Inhibition, Anxiety and the Development of Auditory Hallucinations · Inhibition, Anxiety and the Development of . Auditory Hallucinations . Georgie Paulik . B.Sc. (Hons.) (Psychology)

Inhibition, Anxiety and the Development of

Auditory Hallucinations

Georgie Paulik

B.Sc. (Hons.) (Psychology)

School of Psychology

University of Western Australia

This thesis is presented for the degree of Doctor of Philosophy and

as a partial requirement for the degree of Masters of Psychology (Clinical)

of the University of Western Australia.

2008

ii

iii

ABSTRACT

Auditory hallucinations (AHs) are one of the most common symptoms of

schizophrenia, and are associated with high levels of distress, functional impairment,

and need for care. However, current understanding of the exact causes – and thus

treatment – of AHs is still in its infancy. Recently, Badcock and colleagues proposed a

cognitive dual-deficit model of AHs, which stipulates that intentional inhibition deficits

underlie the intrusive and unintentional nature of AHs, while context memory binding

deficits explain the source misattribution (Waters, Badcock, Michie, & Maybery, 2006).

While this model seems to best explain the different features of AHs, the precise

components of inhibitory control involved, and the evident role of negative affect in the

production of AHs, have not been empirically examined. Thus, the first two aims of this

thesis were to clarify the critical component(s) of inhibitory control specifically related

to AHs, and to examine the relationships between negative affect (chiefly anxiety), AHs

and inhibitory control. Finally, AHs are also commonly reported by individuals in the

general population, consistent with a continuum approach to AHs. Accordingly, the

third aim of this thesis was to investigate whether similar relationships exist between

hallucinatory-type experiences, inhibitory processes and negative affect in both

hallucination predisposition and schizophrenia.

The first study presents the findings from two related investigations of

hallucination predisposition. The first of these investigations used confirmatory factor

analysis (N = 589) to identify the specific features of hallucination predisposition in the

general population (measured using the revised Launay-Slade Hallucination Scale;

Bentall & Slade, 1985), and found that intrusiveness was a defining feature of all three

components obtained. The second investigation examined relationships between

negative affect and separate components of hallucination predisposition (N = 462), and

identified a consistent association between anxiety – but not depression or stress – and

all three components, possibly reflecting a relationship with the intrusiveness of

experiences in hallucination predisposition.

Empirical studies have shown that intrusive mental events are the product of

failed cognitive inhibition (Friedman & Miyake, 2004). Given the intrusive nature of

hallucination preposition, the second and third studies, together, aimed to dissociate the

critical inhibitory components involved in hallucination predisposition. This was

achieved through the administration of tasks differentially assessing intentional

inhibition (Inhibition of Currently Irrelevant Memories [ICIM] task; Schnider, Valenza,

iv

Morand, & Michel, 2002), unintentional inhibition (Brown-Peterson [B-P] variant task;

Kane & Engle, 2000) and intentional resistance to interference (directed ignoring task

[DI] task; Connelly, Hasher, & Zacks, 1991) to high (N = 26) and low (N = 25)

hallucination predisposed participants. The findings support the Badcock et al. model of

– and thus the continuum approach to – AHs, since the hallucination predisposed group

exhibited difficulties with intentional, but not unintentional, forms of cognitive control,

with intentional inhibition being the only form of cognitive control uniquely related to

hallucination predisposition.

Anxiety has been empirically linked to both intrusive cognitions and inhibition

difficulties (Wood, Mathews, & Dalgleish, 2001). The fourth study aimed to investigate

whether anxiety exacerbates intentional inhibition difficulties in both high (N = 28) and

low (N = 33) hallucination predisposed participants. A music mood induction paradigm

was used to compare participants’ performance on the ICIM task following an anxious

induction in one condition and a neutral induction in another. Overall there was a non-

significant pattern of effects of state anxiety on intentional inhibition, possibly due to

the modest magnitude and duration of the induced mood states. However, the study

revealed a significant relationship between intentional inhibition and trait anxiety

(which was independent of hallucination predisposition) allowing the possibility that

more severe or longer lasting changes in anxiety may indeed exacerbate difficulties with

intentional inhibition.

The final study sought to determine whether the pattern of relationships between

AHs, inhibitory impairments and anxiety in schizophrenia are similar to those found in

hallucination predisposition. The same three cognitive tasks previously employed

(ICIM, B-P, and DI) were administered to schizophrenia (N = 61) and healthy control

(N = 34) participants. Schizophrenia participants overall exhibited difficulties

intentionally resisting interference from distracting stimuli, however did not have

difficulties [intentionally or unintentionally] inhibiting task-irrelevant memory traces.

Consistent with the continuum approach, AHs were related only to difficulties with

intentional inhibition, and these difficulties existed independently from anxiety

(although anxiety was related to intentional inhibition) and were unrelated to other

schizophrenia symptoms.

Together, the studies support the first component of Badcock et al.’s dual-deficit

model of AHs, with hallucinatory experiences in both hallucination predisposition and

schizophrenia associated with specific intentional inhibition impairments. The findings

also suggest that while anxiety may contribute to the production of AHs by exacerbating

v

existing intentional inhibition impairments, it is likely that anxiety has additional routes

of influence. These findings provide strong support for the continuum approach to AHs.

The implications of these findings and possible avenues for future research are

discussed.

vi

REFERENCES

Bentall, R. P., & Slade, P. D. (1985). Reliability of a scale measuring disposition

towards hallucination: A brief report. Personality and Individual Differences, 6,

527-529.

Connelly, S. L., Hasher, L., & Zacks, R. T. (1991). Age and reading: The impact of

distraction. Psychology and Aging, 6, 533-541.

Friedman, N. P., & Miyake, A. (2004). The relations among inhibition and interference

control functions: A latent-variable analysis. Journal of Experimental

Psychology: General, 133, 101-135.

Kane, M. J., & Engle, R. W. (2000). Working-memory capacity, proactive interference,

and divided attention: Limits on long-term memory retrieval. Journal of

Experimental Psychology: Learning, Memory, and Cognition, 26, 336-358.

Schnider, A., Valenza, N., Morand, S., & Michel, C. M. (2002). Early cortical

distinction between memories that pertain to ongoing reality and memories that

don't. Cerebral Cortex, 12, 54-61.

Waters, F. A. V., Badcock, J. C., Michie, P. T., & Maybery, M. T. (2006). Auditory

hallucinations in schizophrenia: Intrusive thoughts and forgotten memories.

Cognitive Neuropsychiatry, 11, 65-83.

Wood, J., Mathews, A., & Dalgleish, T. (2001). Anxiety and cognitive inhibition.

Emotion, 1, 166-181.

vii

TABLE OF CONTENTS

Abstract……………………………………………………………………………… iii

(Table of Contents)

Manuscripts and publications generated from this thesis…………………………… xiii

Declaration for theses containing published work ……………………………….… xv

Acknowledgements…………………………………………………………………. xvii

INTRODUCTION………………………………………………………………..... 1

Chapter 1: An overview of schizophrenia, auditory hallucinations, inhibition and

negative affect………………………………………………………………………. 3

Abstract……………………………………………………………………………… 3

Schizophrenia…………………………………...…………………………………... 4

Auditory hallucinations…………………………………………………………...… 8

Definition……………………………………………………………………. 8

Auditory hallucinations in schizophrenia..……………...………..………..… 8

Auditory hallucinations in other clinical populations……………………….. 9

Auditory hallucinations in the general population………………………..… 10

Explanatory models of auditory hallucinations …………………………..… 13

Mental imagery…………………………………………...……….… 13

Inner speech…………………………………..…………………...… 14

Socio-psychological theories……………………………………...… 16

Dopamine……………………………………………………………. 17

Dual deficit model: Intentional inhibition and context memory…….. 19

Negative affect…………………………………………………………………….… 22

Definition………………………………………………………………….… 22

Negative affect and schizophrenia…………………………………….......… 23

Negative affect and auditory hallucinations ……….……………………...… 24

The role of negative affect in the onset and maintenance of auditory

hallucinations………………………………………………………... 24

Negative affect and the phenomenology of auditory hallucinations… 26

Key processes under investigation…………………………………………………... 29

Cognitive inhibition…………………………………………………………. 29

Anxiety and depression …………………………………………………….. 31

viii

Aims and organization of thesis………………………………………………….…. 33

References…………………………………………………………………………... 36

PREDISPOSITION TO HALLUCINATIONS………………………………….. 59

Foreword to Chapter 2…………………………………………………………….… 61

Chapter 2: The multifactorial structure of the predisposition to hallucinate and

associations with anxiety, depression and stress………………………………..... 63

Abstract…………………………………………………………………………….... 63

Introduction………………………………………………………………………….. 64

Study 1……………………………………………………………………………..... 65

Method………………………………………………………………………. 66

Participants………………………………………………………...... 66

Measures…………………………………………………………….. 66

Model definition for confirmatory factor analysis………………...... 66

Results and discussion…………………………………………………….… 67

Study 2………………………………………………………………………………. 68

Method………………………………………………………………………. 69

Participants………………………………………………………….. 69

Measures…………………………………………………………….. 69

Results and discussion………………………………………………………. 70

General discussion………………………………………………………………….. 72

Acknowledgements……………………………………………………………….… 75

References…………………………………………………………………………… 76

PREDISPOSITION TO HALLUCINATIONS AND INHIBITORY CONTROL… 79

Foreword to Chapters 3 and 4……………………………………………………..… 81

Chapter 3: Poor intentional inhibition in individuals predisposed to

hallucinations……………………………………………………………………….. 83

Abstract……………………………………………………………………………… 83

Introduction………………………………………………………………………….. 84

Method………………………………………………………………………………. 85

Participants……………………………………………………………...…… 85

Measures………………………………………………………………..…… 86

ix

Inhibition of currently irrelevant memories (ICIM) task……………. 86

Additional measures……………………………………………….... 87

Procedure…………………………………………………………………………..... 87

Results………………………………………………………………………….….… 88

Descriptive statistics……………………………………………………….… 88

ICIM task………………………………………………………………….… 88

Encoding and recognition in run 1…………………………...……… 89

Target detection in runs 2 and 3…………………………………….. 89

Intentional inhibition in runs 2 and 3……………………………...… 90

Signal detection analysis…………………………………………..… 90

Response times for run 1……………………………………………. 90

Response times for runs 2 and 3…………………….…………….… 91

Discussion…………………………………………………………………………… 92

Acknowledgements………………………………………………………….……… 96

References…………………………………………………………………………… 97

Chapter 4: Dissociating the components of inhibitory control involved in

predisposition to hallucinations………………………………………………...…. 101

Abstract……………………………………………………………………………… 101

Introduction……………………………………………………………………..…... 102

Method……………………………………………………………………………..... 104

Participants………………………………………………………………….. 104

Measures…………………………………………………………………...… 105

Directed ignoring………………………………………………….… 105

Brown-Peterson variant……………………………………………… 105


Procedure……………………………………………………………………. 107

Results…………………………………………………………………………….… 107

Descriptive statistics……………………………………………………….... 107

Directed ignoring task………………………………………………………. 108

Reading time……………………………………………………….... 108

Intrusions…………………………………………………………..... 109

Multiple choice questions: Foil errors and accuracy…………….….. 110

Brown-Peterson Variant Task…………………………………………….… 110

Word recall………………………………………………………….. 110

x

Intrusions in recall………………………………………………...… 111

Discussion…………………………………………………………………………… 111

Acknowledgements…………………………………………………………………. 115

References…………………………………………………………………………… 116

ANXIETY, INHIBITION, AND HALLUCINATION PREDISPOSITION…… 119

Foreword to Chapter 5………………………………………………………………. 121

Chapter 5: Effects of anxiety on the intentional inhibition of currently irrelevant

memories: A hallucination predisposition study ………….……….……………. 123

Abstract……………………………………………………………………………… 123

Introduction…………………………………………………………………………. 124

Method…………………………………………………………………………..…... 126

Participants……………………………………………………………..……. 126

Measures…………………………………………………………………..… 126

Inhibition of currently irrelevant memories (ICIM) task……………. 126

Mood induction procedure………………………………………..…. 127

Mood measures……………………………………………………… 127


Procedure……………………………………………………………………. 128

Results………………………………………………………………………….…… 129

Descriptive statistics………………………………………………..……….. 129

Efficacy of mood induction procedure…………..…………………….……. 130

Intentional inhibition and hallucination predisposition..…………………….. 131

Effects of anxiety on ICIM task performance…………………….…..…...… 132

Encoding and recognition………………………………………..….. 132

Intentional inhibition and target detection in run 2…………….…… 133

Response times for run 1………………………………..…………… 133

Response times for run 2………………………………..…………… 134

Trait anxiety and intentional inhibition in run 2…………..………… 134

Discussion…………………………………………………………………………… 134

Acknowledgements……………………………………………………………….… 138

References………………………………………………………………………..…. 139

xi

AUDITORY HALLUCINATIONS, INHIBITION AND ANXIETY IN

SCHIZOPHRENIA……………………………………………………………….. 145

Foreword to Chapter 6………………………………………………………….…… 147

Chapter 6: Inhibitory dysfunction, anxiety and auditory hallucinations…….… 149

Abstract……………………………………………………………………………… 149

Introduction……………………………………………………………………..…... 150

Anxiety and inhibitory control…………………………………………….... 151

Anxiety and auditory hallucinations………………………………………… 152

Hypotheses……………………………………………………………...…… 153

Method……………………………………………………………………………..... 153

Participants………………………………………………………………..… 153

Measures…………………………………………………………………….. 154

Inhibition of currently irrelevant memories (ICIM) task…………… 154

Directed ignoring (DI) task…………………………………………. 155

Brown-Peterson variant (B-P) task...……………………………….. 156

Clinical interviews…………………………………………………... 157


Procedure……………………………………………………………………. 158

Data Analysis………………………………………………………………... 158

Results………………………………………………………………………………. 159

Descriptive statistics………………………………………………………… 159

Schizophrenia- and control group comparisons…………………………….. 160

ICIM task performance………………..……………………………. 160

Intentional inhibition (false alarms: FA)………………….… 160

Target detection (Hits)…………………………………….… 160

DI task performance………………………………………………… 161

Reading time (RT)…………………………………………... 162

Intrusions……………………………………………….…… 162

Comprehension…………………………………………….... 162

B-P task performance……………………………………………..… 163

Correlations between anxiety and inhibition indices…………………...…… 163

Correlations between anxiety and schizophrenia-related symptoms………... 163

Correlations between schizophrenia-related symptoms and inhibition

indices..…………………………………………………………………...…. 164

xii

Discussion…………………………………………………………………………… 165

Acknowledgements…….…………………………………………………………… 171

References…………………………………………………………………………... 172

GENERAL DISCUSSION……………………………………………………….... 177

Chapter 7: General Discussion………………………………………………….… 179

Review of thesis aims…………………………………………………………..…… 179

Cognitive control and hallucinatory experiences…………………………………… 180

Summary of findings and interpretation.………………………………….… 180

Critical examination of findings……………………………………….……. 183

Strengths, limitations and implications for future research……………….… 186

Clinical implications………………………………………………………… 189

Summary………………………………………………………………….…. 190

Anxiety and hallucinatory experiences……………………………………………… 190

Summary of findings and interpretation.……………………………….…… 190

Critical examination of findings ………………………………………...….. 193

Strengths, limitations and implications for future research……………….… 195


Summary…………………………………………………………………..… 197

The hallucination continuum………………………………………………………... 198

Summary of findings and interpretation.……………………………………. 198

Critical examination of findings …………………………………………..... 200

Strengths, limitations and implications for future research…………….…… 200


Summary………………………………………………………………..…… 203

Final comments…………………………………………………………………..….. 204

References…………………………………………………………………………… 206

APPENDICES……………………………………………………………………… 217

Appendix A: Words used in the Brown-Peterson variant task (Chapters 4 and 6).… 218

Appendix B: Stories and comprehension questions used in the directed ignoring task

(Chapter 4)…………………………………………………………………………… 221

Appendix C: Stories and comprehension questions used in the directed ignoring task

(Chapter 6)………………………………………………………………………...… 232

Appendix D: Dissociating the components of inhibitory control associated with

auditory hallucinations in schizophrenia…………………………………………….. 247

xiii

MANUSCRIPTS AND PUBLICATIONS GENERATED FROM THIS THESIS

This thesis consists of a collection of papers prepared in journal format, supplemented

by a general introduction, chapter forewords connecting the papers, and a general

discussion. The papers and publications presented in this thesis are as follows:

Chapter 2

Paulik, G., Badcock, J., & Maybery, M. (2006). The multifactorial structure of the

predisposition to hallucinate and associations with anxiety, depression and

stress. Personality and Individual Differences, 41, 1067 – 1076.

Chapter 3

Paulik, G., Badcock, J., & Maybery, M. (2007). Failure to inhibit currently irrelevant

memories in individuals predisposed to hallucinations. Cognitive

Neuropsychiatry, 12, 457-470.

Chapter 4

Paulik, G., Badcock, J., & Maybery, M. (2008). Dissociating the components of

inhibitory control involved in predisposition to hallucinations. Cognitive


Chapter 5

Paulik, G., Badcock, J., & Maybery, M. (2008). Effects of anxiety on the intentional

inhibition of currently irrelevant memories: A hallucination predisposition study.

Unpublished manuscript, University of Western Australia.

Chapter 6

Paulik, G., Badcock, J., & Maybery, M. (2007). Inhibitory dysfunction, anxiety and

auditory hallucinations. Manuscript submitted for publication to the Journal of

Abnormal Psychology (October 2007).*

* Based on feedback from two journal reviwers a revised version of this manuscript was

written and is included in the Appendices (Appendix D): Paulik, G., Badcock, J., &

Maybery, M. (2007). Dissociating the components of inhibitory control associated with auditory

hallucinations in schizophrenia. Manuscript submitted for publication to Cognitive

Neuropsychiatry (May 2008).

xiv

xv

DECLARATION FOR THESES CONTAINING PUBLISHED WORK AND/OR

WORK PREPARED FOR PUBLICATION

Please sign one of the statements below.

1. This thesis does not contain work that I have published, nor work under review for

publication.

2. This thesis contains only sole-authored work, some of which has been published

and/or prepared for publication under sole authorship.

3. This thesis contains published work and/or work prepared for publication, some of

which has been co-authored.

In all of the studies included in this thesis (see the previous section Manuscripts and

Publications Generated From This Thesis for details), study design, task development,

participant recruitment and testing, data entry, analysis, interpretation, and preparation

and revision of manuscripts were conducted by the candidate. There are two minor

exceptions. The original software programs for the computer-administered tasks

reported in Chapters 2 to 6 were developed with the assistance of Matt Huitson,

however the candidate was in charge of task development/design and made most

subsequent modifications to the programs. In addition, approximately half of the

experimental testing for the study reported in Chapter 5 was completed by a research

assistant (trained and supervised by the candidate) since the testing phases for the

experiments reported in Chapters 5 and 6 unavoidably overlapped.

The additional authors on the included manuscripts give permission for the publications

produced during the primary author’s candidature to be included in this thesis.

___________________________ ________________________

Georgina Paulik (candidate) Date

___________________________ ________________________

Johanna Badcock (co-supervisor) Date

___________________________ ________________________

Murray Maybery (co-supervisor) Date

xvi

xvii

ACKNOWLEDGEMENTS

I would like to sincerely thank the following people, for without their wisdom,

encouragement and humour, the fruition of this thesis may never have been.

First and foremost, I would like to thank my two supervisors, Johanna Badcock

and Murray Maybery. I greatly admire Jo’s unmatched drive and dedication to research,

which have inspired me to further pursue my own passion for schizophrenia research

and clinical practice. Her razor sharp intellect, enthusiasm, and compassion have been

invaluable. Murray has been my stable rock. His door has always been open to me,

whether for thesis guidance, calamity control or to share a laugh. His encouragement,

patience and calmness have been instrumental to the development of this thesis. I would

also like to thank both Jo and Murray for having trust and confidence in me to complete

the final six months of this thesis interstate. This has brought me tremendous happiness.

I am also indebted to the Schizophrenia Research Institute and the Ron and

Peggy Bell Foundation, who provided encouragement and financial support for this

project; Matt Huitson, for his programming assistance and infinite patience; Flavie

Waters, for setting the bar extremely high; Alan Bland and Sarah Howell, for their

recruitment expertise; and John Dean, for his enthusiastic diagnostic interview training.

My most heartfelt thanks goes out to all of the project’s participants, especially

to the individuals who confided in me their intimate experiences of life and the trials of

schizophrenia. Thank you to these people for their inspirational courage. I truly hope

that this research may contribute to these individuals finding hope and relief.

My friends have also played a vital role in the fruition of this thesis. I would like

to say a special thank you to: my psychology gals, Mel, Suzie, Sian, and Amanda, for

the endless support and countless laughs we have shared over our monthly ‘co-

supervision’ dinners; Russell and Nic, for enforcing Friday beer o’clock; my Capoeira

family, who have helped me to find the balance I so needed; and my dear friend

Hannah, for the laughs, the beer, the backgammon and for most generously

transforming her home into my office.

Finally, I would like to thank the people who I hold most dear to my heart: my

partner and best friend, Johnny Pascall, who challenges me everyday to seek the

unattainable and give back my weight in love; and my family, in particular my mum

Debbie, who has been my pillar of strength and inspiration throughout life. I am

beholden to these people, and eternally thankful for their immeasurable contributions to

my life.

xviii

Chapter 1

1

INTRODUCTION

Chapter 1

2

Chapter 1

3

Chapter 1

An overview of schizophrenia, auditory hallucinations,

inhibition and negative affect

ABSTRACT

The aim of this chapter is to summarize the relevant theoretical and empirical

literature pertaining to the critical phenomena under investigation in this thesis: namely,

auditory hallucinations, cognitive inhibition, and negative affect. In the first section, the

epidemiology and clinical characteristics of schizophrenia will be briefly reviewed,

followed by a more detailed literature analysis of auditory hallucinations (AHs). The

phenomenological findings from studies of AHs in schizophrenia, other clinical

populations, and the general population will be reviewed in turn. The most widely

debated and researched cognitive, socio-psychological, and biological-based models of

AHs will then be reviewed. The third section examines the literature on negative affect

in schizophrenia, and and its potential roles in AHs more specifically. In this section,

the literature regarding negative affect as a trigger, a maintenance mechanism, a

determinant of content, and a by-product of AHs will be sequentially reviewed. The

fourth section discusses the literature (from studies of the healthy population) pertaining

to the two key constructs related to AHs that are under investigation in this thesis:

cognitive inhibition and negative affect. Finally, an outline, and the aims, of the

proceeding chapters will be presented.

Chapter 1

4

SCHIZOPHRENIA

Schizophrenia, from the Greek roots schizo ("split") and phrene ("mind"), is a

common and often disabling mental disorder which occurs in all races and cultures at an

incidence rate of between 0.4% and 0.6%, and is equally common in men and women

(American Psychiatric Association [APA], 2000; Bhugra, 2005; Goldner, Hsu, Waraich,

& Somers, 2002). Sufferers commonly have low social and occupational functioning,

widespread neuro-cognitive impairment, poor quality of life, and a reduced life

expectancy (Elvevag & Goldberg, 2000; Huppert, Weiss, Lim, Pratt, & Smith, 2001;

Jablensky et al., 1999). Needless to say, the costs of schizophrenia to the sufferer, the

sufferer‟s family and their social network are immense, both emotionally and

financially. The costs of schizophrenia however do not end there. Despite its relatively

low prevalence, the direct annual financial costs of schizophrenia to the Australian

government ranks in the top three of mental illnesses, costing government around $653

million per annum (based on calculations from 2001; Australian Institute of Health and

Welfare, 2002). The poor quality of life had by most individuals with schizophrenia, as

well as the financial costs of the disorder, emphasise the importance of improving our

understanding, and thus prevention and treatment, of schizophrenia and the associated

distressing and disabling symptoms, such as hallucinations.

Schizophrenia is diverse in symptom presentation and course. The prodromal

phase – that is, the period of time prior to the first full-blown psychotic episode when

there is some evidence of social, cognitive, and affective changes taking place – most

commonly begins during late adolescence, and lasts anywhere between several weeks

and several years (Addington et al., 2007). Most individuals who develop schizophrenia

will have their first full-blown psychotic episode in young adulthood (Castle, Wessely,

Der, & Murray, 1991). The primary symptoms in schizophrenia have been classified or

described in terms of positive (or productive) symptoms and negative (or deficit)

symptoms (Crow, 1980; Liddle, 1987). Positive symptoms include hallucinations (a

perceptual experience in the absence of corresponding external stimuli, including

auditory, visual, tactile, olfactory and gustatory percepts), delusions (a strongly held and

fixed belief that is not founded on true evidence and is not ordinarily accepted by other

members of the person's culture), and thought disorder (disorganised thinking and

speech), although the latter of these is often classified in a third class of symptoms aptly

termed disorganised symptoms, which includes chaotic and catatonic speech, thought,

and behaviour (Peralta & Cuesta, 2001). Negative symptoms are so-named because they

Chapter 1

5

are considered to be the loss or absence of normal traits or abilities, and include features

such as flat or blunted affect, poverty of speech (alogia), an inability to experience

pleasure (anhedonia), and lack of motivation (avolition).

The diverse range of symptoms and symptom groupings has led to the

development of a sub-classificatory system for schizophrenia specified in the

Diagnostic and Statistical Manual of Mental Disorders (DSM; APA, 2000).

Accordingly, five sub-types of schizophrenia are recognised: paranoid type,

disorganized type, catatonic type, undifferentiated type, and residual type (where

positive symptoms are present, but of low intensity). Reflecting the vast clinical

diversity of schizophrenia, several other classificatory systems have been developed

(e.g., Harris, Gordon, Bahramali, & Slewa-Younan, 1999; Liddle, 1987; Peralta &

Cuesta, 2001), including the proposal that the standard diagnostic criteria for

schizophrenia be modified to include cognitive impairments (Keefe & Fenton, 2007). In

addition to the diverse primary symptoms of schizophrenia, many secondary symptoms

and co-morbid disorders also occur in schizophrenia, including substance abuse, mood

disorders, anxiety disorders, and personality disorders (Kavanagh et al., 2004;

McGlashan, 1987; Svirskis et al., 2005; also see the Negative Affect and Schizophrenia

section). Many of these symptoms/disorders appear to develop in response to the

primary symptoms (i.e., substance abuse as a coping strategy), while others may reflect

some shared etiological components (be it genetics, neurological, cognitive, or psycho-

social) between the two disorders/symptoms. One of the central aims of the present

thesis was to explore the co-morbidity between heightened negative affect and

hallucinations specifically (the literature pertaining to this area will be explored later in

this chapter).

