerized aphasia treatment study has beenreported, one could be conducted by using the Internet, where a large numberof patients and former patients could be solicited through their clinicians toparticipate in the study. Referring clinicians could administer all pre- andpost-testing, and testing could be validated by videotaping or videoconfer-encing randomly selected test administrations. Standardized language, func-tional, and quality of life tests would serve as outcome measures to evaluatethe effectiveness of treatment.

For example, in a Phase IV study developed from Katz and Wertz (1997)computer reading treatment program, all subjects would receive the com-puterized treatment and be tested before beginning and after completing treat-ment. The goal would be to evaluate the treatment of “typical” patientsunder “real-world” conditions. Exclusion criteria would be minimal to include


patients typically found in clinics. Data from subjects unable to maintainthe prescribed treatment schedule (i.e., treatment dosage) would not bedropped from the study, as under “optimal” conditions tested in Phase IIIresearch. Positive outcomes from Phase IV research would provide clinicianswith support to justify funding and resources to provide treatment.

Phase V

Additional research is continued in Phase V, initiating studies to test thetreatment’s effectiveness and efficiency. Continued effectiveness researchmight examine the cost–benefit, or cost effectiveness, of the treatment. Or,additional outcome measures might be employed to determine the patient’sand family’s satisfaction with the intervention and the influence of the treat-ment on the patient’s quality of life. Large group studies and/or single-subjectdesigns with multiple replications across patients are appropriate for Phase Vresearch, and, usually, external control is not required. However, some effi-ciency studies require control through random assignment. For example,comparing the efficiency of two treatments that have been demonstrated to beefficacious in Phase III research requires a comparison of treatments design,where study participants who meet selection criteria are assigned randomly toone treatment or the other. Similarly, an efficiency study designed to compareone intensity and/or duration with another intensity and/or duration wouldrequire random assignment of study participants to the different schedules.For example, a Phase V study could compare the two comprehensiontreatments described above, auditory and reading, and determine whethersubjects receiving one treatment or the other report and demonstrate betterfunctional outcomes.

Loverso and his colleagues provided examples of Phase I and Phase IIresearch, describing the development and testing of a model-driven, clinician-provided treatment approach, the “verb as core” (Loverso, 1987; Loverso,Prescott, & Selinger, 1988; Loverso, Selinger, & Prescott., 1979). These led toa comparison study of clinician-provided treatment with a computer-providedand clinician-assisted version of the treatment (Loverso, Prescott, & Selinger,1992; Loverso, Prescott, Selinger, & Riley, 1988; Loverso, Prescott, Selinger,Wheeler, & Smith, 1985). However, the efficacy of neither treatment had beentested in Phase III efficacy research. Consequently, neither treatment hadbeen demonstrated to be effective in Phase IV research. A comparison of twotreatments of unknown efficacy will not demonstrate the efficacy of eithertreatment (Wertz & Irwin, 2001).

In both the clinician-provided and the computer/clinician-assisted versionsof “verb as core” treatment protocol, verbs were presented as starting pointsand paired with different wh-question words to provide cues to elicit sen-tences in an actor–action–object framework. Thirty verbs were used in eachof six modules. The hierarchy was divided into two major levels, each consist-ing of an initial module and two sub-modules that provided additional cuing

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for subjects unable to achieve 60% or better accuracy on the initial module.Level I presented stimulus verbs and the question words “who” or “what” toelicit an actor–action sentence. Level II elicited actor–action–object sentencesby presenting stimulus verbs and the question words “who” or “what” for theactor, and the question words “how,” “when,” “where,” and “why” for theobject. Subjects responded verbally and graphically. Subjects were scheduledfor treatment three to five times per week. During each session, 30 stimulusverbs were presented for generation of sentences.

Loverso et al. (1985) compared the effects of the “verb as core” treatmentapproach when treatment was provided by a clinician and when it was pro-vided by a computer and speech synthesizer assisted by a clinician. The apha-sic subject responded in the clinician-only condition by speaking and writing,and in the clinician–computer condition by speaking and typing. Stimuluspresentation and feedback in the clinician–computer condition was normallyprovided only by the computer. The clinician intervened only if the patient’styped response was correct but the spoken response was in error. The subjectimproved on the task under both conditions, but took longer to reach criteriaunder the computer and clinician-assisted condition. Based on the subject’simprovement, both on the treatment task and on “clinically meaningful”changes on successive administrations of the PICA (p < .01), the authorsconcluded that their listening, reading, and typing activities under theclinician–computer condition had a positive influence on the patient’s lan-guage performance. They suggested that, although still in the early stages ofdevelopment, aphasia treatment administered by computers is practical andhas the capacity for success. Loverso, Prescott, Selinger, and Riley (1988)replicated the study by Loverso et al. (1985) with five fluent and five non-fluent aphasic subjects for the purpose of examining whether treatment pro-vided under the computer–clinician condition was as effective as a clinicianalone when treating various types and severities of aphasia using theircuing–verb–treatment technique. The 10 subjects required 28% more sessions(p < .05) to reach criteria under the computer–clinician condition than underthe clinician-only condition. Fluent subjects required 24% more sessions, andnonfluent subjects required 33% more sessions under the computer–clinicianconditions than under the clinician-only condition. Of the 10 subjects,8 showed significant improvement (p < .05) on the PICA overall percentilemeasure, on the verbal modality measure, and on the graphic modality meas-ure. All subjects retained these gains after a maintenance phase of 1 monthpost-treatment or longer. Similar results were reported following a replicationof the study using 20 subjects (Loverso et al., 1992).

To our knowledge no additional studies examining the efficacy of com-puter-provided treatment for aphasia have been conducted. As indicatedabove, any effectiveness or efficiency research would require that the treat-ments being evaluated have been demonstrated to be efficacious in Phase IIIresearch.


A proposal

Previous computer-provided aphasia treatment outcome research has beenplagued by the problem that affects clinician-provided aphasia treatment out-come research. Programmatic research, where a treatment is tested system-atically in each phase of the five-phase treatment outcomes research model,is, if not nonexistent, extremely rare (Wertz & Irwin, 2001). NumerousPhase I computer-provided aphasia treatment studies have been reported.Few Phase II studies, building on Phase I research, exist. Only one Phase IIIinvestigation (Katz & Wertz, 1997) has tested the efficacy of a computer-provided intervention, and there have been no Phase IV and V effectivenessinvestigations. The tendency has been to develop new computer interventionsthat are prompted by new technology or to adapt clinician-provided treat-ment into computer applications, rather than to build and expand on previouscomputer-provided treatment research.

There are a number of computer-provided treatments that imply thetreatment appears to be “active” in Phase I research. The work to be done isto select the most promising of these and test them in Phase II research. Ifresults are positive, subsequent Phase III efficacy testing, and eventuallyPhases IV and V effectiveness and efficiency testing, is essential. Until webecome programmatic and systematic in our evaluation of computerizedaphasia treatment, we are not documenting, we are dabbling.

References

Duffy, R. J., & Coelho, C. A. (2001). Schuell’s stimulation approach to rehabilitation.In R. Chapey (Ed.), Language intervention strategies in aphasia and related neurogeniccommunication disorders. New York: Lippincott, Williams, & Wilkins.

Katz, R. C., & Nagy, V. T. (1982). A computerized treatment system for chronicaphasic adults. In R. H. Brookshire (Ed.), Clinical aphasiology: 1982 conferenceproceedings (pp. 153–160). Minneapolis, MN: BRK.

Katz, R. C., & Nagy, V. T. (1983). A computerized approach for improving wordrecognition in chronic aphasic patients. In R. H. Brookshire (Ed.), Clinical aphasi-ology: 1983 conference proceedings (pp. 65–72). Minneapolis, MN: BRK.

Katz, R. C., & Nagy, V. T. (1984). An intelligent computer-based task for chronicaphasic patients. In R. H. Brookshire (Ed.), Clinical aphasiology: 1984 conferenceproceedings (pp. 159–165). Minneapolis, MN: BRK.

Katz, R. C., & Nagy, V. T. (1985). A self-modifying computerized reading program forseverely-impaired aphasic adults. In R. H. Brookshire (Ed.), Clinical aphasiology:1985 conference proceedings (pp. 184–188). Minneapolis, MN: BRK.

Katz, R. C., & Wertz, R. T. (1997). The efficacy of computer-provided reading treat-ment for chronic aphasic adults. Journal of Speech, Language and Hearing Research,40 (3), 493–507

Kertesz, A. (1982). Western aphasia battery. New York: Grune & Stratton.Loverso, F. L. (1987). Unfounded expectations: Computers in rehabilitation. Aphasi-

ology, 1 (2), 157–160.Loverso, F. L., Prescott, T. E., & Selinger, M. (1988). Cueing verbs: A treatment

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strategy for aphasic adults. Journal of Rehabilitation Research and Development, 25,47–60.

Loverso, F. L., Prescott, T. E., & Selinger, M. (1992). Microcomputer treatmentapplications in aphasiology. Aphasiology, 6 (2), 155–163.

Loverso, F. L., Prescott, T. E., Selinger, M., & Riley, L. (1988). Comparison of twomodes of aphasia treatment: Clinician and computer-clinician assisted. In T. E.Prescott (Ed.), Clinical aphasiology (Vol. 18, pp. 297–319). Austin, TX: Pro-Ed.

Loverso, F. L., Prescott, T. E., Selinger, M., Wheeler, K. M., & Smith, R. D. (1985).The application of microcomputers for the treatment of aphasic adults. In R. H.Brookshire (Ed.), Clinical aphasiology: 1985 conference proceedings (pp. 189–195).Minneapolis, MN: BRK.

Loverso, F. L., Selinger, M., & Prescott, T. E. (1979). Application of verbing strategiesto aphasia treatment. In R. H. Brookshire (Ed.), Clinical aphasiology: 1979conference proceedings (pp. 229–238). Minneapolis, MN: BRK.

Mills, R. H. (1982). Microcomputerized auditory comprehension training. In R. H.Brookshire (Ed.), Clinical aphasiology: 1982 conference proceedings (pp. 147–152).Minneapolis, MN: BRK.

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18 Traumatic brain injuryrehabilitationAdvanced communicationtraining perspectives

Leanne Togher

This chapter presents part of an ongoing research programme that has beendeveloped with the guidance of Professor Chris Code. Chris’ influence onmy work has been far reaching; he was my PhD supervisor during his stayin Australia as the Foundation Chair of Communication Sciences andDisorders at the University of Sydney, my mentor during my postdoctoralfellowship and we continue to work together on current and new projects.Chris’ breadth of knowledge in the field of adult neurological communica-tion disorders has been invaluable in the development of my research ideasand my research career. He has that special talent of being able to improve aresearch proposal, a grant application or a manuscript in preparation withapparent ease. Chris has taught me a great deal about editing and reviewingjournal articles, and has given me an appreciation of the work entailed inmanaging a specialist journal such as Aphasiology. Perhaps his greatest gifthas been teaching me the value of collaboration and communication withcolleagues in the development and critique of my ideas. Chris’ contributionsto the numerous conferences he attends are always insightful and generous.His extraordinary international network is testament to his keen interest in allapproaches to neurological communication disorders and his willingness toexplore all ideas.

My research focus has been the application of novel methods, such asthe use of Systemic Functional Linguistic (SFL) theory (Halliday, 1994) toelucidate the nature of everyday interactions of people with traumatic braininjury (TBI). While TBI and SFL are not Chris’ specific area of interest, heencouraged me to pursue this area, to publish, to present at internationalconferences, and to apply for research grants. His guidance, mentorship, wisecounsel and encouragement are immeasurable, and I am honoured to be ableto pay tribute to him in this Festschrift.

Traumatic brain injury is the leading cause of disability in youngAustralians, and is particularly prevalent in young men. The condition dis-turbs, inter alia, thinking and problem solving. Ultimately, these problemsmanifest in impaired verbal communication. Communication problems fol-lowing TBI can make critical relationships – such as father, husband, andemployee – impossible to sustain. Those affected are socially inappropriate

and uncomfortable to be around, which causes a lifetime of lost friendships,unemployability, and social isolation. Minimization of these lifelong effectsis of the utmost importance to the health of those affected, and is critical toreducing the economic burden of the condition.

Traumatic brain injury (TBI) results from an external insult to the brain,and in severe cases, can lead to life-long devastating disability. Seventy percent of TBI cases are a result of motor vehicle accidents, with most being inthe 15–24 year age range (Tate, McDonald, & Lulham, 1998). With normallife expectancies and the addition of more casualties each year, the socialburden of TBI is cumulative. Most people with moderate-severe TBI havechronic communication and cognitive problems that result in a breakdownin family relationships, loss of friends, a failure to return to work, and socialisolation.

Communication difficulties for people with TBI include word findingproblems, excessive talkativeness, poor turn taking and repetitiveness (Snow,Douglas, & Ponsford, 1995). These communication difficulties are substan-tially different to the sequelae of aphasia and have been termed cognitive-communication impairments (Hartley, 1995). While some communicationproblems after TBI reflect disorders of language function, the majority arisefrom more generic cognitive deficits reflecting fronto-temporal pathologyand diffuse axonal injuries. Slowed information processing, impaired workingmemory/attention and executive dyscontrol may translate into deficiencies(e.g., inertia, rigidity, poor conceptualization and planning) or excesses(such as disinhibition) of cognition and behaviour (Tate, 1999; Tate, Lulham,Broe, Strettles, & Pfaff, 1989). Inertia and rigidity can lead to flat presen-tation, seeming disinterest in the conversation, and an inability to generateand maintain topics. Alternatively, excesses can interfere due to frequentinterruptions, disinhibited responses, swearing and perseveration on topics.These inappropriate and disturbing communicative behaviours are difficultto manage, particularly when in a community setting such as a shoppingcentre.

Overall, loss of communicative competence presents a major obstacle toreintegration into the community because it makes the person more taxingand less rewarding to interact with socially (Bond & Godfrey, 1997). Friends,carers and family begin avoiding them and this generally limits their ability tomaintain pre-injury relationships (Elsass & Kinsella, 1987; Tate et al., 1989).In addition, they often misjudge social situations, appearing to be overlyfamiliar with potential acquaintances thus interfering with their ability toestablish new relationships. As a result of diminished communication skills,people with TBI become socially isolated, have reduced opportunities foremployment and may even require care-givers to help them with everydaytasks such as shopping or pursuing leisure options. But even with care-givers,the poor communication skills of people with TBI are problematic. Caringfor people with TBI is stressful, with high levels of care-giver burden anddepression (Knight, Devereux, & Godfrey, 1998). The main sources for this

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stress have been identified as problems communicating with the person withTBI (MAA, 1998), behavioural disturbance (Knight et al., 1998; Marsh,Kersel, Havill, & Sleigh, 1998) and the level of cognitive processing difficul-ties of the person with TBI (Wallace, Bogner, Corrigan, Clinchot, Mysiw, &Fugate, 1998). Training programmes to provide communication strategies forcare-givers, while needed, are currently non-existent, and are urgently calledfor (Holland & Shigaki, 1998).

Improving the communication skills of the person with TBI

Despite its pivotal role in social reintegration there has been surprisingly littleresearch to examine the effectiveness of remediation of communication dis-orders after TBI. However, there is reason for optimism in this area. Recentstudies suggest that behavioural and cognitive deficits suffered by TBIpatients, thought to contribute to their loss of communicative competence,are amenable to remediation (Cannizzaro & Coelho, 2002; Cramon &Cramon, 1992, Flanagan, McDonald, & Togher, 1995, Helffenstein &Wechsler, 1982, Medd & Tate, 2000, Tate, 1987). Furthermore, a systematicreview of treatment outcomes in TBI indicated that the broad area of socialskills, which encompasses communication skills, was one of only two areasthat proved amenable to treatment (Cicerone et al., 2000). However, properlycontrolled treatment studies in this area are virtually non-existent. In orderto redress the lack of research into social skills remediation, we developeda social skills treatment approach (Flanagan et al., 1995). In this study, weevaluated the effectiveness of a social skills training programme with fivemales in the chronic stage following severe TBI. The participants’ perform-ance was judged using the six verbal scales of the Behaviourally ReferencedRating System of Intermediate Social Skills (BRISS; Wallander, Conger, &Cohen Conger, 1985; see also Farrell, Rabinowitz, Wallander, & Curran,1985) during three naturalistic interactions with an opposite-sex stranger.Ratings from the initial interaction were used to develop individualized inter-vention plans for each of the five TBI participants. Following the threeassessment interactions and the development of the intervention plans, theTBI patients took part in a group-based social skills training programme thatallowed for each individual’s specific deficits to be addressed. This promotedthe incorporation of individual goals into a group treatment process. Thetraining consisted of weekly 2-hour group sessions held over a 3-monthperiod. The instruction methods included modelling, role-play, feedback andhomework assignments. As the group was severely cognitively impaired, thesessions were highly structured, with repetition, frequent rest breaks, and avariety of interactive activities. Role plays were frequently videotaped andimmediately replayed to facilitate the provision of feedback. In addition topractising specific social skills, the participants were encouraged to attendto social cues. Following the treatment, the post-assessment tasks were thesame procedure as pre-intervention assessment. As expected, there was

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significant variability across participants on some scales pre-intervention.A significant finding, however, was the improvement shown by one of theparticipants on three of the BRISS scales, which was socially validated. Afurther participant also improved on one of the BRISS scales.

While this study demonstrated that positive changes can occur in inter-actions of people with severe chronic TBI, there have been no treatmentsdesigned and empirically evaluated to specifically target communication ineveryday situations for people with TBI. There has also been a paucity ofcommunication treatment studies using broader models of disability andsocial participation. These models are acquiring considerable currency inthe field of aphasia, but are yet to be applied to the everyday communicationfor people with TBI. There is recognition that social participation should bean outcome of rehabilitation following TBI (Cicerone, 2004), however therehas been no explicit examination of the relationship between communityreintegration and communication outcomes.

In discussing the communication outcomes necessary for community inte-gration, the question arises as to which communication tasks are necessaryfor the person with TBI to reintegrate into their own community. In anobservational study of 10 individuals with TBI in New Zealand, participantswere observed for 5 hours within a 1-week time frame to establish the com-munication activity range, frequency and domain of interaction (Larkins,Worrall, & Hickson, 1999). The most frequently occurring communicationactivity was social chat, an interactional communication activity that wasdefined as “communication interactions that maintain social relationships”(p. 188). Speech pathologists spend much of their clinical energy focusing onthe transactional features of communication; that is, getting the messageacross, rather than helping the person to engage in social chat or small talk.This poses difficulty for the clinician in a brain injury unit when working onsocial chat.

The first problem is that people with TBI are typically young males ofworking age, who are usually treated by young women with starkly differentcommunication styles and preferences in conversation. A second difficulty isthe social barrier of clinician–patient power imbalance (Togher, Hand, &Code, 1996). Nonetheless, therapy to improve social chat is imperative givenLarkins et al.’s (1999) findings. One solution to this dilemma is to includeother conversational partners in the therapy process.

Training communication partners of people with neurogeniccommunication disorders

A wide range of theoretical perspectives have been used to study the issue oftraining communication partners of people with neurogenic communicationdisorders, with the majority being completed in the field of aphasia. Theyinclude Conversational Analysis (CA) (Booth & Perkins, 1999; Wilkinsonet al., 1998), functional perspectives (Lyon et al., 1997; Worrall & Yiu,


2000), pragmatic models of communication (Newhoff, Bugbee, & Ferreira,1981), behavioural approaches (Simmons, Kearns, & Potechin, 1987) andsocial models of disability (Byng, Pound, & Parr, 2000; Kagan, Black,Duchan, Simmons-Mackie, & Square, 2001; Simmons-Mackie, 2000). Thecore principles of these approaches are similar. They all focus on improvingconversational interaction by training the communication partner and/orthe communication interaction rather than the person with communicationproblems.

Conversational analysis of interactions provides a rich source of informa-tion about areas such as the way participants repair communication break-down, take turns and introduce topics (Schiffrin, 1987). Booth and Perkins(1999) presented a single case study where the brother of an aphasic man wastrained over a 6-week period in collaborative repair management. This manwas part of a larger group who participated in training for carers of peoplewith aphasia (Booth & Swabey, 1999). During this training the potentialnegative consequences of focusing on the correction of aphasic errors wasdiscussed. One of the clearest outcomes in the post-intervention conversationwas the absence of correction. The brother permitted aphasic errors to passand collaborated to resolve sources of trouble. This study is an importantpreliminary foray into the value of individualized advice for communicationpartners in facilitating everyday conversation. With the publication of theSPPARC (Supporting Partners of People with Aphasia in Relationships andConversation; Lock, Wilkinson, & Bryan, 2001), a therapy resource for clini-cians to use with communication partners, this type of intervention is nowreadily accessible.

Functional perspectives have also been used in designing training studiesfor communication partners of people with aphasia (Lyon et al., 1997;Worrall & Yiu, 2000). The functional approach has developed partly inresponse to financial pressures (Frattali, 1993), a belief within the speechpathology profession that functional outcomes are important (Smith & Parr,1986) and a recognition of the WHO (2001) guidelines that differentiatebetween the dimensions of Impairment, Activity and Participation. Worralland Yiu (2000) incorporated these underlying tenets into a training pro-gramme for volunteers called “Speaking Out”, which focused on 10 generalcommunication domains such as banking and using a telephone. Scriptedmodules consisted of a “trigger” to raise awareness of participants regardingthe topic of the module. For example, in the banking module, participantsengaged in a discussion around electronic banking and the possible benefitsof this for a person with aphasia. A discussion ensued with the volunteerregarding ways a person with aphasia could remain involved in managing hisor her finances, and a plan was set up for the volunteer to assist the personwith aphasia during the following week. This planning was accompanied bypractical information handouts, which gave general strategies for the volun-teers. The training continued over a 10-week training period. Functionalmeasures showed small changes post-training; however, the authors point out

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that these changes were nonetheless clinically significant. It was also suggestedthat a more individualized training approach may have further increased theeffects of training.

The social approach to disability is a more recent movement in the wayintervention is viewed in relation to people with aphasia (Pound, Parr,Lindsay, & Woolf, 2000). This approach takes the broader view that therapyshould identify social barriers for people with aphasia, including the waycommunication partners may interact. The Conversation Partners programmedescribed by Pound et al. (2000) is a relatively new scheme where studentspeech pathologists and some members of the community commit to spend-ing 2 hours per fortnight for at least 6 months with a person with aphasia.Volunteers attend group training sessions before meeting their aphasic part-ner. Training is focused on giving information about aphasia, its communica-tive and social consequences, and basic communication techniques. Althoughthis programme has not been evaluated empirically, Pound et al. (2000) pre-sented a case study demonstrating the value of regular visits by a studentspeech pathologist with regard to increased communicative opportunities fora person with aphasia.

The value of these partner-focused treatment regimes is that communica-tion partners, when suitably skilled, can reveal the inherent competence ofthe person with brain injury by providing communicative opportunity(Kagan et al., 2001, Ylvisaker, Feeney, & Urbanczyk, 1993). In other words,when provided with the opportunity, people with acquired communicationproblems can capitalize on their preserved cognitive and social abilities toparticipate in conversation. Kagan et al. (2001) reported empirical evidenceof the positive communication and social outcomes of training communica-tion partners of people with severe aphasia. In a randomized controlled trial,20 communication partners were trained in how to keep talk as natural aspossible, to avoid being patronizing and to explicitly let the person know thathis or her competence was not in question. Partners were also trained toimprove the exchange of information. Results provided experimental supportfor the efficacy of communication partner training in improving the com-munication skills of conversation partners. Their brain-impaired partnersalso improved significantly, even though they did not receive specific training.

Communication partners of a range of participants with communicationproblems have taken part in training programmes. These include volunteerstalking with people with aphasia (Kagan et al., 2001; Lyon et al., 1997),nursing staff who were trained to use memory aids as an augmentativeand alternative communication device with people with Alzheimer’s disease(Bourgeois, Dijkstra, Burgio, & Allen-Burge, 2001; Burgio et al., 2000) andcaregivers who underwent communication training to facilitate communica-tion with people with Alzheimer’s disease (Ripich, Ziol, Fritsch, & Durand,1999). The type and amount of training has also varied across studies,ranging from 1-hour in-service training for nursing staff (Bourgeois et al.,2001), a one and a half day workshop format for volunteers (Kagan et al.,


2001), a 4-week training programme for nursing staff on memory book useand general communication skills (Burgio et al., 2000), a small group trainingformat where four carers of adults with aphasia attended 2-hour sessionsonce a week for 6 consecutive weeks (Booth & Perkins, 1999; Booth &Swabey, 1999), up to a 10-week training programme for volunteers (Worrall& Yiu, 2000). The length of training programmes for communication part-ners that is required for effective communication modification has not beenspecifically investigated to date.

Communication partner training in traumatic brain injury

In a similar vein to the work done in aphasia, training programmes are nowbeginning to emerge to help families and other care-givers deal with theongoing problems that can follow TBI (Carnevale, 1996; Holland & Shigaki,1998; Ylvisaker et al., 1993). Ylvisaker et al. (1993) describe the importanceof providing a positive communication culture within the rehabilitation con-text. They suggest that role-playing and modelling combined with ongoingcoaching and support in vivo are appropriate methods to facilitate communi-cation training for communication partners of people with TBI. Furtherwork is needed, however, to develop such training programmes to addressindividual communication profiles in collaboration with the family and peernetwork of the person with TBI. Importantly, there has been no descriptionof training programmes that may be appropriate for community groups whointeract with people with TBI. Thus, although community reintegration isfrequently suggested as the primary objective of TBI rehabilitation (Coelho,DeRuyter, & Stein, 1996; Ylvisaker, 1998), there are few documented caseswhere community agencies have been assisted to encourage more appropriateparticipation for these clients, and none where the efficacy of such anapproach has been demonstrated. This is despite the fact that there are now anumber of studies that have clearly documented the nature of social inter-action difficulties that commonly occur when people with TBI communicatein everyday settings.

Focus on the conversational partners of people with TBI

In any conversation, the person with communication difficulties representsonly one side of the interaction. The behaviour of their conversational part-ner is important; facilitating, or diminishing opportunities for the individualwith brain injury to continue the conversation in a successful manner. Indeed,it has been found that TBI individuals are often disadvantaged in interactionsbecause of the way their communication partners interact with them. Forexample, in a study of telephone conversations where TBI participantsrequested information from a range of communication partners, they wereasked for and were given less information than matched control participants(Togher, Hand, & Code, 1996, 1997a, 1997b). Therapists and mothers never

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asked people with TBI questions to which they did not already know theanswer. Additionally, TBI participants were more frequently questionedregarding the accuracy of their contributions, and contributions were fol-lowed up less often than matched control participants. Communicationpartners used patronizing comments, flat voice tone and slowed speechproduction when talking to people with TBI. This was in contrast to thecontrol interactions, where participants were asked for unknown information,encouraged to elaborate, did not have their contributions checked frequently,and had their contributions followed up.

Importantly, we found that communication can be improved by manipulat-ing the speaking situation for the person with TBI. For example, when peoplewith TBI were placed in a powerful information-giving role, such as a guestspeaker talking about the experience of having a serious injury, their com-munication approximated matched control participants (who had a spinalinjury) (Togher, 2000; Togher & Hand, 1998). Thus, when provided with afacilitative context such as an equal communicative opportunity, TBI partici-pants were primed to match the performance of control participants. Theseresults suggest that greater opportunities and increased conversational com-petence can be created for the person with TBI by specifically training theircommunication partner.

To examine the effect of training communication partners we developeda training programme for carers, which was piloted with a single case in2000 (Togher & Grant, 2001). We trained a paid attendant care-giver whosupported the daily activities of a 28-year-old man with TBI. The maincommunication problems reported separately by the care-giver and the per-son with TBI were keeping conversations going and staying on topic. Afteridentifying target speaking situations (e.g., lunch at the shopping centre), wetaught the structure of casual conversation (Ventola, 1979) in combinationwith the strategies of collaboration and elaboration (Ylvisaker, 1998). Pilotdata indicated that the care-giver improved his ability to facilitate communi-cation by using collaborative statements, explicitly acknowledging difficultyin the interaction, confirming his partner’s contribution and asking questionsin a supportive manner.

We expanded this approach by developing and evaluating a communication-training programme for police officers, as members of a service industry whoare likely to encounter people with TBI. We trained the police officers tomanage specific service encounters with people with TBI who they had notpreviously met. This was evaluated in a randomized controlled trial (Togher& Grant, 2001; Togher, McDonald, Code, & Grant, 2004). The TBI speakersrang the police to ask their advice both before and after the police had beentrained. Training resulted in more efficient, focused interactions. In otherwords, this study confirmed that training communication partners improvedthe competence of people with TBI. What is unknown is whether this approachis better than, or equal to, the efficacy of direct remediation work with theperson with TBI, or whether a combined approach is more effective still.


Measuring the interaction – the value of sociolinguistics

One of the problems in examining the interactions of people with TBI hasbeen finding sensitive measures that reflect the two-way nature of inter-actions. This was one of the driving forces in the early research Chris Codeand I completed in the mid-1990s; to find an alternative way to examineeveryday interactions. This led us to use sociolinguistic analyses to providenew insights into the communication of people with TBI (Togher, 2000;Togher & Hand, 1998; Togher et al., 1997a, 1997b), and became the basisfor a successful training programme for communication partners (Togheret al., 2004). This approach has been innovative in that it focuses on not onlythe speaker with TBI, but also the conversational behaviour of their speakingpartner.

We have found analytic frameworks based on Systemic FunctionalLinguistics (Halliday, 1994), specifically Generic Structure Potential (GSP),to be useful in measuring the interactions of people with TBI (Togher &Hand, 1999; Togher et al., 1997b) and in revealing areas of difficulty thatcan be targeted in remediation. GSP analysis examines oral texts as genre(Hasan, 1985). Genres in literary terms describe typical realizations of par-ticular types of texts. Some examples of genres include letters to the editor,appointment making and service encounters. In each of these, the contentvaries according to the activity (known as field) and the participants involved(known as tenor), however there is a common core of structural elements.There are a number of already established spoken genres, some of which arewell known to speech pathologists. These include narrative, recount, pro-cedure, exposition, discussion and casual conversation. All these genres canbe used to train communication partners to facilitate the interactions ofpeople with TBI. We chose the service encounter genre to train police officersin ways of dealing with people with TBI for a number of reasons. This highlystructured genre is familiar to most people, and has well-defined parameters.Once communication partners are aware of these parameters, it is easy forthem to identify deviations from the regular format and to respond accord-ingly. The service encounter genre has face and social validity, and was easilyapplied to the goal of measuring an everyday activity that contributes tocommunity reintegration. In broad terms, the service encounter genre wasfirst proposed by Hasan (1985) as shown in the table opposite.

This example represents a simple service encounter on the telephone.Telephone inquiries, however, are not always this straightforward. Someelements recur with more than one service request and a number of serviceinquiries before the interaction is completed (Eggins & Slade, 1997; Hasan,1985). Other features that may occur include a query by either participant iftheir communication partner has left the call (e.g., “Are you there?”) as wellas a statement of action (e.g., “I’ll just write that down”). The interactions ofpeople with TBI have previously been found to consist of other elements notaccounted for in traditional SFL analyses (Togher et al., 1997b). These

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include the aberrant moves of unrelated elements, incomplete or inappro-priate elements, and repetition of elements. This way of examining serviceencounter interactions has proved to be a sensitive measure of everydayinteractions as it differentiates TBI participants’ interactions from controlparticipants’ interactions.

As well as providing direction for the clinician in designing treatment forthe person with TBI, we have shown that it can be used successfully in train-ing communication partners. The police officers who underwent trainingquickly grasped the notion of an interaction being divided into chunks, andtherefore knew the expected structure of their service encounter interactions.In the case of a person with TBI deviating from this, the police officer couldthen use a range of conversational strategies to prompt the person with TBIback to the task, and therefore promote a productive, timely interaction.

Conclusion

Improving the communication of a person with TBI is neither straight-forward nor easy. Similar to treatment approaches for people with aphasia,therapy has traditionally focused on improving the person’s ability to get theirmessage across, usually to a clinician in a clinic room. There are a number ofproblems with this approach, however, including the fact that the most com-mon communication activity for people with brain injury, and for those whohave not had a brain injury, is social chat. This interactional task is difficult toreplicate in the clinical setting because of the power imbalance inherent in theclinical interaction, and the probable cultural and gender differences betweenthe clinician and the patient. A possible solution to this dilemma is to includeother communication partners in treatment, and to train them to facilitatethe person’s everyday interactions. One proven way to measure this processis generic structure potential analysis. Training communication partners is arelatively novel approach in the field of TBI, but offers a great deal of prom-ise in engaging the person with brain injury in a socially valid treatment

Generic structural element Example

GREETING A: Hello Optus AustraliaB: Hello

SERVICE REQUEST B: Could you tell me what the time is in London?SERVICE ENQUIRY A: Do you mean at the moment?

B: YesSERVICE COMPLIANCE A: Yes it’s 10AMCLOSE B: OK thanks very much, you’ve been very helpful

A: No problemA: Bye

GOODBYE B: Bye


process designed to improve social participation, community integration,quality of life and overall satisfaction. There is also potential for this approachto be adapted for use with communication partners of people with aphasia;an avenue that Chris Code and I hope to pursue in the future.

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19 The future of our knowledgeabout communicationimpairments following aright-hemisphere lesion

Yves Joanette, Maud Champagne-Lavau,Karima Kahlaoui andBernadette Ska

The question of the asymmetrical nature of the neurobiological bases ofhuman communication has been fascinating researchers for more than acentury. The initial step in this discovery revealed that, in right-handers, theessence of the cerebral representation of language was confined to the lefthemisphere. The second act was to come later in the twentieth century whensome clever clinical observations were reported by certain visionaries – suchas Eisenson (1962), Weinstein (1964) and Critchley (1962) – who raised thepossibility that a lesion to the right hemisphere might also interfere with someaspects of communicative abilities. Since that time, the fact has not beenchallenged: the right hemisphere undeniably contributes in some way to theability we have to communicate with others, and when the right hemisphere islesioned, this ability can be altered in various ways. The first book to capture,summarize and critique the different observations suggesting that the righthemisphere makes such a contribution to communicative abilities, as well asto a patient’s recovery after aphasia, was written by another visionary, Pro-fessor Chris Code. In 1987, Professor Code published a monograph entitledLanguage, aphasia and the right hemisphere. In that book, he provided aunique overview of the different sources of observations addressing the ques-tion of the right hemisphere’s participation in language. Although thesummary of these observations was in itself a first, Professor Code did notcontent himself with a synthesis of the then available knowledge. This bookalso makes unique theoretical statements and proposals about the nature ofthe right hemisphere’s contribution to language and communication, and thefuture studies needed to address these issues.

The goal of this chapter is twofold. First, 20 years after the publication ofProfessor Code’s monograph, a summary of current knowledge of the con-tribution the right hemisphere of right-handers makes to communicativeabilities is offered. Then, some future research directions are discussed withreference to those delineated by Professor Code in his 1987 monograph.

Current status of our knowledge of communication impairmentsafter a right-hemisphere lesion

The occurrence of a right-hemisphere (RH) lesion can interfere with com-municative abilities at different levels of human communication. Apart fromits impact on the processing of emotional prosody and aspects of linguisticprosody that require the processing of large time-scales (e.g., modalities) theimpact of an RH lesion is essentially semantic in the broadest sense of theterm. This includes the semantic processing of words and discourse, as well aspragmatics.

Semantic processing of words

The occurrence of an RH lesion can interfere with word production asRH-lesioned individuals may exhibit poorer performance on picture-namingtasks (Joanette & Brownell, 1990) and verbal fluency tasks (Cardebat, Doyon,Puel, Goulet, & Joanette, 1990; Goulet, Joanette, Sabourin, & Giroux, 1997;Joanette & Goulet, 1986; Koivisto & Laine, 1999). Studies have consistentlyshown that the verbal fluency of RH-lesioned individuals is impaired, mostlywhen the production criterion was semantic in nature as opposed to literal ororthographic. This result emphasizes the fact that the RH’s contribution tothe production of words has to do with word access in semantic memorymore than the production of their morphological or phonological form. Anumber of converging clues – including priming studies (Gagnon, Goulet, &Joanette, 1994) and time-course analyses of verbal fluency tasks (Joanette,Goulet, & Le Dorze, 1988) – suggest that this deficit does not reflect primarilyan impairment of the semantic representation itself, but rather a deficiencyaffecting access to the semantic representation, as is the case in aphasia. Oneaspect of verbal fluency impairment that has been suggested to be specific toRH-lesioned individuals is a certain tendency to produce words that are“unexpected,” that is, less prototypical of their semantic category (LeBlanc &Joanette, 1996). If this is confirmed, it would mean that a lesion to the RHnot only interferes with normal access to the lexicon, but also has a specificimpact on the nature of the activation of the semantic network, favoring theactivation of less central, more peripheral exemplars of a given semanticcategory.

A larger number of studies have addressed the nature of the impairmentRH-lesioned individuals exhibit when processing the meaning of words.Again, the quest for the specific nature of the semantic impairment followingan RH lesion is still ongoing. At this point, a number of potential candidateshave been raised:

• Impairments of the ability to process the metaphorical alternativemeaning of words (Brownell, Simpson, Bihrle, Potter, & Gardner, 1990;Gagnon, Goulet, Giroux, & Joanette, 2003): this feature was one of the

Communication impairments following a right-hemisphere lesion 285

first to be mentioned as a putative characteristic of an RH lesion. Thequestion regarding the exact nature of this deficit remains a matter ofdebate. Future studies should try to explore the impact of RH lesionswith reference to the depth/nature of the semantic activation of eachhemisphere. According to Beeman (1998) and Chiarello (1998), the righthemisphere sustains more shallow, less focal, coarser semantic dimen-sions of words. This proposal has direct consequences on the nature ofthe semantic impairments likely to follow an RH lesion that still need tobe investigated. However, a major loophole for the proponents of such aspecific impairment resides in the fact that, most of the time, the poly-semic words that appear to be most affected in RH-lesioned individualsare also those that are the most demanding in terms of cognitiveresources (Monetta & Joanette, 2001, 2003). Consequently, the specificityof such impairments still needs to be fully demonstrated in contrast to amore general impact of an RH lesion on the overall pool of cognitiveresources or access; in this context, an RH lesion would interfere withlanguage’s most complex dimensions.

• Other possible candidates for a specific impairment of word semanticsafter an RH lesion concern the nature of the semantic relationships to beaffected. Inspired by the initial proposal by Drew (1987), Nocentini,Goulet, Roberts, and Joanette (2001) provided only partial support forthe idea that an RH lesion may have more of an impact on inter- ratherthan intra-conceptual relationships. Even if it were confirmed, such a spe-cific constraint on the nature of the semantic relationships affected mightreflect a more general characteristic of impairments of semantic relation-ships after an RH lesion. For example, Burgess and Simpson (1988) andKoivisto (1997) suggest that the activation spreading in the semantic net-work supported by RH-based neural networks appears to operate over alarger time-scale, in more remote areas of the network, and on a smallernumber of nodes/items. If this is the case, then predictions could be maderegarding the specificity of the impact of an RH lesion on the nature ofthe resulting impairments of semantic relationships.