Similar to symptom presentation, the course of schizophrenia is also highly

variable. A large scale Australian study recently showed that only 8% of individuals

with psychosis have a single psychotic episode with full recovery, 49% have multiple

psychotic episodes with either good recovery (21%) or partial recovery (28%) during

phases of remission, and 43% remain chronically ill but experience little deterioration

(20%) or constant functional decline and increase in symptom severity (23%)

(Jablensky, 2000; Jablensky et al., 2000). These statistics are similar to the outcomes

reported by the World Health Organisation (Barbato, 1998). The global standard

treatment for schizophrenia is psychoactive („antipsychotic‟) medications, which are

commonly classified as either „typical‟ (traditional) or „atypical‟ (novel) and take

around 7-14 days to have an effect. Antipsychotic medications are found to be most

Chapter 1

6

effective at reducing or eliminating positive symptoms, however they have little impact

on negative symptoms (Leucht, Wahlbeck, Hamann, & Kissling, 2003). A large

minority of individuals will respond well to antipsychotic medications, having few if

any symptoms when medicated. However, the current available medications do not

resolve all psychotic symptoms for most schizophrenia individuals, and often the side

effects can be more disabling than the symptoms themselves (side effects can include

headaches, dizziness, weight gain, anxiety, aggression, suicidal acts, sedation, blurred

vision, and salivation, movement, urinary, cardiovascular and endocrine problems),

resulting in poor compliance and consequential relapse (Barbato, 1998; Conley & Kelly,

2001). In addition to medications, numerous socio-psychological interventions have

also been found effective in increasing the quality of life of individuals with

schizophrenia, often by increasing coping and social resources, decreasing the level of

associated distress and functional impairment, treating co-morbid disorders, and even

helping to reduce the severity of positive symptoms (e.g., Farhall, Greenwood, &

Jackson, 2007; Jenner & van de Willige, 2001; Jenner, van de Willige, & Wiersma,

1998; Kuipers et al., 1998; Mihalopoulos, Magnus, Carter, & Vos, 2004; Mojtabai,

Nicholson, & Carpenter, 1998; Pilling, Bebbington, Kuipers, & etal, 2002; Turkingtona

et al., 2008; Wiersma, Jenner, Nienhuis, & van de Willige, 2004; Wiersma, Jenner, van

de Willige, Spakman, & Nienhuis, 2001; Wykes et al., 2003). Of the most common and

efficacious of these socio-psychological interventions are cognitive behaviour therapy,

social skills training, psycho-education, family therapy, cognitive remediation training,

and vocational rehabilitation. Despite their shown clinical and cost effectiveness,

government supported standard treatment for schizophrenia does not include socio-

psychological interventions in most countries (Milner & Valenstein, 2002).

As with many other complex disorders, such as cancer and HIV, there is still

much to learn about the underlying causes of schizophrenia. Studies suggest that

genetics, early environment, neurobiology, cognitive and socio-psychological processes

are all important contributing factors. Genetic studies suggest that multiple genes are

involved in schizophrenia inheritance, some of which may also contribute to the

diathesis of other psychological disorders, such as bipolar disorder (Craddock,

O'Donovan, & Owen, 2006; O'Donovan, Williams, & Owen, 2003; Owen, Craddock, &

O'Donovan, 2005). Prenatal research has found an increased risk of schizophrenia

linked to winter and spring births (Davies, Welham, Chant, Torrey, & McGrath, 2003)

and prenatal exposure to infections (Brown, 2006). Studies examining neurotransmitters

(chemical messengers responsible for transmitting information within the central

Chapter 1

7

nervous system) in schizophrenia have implicated the dysregulation of dopamine

(Laruelle, Abi-Dargham, Gil, Kegeles, & Innis, 1999) and other related

neurotransmitters, such as glutamate (Konradi & Heckers, 2003), in the onset and

maintenance of psychosis. Neuroimaging studies have shown structural and functional

differences between the central nervous system of individuals with schizophrenia and

healthy controls (at a group level of comparison). The most commonly reported

structural difference is the enlargement of the ventricles (Johnstone, Crow, Frith,

Husband, & Kreel, 1976), and the most common functional differences are found in the

frontal lobes, temporal lobes, and hippocampus (Green, 2001). These functional

differences are linked to the specific cognitive deficits associated with schizophrenia,

including impairments in the mental processes involved in executive control, language

and memory (for reviews, see Aleman, Hijman, de Haan, & Kahn, 1999; Elvevag &

Goldberg, 2000; Green, 2006; Harrison et al., 2007; McCarley, Niznikiewicz et al.,

1999; Merlotti, Piegari, & Galderisi, 2005; Ragland, Yoon, Minzenberg, & Carter,

2007). Many of these cognitive difficulties have been documented in prodromal and at-

risk individuals, who have not yet transitioned into full-blown psychosis (e.g., Eastvold,

Heaton, & Cadenhead, 2007; Niendam et al., 2006; Smith, Sohee, & Cornblatt, 2006).

Furthermore, different cognitive difficulties have been empirically linked to specific

symptoms seen in schizophrenia, implicating a role of cognition in the production of

those symptoms (e.g., Carter, Robertson et al., 1996; Garety & Freeman, 1999; Langdon

& Coltheart, 2000; Waters, Badcock, Michie, & Maybery, 2006). Finally, socio-

psychological stressors, such as bereavement/loss, trauma, poverty, migration, family

dysfunction, and unemployment, are associated with increased risk of developing

schizophrenia, with such stressors often preceding the onset of the first psychotic

episode (Read, van Os, Morrison, & Ross, 2005; Selten, Cantor-Graae, & Kahn, 2007;

van Os, Krabbendam, Myin-Germeys, & Delespaul, 2005). Most theories of

schizophrenia aetiology propose a diathesis-stress type model, which contends that

individuals will be “at-risk” when certain genetic/biological markers are present (the

„diathesis‟), however the disorder will only be “triggered” in the occurrence of a

significant life stressor (the „stress‟), which pushes the individual beyond some sort of

critical threshold.

Despite the continual progression in our understanding of schizophrenia, there is

growing debate over the validity and usefulness of studying schizophrenia as a unitary

condition, since both the genotypic and phenotypic presentation of the disorder seems to

vary. Thus, many researchers have instead sought to understand the underlying causes

Chapter 1

8

of specific symptoms or symptom groupings of schizophrenia (Bentall, 2003), such as

auditory hallucinations, and thus far, the cognitive literature has provided much support

for this method of research (e.g., Carter, Robertson, Chaderjian, O'Shora-Celaya, &

Nordahl, 1994; Seal, Aleman, McGuire, & Seal, 2004). The present thesis has adopted

this approach, endeavouring to further identify and dissociate the cognitive and affective

processes involved in the onset of auditory hallucinations.

AUDITORY HALLUCINATIONS

Definition

Auditory hallucinations (AHs) are broadly defined as auditory sensory

experiences that occur in the absence of external stimuli that is perceived by the

individual as a true perception (Gelder, Gath, & Mayou, 1993), that is of non-self origin

(Nayani & David, 1996a), and beyond the individual‟s control (Bentall, 1990). The

defining features that hallucinatory experiences share with other everyday unwanted

mental events (including thoughts, impulses and images), are that they are intrusive,

unwanted, uncontrollable, and interrupt ongoing reality (Morrison, 2005; Slade &

Bentall, 1988).

Auditory Hallucinations in Schizophrenia

AHs are one of the most common symptoms experienced by individuals with

schizophrenia, with approximately 74% of individuals with schizophrenia experiencing

an AH at some stage during the course of their illness (Sartorius, Shapiro, & Jablensky,

1974). In schizophrenia, although non-verbal AHs are frequently experienced (i.e.,

music and environmental sounds), the hearing of voices is the most common form of

AH, and are typically personal and negative in content, with individuals commonly

reporting that their voices are commanding, critical and even abusive (Haddock,

McCarron, Tarrier, & Faragher, 1999; Nayani & David, 1996a). Thus, it is not

surprising that the experience of AHs is often confronting and distressing, possibly

accounting – at least in part – for the high rates of co-morbid psychopathology and

heightened risk of suicide (Alpert & Silvers, 1970; Carter, Mackinnon, & Copolov,

1996; Close & Garety, 1998; Delespaul, deVries, & van Os, 2002; Hustig & Hafner,

Chapter 1

9

1990; Johns, Hemsley, & Kuipers, 2002; Walsh et al., 1999). Active voice hearers

typically hear their voices between once a week to continuously, voices can be

perceived to originate from either outside or inside the head, and voices can vary

according to gender (though male voices predominate), identity (though most often the

identity is of someone known to the individual) and even accent (Haddock et al., 1999;

Nayani & David, 1996a). The grammatical construction of voices also varies; second

person (i.e. “you are a slob”), third person (i.e. “he‟s going to bed”), or purely

descriptive non-personal comments (i.e. “the grass is green”) are most common, though

first person narration also occurs. Despite the diversity of AHs, voice hearers most

commonly report that they have limited control over their AHs, that the voices are most

likely to occur when alone, and that their voices are a similar loudness to one‟s own

speaking voice (Haddock et al., 1999; Nayani & David, 1996a).

Auditory Hallucinations in Other Clinical Populations

Although typically associated with schizophrenia, auditory hallucinations can

also occur in mood disorders - during major depressive and manic episodes – and

anxiety disorders, in particular posttraumatic-stress disorder (PTSD). For instance,

research has shown that between 50% and 80% of individuals with bipolar disorder

(during a manic episode), and between 10% and 30% of individuals with major

depressive disorder, experience psychotic symptoms, including AHs (Carlson &

Goodwin, 1973; Johnson, Horwath, & Weissman, 1991; Ohayon & Schatzberg, 2002),

and that the presence of psychotic symptoms is related to the severity of the manic or

depressive episode (Abrams & Taylor, 1981; Ohayon & Schatzberg, 2002). A recent

study of AHs in schizophrenia and „psychotic depression‟, reported similar

phenomenological qualities of AHs for both diagnostic groups, and moreover, anxiety

was the strongest predictor of hallucination intensity irrespective of diagnosis,

suggesting that anxiety may play a similar role in the production of AHs in

schizophrenia and mood disorders (Delespaul et al., 2002). The most consistently

reported difference between the AHs experienced in schizophrenia and mood disorders

is that a greater percentage of hallucinations are mood-congruent in mood disorders than

in schizophrenia, such that the content of the hallucination is consistent with depressive

or manic themes (e.g., Coryell & Tsuang, 1985; Coryell, Tsuang, & McDaniel, 1982;

Fennig, Bromet, Karant, Ram, & Jandorf, 1996; Winokur, Scharfetter, & Angst, 1985).

For instance, in depression hallucinated voices are typically negative in content,

Chapter 1

10

berating the voice hearer for his/her short comings, while in mania the voices are

typically grandiose in content, commonly taking the identity of God or other

influential/famous individuals (APA, 2000).

The predisposition to hallucinations and the occurrence of AHs in individuals

with schizophrenia have also been linked to traumatic life experiences (e.g., Hardy et

al., 2005; Morrison & Petersen, 2003; Read et al., 2005). Consistent with this, PTSD is

characterised by intrusive hallucinatory-type flashbacks of the trauma, and – although

less common – full-blown hallucinatory experiences, with the content of most AHs

related to the trauma (APA, 2000; Hamner, 1997; Hamner et al., 2000; Kastelan et al.,

2007). It has been documented that as many as 40% of combat veterans with PTSD

have co-morbid psychotic symptoms, and that the severity of PTSD and psychotic

symptoms correlate (Hamner, 1997).

Hallucinations are also frequently reported by individuals with tinnitus

(predominantly non-verbal AHs; Johns et al., 2002), Alzheimer‟s disease (both visual

and auditory hallucinations; Bassiony & Lyketsos, 2003), and patients with traumatic

brain injury, primarily associated with damage to the temporal and frontal areas

(predominantly verbal AHs; Fujii & Ahmed, 2002a, 2002b). Intoxication from psycho-

active substances (such as LSD, amphetamines, steroids and cocaine) and medications

that increase dopamine activity in the brain (such as Levodopa – an anti-Parkinson‟s

medication) also often produce psychotic-like symptoms, including AHs (Aggernaes,

1972; Kershner & Wang-Cheng, 1989; Laruelle et al., 1999).

Auditory Hallucinations in the General Population

There is strong evidence that a symptom continuum exists for AHs between

individuals from the general population and individuals with full-blown psychosis

(Choong, Hunter, & Woodruff, 2007; Shevlin, Murphy, Dorahy, & Adamson, 2007).

Numerous large scale community projects have reported an annual prevalence rate for

AHs of around 4%, and that between 10% and 25% of individuals in the general

population report having experienced an hallucination (not including hallucinatory

experiences during altered states of consciousness) at some stage during their lives, of

whom less than half have received any psychological services or met diagnosis for a

mental illness (Johns, Nazroo, Bebbington, & Kuipers, 1998; Kendler, Gallagher,

Abelson, & Kessler, 1996; Ohayon, 2000; Romme, Honig, Noorthoorn, & Escher,

1992; Sidgewick, Johnson, Myers, & et-al., 1894; Tien, 1991). These prevalence rates

Chapter 1

11

are similar for children and adolescents (Altman, Collins, & Mundy, 1997; Escher,

Delespaul, Romme, Buiks, & Van Os, 2003; McGee, Williams, & Poulton, 2000). It has

been found that the AHs experienced by healthy non-clinical individuals have all the

reality characteristics necessary to classify them as actual hallucinations according to

Slade and Bentall‟s (1988) definition: namely, they (a) occur in the absence of

corresponding external stimuli, (b) have the full impact of a real perception, and (c) are

not amenable to direct voluntary control (Barrett & Caylor, 1998).

There is considerable support for the conjecture that hallucinatory experiences

occur in a continuous – rather than discontinuous – fashion. For instance, the life

experiences preceding the first hallucinatory experience (i.e. trauma, stress and drug

use) and demographic characteristics (i.e. age, education, occupational and marital

status) are similar for hallucinating individuals in the general population and those who

have schizophrenia (e.g., Honig et al., 1998; Ohayon, 2000; van Os, Hanssen, Bijl, &

Ravelli, 2000; van Os, Park, & Jones, 2001). Furthermore, the AHs experienced by non-

clinical and clinical individuals share many phenomenological characteristics, such as

type, form, pragmatics and perceived reality characteristic (Barrett & Caylor, 1998;

Choong et al., 2007; Honig et al., 1998; Leudar, Thomas, McNally, & Glinski, 1997).

Nevertheless, several differences have been documented, possibly contributing to, or

predicting the need for care. For instance, Honig et al. (1998) interviewed patient voice

hearers (schizophrenia or dissociative disorder diagnoses) and healthy non-patient voice

hearers about the characteristics of – and affective responses to – their AHs. Although

the hallucinatory experiences of the groups were similar in form, there were some

significant differences: more of the voices experienced by patients had a negative

content, while the voices of non-patient participants were predominantly positive;

patients were also afraid of their voices, while non-patients were not upset by their

voices; and patients reported having less control over their voices than non-patients.

Similar differences in appraisals and emotional consequences have been reported

between child patient and non-patient voice hearers (Escher, Romme, Buiks, Delespaul,

& van Os, 2002). Also consistent with this finding, a large scale community study

conducted by Tien (1991) found that the majority of healthy individuals who

experienced AHs reported that their AHs were not distressing or functionally impairing.

Despite the reported differences in emotional content and affective responses to AHs by

patient and non-patient voice hearers, high levels of anxiety and depression are reported

in both hallucinating groups (Barrett & Etheridge, 1994; McGee et al., 2000; Ohayon,

Chapter 1

12

2000), suggesting that affective disturbance may play a similar role in the onset and/or

maintenance of AHs across the continuum.

Given the high prevalence of hallucinatory experiences reported in the general

population, the Launay-Slade Hallucination Scale (LSHS: Launay & Slade, 1981,

revised by Bentall & Slade, 1985; LSHS-R) was developed to identify and study

healthy individuals „predisposed‟ to hallucinatory experiences. The scale includes items

that enquire about vivid and intrusive everyday cognitions (i.e. “no matter how hard I

try to concentrate, unrelated thoughts always creep into my mind”) as well as full-blown

hallucinatory experiences (i.e. “I often hear a voice speaking my thoughts aloud”). This

scale has since been used in over 40 published studies, translated into several different

languages, and used in both non-clinical and clinical (including schizophrenia) samples.

Serper and colleagues (Serper, Dill, Chang, Kot, & Elliot, 2005) administered the

LSHS-R to healthy undergraduate students, and schizophrenia individuals who did and

did not experience AHs, and found an almost identical factor-analytic solution of the

LSHS-R items for all three groups, suggesting a similar architecture of hallucinatory

experiences in schizophrenia and the general population.

The research suggests that although the experience of AHs in the general

population may predispose people to developing psychosis, it is not indicative of

psychosis (Barrett & Etheridge, 1994), further indicating that AHs occur on a symptom

– rather than a disorder-based – continuum. The overwhelming evidence that

hallucinatory-type experiences span across a continuum suggests that similar cognitive

and affective processes may underlie the development of AHs in both the general

population („hallucination predisposed‟ individuals) and schizophrenia (Johns & van

Os, 2001; Verdoux & van Os, 2002). Indeed, several studies have already found

evidence of this (e.g., Aleman, Nieuwenstein, Bocker, & de Haan, 2000; Allen,

Freeman, Johns, & McGuire, 2006; Allen et al., 2005; Laroi, Van der Linden, &

Marczewski, 2004; Levine, Jonas, & Serper, 2004; Morrison & Petersen, 2003; van't

Wout, Aleman, Kessels, Laroi, & Kahn, 2004). These observations support the study of

hallucinatory-type experiences in the general population, which is useful since it not

only helps to avoid over testing schizophrenia samples, but also permits the study of

AHs in the absence of confounding variables associated with schizophrenia, such as the

effects of medication, other symptoms, institutionalisation, and the associated general

cognitive impairments. In this thesis, specific cognitive and affective variables

associated with AHs will be investigated in both hallucination predisposition and

schizophrenia.

Chapter 1

13

Explanatory Models of Auditory Hallucinations

Several different classes of explanatory models have been developed to explain

the onset and maintenance of AHs in schizophrenia. The most widely debated of these

include two single-deficit cognitive accounts (mental imagery theories and inner speech

theories), socio-psychological accounts, and the biological-based theories involving

dopamine. Finally, I will present a dual-deficit cognitive account of AHs based on

deficits in intentional inhibition and context memory, which I will advocate best

accounts for the complex nature of AHs.

Mental Imagery

One of the earliest explanatory models of AHs posited that such experiences are

the product of aberrantly vivid auditory imagery. According to this conjecture, these

vivid imaginal auditory experiences are so life-like that the individual assumes, without

doubt, that the experience is real; that they are actually hearing someone speaking

(Laroi & Woodward, 2007; Seal et al., 2004). Of the 20 or so studies that have

empirically tested this model of AHs in schizophrenia, only two have provided concrete

support for this account (for a review, see Seal et al., 2004). Mintz and Alpert (1972)

reported that significantly more schizophrenia participants who experienced AHs rated

an imaginal auditory exercise (imaginal listening to the song „White Christmas‟) as

more vivid than did schizophrenia participants who did not experience AHs. Similarly,

Young and colleagues (Young, Bentall, Slade, & Dewey, 1987) found that both

hallucinating psychiatric patients and hallucination predisposed individuals were more

likely to hear suggested sounds than control participants; although such findings could

equally denote increased suggestibility. However, studies using other auditory imagery

tasks and subjective ratings of auditory imagery have not been able to substantiate the

implications drawn from these studies (e.g., Aleman, Bocker, Hijman, de Haan, &

Kahn, 2003; Evans, McGuire, & David, 2000; Slade, 1976a; Starker & Jolin, 1982). By

and large, these studies have reported that hallucinating individuals have normal

vividness of auditory imagery.

The dearth of empirical support for the vivid auditory imagery model of AHs led

to a contrasting mental imagery account: reduced vividness of visual imagery.

Chapter 1

14

According to this account, if individuals have reduced vividness of visual imagery, and

the visual modality is the preferred imaginal modality, then bizarre auditory imagery

with normal vividness would – by comparison – seem vivid and consequently

misinterpreted as a true perception (Slade, 1976a; Starker & Jolin, 1982). This model of

AHs has also received limited empirical support (e.g., Aleman et al., 2003). Moreover,

the theoretical basis of mental imagery accounts has been criticised for not adequately

explaining the source misattribution aspect of AHs: namely, there is no evidence that

the vividness of imagined events has any impact on an individuals‟ interpretation of an

event as imagined or real (Bentall, 1997). However the strength of these theories lies in

their ability to explain the varying perceptual qualities of AHs (such as the variation in

identity and narrative stance of verbal AHs, and the presence of non-verbal AHs) which

other single deficit theories struggle to do; perhaps explaining how these accounts have

held their position amongst the most debated models of AHs to date (Laroi &

Woodward, 2007).

Inner Speech

Possibly the most widely researched explanatory approach to AHs to date is the

inner speech (or „verbal self-monitoring‟) model, which conceptualises AHs as inner

speech that has been misattributed to a non-self origin due to self-monitoring

dysfunction (e.g., Frith, 1996; see Allen, Aleman, & McGuire, 2007 for review).

Several different accounts of how, and at what stage, this breakdown in self-monitoring

occurs have been proposed, however they all share the basic premise that the system

(often referred to as forward modelling or corollary discharge) which monitors our

intention to produce action/speech/thought is defective, and thus inner speech appears

unintended, and consequently is not identified as belonging to the self (Blakemore,

Wolpert, & Frith, 2002; Seal et al., 2004).

The empirical findings pertaining to the inner speech model have been

somewhat inconsistent. Although – as the inner speech account would predict – studies

have reported low subjective ratings of control and intentionality of self-generated

words during experimental tasks given by hallucinating individuals with schizophrenia

(Baker & Morrison, 1998; Morrison & Haddock, 1997), these studies have been

criticised for their reliance on the assumption that humans are capable of consciously

and reliably reporting on complex cognitive processes (Seal et al., 2004). More

objective measures of verbal self monitoring have required participants to discriminate

Chapter 1

15

between self-generated and other-generated speech while they are talking, with

uncertainty experimentally manipulated in various ways (Cahill, 1996; Goldberg, Gold,

Coppola, & Weinberger, 1997; Johns & McGuire, 1999; Johns et al., 2001). Only two

of the four studies using this paradigm found that hallucinating schizophrenia

participants were more likely to misattribute self-generated speech than non-

hallucinating schizophrenia participants (Johns & McGuire, 1999; Johns et al., 2001).

However, both of these studies reported self-generated speech recognition difficulties in

all schizophrenia participants relative to healthy control participants, which is difficult

to reconcile with a single deficit account of AHs, since one would expect all individuals

with verbal self-monitoring deficits to experience AHs. Interestingly, Allen et al. (2004)

found that hallucinating schizophrenia participants had greater propensity to

misattribute self-generated speech than non-hallucinating schizophrenia participants and

healthy controls when the speech was played back to the participant after a delay (not

while the participant was speaking), thus not requiring immediate verbal self-

monitoring. This raises the possibility that the previous studies findings may instead

reflect an external source attribution bias.

Imaging studies have documented activation of the temporal cortical areas of the

brain during AHs (see Allen et al., 2007 for review), which are usually activated during

auditory-verbal perception and imagery (McGuire, Silbersweig, & Frith, 1996;

McGuire, Silbersweig, Murray et al., 1996). These findings have been interpreted as

evidence supporting both the inner speech and vivid mental imagery (as outlined above)

accounts of AHs. Likewise, imaging studies have also found that language production

areas of the brain, such as Broca‟s area (e.g., McGuire, Shah, & Murray, 1993; McGuire

et al., 1995), are activated during AHs. However, these neural associations have not

been consistently reported (e.g., Woodruff et al., 1997), and furthermore, these areas of

the brain are often activated in tasks not eliciting inner speech (Silbersweig & Stern,

1996), giving rise to doubts about the inner speech implications drawn from these

neurological findings.

One of the greatest limitations to the inner speech accounts of AHs, is that they

do not cope well with explaining several of the phenomenological features of AHs: for

instance, why the perceptual qualities of AHs can vary, why voices are often

familiar/known to the voice hearer, why most hallucinated voices speak in second or

third person (since inner speech is typically first person), why AHs can be perceived as

originating outside the head, or the occurrence of non-verbal AHs. In addition, such

accounts do not adequately explain why some thoughts are perceived by the voice

Chapter 1

16

hearer as their own while other thoughts are perceived as having a non-self origin, and

furthermore, how the voice hearer can converse (using correctly identified inner speech)

with the „voices‟. Consequently, a single-deficit inner speech account does not provide

an adequate explanation of AHs, although the research pertaining to this conjecture has

contributed immensely to our current understanding of AHs. Furthermore, while it

seems evident that inner-speech mechanisms cannot be the primary (or only) cause of

AHs per se, it is acknowledge that AHs may be made up of misidentified inner-speech

(in addition to other misidentified cognitions, such as memories).

Socio-Psychological Theories

Several models of AHs have highlighted the social and psychological aspects of

the experience of AHs, rather than the cognitive and neurological processes traditionally

speculated on. These theories generally emphasise the involvement of cognitive biases –

maladaptive beliefs, evaluations and interpretations about their aberrant experiences - in

the generation and maintenance of AHs (e.g., Beck & Rector, 2003; Garety, Kuipers,

Fowler, Freeman, & Bebbington, 2001). For instance, numerous socio-psychological

models have been proposed – and some supporting evidence has been found – that

positive symptoms (including AHs) are maintained by (1) cognitive biases, such as an

externalising attribution bias, jumping to conclusions, belief inflexibility, belief

confirmation bias, abnormal meta-cognitive beliefs regarding the uncontrollability of

thoughts, increased self-focused attention, and circular and emotion-based reasoning;

(2) impaired problem solving processes causing the individual to fail to collect more

data, look for errors, search for alternative explanations, or reappraise attributions; and

(3) social isolation and other „safety behaviours‟ (behaviours which assist avoidance of,

and escape from, feared situations), which prevent the individual from obtaining counter

evidence (Baker & Morrison, 1998; Beck & Rector, 2003; Bentall, 1990; Bentall,

Baker, & Havers, 1991; Garety & Freeman, 1999; Garety et al., 2001; Morrison, 1998;

Morrison, 2001; Morrison & Haddock, 1997). These socio-psychological processes are

thought to contribute to AHs by increasing the likelihood that a percept will be

attributed to an external source and prevent the individual from questioning this

attribution. Many of the proposed cognitive biases are also thought to increase resulting

negative affect, which in turn acts to trigger further AHs (Morrison, 1998). Langdon

and Coltheart (2000) have posited that different cognitive biases lead to different types

of delusions and hallucinatory experiences.

Chapter 1

17

Originating from psychoanalytic explanations of AHs (Freud, 1924; Gillibert,

1968), several alternative modern socio-psychological models of AHs propose that

intrusive cognitions that threaten the integrity of the individual (causing „cognitive

dissonance‟) are automatically rejected by the individual as belonging to – or a product

of – one‟s own mind, and consequently are attributed to an external source (e.g., Baker

& Morrison, 1998; Kapsambelis, 2005; Morrison, 2001; Morrison & Wells, 2003).

Although Morrison and colleagues have found evidence that voice hearers have meta-

cognitive beliefs regarding punishment, responsibility, uncontrollability, and the

unacceptability of negative thoughts (Baker & Morrison, 1998; Morrison & Wells,

2003), there has been no documented evidence that meta-cognitive beliefs impact on an

individuals‟ attribution of the source of an event to self or other.