Semantic processing of discourse

Discourse production and comprehension require a set of cognitive contribu-tions that make it possible to extract/encode the important pieces of informa-tion in a narrative, for example, and to generate the relevant and necessarylinks/inferences that make it possible to grasp the gist of a story and itssituational model. An RH lesion can interfere with many of these levels.Typically, narrative discourse production after an RH lesion includes impov-erished informative content, a tendency to digress, unexpected shifts towardsa tangential topic, and some level of incoherence reflecting a lack of, orinadequate, relation markers. Discourse comprehension may be affected bythe difficulties RH-lesioned individuals have with making proper inferences,

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extracting the macro-structure of the narrative and, above all, revising thesituational model when required by the story (e.g., Delis, Wapner, Gardner, &Moses, 1983; Hough, 1990; Huber & Gleber, 1982; Schneiderman, Murasugi,& Saddy, 1991; Stemmer & Joanette, 1998).

Obviously, the RH’s contribution to discourse processing is not exclusive.Such a complex and high-level ability depends on numerous basic cognitiveabilities, including inference making, inhibition, cognitive flexibility, verbalworking memory, and so on. The reason why RH-lesioned individuals fre-quently appear to be impaired in their discourse abilities may reflect at leasttwo things. First, the presence of discourse impairments in RH-lesionedindividuals is not overshadowed by more basic syntactic or phonologicalimpairments, as it is in aphasia. Second, it could be the case that RH-basedneural networks are important for sustaining a number of cognitive processes(e.g., inference making) that are particularly critical for discourse processing.This possibility does not preclude the possibility, however, that left-hemi-sphere-based neural networks are also necessary for some other importantcognitive processes. Consequently, both left- and right-hemisphere lesionswould interfere with discourse abilities, though isolated discourse impair-ments would be more frequent following an RH lesion. The cognitive pro-cesses that are sustained more by the neural networks present in the rightrather than the left hemisphere still need to be identified.

Processing communicative intent: Pragmatics

The ability to encode or decode communicative intent is a very importantdimension of interpersonal communication. Indeed, in natural communica-tion it is frequently the case that not all the relevant information is provided,a situation referred to as non-literal language. Consequently, interlocutorsconstantly have to rely on their knowledge of the world, or on the immediatecontext, to fully process a speaker’s communicative intent. In doing so,human beings seem to stimulate interest in the act of communicating withothers, since providing each and every piece of information overtly tendsto make communication boring; this is the case when automated devicesattempt to offer pseudo-natural communicative environments (e.g., phoneanswering systems). In any case, ever since the first systematic descriptions ofcommunicative impairments following an RH lesion, it has been reportedthat RH-lesioned individuals display improper and/or unexpected communi-cation behavior when engaged in everyday natural communication (e.g.,Gardner, Brownell, Wapner, & Michelow, 1983). These deficits can best bedescribed as affecting the pragmatic dimension of communication. Deficitsaffecting many aspects of non-literal language have thus been reported, suchas indirect speech acts, humor, sarcasm, and the ability to take shared know-ledge into account (e.g., Chantraine, Joanette, & Ska, 1998; Foldi, 1987;Gardner, Ling, Flamm, & Silverman, 1975; Kaplan, Brownell, Jacobs, &Gardner, 1990; Stemmer, Giroux, & Joanette, 1994; Vanhalle, Lemieux,


Joubert, Goulet, Ska, & Joanette, 2000; Wapner, Hamby, & Gardner, 1981;Winner, Brownell, Happe, Blum, & Pincus, 1998).

The reasons why such a pragmatic deficit may occur following RH damageare still unclear. It is, however, quite clear that there is no such thing as aspecific “pragmatic cognitive module” that is impaired in those cases. Rather,an impairment of one or more known cognitive processes may result indifficulties processing the communicative intent. Thus, Champagne andJoanette (2004) suggest that the pragmatic deficit in RH-lesioned individualsis probably determined by some lack of inhibition, whereas similar pragmaticdeficits in schizophrenic individuals reflect a lack of mental flexibility. Hereagain, given the cognitive demand of pragmatic abilities, it might be the casethat part of the picture in RH-lesioned individuals is related to a lack ofcognitive resources or ability to access them. Cues favoring this possibilityhave been provided by Monetta and Joanette (2003), who showed that nor-mal young individuals given a pragmatic task in a limited resource context(dual task) exhibited patterns of performance similar to those frequentlyfound in RH-lesioned individuals. Consequently, at this level as at otherlevels, it is still not known whether an RH lesion has a specific or a non-specific impact on the ability to process the pragmatic aspects of languageand communication. The answer will probably reflect both possibilities, butthe underlying cognitive impairments have still to be identified (McDonald,2000).

Clinical management of individuals with communicativeimpairments following an RH lesion

The clinical management of individuals with communicative impairmentsfollowing an RH lesion is still a new field of practice for speech-languagepathologists and other members of interdisciplinary teams in acute orrehabilitation-oriented health centers. Though many recent articles on thesubject insist on the importance of such clinical management (e.g., Myers,1999; Tompkins, 1995), there is still a lack of clinical descriptions and ofevaluation tools and management strategies. Professor Chris Code himselfinsisted on the importance of this aspect in his 1987 monograph. Our group’sexperience in this respect has further convinced us of the relevance of suchclinical management, and the importance of providing those tools and strat-egies. One very important question has to do with the incidence and clinicalprofile of communicative impairments among individuals suffering from RHlesions. It has to be stressed that, as with left-hemisphere-lesioned individuals,not all RH-lesioned individuals suffer from communicative impairments.According to our studies, the proportion of individuals with RH lesions whoexhibit communicative impairments is between 50% and 80% (Côté, Payer,Giroux, & Joanette, 2006; Joanette, Goulet, & Daoust, 1991). Moreover,when present, these impairments do not always affect all the possible dimen-sions of communication described in the first part of this chapter. Indeed, not

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only do RH-lesioned individuals with communication impairments not allexhibit the same pattern of impairment, but there are double-dissociationswhereby different individuals exhibit patterns of clinical impairment that arethe reverse of each other (Joanette et al., 1991). These pieces of informationare crucial for the development of a clinical management strategy. Indeed, itfollows that RH-lesioned individuals suspected to exhibit communicationimpairments must be evaluated in order to describe the nature of the clinicalprofile in each case, as is the case for left-hemisphere-lesioned individualssuspected of having aphasia. The exact clinical description of the impaireddimensions of communication is extremely important in that it allows forcrucial counseling with the affected individual and his or her family members.Indeed, despite the fact that these communication impairments are the causeof a major communicative disability, they are poorly recognized by the familyand the individual himself or herself since they affect dimensions of com-munication that are themselves poorly recognized (e.g., discourse abilities,pragmatic abilities).

Since the publication of Professor Code’s book, a number of clinicalbatteries have been proposed in order to help clinicians to conduct such anevaluation. Most of these batteries, however, focus on the evaluation of cog-nitive impairments, such as neglect, which may accompany communicativeimpairments in RH-lesioned individuals. One of the most interesting batter-ies published in English to date is that of Bryan (1988). The proposed tasksaddress most of the aspects of communication that can be impaired after anRH lesion. More recently, our group has published such a battery in French(Joanette, Ska, & Côté, 2004), which incorporates the most recent theoreticaldevelopments in the field. Adaptations are being finalized in Portuguese,Spanish and Italian; an English version prepared with the collaboration ofLeonard LaPointe and his team will soon be available with norms.

Although the question of the evaluation of the communication impair-ments that can follow an RH lesion is starting to penetrate the field of speech-language pathology, that of rehabilitation strategies is still in its infancy. In arecent review, Moix and Côté (2004) report that only a small proportion ofspeech-language pathologists in rehabilitation centers in Québec engage insystematic rehabilitation strategies with individuals suffering from an RHcommunication impairment. Among the few who do, dissatisfaction is com-mon as there is no evidence-based practice in this area. Both Tompkins (1995)and Myers (1999) suggest some possible rehabilitation strategies, but the fieldremains to be investigated, and systematic observations are still required.

Future directions, now and then

In his 1987 monograph, Chris Code identified a number of areas in which itwas felt that the field of RH and language would evolve. Some of thesepredictions became reality, whereas a number of subsequent developmentshad not been predicted. The following is a selection of topics largely inspired


by the conclusion of the 1987 monograph, and discussed with reference tofuture directions as we currently perceive them.

The impact of interindividual differences

The presence of interindividual differences, which modulate the nature of theRH’s contribution to verbal communication in a given individual, was rightlypointed at by Professor Code in 1987. Since then, it has been demonstratedthat a number of factors can impact on the nature of the RH’s contribution.Apart from the classical factors linked to genetics (e.g., familial history ofleft-handedness) or to the nature of the exposure to language (e.g., character-istics of the spoken or written language), Professor Code already foresaw theimportance of aging. Indeed, it is now well known that age represents a factorthat significantly influences the nature of interhemispheric cooperation and,hence, the RH’s contribution to communication. Summarizing the literatureand his own personal observations, Roberto Cabeza (2002) introduced theHAROLD (Hemispheric Asymmetry Reduction in Older Adults) model,which essentially describes the presence of an age-related functional dedif-ferentiation in the respective contributions of the left and right hemispheresfor abilities such as working memory, episodic memory, and inhibition con-trol. Although Cabeza (2002) did not directly report data involving languagebehavior, the phenomenology described is presumed to be universal. In otherwords, the neural network subserving a given ability is more widespreadover both hemispheres in older adults. This appears to be true only whenbehavioral performance is maintained at a good level. Older adults withdecreased performance would not exhibit this pattern. If this phenomenon isalso found for components of communication with which the RH is involved,it would mean that the impact of an RH lesion could be expected to beproportionally greater in older adults. Recently, our group has provided pre-liminary data using language tasks that could force a reformulation of theHAROLD phenomenology for the neural bases of language. Indeed, usinga word semantic category judgment task, Ouellet-Plamondon, Monchi,Senhadji, and Joanette (2006) have shown that the reorganization of neuralactivations with age not only follows a hemispheric dedifferentiation trend,but also – and most markedly – evolves along an anterior–posterior axis. Inother words, in order to maintain performance with age, the neural networksnecessary for the semantic processing of words are much more posterior, andsomewhat more bilateral. Again, if this is confirmed, it would imply not onlythat RH lesions would be more frequently associated with word semanticimpairments with age, but that posterior lesions would probably have moreimpact than anterior ones. These predictions must, of course, be validated.However, one fact remains: as Professor Code predicted in 1987, age is afactor that probably influences the nature and extent of communicativeimpairments after an RH lesion.

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The nature of the right hemisphere’s contribution

Another comment in the conclusion of Professor Code’s 1987 monographhas to do with the basic question regarding the association between the righthemisphere and communication. As Professor Code rightly wrote (p. 169),“the question concerns the nature and the extent of that involvement,” andnot whether or not the RH does contribute to communication. In 1987,Professor Code stated that there was no satisfying answer to both aspects ofthe question; since then, the situation has certainly evolved, but not verymuch. There is still debate as to whether the RH’s contribution to communi-cation is in terms of specific basic cognitive processes that characterizeRH-based neural networks, within an interhemispheric cooperation model,or whether this contribution should be conceived more in terms of a sourceof possible quantitative addition to the pool of neural networks necessaryto process some of the more complex dimensions of communication. As isfrequently the case when the human mind tries to polarize the answer to acomplex question around two opposite points, the reality probably fallssomewhere in the middle; in other words, both mechanisms are probablyinvolved, with different representations according to specific components ofcommunication. For instance, as briefly alluded to earlier, the semantic repre-sentations in the brain’s neural networks that appear to be sustained on theright side of the brain tend to be characterized differently, both quantitativelyand qualitatively. There is sufficient convergence regarding what is sus-pected to be the nature of the semantic representations (shallow, less focal,coarse semantic representation; Beeman, 1998; Chiarello, 1998) as well as thespecific types of semantic relationships (e.g., interconceptual relationships;Drew, 1987; Nocentini et al., 2001) and the time-course of activation(Koivisto, 1997), to support the idea that the RH’s neural networks make aspecific contribution to the semantic processing of words, and maybe beyond.At the same time, there is also converging evidence at the word level(e.g., Monetta & Joanette, 2001, 2003) as well as at the pragmatic level (e.g.,Champagne & Joanette, 2004) to support the idea that the involvement of theRH’s neural networks could also be viewed as a general contribution to apool of cognitive resources needed to handle the most complex, demandingcomponents of communication. Consequently, we are still left with the samequestion that Professor Code raised 20 years ago, although a number ofconverging lines of evidence suggest that the RH’s contribution is bothqualitative and quantitative.

The advent of new methodologies and techniques

Without taking too much of a risk, Professor Code also predicted in his 1987work that future methodologies and techniques would contribute to dimin-ishing our uncertainty about the RH’s role in communication. He was, ofcourse, quite right. Over the last two decades, functional neuroimagery has


revolutionized the field of cognitive neuroscience of language. Many innova-tive techniques are now contributing to our knowledge of the extent andnature of the RH’s contribution to communication. Some of these tech-niques are especially good at spatial resolution and the identification of lociof activation (e.g., PET, fMRI); others contribute essentially to the time-lineof processing, given their temporal resolution (e.g., ERPs); while still othersappear to be able to contribute to both spatial and temporal resolution(MEG, Near Infrared Spectroscopy optical imaging or NIRS/OI). Each ofthese techniques has its limitations, and the quest for convergence is import-ant. Functional imaging initially provided converging evidence in favor of aspecific role for RH-based neural networks in the processing of metaphoricutterances (e.g., Bottini, Corcoran, Sterzi, & Schenone, 1994; Seger, Desmond,Glover, & Gabrieli, 2000; St. George, Kutas, Martinez, & Sereno, 1999).Contrary to Bottini and colleagues (1994), who reported right lateral tem-poral and frontal PET activation during the processing of metaphors, Rapp,Leube, Erb, Grodd, and Kircher (2004) conclude that the RH’s involvementmay be neither essential nor specific for metaphor understanding. LikeLee and Dapretto (2006), Rapp and colleagues (2004) suggested that theRH’s involvement in the processing of metaphorical language might reflectprimarily the increased complexity of non-literal language rather than an RHspecialization in metaphor comprehension.

In general, the contribution made by modern neuroimagery has beenlimited by the fact that many of the components of communication for whichthe RH is suspected to make a specific contribution are not particularly easyto study with these techniques. Indeed, discourse processing and pragmaticabilities have been much less studied than the processing of words or otherunitary events. Moreover, the setting in which data are acquired (e.g., thenoise and spatial constraints of fMRI) does not allow the use of naturalisticcontexts. Emerging techniques such as NIRS/OI already appear to be fillingthe gap between the spatial and temporal resolution needed, and the ability toallow for a noise-free, quasi physical-constraint-free setting compatible withmore naturalistic communication situations. For example, Scherer, Ska, andJoanette (2006) have been able to study narrative discourse abilities, trying todisentangle the nature of interhemispheric cooperation for distinct com-ponents such as the micro- and macro-propositional levels and the situationalmodel. Their results indicate that the RH’s contribution is optimal at themacro-propositional level and for the appreciation of a situational model. Itcan therefore be concluded that current neuroimaging techniques are con-tributing to identifying the nature and extent of the RH’s contribution tosemantic processing.

The introduction of new data acquisition techniques should not over-shadow the immense change that has already taken place in these techniques,which now allows us to address such fundamental questions as the role ofRH-based networks in global cerebral connectivity for a given communica-tive process or ability. Indeed, functional neuroimaging data can now be

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analyzed in such a way as to allow for the exploration of the functionalnetworks associated with a given ability or task. Those networks are referredto as having functional connectivity or effective connectivity, depending onwhether or not they include causality indications. The type of comple-mentary information they offer is crucial to our understanding of the integra-tion of RH-based neural networks within a more general brain functionalnetwork. For example, although it has been known for some time that RHactivation is reported when a subject is engaged in the semantic processingof words, it was only recently that evidence was provided of the integrationof the RH activations into a more general cerebral network involving bothright- and left-hemisphere-based areas (Walter, Jbabdi, Marrelec, Benali, &Joanette, 2006).

In sum, Professor Code (1987) was right in anticipating that new tech-niques and methodologies would help us understand the nature and theextent of the RH’s contribution to communication. Not only has thisoccurred over the last two decades, but it has allowed us to situate the ques-tion regarding the RH exactly where it should be, namely at the level of acontribution nested within a more general question regarding the nature ofinterhemispheric cooperation for the different components of cognition.

The unpredicted changes

Although it commands admiration and respect, Professor Code’s 1987monograph manifestly did not predict all the developments that haveoccurred since its publication. One of the unpredicted changes has to do withthe discussion concerning what constitutes a linguistic component of com-munication and what is extralinguistic [sic]. Indeed, since the first descriptionsby pioneers such as Eisenson in 1962, there has been a malaise affecting someof the concepts of language. Eisenson (1959), for example, used the conceptof super-ordinary aspects of language to refer to subtle word-processingimpairments for which he did not have the appropriate conceptual tools andtheoretical background to describe adequately. It should be kept in mind thatthe early 1960s were also the years when the first writings were published onwhat was to become pragmatics, including the concept of direct and indirectspeech acts (e.g., Austin, 1962; Searle, 1969). In the 1960s, language was stillconsidered to be limited to certain specific components, ranging from articu-lation to morphosyntactic processes. These components were more or lessthe same in the 1980s as they had been a century before, when the firstdescriptions of aphasia following a left-hemisphere lesion were introducedand crystallized in a number of classical aphasia syndromes. Professor Codein 1987 was therefore still largely influenced by this long-standing tradition,as the mutual relationships between components such as pragmatics andlanguage were not yet felt to be reconcilable. This is why he maintained theuse of concepts such as linguistic and extralinguistic, since the components oflanguage affected by an RH lesion were not part of the traditional definition


of language. The 1990s saw a proliferation of research on pragmatics and itsrelationship with language. In 1999, a special issue of Brain and Languagemade it obvious that nontraditional components such as pragmatics were notto be considered as being above, beside or apart from language; for instance,Gibbs (1999) considers pragmatics to be an inherent component of language.Even Noam Chomsky, whose opinion is reported by Stemmer (1999) in thesame special issue, states that “pragmatics must be a central component ofany theory of language that aims to be comprehensive.” Consequently, itmust be acknowledged that the concept of language has evolved somewhatsince the birth of aphasiology in the late nineteenth century; it now includes alarger set of cognitive processes that, together, make verbal communicationpossible. In this context, some of us (e.g., Joanette & Ansaldo, 1999, 2000)think that the evolution of the concept of language, which now encompassesall components typically affected following an RH lesion, requires a logicalextension of the concept of aphasia. Indeed, given that the universal defin-ition of aphasia refers to the notion of an acquired language impairmentfurther to an acquired brain lesion – whatever its etiology, nature or localiza-tion – it follows that acquired language impairments further to an RH lesionconstitute forms of aphasia that will have to be defined with reference to thecomponents of the revised concept of language. This will give the field ofspeech-language pathology further arguments to convince health service pro-viders to offer clinical management to individuals with such impairments.The challenge of evaluating and identifying adaptive and rehabilitation strat-egies is not a small one; clinical research will have to address these issues in anevidence-based practice manner. In our view, there are no arguments formaintaining the exclusion of RH-lesion communicative impairments fromthe concepts of language and aphasia, other than arguments based on an apriori excluding definition. Thus concepts such as extralinguistic appear to beuseless, as would be the introduction of equivalent concepts such as extra-magnesic or extra-agnosic to refer to recently introduced cognitive concepts inthe field of memory or perception. This development was not expected byProfessor Code in 1987, but will certainly find a receptive ear nowadays.

Conclusion

The role of the RH in everyday verbal communication and the impact of RHlesions on such abilities, were expertly summarized and predicted by ProfessorCode in his 1987 monograph. Professor Code delineated the future of the field20 years ago. His writings will remain an inspiration for a long time. In fact,the future lies partly in his inspired and perspicacious reflections and output.

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20 Progressive language andspeech disorders in dementia

Maria Pachalska

Introduction

Disturbances of speech and language, ranging from dysarthria throughaphasia to mutism, are a common feature of dementia, though often over-shadowed by other symptoms of mental deterioration. The symptoms are sodiverse and changeable, however, that very few unqualified statements can bemade. Some patients present symptoms that can be easily classified as phono-logical, semantic, or syntactic, while in other cases there are relatively non-specific communication breakdowns, perhaps related to other cognitive orbehavioral deficiencies (Kempler, 1995). The disturbances in verbal com-munication are sometimes mild, sometimes severe; they may appear late inthe course of the disease, or they may be the first presenting symptom ofdementia. This diversity results from a complex calculus, whose main factorsinclude the pathogenesis of the disease itself, the characteristics of the speechand language behavior of the affected individual prior to onset, and thecognitive reserves available to cope with and compensate for the loss ofspeech and language functions (Stern, 2002). Moreover, by the end stages, asthe disease progresses, these and other distinctions (even the differencesbetween “cortical” and “subcortical” dementias) are gradually wiped outas the deterioration (both structural and functional) becomes increasinglyglobal. The beginning point and initial course of each dementive illness isrelatively specific, but they all converge to a common end point.

For a variety of reasons, speech and language has tended to be at best asecond-order concern in the study of dementia, while dementia remaineduntil fairly recently an area of only secondary interest for aphasiology(Harciarek & Jodzio, 2005; Ross, Cummings, & Benson, 1990). Nevertheless,the negative impact of these disturbances on the quality of life of dementedindividuals is in many cases far greater than might be indicated by the relativepaucity of scientific literature on the topic. Moreover, the complex patternsof speech and language decay in dementia, though often difficult to interpret,provide invaluable insights, not only into the relation between neuronal struc-tures and language, but also into the relationship of language to otherdomains of cognition and behavior.

Regardless of the specific etiology of dementia in a given case, the cognitivedeficits that define dementia typically result from atrophy of brain tissue anda consequent decline in mental efficiency. The course of dementia (i.e., howrapidly this decline occurs, and what cognitive, affective, and behavioralsymptoms occur in what order) depends in each case on the nature of thetissue destruction caused by the basic pathomechanism, the point at whichthe degenerative process begins, and the general direction in which it spreads,not to mention the patient’s premorbid intelligence, habits, and predisposi-tions. At the cellular level, each disease is accompanied by particular, pathog-nomonic neuropathological signs, but the clinical picture in vivo is seldomclear-cut, especially since neuroimaging techniques rarely give an unequivo-cal answer to the basic nosological questions. Though the search for non-invasive tests based on biological markers continues (Leszek, Malyszczak,Janicka, Kiejna, & Wiak, 2003), at present a definitive diagnosis of almost alldementive illnesses is only made possible by neuropathological resultsshowing the characteristic cellular features of a given disease. The clinicaldiagnosis is always at best a reasonable inference awaiting neuropathologicalconfirmation.

There do exist, however, identifiable neuropsychological syndromes ofdementia that have been found to correlate at least roughly with particulardementive illnesses. For example, “Dementia of the Alzheimer’s type” (DAT)is characterized by the insidious onset of problems with working memoryappearing after age 55, often followed by depressive symptoms and confu-sion, then gradual loss of other memory domains and a general cognitivedecline, with language disturbances and other neurological signs appearingrelatively late. A diagnosis of DAT gives roughly 75% confidence that thepatient actually has Alzheimer’s disease (AD) in the neuropathological sense.Thus the neuropsychological diagnosis describes a clinical syndrome ofdementia bearing certain characteristic features, not unrelated to the ultimateneuropathological diagnosis, but in an important sense independent of it. Forexample, a post mortem neuropathological finding that the patient did nothave the amyloid plaques and neurofibrillary tangles characteristic of ADdoes not mean that the neuropsychological diagnosis of DAT was in error,but only that the neuropathology underlying the observed symptoms provedto be something other than AD.

In order to keep the discussion within reasonable limits, only four demen-tive syndromes will be described here:

• dementia of the Alzheimer’s type (DAT);• fronto-temporal dementia (FTD);• Creutzfeldt-Jakob disease (CJD);• the MELAS syndrome.

Each of these descriptions will be supported by a brief case study, drawnfrom the author’s own clinical material.

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Alzheimer’s dementia (DAT)

Though there are several different schemes of staging in DAT, for the presentpurposes it is most convenient to speak simply of an early phase, a middlephase, and a late phase (Gustafson, Elfgren, & Passant, 2004). The earlyphase is usually pre-clinical, with loss of short-term memory attended byconfusion, which becomes increasingly troublesome until it finally promptsthe patient (or the family) to seek medical attention. The late phase is virtu-ally complete loss of logical contact, accompanied by increasingly severeneurological disorders and terminating in death. What we are calling the“middle phase,” then, is not so much a clearly delineated stage as a series oftransitions that lead from the early (pre-clinical) stage to the late (terminal)stage.

Aphasia usually appears relatively late in the course of DAT. In the clas-sical presentation, speech remains largely unaffected until the transition fromthe middle stage to the late stage, when aphasia joins other neurologicalsymptoms, including motor problems. However, even in early DAT, althoughordinary conversation may seem unaffected, patients often have more word-finding problems than do healthy elderly, and typically show below-normalscores in verbal fluency (Cerhan, Ivnik, Smith, Tangalos, Petersen, & Boeve,2002; Harciarek & Jodzio, 2005). The task of naming as many animals aspossible in one minute is usually easier for DAT patients than the task oflisting words that begin with a certain letter, and shifting from the one task tothe other almost always produces perseveration of the first task into thesecond.

The steady cognitive decline of the middle-stage AD patient is accompaniedby impoverished vocabulary, leading to increasingly severe word-findingproblems and ending in the organic mutism of the late stage. Automatismsand meta-linguistic comments occupy an increasing amount of the patient’sdiscourse. At the same, the mental confusion typical of AD at this stage leadsto apparently nonsensical utterances that begin to take on the features ofaphasic jargon (Mendez & Cummings, 2003). Some authors (Gates, Beiser,Rees, D’Agostino, & Wolf, 2002) have compared the typical picture at thisstage to transcortical sensory aphasia. A characteristic feature is logoclonia:that is, the tendency to overuse a particular word, substituting it for a numberof different target words.

Case study: JG

This patient, a right-handed Polish female, age 67 at first contact, wasreferred for neuropsychological testing by her family, whose concern wasaroused when on several different occasions she seemed to become com-pletely lost in her own neighborhood, unable to find her way home when shewas only a block away from her home of 20 years. Since she had recentlyexperienced the loss of her younger brother, the family at first attributed the

Progressive language and speech disorders in dementia 301

problems to emotional stress, and indeed the first diagnostic task (often adifficult one in early DAT, see Dierckx, Ponjaert-Kristoffersen, Verté, & DeRaedt, 2004) was to differentiate between depression and dementia. The pos-sibility that JG was suffering from depression rather than a neurodegenera-tive disease was made more likely by the fact that her score on the MiniMental State Examination (MMSE) in the first test was at the low end ofnormal. On her first attempt to draw a clock face (a widely used screening testfor dementia) she drew a circle with marks at 12:00, 3:00, 6:00 and 9:00, butthen the examiner noticed that she was looking at a clock on the kitchencounter (she was first examined at her home). When the clock test wasrepeated 30 minutes later and the clock was removed from her line of sight,she drew the clock face correctly, but when asked to show “3:05,” she drewfour different hands (none in the right place), then expressed frustration thatshe “couldn’t make it come out right” (see Figure 20.1).

Her conversation seemed normal and her mood actually improved con-siderably during the first examination session. The Frenchay Aphasia Screen-ing Test did not indicate aphasia. However, on the Boston Naming Test(BNT; Kaplan, Goodglass, & Weintraub, 1983) she showed a sub-normalscore (45/60 items properly named), and prompting (whether semantic orverbal) did not help her recover the names of objects she could not remember.In some cases, she indicated by periphrasis or gesture that she knew what the

Figure 20.1 Clock faces drawn by JG over the course of her illness: (A)first examination, May 2005, (B) June 2005, (C) August 2005, (D)September 2005 (one month before her death).

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object was but could not think of its name. However, she called many of theanimals simply “animal,” and all the vegetables or fruits were “onions” (thefirst vegetable encountered on the Polish version of the BNT). When herattention was called to this after the test, she complained that she could notsee (when later examined by an ophthalmologist, no abnormalities werefound apart from a mild myopia, corrected by eyeglasses). On the test ofverbal fluency, she did not reach norms in either task (category or initialletter), but her performance in the “words that begin with P” task was muchworse (see Henry, Crawford, & Phillips, 2004). Significantly, she fretted thatshe could not think of the names of any animals (the first, “category” task)that begin with P, and even after being reminded several times that the wordsdid not have to be the names of animals, she clung to this restriction andcould think of only two, which she repeated over and over.

When re-examined a month later, her mood was generally improved, andshe remembered the examiners from the first meeting. However, her perform-ance on the MMSE was now much worse (19), and all cognitive parameterswere likewise reduced; her clock drawing was noticeably disturbed (see Figure20.1B). For the present purposes, however, most important is the fact that,although her score on the Frenchay Aphasia Screening Test was still withinthe normal range, conversation had become more difficult. She often leftsentences unfinished or expressed herself so vaguely that it was not alwayspossible to ascertain what she meant to say. The family likewise complainedthat it was becoming increasingly difficult to follow her meaning. When ques-tioned as to her meaning she became flustered and occasionally expressedannoyance, sometime at her own inability to say what she wanted to say,sometimes at the obtuseness of the interlocutor, who in her opinion ought toknow what she meant.

By the next monthly examination, the score on the Frenchay AphasiaScreening Test was now in the subnormal range (the task of identifying itemson the “bridge” picture from that test now seemed entirely beyond her ca-pabilities). There was now slight dysarthria (slurring), as well as logoclonia;during the Boston Naming Test almost half the prompts were now called“onions,” and the word “onion” recurred in her conversation as well. Hermood was generally good, but she was often confused and was unable to staywith even simple tasks, though she tried hard to concentrate and was eager toplease. Her writing was more agrammatic than her speech, with letter distor-tions and a general inability to maintain an even line. Her clock drawing nowbore little resemblance to a clock (see Figure 20.1C).

By six months after the first examination, her speech was nearly incompre-hensible (see Ball, Code, Tree, Dawe, & Kay, 2004). Logical contact wasfleeting and most standard neuropsychological tests had become difficult orimpossible to administer. When asked to draw a clock, she made only a seriesof strokes, which she did not stop making until the paper was taken from her(see Figure 20.1D). By 8 months she required hospitalization, and after 6weeks of steady deterioration she died. A post mortem neuropathological


examination found the amyloid plaques and neurofibrillary tangles character-istic of Alzheimer’s disease.

The relatively rapid progress of the disease in this case, dramaticallydocumented by Figure 20.1, is unusual for AD and requires some comment.Clinicians have long noted that AD tends to have a more severe course inpersons of above-average intelligence (JG was a teacher, known before herillness for her wit and tendency to take a lively interest in things). It is nowsuggested by some authors (Stern, 2002; Stern, Zarahn, Hilton, Flynn,DeLaPaz, & Rakitin, 2003) that the reason for this counterintuitive phenom-enon is that these patients, due to their high level of cognitive reserves, oftendo not show any clinical symptoms of illness until the disease progress is welladvanced.

Fronto-temporal dementia

In fronto-temporal dementia (FTD), personality changes (consistent withthe well-known picture of “frontal syndrome”) usually play a much moreimportant role than specific cognitive deficits (Borkowska & Sobow, 2005;Mendez & Cummings, 2003; Pasquier & Delacourte, 1998). The diagnosisof FTD is most often based on the Lund and Manchester clinical criteria(Lund and Manchester Groups, 1994), combined with a neuroradiologicalfinding of frontotemporal atrophy consistent with corticobasal degeneration(Boccardi et al., 2002, 2003; Miller, Boone, Mishkin, Schwartz, Koras, &Kushii, 1998; Varma et al., 2002). Among the most important diagnosticcriteria listed by the Lund and Manchester study (Gustafson et al., 2004) arethe following:

• insidious onset with slow progression;• early loss of insight;• early signs of disinhibition and impulsivity;• loss of mental flexibility (inability to adjust to changes of plans or

circumstances);• stereotyped, perseverative behavior (motor and verbal);• utilization behavior (a tendency to pick up and manipulate all objects

lying within arm’s reach);• hyperorality (frequently manifested in compulsive eating and drinking);• difficulty in staying focused on the task at hand.

Nevertheless, every one of these criteria has been challenged in the literature,especially since the difference between the clinical picture of FTD and that ofDAT or other dementias may be more the timing (i.e., when the given symp-tom appears) than the specific symptomatology (Harciarek & Jodzio, 2005).Thus the disputes between “lumpers” and “splitters” rage on to the present(Kertesz, 2005). For the present purposes, however, it is not essential to sortout the “alphabet soup” of proposed nosological entities that may or may not

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fall within the general category of FTD. It is surely safe to say that, since theneuronal loss associated with fronto-temporal lobar degeneration and itsmany variants causing FTD often occurs in areas critical for speech andlanguage, aphasia symptoms tend to appear earlier in the frontal-temporaldementias than in DAT, and not infrequently constitute the first presentingsymptom (Knopman, Mastri, Frey, Sung, & Rustan, 1990; Neary, Snowden,Northen, & Goulding, 1998; Snowden & Neary, 1993).

Aphasia often begins with the loss of verbal spontaneity (the family com-plains that the patient has grown taciturn and uncommunicative), whichnot surprisingly is accompanied by diminished verbal fluency in neuro-psychological testing, particularly when the task involves listing words thatbegin with the same letter (Kertesz, 2003). There are frequent stereotypedcomments and a marked tendency to repeat a limited number of stockphrases, not always relevant to the context in which they are used (see Code,1997 for a comparison to the repetition of stock phrases in popular music).The combination of palilalia (repeating the same word over and over), echo-lalia (repeating the conversation partner’s last words before beginning one’sown utterance; see Lebrun, 2003), late mutism and amimia (loss of spon-taneous mimicry), known as the PEMA syndrome (Guiraud, 1956), is typicalof FTD; logoclonia, however, is rare. A particularly salient feature of aphasiain FTD is difficulty in understanding sentence structure (Grossman, Rhee, &Moore, 2005).

In some such cases, the development of further symptoms of dementiamay be delayed, sometimes for many years, in which case we speak of “Pri-mary Progressive Aphasia” (PPA), though the term itself and the relation ofthis syndrome to FTD remain controversial (Knibb & Hodges, 2005; Selnes& Harciarek, 2005). Already in the nineteenth century Arnold Pick hadpointed out that progressive atrophy in the frontal and temporal lobes evokeda constellation of symptoms that included personality change and dysphasia(Kertesz, 1998b; Selnes & Harciarek, 2005), but Mesulam (1982) was the firstmodern author to demonstrate the existence of a syndrome of aphasia devel-oping slowly in the absence of other symptoms of dementia or neurologicalsigns. Luzzatti and Poeck (1991), Kempler (1995), and Mesulam (2001) thusidentify the most common clinical features of PPA as follows:

• a non-fluent aphasia with hesitant, dysprosodic speech, phonemic para-phasias, and impaired syntax;

• poor repetition;• generally preserved comprehension;• normal or near-normal performance on tests of other cognitive

functions.

Another variant of FTD that has a noticeable and early effect on speechand language is semantic dementia. Hodges, Patterson, Oxbury, and Funnell(1992; see Garrard & Hodges, 1999) described the insidious onset and


progressive breakdown of semantic knowledge, which affects not only lan-guage, but also memory, general knowledge, and object recognition. Theresult is usually a fluent aphasia, involving anomia with circumlocution andsemantic paraphasia, single-word comprehension deficits, and reduced cat-egory fluency, typically accompanied by visual agnosia and other symptomsof a generalized inability to abstract conceptual meaning from concrete signsand symbols (Knibb & Hodges, 2005).

In recent years the term Pick’s complex (Ioannides, Karacostas, Hatzipan-tazi, & Ioannis, 2005; Kertesz, 1998a) has come into use to denote thesignificant clinical and pathological overlapping between primary progres-sive aphasia, frontal lobe dementia and corticobasal degeneration. Kertesz(2005) argues that despite the diversity of the clinical picture, FTD is a clin-ical syndrome, within which one can further specify variants, including abehavioral variety with features of frontal syndrome, progressive aphasia,semantic dementia, corticobasal degeneration and progressive supranuclearpalsy (PNP, also known as Steele-Richardson-Olszewski syndrome).

Case study: ZE

This patient, a right-handed Polish female, was 72 years old at the momentwhen the first symptoms appeared. ZE was a prominent professor of medi-cine, a cardiosurgeon of international stature in her field of specialization,who spoke several languages fluently enough to lecture around the world. Shehad always been remarkable not only for her high professional and scientificqualifications, but also for her warm and outgoing personality. Her home hadalways been an international “salon” of sorts, and her dinners for speciallyinvited guests were once legendary in Cracow. She had always enjoyedremarkably good health until the spring of 1999, when she noticed that shewas more and more often forgetting daily tasks and leaving personal objectsin unlikely places. Since her mother had died of Alzheimer’s disease severalyears earlier, ZE was alarmed by this and reported it to her family, but no onefelt that the problems were sufficiently severe to merit attention. Later, shebegan to have sudden, unmotivated (and highly uncharacteristic) outburstsof rage, but again, her friends and family interpreted these incidents as theresult of stress and fatigue associated with her busy professional calendar(which despite her nominal retirement would have exhausted someone halfher age). She herself attributed her emotional lability to her latent fear of AD.

The first neurological symptoms appeared in late 2001, when her gaitslowed and became ataxic, so that she had several falls (early falls are con-sidered a sign of progressive supranuclear palsy; see Litvan et al., 1996). Sincethe earlier behavioral symptoms were not taken seriously, and ZE developed,in addition to the motor symptoms, a Parkinsonian “mask,” she was initiallydiagnosed with Parkinson’s disease. However, dopaminergic treatment provedcompletely ineffective and even counterproductive (another sign of PSP).The final piece of the puzzle fell into place in May of 2002, when during

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neuropsychological testing the present author observed that EZ was unableto look upward or downward without moving her head (“vertical ophthal-moplegia” is virtually pathognomonic for PSP).

Neuropsychological testing showed:

• progressive subcortical dementia, with difficulty in planning activities,reduced criticism, impaired working memory, dysexecutive syndrome,and personality changes;

• disturbances in spatial orientation;• limb apraxia;• verbal and motor perseverations;• constructional apraxia.

The speech and language disturbances presented by ZE (with the exceptionof slowed speech tempo and slight, barely noticeable slurring, consistent withhypokinetic dysarthria; see Darley, Aronson, & Brown, 1975), accompaniedby dysphagia, appeared considerably later than the motor symptoms. Therewas also dysgraphia, manifested in distortion of letter shapes and difficultykeeping the written text on the lines of the paper. Later she began to makeorthographical errors. The progress of dysgraphia is illustrated by Figure 20.2.