Socio-psychological theories are important as they incorporate aspects of how

the individual relates to their hallucinatory experiences, which most cognitive models

neglect to do, and importantly, most of these approaches provide clear targets for socio-

psychological therapeutic intervention. However, by and large, socio-psychological

models do not account for many of the existing neurological anomalies associated with

AHs, nor do they explain much of the phenomenological variation in AHs. In addition,

while these theories contribute to our understanding of the possible maintaining factors

involved in AHs, their ability to explain the onset of AHs is often limited (or omitted

altogether), and those models which have speculated on the possible processes involved

in the onset of AHs have not been adequately tested (e.g., Beck & Rector, 2003).

Dopamine

Aberrant hypo-activity of dopamine D2 receptors has been implicated in the

onset and maintenance of positive symptoms, along with the dysregulation of other

neurotransmitters, such as γ-amino butyric acid (commonly referred to as GABA), that

interact with dopamine receptors (see David, 1999, for review). The neurotransmitter

dopamine has been implicated in a wide range of functions, including memory,

attention, problem-solving, reward prediction and incentive salience attributions derived

from pleasure (Berridge & Robinson, 1998). Kapur has provided an explanatory

account of the mechanism of dopamine in the production of psychotic symptoms

(Kapur, 2003; Kapur, Mizrahi, & Li, 2005) – namely, that the excess of dopamine in

schizophrenia results in the assignment of aberrant salience to external objects/events

and internal representations in the absence of a contextual drive, causing irrelevant and

Chapter 1

18

unrelated events and cognitions to appear pertinent and related. According to Kapur

(2003, p. 13), „hallucinations reflect a direct experience of the aberrant salience of

internal representations‟, while delusions are the individual‟s attempt to make sense of

the aberrantly salient experience.

The majority of evidence linking aberrant dopamine activity to AHs comes from

the finding that drugs that increase dopamine activity (including amphetamines,

cocaine, and Levodopa) can produce hallucinations (e.g., Laruelle et al., 1999).

Likewise, neuroleptic medications (e.g., some antipsychotics) found to decrease

dopamine activity have been found to reduce or stop AHs in many – though not all –

individuals with schizophrenia (Lieberman, Kane, & Alvir, 1997). Schizotypal

personality studies have demonstrated significant correlations between levels of plasma

and cerebrospinal fluid homovanillic acid (HVA; used as an indirect measure of

dopamine) and psychotic-like symptoms (Siever et al., 1991; Siever et al., 1993). Some,

though little, empirical attention has been given to the operational workings of

dopamine on the cognitive or affective processes involved in the production of AHs. In

one of these studies, Myin-Germeys and colleagues (Myin-Germeys, Marcelis,

Krabbendam, Delespaul, & van Os, 2005) used an experience sampling method to

measure momentary fluctuations in stress and psychotic experiences, and measured

indirect changes in dopamine activity through plasma HVA levels, in first-degree

relatives of schizophrenia individuals and control participants. In first-degree relatives,

but not control participants, HVA reactivity modified the relationship between

psychotic experiences and daily stress. These results were interpreted as evidence that

dopamine may mediate the trigger-type role of stress in the onset and maintenance of

psychotic experiences (i.e., less stress may be necessary to trigger the psychotic

experience), which is consistent with Kapur‟s aberrant salience account.

While it is indisputable that dopamine plays an important role in the production

of AHs, the particular cognitive process(es) on which it exerts its influence in

schizophrenia is still largely unknown. However, the finding that medications thought to

regulate dopamine activity are not effective at ceasing AHs altogether or in all

individuals suggests that dopamine may not influence all (or indeed perhaps any)

cognitive processes involved in AHs, but rather – as Kapur (2003) posits – make

internal cognitions aberrantly salient, rendering them more difficult to dismiss or

inhibit, thus contributing to their intrusive, unintentional and uncontrollable nature.

Chapter 1

19

Dual Deficit: Intentional Inhibition and Context Memory Deficits

There has been growing concern that single-deficit accounts of AHs are

insufficient at explaining such complex and diverse mental events (e.g., Nayani &

David, 1996b; Waters, Badcock, Michie et al., 2006). This led Badcock, Waters,

Maybery and Michie to formulate and test a dual-deficit account of AHs (Badcock &

Maybery, 2005; Waters, Badcock, Michie et al., 2006). Their model argues that at least

two cognitive deficits are critical to experiencing AHs: an intentional cognitive

inhibition deficit (Badcock, Waters, Maybery, & Michie, 2005; Waters, Badcock,

Maybery, & Michie, 2003) and a deficit in binding of contextual memory (Waters,

Badcock, & Maybery, 2006b; Waters, Maybery, Badcock, & Michie, 2004). This model

posits that a failure to inhibit or suppress irrelevant cognitions (including memories and

other currently active mental associations) results in this information intruding into

conscious thought. This component of the model explains the intrusive, involuntary and

uncontrollable aspects of the hallucinatory experience. Accordingly, these intrusive

cognitions are then misidentified as being of non-self origin because the contextual

information required for correct recognition and identification is missing or incomplete

due to a deficit in contextual binding. The binding of all three crucial sources of

contextual information (source, spatial, temporal) to memories is essential for correct

identification of retrieved memories since it informs the individual, for example, who

the memory is of (source), where the recalled event took place (spatial), and when the

recalled event took place (temporal) (Chalfonte & Johnson, 1996). According to

Badcock and colleagues, in most cases the loss of contextual information is not absolute

(since the context memory difficulties stem specifically from defective binding of

contextual information, as opposed to a complete failure to encode, store or retrieve

contextual information), explaining why some parts of the original memory may be

retained and recognised, such as the identity of the voice.

Badcock and colleagues have tested and provided empirical support for both

components of their dual-deficit model. They demonstrated a specific relationship

between AH severity and intentional cognitive inhibition in individuals with

schizophrenia using two different cognitive control tasks (Badcock et al., 2005; Waters

et al., 2003). In the first of these tasks, the Hayling Sentence Completion Test (Burgess

& Shallice, 1996), participants were required to provide a single word ending to a

sentence that was neither the most suited response (Type A errors) nor semantically

related (Type B errors). Waters et al. (2003) found that the severity ratings of AHs – but

Chapter 1

20

not delusions or negative symptoms – correlated significantly with Type A errors,

suggesting that people with frequent AHs find it more difficult to actively inhibit

prepotent responses than those with less severe or no AHs. In the second intentional

inhibition task, the Inhibition of Currently Irrelevant Memories task (ICIM; Schnider &

Ptak, 1999), participants were presented with a series of pictures and were asked to

identify when a picture was repeated within the current run. As there were several runs

and the same pictures were presented on each run, participants had to intentionally

suppress the memory traces of pictures shown in previous runs in order to avoid

mistaking previous-run items as having already been presented on the current run (with

failed inhibition measured by the number of false alarms made on runs subsequent to

run 1). As predicted, Waters et al. (2003) found that the severity of AHs – but not

delusions or negative symptoms – was significantly correlated with the number of false

alarms made on runs 2-4, but not run 1 (which does not require inhibition, since items

are novel). In a more recent paper, Badcock et al. (2005) re-analysed the results from

the ICIM task using a between group approach and found that intentional inhibition

difficulties were specific to hallucinating individuals. Specifically, they reported that

hallucinating schizophrenia participants made significantly more FAs on the inhibitory

runs than either non-hallucinating schizophrenia participants or healthy control

participants, while the inhibitory performance of non-hallucinating schizophrenia

participants and control participants did not significantly differ.

Additional evidence supporting the inhibitory control aspect of the Badcock et

al. model comes from the neuro-imaging literature. Regions in the frontal lobes, such as

dorsolateral prefrontal cortex, the cingulate gyrus, and the orbitofrontal cortex (OFC),

have been associated with different forms of inhibitory control (e.g., Aron, Robbins, &

Poldrack, 2004; Dias, Robbins, & Roberts, 1997; Fuster, 1997; Konishi et al., 1999;

Wyland, Kelley, Macrae, Gordon, & Heatherton, 2003), with the OFC found to be

involved in ICIM task performance (Schnider & Ptak, 1999; Schnider, Treyer, & Buck,

2000; Treyer, Buck, & Schnider, 2003). Furthermore, imaging research has found that

the OFC and cingulate gyrus are activated during AHs (e.g., Copolov et al., 2003;

Lennox, Park, Jones, & Morris, 1999; Silbersweig et al., 1995), supporting the link

between AHs and inhibitory control.

While contextual binding deficits associated with AHs were first investigated by

Badcock and colleagues, context memory difficulties more broadly have been

documented extensively in the schizophrenia literature, and more recently, have been

specifically linked to hallucinations following the single-deficit context memory

Chapter 1

21

conjecture developed by Nayani and David in 1996 (Brebion et al., 1999; Brebion,

Gorman, Amador, Malaspina, & Sharif, 2002; Guillem et al., 2003; Servan-Schreiber,

Cohen, & Steingard, 1996). Nayani and David (1996b) theorized that auditory

hallucinations are composed of fragments of memories of speech which fail to be

correctly recognised as memories because the information needing to identify the

memory‟s origins and context is missing or fragmented due to context memory

impairments. Furthermore, much of the cognitive evidence used to support the inner

speech models of AHs equally supports the context memory conjecture. For instance,

the documented failure of hallucinating individuals to correctly identify the source of

speech/actions/thoughts after a period of delay could be the product of faulty context

memory for these prior events/cognitions, particularly given that several of these studies

have also found that hallucinating individuals have difficulties with source

identification of actions/speech generated by another person (e.g., Brebion et al., 2000;

also see the Inner Speech section).

To overcome the ambiguity of the principal mechanism causing difficulties on

source attribution tasks, Badcock and colleagues manipulated the source attribution

paradigm to isolate deficits of contextual memory binding (Waters et al., 2004). The

context binding task they developed was administered over two test sessions. In each

session participants performed or watched pairings of household items. Five minutes

after the end of the second session, participants‟ memory for pairs of items (content), for

who paired the items (source) and for when the items were paired (temporal) was tested.

In their first publication, individuals with schizophrenia were shown to retrieve fewer

individual contextual (source or temporal) features of the event than healthy controls

(Waters et al., 2004). In a second publication (Waters, Badcock et al., 2006b) they

reported that significantly more hallucinating schizophrenia participants had context

memory impairments on this task than non-hallucinating schizophrenia participants,

although many participants in the non-hallucinating group still exhibited such

difficulties. However, one of the key strengths of multi-deficit models is that they

account for how an individual with schizophrenia who does not experience AHs could

have one (but not all) of the contributing cognitive deficits, since the experience of AHs

requires the specific combination of all principal deficits involved. Likewise, it can

explain the overlap of cognitive deficits with similar schizophrenia symptoms, such as

delusions and other intrusive cognitions (e.g., Badcock, Waters, & Maybery, 2007).

The proposal that AHs are fragments of memories can explain many of the well

documented variations in the perceptual qualities of AHs, such as identity/familiarity,

Chapter 1

22

gender, form of verb (i.e., first, second or third person), loudness, location, and accent,

as well as the occurrence of non-verbal AHs. This proposal of AHs as misidentified

memories is supported by neuroimaging studies that that have found hippocampal

activation during AHs (Copolov et al., 2003; Silbersweig et al., 1995; Takebayashi,

Takei, Mori, & Suzuki, 2002), since the hippocampus plays a critical role in the

formation and retrieval of relational memories (see Aggleton & Brown, 1999 for

review). In addition, a recent neuroimaging study of perception of externally generated

human speech in schizophrenia found that the pattern of brain activation associated with

AHs was most consistent with models of AHs as mis-remembered memories of speech

(Copolov et al., 2003). Although, for the said reasons, I believe that the Badcock et al.

dual-deficit model of AHs represents a significant improvement on earlier models and

more readily explains the complexity and diversity of AH experiences, the model does

not (yet) adequately address the well documented involvement of negative affect

(namely, anxiety and depression) in the onset and maintenance of AHs (Freeman &

Garety, 2003; also see the Negative Affect section). Furthermore, although the model

argues that a specific form of cognitive control impairment is associated with AHs,

namely intentional cognitive inhibition, the specificity of this claim has not yet been

empirically examined (although previous research has failed to document a link

between AHs and unintentional forms of inhibitory control; e.g., Peters et al., 2000).

These two aspects of the model will be investigated in this thesis.

NEGATIVE AFFECT

Definition

The term affect will be used throughout this thesis to encompass a wide range of

emotion-related phenomena, with the preceding term negative describing emotion-

related experiences that are generally perceived as being unpleasant. According to Gross

(1998), affect is the „superordinate category for valanced states, including emotions

such as anger and sadness.., moods such as depression and euphoria, dispositional states

such as liking and hating, and traits such as cheerfulness and irascibility‟ (p. 273). The

following review will focus primarily on depression and anxiety, since these affective

states have been linked most closely to the positive symptoms of schizophrenia.

Chapter 1

23

Negative Affect and Schizophrenia

Given the intrusive nature of positive symptoms and the negative impact the

disorder typically has on the individual‟s social and occupational life, it is not surprising

that high rates of co-morbid depression and anxiety have been documented across the

lifespan of the disorder. Some schizophrenia studies have shown as many as two thirds

of individuals report being depressed and/or anxious (Huppert & Smith, 2001; Siris,

1995). Furthermore, the rate of suicide in schizophrenia is 10 times higher than in the

general population, with 10% of sufferers taking their own lives (APA, 2000; Limosin,

Loze, Philippe, Casadebaig, & Rouillon, 2007). Other studies have shown that

depression and anxiety are characteristic of the prodromal phase of psychosis, evident

even prior to symptom onset. Two large-scale prodromal studies reported that between

57% and 76% of individuals had depressive symptomatology, and between 62% and

86% of individuals had high levels of anxiety (Birchwood et al., 1989; Herz & Melville,

1980). Such findings suggest that negative affective disturbances may not only be a

consequence of the frightening and disabling symptoms of schizophrenia but may be

important causal factors. Furthermore, neuroimaging studies of individuals with

schizophrenia have shown abnormal volumes in areas of the brain involved in the

production and modulation of emotion and storing of emotion-cued memories: the

amygdala, thalamus, hippocampus and insula (Aleman & Kahn, 2005; McCarley, Wible

et al., 1999; Wright et al., 2000).

Until recently, the study of affective disturbance in schizophrenia has almost

exclusively focused on negative symptoms, since the most common negative symptoms,

namely flat affect and anhedonia, respectively mimic the behavioural and subjective

emotional experience of depression (Bentall, 2003). Researchers in the area have sought

to determine whether these symptoms are independent of, or merely part of, the high co-

morbidity of depression in schizophrenia. Refuting the speculated link between negative

symptoms and negative affect, empirical studies have typically found that schizophrenia

individuals with these negative symptoms do not differ from controls or schizophrenia

individuals without negative symptoms on subjective ratings of the valence and arousal

of their experiences of emotional stimuli (e.g., Berenbaum & Oltmanns, 1992;

Burbridge & Barch, 2007; Myin-Germeys, Delespaul, & deVries, 2000). Despite this

empirical focus, studies have consistently found depression and anxiety to be more

closely related to positive symptoms than negative symptoms (e.g., Guillem,

Pampoulova, Stip, Lalonde, & Todorov, 2005; Norman & Malla, 1991; Norman, Malla,

Chapter 1

24

Cortese, & Diaz, 1998; Norman & Malla, 1994; Smith, Fowler et al., 2006; Tibbo,

Swainson, Chue, & LeMelledo, 2003). The literature pertaining to affect and delusions

will not be reviewed in this thesis, however in a recent literature review, Freedman and

Garety (2003) concluded that the content of delusions „are a direct representation of

emotional concerns, and that emotion contributes to delusion formation and

maintenance‟ (pg. 923). The following subsection will review the literature which has

examined the specific relationship(s) between negative affect and AHs.

Negative Affect and Auditory Hallucinations

Auditory hallucinations are predominantly pessimistic in content and intrusive in

nature, and are most often perceived by the individual as confronting and distressing

(Nayani & David, 1996a), potentially explaining the high co-occurrence of AHs with

depression, anger, fear, anxiety, low self-esteem, and suicide (Alpert & Silvers, 1970;

Carter, Mackinnon et al., 1996; Close & Garety, 1998; Delespaul et al., 2002;

Gallagher, Dinan, Sheehy, & Baker, 1995; Hustig & Hafner, 1990; Johns et al., 2002;

Walsh et al., 1999). However, in recent years it has become increasingly evident that

negative affect plays more than one role in an hallucinatory event. Negative affect may

be a trigger, a maintenance mechanism, a determinant of content, and a by-product. The

literature pertaining to each of these roles will be reviewed.

The Role of Negative Affect in the Onset and Maintenance of Auditory Hallucinations

Depression and anxiety have not only been found to accompany the experience

of AHs, but have also been found to precede the initial – and subsequent – onset of

AHs, suggesting that emotional disturbance plays a direct causal role in the onset of

AHs (e.g., Allen & Agus, 1968; Delespaul et al., 2002; Myin-Germeys, Delespaul, &

van Os, 2005; Nayani & David, 1996a; Slade, 1976b). For instance, in a

phenomenological survey of AH experiences in individuals with a psychotic disorder

conducted by Nayani and David (1996a), 52% reported feelings of sadness and 45%

reported having anxiety-related bodily sensations (i.e., churning or butterfly sensations

in their stomach) prior to the onset of hallucinatory episodes. Overcoming the potential

limitations of using a retrospective design, Delespaul and colleagues (2002) employed a

time-sampling procedure and found that hallucinating individuals with schizophrenia or

Chapter 1

25

„psychotic depression‟ reported a rise in anxiety levels immediately prior to the onset of

a hallucinatory episode, with anxiety restoring to baseline levels shortly after the

episode ceased. Furthermore, this study found that anxiety was the strongest predictor

of hallucination severity – more so than depression-related mental states – irrespective

of diagnosis. Another time-sampling study found that increases in psychosis intensity

(including AHs) was associated with daily life stress in both schizophrenia participants

and their first degree relatives, but not control participants (Myin-Germeys, Delespaul et

al., 2005), providing further evidence of an interplay between negative affect and the

mechanisms or „diathesis‟ underlying psychotic symptoms. In a much earlier study,

Allen and Agus (1968) demonstrated in a series of case studies that AHs could be

induced in individuals with schizophrenia by stimulating the somatic symptoms that

often accompany anxiety and panic attacks. Providing further support, clinical studies

have found that by effectively reducing anxiety and depression in patients with

schizophrenia through cognitive-behavioural intervention or antidepressant medication,

the severity of AHs is also reduced (e.g., Cornblatt, Lencz, & Obuchowski, 2002;

Cornblatt et al., 2007; Kuipers et al., 1998; Slade, 1972, 1973).

Studies examining the emergence of psychosis in at-risk and community

samples have largely found that depression, anxiety, stress and trauma are amongst the

strongest predictors of psychosis onset (e.g., Bebbington et al., 1993; Cunningham,

Miller, Lawrie, & Johnstone, 2005; Goodwin, Fergusson, & Horwood, 2004; Jones,

Rodgers, Murray, & Marmot, 1994; Svirskis et al., 2005; Tien & Eaton, 1992; Yung et

al., 2003). Studies examining the temporal order of symptom emergence in the

prodromal phase have reported that depressive symptoms precede all other

schizophrenia-specific and non-specific symptoms, while anxiety symptoms do not

appear until prior to positive symptom onset (Hafner et al., 2005). In line with this

finding, the few studies that have examined the initial onset of hallucinations

specifically, report that anxiety disorders and anxious mood are strong predictors of

hallucination onset, more so than depression (e.g., Krabbendam et al., 2002; Nayani &

David, 1996a; Tien & Eaton, 1992), while both anxiety and depression are related to the

continuation of AHs (Escher et al., 2002). Furthermore, in a series of studies conducted

by Krabbendam and colleagues, they reported that the presence of depressed mood was

able to predict the onset of psychosis in individuals who already experience AHs in the

general population, and furthermore that this relationship was partly mediated by

negative and delusional appraisals of hallucinatory experiences (Krabbendam et al.,

2005; Krabbendam & van Os, 2005). Taken together, these separate findings implicate

Chapter 1

26

the involvement of anxiety in the initial and subsequent onset of AHs, and the

involvement of depression in the onset of psychosis more generally, with both likely to

contribute to the maintenance of hallucinations by shaping cognitive appraisals of

aberrant experiences (Freeman & Garety, 2003; Garety et al., 2001; Kuipers et al., 2006;

Yung & McGorry, 1996).

Several socio-psychological and cognitive theories have been proposed to

explain the involvement of negative affect in the onset and maintenance of AHs, which

can be organised into two main categories: (1) direct theories, those that argue that

affect may trigger the underlying mechanisms (or some of) involved in the development

of AHs (rather than advocating that affect is the underlying mechanism), and (2)

indirect theories, those that argue that hallucinations are a form of defence mechanism

against negative emotion (for an example, see the „cognitive dissonance‟ conjecture

briefly explained in the section on Socio-Psychological Theories of AHs) (Freeman &

Garety, 2003). Direct theories have received the most support in the literature (Freeman

& Garety, 2003). These models typically propose some form of maintenance cycle,

often in which negative affect influences or biases a person‟s interpretations/

appraisals/beliefs about their AHs (i.e., beliefs regarding malevolence, omnipotence,

and controllability of voices) which further exacerbates negative affect, and in turn

triggers further AHs (e.g., Chadwick & Birchwood, 1994; Garety et al., 2001; Morrison,

1998; Morrison, 2001; Slade, 1976a). While these theoretical accounts address how

negative affect may contribute to the maintenance of AHs and further affective distress,

there has been little explanation of how – the precise mechanisms by which – emotions

contribute to the onset of AHs (Bentall, 2003; Freeman & Garety, 2003).

Negative Affect and the Phenomenology of Auditory Hallucinations

It has been proposed that the mood state preceding an AH may have a direct

influence on the phenomenological characteristics of the hallucinatory experience

(Freeman & Garety, 2003; Nayani & David, 1996b). For instance, Garety et al. (2001)

proposed that the emotions which trigger AHs and the emotions caused by AHs, feed

back into the content of voices, such that the content of an AH is a reflection of the

affective state. Nayani and David‟s (1996b) model of AHs as misidentified memories

(resulting from contextual memory deficits) presented earlier, has been used to explain

the mechanisms involved. They propose that because memories are organised in a

Chapter 1

27

semantic network, affect laden memories that are congruent with an individual‟s current

mood state will be automatically activated and retrieved if the emotional intensity of the

current mood is above the critical activation threshold. Accordingly, a mood such as

anxiety or paranoia may result in the automatic retrieval of memories of threat or abuse.

According to Nayani and David (1996b), a vicious cycle emerges making AHs

increasingly more frequent and severe, since the re-pairing of the emotion with the

memory reinforces the triggering emotion, the memory (or at least the misidentification

of the memory as a „voice‟), and the memory-emotion link, making the memory more

readily accessible.

Numerous studies have provided partial empirical support for Nayani and

David‟s (1996b) conjecture that AHs are misidentified memories. For instance, Nayani

and David‟s (1996a) survey study found that 61% of voice hearers can identify their

voices as people they know (and a further 15% report familiarity). Additionally, several

studies have found that the content of AHs experienced by individuals who have

experienced trauma are predominantly negative and paranoid, and are typically related

to – or flash backs of – the traumatic event itself (Hardy et al., 2005; Honig et al., 1998;

Read & Argyle, 1999). However, the empirical evidence supporting the specific link

between mood state and AH content has been somewhat inconsistent. In support,

several studies have reported significant correlations between depression/self-esteem

and negative/distressing content of AHs in schizophrenia (e.g., Smith, Fowler et al.,

2006). However, studies that have examined the prevalence of mood-congruent AHs in

different clinical populations have reported that while most AHs experienced in mood

disordered samples are mood-congruent, the AHs experienced in schizophrenia are both

mood-congruent and mood-incongruent (e.g., Fennig et al., 1996; Winokur et al., 1985).

However, a limitation of mood congruency studies is that „mood‟ is typically

determined by a single trait measure or by diagnostic label, rather than a measure of

ones mood state at the time of the hallucinatory episode. Similar to Nayani and David‟s

(1996b) conjecture, it has been proposed that the content of AHs reflect affect-triggered

self-schemas (Freeman & Garety, 2003), and indeed several studies have found that the

content of AHs reported by individuals with schizophrenia is closely tied to the

individual‟s self-schema, self esteem and social status (e.g., Close & Garety, 1998;

Hayward, 2003). However, these findings are not inconsistent with Nayani and David‟s

proposal, since memories are thought to be linked to a person‟s self-schema,

reciprocally activating one another.

Chapter 1

28

The relationship between negative affect and the phenomenology of AHs is

thought to be a reciprocal one, with several aspects of the AH experience contributing to

one‟s affective response. It has long been assumed that the predominantly negative

content of AHs is primarily responsible for the resulting distress. However, research

findings suggest that the relationship between AH phenomenology and affective

responding is more complex than this (Soppitt & Birchwood, 1997). Honig et al. (1998)

compared the AHs of patient and non-patient voice hearers and reported that only

patients found their voices distressing. The two AH features distinguishing these groups

was the amount of negative content (patients reported predominantly negative content)

and perceived control over voices (patients reported little control), suggesting that

content and control may influence affective responding. Similar findings have also been

reported in samples of patient and non-patient adolescent voice hearers (Escher et al.,

2002). Similarly, one study reported that 26% of schizophrenia participants experienced

enjoyable AHs, and that these AHs were positive or neutral in content and controllable

(Sanjuan, Gonzalez, Aguilar, Leal, & van Os, 2004). It is possible however that

perceived control over AHs is more integral to the affective response than content

(Nayani & David, 1996a). Johns et al. (2002) compared the AHs experienced by

individuals with tinnitus and schizophrenia, and found that the tinnitus participants

predominantly experienced non-verbal AHs (music, singing, birds, etc) with positive or

neutral content, while the schizophrenia participants mainly head voices with negative

content. Despite these differences in form and content, both groups reported high levels

of resulting distress, which was primarily attributed in both groups to the perceived

uncontrollability of their AHs.

In addition to content and control, studies have also linked affective responses to

AHs to the individual‟s beliefs regarding the voice‟s omnipotence and

malevolence/benevolence (Birchwood & Chadwick, 1997; Chadwick & Birchwood,

1994; Morrison, Nothard, Bowe, & Wells, 2004; Soppitt & Birchwood, 1997) and the

perceived social rank/social power of the voice relative their own (Birchwood et al.,

2004; Birchwood, Iqbal, & Upthegrove, 2005; Vaughan & Fowler, 2004).

In sum, these studies have taught us that the relationship between affect and AH

phenomenology is both complex and reciprocal in nature. It is clear however that

emotion is an important precursor to the onset on AH, yet the precise mechanisms by

which emotions contribute to the production of AHs is still unknown (Bentall, 2003;

Freeman & Garety, 2003). The relationship between negative affect and the cognitive

Chapter 1

29

processes purportedly involved in the onset of AHs will thus be investigated in this

thesis.