Until very late in the progress of the disease ZE had no pathological scoreson any aphasia tests, though it was noticed that, in comparison to her pre-morbid speech habits, her lexicon was distinctly impoverished. She becamemarkedly less spontaneous, often smiling and nodding instead of speaking,even in response to a direct question. She seemed at that point to be movingin the direction of Luria’s “dynamic aphasia” (Esmonde, Giles, Xuereb, &Hodges, 1996; Luria, 1977), characterized by markedly diminished verbaloutput with relatively few patent errors.

One of the most salient features of ZE’s speech at this stage was an increas-ing tendency to fall into various forms of pathological repetition, a commonfeature of both PSP (Lebrun, Devreux, & Rousseau, 1986) and Parkinson’sdisease (Benke, Hohenstein, Poewe, & Butterworth, 2000). Initially, ZE inconversation often repeated the question she had just been asked beforeanswering it, as though wanting to be sure that she had understood itcorrectly. For example:

Examiner: What time is it?ZE: What time is it? Oh, ten o’clock.

Over time this habit developed into echolalia, and the repetition of theinterlocutor’s speech was less and less often motivated or followed by anappropriate response, as follows:

Examiner: It’s very cold today.ZE: It’s very cold today. Yes, it’s very cold.


Later, she also developed palilalia, first involving the repetition of words,then syllables, then single phonemes, rendering it difficult to determine asharp boundary between palilalia and stuttering (Lebrun, 2003). Unlike typ-ical stuttering, however, she most often repeated the last syllable or phonemeof a word she was trying to use, rather than the first.

It is of particular interest to note that until a relatively late stage in herillness ZE was not only able to converse in English, but in fact showed less

Figure 20.2 Writing samples from patient ZE in October (A), November (B) andDecember (C) 2002. The prompt text was identical in each case.

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dysarthria and echolalia in this language than in her native Polish. Sheenjoyed speaking English and often spontaneously shifted languages duringtesting. However, as the disease progressed she fell into a global aphasia andultimately ceased to display any verbal behavior at all.

Creutzfeldt-Jakob disease

Although Creutzfeldt-Jakob disease (CJD) was first described in the early1920s (Creutzfeldt, 1920; Jakob, 1921), it was not until the 1990s that StanleyPrusiner discovered the basic pathogen of this disease: a “contagious protein”for which he coined the term “prion.” In the present state of our knowledge,however, the process by which prions lead to spongiform encephalopathy(SE) can only be sketched in outline. Prions originate from the protein knownas PrP, genetically coded by the PRNP gene in the human chromosome.Normal PrP molecules (designated PrPC) are distributed primarily in thecentral nervous system, but their exact function remains unknown (Büeleret al., 1992; Mastrianni & Roos, 2000). When pathogenic prions (designatedPrPSc) are introduced into the nervous system, they adhere to healthy PrPCmolecules and transform them into pathogenic PrPSc, the accumulation ofwhich in the central nervous system leads to neuron death and spongiformencephalopathy. A phenotypically diverse family of prion diseases is known,among which BSE (bovine spongiform encephalopathy, the famous “madcow disease”) has attracted much attention in the popular press in recentyears. The appearance of BSE in England and the later appearance of apreviously unknown variant of CJD among younger patients (the previouslyknown spontaneous variants were not known to appear before age 60) ledto the conjecture that the new variant (nvCJD) was simply BSE transmittedto humans through the consumption of prion-contaminated beef products.As is often the case, the popular press has largely forgotten about CJD inrecent years, in part due to the effectiveness of the rather dramatic counter-measures taken to prevent the further spread of BSE, since it does notappear that prions can be transmitted from human to human (Mastrianni &Roos, 2000).

By far the rarest form of CJD is the Heidenhain variant (HvCJD), in whichvision disturbances are the first presenting symptoms (Heidenhain, 1929).These patients typically present at an early stage with hemianopsia, notaccompanied by pyramidal symptoms or lesion detectable by neuroimaging(Brazis, Lee, Graff-Radford, Desai, & Eggenberger, 2000), followed by pro-gressive metamorphopsia (Kropp et al., 1999), visual hallucinations anddiminished visual acuity, culminating in cortical blindness without remarkableocular pathology.

The characteristic feature of dementia in Creutzfeldt-Jakob disease is itsrapid progression, with death most often occurring from 6 to 18 months afterthe first clinical symptoms are noticed. Ataxia, myoclonus, and hyperkinesiaare common. Ironically enough, this dramatic course may well result from the


extremely long incubation period of prion diseases (from 8 to 15 years),since the conformation of normal PrPC to the pathogenic PrPSc beginsvery slowly but proceeds logarithmically, so that by the time clinical symp-toms appear the patient is already well advanced. The transition from aclinical status similar to “early” AD to a status almost identical to “late”AD may take only a few months, or even a few weeks. When the diseaseprocess hits the period of acceleration, speech and language may changefrom normal to organic mutism in a matter of a few weeks (Hillis & Selnes,1999). This is not a sudden change, however, as in a post-stroke aphasia, butrather a series of accelerating transitions. Various aphasic syndromes mayappear for a day or two before they give way to another, more profoundsyndrome.

Case study: JR

The patient, a right-handed Polish female, was 68 years old at onset,widowed, with no family history of neurological illnesses and generally ingood health. She very seldom ate beef, but as a young woman she had exten-sive close contact at work with animal byproducts (including bovine) andchemical agents of various kinds.

In July of 2000, her writing began to show orthographical errors (rare inPolish), perseveration and disorganization, but JR successfully hid the prob-lem and the family did not notice. Only later, when looking over her papers, aprogressive dysgraphia was noticed in her monthly accounts (see Figure 20.3).

In mid-September 2000 she sought medical attention when she began toexperience vision disorders, ophthalmologically diagnosed as hemianopsia,without pyramidal symptoms. By early October she had lost all senseof visual perspective, and the visual images also began to be seriously dis-torted, as micropsia and macropsia turned into metamorphopsia. She alsomanifested hypersensitivity to bright colors, especially red.

Figure 20.3 JR’s monthly budget from October (A) and November (B) 2000 (used bypermission of the patient’s family).

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Systematic neuropsychological testing began in early October. The patientinitially had normal scores on the Western Aphasia Battery–Revised (WAB-R; Kertesz & Poole, 1974), for both the Cortical Quotient and the AphasiaQuotient; however, she showed a low-normal score on the BNT. She haddifficulties with simple arithmetical operations and was unable to completeall but the very simplest block pattern tests in the Wechsler Adult IntelligenceScale–Revised (Wechsler, 1981). Delayed verbal and visual recall were belownormal for her age group on the Wechsler Memory Scale–Revised (WMS-R;Wechsler, 1986). On selected subtests from the Cracow Right HemisphereDiagnostic Battery (Pachalska & MacQueen, 1998) her scores were border-line for agnosia, constructive apraxia, and dyspragmatism. There was alsoslight left-sided hemispatial neglect.

In early October she reported seeing black spots before her eyes; by lateOctober she was seeing the black spots as insects climbing the walls. She wasstill aware, however, that these were hallucinations.

In mid-November she was hospitalized in the Department of Neurology atthe Ministerial Hospital of the Polish Ministry of Internal Affairs andAdministration (MSWiA) in Cracow. She never left the hospital again. Herdifficulties with naming increased considerably, and in conversation shetended to ramble. An MRI performed after admission showed numerous,dispersed changes characteristic of spongiform encephalopathy (Pachalska,Kurzbauer, MacQueen, Forminska-Kapuscik, & Herman-Sucharska, 2003).By mid-December JR had ceased to be critical of her hallucinations, andoften fell into panic when the “big black bugs” began to crawl over her foodand her body. She now showed aphasia on the WAB-R, and verbal contactwith the examiners began to be difficult. When actively hallucinating she wasdisoriented and unresponsive. The tempo of mental and physical deterior-ation began to accelerate in late December and early January. Neuro-psychological testing was possible for the last time in mid-January. By thistime her verbal output was scarce and barely audible. She showed severe left-sided neglect in a figure cancellation task (the test had to be specially adaptedto use large figures entirely in red, the only color to which she still reacted). Bythis time laboratory tests had confirmed the presence of protein 14–3–3 inJR’s cerebrospinal fluid, a highly sensitive (but unfortunately not highly spe-cific) test for CJD.

By late January 2001 logical and verbal contact was irreversibly lost.Myoclonus and hyperkinesia (common features of CJD) had become verypronounced and nearly constant. An ophthalmological examination con-firmed cortical blindness. Although it seemed at this point that death wasimminent, she lingered for 16 months, never regaining consciousness. Anautopsy confirmed spongiform encephalopathy without any of the neuro-pathological features characteristic of other dementive illnesses. In viewof these results, along with the prominence and early appearance of visionproblems, JR was diagnosed with the Heidenhain variant of CJD (Kroppet al., 1999).


For the present purposes, the most salient features of this case are thefollowing:

• early appearance of agraphia (initially not detected by the family), whichmay well be related to the specific features of the Heidenhain variant ofCJD;

• the process by which metaphors (black spots that “look like bugs”)concretized into visual hallucination (“bugs” crawling on the wall; seePachalska, Kurzbauer, & MacQueen, 2002);

• the rapid but not sudden deterioration of linguistic competence (Hillis &Selnes, 1999) when the disease progressed to the crisis point.

The MELAS syndrome

MELAS (an abbreviation for mitochondrial encephalopathy, lactic acidosis,and stroke-like episodes) is a relatively rare disease, though in reality it maybe more common than the available statistics would indicate. Because of theconsiderable difficulties involved in establishing a diagnosis, MELAS is oftenmistaken for a range of other neurological disorders.

The course of this mitochrondrial cytopathy is remarkable for the combin-ation of a steadily progressive dementia punctuated by the sudden appear-ance and equally sudden disappearance of acute neurological symptoms(caused by the so-called “stroke-like episodes”). It is not at all uncommon forMELAS patients to be admitted to the emergency room with every neuro-logical indication of an ischemic stroke, and then to be discharged a few dayslater with no apparent deficits.

The basic pathomechanism of MELAS is an energy deficiency on the cellu-lar level, caused by insufficient output from the mitochondria, which triggersa shift to anaerobic respiration and lactic acidosis. In the brain, the repeatedmitochondrial crises over time produce spongiform encephalopathy, whichmay be concentrated in one or several regions (appearing as a hypodenselesion in neuroradiological testing), or may affect the entire brain more or lessevenly (visible in CT scans or MRI as generalized atrophy). Each stroke-likeepisode produces mostly transient effects, but the cumulative effect is neuronloss and atrophy.

Unlike the other dementive illnesses presented here, MELAS is not primar-ily or even commonly a disease of the elderly. A normal childhood is typical,with the first symptoms usually appearing between puberty and young adult-hood. The first episode is often triggered by psychological stress or an other-wise unrelated illness (e.g., flu) that increases the body’s energy demands,which the inefficient mitochondria cannot meet. The combination of periodicacute episodes against the background of slowly progressive atrophy gives acomplex neuropsychological picture, characterized by a combination of“stroke-like” and “dementia-like” features, not always consistent with eachother (Pachalska & MacQueen, 2002).

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Case study: KS

KS, a right-handed Polish female, was born in 1978 without perinatal com-plications, and her psychomotor development was fully normal to age 15.Her mother is of unusually short stature and suffers from migraine head-aches, a typical pattern in MELAS families (DiMauro, personal information),since the mutation is likely to have been present over several generations, withearlier and more severe symptoms in each successive generation. She wasan outstanding student in secondary school, gregarious and popular. Therewas no history of substance abuse or promiscuity. At the age of 16, she beganto experience an array of apparently inexplicable, continually worsening“attacks”: acute headaches, weakness (exercise intolerance), nausea andvomiting, and periodic fevers without apparent cause reaching 40°C. Whilepreparing for her final examinations in her last year of secondary school, shehad a neurological episode now recognized as having been a stroke-like epi-sode, resulting in transient hemianopsia, moderate non-fluent aphasia andmild left hemiparesis, followed by vision and hearing disturbances and cogni-tive dysfunctions. An MRI revealed changes, not of vascular origin, in theright posterior parietal and occipital lobes, and in the left hemisphere of thecerebellum. In 1998, during the first of four lengthy stays under the presentauthor’s care at the Cracow Rehabilitation Center, the clinical diagnosis ofMELAS was advanced, since the patient exhibited all the clinical signs andsymptoms, including lactic acidosis. At the same time, intensive genetictesting was begun at Columbia University, which bore fruit in mid-2000with the discovery of a novel mutation (C8293T in mitochondrial DNA; seePachalska & MacQueen, 2001).

KS was treated with Neurotop (carbamazepine) to control epilepticseizures, and co-enzyme Q10 combined with L-carnitine to support herenergy metabolism. In addition, she received a comprehensive program ofneurorehabilitation, which seems to have delayed the progress of the disease(Pachalska & MacQueen, 2001). The number and intensity of the stroke-likeepisodes diminished considerably after 1999, but dementia progressed stead-ily. Until her death in June of 2005, KS lived at home with her parents, butrequired increasing supervision due to paranoid delusions of persecution byher younger brother.

The overall course of each mitochondrial crisis experienced by KS wasessentially similar. The prodrome consisted of severe headache, protractedspells of nausea and vomiting, followed by epileptic seizures (initially focal,later sometimes generalized), narrowing of the field of vision and deteriorat-ing visual acuity, culminating either in a grand mal epileptic seizure (some-times status epilepticus) or stroke-like neurological symptoms, includingserious disturbances of hearing and vision, occasional paresthesia or paresis,and aphasia-like symptoms. Within days or even hours after the onset of theepisode, however, most of these symptoms receded, though residual effectswere often noted. The effects can be seen in Figure 20.4.


Figure 20.4A shows the results from a battery of selected subtests that wereadministered to KS on a daily basis when prodromal symptoms appeared,pointing to an imminent stroke-like episode (see Pachalska & MacQueen,2001). This battery (which had to be kept short due to the patient’s lowfatigue threshold) included the following six elements:

• naming (BNT);• repetition of high probability (i.e., commonly used) words (Cracow

Neurolinguistic Aphasia Battery, CNAB; Pachalska, Kaczmarek, &Knapik, 1995);

• repetition of low probability (i.e., infrequent) words (CNAB);• sequential commands (WAB);• reading (CNAB);• writing (CNAB).

As can be seen, repetition of high probability words, reading, and writingwere at normal levels when testing began, while repetition of low probabilitywords, naming, and sequential commands were already showing some path-ology at about 80% of normal. Since by 1998 KS never showed 100% resultson these three subtests, the examination of September 10, 1998, though pro-dromal symptoms were already occurring, can safely be taken as baseline. Bythe afternoon of September 16, KS was nearly mute, with minimal responses(about 20% of normal) on naming and sequential commands, and noresponse at all on the remaining tests. This state only lasted for 1 day, how-ever, and the recovery was nearly as dramatic as the loss of function. Other

Figure 20.4 Speech and language results obtained by KS: (A) the course of a typicalstroke-like episode (courses converted to percentages to facilitate com-parison), (B) overall decline in language and mentation.

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episodes show a very similar profile in terms of the overall shape, but in eachcase the various parameters are affected in different ways (Pachalska &MacQueen, 2001).

Figure 20.4B, by contrast, shows the steady decline over the years ofKS’s illnesses, independent of the dramatic course of the episodes. By mid–2004, her language capacity had fallen to the point that further testingwas pointless. As her hearing deteriorated, she developed slight dysarthria,but as the disease progressed her speech became more and more difficultto understand (see Ball et al., 2004). In the last year of her life KS spokeonly a few mumbled words; on the Boston Naming Test, she identified thecat but no other pictures (1/60). She spoke of herself (when she couldbe induced to speak at all) in the third person singular (see Pachalska &MacQueen, 2002), which is a common feature of the speech of the dementedin a late stage, when disturbances of consciousness and identity becomecommon.

Discussion

In a modular approach to brain work (Jackendoff, 2000), one assumes that,somewhere in the brain, there is a thought module, which is both the origin ofdata presented to the language module to be transformed into a speech act,and the destination of information decoded by the process of comprehen-sion. In such a view, the language module (whether it is conceived of as asingle module or as a set of modules forming a processing unit; see Jackendoff,2000) receives input in the form of thoughts, concepts, images, or the like, andproduces a speech act as output, or, in reverse, receives phonemes or graph-emes and transforms them through the application of linguistic rules intothoughts (or cognitions). Its function, then, is one of mediation betweenself and the world, inner and outer, a center for encoding and decodinginformation that can be sent and received.

Postulating the existence of a “thinking module” at the apex of brainfunctioning seems reasonable enough, virtually instinctive, but it is attendedby some serious problems, not the least of which is the difficulty in establish-ing where in the brain such a “thinking module” would be located. Couldthinking be one of the executive functions performed by the frontal lobes,or is it kind of meta-cognition situated in the strategic temporo-parieto-occipital (TPO) region? Or are there two thinking modules, one anterior andone posterior? If so, how are they related to each other? The problembecomes more difficult the longer it is pursued. Perhaps it would be moreexpedient to question the necessity to postulate a distinct thought module, asLuria did (1977). There is really no such thing as “thinking,” one mightargue. Mentation would then be reduced to inner speech; that is, a speechact that has not been realized through the motor segment (Brown, 2004),or to imagination, assuming that the “stuff” of thought consists of wordsand pictures. This alternative has the further advantage of avoiding the


“homunculus” fallacy, which necessarily emerges whenever a thought moduleis postulated.

Attempts to tease thought processes away from language-related pro-cesses begin by searching for a kind of “pure” aphasia (or dyslexia, ordysgraphia), in which thought processes are intact but specific languagefunctions are disturbed, so that:

• on the active side, the content of the intended speech act is normal, butthe language module is unable to process this content into a comprehen-sible and fluent speech act;

• on the passive side, there is a retained ability to receive the signals thatmake up another person’s speech act (or written text) as sensory data,but the meaning is not extracted from the signals.

The principle of double dissociation can perhaps be used to argue that inpatients with focal lesions there are indeed “purely” cognitive processes and“purely” linguistic processes that are selectively disturbed, but even so thisactually requires some mental gymnastics. The incessant disputes in clinicalpsychology over the problem of defining and measuring intelligence shouldmake us cautious about naively assuming that we know how to assess thequality of thinking in a manner that is not in some way dependent on lan-guage. In clinical practice, it is possible to be sure that there is intact thinkingwith disturbed speech only when the disorder is rather obviously peripheralin nature, sensory or motor, as in a hearing defect or dysarthria; that is,affecting the receptor or effector responsible for receiving sensory signals orexecuting motor programs. The more central the point of disturbance, how-ever, the more difficult it becomes to disentangle language from thinking.This is difficult to explain in the light of a modular system, in which thelanguage module is conceived of as a center for encoding and decoding,mediating between the inner world of thought and the outer world ofbehavior. If the language module is content neutral, as much of contempor-ary linguistics seems to assume, then it is only a messenger between “inner”and “outer” domains of information; if it is not content neutral, then theproblem of distinguishing language from mentation becomes much moredifficult.

This is why dementia-related aphasia is “messy,” enough so that for sometime no one was willing to allow the speech and language disturbances occur-ring in conjunction with dementia to be classified as “aphasia” (Ross et al.,1990). It seems an obvious conclusion that from the perspective of aphasiathe basic speech and language problem in dementia is similar to what occursin schizophrenia: there is disordered speech because there is disordered think-ing. Problems arise, however, when these concepts are tested critically in theclinic. A strictly psychometric approach can sometimes give us the illusionthat mentation can collapse while leaving speech and language intact, or viceversa, but a careful observation of the patient’s behavior, in and out of

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the clinical setting, very often gives the lie to this conclusion. In what sensecan a nonsensical sentence be linguistically correct? For analogous reasons,semantics and syntax may seem to be separate processors within the languagemodule, but when we examine what the brain actually does in real time totake in a sentence (MacQueen, 2003), it turns out to be inordinately difficultto find “purely” syntactical or “purely” semantic operations.

We seem to be faced with a significant conceptual dilemma:

• On the one hand, many patients and their families, and a good part ofthe general public, cannot dissociate disordered speech from disorderedthinking. The patient is (or is not) mentally ill, “crazy,” and the test iswhether or not speech is coherent. The one who talks “crazy” is “crazy.”Clinicians know the problems faced by the aphasic patient who, on com-ing into casual verbal contact with strangers, is immediately categorizedas inebriated, mentally ill, or mentally retarded, and who often reacts tothat perceived stigma simply by avoiding such contacts. As mental healthprofessionals we fight this attitude on a daily basis.

• On the other hand, currently fashionable modular approaches force usinto a dissociation that, as previously mentioned, is much easier to main-tain in theory than it is in practice. If, for example, the patient is unable toform a grammatical sentence, is this simply a defect of a specific functionin the language system, perhaps due to the loss of one particular syn-tactic rule, or is there an underlying loss of the ability to form a logicalproposition? Could we find a way to test one hypothesis or the other,without making a series of simplifying assumptions regarding either thenature of syntax or the nature of logical thinking?

The problem raised here is far too complex and far-reaching to solve inthis chapter, though indeed dementia is a good point at which to begin thediscussion, precisely because we are forced to ask the basic question: What isthinking? The very derivation of the word dementia (in past centuries a verygeneral term for mental illness) points to “losing [one’s] mind,” which isechoed even in ordinary speech. The fact that we have narrowed the definitionconsiderably and have a generally more “enlightened” attitude towards theproblem should not disguise the fact that the patient ordinarily experiencesthe progress of dementia as rather literally a loss of mind. Moreover (again,setting aside for the moment our scientific predispositions), it is hard toimagine that one could lose one’s mind (whatever we understand that tomean) without that fact finding some reflection in speech and language – andvice versa.

The wall of separation that we have erected between thinking (the contentsof our minds) and speaking (the production of a speech act) is built into ourlanguage, and for that reason alone seems to us perfectly natural and obvious.Those post-modernist theories (such as deconstructionism) that questionwhether discourse can ever actually get to the truth, though ordinarily taken


as an attack on logocentrism, in fact reflect a cry of despair, which wouldmake no sense at all if there were not still an implicit assumption, indeedan act of faith, that there could be a truth that would exist independent ofthe words we use to describe it. Yet in that same ancient Greek languagethat gave us the “logo-” of logocentrism there is no verb that denotes “think-ing” independent of speech. Indeed, the basic noun logos, from which arederived such apparently disparate concepts as logic, analogy, catalogue,and the names of most of our sciences, does not mean “thought,” but rather“word,” or better, “discourse.” Thus the gospel of St. John begins, “Inthe beginning was the logos,” meaning the Word – and not, as our psycho-logical theories would incline us to assume, “In the beginning was theThought.” The thought and the speech act that embodies it evolve together,emerging from depth (drive and affect) through various phases of verbaliza-tion to the surface, the level of consciousness and behavior. Separating themsimplifies analysis, to be sure, but at the cost of obscuring the nature of ourmental life.

In microgenetic theory (Brown, 1988, 2005) the process of forming aspeech act is understood as a continuous stream, leading from drive throughmotivation to behavior, where specific mental functions are not “processors”in a data-processing system, but rather moments when the diversion or inter-ruption of the flow produces particular consequences. The process of formu-lating a thought flows into the process of formulating a speech act in innerspeech (Brown, 2004), which in turn flows into a realized speech act. Themental process that leads to comprehension is a parallel flow, with innerspeech mediating between rules and specific mental states. Just as a mutationand a change in the environment may cause the tree of evolution to branch ata given moment, so changes in circumstances or context, both inner (withinthe brain) and outer (in the world “outside”), cause the microevolution of amental state to branch in a particular way. In such a system, nothing isentirely predetermined, but then again, nothing is entirely random. Braindamage, then, including neuron loss resulting from a degenerative process,affects the ensuing mental state(s) much as the damage to a branch affects thegrowth of the tree. Further growth (i.e., the appearance of further stages inthe affected process) may be stopped, but more often growth continues down-stream from the point of damage, though its direction and force are likely tobe changed. The nature of the symptom is not merely an absence, a failure toperform, defective output from a damaged function, but a vital clue to thenature of the process itself (Brown & Pachalska, 2003). Involution revealsthe process by which evolution works.

In microgenetic theory, then, the difference between disturbances of think-ing and disturbances of speech and language is as much or more a matter of“when” as “where.” The closer the damage to the surface, the more its effectsare felt in the fine articulation of the affected behavior, the last stages ofmicrogenesis, and conversely: the deeper the damage, the greater the numberof functions that are disturbed at the outset. It is essential to emphasize that

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in this approach the concepts of “depth” and “surface” are not used ina purely metaphorical sense, but pertain rather to the basic structure of thecentral nervous system, with the brainstem and midbrain at the core and thecortex at the surface. Mental states emerge along the paths laid down byevolution, from deeper, older, simpler structures, upward and outward to theyoungest and most specialized regions of the cortex. In a cortical dementia,then, involution begins at the point where evolution concluded, while a sub-cortical dementia begins deeper, undermining the surface structures, which“cave in” as a result.

If the organism survives an insult, it tries to adapt; if it does not adapt, itdoes not survive (Goldstein, 1995). Adaptation rarely succeeds, however, inremoving the obstacle, erasing the damage; indeed, that is not what adapta-tion is all about. The damaged brain goes about its work differently, butneither that which is the same, nor that which is different, simply appearedout of nowhere. Nihil de nihilo gignitur, said the Roman poet Lucretius, fol-lowing his master, the Greek philosopher Epicurus: “Nothing ever happensfrom nothing.” The reasons for the behavior we see in the clinic must besought not only in the disease, but also in the premorbid brain (Brown &Pachalska, 2003). In dementia, then, what we are seeing is an involution ofmental processes. Dementia is ontogenesis in reverse, unraveling the fabricthat evolution and growth have woven. Symptoms appear as entropy expandsto take in ever larger segments of mental processing. Whether this emerges asa cortical or subcortical dementia, with or without motor disturbances, withor without aphasia, depends on the point at which the entropy begins and thedirection in which it spreads, whether from depth to surface or surface todepth, posterior to anterior or anterior to posterior, and so forth. The strug-gle to adapt, to compensate for what has been lost, is ultimately lost, and asthe entropy spreads, the differences between the various diseases are grad-ually effaced. This is why all the roads traveled by the various dementivesyndromes begin very differently and end very much the same. The speech actmay become first inarticulate in its execution, then disordered in its contents,or the reverse; this may happen early or late, and it may take place quickly orslowly. In the end, however, the patient falls into global aphasia and thenmutism. Logical contact is then irretrievably lost.

Conclusion

There is, of course, no cure for dementia, as there is no cure for the variousdiseases that cause it. It is possible, however, to slow its progress and mitigateits effects. In many cases, too, it may well be possible to prevent the involu-tionary processes from beginning. There is some evidence, though contro-versial, that regular mental and physical stimulation throughout life mayprevent neural degeneration from beginning, even when there is a geneticpredisposition (Stern, 2002). In my opinion, one of the great challengesfacing neuropsychology in the century to come, as the world population ages


(especially in Europe and the United States), is to develop therapeutic andpreventive interventions that can keep a larger percentage of the world’spopulation from “losing their minds” before their natural lifespan is over.This may require some discussion and debate about where and how researchresources are allocated, especially since at present the involvement of neuro-psychology with dementia has been almost exclusively in the area of diag-nosis. What Dylan Thomas said about death in his poem Do not go gentle intothat good night (1951) could well serve as a motto for the neuropsychology ofdementia in the twenty-first century:

Do not go gentle into that good night!Rage, rage! against the passing of the light!

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324 Pachalska

Author index

Page entries in bold refer to tables/figures.

Adams, J. H. 45Adams, W. 304Adolphs, R. 49, 52Agid, Y. 147, 306Agliotti, S. 236, 236Aharon-Peretz, J. 46Ahlskog, J. E. 145Alajouanine, T. 3, 4, 169Alarcon, N. B. 74Albert, M. 141, 169, 178Alexander, G. E. 137, 138, 140, 141, 142,

143, 146Allen-Burge, R. 275, 276Amparo, E. 45Andelman, F. 198Andresen, E. M. 83Ansaldo, A. I. 294Arabia, C. 161Archer, B. 224, 238Armstrong, E. 8, 93, 97, 100, 172, 181,

182, 188, 189, 195, 198, 199, 204, 205,225

Aronson, A. E. 307Aten, J. L. 184Auer, P. 235Aust, C. 24Austin, J. 117, 293Auther, L. 226Avent, J. R. 184Azrin, N. A. 73

Baer, D. M. 79, 80, 81Bainton, D. 246Bakay, R. A. E. 141Baker, E. 157Ball, M. J. 1, 3, 4, 5, 6, 8, 92, 168, 303, 315Bara, B. G. 44, 48

Baresi 247Barnes, M. A. 44, 46, 49, 51Baron-Cohen, S. 48, 49Barry, C. 59, 161, 164Bartels, C. 19, 22Bassich, C. J. 169Basso, A. 39Bastiaanse, R. 224, 245, 249, 250, 251,

253Baum, S. R. 126Bayles, K. A. 130Bayley, K. 273Bayley, M. 84Beblo, Th. 22Bechara, A. 49Beeke, S. 182, 183, 233Behrens, S. J. 125Beiser, A. 301Béland, R. 110Benali, H. 292Benecke, R. 169Benke, T. 307Benson, D. F. 168, 299, 316Benzing, L. 157, 164Berger, J. 170Berger, P. L. 95, 96Bergquist, T. 272Berndt, R. S. 230, 249, 251Bernstein, B. 108Bernstein-Ellis, E. 98, 189Besse, J.-M. 108Bester, S. 79, 194, 218Beukelman, D. R. 77, 171Bibby, H. 49Biber, D. 196Biddle, K. R. 54Bihrle, A. M. 285

Binder, G. M. 33, 59Bishara, S. M. 59, 60Bitensky, J. 84Biuethmann, H. 309Black, S. E. 185, 274, 275Blanken, G. 4, 20, 156, 161, 162, 164Bliss, L. S. 54Blum, A. 288Bobholz, J. A. 149, 150Boccardi, M. 304Body, R. 53, 55, 61, 168Boeve, B. F. 301Bogner, J. 272Boller, F. 169, 178Bollinger, R. L. 184Bond, F. 60, 271Boone, K. 304Boongird, P. 130, 131, 132Boonklam, R. 130, 131, 132Booth, S. 182, 273, 274, 276Borke, R. C. 141Borkowska, A. 304Bormann, T. 156, 162Bornhofen, C. 46, 47, 49Borod, J. C. 198Boshart, J. 49Bottini, G. 292Boulton, C. 148Bourgeois, M. 84, 275, 276Bowler, D. M 48Boylstein, C. 197Bracy, C. A. 54Braden, C. L. 84Brain, R. 169Branford, W. 232Brassard, C. 93Brazis, P. W. 309Brinson, G. 146Britz, A. 19, 22Broadbent, G. 137Broca, P. 92Broe, G. A. 271Brookshire, B. L. 55, 56, 57, 58, 62Brown, J. W. 6, 307, 315, 318, 319Brown, P. 43, 45Brownell, H. H. 285, 287, 288Bruce, C. 273Brumfitt, S. 184, 194Brunner, R. J. 140Bryan, K. 178, 255, 273, 274, 289Buckingham, H. W. 28, 29, 30, 35, 169Büeler, H. 309Buell, U. 146Bugbee, J. K. 274

Bunning, S. 48Burgio, L. 275, 276Burt, D. M. 52Buskell, R. 188, 189Butterworth, B. 35, 36, 157, 160, 307Button, G. 100Buttsworth, D. L. 57Byng, S. 72, 77, 198, 199, 274

Cabeza, R. 149, 290Caine, E. D. 169Caligiuri, M. P. 184Calne, D. 306Campbell, G. 306Candlin, C. N. 186Canetti 10Cannito, M. P. 50Capaso, R. 40Cappa, S. F. 137, 139, 140, 141, 143, 147,

148Caramazza, A. 40, 157, 158, 159, 160,

161, 164, 249Cardebat, D. 285Cariski, D. 79, 273, 274, 275Carpenter, C. M. 225Carrol, J. M. 115Carson, K. J. 304Carter, R. 196Cavallotti, G. 140Cerhan, J. H. 301Chafe, W. L. 232Champagne, M. 116, 119, 284, 288, 291Chan, J. L. 127, 128, 130Channon, S. 44, 47, 49Chantraine, Y. 287Chapey, R. 3, 83Chapman, S. B. 53, 55, 56, 57, 58, 62,

168Charolles, M. 118Cherney, H. J. 140, 150Chiarello, C. 286, 291Chipere, N. 251Chomsky, N. 29, 294Christman, S. 28, 29, 35Chung, K. 3, 4, 8Cicerone, K. D. 49, 272, 273Clark, H. H. 44, 118Claughton, J. S. 232Clinchot, D. 272Code, C. 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 17, 18,

20, 21, 23, 24, 25, 28, 29, 42, 55, 60, 87,92, 107, 111, 125, 136, 156, 168, 169,170, 181, 195, 198, 213, 220, 237, 255,259, 270, 272, 276, 277, 278, 280, 284,

326 Author index

288, 289, 290, 291, 293, 294, 303, 305,315

Coelho, C. A. 55, 56, 57, 58, 59, 263, 272,276

Cohen Conger, J. 272Coltheart, M. 248Combrink, J. G. H. 223Conan, M. 181Conger, A. J. 272Cooper, I. S. 139Cooper, L. J. 77Cooper, W. E. 125, 126, 132Copeland, G. 235Copland, D. A. 140, 150Corrigan, J. 272Corrigan, P. W. 49Corso, M. 55Cortazzi, M. 196Côté, H. 288, 289Cowell, S. F. 7, 23Cowin, K. 181Cramon, D. 272Cramon, G. M.-v. 272Crawford, J. R. 49, 50, 303Creutzfeldt, H. G. 309Crisp, J. 182Critchley, H. 52Critchley, M. 169, 173, 177, 284Croker, V. 50Crosson, B. 44, 48, 138, 139, 140, 142,

143, 144, 145, 146, 148, 149, 150Cruice, M. 75, 82Crum, R. 218, 219Crutcher, M. D. 138Culhane, K. A. 53, 55Cummings, J. L. 168, 299, 301, 304, 316Curran, J. P. 272Cutica, I. 48

D’Agostino, R. B. 301Dahlberg, C. 272Damasio, A. R. 52, 139, 140, 141Damico, J. 1, 78, 92, 93, 97, 99, 100, 183,

188, 235Danly, M. 125Daoust, H. 288, 289Dapretto, M. 292Darby, D. 46, 52Dardarananda, R. 128, 130Darley, F. L. 92, 307Dass, R. 218David, R. 246Davis, G. A. 56, 183, 184Davis, H. L. 49

Davis, K. E. 95Davis, L. E. 139Dawe, K. 6, 303, 315de Gaulmyn, M.-M. 108De Long, M. R. 138, 141, 142, 143De Raad, A. O. 77De Raedt, R. 302de Wilde, M. 161DeArmond, S. J. 309Dechongkit, S. 130, 131, 132Delacourte, A. 304DeLaPaz, R. 304Delis, D. C. 287Dell, G. S. 34, 132, 158, 159, 161Deloche, G. 260, 261Denes, G. 169, 178Dennis, M. 44, 46, 49, 51DeRuyter, F. 276Desai, N. P. 309Deser, T. 56Desmond, J. E. 292Devereux, R. 271, 272Dierckx, E. 302Dijkstra, K. 275, 276Dittmann, J. 156, 161, 164Docking, K. 138Dolan, R. J. 52Doody, P. 168Dorian, N. C. 232, 233Douglas, J. M. 53, 57, 61Dow, R. S. 138Doyle, D. 45Doyle, P. 84, 86Doyon, B. 285Drew, E. 291, 286Druks, J. 249Drummond, S. S. 59, 60, 184Dubois, B. 147, 306Duchan, J. F. 3, 75, 83, 185, 190, 198, 274,

275Duffy, R. J. 55, 56, 57, 59, 268Durán, P. 251Durand, E. 275Duranti, A. 96Duvoisin, R. C. 306Dykes, J. C. 225

Eales, C. 181Ebert, M. H. 169Edwards, S. 224, 245, 246, 249, 250, 253Edwards, W. 20Egan, G. F. 7, 23Eggenberger, E. R. 309Eggins, S. 178, 185, 278

Author index 327

Eisenberg, H. M. 24, 45Eisenson, J. 246, 284, 293Elbard, H. 79, 194, 218Elfgren, C. 301, 304Eling, P. 92Ellis, A. W. 36, 161, 163, 248, 249Ellis, G. J. 189Ellmas, J. 246Elman, R. 3, 8, 75, 83, 93, 97, 98, 100,

185, 189, 255Elsass, L. 271Emig, J. 98Enderby, P. 246Engedal, K. 129Engell, B. 80,Erb, M. 292Erlich, J. S. 53, 55, 59Esmonde, T. 307Ewing-Cobbs, L. 53, 55

Fabbro, F. 235, 236Faircloth, C. A. 197Farrell, A. D. 272Fatkenheuer, G. 170Fazio, F. 147Federmeier, K. D. 235Feeney, T. J. 275, 276Feeny, D. H. 83Fehr, T. 17Feinn, R. 55Fenelon, B. 45, 46Ferguson, A. 93, 181, 182, 188, 189, 190Ferreira, A. 274Ferstl, E. C. 46Finegan, E. 196Finger, S. 30Finkenstaedt, M. 309Finlayson, A. 79, 194Fischer, M. 309Fisher, C. M. 137Flamm, L. 287Flanagan, S. 44, 48, 49, 50, 57, 60, 272Flynn, J. 304Fok, A. Y.-Y. 128, 130Foldi, N. S. 287Foley, N. C. 84Ford, I. 45Fordyce, D. J. 53Forminska-Kapuscik, M. 311Fox, P. T. 145, 149Frackowiak, R. S. 150Frame, S. R. 232Frank, A. 201Frank, E. 50

Franklin, S. 250Frattali, C. 87, 88, 274Frazer, W. 140Freedman-Stern, R. 225, 235Frege, G. 118Freud, S. 28, 32, 39, 87, 92, 245Frey, W. H. 305Fridriksson, J. 217Friedland, D. 188Friston, K. J. 150Frith, C. D. 52Frith, U. 48Fritsch, T. 275Fromkin, V. 127, 129, 158Fuchs, S. 49, 50Fugate, L. 272Fujita, I. 235Fukuda, M. 148Fünfgeld, M. 19Funnell, E. 163, 305

Gabrieli, J. D. E. 292Gagnon, D. A. 34, 158, 159Gagnon, J. 285Gall, F. 92Galski, T. 53, 56, 57, 58, 62Gamble, A. 55Gandour, J. 126, 127, 128, 129, 130, 131,

132Gannaelli, T. A. 45Gannaway, R. 232Garcia, L. 3, 83Gardner, H. 285, 287, 288Garfinkel, H. 94, 96Garmen, M. 250Garratt, H. 178Garrett, M. F. 158, 165Gates, G. A. 301Gennarelli, T. 45Gergen, K. J. 95Gerhand, S. 164Geroldi, C. 304Gersh, F. 141Gersh, S. 140Gerstle, J. 275, 276Geschwind, N. 43, 92, 140, 157Gibbs, R. W. 48Giles, E. 307Gilpin, S. 72, 77, 198Ginet, D. 108Giroux, F. 285, 287, 288Gleber, J. 287Glindemann, R. 184Glosser, G. 56