KEY PROCESSES UNDER INVESTIGATION

Cognitive Inhibition

The group of cognitive processes that will be explored in relation to

hallucinatory-type experiences in this thesis is inhibition, which forms part of the

Badcock and colleagues dual-deficit model of AHs (Waters, Badcock, Michie et al.,

2006). The term „inhibition‟ is often used as an umbrella term to cover a family of

cognitive processes which permit the suppression of previously activated – but currently

goal-irrelevant – cognitive contents, cognitive processes (such as attention), and

behavioural or motor actions, and the resistance to goal-competing distracting stimuli

(Harnishfeger, 1995; Wilson & Kipp, 1998). There is considerable evidence that the

processes included under this umbrella term primarily operate independently of one

another. Firstly, performance scores on many (if not most) tasks theorised to measure

„inhibition‟ do not correlate significantly with one another, however performance scores

on „inhibition‟ tasks found to share certain critical features (such as the level of

involvement of working memory and conscious thought, and the nature of the to-be-

suppressed event/stimuli) have been found to correlate significantly (Friedman &

Miyake, 2004; Kramer, Humphrey, Larish, Logan, & Strayer, 1994; Tipper & Baylis,

1987). Secondly, different clinical populations thought to be characterised by

„inhibition‟ deficits (such as Attention-deficit hyperactivity disorder [ADHD] and

Alzheimer‟s) are only impaired on some types of inhibition tasks (e.g., Amieva,

Phillips, Della Sala, & Henry, 2004; Nigg, Butler, Huang-Pollock, & Henderson, 2002).

Thirdly, different forms of inhibitory control are found to develop at different stages in

childhood (Dempster, 1993; Harnishfeger, 1995; Hasher, Lustig, & Zacks, 2007;

Wilson & Kipp, 1998). Finally, neuro-imaging and brain lesion studies have shown that

different forms of inhibitory control correspond with different neural circuits and

regions, all primarily located in the prefrontal cortex (e.g., Aron et al., 2004; Dias et al.,

1997; Fuster, 1999; Konishi et al., 1999; Starkstein & Robinson, 1997; Stuss et al.,

1999; Wyland et al., 2003). This evidence suggests that researchers should specify

which form of inhibitory control is under investigation, and select tasks accordingly. To

facilitate this separation, several theorists have developed inhibition taxonomies, and

Chapter 1

30

although they use different terminology, the key components largely overlap (e.g.,

Clark, 1996; Dempster, 1993; Friedman & Miyake, 2004; Harnishfeger, 1995; Nigg,

2000).

One of the most applied and empirically supported taxonomies of inhibitory

processes was proposed by Harnishfeger (1995). According to this system, inhibitory-

related processes can be classified according to three dimensions. The first dimension

concerns whether the to-be-suppressed event/stimuli is inhibited intentionally (when an

event/stimulus is recognised by the individual as being goal-irrelevant and consequently

is consciously suppressed) or unintentionally (occurring prior to/without conscious

awareness). Evidence for this distinction comes from the findings that unintentional

forms of inhibition develop earlier (around age 5) than intentional forms of inhibition

(around age 7; see Wilson & Kipp, 1998 for review), and secondly, from studies

reporting impaired performance on measures of intentional, but not unintentional,

inhibition in ADHD and Alzheimer‟s disease (Amieva et al., 2004; Nigg et al., 2002).

The second dimension concerns whether inhibition operates on or at a cognitive

(controlling mental processes) or behavioural (controlling impulses or motor responses)

level. Supporting this distinction, (1) cognitive and behavioural control tasks have been

shown to load on separate factors using latent-variable analysis (Friedman & Miyake,

2004), (2) developmental studies have shown that the acquisition of behavioural

inhibitory control begins earlier (from the first year of life) than cognitive inhibitory

control (which begins in the elementary years; see Harnishfeger, 1995 for review), and

(3) cognitive and behavioural control processes are thought to involve different neural

areas, for example the OFC is involved in cognitive inhibition, and the dorsolateral

prefrontal cortex is involved in behavioural inhibition (Dias et al., 1997; Friedman &

Miyake, 2004; West, 1996). The final dimension concerns the distinction between

processes that require inhibition (an active suppression process operating in working

memory) or resistance to interference (a gating mechanism that prevents irrelevant

information from entering working memory). Evidence for this distinction comes from

several sources: (1) neuro-imaging research has found distinct neural regions involved

in these two control processes (e.g., Stuss et al., 1999); (2) studies have found

differences in the involvement of working memory in these related processes (Kramer et

al., 1994); (3) developmental research has reported that the development of interference

control (but not inhibition) relies on/coincides with the increase in memory capacity

(see Harnishfeger, 1995 for review); and (4) inhibition and interference control tasks

Chapter 1

31

have been shown to load on separate factors using latent-variable analysis (Friedman &

Miyake, 2004).

According to the Badcock et al. dual-deficit model of AHs, the inhibitory

control impairments specific to AHs in schizophrenia would be classified, according to

Harnishfeger‟s (1995) taxonomy, as impairments in intentional cognitive inhibition,

since an AH is operating on a conscious and cognitive level and prevention of the

experience requires the inhibition of cognitions already held within working memory

(Badcock et al., 2005). Additional reasoning for this distinction comes from the neuro-

imaging research which has implicated the involvement of the OFC in both AHs and

this specific form of inhibitory control (Schnider et al., 2000; Silbersweig et al., 1995).

Although Badcock and colleagues have provided evidence connecting AHs to

intentional cognitive inhibition impairments in individuals with schizophrenia (see the

previous section: Dual Deficit: Intentional Inhibition and Context Memory Deficits), the

specificity of their proposal has not yet been tested. Consequently, the specificity of this

component of the dual-deficit model of AHs will be investigated in this thesis.1

Anxiety and Depression

The second domain under investigation in this thesis in relation to AHs and

inhibition processes is affective disturbance – specifically, anxiety and depression.

Anxiety and depression are similar, yet distinct affective constructs (Endler,

Macrodimitris, & Kocovski, 2003). It has been proposed that anxiety and depression

have both shared features (namely, general distress) and distinct features, which include

the somatic tension and arousal specific to anxiety and the anhedonia and low positive

affect specific to depression (Clark & Watson, 1991). Evidence that anxiety and

depression are distinct constructs comes not only from factor analyses of related

symptoms (e.g., Endler et al., 2003), but also from the documentation of distinct

cognitive biases associated with each, such as the automatic selective attention to, and

selective memory for, threat-related stimuli in anxiety, and the conscious/strategic

1 Because Harnishfeger‟s (1995) taxonomy makes the distinction between processes requiring

„inhibition‟ and „resistance to interference‟, the terms „cognitive control‟ and „inhibitory

control‟ will be used throughout this thesis when referring to the full range of inhibition-related

cognitive processes.

Chapter 1

32

selective memory for negative events in depression (see MacLeod & Rutherford, 1998;

Mathews & MacLeod, 2005 for reviews). However, possibly reflecting the symptom

overlap, the normal positive interpretation bias is absent in both anxiety and depression

(see Mathews & MacLeod, 2005 for a review). The distinction between state (current

emotion/mood) and trait (emotional temperament or disposition) forms – and thus,

measures – of both anxiety and depression has received empirical support in the

literature (e.g. Endler et al., 2003; Heinrich & Spielberger, 1982; Puliafico & Kendall,

2006). Despite this, most studies of affect do not address this conceptual distinction

(hence, it was excluded from the Negative Affect literature review).

Intrusive, task-irrelevant cognitions (i.e. thoughts, images and impulses) have

been widely documented in clinical and non-clinical studies of anxiety and depression

(e.g., Freeston et al., 1994; Hackmann, Surawy, & Clark, 1998; Seibert & Ellis, 1991;

Wegner & Zanakos, 1994). In anxiety disorders, the nature and content of the intrusion

varies (i.e., images or flashbacks of trauma in PTSD, compulsions often related to

cleanliness in obsessive-compulsive disorder, and worrisome thoughts about daily life

in generalised anxiety disorder), while in depression, the intrusions are typically

ruminative thoughts and memories that are self-deprecating in content. Importantly,

intrusive cognitions have been both theoretically and empirically linked to impaired

inhibitory control (Friedman & Miyake, 2004; Kramer et al., 1994; Schnider & Ptak,

1999), and thus, it is not surprising that studies have found inhibition difficulties in both

anxious and depressed populations (Mathews & MacLeod, 2005). However, the few

studies which have shown inhibitory difficulties in depression have found that they are

specific to the inhibition of emotional stimuli (Hertel & Gerstle, 2003; Joormann, 2004;

Lau, Christensen, Hawley, Gemar, & Segal, 2007; Power, Dalgleish, Claudio, Tata, &

Kentish, 2000; Waters, Badcock, & Maybery, 2006a), rather than a general inhibition

difficulty as documented in hallucinating individuals with schizophrenia (Badcock et

al., 2005). The inhibitory difficulties linked to anxiety on the other hand are more

robust, with studies showing both threat-specific and non-specific inhibition difficulties,

seemingly dependant on the type of inhibitory process under investigation and possibly

on the anxiety population tested (e.g., Amir, Coles, & Foa, 2002; Amir, Foa, & Coles,

1998; Badcock et al., 2007; Dorahy, McCusker, Loewenstein, Colbert, & Mulholland,

2006; Enright & Beech, 1993; Hopko, Ashcraft, Gute, Ruggiero, & Lewis, 1998; Wood,

Mathews, & Dalgleish, 2001). For instance, anxiety-related difficulties on unintentional

inhibition tasks are primarily threat-specific (Amir, Coles, Brigidi, & Foa, 2001;

Heinrichs & Hofmann, 2004), and different diagnostic (anxiety) groups show different

Chapter 1

33

patterns of difficulties on „resistance to interference‟ tasks (i.e., social phobia studies

show threat-specific impairments, while trauma studies show general non-specific

impairments; Amir et al., 2002; Amir et al., 1998; Wood et al., 2001).

As reviewed, both anxiety and depression have been differentially linked to

different stages across the development of schizophrenia, and AHs more specifically. It

is likely that these affective constructs have numerous different roles and operational

relationships within schizophrenia, some of which may be related to their shared- and

others to their distinct characteristics, most likely explaining why anxiety has been more

consistently linked to the onset of hallucinatory episodes than depression (e.g.,

Delespaul et al., 2002). This thesis will investigate – in both hallucination predisposition

and schizophrenia – the relationship between these affective states, cognitive inhibitory

processes, and AHs.

AIMS AND ORGANISATION OF THESIS

There were three general aims of this thesis. The first aim was concerned with

the intentional inhibition component of Badcock and colleague‟s dual-deficit model for

AHs: specifically, to dissociate the particular components of cognitive control (defined

using Harnishfeger‟s (1995) inhibition taxonomy) related to AHs in both hallucination

predisposition and schizophrenia. The second aim was to investigate the role of negative

affect (namely, anxiety and depression) in AHs, specifically with relation to the

cognitive control processes thought to contribute to the production of AHs. The third

aim was to investigate the continuum approach to hallucinatory-type experiences with

respect to the key constructs under investigation. The continuum approach predicts that

similar, though less severe, cognitive and affective disturbances may underlie the

development of hallucinatory-type experiences in healthy hallucination predisposed

individuals, as found in hallucinating individuals with schizophrenia.

The study presented in Chapter 2 of this thesis confirmed the multifactorial

structure of hallucinatory predisposition assessed with the LSHS-R, and further found

that anxiety (but not depression or stress) was consistently related to all components of

hallucination predisposition, even when controlling for the shared variance with

depression and stress. Consequently, the following studies in this thesis focused

exclusively on the role of anxiety in hallucinatory-type experiences. This decision was

also supported by the documentation of heightened anxiety at the onset of AH episodes

Chapter 1

34

and the established links between anxiety and general (non-threat specific) inhibitory-

related impairments.

Chapter 3 and Chapter 4 aimed to dissociate the components of cognitive

control involved in hallucination predisposition. The study presented in Chapter 3

provided support for the continuum approach to AHs, presenting findings of intentional

inhibition difficulties in healthy hallucination predisposed individuals – similar to those

documented in hallucinating individuals with schizophrenia (Badcock et al., 2005;

Waters et al., 2003). These intentional inhibition difficulties could not be explained by

other schizophrenia-related symptoms or state anxiety, suggesting that this inhibition

difficulty is specific to AHs and exists even in the absence of anxiety (though does not

rule out the possibility that anxiety may exacerbate these difficulties). In the study

reported in Chapter 4, we administered tasks measuring intentional resistance to

interference and unintentional inhibition to the same high and low hallucination

predisposed participants tested in Chapter 3. The study found evidence implicating the

involvement of intentional, rather than unintentional, forms of cognitive control in

hallucination predisposition. However, unlike the findings of intentional inhibition

difficulties reported in Chapter 3, the findings from Chapter 4 suggest that difficulties

with intentional resistance to interference may be a common mechanism underlying

anxiety and positive schizophrenia symptoms more generally.

The study presented in Chapter 5 sought to examine the possible effects of state

anxiety on the intentional inhibitory performance of healthy non-clinical individuals

using a music mood induction paradigm, and furthermore, to investigate whether

anxiety‟s effects were similar for hallucination predisposed individuals. The study

replicated the findings of intentional inhibition difficulties in hallucination

predisposition (as reported in Chapter 3), however did not find strong evidence that

state anxiety impairs intentional inhibition. However, whilst the mood induction

procedure was shown to be effective, the size and duration of the effects were modest.

Thus, either more marked or longer lasting changes in anxiety may impair inhibition

performance. Trait anxiety, however, was related to intentional inhibition, even when

controlling for state anxiety and hallucination predisposition.

The study reported in Chapter 6, sought to dissociate the specific components of

cognitive control related to AHs in schizophrenia, and further investigate the

involvement of anxiety in this relationship, by administering the same cognitive control

tasks employed in Chapters 3 and 4 to schizophrenia participants and healthy control

participants. Similar to the findings reported in the hallucination predisposition

Chapter 1

35

investigations, AH severity (but not delusions or negative symptoms) in schizophrenia

participants was specifically related to intentional inhibition, however unlike the

findings from Chapter 4, neither AHs nor delusions were related to intentional

resistance to interference. Although anxiety was related to both AH severity and

intentional inhibition, the correlations between each of these constructs remained

significant when partialling out the shared variance for the third construct. The findings

suggest that while anxiety may exacerbate existing impairments in intentional

inhibition, anxiety must also contribute to the production of AHs through a separate, as

yet unknown, mechanism.

The findings of this thesis and implications for the Badcock and colleagues dual-

deficit model of AHs are discussed in Chapter 7. Methodological strengths and

limitations of the studies, as well as clinical implications and suggestions for future

research are also discussed.

Chapter 1

36

REFERENCES

Abrams, R., & Taylor, M. A. (1981). Importance of schizophrenic symptoms in the

diagnosis of mania. American Journal of Psychiatry, 138, 658-661.

Addington, J., Cadenhead, K. S., Cannon, T. D., Cornblatt, B., McGlashan, T. H.,

Perkins, D. O., et al. (2007). North American prodrome longitudinal study: A

collaborative multisite approach to prodromal schizophrenia research.

Schizophrenia Bulletin, 33, 665-672.

Aggernaes, A. (1972). The difference between the experienced reality of hallucinations

in young drug abusers and schizophrenic patients. Acta Psychiatrica

Scandinavia, 48, 287-299.

Aggleton, J. P., & Brown, M. W. (1999). Episodic memory, amnesia, and the

hippocampal-anterior thalamic axis. Behavioral and Brain Sciences, 22, 425-

489.

AIHW. (2002). Mental Health Services in Australia 1999-00, Cat. No. HSE-19.

Canberra: Australian Institute of Health and Welfare.

Aleman, A., Bocker, K. B., Hijman, R., de Haan, E. H., & Kahn, R. S. (2003).

Cognitive basis of hallucinations in schizophrenia: Role of top-down

information processing. Schizophrenia Research, 64, 175-185.

Aleman, A., Hijman, R., de Haan, E. H., & Kahn, R. S. (1999). Memory impairment in

schizophrenia: A meta-analysis. American Journal of Psychiatry, 156, 1358-

1366.

Aleman, A., & Kahn, R. S. (2005). Strange feelings: Do amygdala abnormalities

dysregulate the emotional brain in schizophrenia? Progress in Neurobiology, 77,

283-298.

Aleman, A., Nieuwenstein, M. R., Bocker, K. B., & de Haan, E. H. (2000). Mental

imagery and perception in hallucination-prone individuals. Journal of Nervous

and Mental Disease, 188, 830-836.

Allen, P., Aleman, A., & McGuire, P. K. (2007). Inner speech models of auditory verbal

hallucinations: Evidence from behavioral and neuroimaging studies.

International Review of Psychiatry 19, 409-417.

Allen, P., Freeman, D., Johns, L., & McGuire, P. (2006). Misattribution of self-

generated speech in relation to hallucinatory proneness and delusional ideation

in healthy volunteers. Schizophrenia Research, 84, 281-288.

Chapter 1

37

Allen, P., Freeman, D., McGuire, P., Garety, P., Kuipers, E., Fowler, D., et al. (2005).

The prediction of hallucinatory predisposition in non-clinical individuals:

Examining the contribution of emotion and reasoning. British Journal of

Clinical Psychology, 44, 127-132.

Allen, P. P., Johns, L. C., Fu, C. H., Broome, M. R., Vythelingum, G. N., & McGuire,

P. K. (2004). Misattribution of external speech in patients with hallucinations

and delusions. Schizophrenia Research, 69, 277-287.

Allen, T. E., & Agus, B. (1968). Hyperventilation leading to hallucinations. American

Journal of Psychiatry, 125, 632-637.

Alpert, M., & Silvers, K. N. (1970). Perceptual characteristics distinguishing auditory

hallucinations in schizophrenia and acute alcoholic psychoses. American


Altman, H., Collins, M., & Mundy, P. (1997). Subclinical hallucinations and delusions

in nonpsychotic adolescents. Journal of Child Psychology and Psychiatry, 38,

413-420.

Amieva, H., Phillips, L. H., Della Sala, S., & Henry, J. D. (2004). Inhibitory functioning

in Alzheimer's disease. Brain, 127, 949-964.

Amir, N., Coles, M. E., Brigidi, B., & Foa, E. B. (2001). The effect of practice on recall

of emotional information in individuals with generalized social phobia. Journal

of Abnormal Psychology, 110, 76-82.

Amir, N., Coles, M. E., & Foa, E. B. (2002). Automatic and strategic activation and

inhibition of threat-relevant information in posttraumatic stress disorder.

Cognitive Therapy and Research, 26, 645-655.

Amir, N., Foa, E. B., & Coles, M. E. (1998). Automatic activation and strategic

avoidance of threat-relevant information in social phobia. Journal of Abnormal

Psychology, 107, 285-290.

APA. (2000). Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) (4th

ed.). Washington DC: American Psychiatric Association.

Aron, A. R., Robbins, T. W., & Poldrack, R. A. (2004). Inhibition and the right inferior

frontal cortex. Trends in Cognitive Science, 8, 170-177.

Badcock, J. C., & Maybery, M. T. (2005). Common or distinct deficits for auditory and

visual hallucinations? [Open Peer Commentary]. Behavioral and Brain

Sciences, 28, 757-758.

Chapter 1

38

Badcock, J. C., Waters, F. A. V., & Maybery, M. T. (2007). On keeping (intrusive)

thoughts to one's self: Testing a cognitive model of auditory hallucinations in

obsessive compulsive disorder. Cognitive Neuropsychiatry, 12, 78-89.

Badcock, J. C., Waters, F. A. V., Maybery, M. T., & Michie, P. T. (2005). Auditory

hallucinations: Failure to inhibit irrelevant memories. Cognitive


Baker, C. A., & Morrison, A. P. (1998). Cognitive processes in auditory hallucinations:

Attributional biases and metacognition. Psychological Medicine, 28, 1199-1208.

Barbato, A. (1998). Schizophrenia and public health. Geneva: World Health

Organization (Division of Mental Health and Prevention of Substance Abuse).

Barrett, T. R., & Caylor, M. R. (1998). Verbal hallucinations in normals, V: Perceived

reality characteristics. Personality and Individual Differences, 25, 209-221.

Barrett, T. R., & Etheridge, J. B. (1994). Verbal hallucinations in normals: III.

Dysfunctional personality correlates. Personality and Individual Differences, 16,

57-62.

Bassiony, M. M., & Lyketsos, C. G. (2003). Delusions and hallucinations in

Alzheimer's disease: Review of the brain decade. Psychosomatics, 44, 388-401.

Bebbington, P., Wilkins, S., Jones, P., Foerster, A., Murray, R., Toone, B., et al. (1993).

Life events and psychosis. Initial results from the Camberwell Collaborative

Psychosis Study. British Journal of Psychiatry, 162, 72-79.

Beck, A. T., & Rector, N. A. (2003). A cognitive model of hallucinations. Cognitive

Therapy and Research, 27, 19-52.

Bentall, R. P. (1990). The illusion of reality: A review and integration of psychological

research on hallucinations. Psychological Bulletin, 107, 82-95.

Bentall, R. P. (1997). The syndromes and symptoms of psychosis: Or why you can't

play 'twenty questions' with the concept of schizophrenia and hope to win. In R.

P. Bentall (Ed.), Reconstructing schizophrenia (pp. 23-60). London: Routledge.

Bentall, R. P. (2003). Madness explained: Psychosis and human nature. London:

Penguin Books Ltd.

Bentall, R. P., Baker, G. A., & Havers, S. (1991). Reality monitoring and psychotic

hallucinations. British Journal of Clinical Psychology, 30, 213-222.



527-529.

Chapter 1

39

Berenbaum, H., & Oltmanns, T. F. (1992). Emotional experience and expression in

schizophrenia and depression. Journal of Abnormal Psychology, 101, 37-44.

Berridge, K. C., & Robinson, T. E. (1998). What is the role of dopamine in reward:

Hedonic impact, reward learning, or incentive salience? Brain Research: Brain

Research Review, 28, 309-369.

Bhugra, D. (2005). The global prevalence of schizophrenia. Medicine, 2, 372-373.

Birchwood, M., & Chadwick, P. (1997). The omnipotence of voices: Testing the

validity of a cognitive model. Psychological Medicine, 27, 1345-1353.

Birchwood, M., Gilbert, P., Gilbert, J., Trower, P., Meaden, A., Hay, J., et al. (2004).

Interpersonal and role-related schema influence the relationship with the

dominant 'voice' in schizophrenia: A comparison of three models. Psychological

Medicine, 34, 1571-1580.

Birchwood, M., Iqbal, Z., & Upthegrove, R. (2005). Psychological pathways to

depression in schizophrenia: Studies in acute psychosis, post psychotic

depression and auditory hallucinations. European Archives of Psychiatry and

Clinical Neuroscience, 255, 202-212.

Birchwood, M., Smith, J., Macmillan, F., Hogg, B., Prasad, R., Harvey, C., et al.

(1989). Predicting relapse in schizophrenia: The development and

implementation of an early signs monitoring system using patients and families

as observers. Psychological Medicine, 19, 649-656.

Blakemore, S. J., Wolpert, D. M., & Frith, C. D. (2002). Abnormalities in the awareness

of action. Trends in Cognitive Sciences, 6, 237-242.

Brebion, G., Amador, X., David, A., Malaspina, D., Sharif, Z., & Gorman, J. M. (2000).

Positive symptomatology and source-monitoring failure in schizophrenia--an

analysis of symptom-specific effects. Psychiatry Research, 95, 119-131.

Brebion, G., Amador, X., Smith, M. J., Malaspina, D., Sharif, Z., & Gorman, J. M.

(1999). Opposite links of positive and negative symptomatology with memory

errors in schizophrenia. Psychiatry Research, 88, 15-24.

Brebion, G., Gorman, J. M., Amador, X., Malaspina, D., & Sharif, Z. (2002). Source

monitoring impairments in schizophrenia: Characterisation and associations with

positive and negative symptomatology. Psychiatry Research, 112, 27-39.

Brown, A. S. (2006). Prenatal infection as a risk factor for schizophrenia. Schizophrenia

Bulletin, 32, 200-202.

Burbridge, J. A., & Barch, D. M. (2007). Anhedonia and the experience of emotion in

individuals with schizophrenia. Journal of Abnormal Psychology, 116, 30-42.

Chapter 1

40

Burgess, P. W., & Shallice, T. (1996). Response suppression, initiation and strategy use

following frontal lobe lesions. Neuropsychologia, 34, 263-272.

Cahill, C. (1996). Psychotic experiences induced in deluded patients using distorted

auditory feedback. Cognitive Neuropsychiatry, 1, 201-211.

Carlson, G. A., & Goodwin, F. K. (1973). The stages of mania. A longitudinal analysis

of the manic episode. Archives of General Psychiatry, 28, 221-228.

Carter, C., Robertson, L., Nordahl, T., Chaderjian, M., Kraft, L., & O'Shora-Celaya, L.

(1996). Spatial working memory deficits and their relationship to negative

symptoms in unmedicated schizophrenia patients. Biological Psychiatry, 40,

930-932.

Carter, C. S., Robertson, L. C., Chaderjian, M. R., O'Shora-Celaya, L., & Nordahl, T. E.

(1994). Attentional asymmetry in schizophrenia: The role of illness subtype and

symptomatology. Progress in Neuropsychopharmacology and Biological

Psychiatry, 18, 661-683.

Carter, D. M., Mackinnon, A., & Copolov, D. L. (1996). Patients' strategies for coping

with auditory hallucinations. Journal of Nervous and Mental Disease, 184, 159-

164.

Castle, E., Wessely, S., Der, G., & Murray, R. M. (1991). The incidence of

operationally defined schizophrenia in Camberwell 1965-84. British Journal of


Chadwick, P., & Birchwood, M. (1994). The omnipotence of voices: A cognitive

approach to auditory hallucinations. British Journal of Psychiatry, 164, 190-201.

Chalfonte, B. L., & Johnson, M. K. (1996). Feature memory and binding in young and

older adults. Memory and Cognition, 24, 403-416.

Choong, C., Hunter, M. D., & Woodruff, P. W. (2007). Auditory hallucinations in those

populations that do not suffer from schizophrenia. Current Psychiatry Reports,

9, 206-212.

Clark, J. M. (1996). Contributions of inhibitory mechanisms to unified theory in

neuroscience and psychology. Brain and Cognition, 30, 127-152.

Clark, L. A., & Watson, D. (1991). Tripartite model of anxiety and depression:

Psychometric evidence and taxonomic implications. Journal of Abnormal


Close, H., & Garety, P. (1998). Cognitive assessment of voices: Further developments

in understanding the emotional impact of voices. British Journal of Clinical

Psychology, 37 173-188.

Chapter 1

41

Conley, R. R., & Kelly, D. L. (2001). Management of treatment resistance in

schizophrenia. Biological Psychiatry Research, 50, 898-911.

Copolov, D. L., Seal, M. L., Maruff, P., Ulusoy, R., Wong, M. T., Tochon-Danguy, H.

J., et al. (2003). Cortical activation associated with the experience of auditory

hallucinations and perception of human speech in schizophrenia: A PET

correlation study. Psychiatry Research, 122, 139-152.