328 Author index

Glover, G. H. 292Goda, A. J. 86Godfrey, H. P. 59, 60, 271, 272Goffman, E. 94, 95, 186Goins, K. E. 205Gokay, D. 149, 150Goldstein, H. 78, 80, 84Goldstein, K. 223, 319Goloskie, S. 125, 132Goodglass, H. 157, 247, 252, 302Goodwin, C. 93, 96, 97, 99, 185, 233Gordon, A. C. L. 49Gordon, D. 45, 46Gordon, J. K. 161Gotts, S. J. 28, 39Goulding, P. J. 162, 305Goulet, P. 285, 286, 288, 289, 291Graff-Radford, N. R. 126, 139, 309Grafman, J. 52Graham, D. I. 45Graham, K. S. 163Graham, N. 100, 163Grant, S. 277Graybiel, A. M. 138Green, C. D. 31Green, R. E. A 50Gregory, R. 148Grela, B. 55Grice, H. P. 44, 45, 47, 50, 53, 116, 117Grodd, W. 292Gross, R. E. 148Grossman, M. 305Grossman, R. G. 43, 48Gubrium, J. 197Guendouzi, J. A. 168Guger, S. 46Guidotti, M. 140Guiraud, P. 305Gumperz, J. J. 190Gustafson, L. 301, 304Guthke, T. 46Guyatt, G. H. 83

Haak, N. J. 57Haas, J. C. 156Hadar, U. 149Hagan, C. 53Hale, S. 86Hall, B. 138, 149Halliday, G. M. 7Halliday, M. A. K. 43, 56, 59, 172, 173,

178, 190, 206, 270, 278Hallowell, B. 8, 181Halson, D. 48

Hand, L. 51, 55, 60, 61, 273, 276, 277,278

Hanson, W. R. 147Happé, F. 48, 288Harasty, J. 7, 23Harciarek, M. 299, 301, 304, 305Harding-Clark, J. 149Harley, T. 28, 29, 34, 35, 36, 37, 38, 39Harris, Z. 119, 120Harrison, J. 140, 148Hartley, D. 30Hartley, L. L. 53, 55, 56, 58, 271Harward, H. 53, 54, 55Hasan, R. 56, 59, 278Hatzipantazi, M. 306Haverkate, H. 48Havill, J. H. 272Hayashi, M. 235Haynes, W. O. 57Head, H. 245Hebb, D. O. 33Hecaen, H. 169Heeschen, C. 182Heidenhain, A. 309, 311, 312Heilman, K. M. 43, 139Helasvuo, M. 182Helffenstein, D. A. 272Heling, G. 224,Helm-Estabrooks, N. 140, 141Helmick, J. W. 20Hemsley, G. 2, 3, 23, 181, 198Hengst, J. A. 182, 190, 232Henry, J. D. 303Henschen, S. E. 137Heritage, J. C. 96, 97, 99, 186Herman-Sucharska, I. 311Herrmann, M. 2, 3, 17, 18, 19, 20, 21, 22,

23, 24, 87, 181, 198Herzig, A. 116, 119Hickey, E. M. 84Hickin, J. 181Hickson, L. 75, 82, 272, 273Hier, D. B. 168High, W. M. Jr. 45Hill, C. L. 182, 233Hill, M. A. 168Hillis, A. E. 157, 160, 161, 164, 310Hilton, H. J. 304Hinckley, J. J. 85Hirsh, K. W. 161, 163Hodges, J. R. 162, 163, 305, 306, 307Hoffmann, C. 170Hogan, A. 3, 21, 181Hohenstein, C. 307

Author index 329

Hojgaard, K. 147Holderbaum, C. S. 120Holland, A. 3, 75, 80, 81, 84, 93, 98, 109,

184, 213, 217Holland, D. 272, 276Hollerbach, B. 140Holmes, J. 201Homskaya, E. D. 32, 39Hopper, T. 84Hough, M. S. 56, 287Howard, D. 157, 160, 161, 164, 247Huber, W. 80, 162, 169, 247, 287Hughes, C. 49Humphreys, G. W. 150, 159Hunston, S. 196, 201Hunter, M. 45, 46Hurkmans, J. 250Hutter, B. 80Hydén, L.-C. 195, 197

Ioannides, P. 306Ioannis, M. 306Ireland, C. 72, 77, 198Irwin, W. H. 266, 268Israel, D. 115Ivnik, R. J. 301

Jackson, H. F. 50Jackson, J. H. 32, 39, 92, 245, 246Jacob, S. 24Jacobs, B. J. 84Jacobs, J. R. 287Jahn, H. 24Jakob, A. 309James, W. 33Janicka, B. 300Jbabdi, S. 292Jefferson, G. 184Jenkins, J. J. 139, 263Jensen, P. J. 53, 55, 56, 58Jescheniak, J. D. 158, 160,Jiménez-Pabón, E. 139, 263Jin, L. 196Joanette, Y. 7, 8, 29, 119, 125, 284, 285,

286, 287, 288, 289, 290, 291, 292, 293,294

Jodzio, K. 299, 301, 304Johannsen-Horbach, H. 18, 19, 22Johnson, A. F. 184, 189Johnson, C. J. 46Johnson, D. A. 60Johnston, M. V. 53, 56, 57, 58, 62Johnston, R. A. 161Jonas, S. 139

Jones, R. H. 190Jones, R. J. 73Jonkers, R. 224, 249Jordan, F. M. 57Jordens, C. F. C. 197Jutai, J. W. 83

Kaczmarek, B. L. J. 29, 314Kagan, A. 3, 83, 185, 198, 274, 275Kalinyak, M. 86Kalmar, K. 272Kalmek, L. 224, 238Kameyama, S. 148Kamio, A. 235Kampe, K. K. W. 52Kaplan, E. 247, 252Karacostas, D. 306Karafin, M. S. 52Kaszniak, A. W. 130Katz, R. C 8, 84, 181, 259, 260, 261, 263,

264, 265, 268Kaufman, S. 197Kaufmann, P. M. 44, 47, 62Kay, J. 6, 248, 249, 303, 315Kazdin, A. E. 72, 73, 78Keebler, M. W. 182, 205, 233Keenan, T. 49Keisler, L. 79, 273, 274, 275Kelly, P. J. 145Kemmerer, D. 249Kemper, T. D. 96Kempler, D. 299, 305Kendall, E. 48Kennedy, C. H. 74, 78, 81Kennedy, M. 139, 140Kenstowicz, M. 131Kent, R. D. 177Kersel, D. A. 272Kertesz, A. 29, 35, 74, 126, 225, 247, 264,

304, 305, 306, 311Keyser, A. 224Khunadorn, F. 130, 131, 132Kiejna, A. 300Kimura, M. 138Kinch, J. 44, 50, 60Kinsella, G. 271Kintsch, W. 57Kircher, T. T. J. 292Kirchner, D. M. 53Kiss, K. 249Klippi, A. 93, 182, 183, 185, 189, 235Klouda, G. V. 125, 126, 134Knibb, J. A. 305, 306Knight, R. T. 49, 60

330 Author index

Knight, R. G. 49, 59, 60, 271, 272Knopman, D. S. 305Knott, R. 250Koch, U. 18Kodras, J. E. 85Kohn, S. E. 249Koivisto, M. 285, 286Kolk, H. 224Koras, N. 304Kornhuber, H. H. 140Kozleski, E. B. 81Kozlowski, A. 168Krampe, H. 24, 161Kril, J. J. 7Kroes, H. 223Kropp, S. 309, 311Kubler-Ross, E. 217Kubo, S. 116Kufera, J. A. 54Kuhl, D. E. 147Kulke, F. 162Kumpula, J. 79, 273, 274, 275Kunz, T. 140Kurzbauer, H. 311Kushii, J. 304Kutas, M. 236, 292

Laakso, M. 182, 183, 304Labonde, E. 161Labov, W. 196, 200, 203, 205, 225, 232,

235Lahire, B. 108Lakoff, G. 45, 46Lambon Ralph, M. A. 163Lang Y. 309Lang, A. E. 148Lange, K. L. 230, 249, 251Langenbahn, D. 272LaPointe, L. L. 72, 75, 82, 84, 85, 86, 198,

289Larkins, B. 272, 273Lashley, K. S. 92Lasker, J. P. 77, 85Lassen, N. A. 147Laughlin, S. A. 140Lavizzo-Mourey, R. 141Lawler, E. N. 161Lawrence, A. E. 45Le Blanc, B. 285Le Dorze, G. 285Lebrun, Y. 305, 307, 308Lecours, A.-R. 7, 8, 29, 36, 111, 125LeDorse, G. 93Lee, A. G. 309

Lee, S. S. 292Leer, E. V. 56, 58Lehmann, C. 170Leiner, A. L. 138Leiner, H. C. 138Leiwo, M. 235Lemarié, J. 113Lemieux, S. 287Lenay, Ch. 113Lenius, K. L. 72Leonard, C. M. 149, 150Lesser, R. 168, 248Leszek, J. 300Leube, D. T. 292Levelt, W. J. M. 157, 158, 159, 160, 164Levin, H. S. 43, 45, 48, 53, 55, 56, 57, 58,

62Levine, H. L. 140Levine, R. 79, 273, 274, 275Levinson, S. C. 43, 45, 184Levita, E. 43Liang, J. 127, 131, 132Lichtheim, L. 137, 246Liles, B. Z. 55, 56, 57, 59Lind, M. 253Lindgren, A. G. H. 168Lindsay, J. 182, 275Ling, P. K. 287Links, P. 250Lipp, H. P. 309Little, J. 197Litvan, I. 306Lloyd, J. J. 304Lock, S. 273, 274Lomas, J. 79, 194, 218Lombardi, W. J. 148Long, E. 46, 47, 49Longacre, R. E. 203Longin, D. 119Lorch, M. P. 248Lorenz, A. 161LoVerme, S. R. 140Loverso, F. L. 266, 267Lozano, A. M. 148Lu, L. 146Lubinski, R. 75, 87, 190Lucius-Hoene, G. 18Luckmann, T. 95, 96Ludlow, C. L. 169Lulham, J. M. 271Luria, A. 28, 29, 32, 33, 37, 38, 39, 92,

139, 247, 307, 315Lustig, A. P. 76, 84Luzzatti, C. 305

Author index 331

Lyon, J. G. 3, 13, 75, 79, 83, 86, 98, 273,274, 275

Macaluso-Hayes, S. 225, 235MacAndrew, S. B. G. 34, 35, 36, 37, 38,

39Machetanz, J. 169Macken, E. 115MacQueen, B. D. 311, 312, 313, 314, 315,

317Malapani, C. 147Malec, J. 272Malvern, D. D. 251Malyszczak, K. 300Mann, W. 120Manning, M. L. 45, 46Marie, P. 137, 246Marquardt, T. P. 50, 235Marrelec, G. 292Marsh, N. V. 59, 60, 272Martin, I. 46, 47, 48, 49, 60Martin, J. R. 172, 173, 196, 204Martin, N. 34, 158, 159Martinez, A. 292Masterson, J. 249Mastri, A. R. 305Mastrianni, A. 309Matejka, J. 54Matthiessen, C. M. I. M. 172, 173, 178Maurel, F. 113Maxim, J. 178, 182, 273Mayley, Y. 186McArdle, C. B. 45McCabe, A. 54, 55, 170, 196McCarney, C. T. 184, 189McCormick, K. 224, 229, 232, 235McDonald, S. 42, 44, 46, 47, 48, 49, 50,

51, 53, 55, 56, 57, 58, 60, 62, 271, 272,277, 288

McFall, R. M. 43, 59, 60, 61McFarling, D. 139McKevitt, C. 197, 199McLellan, D. R. 45McPhee, J. 188, 189Medd, J. 272Mega, M. S. 140, 146Mendelsohn, D. 53, 55Mendez, M. F. 301, 304Menn, L. 235Messa, C. 147Mesulam, M. M. 149, 305Metter, E. J. 147Meyer, A. S. 157, 158Meyers, A. R. 83

Mezirow, J. 218, 219Miceli, G. 40, 160, 249Michelow, D. 125, 132, 287Middleton, F. A. 138Milders, M. 49, 50Miller, B. L. 304Miller, D. 36Miller, G. A. 48Mills, R. H. 260, 262, 263Milne, E. 52Milton, S. B. 44, 53, 59Mintum, M. 149Miozzo, M. 159Mishkin, F. 304Mitchum, C. C. 230Moen, I. 125, 127, 128, 129, 130, 131,

132, 253Moffat, N. J. 50Mohr, C. M. 149, 150Mojahid, M. 113Monakow, C. von. 137Monchi, O. 290Monetta, L. 286, 288, 291Monory, B. 59, 60Monrad-Krohn, G. H. 125Montgomery-West, P. 86Moore, C. 150Moore, P. 305Moreau, N. 110Moreno, E. M. 236Morgan, J. 117Morris, J. 250Moses, J. A. 287Moss, B. 199Moulard, G. 260, 261Moutier, F. 137Mugford, J. 2, 3, 18Müller, D. 1, 2, 3, 4, 6, 18, 20, 21, 92, 168,

181Müller, N. 4, 6Munoz, M. L. 235Murasugi, K. G. 287Murdoch, B. E. 56, 57, 136, 1371, 138,

139, 140, 149, 150Murison, R. 75, 82Musson, N. D. 184Myers, P. S. 288, 289Mysiw, W. 272

Nabeemeah, K. 224, 238Nadeau, S. E. 139, 140, 142, 145, 146Naeser, M. A. 128, 130, 140, 141, 142Nagy, V. T. 261, 263, 264Narabayashi, H. 146

332 Author index

Nash, W. 196Neary, D. 162, 305Nespoulous, J. L. 7, 55, 59, 107, 108, 109,

110, 111, 113, 116, 119, 120Neulinger, K. 46, 47, 49Neuman-Stritzel, T. 232Newhoff, M. 217, 251, 274Newman, J. R. 20Newton, A. 60Nickels, L. 157, 161, 164Nicol, J. 126, 132Nielsen, J. M. 137Nocentini, U. 286, 291Noe, A. 113Norris, S. 190Nyberg, L. 149

O’Brien, J. 48O’Doherty, J. 52O’Flaherty, C. A. 53O’Regan, J. K. 113Obler, L. K. 198Ochberg, R. L. 197Oelschlaeger, M. L. 93, 97, 99, 100, 183,

188Ogilvy, D. 226, 238Ojemann, G. A. 139, 143, 145Okasha, S. 100Oksengaard, A. R. 129Olness, G. S. 182, 198, 199, 205, 225, 226,

233, 234Olsen, D. R. 49Olsen, T. 147Olswang, L. B. 74, 84Orchard-Lisle, V. 157Osvaldsson, K. 184, 185Ouellet-Plamondon, C. 290Oxbury, S. 163, 305Ozonoff, S. 48

Pachalska, M. 311, 312, 313, 314, 315,318, 319

Packard, J. L. 130Page, R. E. 201Painter, C. 172, 173Palmer, J. M. 20Palumbo, C. L. 137, 141, 142Papagno, C. 4, 138, 139, 140, 142, 144,

156Papineau, D. 100Paradis, C. 110, 111Paradis, M. 225, 245, 254Parker, M. 53, 168Parkin, S. 148

Parr, S. 72, 75, 77, 198, 199, 274, 275Pasquier, F. 304Passant, U. 301, 304Patrick, D. L. 83Patterson, K. 162, 163, 305Paul, K. 197Pavard, P. 117Pavlov, I. 28, 29, 30, 31, 32, 36, 37, 38, 39,

40Payer, M. 288Pearce, S. 44, 47, 48, 50, 51, 53, 57, 58, 62Pearl, G. 181Pell, M. D. 126Pellijeff, A. 44, 49Penfield, W. 137, 139Penn, C. 93, 188, 222, 226, 232, 235, 237Pennanen, C. M. 304Perani, D. 147Perkins, M. 53, 55, 61, 98, 99, 168, 182,

273, 274, 276Perrett, D. 52Perrier, D. 161Perry, J. 115Petersen, R. C. 301Peterson, P. M. 149Petheram, B. 199Petty, S. H. 130Pfaender, F. 113Pfaff, A. 271Phelps, M. E. 147Phillips, L. H. 303Pick, L. H. 198Pickard, L. 79, 194, 218Pillon, B. 147Pimentel, J. I. 55, 57, 58, 62Pincus, D. 288Plaut, D. C. 28, 39Poeck, K. 162, 169, 247, 305Poewe, W. 307Polinsky, R. J. 169Pollock, M. 117Ponglorpisit, S. 130, 131, 132Ponjaert-Kristoffersen, I. 302Ponsford, J. 53, 56, 57, 59, 61Porch, B. 8, 92, 262Porter, G. 247Posner, M. I. 149Potter, H. H. 285Pouk, J. A. 48Pound, C. 8, 75, 181, 274, 275Prescott, T. E. 266, 267Prevignano, C. L. 190Pribram, K. H. 50Price, C. J. 149, 150

Author index 333

Prigatano, G. P. 44, 50, 53Prince, S. 57Prins, R. S. 250, 251Proctor, A. 55, 56Prutting, C. A. 53, 56, 59Puel, M. 285Purvis, K. 44, 49

Quinlan, P. T. 159

Rabinowitz, J. A. 272Raichle, M. E. 149Rakitin, B. 304Ramsey, S. 149Rapp, A. M. 292Rapp, B. 157, 158, 160, 164Read, S. 168Reason, J. 117Rees, T. S. 301Reiche, W. 146Reichle, T. 18Reilly, K. F. 235Reimers, T. M. 77Reinvang, I. 130Reivich, K. 214Rewega, M. 84Reynolds, A. F. 139Rhee, J. 305Richards, B. J. 251Richburg, T. 50Riddoch, M. J. 159Riedemann, C. 309Riege, W. H. 147Riklan, M. 139Riley, L. 266, 267Ringelstein, E. B. 146Rios-Brown, M. 50Ripich, D. 275Rispens, J. 249, 250, 253Rittman, M. 197Rizzo, M. 140, 141Roberge, P. T. 223Roberts, J. 233Roberts, L. 137, 139Roberts, P. M. 8, 181, 286, 291Robey, R. R. 259Robin, D. A. 126Rochon, E. 251Rodman, R. 127Roelofs, A. 157, 158Roger, P. 8Rogers, M. A. 74Rogers, M. F. 95Rollins, J. 44, 50, 60

Romani, C. 157Roncadin, C. 46Rondeau, G. 85Roos, R. P. 309Rorie, K. D. 198Rose, J. E. 43, 48Rosenbek, J. 273, 274, 275Rosenbek, J. 79, 273, 274, 275Ross, G. W. 299, 316Ross, K. B. 75, 86Roth, D. 275, 276Rothi, L. J. 139Roueche, J. R. 53Rousselle, M. 260, 261Rowley, D. 29Rule, A. 44, 49Ruml, W. 40Rustan, T. 305Rutter, B. 4, 6Ryalls, J. H. 125, 130, 132