Cornblatt, B., Lencz, T., & Obuchowski, M. (2002). The schizophrenia prodrome:

Treatment and high-risk perspectives. Schizophrenia Research, 54, 177-186.

Cornblatt, B. A., Lencz, T., Smith, C. W., Olsen, R., Auther, A. M., Nakayama, E., et

al. (2007). Can antidepressants be used to treat the schizophrenia prodrome?

Results of a prospective, naturalistic treatment study of adolescents. Journal of

Clinical Psychiatry, 68, 546-557.

Coryell, W., & Tsuang, M. T. (1985). Major depression with mood-congruent or mood-

incongruent psychotic features: Outcome after 40 years. American Journal of


Coryell, W., Tsuang, M. T., & McDaniel, J. (1982). Psychotic features in major

depression. Is mood congruence important? Journal of Affective Disorders, 4,

227-236.

Craddock, N., O'Donovan, M. C., & Owen, M. J. (2006). Genes for schizophrenia and

bipolar disorder? Implications for psychiatric nosology. Schizophrenia Bulletin,

32, 9-16.

Crow, T. J. (1980). Positive and negative schizophrenic symptoms and the role of

dopamine. British Journal of Psychiatry, 137, 383-386.

Cunningham, O. D., Miller, P., Lawrie, S., & Johnstone, E. (2005). Pathogenesis of

schizophrenia: A psychopathological perspective. British Journal of Psychiatry,

186, 386-393.

David, A. S. (1999). Auditory hallucinations: Phenomenology, neuropsychology and

neuroimaging update. Acta Psychiatrica Scandinavica, 395, 95-104.

Davies, G., Welham, J., Chant, D., Torrey, E. F., & McGrath, J. (2003). A systematic

review and meta-analysis of Northern Hemisphere season of birth studies in

schizophrenia. Schizophrenia Bulletin, 29, 587-593.

Delespaul, P., deVries, M., & van Os, J. (2002). Determinants of occurrence and

recovery from hallucinations in daily life. Social Psychiatry and Psychiatric

Epidemiology, 37, 97-104.

Chapter 1

42

Dempster, F. N. (1993). Resistance to interference: Developmental changes in a basic

processing mechanism. In M. L. Howe & R. Pasnak (Eds.), Emerging themes in

cognitive development (Vol. 1). New York: Springer-Verlag.

Dias, R., Robbins, T. W., & Roberts, A. C. (1997). Dissociable forms of inhibitory

control within prefrontal cortex with an analog of the Wisconsin Card Sort Test:

Restriction to novel situations and independence from "on-line" processing.

Journal of Neuroscience, 17, 9285-9297.

Dorahy, M. J., McCusker, C. G., Loewenstein, R. J., Colbert, K., & Mulholland, C.

(2006). Cognitive inhibition and interference in dissociative identity disorder:

The effects of anxiety on specific executive functions. Behaviour Research and

Therapy, 44, 749-764.

Eastvold, A. D., Heaton, R. K., & Cadenhead, K. S. (2007). Neurocognitive deficits in

the (putative) prodrome and first episode of psychosis. Schizophrenia Research,

93, 266-277.

Elvevag, B., & Goldberg, T. E. (2000). Cognitive impairment in schizophrenia is the

core of the disorder. Critical Reviews in Neurobiology, 14, 1-21.

Endler, N. S., Macrodimitris, S. D., & Kocovski, N. L. (2003). Anxiety and depression:

Congruent, separate, or both? Journal of Applied Biobehavioral Research, 8, 42-

60.

Enright, S. J., & Beech, A. R. (1993). Reduced cognitive inhibition in obsessive-

compulsive disorder. British Journal of Clinical Psychology, 32 67-74.

Escher, S., Delespaul, P., Romme, M., Buiks, A., & Van Os, J. (2003). Coping defence

and depression in adolescents hearing voices. Journal of Mental Health (UK),

12, 91-99.

Escher, S., Romme, M., Buiks, A., Delespaul, P., & van Os, J. (2002). Independent

course of childhood auditory hallucinations: A sequential 3-year follow-up

study. British Journal of Psychiatry, 181, 10-18.

Evans, C. L., McGuire, P. K., & David, A. S. (2000). Is auditory imagery defective in

patients with auditory hallucinations? Psychological Medicine, 30, 137-148.

Farhall, J., Greenwood, K. M., & Jackson, H. J. (2007). Coping with hallucinated voices

in schizophrenia: A review of self-initiated strategies and therapeutic

interventions. Clinical Psychology Review, 27, 476-793.

Fennig, S., Bromet, E. J., Karant, M. T., Ram, R., & Jandorf, L. (1996). Mood-

congruent versus mood-incongruent psychotic symptoms in first-admission

patients with affective disorder. Journal of Affective Disorders, 37, 23-29.

Chapter 1

43

Freeman, D., & Garety, P. A. (2003). Connecting neurosis and psychosis: The direct

influence of emotion on delusions and hallucinations. Behaviour Research and

Therapy, 41, 923-947.

Freeston, M. H., Gagnon, F., Ladouceur, R., Thibodeau, N., Letarte, H., & Rheaume, J.

(1994). Health-related intrusive thoughts. Journal of Psychosomatic Research.

Freud, S. (1924). The Loss of Reality in Neurosis and Psychosis. In J. Strachey (Ed.),

The standard edition of the complete psychological works of Sigmund Freud

(Vol. 19, pp. 181-188). London: Hogarth Press.




Frith, C. (1996). The role of the prefrontal cortex in self-consciousness: The case of

auditory hallucinations. Philosophical Transactions of the Royal Society of

London, 351, 1505-1512.

Fujii, D., & Ahmed, I. (2002a). Characteristics of psychotic disorder due to traumatic

brain injury: An analysis of case studies in the literature. Journal of

Neuropsychiatry and Clinical Neuroscience, 14, 130-140.

Fujii, D., & Ahmed, I. (2002b). Psychotic disorder following traumatic brain injury: A

conceptual framework. Cognitive Neuropsychiatry, 7, 41-62.

Fuster, J. M. (1997). The prefrontal cortex: Anatomy, physiology, and neuropsychology

of the frontal lobe (3rd ed.). Philadelphia: Lippincott-Raven.

Fuster, J. M. (1999). Synopsis of function and dysfunction of the frontal lobe. Acta

Psychiatrica Scandinavia, 395, 51-57.

Gallagher, A. G., Dinan, T. G., Sheehy, N., & Baker, L. (1995). Chronic auditory

hallucinations and suicide risk factors in schizophrenia. Irish Journal of


Garety, P., Fowler, D., Kuipers, E., Freeman, D., Dunn, G., Bebbington, P., et al.

(1997). London-East Anglia randomised controlled trial of cognitive-

behavioural therapy for psychosis. II: Predictors of outcome. British Journal of


Garety, P. A., & Freeman, D. (1999). Cognitive approaches to delusions: A critical

review of theories and evidence. British Journal of Clinical Psychology, 38,

113-154.

Chapter 1

44

Garety, P. A., Kuipers, E., Fowler, D., Freeman, D., & Bebbington, P. E. (2001). A

cognitive model of the positive symptoms of psychosis. Psychological Medicine,

31, 189-195.

Gelder, M., Gath, D., & Mayou, R. (1993). Oxford textbook of psychiatry (2nd ed.).

Oxford: Oxford University Press.

Gillibert, J. (1968). Thoughts on hallucination. Interpretation, 2, 65-79.

Goldberg, T. E., Gold, J. M., Coppola, R., & Weinberger, D. R. (1997). Unnatural

practices, unspeakable actions: A study of delayed auditory feedback in

schizophrenia. American Journal of Psychiatry, 154, 858-860.

Goldner, E. M., Hsu, L., Waraich, P., & Somers, J. M. (2002). Prevalence and incidence

studies of schizophrenic disorders: a systematic review of the literature.

Canadian Journal of Psychiatry, 47, 833-843.

Goodwin, R. D., Fergusson, D. M., & Horwood, L. J. (2004). Panic attacks and

psychoticism. American Journal of Psychiatry, 161, 88-92.

Green, M. F. (2001). Schizophrenia revealed: From neurons to social interactions. New

York: W.W. Norton.

Green, M. F. (2006). Cognitive impairment and functional outcome in schizophrenia

and bipolar disorder. Journal of Clinical Psychiatry, 67, 3-8.

Guillem, F., Bicu, M., Pampoulova, T., Hooper, R., Bloom, D., Wolf, M. A., et al.

(2003). The cognitive and anatomo-functional basis of reality distortion in

schizophrenia: A view from memory event-related potentials. Psychiatry

Research, 117, 137-158.

Guillem, F., Pampoulova, T., Stip, E., Lalonde, P., & Todorov, C. (2005). The

relationships between symptom dimensions and dysphoria in schizophrenia.

Schizophrenia Research, 75, 83-96.

Hackmann, A., Surawy, C., & Clark, D. M. (1998). Seeing yourself through others'

eyes: A study of spontaneously occurring images in social phobia. Behavioural

and Cognitive Psychotherapy, 26, 3-12.

Haddock, G., McCarron, J., Tarrier, N., & Faragher, E. B. (1999). Scales to measure

dimensions of hallucinations and delusions: The psychotic symptom rating

scales (PSYRATS). Psychological Medicine, 29, 879-889.

Hafner, H., Maurer, K., Trendler, G., an der Heiden, W., Schmidt, M., & Konnecke, R.

(2005). Schizophrenia and depression: Challenging the paradigm of two separate

diseases--A controlled study of schizophrenia, depression and healthy controls.


Chapter 1

45

Hamner, M. B. (1997). Psychotic features and combat-associated PTSD. Depression

and Anxiety, 5, 34-38.

Hamner, M. B., Frueh, B., Ulmer, H. G., Huber, M. G., Twomey, T. J., Tyson, C., et al.

(2000). Psychotic features in chronic posttraumatic stress disorder and

schizophrenia: Comparative severity. Journal of Nervous and Mental Disease,

188, 217-221.

Hardy, A., Fowler, D., Freeman, D., Smith, B., Steel, C., Evans, J., et al. (2005).

Trauma and hallucinatory experience in psychosis. Journal of Nervous and

Mental Disease, 193, 501-507.

Harnishfeger, K. K. (1995). The development of cognitive inhibition: Theories,

definitions, and research evidence. In F. N. Dempster & C. J. Brainerd (Eds.),

Interference and inhibition in cognition (pp. 175-204). San Diego, CA:

Academic Press.

Harris, A. W. F., Gordon, L. W., Bahramali, H., & Slewa-Younan, S. (1999). Different

psychopathological models and quantified EEG in schizophrenia. Psychological

Medicine, 29, 1175-1181.

Harrison, B. J., Yucel, M., Fornito, A., Wood, S. J., Seal, M. L., Clarke, K., et al.

(2007). Characterizing anterior cingulate activation in chronic schizophrenia: A

group and single-subject fMRI study. Acta Psychiatrica Scandinavia, 116, 271-

279.

Hasher, L., Lustig, C., & Zacks, R. (2007). Inhibitory mechanisms and the control of

attention. In A. R. A. Conway, C. Jarrold, M. J. Kane, A. Miyake & J. N. Towse

(Eds.), Variation in Working Memory. Oxford: Oxford University Press.

Hayward, M. (2003). Interpersonal relating and voice hearing: To what extent does

relating to the voice reflect social relating? Psychology and Psychotherapy, 76,

369-383.

Heinrich, D. L., & Spielberger, C. D. (1982). Anxiety and complex learning. Series in

Clinical & Community Psychology: Achievement, Stress, & Anxiety, 145-165.

Heinrichs, N., & Hofmann, S. G. (2004). Encoding processes in social anxiety. Journal

of Behavior Therapy and Experimental Psychiatry, 35, 57-74.

Hertel, P. T., & Gerstle, M. (2003). Depressive deficits in forgetting. Psychological

Science, 14, 573-578.

Herz, M. I., & Melville, C. (1980). Relapse in schizophrenia. American Journal of


Chapter 1

46

Honig, A., Romme, M. A., Ensink, B. J., Escher, S. D., Pennings, M. H., & deVries, M.

W. (1998). Auditory hallucinations: A comparison between patients and

nonpatients. Journal of Nervous and Mental Disease, 186, 646-651.

Hopko, D. R., Ashcraft, M. H., Gute, J., Ruggiero, K. J., & Lewis, C. (1998).

Mathematics anxiety and working memory: Support for the existence of a

deficient inhibition mechanism. Journal of Anxiety Disorders, 12, 343-355.

Huppert, J. D., & Smith, T. E. (2001). Longitudinal analysis of subjective quality of life

in schizophrenia: Anxiety as the best symptom predictor. Journal of Nervous

and Mental Disease, 189, 669-675.

Huppert, J. D., Weiss, K. A., Lim, R., Pratt, S., & Smith, T. E. (2001). Quality of life in

schizophrenia: Contributions of anxiety and depression. Schizophrenia

Research, 51, 171-180.

Hustig, H. H., & Hafner, R. J. (1990). Persistent auditory hallucinations and their

relationship to delusions and mood. Journal of Nervous and Mental Disease,

178, 264-267.

Jablensky, A. (2000). Prevalence and incidence of schizophrenia spectrum disorders:

Implications for prevention. Australian and New Zealand Journal of Psychiatry,

34 Suppl, S26-34.

Jablensky, A., McGrath, J., Herrman, H., Castle, D., Gureje, O., Evans, M., et al.

(2000). Psychotic disorders in urban areas: An overview of the Study on Low

Prevalence Disorders. Australian and New Zealand Journal of Psychiatry, 34,

221-236.

Jablensky, A., McGrath, J., Herrman, H., Castle, D., Gureje, O., Morgan, V., et al.

(1999). People living with psychotic illness: An Australian study 1997-98. In

National Mental Health and Wellbeing Report 4. Canberra, Australia:

Commonwealth of Australia (Department of Health and Aged Care).

Jenner, J. A., & van de Willige, G. (2001). HIT, hallucination focused integrative

treatment as early intervention in psychotic adolescents with auditory

hallucinations: A pilot study. Acta Psychiatrica Scandinavica, 103, 148-152.

Jenner, J. A., van de Willige, G., & Wiersma, D. (1998). Effectiveness of cognitive

therapy with coping training for persistent auditory hallucinations: A

retrospective study of attenders of a psychiatric out-patient department. Acta

Psychiatrica Scandinavica, 98, 384-389.

Chapter 1

47

Johns, L. C., Hemsley, D., & Kuipers, E. (2002). A comparison of auditory

hallucinations in a psychiatric and non-psychiatric group. British Journal of


Johns, L. C., & McGuire, P. K. (1999). Verbal self-monitoring and auditory

hallucinations in schizophrenia. Lancet, 353, 469-470.

Johns, L. C., Nazroo, J. Y., Bebbington, P., & Kuipers, E. (1998). Occurrence of

hallucinations in a community sample. Schizophrenia Research, 29, 23-23.

Johns, L. C., Rossell, S., Frith, C., Ahmad, F., Hemsley, D., Kuipers, E., et al. (2001).

Verbal self-monitoring and auditory verbal hallucinations in patients with

schizophrenia. Psychological Medicine, 31, 705-715.

Johns, L. C., & van Os, J. (2001). The continuity of psychotic experiences in the general

population. Clinical Psychology Review, 21, 1125-1141.

Johnson, J., Horwath, E., & Weissman, M. M. (1991). The validity of major depression

with psychotic features based on a community study. Archives of General

Psychiatry, 48, 1075-1081.

Johnstone, E. C., Crow, T. J., Frith, C. D., Husband, J., & Kreel, L. (1976). Cerebral

ventricular size and cognitive impairment in chronic schizophrenia. Lancet, 30,

924-926.

Jones, P., Rodgers, B., Murray, R., & Marmot, M. (1994). Child development risk

factors for adult schizophrenia in the British 1946 birth cohort. Lancet, 344,

1398-1402.

Joormann, J. (2004). Attentional bias in dysphoria: The role of inhibitory processes.

Cognition and Emotion, 18, 125-147.

Kapsambelis, V. (2005). Is hallucination an external excitation? Revue Francaise de

Psychanalyse, 69, 137-157.

Kapur, S. (2003). Psychosis as a state of aberrant salience: A framework linking

biology, phenomenology, and pharmacology in schizophrenia. American


Kapur, S., Mizrahi, R., & Li, M. (2005). From dopamine to salience to psychosis -

linking biology, pharmacology and phenomenology of psychosis. Schizophrenia

Research, 79, 59-68.

Kastelan, A., Franciskovic, T., Moro, L., Roncevic-Grzeta, I., Grkovic, J., Jurcan, V., et

al. (2007). Psychotic symptoms in combat-related post-traumatic stress disorder.

Military Medicine, 172, 273-277.

Chapter 1

48

Kavanagh, D. J., Waghorn, G., Jenner, L., Chant, D. C., Carr, V., Evans, M., et al.

(2004). Demographic and clinical correlates of comorbid substance use

disorders in psychosis: Multivariate analyses from an epidemiological sample.


Keefe, R. S., & Fenton, W. S. (2007). How should DSM-V criteria for schizophrenia

include cognitive impairment? Schizophrenia Bulletin, 33, 912-920.

Kendler, K. S., Gallagher, T. J., Abelson, J. M., & Kessler, R. C. (1996). Lifetime

prevalence, demographic risk factors, and diagnostic validity of nonaffective

psychosis as assessed in a US community sample. The National Comorbidity

Survey. Archives of General Psychiatry, 53, 1022-1031.

Kershner, P., & Wang-Cheng, R. (1989). Psychiatric side effects of steroid therapy.

Psychosomatics, 30, 135-139.

Konishi, S., Nakajima, K., Uchida, I., Kikyo, H., Kameyama, M., & Miyashita, Y.

(1999). Common inhibitory mechanism in human inferior prefrontal cortex

revealed by event-related functional MRI. Brain, 122, 981-991.

Konradi, C., & Heckers, S. (2003). Molecular aspects of glutamate dysregulation:

Implications for schizophrenia and its treatment. Pharmacology and

Therapeutics, 97, 153-179.

Krabbendam, L., Janssen, I., Bak, M., Bijl, R. V., de Graaf, R., & van Os, J. (2002).

Neuroticism and low self-esteem as risk factors for psychosis. Society of

Psychiatry and Psychiatric Epidemiology, 37, 1-6.

Krabbendam, L., Myin-Germeys, I., Hanssen, M., de Graaf, R., Vollebergh, W., Bak,

M., et al. (2005). Development of depressed mood predicts onset of psychotic

disorder in individuals who report hallucinatory experiences. British Journal of


Krabbendam, L., & van Os, J. (2005). Affective processes in the onset and persistence

of psychosis. European Archives of Psychiatry and Clinical Neuroscience, 255,

185-189.

Kramer, A. F., Humphrey, D. G., Larish, J. F., Logan, G. D., & Strayer, D. L. (1994).

Aging and inhibition: Beyond a unitary view of inhibitory processing in

attention. Psychology and Aging, 9, 491-512.

Kuipers, E., Fowler, D., Garety, P., Chisholm, D., Freeman, D., Dunn, G., et al. (1998).

London-east Anglia randomised controlled trial of cognitive-behavioural therapy

for psychosis. III: Follow-up and economic evaluation at 18 months. British


Chapter 1

49

Kuipers, E., Garety, P., Fowler, D., Freeman, D., Dunn, G., & Bebbington, P. (2006).

Cognitive, emotional, and social processes in psychosis: Refining cognitive

behavioral therapy for persistent positive symptoms. Schizophrenia Bulletin, 32,

S24-31.

Langdon, R., & Coltheart, M. (2000). The cognitive neuropsychology of delusions.

Mind and Language, 15, 184-218.

Laroi, F., Van der Linden, M., & Marczewski, P. (2004). The effects of emotional

salience, cognitive effort and meta-cognitive beliefs on a reality monitoring task

in hallucination-prone subjects. British Journal of Clinical Psychology, 43, 221-

233.

Laroi, F., & Woodward, T. S. (2007). Hallucinations from a cognitive perspective.

Harvard Review of Psychiatry, 15, 109-117.

Laruelle, M., Abi-Dargham, A., Gil, R., Kegeles, L., & Innis, R. (1999). Increased

dopamine transmission in schizophrenia: Relationship to illness phases.

Biological Psychiatry, 46, 56-72.

Lau, M. A., Christensen, B. K., Hawley, L. L., Gemar, M. S., & Segal, Z. V. (2007).

Inhibitory deficits for negative information in persons with major depressive

disorder. Psychological Medicine, 37, 1249-1259.

Launay, G., & Slade, P. D. (1981). The measurement of hallucinatory predisposition in

male and female prisoners. Personality and Individual Differences, 2, 221-234.

Lennox, B. R., Park, S. B., Jones, P. B., & Morris, P. G. (1999). Spatial and temporal

mapping of neural activity associated with auditory hallucinations. Lancet, 353,

644.

Leucht, S., Wahlbeck, K., Hamann, J., & Kissling, W. (2003). New generation

antipsychotics versus low-potency conventional antipsychotics: A systematic

review and meta-analysis. The Lancet, 36, 1581-1589.

Leudar, I., Thomas, P., McNally, D., & Glinski, A. (1997). What voices can do with

words: Pragmatics of verbal hallucinations. Psychological Medicine, 27, 885-

898.

Levine, E., Jonas, H., & Serper, M. R. (2004). Interpersonal attributional biases in

hallucinatory-prone individuals. Schizophrenia Research, 69, 23-28.

Liddle, P. F. (1987). Schizophrenic syndromes, cognitive performance and neurological

dysfunction. Psychological Medicine, 17, 49-57.

Lieberman, J. A., Kane, J. M., & Alvir, J. (1997). Provocative tests with

psychostimulant drugs in schizophrenia. Psychopharmacology, 91, 415-433.

Chapter 1

50

Limosin, F., Loze, J.-Y., Philippe, A., Casadebaig, F., & Rouillon, F. (2007). Ten-year

prospective follow-up study of the mortality by suicide in schizophrenic

patients. Schizophrenia Research, 94, 23-28.

MacLeod, C., & Rutherford, E. M. (1998). Automatic and strategic cognitive biases in

anxiety and depression. In K. Kirsner, C. Speelman, M. Mayberry, A. O‟Brien-

Malone, M. Anderson & C. MacLeod (Eds.), Implicit and explicit mental

processes (pp. 233-254). Mahwah, NJ: Lawrence Erlbaum.

Mathews, A., & MacLeod, C. (2005). Cognitive vulnerability to emotional disorders.

Annual Review of Clinical Psychology, 1, 167-195.

McCarley, R. W., Niznikiewicz, M. A., Salisbury, D. F., Nestor, P. G., O'Donnell, B. F.,

Hirayasu, Y., et al. (1999). Cognitive dysfunction in schizophrenia: Unifying

basic research and clinical aspects. European Archives of Psychiatry and

Clinical Neuroscience, 249, S69-82.

McCarley, R. W., Wible, C. G., Frumin, M., Hirayasu, Y., Levitt, J. J., Fischer, I. A., et

al. (1999). MRI anatomy of schizophrenia. Biological Psychiatry, 45, 1099-

1119.

McGee, R., Williams, S., & Poulton, R. (2000). Hallucinations in nonpsychotic

children. Journal of the American Academy of Child and Adolescent Psychiatry,

39, 12-13.

McGlashan, T. H. (1987). Testing DSM-III symptom criteria for schizotypal and

borderline personality disorders. Archives of General Psychiatry, 44, 15-22.

McGuire, P. K., Shah, G. M., & Murray, R. M. (1993). Increased blood flow in Broca's

area during auditory hallucinations in schizophrenia. Lancet, 342, 703-706.

McGuire, P. K., Silbersweig, D. A., & Frith, C. D. (1996). Functional neuroanatomy of

verbal self-monitoring. Brain, 119, 907-917.

McGuire, P. K., Silbersweig, D. A., Murray, R. M., David, A. S., Frackowiak, R. S., &

Frith, C. D. (1996). Functional anatomy of inner speech and auditory verbal

imagery. Psychological Medicine, 26, 29-38.

McGuire, P. K., Silbersweig, D. A., Wright, I., Murray, R. M., David, A. S.,

Frackowiak, R. S., et al. (1995). Abnormal monitoring of inner speech: A

physiological basis for auditory hallucinations. Lancet, 346, 596-600.

Merlotti, E., Piegari, G., & Galderisi, S. (2005). Cognitive impairment as a core feature

of schizophrenia. Minerva Psichiatrica, 46, 67-77.

Mihalopoulos, C., Magnus, A., Carter, R., & Vos, T. (2004). Assessing cost-

effectiveness in mental health: Family interventions for schizophrenia and

Chapter 1

51

related conditions. Australian and New Zealand Journal of Psychiatry, 38, 511-

519.

Milner, K. K., & Valenstein, M. (2002). A comparison of guidelines for the treatment of

schizophrenia. Psychiatric Services, 53, 888-890.

Mintz, S., & Alpert, M. (1972). Imagery vividness, reality testing, and schizophrenic

hallucinations. Journal of Abnormal Psychology, 79, 310-316.

Mojtabai, R., Nicholson, R. A., & Carpenter, B. N. (1998). Role of psychosocial

treatments in management of schizophrenia: A meta-analytic review of

controlled outcome studies. Schizophrenia Bulletin, 24, 569-587.

Morrison, A., & Petersen, T. (2003). Trauma, metacognition and predisposition to

hallucinations in non-patients. Behavioural & Cognitive Psychotherapy, 31,

235-246.

Morrison, A. P. (1998). A cognitive analysis of the maintenance of auditory

hallucinations: Are voices to schizophrenia what bodily sensations are to panic?

Behavioural and Cognitive Psychotherapy, 26, 289-302.

Morrison, A. P. (2001). The interpretation of intrusions in psychosis: An integrative

cognitive approach to hallucinations and delusions. Behavioural and Cognitive

Psychotherapy, 29, 257-276.

Morrison, A. P. (2005). Psychosis and the phenomenon of unwanted intrusive thoughts.

In D. A. Clark (Ed.), Intrusive thoughts in clinical disorders: Theory, research,

and treatment (pp. 175-198). New York: The Guilford Press.

Morrison, A. P., & Haddock, G. (1997). Cognitive factors in source monitoring and

auditory hallucinations. Psychological Medicine, 27, 669-679.

Morrison, A. P., Nothard, S., Bowe, S. E., & Wells, A. (2004). Interpretations of voices

in patients with hallucinations and non-patient controls: A comparison and

predictors of distress in patients. Behaviour Research and Therapy, 42, 1315-

1323.

Morrison, A. P., & Wells, A. (2003). A comparison of metacognitions in patients with

hallucinations, delusions, panic disorder, and non-patient controls. Behaviour

Research and Therapy, 41, 251-256.

Myin-Germeys, I., Delespaul, P., & deVries, M. W. (2000). Schizophrenia patients are

more emotionally active than is assumed based on their behavior. Schizophrenia

Bulletin, 26

Myin-Germeys, I., Delespaul, P., & van Os, J. (2005). Behavioural sensitization to daily

life stress in psychosis. Psychological Medicine, 35, 733-741.

Chapter 1

52

Myin-Germeys, I., Marcelis, M., Krabbendam, L., Delespaul, P., & van Os, J. (2005).

Subtle fluctuations in psychotic phenomena as functional states of abnormal

dopamine reactivity in individuals at risk. Biological Psychiatry, 58, 105-110.

Nayani, T. H., & David, A. S. (1996a). The auditory hallucination: A phenomenological

survey. Psychological Medicine, 26, 177-189.

Nayani, T. H., & David, A. S. (1996b). The neuropsychology and neurophenomenology

of auditory hallucinations. In C. Peantelis, H. E. Nelson & T. R. E. Barnes

(Eds.), Schizophrenia: A neuropsychological perspective (pp. 345-369). New

York: John Wiley & Sons Ltd.

Niendam, T. A., Bearden, C. E., Johnson, J. K., McKinley, M., Loewy, R., O'Brien, M.,

et al. (2006). Neurocognitive performance and functional disability in the

psychosis prodrome. Schizophrenia Research, 84, 100-111.

Nigg, J. T. (2000). On inhibition/disinhibition in developmental psychopathology:

Views from cognitive and personality psychology and a working inhibition

taxonomy. Psychological Bulletin, 126, 220-246.

Nigg, J. T., Butler, K. M., Huang-Pollock, C. L., & Henderson, J. M. (2002). Inhibitory

processes in adults with persistent childhood onset ADHD. Journal of

Consulting Clinical Psychology, 70, 153-157.

Norman, R. M., & Malla, A. K. (1991). Dysphoric mood and symptomotology in

schizophrenia. Psychological Medicine, 21, 897-903.

Norman, R. M., Malla, A. K., Cortese, L., & Diaz, F. (1998). Aspects of dysphoria and

symptoms of schizophrenia. Psychological Medicine, 28, 1433-1441.

Norman, R. M. G., & Malla, A. K. (1994). Correlations over time between dysphoric

mood and symptomatology in schizophrenia. Comprehensive Psychiatry, 35, 34-

38.

O'Donovan, M. C., Williams, N. M., & Owen, M. J. (2003). Recent advances in the

genetics of schizophrenia. Human Molecular Genetics, 12, 125-133.

Ohayon, M. M. (2000). Prevalence of hallucinations and their pathological associations

in the general population. Psychiatry Research, 97, 153-164.

Ohayon, M. M., & Schatzberg, A. F. (2002). Prevalence of depressive episodes with

psychotic features in the general population. American Journal of Psychiatry,

159, 1855-1861.

Owen, M. J., Craddock, N., & O'Donovan, M. C. (2005). Schizophrenia: Genes at last?

Trends in Genetics, 21, 518-525.

Chapter 1

53

Peralta, V., & Cuesta, M. J. (2001). How many and which are the psychopathological

dimensions in schizophrenia? Issues influencing their ascertainment.


Peters, E. R., Pickering, A. D., Kent, A., Glasper, A., Irani, M., David, A. S., et al.

(2000). The relationship between cognitive inhibition and psychotic symptoms.

Journal Of Abnormal Psychology, 109, 386-395.

Pilling, S., Bebbington, P., Kuipers, E., & etal. (2002). Psychological treatments in

schizophrenia: II. Metaanalyses of randomized controlled trials of social skills

training and cognitive remediation. Psychological Medicine, 32, 783-791.

Power, M. J., Dalgleish, T., Claudio, V., Tata, P., & Kentish, J. (2000). The directed

forgetting task: Application to emotionally valent material. Journal of Affective

Disorders, 57, 147-157.

Puliafico, A. C., & Kendall, P. C. (2006). Threat-related attentional bias in anxious

youth: A review. Clinical Child and Family Psychology Review, 9, 162-180.

Ragland, J. D., Yoon, J., Minzenberg, M. J., & Carter, C. S. (2007). Neuroimaging of

cognitive disability in schizophrenia: Search for a pathophysiological

mechanism. International Review of Psychiatry, 19, 417-427.

Read, J., & Argyle, N. (1999). Hallucinations, delusions, and thought disorder among

adult psychiatric inpatients with a history of child abuse. Psychiatric Services,

50, 1467-1472.

Read, J., van Os, J., Morrison, A. P., & Ross, C. A. (2005). Childhood trauma,

psychosis and schizophrenia: A literature review with theoretical and clinical

implications. Acta Psychiatrica Scandinavica, 112, 330-350.

Romme, M. A., Honig, A., Noorthoorn, E. O., & Escher, A. D. (1992). Coping with

hearing voices: An emancipatory approach. British Journal of Psychiatry, 161,

99-103.

Sanjuan, J., Gonzalez, J. C., Aguilar, E. J., Leal, C., & van Os, J. (2004). Pleasurable

auditory hallucinations. Acta Psychiatrica Scandinavica, 110, 273-278.

Sartorius, N., Shapiro, R., & Jablensky, A. (1974). The international pilot study of

schizophrenia. Schizophrophrenia Bulletin, 8, 21-34.

Schnider, A., & Ptak, R. (1999). Spontaneous confabulators fail to suppress currently

irrelevant memory traces. Nature Neuroscience, 2, 677-681.

Schnider, A., Treyer, V., & Buck, A. (2000). Selection of currently relevant memories

by the human posterior medial orbitofrontal cortex. Journal of Neuroscience, 20,

5880-5884.

Chapter 1

54

Seal, M. L., Aleman, A., McGuire, P. K., & Seal, M. L. (2004). Compelling imagery,

unanticipated speech and deceptive memory: Neurocognitive models of auditory

verbal hallucinations in schizophrenia. Cognitive Neuropsychiatry, 9, 43-72.

Seibert, P. S., & Ellis, H. C. (1991). Irrelevant thoughts, emotional mood states, and

cognitive task performance. Memory and Cognition, 19, 507-513.

Selten, J. P., Cantor-Graae, E., & Kahn, R. S. (2007). Migration and schizophrenia.

Current Opinion in Psychiatry, 20, 111-115.

Serper, M. P., Dill, C. A. P., Chang, N. M. A., Kot, T. P., & Elliot, J. M. A. (2005).

Factorial structure of the hallucinatory experience: Continuity of experience in

psychotic and normal Individuals. Journal of Nervous and Mental Disease 193,

265-272.

Servan-Schreiber, D., Cohen, J. D., & Steingard, S. (1996). Schizophrenic deficits in the

processing of context. A test of a theoretical model. Archives of General

Psychiatry, 53, 1105-1112.

Shevlin, M., Murphy, J., Dorahy, M. J., & Adamson, G. (2007). The distribution of

positive psychosis-like symptoms in the population: A latent class analysis of

the National Comorbidity Survey. Schizophrenia Research, 89, 101-109.

Sidgewick, H., Johnson, A., Myers, F. W. H., & et-al. (1894). Report on the census of

hallucinations. Proceedings of the Society for Psychiatric Research, 26, 259-

394.

Siever, L. J., Amin, F., Coccaro, E. F., Bernstein, D., Kavoussi, R. J., Kalus, O., et al.

(1991). Plasma homovanillic acid in schizotypal personality disorder. American


Siever, L. J., Amin, F., Coccaro, E. F., Trestman, R., Silverman, J., Horvath, T. B., et al.

(1993). CSF homovanillic acid in schizotypal personality disorder. American


Silbersweig, D., & Stern, E. (1996). Functional neuroimaging of hallucinations in

schizophrenia: Toward an integration of bottom-up and top-down approaches.

Molecular Psychiatry, 1, 367-375.

Silbersweig, D. A., Stern, E., Frith, C., Cahill, C., Holmes, A., Grootoonk, S., et al.

(1995). A functional neuroanatomy of hallucinations in schizophrenia. Nature,

378, 176-179.

Siris, G. G. (1995). Depression and schizophrenia. In S. R. Hirsch & D. R. Weinberger

(Eds.), Schizophrenia (pp. 128–146). Oxford: Blackwell Science Ltd.

Chapter 1

55

Slade, P. D. (1972). The effects of systematic desensitisation on auditory hallucinations.

Behaviour Research and Therapy, 10, 85-91.

Slade, P. D. (1973). The psychological investigation and treatment of auditory

hallucinations: A second case report. British Journal of Medical Psychology, 46,

293-296.

Slade, P. D. (1976a). An investigation of psychological factors involved in the

predisposition to auditory hallucinations. Psychological Medicine, 6, 123-132.

Slade, P. D. (1976b). Towards a theory of auditory hallucinations: Outline of an

hypothetical four-factor model. British Journal of Social and Clinical

Psychology 15, 415-423.

Slade, P. D., & Bentall, R. P. (1988). Sensory deception: A scientific analysis of

hallucination. London: Croom Helm.

Smith, B., Fowler, D. G., Freeman, D., Bebbington, P., Bashforth, H., Garety, P., et al.

(2006). Emotion and psychosis: Links between depression, self-esteem, negative

schematic beliefs and delusions and hallucinations. Schizophrenia Research, 86,

181-188.

Smith, C. W., Sohee, P., & Cornblatt, B. (2006). Spatial working memory deficits in

adolescents at clinical high risk for schizophrenia. Schizophrenia Research, 81,

211-215.

Soppitt, R. W., & Birchwood, M. (1997). Depression, beliefs, voice content and

topography: A cross-sectional study of schizophrenic patients with auditory

verbal hallucinations. Journal of Mental Health, 6, 525-532.

Starker, S., & Jolin, A. (1982). Imagery and hallucination in schizophrenic patients.

Journal of Nervous and Mental Disease, 170, 448-451.

Starkstein, S. E., & Robinson, R. G. (1997). Mechanism of disinhibition after brain

lesions. Journal of Nervous and Mental Disease, 185, 108-114.

Stuss, D. T., Toth, J. P., Franchi, D., Alexander, M. P., Tipper, S., & Craik, F. I. (1999).

Dissociation of attentional processes in patients with focal frontal and posterior

lesions. Neuropsychologia, 37, 1005-1027.

Svirskis, T., Korkeila, J., Heinimaa, M., Huttunen, J., Ilonen, T., Ristkari, T., et al.

(2005). Axis-I disorders and vulnerability to psychosis. Schizophrenia Research,

75, 439-446.

Takebayashi, H., Takei, N., Mori, N., & Suzuki, S. (2002). Unilateral auditory

hallucinations in schizophrenia after damage to the right hippocampus.


Chapter 1

56

Tibbo, P., Swainson, J., Chue, P., & LeMelledo, J. M. (2003). Prevalence and

relationship to delusions and hallucinations of anxiety disorders in

schizophrenia. Depression and Anxiety, 17, 65-72.

Tien, A. Y. (1991). Distribution of hallucinations in the population. Psychiatric


Tien, A. Y., & Eaton, W. W. (1992). Psychopathologic precursors and

sociodemographic risk factors for the schizophrenia syndrome. Archives of

General Psychiatry, 49, 37-46.

Tipper, S. P., & Baylis, G. C. (1987). Individual-differences in selective attention: The

relation of priming and interference to cognitive failure. Personality and

Individual Differences, 34, 285-292.

Treyer, V., Buck, A., & Schnider, A. (2003). Subcortical loop activation during

selection of currently relevant memories. Journal of Cognitive Neuroscience, 15,

610-618.

Turkingtona, D., Senskyb, T., Scottc, J., Barnesb, T. R. E., Nurb, U., Siddled, R., et al.

(2008). A randomized controlled trial of cognitive-behavior therapy for

persistent symptoms in schizophrenia: A five-year follow-up. Schizophrenia

Research, 98, 1-7.

van't Wout, M., Aleman, A., Kessels, R. P. C., Laroi, F., & Kahn, R. S. (2004).

Emotional processing in a non-clinical psychosis-prone sample. Schizophrenia

Research, 68, 271-281.

van Os, J., Hanssen, M., Bijl, R. V., & Ravelli, A. (2000). Strauss (1969) revisited: A

psychosis continuum in the general population? Schizophrenia Research, 45, 11-

20.

van Os, J., Krabbendam, L., Myin-Germeys, I., & Delespaul, P. (2005). The

schizophrenia envirome. Current Opinion in Psychiatry, 18, 141-145.

van Os, J., Park, S. B., & Jones, P. B. (2001). Neuroticism, life events and mental

health: Evidence for person-environment correlation. British Journal of

Psychiatry, 40, S72-77.

Vaughan, S., & Fowler, D. (2004). The distress experienced by voice hearers is

associated with the perceived relationship between the voice hearer and the

voice. British Journal of Clinical Psychology, 43, 143-153.

Verdoux, H., & van Os, J. (2002). Psychotic symptoms in non-clinical populations and

the continuum of psychosis. Schizophrenia Research, 54, 59-65.

Chapter 1

57

Walsh, E., Harvey, K., White, I., Manley, C., Fraser, J., Stanbridge, S., et al. (1999).

Prevalence and predictors of parasuicide in chronic psychosis. UK700 group.

Acta Psychiatrica Scandinavica, 100, 375-382.

Waters, F. A., Badcock, J. C., & Maybery, M. T. (2006a). Selective attention for

negative information and depression in schizophrenia. Psychological Medicine,

36, 455-464.

Waters, F. A. V., Badcock, J. C., & Maybery, M. T. (2006b). The 'who' and 'when' of

context memory: Different patterns of association with auditory hallucinations.


Waters, F. A. V., Badcock, J. C., Maybery, M. T., & Michie, P. T. (2003). Inhibition in

schizophrenia: Association with auditory hallucinations. Schizophrenia

Research, 62, 275-280.




Waters, F. A. V., Maybery, M. T., Badcock, J. C., & Michie, P. T. (2004). Context

memory and binding in schizophrenia. Schizophrenia Research, 68, 119-125.

Wegner, D. M., & Zanakos, S. (1994). Chronic thought suppression. Journal of

Personality, 62, 615-640.

West, R. L. (1996). An application of prefrontal cortex function theory to cognitive

aging. Psychological Bulletin, 120, 272-292.

Wiersma, D., Jenner, J. A., Nienhuis, F. J., & van de Willige, G. (2004). Hallucination

focused integrative treatment improves quality of life in schizophrenia patients.


Wiersma, D., Jenner, J. A., van de Willige, G., Spakman, M., & Nienhuis, F. J. (2001).

Cognitive behaviour therapy with coping training for persistent auditory

hallucinations in schizophrenia: A naturalistic follow-up study of the durability

of effects. Acta Psychiatrica Scandinavica, 103, 393-399.

Wilson, S. P., & Kipp, K. (1998). The development of efficient inhibition: Evidence

from directed-forgetting tasks. Developmental Review, 18, 86-123.

Winokur, G., Scharfetter, C., & Angst, J. (1985). The diagnostic value in assessing

mood congruence in delusions and hallucinations and their relationship to the

affective state. European Archives of Psychiatry and Neurological Sciences,

234, 299-302.

Chapter 1

58


Emotion, 1, 166-181.

Woodruff, P. W., Wright, I. C., Bullmore, E. T., Brammer, M., Howard, R. J., Williams,

S. C., et al. (1997). Auditory hallucinations and the temporal cortical response to

speech in schizophrenia: A functional magnetic resonance imaging study.

American Journal of Psychiatry, 154, 1676-1682.

Wright, I. C., Rabe-Hesketh, S., Woodruff, P. W., David, A. S., Murray, R. M., &

Bullmore, E. T. (2000). Meta-analysis of regional brain volumes in

schizophrenia. American Journal of Psychiatry, 157, 16-25.

Wykes, T., Reeder, C., Williams, C., Corner, J., Rice, C., & Everitt, B. (2003). Are the

effects of cognitive remediation therapy (CRT) durable? Results from an

exploratory trial in schizophrenia. Schizophrenia Research, 61, 163-174.

Wyland, C. L., Kelley, W. M., Macrae, C. N., Gordon, H. L., & Heatherton, T. F.

(2003). Neural correlates of thought suppression. Neuropsychologia, 41, 1863-

1867.

Young, H. F., Bentall, R. P., Slade, P. D., & Dewey, M. E. (1987). The role of brief

instructions and suggestibility in the elicitation of auditory and visual

hallucinations in normal and psychiatric subjects. Journal of Nervous and

Mental Disease, 175, 41-48.

Yung, A. R., & McGorry, P. D. (1996). The prodromal phase of first-episode psychosis:

Past and current conceptualizations. Schizophrenia Bulletin, 22, 353-370.

Yung, A. R., Phillips, L. J., Yuen, H. P., Francey, S. M., McFarlane, C. A., Hallgren,

M., et al. (2003). Psychosis prediction: 12-month follow up of a high-risk

("prodromal") group. Schizophrenia Research, 60, 21-32.

59

PREDISPOSITION TO HALLUCINATIONS

60

Foreword to Chapter 2

61

FOREWORD TO CHAPTER 2

It is commonly believed that hallucinatory experiences exist on a continuum,

with normal mental events experienced by healthy individuals on one end (including

intrusive and vivid thoughts, memories or day dreams), and full-blown auditory

hallucinations (AHs) experienced by individuals with schizophrenia on the other (e.g.,

Bentall & Slade, 1985; Choong, Hunter, & Woodruff, 2007; Johns & van Os, 2001;

Shevlin, Murphy, Dorahy, & Adamson, 2007; Verdoux & van Os, 2002). Supporting

this conjecture, it has been found that a large minority of healthy individuals (10 to

25%) who do not meet criteria for schizophrenia also report having had one or more

hallucinatory experiences when not in an altered state of consciousness (Johns, Nazroo,

Bebbington, & Kuipers, 1998; Tien, 1991). The continuum approach to AHs predicts

that analogous experiences across the continuum share similar features and underlying

mechanisms, contributing to the rationale behind the study of AHs in a non-clinical

population. An advantage of studying hallucinatory-type experiences in the general

population (termed ‘hallucination predisposition’) is that it permits the examination of

these experiences in the absence of possible confounds associated with schizophrenia.

The Launay-Slade Hallucination Scale (LSHS: Launay & Slade, 1981, revised by

Bentall & Slade, 1985; LSHS-R) was developed specifically to facilitate this type of

research.

Chapter 2 presents the findings from two related studies into the features of, and

affective associations with, hallucination predisposition. The aim of the first study was

to clarify the defining characteristics of the components underlying hallucination

predisposition (measured using the LSHS-R) in a large non-psychiatric sample using

confirmatory factor analysis. The aim of the second study was to examine the

association between depression, anxiety, and stress and the separate components of

hallucinatory predisposition. The results from these two studies helped to identify the

affective construct most consistently associated with hallucination predisposition, and

furthermore, facilitated speculation into the underlying mechanisms involved in the

examined relationships.


62

REFERENCES



527-529.



9, 206-212.



Johns, L. C., & van Os, J. (2001). The continuity of psychotic experiences in the general

population. Clinical Psychology Review, 21, 1125-1141.



Shevlin, M., Murphy, J., Dorahy, M. J., & Adamson, G. (2007). The distribution of

positive psychosis-like symptoms in the population: A latent class analysis of

the National Comorbidity Survey. Schizophrenia Research, 89, 101-109.



Verdoux, H., & van Os, J. (2002). Psychotic symptoms in non-clinical populations and

the continuum of psychosis. Schizophrenia Research, 54, 59-65.

Chapter 2

63

Chapter 2

The multifactorial structure of the predisposition to hallucinate

and associations with anxiety, depression and stress 1

ABSTRACT

Depression, anxiety and stress are commonly experienced by individuals

predisposed to hallucinations and often accompany hallucinations in patients with

schizophrenia. Analogous to hallucinatory experiences themselves, hallucination

predisposition is measured as a multidimensional construct, though many competing

structures have been proposed. Few studies have examined the association between

negative affect and the individual subcomponents of hallucination predisposition. This

paper describes two related studies: the first aimed to confirm the multifactorial

structure of hallucinatory predisposition assessed with the Launay-Slade Hallucination

Scale-Revised (LSHS-R; Bentall & Slade, 1985); the second study aimed to examine

the association between depression, anxiety, and stress and the separate components of

hallucinatory predisposition in a non-psychiatric population. The first study showed that

a 3-factor model of hallucination predisposition (Waters, Badcock, & Maybery, 2003a)

was superior to two competing models. The second study showed that anxiety was most

consistently related to the predisposition to hallucinate, being associated with all three

of the LSHS-R components, even after the variance shared with the other two affective

constructs was partialled out. The possible influence of anxiety on cognitive

mechanisms (in particular, intentional inhibition) potentially involved in hallucination

predisposition was discussed.

Keywords: Hallucination predisposition; Launay-Slade Hallucination Scale-Revised

(LSHS-R); Inhibition; Affect; Depression; Anxiety; Stress

1 This chapter is a reproduction of the following article: Paulik, G., Badcock, J., & Maybery, M.

(2006). The multifactorial structure of the predisposition to hallucinate and associations with

anxiety, depression and stress. Personality and Individual Differences, 41, 1067 – 1076.

Chapter 2

64

Auditory hallucinations occur in patients with schizophrenia and in a substantial

minority (10 to 25%) of the general population (e.g., Tien, 1991), suggesting that

hallucinatory experiences form a continuum with normal psychological functioning

(Slade & Bentall, 1988). Recently there has been a growing interest in the empirical

examination of hallucinations in healthy individuals predisposed to hallucinations. Such

individuals do not have any form of psychosis, but may experience ‘clinical’

hallucinations and/or a high frequency/severity of ‘subclinical’ hallucinatory-type

experiences, which refer to cognitions (thoughts, memories or day dreams) similar to

hallucinations in their intrusiveness, vividness, and seemingly uncontrollable nature,

though distinguishable from hallucinations in their intact source information (i.e.,

recognised as being of self origin) (Serper, Dill, Chang, Kot, & Elliot, 2005).

One of the most frequently used measures of hallucinatory predisposition in the

general population is the Launay-Slade Hallucination Scale (LSHS: Launay & Slade,

1981), as revised by Bentall and Slade in 1985 (LSHS-R). Analogous to hallucinatory

experiences themselves, hallucination predisposition is measured by the LSHS-R as a

multidimensional construct, assessing both clinical and sub-clinical hallucinatory-type

experiences (e.g., Aleman, Nieuwenstein, Boecker, & De Haan, 2001; Levitan, Ward,

Catts, & Hemsley, 1996; Serper et al., 2005; Waters, Badcock, & Maybery, 2003a).

However, the precise number and nature of the subcomponents describing hallucination

predisposition is debateable and reported factor structures of the LSHS-R are

inconsistent (Aleman et al., 2001; Serper et al., 2005; Waters et al., 2003a), making it

difficult to investigate how the different components of hallucination predisposition

(based on the LSHS-R) differentially relate to other constructs, such as emotions.

High levels of negative affect, especially depression, anxiety and stress, have

been documented consistently both prior to and in association with hallucinatory

experiences (Delespaul & Van Os, 2005; for review see Freeman & Garety, 2003). Such

findings suggest that emotional disturbance may play a direct role in the onset of

hallucinations or that some of the processes involved in hallucinations may be mediated

or moderated by affective arousal (Slade & Bentall, 1988). This does not, however,

preclude the experience of emotion as a bi-product of the hallucinatory experience,

which to date has received the majority of attention in the research literature (e.g., Close

& Garety, 1998). In addressing the paucity of research on the role of negative affect in

the onset of hallucinations, Freeman and Garety (2003) recommended examining the

role of emotions in individuals prior to full symptom development. Indeed, high levels

of negative affect have also been shown in healthy individuals predisposed to

Chapter 2

65

hallucinations (e.g., Allen et al., 2005; Lewandowski et al., 2006; Morison, Wells, &

Nothard, 2000, 2002; van't Wout, Aleman, Kessels, Laroi, & Kahn, 2004; Young,

Bentall, Slade, & Dewey, 1986). However, limited research has been conducted to

examine whether negative affect relates to all, or only some, of the components of


This paper presents two related studies. The aim of Study 1 was to evaluate the

different factor structures of the LSHS-R reported in previous non-patient studies. The

aim of the second study was to investigate whether all or only some of the

subcomponents characteristic of hallucination predisposition relate to separate measures

of negative affect - namely depression, anxiety and stress – in an undergraduate sample.

STUDY 1

Three previous factor analytic studies of the 12-item LSHS-R have reported that

either a two-factor structure or (different) three-factor structures best capture the multi-

dimensional nature of the experience in healthy (non-patient) individuals. Waters et al.

(2003a) administered the LSHS-R to 562 undergraduate students and, using principal

components analysis (PCA), obtained three factors: (1) vivid mental events (items 1-7);

(2) hallucinations with a religious theme (items 10-12); and (3) auditory and visual

(perceptual) hallucinatory experiences (items 7-9 and 12). More recently, Serper et al.

(2005) administered the LSHS-R to 363 undergraduate students and, using principal

axial factor analysis, reported two factors: (1) a ‘subclinical’ factor (items 1-7; similar to

the Waters et al. ‘vivid mental events’ component); and (2) a ‘clinical’ factor (items 7-

12; a composite of the Waters et al. ‘perceptual hallucinatory experiences’ and

‘religious hallucinatory experiences’ components). In contrast, Aleman et al. (2001)

administered a Dutch version of the LSHS-R to 243 undergraduate students and, using

PCA, obtained three components dissimilar to those obtained in the other two studies:

(1) tendency towards hallucinatory experiences (items 1, 2, 7-10, and 12); (2) subjective

externality of thought (items 3, 4 and 11); and (3) vivid daydreams (items 5, 6 and 12).

The aim of Study 1 was to consolidate the latent structure of the LSHS-R in a

large English speaking undergraduate sample, by using confirmatory factor analysis to

compare the different factor structures reported in these three previous studies to find

the model of best fit.

Chapter 2

66

Method

Participants

Participants were 589 first year psychology students (384 females). This

imbalanced gender ratio is common in studies using an undergraduate psychology

sample (e.g., Aleman et al., 2001; P. F. Lovibond & S. H. Lovibond, 1995; Waters et

al., 2003a). Mean age was 19 years (SD = 4.12 years).

Measures

The 12 LSHS-R items are scored on a 5-point scale (from 0 = certainly does not

apply to me, to 4 = certainly applies to me) (Bentall & Slade, 1985) and describe either

clinical hallucinatory experiences (e.g., item 8 ‘In the past, I have had the experience of

hearing a person’s voice and then found that no one was there’ and item 11 ‘In the past I

have heard the voice of God speaking to me’) or sub-clinical, intrusive mental events

(e.g., item 5 ‘The sounds I hear in my daydreams are usually clear and distinct’). The

LSHS-R has good reliability and validity (Aleman, Nieuwenstein, Bocker, & de Haan,

1999; Levitan et al., 1996).

Model Definition for Confirmatory Factor Analysis

Allocation of LSHS-R items to factors for the three models was based on the

heaviest loading, to avoid overlap of factors. The one exception was for item 12 in the

Waters et al. (2003a) model, as there was only a .01 difference in loadings on the

second and third factors (the next smallest difference in cross loadings was .10).

Consequently, item 12 was assigned to both factors 2 and 3 for this model. Accordingly,

items 1-6, items 7-9 and 12, and items 10-12 formed the three factors in the Waters et

al. (2003a) model, items 1-6 and items 7-12 formed the two factors in the Serper et al.