Sabourin, L. 285Sacks, H. 99, 184Sacks, O. 195Saddy, J. D. 287Sadek, J. R. 146, 149, 150Saffran, E. M. 34, 158, 159, 235, 251Safran, A. 43Saint-Cyr, J. A. 146St. George, M. 292Salembier, P. 117Salmon, D. P. 162Salter, K. 83Samson, A. 205Sands, D. J. 81Santoro, J. M. 48, 49Sarno, M. T. 43Sasanuma, S. 235Saunders, C. 46, 47, 48, 49, 60Sayers, E. J. 197Schachar, R. 46Scheff, T. J. 95, 99Schegloff, E. A. 99, 182, 184Schenone, P. 292Scherer, L. C. 292Schiffrin, D. 274Schlosser, R. W. 79Schneider, S. L. 230, 249, 251Schneiderman, E. I. 287Schnitzer, M. L. 235Schönle, P. W. 169Schriefers, H. 158Schuell, S. M. 87, 92, 139, 246, 263Schultz, M. C. 259

334 Author index

Schulz-Schaeffer, W. J. 309Schum, D. 46, 48Schumacher, M. 22, 158Schunk, D. H. 44Schwartz, I. F. 79, 80, 81Schwartz, J. R. 304Schwartz, M. F. 34, 158, 159, 251Scott, R. B. 148Searle, J. R. 43, 45, 116, 117, 293Seger, C. A. 292Seibert, L. K. 50Seligman, M. 214Selinger, M. 266, 267Selnes, O. A. 305, 310, 312Senhadji, N. 290Sereno, M. I. 292Seron, X. 260, 261Shadden, B. 3, 75, 77, 83, 87, 198Shallice, T. 157, 158, 159Shamay-Tsoory, S. G. 46Shannon, C. E. 119Shapiro, B. E. 125Shapiro, L. P. 230, 249, 251Shatté, A. 214Sheard, C. 8, 170Sheeran, P. 184, 194Shigaki, C. 272, 276Shindler, A. G. 168Shotter, J. 96Shum, D. 46, 47, 49Sidtis, J. J. 126Silburn, P. A. 138, 149Silver, C. H. 62Silveri, M. C. 160, 249Silverman, J. 287Silverman, S. 251Simmons, N. N. 274Simmons, T. P. 184Simmons-Mackie, N. 3, 8, 75, 78, 79, 81,

92, 93, 97, 98, 100, 185, 255, 274, 275Simonson, H. G. 253Simpson, T. L. 285, 286Singh, S. 177Sjogren, T. 168Ska, B. 284, 287, 288, 289, 292Skrap, M. 235, 236Skriver, E. 147Slade, D. 185, 278Sleigh, J. W. 272Smith, G. E. 301Smith, L. 274Smith, R. D. 266, 267Snow, C. 250Snow, P. C. 53, 54, 56, 57, 59, 61, 271

Snowden, J. S. 162, 304, 305Soares, C. 125, 132Sobow, T. 304Soininen, H. 304Song, J. 53, 55, 56, 57, 58, 62Spell, L. A. 50Spence, S. E. 60Sperber, D. 50, 62Spiers, M. 48, 49Springer, L. 184Square, P. 185, 274, 275Squire, L. R. 147Starr, P. A. 141Stein, M. 276Steinhoff, B. J. 309Stemmer, B. 287, 294Stern, Y. 299, 304, 319Sterzi, R. 141, 148Stiassny-Eder, D. 141Stiegler, L. 8, 255Stone, V. E. 49Stout, C. E. 55, 57, 58, 62Strange, B. A. 52Strawson, P. 117Strettles, B. 271Strick, P. L. 138, 141, 142, 143Stubbs, M. 196Su, M. S. 127Suger, G. 140Sullivan, K. 49Sundet, K. 127, 128, 130, 132Sung, J. H. 305Surian, L. 48Swabey, D. 274, 276Swinburn, K. 247

Tager-Flusberg, H. 49Tanaka, R. 146Tanenbaum, L. N. 49Tangalos, E. C. 301Tate, R. L. 45, 46, 271, 272Teasdale, G. 43, 48Teasell, R. 83Teh, M. 48Testa, C. 304Testa, H. J. 304Theodoros, D. G. 138, 149Thibault, P. J. 190Thompson, C. K. 98, 230, 251Thompson, D. 140Thompson, G. 196, 201Thompson, J. L. 182, 226, 246Thompson, S. 120Thompson, W. F. 50

Author index 335

Thomson, I. V. 43Threats, T. T. 74, 83, 88Thron, A. 146Timberlake, W. H. 169, 178Tirassa, M. 44, 48Togher, L. 42, 48, 51, 55, 57, 60, 61, 188,

189, 270, 272, 273, 276, 277, 278Tomer, R. 46Tompkins, C. A. 53, 56, 57, 58, 62, 76, 80,

84, 288, 289Toomey, R. 49Tranel, D. 52, 249Tree, J. 6, 303, 315Trepanier, L. L. 148Tsironas, D. 86Tsohatzidis, S. L. 116Tucker, K. 250Turkstra, L. S. 44, 47, 56, 57, 58, 62

Ulatowska, H. K. 168, 182, 195, 198, 199,205, 225, 226, 233, 234, 235

Urbanczyk, B. 275, 276

Vallar, G. 137, 139, 140, 141, 143, 147Van Buren, J. M. 141Van der Lely, H. 48van Dijk, T. A. 57van Heuven, V. J. 127, 131, 132Van Hoesen, G. W. 141Van Lancker, D. 126, 129Van Rensburg, C. 224van Sommers, P. 48van Wageningen, B. 224, 250van Zonneveld, R. 224, 249Vanderveken, D. 116Vanhalle, C. 287Varma, A. R. 304Varney, N. 141Venter, A. 224, 226, 238Vermeulen, J. 224, 250Verney, N. 140Verté, D. 302Vignolo, L. A. 139, 140Vigouroux, N. 113Virbel, J. 7, 107, 111, 113, 116, 119, 120Vitek, J. L. 141von Bentheim, I. 224, 226, 238fvon Cramon, D. Y. 46Vygotsky, L. 32

Wacker, D. P. 77Wagenaar, E. 249Waletsky, J. 196Wallace, C. 272

Wallander, J. L. 272Wallesch, C. W. 4, 8, 18, 19, 20, 22, 29,

125, 137, 138, 139, 140, 142, 144, 156,160, 161, 162, 164, 168, 173

Walsh, K. W. 46, 52Walshaw, D. 182Walter, N. 292Wapner, W. 287Warburton, E. 149Ward, E. C. 138Watamori, T. S. 20Watson, D. R. 186Watson, J. D. G. 7, 23Watts, M. 44, 47, 49Wayland, S. 251Weaver, W. 119Webster, E. 215, 217Webster, J. 250Wechsler, F. S. 47, 272, 311Weiller, C. 146, 149Weinstein, E. A. 284Weiss Doyle, A. 225, 235Weitzner-Lin, B. 190Welkowitz, J. 198Wells, A. 78Weniger, D. 162, 169, 247Wenz, C. 19Wepman, J. M. 246Wernicke, C. 92Wertz, R. T. 44, 75, 86, 182, 226, 259, 260,

264, 265, 266, 268Wheeler, K. M. 266, 167Whelan, B.-M. 138, 149Whitaker, H. A. 169Whitworth, A. 168, 249Wiak, A. 300Wight, H. H. 251Wilcox, J. 183, 184Wilkes-Gibbs, D. 118Wilkinson, M. 44, 49Wilkinson, R. 93, 97, 182, 185, 233, 273,

274Williams, C. L. 161Williams, D. H. 45Williams-Hubbard, L. J. 225Willmes, K. 80, 162, 247Wilson, B. M. 55, 56Wilson, D. 50, 62Wilson, J. 148Windl, O. 309Winner, E. 44, 49, 288Winston, J. S. 52Wise, R. J. S. 149Wolf, M. M. 72, 73, 74

336 Author index

Wolf, P. A. 301Wolfson, N. 230, 232Woolf, C. 275Worrall, L. E. 3, 75, 80, 81, 82, 83, 88, 93,

184, 188, 189, 272, 273, 274, 276Wright, H. H. 251Wyen, C. 170

Xuereb, J. 307

Yamada, T. 139Yeterian, E. H. 141Yiu, E. M.-L. 128, 129, 130, 133, 273,

274, 276Ylvisaker, M. 61, 275, 276, 277

Yorkston, K. M. 55, 57, 58, 62, 171Yoshino, M. 146Young, A. W. 248Young, M. E. 197Youse, K. M. 58

Zalagens, M. R. 56, 57Zarahn, E. 304Zawacki, T. 146Zettin, M. 44Zieper, I. 169, 178Zingeser, L. 249Ziol, E. 275Zoghaib, C. 79, 194

Author index 337

Subject index

Page entries in bold refer to tables/figures.

Acquired Immune Deficiency Syndrome(AIDS) 170

Adjectivesin evaluation 204in word repetition 173, 176

Ageand dementia 300, 309in testing 76, 77

Agrammatism 224definition of 109–110illustration 110writing 303

Agraphia 312Alzheimer’s disease see DementiaAmimia 305Amyotrophic lateral sclerosis 83, 216Anartria 137Anomia 33, 110, 157, 160, 306Aphasia

amnesic 162anomic 128, 131, 157,Broca’s 125, 128, 130, 131, 132, 133,

140, 205, 246, 251conduction 128, 130, 137definition of 294expressive 246fluent 162, 187, 306,global 140, 164, 309, 314jargon 301mixed transcortical sensory 139motor see transcortical motornonfluent 18, 22, 130, 305, 313progressive 162, 216, 305, 306receptive 246semantic 162sensory see transcortical sensorystriatocapsular 139, 140

subcortical 136–150thalamic 139–140transcortical motor 128, 140, 142transcortical sensory 301Wernicke’s 125, 128, 130, 140, 162

Aphasia quotient 182, 264, 311Apraxia of speech 5–6Artery

carotid 146middle cerebral 146

Articulation 141, 146imprecise 170in microgenetic theory 318

Asperger’s syndrome 48Ataxia

in Creutzfeldt-Jakob disease 309Atrophy 300, 312

of the temporal lobe 162, 304, 305Attitude

in clinicians 317in speakers 44, 48, 50, 51, 208

Auditory association cortex 143Auditory comprehension

in assessment 261in the subcortical white matter

pathways model 142–143in treatment 261–263vs. visual comprehension 23

Augmentative alternativecommunication (AAC) 77, 85

Basal Ganglia see also Subcortical region22, 136, 137, 138, 140, 141, 145, 146,149, 150, 170

Behaviourally Referenced Rating Systemof Intermediate Social Skills(BRISS) 272

Bilingualism 223, 224, 225, 226, 234–237,254

Body language 219Boston Diagnostic Aphasia Examination

(BDAE) see Standardized testsBrain damage

and depression 216knowledge of 33, 92psychosocial adjustment to 2–3and tone 127–132

Brain stem 170Broca’s area 142

Caudate nucleus 137, 144, 150lesion of 142

Cerebellum 138, 170, 313Classical view of aphasia 246, 247, 293Code-Müller Protocols (CMP) 2–3, 18,

20–22Code-switching 225, 233, 234, 235, 236,

237Communication Abilities in Daily Living

(CADL) see Standardized testsCommunication Readiness and Use

Index (CRUI) 79, 86Compensatory strategies 18, 223, 224,

235Comprehension 7, 44, 46, 49–50, 62, 75,

118–120, 139–143, 146, 149, 163,246–253, 261–266, 286, 292,305–306, 315, 318

Comprehensive Aphasia Test (CAT) seeStandardized tests

Conversation analysis (CA) 94, 100, 183,188, 274

Coprolalia 169Corpus callosum 126Counseling 181, 186, 213, 289

definition of 215

Deafness, and aphasia 113Dementia 168, 215, 216, 299–320

and age 300, 309Creutzfeldt-Jakob disease (CJD) 300,

309–312definition of 317dementia of the Alzheimer’s type

(DAT) 129, 162–163, 168, 275, 300,301–304

and depression 302fronto-temporal dementia (FTD) 300,

304–309history 317MELAS syndrome 300, 312–315

semantic dementia (SD) 162–163subcortical dementia 307

Depression 2, 20, 216–217, 271, 302post-stroke 22–23

Discourse analysis 54–55, 100, 196Dominance, in tonal perception 127Dysarthria 5, 140, 170, 171, 177, 303,

307, 315, 316Dysgraphia 307, 310

Echolalia 169, 309Efficiency, in testing 259, 266, 267Employment, prognosis and 85,

271Epenthesis 111Evaluation

factors influencing 199of patient 120, 288, 289

Executive dysfunction 46

FACS see Standardized testFamily

affect of aphasia on 87as conversational partners 276–277counseling of 218, 220, 289treatment and 78, 81, 213, 276

Feedbackin treatment 260, 263, 267, 272in models of word production 159in the response-release semantic

feedback model 143Fluency 146, 247, 285, 301, 303, 305Frontal lobe 51, 144, 145, 236, 315Frontostriatal circuits 22Functional approach to treatment 75, 98,

274Functional Assessment of

Communication Skills (FACS) forAdults see Standardized tests

Functional magnetic resonance imaging(fMRI) 23, 149, 150, 292

Function words 160, 173

Generalization 79, 84, 261Genetic factors 290, 319Gesture 110, 171, 182Grammar, evaluation of 250Grice’s Maxims 52–53, 54, 55Group therapy see Therapy

Handedness 290Handicap, definition of 107–108Helm Elicited Language Program for

Syntax Stimulation (HELPSS) 84

340 Subject index

Hemispheric Asymmetry Reduction inOlder Adults (HAROLD) 290

History, evaluation and 233, 237,of family 290, 310

Human Immunodeficiency Virus (HIV)170

Hypokinetic dysarthria 170, 307

Infarction 146, 147Inferential reasoning 46Informational theory 120Inflectional morphology 109–110Inner speech 315, 318Intonation see also Prosody 125, 127,

132, 219Iteration 169, 173

Jargon, as symptom of aphasia 36, 301

Languageacquisition 118, 161contact 224deficits 18, 44, 137, 142, 143, 144, 145,

146, 248, 249impairment 45, 140, 143, 182, 195, 198modality 39, 59, 160neurophysiology of 28, 32, 108, 292processing 6, 7, 101, 136, 137, 139, 150,

158, 183, 213, 223, 248rehabilitation 7written 157

Left hemisphere 22, 119, 125, 126, 127,128, 129, 133

Lexicon 110, 130, 132, 157, 163, 224, 285Life Participation Approach 3, 74, 83Linguistics 116,

clinical linguistics 125psycholinguistics 116

Logoclonia 301, 303, 305

Magnetencephalography (MEG) 23Memory

episodic memory 290in assessment 149semantic memory 130, 157, 285short-term memory 301verbal memory 139, 287working memory 271, 287, 290, 300,

307Mental calculation see number

processingMetaphoric language 199, 206Microgenetic theory 318–319Multiple sclerosis 216

Multilingualism see also Bilingualism222, 223, 225, 237

Mutism 110, 299, 301, 305, 310, 319

Near Infrared Spectroscopy OpticalImaging (NIS/OI) 292

Neologisms 35, 36Neural networks 33, 286, 287, 290, 291,

292, 293Nouns 244, 253, 254

in assessment 249Number processing 23–24

Palilalia 169, 173, 178, 308PALPA see Standardized testsParkinsonism 216Parkinson’s disease 148, 307Perseveration 35, 39, 46, 139, 169, 205,

301of topics 271

Personalityin evaluation 199change of 304, 305, 307

Phoneme, perseveration of 35Phonemic decoding 130Phonemic errors 110, 157Phonetic decoding 130Phonology 5, 163, 224, 250

expressive 232, 234, 242gestural 5government 5and phonetics 5underspecification in 131usage based 5

PICA see Standardized testsPorch Index of Communicative Ability

see Standardized testsPositron emission tomography (PET)

149, 150, 292Pragmatics 183, 224, 287–288, 294

Pragmatic Theory 43Progressive speech deterioration 6Progressive supranuclear palsy (PNP) 306Proposition 204, 317

definition of 111Prosody

definition of 125–126emotional 285in speech perception 219

Psycholinguistic Assessment ofLanguage Processing in Aphasia(PALPA) see Standardized tests

Psychosocial factors 18–19, 20–22, 79,86–87

Subject index 341

Psychosocial Well-Being Index (PWI) 86Putamen 137, 138, 141, 142, 143, 146, 150

Quality of life 3, 9, 78–79, 80–81, 82, 85,170, 266, 299

Health Related Quality of Life(HRQOL) 83

World Heath Organization (WHO)definition of 82

Readingcomprehension 140intervention 75, 263–265testing 132, 246, 247, 252

Recurrent utterances 3–5, 169, 271Repetitive utterances see Recurrent

utterancesRecovery

predictions in 29psychosocial factors in 87the role of the right hemisphere in 7spontaneous 216

Rehabilitation 6–7, 17, 19, 20–21, 72goals in 21–22, 82, 273maintenance of 80social validation of 88stages in 22stimuli for 76strategies for 289, 294

Rhetorical Structure Theory (RST)120

Right hemispherelesion 118, 128–129, 133, 216, 285role in communication 5, 6–7, 126,

284, 291

Semiological substitution 113Semantics 114, 157, 252, 285, 286, 317Science and Technology of Information

and Communication (STIC) 115Speech

apraxia of, see Apraxia of speechinstrumental analysis of 5speech automatisms see Speech

automatismsSpeech Act(s) Theory (SAT) 43, 62,

116–119Standardized tests

Boston Diagnostic AphasiaExamination (BDAE) 86, 247

Communication Abilities in DailyLiving (CADL) 86

Comprehensive Aphasia Test (CAT)247

Functional Assessment ofCommunication Skills (FACS) forAdults 182

Porch Index of CommunicativeAbility (PICA) 262

Psycholinguistic Assessment ofLanguage Processing in Aphasia(PALPA) 245, 248–249, 252–253

Verb and Sentence Test (VAST) 245,249, 250, 253–254

Western Aphasia Battery (WAB) 74,247

Stereotypy 169Stroke 4, 18, 19, 195–209

depression following 22–23Sonority sequencing principle 4Speech automatisms 3–5, 169

origins of 4Speech tics 169Spinal cord, results of lesion in 170Stuttering 5, 73, 308Subcortical region, neuroanatomy of 138

models of participation in language141–147

Suprasegmental characteristics 6Systemic Functional Linguistics (SFL)

59, 172, 270, 278Syntax 84, 163, 224, 305, 317

TBI see Traumatic brain injuryTraumatic brain injury (TBI) 42–63, 216,

270, 271in children 44, 46, 51, 56, 58

Treatment see also Rehabilitationsocial validation of 2, 73

Thalamusaffect of lesion 139–140anatomical function of 138role in language 139, 150role in lexical decision making model

145role in response-release semantic

feedback model 143–144role in selective engagement model

145Therapy

of speech 18, 72occupational 21participants in 273physiotherapy 21neuropsychological 21Group therapy 72, 84, 181, 183–184,

185, 186, 187, 189goals 74, 79, 84–85

342 Subject index

Theory of Mind (ToM) 48–49Token test 182Tone languages 127

VAST see Standardized testsVerb and Sentence Test (VAST) see

Standardized testsVerbs 118, 198, 224, 225, 227, 229, 249,

252, 253–254, 266, 267, 318copula 76errors 226, 228

Visual impairment 309, 310, 312, 313Visual stimuli 80, 261Vocabulary

in dementia 301measures of 251

Voicing 5Vowels 5, 111, 171

ratio to consonants 4

WAB see Standardized testsWernicke’s Area 143Western Aphasia Battery (WAB) see

Standardized testsWord finding difficulties 54, 57, 139, 142,

143, 163, 182, 206, 271, 301Word frequency 160–161, 163, 249, 252,

263Word length 160, 263Word order 225, 229, 230, 234, 235, 253Word production

models in 156, 158–159Word tics 169Writing 84–85, 140, 171, 246, 247

agrammatism 303computerized 260–261orthographical errors 310samples 78

Written language 157, 172, 246

Subject index 343

Documents

Clinical Aphasiology