(2005) model, and items 1, 2, 7-10 and 12, items 3, 4 and 11, and items 5 and 6 formed

the three factors in the Aleman et al. (2001) model.

Chapter 2

67

Results and Discussion

All 12 LSHS-R items in the current study attained endorsement frequencies

above 1%, consequently no items were excluded from the analysis (Morrison et al.,

2000). The mean LSHS-R total score was 15.79 (SD = 8.18), which is comparable to

data reported for other Australian university samples (Waters et al., 2003a). There was

no significant gender difference in LSHS-R total scores, t (573) = 1.10, p > .05.

To compare the fit of the three different factor structures for the LSHS-R, the

data were analysed in LISREL (version 8.52) using maximum likelihood estimation and

a scaled chi-square statistic was calculated (Satorra & Bentler, 1988). We used the fit

indices recommended by Hu and Bentler

(1998) to evaluate

the results of the

comparative factor analysis. Based on common practice in using these indices, the

following criteria for an acceptable model fit were employed: root mean square error of

approximation (RMSEA) < .05, standardized root mean residual (SRMR) < .08, and

comparative fit index (CFI) > .90.

In the first step of the analyses, the difference in the scaled chi squared statistics

revealed the Aleman et al. (2001) three-factor model to be a better fit than the Serper et

al. (2005) two-factor model (see Table 1)2. In the second step, the Waters et al. (2003a)

three-factor model was found to be a better fit than the Aleman et al. (and thus the

Serper et al.) model. Furthermore, all three fit indices for the Waters et al. (2003a)

model met the set criteria, indicating that this three-factor structure provides an

acceptable fit to the data. Accordingly, hallucination predisposition when measured

using the LSHS-R seems to be best characterized by three features: (1) the experience of

vivid mental events, such as thoughts and day dreams, that are recognized as self-

generated, (2) perceptual (auditory and visual) hallucinatory experiences, and (3)

religious hallucinatory experiences.

2 An alternative model based on Serper et al.’s (2005) theoretical model (rather than assigning

items to factors by loading size) – in which item 7 formed part of the ‘subclinical’ rather than

the ‘clinical’ factor – was also tested. A significantly better fit was obtained for Serper et al.’s

theoretical model than for the Aleman et al. (2001) three-factor solution, although the best fit

remained with the Waters et al. (2003) three-factor model.

Chapter 2

68

Table 1

Goodness-of-Fit Indices for Three Models for the LSHS-R (N = 589)

Serper et al. (2005)

2 factor structure

Aleman et al. (2001)

3 factor structure

Waters et al. (2003)

3 factor structure

S-B χ2 267.45* 261.46* 108.31*

df 53 51 50

χ2

diff - 5.98 153.15*

∆ df - 2 1

RMSEA .08 .08 .04

SRMR .11 .14 .06

CFI .85 .79 .93

Note. S-B χ2

= Satorra-Bentler Scaled Chi-square; df = degrees of freedom; RMSEA =

root mean square error of approximation; SEMR = standardized root mean square

residual; CFI = comparative fit index.

* p < .05.

STUDY 2

As documented in hallucinating patients with schizophrenia (e.g., Delespaul et

al., 2002), high levels of affective disturbance have been reported in healthy individuals

predisposed to hallucinations (e.g., Allen et al., 2005; van't Wout et al., 2004; Young et

al., 1986). While Allen et al. (2005) reported a significant positive correlation between

LSHS-R total scores and measures of anxiety, depression, and stress, Morrison and

colleagues (2000, 2002) reported somewhat different patterns of findings. In the first of

Morrison et al.’s studies (2000), visual, but not auditory, hallucinatory-type experiences

significantly correlated with measures of anxiety and depression when using a 16-item

extension of the LSHS, while in the second study (2002), the reverse was found when

using a 24-item extension of the LSHS. However, on closer inspection, the items

forming the auditory subscales in the two studies were quite different, with most

auditory items in the first study describing ‘subclinical’ experiences, and most auditory

items in the second study describing more ‘clinical’ hallucinatory experiences. These

results raise the possibility that negative affect is related to some, but not all, of the

subcomponents – and underlying mechanisms – of hallucination predisposition.

In addition, whilst previous studies have employed measures of depression,

anxiety and/or stress as model constructs of negative affect, it seems possible that

Chapter 2

69

anxiety may play a particularly important role in hallucination predisposition. Allen et

al. (2005) found that whilst all three affect measures were significantly correlated with

LSHS-R total scores, only anxiety made a significant unique contribution to the

prediction of LSHS-R scores when a regression analysis was performed. Unfortunately,

these authors did not examine the relative importance of anxiety, depression and stress

in terms of the separate components of hallucination predisposition. Consequently, the

current study investigated whether the three subcomponents that best characterize

hallucination predisposition, as shown in Study 1, differentially relate to separate

measures of negative affect - namely depression, anxiety and stress.

Method

Participants

Participants were 462 first year psychology students (324 women), none of

whom participated in Study 1 (slightly lower Ns indicated below reflect missing

responses). Mean age was 18.39 years (SD = 2.76 years).

Measures

The 12-item LSHS-R was administered (Bentall & Slade, 1985) together with

the 21-item state version of the Depression Anxiety Stress Scales (DASS; S. H.

Lovibond & P. F. Lovibond, 1995) to obtain state measures of depression, anxiety, and

stress (stress, as measured by the DASS, is characterised by persistent tension,

irritability, and frustration). For the DASS, participants indicate how much each

statement applied to them over the past week using a 4-point scale (0 = did not apply to

me at all, to 3 = applied to me very much, or most of the time). The items for each scale

are summated and then multiplied by two, yielding a scale score range of 0 to 42. The

DASS scales have excellent internal consistency and good discriminant validity

(Brown, Chorpita, Korotitsch, & Barlow, 1997; S. H. Lovibond & P. F. Lovibond,

1995), and the DASS Depression and Anxiety scales show good convergent validity

with other scales that discriminate between depression and anxiety (P. F. Lovibond & S.

H. Lovibond, 1995).

Chapter 2

70

Results and Discussion

Across the several measures, 38 univariate outliers (scores more than 3 SDs

from the mean) were identified and trimmed to 3 SDs from the mean. No multivariate

outliers (scores with a significant Mahalanobi’s distance, p < .001) were found. Mean

scores on the questionnaires were 14.84 (SD = 7.64, N = 461) for the LSHS-R, 8.60 (SD

= 7.81, N = 459) for DASS-Depression, 7.42 (SD = 6.33, N = 460) for DASS-Anxiety,

and 12.67 (SD = 8.35, N = 459) for DASS-Stress. There was no gender difference in

LSHS-R total scores (t(458) = 0.62, p > .05), DASS-Depression scores (t(456) = 0.20, p

> .05) or DASS-Anxiety scores (t(457) = 0.65, p > .05). There was however, a

significant gender difference on the DASS-Stress scale (t(456) = 2.81, p < .05), with

females (M = 13.37, SD = 8.39) scoring higher than males (M = 11.00, SD = 8.06).

To obtain estimated component scores for each student using the regression

approach, a PCA was performed (pre-selecting three components to be extracted) with

orthogonal rotation (Varimax with Kaiser normalization). The three components

extracted accounted for 57% of the variance and were identical to those obtained by

Waters et al. (2003a). This further confirms the outcome of the comparative factor

analysis in Study 1.

Total scores on the LSHS-R correlated significantly with the DASS-Depression

(r = .29, p < .05, N = 458), DASS-Anxiety (r = .34, p < .05, N = 459), and DASS-Stress

(r = .30, p < .05, N = 458) scores. Next we investigated whether all, or only some, of the

subcomponents characteristic of hallucination predisposition relate to depression,

anxiety and stress (see Table 2). The DASS-Anxiety scale showed modest but

consistent and significant associations with all three LSHS-R components, which

suggests that anxiety may influence a common mechanism underpinning all three

components. In contrast, both DASS Depression and Stress scores correlated

significantly with the LSHS-R vivid mental events component and the perceptual

hallucinations component, but not with the religious hallucinations component. It has

been documented that individuals who attribute religious meaning to hallucinations and

delusions (irrespective of their content) are less distressed by such experiences than

individuals who do not (Davies, Griffin, & Vice, 2001; Peters, Day, McKenna, &

Orbach, 1999). This may explain why individuals who score high on the religious

hallucinations component did not score particularly highly on the DASS Depression and

Stress scales.

Chapter 2

71

Table 2

Pearson Correlations (N = 458) and Partial Correlations (df = 450) Between DASS

Scales and LSHS-R Components

Control

Variables

Vivid mental

events

Perceptual

hallucinatory

experiences

Religious

hallucinatory

experiences

Depression .184* .217* .069

Anxiety .082 .089 -.020

Stress .073 .117* .047

Anxiety .200* .253* .144*

Depression .116* .168* .136*

Stress .096* .170* .149*

Stress .197* .210* .053

Depression .113* .098* .014

Anxiety .100* .066 -.049

* p < .05.

Intercorrelations among the DASS scales ranged from .57 to .62 (p < .05),

consequently partial correlations were obtained (see Table 2) to determine whether the

observed relationships with the LSHS-R components remained significant once the

shared variance of the affective measures was partialled out. The results indicate that the

association between depression and the LSHS-R components was largely shared with

the other affective measures, since the correlations between DASS-Depression and the

LSHS-R components generally failed to reach significance when anxiety or stress were

controlled for (with the exception of the perceptual hallucinations component when

controlling for stress). The most robust association for DASS-Stress was with the vivid

mental events component since it remained significant even when the shared variance

with anxiety or depression was partialled out. This finding is consistent with existing

studies linking stress and intrusive cognitions concerning external events (e.g.,

Horowitz, 1975). Finally, the results indicate that anxiety is most consistently related to

predisposition to hallucinate, as the correlations between DASS-Anxiety and all three

LSHS-R components remained significant when depression or stress were controlled. It

should be noted that although several of the correlations between the LSHS-R

components and the DASS subscales reached significance, the size of these effects was

not large.

Chapter 2

72

GENERAL DISCUSSION

Study 1 showed that hallucination predisposition, when measured using the

LSHS-R, is best characterized by three features: (1) vivid mental events recognized as

self-generated (i.e. day dreams or thoughts), (2) auditory and visual hallucinatory

experiences where the source is externally attributed, and (3) hallucinatory experiences

with a religious theme (again where the source is externally attributed). This model,

previously described by Waters et al. (2003a), demonstrated a significantly better fit to

the data than either Serper et al.’s (2005) two-factor model or Aleman et al.’s (2001)

three-factor model, and was clearly reproduced in the second study, using a new data

set. The multifactorial nature of vulnerability to hallucinations suggests that more than

one mechanism may be involved in the development of hallucinations.

Confirming previous findings (Allen et al., 2005), all three measures of negative

affect based on the DASS scales correlated positively with total scores on the LSHS-R.

Notably, Allen et al. (2005) showed that anxiety was particularly important to

hallucination predisposition since of the DASS subscales, DASS-Anxiety was the only

significant predictor of LSHS-R total scores. Study 2 replicated and extended these

findings, with DASS-Anxiety consistently correlating with all three LSHS-R

components, even when variance shared with DASS Depression or Stress was partialled

out. Previous studies investigating the relationship between symptoms of schizophrenia

and affect have more consistently reported significant correlations between positive

symptoms (such as hallucinations) and anxiety rather than depression (e.g., Norman,

Malla, Cortese, & Diaz, 1998). Particularly relevant to the current study, Tien and Eaton

(1992) conducted a one year follow-up study of at-risk individuals and found that initial

assessment of anxiety, but not depression, predicted the subsequent development of

schizophrenia and the onset of hallucinations and delusions.

The current findings are based on correlations; consequently, the direction of

causality can not be assured. It is plausible, therefore, that people who have

hallucination-type experiences may develop heightened levels of anxiety as a result of

these intrusive cognitions. However, at least two reasons suggest the need to consider

the role of anxiety in the development, rather than solely as a consequence, of

hallucinatory experiences. First, participants in the current study vary only in their

predisposition to hallucinate but are not necessarily currently hallucinating, therefore,

increased anxiety in this sample is not readily explained as a consequence of active

hallucinations. Second, Delespaul and colleagues (2002) showed (in patients) that at the

Chapter 2

73

end of a hallucinatory episode, levels of anxiety tend to fall, rather than rise, whilst

immediately prior to the onset of a hallucination, anxiety increases, suggesting its

involvement in the development of the experience.

Anxiety consistently correlated with all three LSHS-R components suggesting

that it may influence an underlying mechanism common to all three components. One

characteristic that all three LSHS-R components share – and thus, anxiety may

influence – is that they relate to intrusive mental events (what differentiates these

components is the attribution of agency and explanatory themes). It may be, therefore,

that anxiety modulates or exacerbates a primary deficit of cognitive control leading to

intrusive mental events (e.g., by increasing the intensity of this process above a critical

threshold; Slade, 1976; Slade & Bentall, 1988). Previous research has shown that

intrusive cognitions are the product of impaired inhibitory control (Kramer, Humphrey,

Larish, Logan, & Strayer, 1994). Poor inhibition has been documented in anxiety

disordered samples (e.g., Badcock, Waters, & Maybery, 2007; Hopko, Ashcraft, Gute,

Ruggiero, & Lewis, 1998), potentially explaining why some anxiety disordered patients

report experiencing spontaneous intrusive images when under heightened arousal (e.g.,

Hackmann, Surawy, & Clark, 1998). Furthermore, intentional inhibition deficits have

also been documented in hallucinating patients with schizophrenia (Waters, Badcock,

Maybery, & Michie, 2003b). Consequently, one possibility may be that in the onset of

hallucinatory-type experiences, anxiety may operate by directly impairing inhibition or

exacerbating an existing inhibition deficit, a conjecture that warrants further research.

The current study is not without its limitations. Firstly, the findings are based on

an undergraduate psychology student sample, and thus may not be representative of the

healthy population at large. Also, there was a greater number of females than males in

the current study, however similar gender ratios were reported for two of the three

previous LSHS-R factor analytic studies (Aleman et al., 2001; Waters et al., 2003a),

ruling out gender differences as the cause of the different factor structures. Furthermore,

no gender differences were found for mean LSHS-R scores in either study. As a non-

clinical sample was used, it is possible that LSHS-R and DASS scores may have been

attenuated, possibly contributing to the small effect sizes reported in Study 2. Future

studies may wish to replicate this study using a clinical mood-disordered sample to

provide a cleaner examination of the emotion-hallucination predisposition link.

The finding that depression, anxiety and stress correlate with predisposition to

hallucinations has important practical and theoretical implications. Firstly, attaining a

comprehensive cognitive-affective profile of hallucination-prone individuals may help

Chapter 2

74

to guide early interventions for psychosis. It may be important to treat negative affective

states, especially anxiety, in addition to psychotic symptoms in the earliest phases of

psychosis. Secondly, these findings may limit the interpretations of studies employing

the LSHS-R to compare high and low-risk groups on cognitive tasks, since differential

group performance may reflect differences in affective profile, rather than the

vulnerability to hallucinate. In order to avoid this limitation, future studies should

control for differences in negative affect.

Chapter 2

75

ACKNOWLEDGEMENTS

This work was supported by the Neuroscience Institute of Schizophrenia and

Allied Disorders (NISAD), utilising funding from the Ron and Peggy Bell Foundation.

Many thanks to Milan Dragovic for his help with the factor analysis, and Mike Stevens

for his help in the scoring of the DASS data.

Chapter 2

76

REFERENCES

Aleman, A., Nieuwenstein, M. R., Bocker, K. B., & de Haan, E. H. (1999). Temporal

stability of the Launay-Slade Hallucination Scale for high- and low-scoring

normal subjects. Psychological Reports, 85, 1101-1104.

Aleman, A., Nieuwenstein, M. R., Boecker, K. B. E., & De Haan, E. H. F. (2001).

Multi-dimensionality of hallucinatory predisposition: Factor structure of the

Launay-Slade Hallucination Scale in a normal sample. Personality and











527-529.

Brown, T. A., Chorpita, B. F., Korotitsch, W., & Barlow, D. H. (1997). Psychometric

properties of the Depression Anxiety Stress Scales (DASS) in clinical samples.





Davies, M. F., Griffin, M., & Vice, S. (2001). Affective reactions to auditory

hallucinations in psychotic, evangelical and control groups. British Journal of







Therapy, 41, 923-947.

Chapter 2

77




Horowitz, M. J. (1975). Intrusive and repetitive thoughts after experimental stress. A

summary. Archives of General Psychiatry, 32, 1457-1463.

Hu, L., & Bentler, P. M. (1998). Fit indices in covariance structure modeling:

Sensitivity to underparameterized model misspecification. Psychological

Methods, 3, 424 – 451.






Levitan, C., Ward, P. B., Catts, S. V., & Hemsley, D. R. (1996). Predisposition toward

auditory hallucinations: The utility of the Launay-Slade Hallucination Scale in

psychiatric patients. Personality and Individual Differences, 21, 287-289.

Lewandowski, K. E., Barrantes-Vidal, N., Nelson-Gray, R. O., Clancy, C., Kepley, H.

O., & Kwapil, T. R. (2006). Anxiety and depression symptoms in

psychometrically identified schizotypy. Schizophrenia Research, 83, 225-235.

Lovibond, P. F., & Lovibond, S. H. (1995). The structure of negative emotional states:

Comparison of the Depression Anxiety Stress Scales (DASS) with the Beck

Depression and Anxiety Inventories. Behaviour Research and Therapy, 33, 335-

343.

Lovibond, S. H., & Lovibond, P. F. (1995). Manual for the Depression Anxiety Stress

Scales (2nd ed.). Sydney, Australia: Psychology Foundation of Australia.

Morrison, A. P., Wells, A., & Nothard, S. (2000). Cognitive factors in predisposition to

auditory and visual hallucinations. British Journal of Clinical Psychology, 39,

67-78.

Morrison, A. P., Wells, A., & Nothard, S. (2002). Cognitive and emotional predictors of

predisposition to hallucinations in non-patients. British Journal of Clinical




Peters, E., Day, S., McKenna, J., & Orbach, G. (1999). Delusional ideation in religious

and psychotic populations. British Journal of Clinical Psychology, 38, 83-96.

Chapter 2

78

Satorra, A., & Bentler, P. M. (1988). Scaling corrections for chi-square statistics in

covariance structure analysis. American Statistical Association, proceedings of

the Business and Economic Sections, Alexandria VA, American Statistical

Association.



psychotic and normal Individuals. Journal of Nervous and Mental Disease, 193,

265-272.

Slade, P. D. (1976). Towards a theory of auditory hallucinations: Outline of an

hypothetical four-factor model. British Journal of Social and Clinical









van't Wout, M., Aleman, A., Kessels, R. P. C., Laroi, F., & Kahn, R. S. (2004).

Emotional processing in a non-clinical psychosis-prone sample. Schizophrenia

Research, 68, 271-281.

Waters, F. A. V., Badcock, J. C., & Maybery, M. T. (2003a). Revision of the factor

structure of the Launay-Slade Hallucination Scale (LSHS-R). Personality and


Waters, F. A. V., Badcock, J. C., Maybery, M. T., & Michie, P. T. (2003b). Inhibition in


Research, 62, 275-280.

Young, H. F., Bentall, R. P., Slade, P. D., & Dewey, M. E. (1986). Disposition towards

hallucination, gender and EPQ scores: A brief report. Personality and Individual

Differences, 7, 247-249.

79

PREDISPOSITION TO HALLUCINATIONS AND

INHIBITORY CONTROL

80

Foreword to Chapters 3 and 4

81

FOREWORD TO CHAPTERS 3 AND 4

The previous chapter confirmed the multidimensional nature of hallucination

predisposition in a non-psychiatric population, and that anxiety, more so than

depression or stress, was consistently related to all three of the identified dimensions.

We speculated that the feature common to all three of the found components of

hallucination predisposition is intrusiveness. The research literature has linked everyday

intrusive cognitions to impaired inhibition (Friedman & Miyake, 2004; Kramer,

Humphrey, Larish, Logan, & Strayer, 1994), and consistent with this, impaired

intentional inhibition has been linked to auditory hallucinations (AHs) in schizophrenia

(Badcock, Waters, Maybery, & Michie, 2005; Waters, Badcock, Maybery, & Michie,

2003). Thus, leading on from the previous chapter‟s findings, the next two chapters

investigate the proposal that similar impairments in intentional inhibition found in

schizophrenia will be present in healthy hallucination predisposed individuals,

consistent with a continuum approach to AHs. Although anxiety will be measured and

controlled for in the following two chapters (to test the specificity of the findings to

hallucination predisposition), a more detailed investigation of the relationships between

anxiety and both hallucinatory-type experiences and inhibitory control in hallucination

predisposition and schizophrenia will be left until Chapters 5 and 6, respectively.

Chapter 3 investigates whether similar intentional inhibition difficulties are

found in hallucination predisposition as found in hallucinating individuals with

schizophrenia (Badcock et al., 2005; Waters et al., 2003). This was achieved by

administering a modified version of one of the intentional inhibition tasks used in

Badcock and colleagues‟ schizophrenia studies.

Chapter 4 aimed to clarify the critical component(s) of inhibitory control

specifically related to hallucination predisposition, through the administration of

cognitive tasks thought to measure different forms of cognitive control to high and low

hallucination predisposed participants. This study was important since Badcock and

colleagues‟ (Waters, Badcock, Michie, & Maybery, 2006) dual-deficit model of AHs

specifies that the cognitive control difficulties specifically linked to AHs are both

intentional (as opposed to unintentional) and inhibitory (as opposed to resistance to

interference) in nature: however, the specificity of this supposition has not yet been

examined in hallucination predisposition or schizophrenia.

Foreword to Chapters 3 and 4

82

REFERENCES












Research, 62, 275-280.




Chapter 3

83

Chapter 3

Poor intentional inhibition in individuals predisposed to

hallucinations 1

ABSTRACT

Introduction: Intentional inhibition deficits have been found in hallucinating

individuals with schizophrenia using the Inhibition of Currently Irrelevant Memories

(ICIM) task. This study sought to investigate whether similar difficulties are found in

healthy individuals predisposed to hallucinations. Methods: The Launay-Slade

Hallucination Scale-Revised (LSHS-R) was completed by 589 undergraduate students,

from which high- and low-predisposed groups were drawn. On the ICIM task,

participants were asked to identify within-run picture repetitions, requiring them to

inhibit memory traces of the same items seen in previous runs. Results: Compared to the

low LSHS-R group, the high LSHS-R group showed significantly increased false

alarms on critical “inhibitory” runs (incorrectly identifying previous-run items as

within-run repetitions), but no group differences were found in first-run false alarms or

in the identification of within-run targets. These results were specific to hallucination

predisposition and could not be explained by other schizophrenia-related characteristics.

Conclusions: Individuals predisposed to hallucinations show subtle, though consistent

difficulties with intentional inhibition similar to patients with hallucinations. These

findings demonstrate a continuity of cognitive processes in individuals predisposed to

hallucinations and in patients with schizophrenia who hallucinate, consistent with a

common neurodevelopmental pathway.

Keywords: Hallucination predisposition; Hallucinations; Schizophrenia; Intentional

inhibition


(2007). Failure to inhibit currently irrelevant memories in individuals predisposed to

hallucinations. Cognitive Neuropsychiatry, 12 (5), 457-470.

Chapter 3

84

Hallucinations in schizophrenia have been linked to impaired intentional

inhibition both in theory and empirically (e.g. Badcock, Waters, Maybery, & Michie,

2005; Frith, 1979; Waters, Badcock, Maybery, & Michie, 2003; Waters, Badcock,

Michie, & Maybery, 2006). For example, in a recent study conducted by Waters and

colleagues (2003), the frequency of auditory hallucinations, but not other symptoms,

was found to be inversely related to the ability to intentionally suppress irrelevant

memories, assessed using the Inhibition of Currently Irrelevant Memories task (ICIM;

Schnider & Ptak, 1999), suggesting that hallucinations occur when strongly activated

memories intrude into consciousness and become confused with ongoing reality. The

ICIM task is a repeated, continuous recognition task, in which participants are asked to

identify picture repetitions within the current run. Waters et al. (2003) presented four

runs, with the same set of pictures used in each, but with the repeated „target‟ items

varying across runs. Consequently, after the first run participants must intentionally

suppress the memory traces of pictures shown in previous runs (and are explicitly

instructed to “forget that you have already seen the pictures”) to avoid making false

alarms (FAs). Therefore, the number of FAs on the second and subsequent runs

measures one‟s ability to inhibit memories that are no longer relevant. In contrast,

performance on the first run does not require inhibition; rather it depends on the ability

to encode new pictures for recognition (Schnider, Valenza, Morand, & Michel, 2002).

Badcock, Waters, and Maybery (2007) also noted that current hallucinators, relative to

non-hallucinators, made significantly more FAs on distractors that had been targets on

previous runs, suggesting that the presence of auditory hallucinations in patients may

involve a failure to suppress previously relevant memories.

Many researchers have proposed that the symptoms of schizophrenia, such as

hallucinatory experiences, occur on a continuum including schizophrenia patients and

normal individuals with schizotypic traits (Meehl, 1989; Slade & Bentall, 1988). The

Launay-Slade Hallucination Scale – Revised (LSHS-R; Bentall & Slade, 1985; Launay

& Slade, 1981) is commonly used to examine the hallucinatory-type experiences of

individuals in the normal population. Healthy individuals predisposed to hallucinations

may never develop full-blown schizophrenia, however hallucination predisposition may

share a common neuro-developmental pathway with schizophrenia and thus,

predisposed individuals may exhibit similar (though milder) clinical, cognitive,

emotional and biological characteristics as individuals with schizophrenia. Indeed,

studies using the LSHS-R have shown that the features characterising hallucination

predisposition parallel those described in patient populations (e.g. Allen, Freeman,

Chapter 3

85

Johns, & McGuire, 2006; Laroi, Van der Linden, & Marczewski, 2004; Paulik,

Badcock, & Maybery, 2006; Serper, Dill, Chang, Kot, & Elliot, 2005). One of the main

advantages of studying a non-clinical predisposed sample is that it avoids confounding

variables such as medication status, effects of institutionalisation, and other symptoms

and general cognitive deficits associated with the clinical disorder.

The aim of the current study was to investigate whether healthy individuals

predisposed to hallucinations have difficulties with intentional inhibition, consistent

with such difficulties reported for individuals with schizophrenia (Waters et al., 2003).

We used a more difficult version of the ICIM task suitable to assess intentional

inhibition in healthy individuals (as recommended by Schnider et al., 2002) and

predicted that individuals with high LSHS-R scores would produce more FAs on critical

inhibitory runs than would individuals with low LSHS-R scores. Response times were

also examined as a potentially sensitive measure of the relative difficulty involved in

correctly rejecting distractors (CR) and identifying targets (Hits). In addition, we were

interested in whether individuals with high LSHS-R scores also show specific

difficulties suppressing responses to previously relevant (but currently irrelevant) items,

as reported in individuals with schizophrenia (Badcock et al., 2005). We expected that

there would be no group differences in encoding/learning or target recognition, as

assessed by FAs on run 1 or Hits overall.

Finally, the specificity of any inhibition difficulties was assessed by including

measures of other schizotypal characteristics (namely, delusional thinking and

anhedonia) and anxiety. Although high levels of anxiety and depression are common in

individuals with high LSHS-R scores (e.g. Allen et al., 2005; Paulik et al., 2006),

anxiety was of particular interest in the current study as it has been shown to correlate

with all components of the LSHS-R, independent of depression (Paulik et al., 2006),

and has been linked to both intrusive cognitions (Kramer, Humphrey, Larish, Logan, &

Strayer, 1994) and deficits of intentional inhibition (Badcock et al., 2005; Hopko,

Ashcraft, Gute, Ruggiero, & Lewis, 1998).

METHOD

Participants

Five hundred and eighty nine undergraduate psychology students completed the

LSHS-R (Bentall & Slade, 1985). To obtain high and low LSHS-R groups, a random

Chapter 3

86

sample of students who scored in the upper 10% (scores above 26) and lower 10%

(scores below 6), were invited to take part in the study. Twenty-eight high scorers and

25 low scorers responded to this invitation and completed the study. The exclusion

criteria included a personal history of psychosis, poor English, poor visual acuity, head

injury or neurological disorder resulting in marked cognitive dysfunction, or an IQ

below 85. Accordingly, two participants from the high LSHS-R group were excluded

from analysis. The remaining 51 participants comprised 18 females and seven males in

the low LSHS-R group and 17 females and nine males in the high LSHS-R group (see

Table 1 for ages).

Measures

Inhibition of Currently Irrelevant Memories (ICIM) Task

The ICIM task is a continuous recognition task, originally developed by

Schnider and Ptak (1999) for use with a clinical population. The current study used a

version of the task that was adapted by Schnider et al. (2002) for use with a healthy

adult population. The creators of this latter version made it more difficult than the

original version used by Waters et al. (2003), by increasing the number of presentations

from 52 to 85, reducing the maximum number of presentations of target pictures from

seven to three, and increasing the total number of targets from four to 36. The task was

administered on a computer with a touch screen monitor. Our version consisted of three

runs, each involving the sequential presentation of 85 black and white line drawings

(Snodgrass & Vanderwart, 1980). Twenty-eight pictures occurred only once in a run,

whilst six occurred twice, and 15 occurred three times, yielding 49 first presentations in

a run (distractors), 21 second presentations, and 15 third presentations (36 targets in

total). Each picture was presented in the centre of the screen for 2000 ms, with a 700 ms

interstimulus interval. There was a 30 s break between the first and second runs and a

five minute break between the second and third runs. In each run, participants were

asked to indicate as rapidly as possible (by pressing keys marked „yes‟ or „no‟), whether

each picture had been presented previously within the current run. The second and third

runs used the same picture set as the first run; only the presentation order and the

pictures selected to be targets changed. In these runs, participants were explicitly

instructed to “forget that you have already seen the pictures”. The first run required the

learning and recognition of new items, while on the second and third runs participants

Chapter 3

87

were explicitly asked to forget – thus, requiring them to intentionally inhibit – what they

had seen in previous runs. The dependent variables were the number of FAs and Hits,

and the response times for correct responses to targets (Hits) and distractors (correct

rejections, CR) for each of the three runs.

Additional Measures

The LSHS-R (Bentall & Slade, 1985) was used to identify individuals

predisposed to hallucinations. The 12 LSHS-R items are rated on a 5-point scale (0 =

certainly does not apply to me, 4 = certainly does apply to me), yielding a total score of

0 to 48. IQ was estimated from the Wechsler Abbreviated Scale of Intelligence (WASI)

vocabulary and matrix reasoning subtests (Wechsler, 1999). The anxiety subscale of the

short form of the Depression Anxiety Stress Scales (DASS; Lovibond & Lovibond,

1995) assessed state anxiety (score range 0-42). The Peters Delusions Inventory (PDI;

Peters, Joseph, & Garety, 1999) measured delusional thinking (score range 0-402), while

the introvertive anhedonia subscale of the Oxford-Liverpool Inventory of Feelings and

Experiences (O-LIFE; Mason, Claridge, & Jackson, 1995) assessed schizotypal

personality features that closely correspond to negative schizophrenic symptomotology

(score range 0-27).

Procedure

Ethical approval was obtained from the University of Western Australia Human

Research Ethics Committee and written informed consent was obtained from each

participant prior to testing. Participants were tested individually and offered course

credit points or $20 reimbursement for time/expenses.

2 The PDI was administered in the standard way, in which additional ratings are made for items

responded to affirmatively. Data from these additional ratings are not reported.

Chapter 3

88

RESULTS

Descriptive Statistics

Across the 816 data points, 10 single data points (one from the OLIFE, six from

the ICIM FA data set, and three from the ICIM Hit data set) were identified to be

univariate outliers (more than 3 SDs from their respective LSHS-R group mean) and

were removed. No multivariate outliers (Cook‟s distance) were detected.

LSHS-R group means and standard deviations for the additional measures are

summarized in Table 1. Substantial group separation was obtained on the LSHS-R.

There was also a significant group difference on WASI IQ scores favouring the high

LSHS-R group; consequently IQ scores were entered into subsequent analyses as a

covariate. The high LSHS-R group also obtained significantly higher scores on the PDI

and the DASS-Anxiety subscale, but there was no significant group difference on the O-

LIFE introvertive anhedonia subscale. Thus, where significant effects were found, PDI

and DASS-Anxiety scores were used as additional covariates to test the specificity of

the results.

Table 1.

LSHS-R Group Means, SDs, and T-tests for the Additional Measures

* p < .05

ICIM Task

Figure 1 shows the mean number of FAs and Hits for the two groups. Consistent

with Waters et al. (2003) patient study, performance on run 1 was analysed separately

Low LSHS-R Group

(n = 25)

High LSHS-R Group

(n = 26)

Mean SD Mean SD t

Age 19.08 2.63 19.65 3.55 0.65p

LSHS-R 2.80 1.71 31.69 2.74 44.99*

WASI 112.32 8.71 119.15 7.34 3.04*

PDI 4.72 3.45 16.04 6.56 7.67*

DASS-Anxiety 4.32 4.61 10.77 6.88 3.92*

O-LIFE introvertive

anhedonia

3.32 2.93 5.44 4.65 1.93p

Chapter 3

89

from performance on runs 2 and 3 throughout, since the task requirements on the first

run are different from those on subsequent runs (namely, only runs 2 and 3 involve the

inhibition of previously relevant items)

0

0.5

1

1.5

2

2.5

3

3.5

4

4.5

1 2 3

Run

FA

s

g

Low LSHS-R High LSHS-R(a)

24

26

28

30

32

34

36

1 2 3Run

Hits

g

Low LSHS-R High LSHS-R

(b)

Figure 1. Mean number of false alarms (FAs) (a), and Hits (b) in runs 1-3 for the high

and low LSHS-R groups on the ICIM task (error bars represent one SE of the mean).

Encoding and Recognition in Run 1

The two groups did not differ significantly when univariate ANCOVAs were

conducted on the run 1 data for Hits, F(1,49) = 1.67, MSE = 2.12, p > .05, and FAs,

F(1,48) = 2.83, MSE = 0.82, p > .05, suggesting no initial differences in the processing

of targets and distractors.

Target Detection in Runs 2 and 3

Interestingly, when examining the Hits data from runs 2 and 3 using a 2 (LSHS-

R Group: high, low) x 2 (Run: 2, 3) ANCOVA, a main effect of Group was found,

F(1,45) = 7.70, MSE = 17.89, p < .05, with the high LSHS-R group making more Hits

than the low LSHS-R group (Fig. 1b). No other effects were significant. This pattern of

results remained the same with the inclusion of PDI or DASS-Anxiety scores as

covariates.

Chapter 3

90

Intentional Inhibition in Runs 2 and 3

In contrast to run 1, when the number of FAs made on runs 2 and 3 were

examined in a 2 (LSHS-R Group: high, low) x 2 (Previous-run status: target, distractor)

ANCOVA, there was a significant Group main effect, F(1,43) = 7.51, MSE = 8.69, p <

.05, with the high LSHS-R group making more FAs than the low LSHS-R group (Fig.

1a). No effects involving Previous-run status were significant. This pattern of results

remained the same when either PDI or DASS-Anxiety scores were included as

additional covariates.

Signal Detection Analysis

No significant group differences in detection sensitivity (measured using d′) or

response criterion (measured using beta; β) were found when separate univariate

ANCOVAs were performed on run 1. Similarly, a 2 (LSHS-R Group: high, low) x 2

(Run: 2, 3) ANCOVA with d′ as the dependent measure revealed no significant main or

interaction effects. Consistent with the reported group differences for Hit and FA rates

on the inhibitory runs, a 2 (LSHS-R Group: high, low) x 2 (Run: 2, 3) ANCOVA

conducted on the β values showed a significant Group main effect only (F(1,43) = 8.03,

MSE = 15.73, p < .05), with the high LSHS-R group (M = 0.02, SD = 1.10) obtaining a

smaller β (greater inclination to respond „yes‟) than the low LSHS-R group (M = 0.81,

SD = 0.86). This pattern of findings remained unchanged when PDI and DASS-Anxiety

scores were entered into the analyses as additional covariates.

Response Times for Run 1

Response times (RT) were examined using median times for correct responses

(Hits and CR)3. A 2 (LSHS-R Group: high, low) x 2 (Response: CR, Hit) ANCOVA on

run-1 data showed a significant Response main effect, F(1,46) = 7.64, MSE = 1916.23,

p < .05, and a significant Response x Group interaction, F(1,46) = 8.23, MSE =1916.23,

p < .05 (see Fig. 2 for means). Simple effect analyses showed that the high LSHS-R

group took significantly longer to make a CR than the low LSHS-R group, F(2,48) =

6.47, MSE = 8444.61, p < .05, whilst there was no significant group difference on Hit

3 Two participants‟ RT data were excluded due to errors in the RT recording program.

Chapter 3

91

RTs. However, when PDI or DASS-Anxiety scores were added separately into the

analysis as additional covariates, the Response x Group interaction was no longer

significant.

660

680

700

720

740

760

780

800

820

1 2 3Run

Res

po

nse

Tim

e (m

s)

p

CR Hit

(a) Low LSHS-R group

660

680

700

720

740

760

780

800

820

1 2 3Run

Res

po

nse

Tim

e (m

s)

)

pCR Hit

(b) High LSHS-R group

Figure 2. Mean RT for the low LSHS-R group (a) and high LSHS-R group (b) for Hits

and correct rejections (CR) in runs 1-3 of the ICIM task (error bars represent one SE of

the mean).

Response Times for Runs 2 and 3

Similar analyses of RTs on runs 2 and 3 again revealed a significant main effect

for Response, F(1,46) = 5.98, MSE = 3482.34, p < .05, and a significant Group x

Response interaction, F(1,46) = 11.55, MSE = 3482.34, p < .05, with simple effect

analyses showing elevated RTs for the high LSHS-R group relative to the low LSHS-R

on CRs, F(2,48) = 6.95, MSE = 7581.49, p < .05, but not on Hits (see Fig. 2). Unlike the

effects for run 1, these effects remained significant even when PDI and DASS-Anxiety

scores were entered separately into the analysis as additional covariates. As displayed in

Fig. 2, the high LSHS-R group were significantly slower at making CRs than Hits on

runs 2 and 3, F(1,23) = 7.44, MSE = 2955.33, p < .05 (this effect was not significant on

run 1), while the trend (though not significant) for the low LSHS-R group was in the

opposite direction, consistent with that previously reported in the literature of normal

student control groups (Schnider et al., 2002).

Chapter 3

92

DISCUSSION

The hypothesis tested in the current study was that if individuals predisposed to

hallucinations have difficulties intentionally inhibiting strongly activated memory

traces, then the high LSHS-R group would produce more FAs on critical inhibitory runs

(namely, runs 2 and 3) than the low LSHS-R group on the ICIM task. The data obtained

supported this prediction. This group difference could not be explained by (i) poor task

comprehension, (ii) difficulties encoding or identifying repeated pictures, or (iii) an

overall response bias to say „yes‟, since there were no significant group differences in

d′, β, FA or Hit rates on run 1. Furthermore, these findings could not be explained by

group differences in intellectual ability, levels of state anxiety, or other symptom-like

features of schizophrenia (specifically, delusions or anhedonia). Thus, similar to

hallucinating individuals with schizophrenia (Waters et al., 2003), individuals

predisposed to hallucinations show subtle, but consistent difficulties with the voluntary

inhibition of currently irrelevant memories. The current findings may indicate that the

capacity to suppress irrelevant memories varies in a continuous fashion in the healthy

population (i.e. is trait like).

While the present study replicated the link between intentional inhibition

difficulties and hallucinatory experiences, Badcock et al. (2005) reported that

hallucinating patients made significantly more FAs on inhibition runs than non-

hallucinating patients when the distractors had been targets on previous runs, suggesting

that intentional inhibition deficits in hallucinating patients may involve a failure to

suppress previously relevant cognitions. However, the current study found no evidence

that healthy hallucination-predisposed individuals were especially prone to FAs on

previous-run targets. One explanation of this discrepancy in FA patterns may be that

different processes produce intrusions in patients and healthy individuals who

hallucinate. However, the current study used a more difficult version of the ICIM task

to that used in the Waters et al. (2003) patient study, which may also explain this

discrepancy. Namely, in the current study, there were a greater number of targets and

targets were repeated less often. Consequently, all stimuli in the current ICIM task may

have been perceived by participants as „relevant‟, since it was difficult to predict which

items would become targets. It is recommended that future research compare patients

and predisposed individuals on identical versions of the ICIM task to better characterize

similarities and differences in inhibition abilities between these two populations. It

Chapter 3

93

should be noted however, that both experimental and neuroimaging research suggests

that the ICIM version used in the current study involves the same fundamental cognitive

processes as the original version (Schnider & Ptak, 1999; Schnider et al., 2002; Treyer,

Buck, & Schnider, 2003).

Unexpectedly, the high LSHS-R group made significantly more Hits on the

critical inhibitory runs. Together with the increase in FA rates on these runs, this

indicates a change in response bias, which was confirmed in the signal detection

analysis. Importantly, however, the current data also provides novel insight into the

processes driving this change. Examination of response times clearly showed the

relative activation (or salience) of targets was greater in the high LSHS-R group, even

in the first run. Thus at the start of run 2, but not before, individuals in the high LSHS-

group face greater ambiguity in distinguishing highly activated, but currently irrelevant

pictures, from repeated targets in the current run, resulting in an increase in FA and Hit

rates. This view is consistent with Kapur‟s (2003) conjecture that individuals who

hallucinate (or are predisposed to hallucinate) have aberrantly salient memory traces.

Indeed, consistent with this conjecture, the high LSHS-R group were also (i)

significantly slower to make a CR than a Hit on the critical inhibition runs, but not on

run 1, and (ii) significantly slower to make CRs (but not Hits) than the low LSHS-R

group on the inhibitory runs. Furthermore, these results could not be accounted for by

other factors such as intelligence, anxiety, anhedonia or delusional thinking. However,

the high LSHS-R group were also slower to reject distractors than the low LSHS-R

group on run 1, though unlike on the inhibition runs, this effect appeared to be related to

other factors such as heightened anxiety and delusional thinking, both of which

commonly co-occur in individuals at increased risk for schizophrenia and in the

schizophrenia prodrome (Morrison, Wells, & Nothard, 2002; Paulik et al., 2006;

Svirskis et al., 2005). These results point to a mechanism underpinning the conclusion

that “a cognitive style characterized by a tendency to worry increases the risk for newly

developed psychotic symptoms” (Krabbendam & van Os, 2005, p.185), since

difficulties rejecting distracting anxious thoughts may provide the source for intrusions

which hallucination-predisposed individuals have specific difficultly later suppressing.

An alternative explanation of the current study‟s findings may be that the high

LSHS-R group made more FAs on the inhibitory runs because of difficulties monitoring

– or accessing memories of – the temporal context of the stimuli. Although the authors

recognise that this task does require some degree of temporal monitoring,

electrophysiological evidence has shown that the process of inhibiting currently

Chapter 3

94

irrelevant memories involves distinct neural regions from those involved in temporal

monitoring (e.g., Cabeza et al., 1997; Schnider et al., 2002; Treyer et al., 2003), and that

the regions involved in temporal monitoring are not activated during performance of

inhibitory runs of the ICIM task, or related to FAs on these runs (Schnider & Ptak,

1999; Schnider et al., 2002; Treyer et al., 2003). However, it would be advantageous if

future studies employ tasks that tap intentional inhibition where there is minimal

demand on temporal or contextual memory.

Hallucinatory experiences, by nature, are very similar to everyday unwanted

mental intrusions (such as intrusive thoughts, images or impulses), in that they are

intrusive, uncontrollable, unwanted and interrupt ongoing reality (Morrison, 2005;

Nayani & David, 1996). It was been proposed that both the content and an individual‟s

appraisal (interpretation) of an unwanted mental intrusion differentiates the intrusions

experienced by non-clinical individuals from those experienced by individuals with

clinical disorders, such as obsessive-compulsive disorder (OCD) (Clark & Rhyno, 2005;

Morrison, 2005). Accordingly, Morrison (2005) proposed that one of the key

differences between hallucinations and non-psychotic mental intrusions is the

attribution of source, namely, hallucinations are appraised as coming from an external

source rather than one of self-origin. Research conducted by Badcock et al. (2007)

however, suggests that one of the essential differences between hallucinations and non-

psychotic intrusions may also be the form of cognitive control underpinning the

intrusions. While empirical research has shown that both clinical and non-clinical

unwanted mental intrusions are the product of impaired cognitive inhibitory control

(Enright & Beech, 1993; Friedman & Miyake, 2004; Vasterling, Brailey, Constans, &

Sutker, 1998), Badcock et al. (2007) found that the pattern of impaired performance of

an OCD group was qualitatively different to that of a group of hallucinating individuals

with schizophrenia tested on the same measures of intentional inhibitory control. It will

thus be important for future research to investigate the specific components of the

inhibitory process (such as intentionality) that are related to hallucinatory experiences

and those that are related to other unwanted mental intrusions.

It should be noted that the findings reported in the current study are based on an

undergraduate psychology student sample, and thus may not be representative of the

healthy population (including individuals predisposed to hallucinations) at large. Since

the patterns of findings reported suggest that aberrantly salient memory traces may

contribute to the intentional inhibition difficulties found in the high LSHS-R group, it is

recommended that future studies employ tasks that measure the activation of memory

Chapter 3

95

traces independent of intentional inhibition demands. This may help further clarify the

processes involved in the development of hallucinatory-type experiences in both healthy

individuals predisposed to hallucinations and hallucinating individuals with

schizophrenia.

Chapter 3

96

ACKNOWLEDGEMENTS

This work was supported by the Schizophrenia Research Institute, utilising

funding from the Ron and Peggy Bell Foundation. We also thank Matt Huitson for his

help with task programming.

Chapter 3

97

REFERENCES

Allen, P., Freeman, D., Johns, L., & McGuire, P. (2006). Misattribution of self-

generated speech in relation to hallucinatory proneness and delusional ideation

in healthy volunteers. Schizophrenia Research, 84, 281-288.

Allen, P., Freeman, D., McGuire, P., Garety, P., Kuipers, E., Fowler, D., Bebbington,

P., Green, C., Dunn, G., & Ray, K. (2005). The prediction of hallucinatory

predisposition in non-clinical individuals: Examining the contribution of

emotion and reasoning. British Journal of Clinical Psychology, 44, 127-132.









527-529.

Cabeza, R., Mangels, J., Nyberg, L., Habib, R., Houle, S., McIntosh, A. R., et al.

(1997). Brain regions differentially involved in remembering what and when: A

PET study. Neuron, 19, 863-870.

Clark, D. A., & Rhyno, S. (2005). Unwanted intrusive thoughts in nonclinical

individuals. In D. A. Clark (Ed.), Intrusive thoughts in clinical disorders:

Theory, research, and treatment (pp. 1-29). New York: The Guilford Press.






Frith, C. D. (1979). Consciousness, information processing and schizophrenia. British





Chapter 3

98






185-189.




Laroi, F., Van der Linden, M., & Marczewski, P. (2004). The effects of emotional

salience, cognitive effort and meta-cognitive beliefs on a reality monitoring task

in hallucination-prone subjects. British Journal of Clinical Psychology, 43, 221-

233.




Scales (2nd ed.). Sydney: Psychology Foundation of Australia.

Mason, O., Claridge, G., & Jackson, M. (1995). New scales for the assessment of

schizotypy. Personality and Individual Differences, 18, 7-13.

Meehl, P. E. (1989). Schizotaxia revisited. Archives of General Psychiatry, 46, 935-944.



and treatment. New York: The Guilford Press.

Morrison, A. P., Wells, A., & Nothard, S. (2002). Cognitive and emotional predictors of

predisposition to hallucinations in non-patients. British Journal of Clinical


Nayani, T. H., & David, A. S. (1996). The neuropsychology and neurophenomenology




Paulik, G., Badcock, J. C., & Maybery, M. T. (2006). The multifactorial structure of the


stress. Personality and Individual Differences, 41, 1067-1076.

Chapter 3

99

Peters, E. R., Joseph, S. A., & Garety, P. A. (1999). Measurement of delusional ideation

in the normal population: Introducing the PDI (Peters et al. Delusions

Inventory). Schizophrenia Bulletin, 25, 553-576.









265-272.



Snodgrass, J. G., & Vanderwart, M. (1980). A standardized set of 260 pictures: Norms

for name agreement, image agreement, familiarity, and visual complexity.

Journal of Experimental Psychology: Human Learning and Memory, 6, 174-

215.

Svirskis, T., Korkeila, J., Heinimaa, M., Huttunen, J., Ilonen, T., Ristkari, T.,

McGlashan, T., & Salokangas, R. K. (2005). Axis-I disorders and vulnerability

to psychosis. Schizophrenia Research, 75, 439-446.



610-618.

Vasterling, J., Brailey, K., Constans, J., & Sutker, P. (1998). Attention and memory

dysfunction in post-traumatic stress disorder. Neuropsychology, 1, 125-133.



Research, 62, 275-280.




Wechsler, D. (1999). Wechsler Abbreviated Scale of Intelligence. San Antonio, USA:

Psychological Corporation.

100

Chapter 4

101

Chapter 4

Dissociating the components of inhibitory control involved in

predisposition to hallucinations 1

ABSTRACT

Introduction: We have previously linked hallucinations in schizophrenia and

hallucination predisposition to poor intentional inhibition. However, these previous

studies have not systematically investigated the separable dimensions of inhibitory

control involved, namely, intentional versus unintentional, and inhibition versus

resistance to interference. The aim of this study was to clarify the critical component(s)

of inhibitory control specifically related to hallucination predisposition. Methods: The

Launay-Slade Hallucination Scale-Revised (LSHS-R) was completed by 589

undergraduate students, from which high- (n = 28) and low- (n = 25) hallucination

predisposition groups were drawn. Participants were administered tasks measuring

unintentional inhibition (Brown-Peterson variant task) and intentional resistance to

interference (directed ignoring [DI] task). Results: The high LSHS-R group showed

significant difficulties relative to the low LSHS-R group on the DI task only; although

these differences did not remain significant when controlling for anxiety or delusional

thinking. Regression analyses showed that anxiety, but not delusional thinking,

independently contributed to variance in DI task performance above that accounted for

by hallucination predisposition. Conclusions: Intentional rather than unintentional

control of intrusive cognitions appears to play an important role in hallucination

predisposition. The results indicate that difficulties with the intentional resistance to

interference from concurrent external distractors may be a common mechanism

underlying positive schizophrenia symptoms and anxiety. However, given previous

findings reported by Paulik, Badcock and Maybery (2007) we propose that hallucination

predisposition is also characterized by a difficulty with the active suppression of

intrusive cognitions – that is, intentional inhibition – which is not shared with anxiety or

delusional symptoms.


(2008). Dissociating the components of inhibitory control involved in predisposition to

hallucinations. Cognitive Neuropsychiatry, 13, 33-46.

Chapter 4

102

Keywords: Hallucination predisposition; Hallucinations; Schizophrenia; Inhibition;

Resistance to interference; Cognitive intrusions

Hallucinatory experiences have traditionally been linked to psychotic disorders,

such as schizophrenia. However, it is now clear that hallucinatory experiences are

relatively common in the general population, including among children and adolescents

(e.g., Johns, Nazroo, Bebbington, & Kuipers, 1998; McGee, Williams, & Poulton, 2000;

Tien, 1991). Furthermore, compared to other psychotic-like symptoms occurring in the

general community, hearing voices and nonverbal hallucinations are differentially

associated with a need for care (Bak et al., 2005). Given the frequency and significance

of hallucinatory experiences in the normal population it is increasingly important to

understand the cognitive mechanisms underpinning the predisposition to hallucinate.

Unwanted mental intrusions – defined as ‘thoughts, images or impulses that are

experienced as unwanted and uncontrollable and interrupt ongoing reality’ (Morrison,

2005, p. 175) – characterise several different clinical populations, such as obsessive-

compulsive disorder (OCD), generalised anxiety disorder (GAD), and posttraumatic-

stress disorder (PTSD), though are also frequently experienced by individuals in the

general population (Purdon & Clark, 1993; see Clark & Rhyno, 2005, for a review).

Conventional definitions of unwanted mental intrusions stipulate that the experience is

attributed to the self, an internal source (Clark & Rhyno, 2005). However, several

authors have proposed that hallucinations are a form of intrusive cognition, as they are

unwanted, uncontrollable, and interrupt ongoing reality (Morrison, 2001; Nayani &

David, 1996). Adopting a meta-cognitive approach, Morrison (2005) proposed that a

key difference between hallucinations and non-psychotic unwanted mental intrusions is

the attribution (or appraisal) of source: hallucinations are appraised as coming from an

external source.

Whilst source attribution is clearly an important factor distinguishing between

everyday (non-psychotic) intrusions and hallucinations, this postulation may downplay

important differences in dysfunctional mechanisms of cognitive control underlying

different forms of intrusions. Empirical findings suggest that everyday intrusive

cognitions are a product of poor inhibitory control (e.g., Friedman & Miyake, 2004;

Kramer, Humphrey, Larish, Logan, & Strayer, 1994), and that inhibition deficits occur

in clinical populations characterised by intrusive cognitions, such as OCD (e.g.,

Badcock, Waters, & Maybery, 2007; Enright & Beech, 1993) and PTSD (e.g.,

Vasterling, Brailey, Constans, & Sutker, 1998). Although impaired intentional

inhibition has also been empirically linked to the frequency of auditory hallucinations in

Chapter 4

103

individuals with schizophrenia (e.g., Badcock, Waters, Maybery, & Michie, 2005;

Waters, Badcock, Maybery, & Michie, 2003; Waters, Badcock, Michie, & Maybery,

2006), Badcock et al. (2007) found that the pattern of impaired performance for this

group was qualitatively different to that of an OCD group tested on the same measures.

This finding suggests that hallucinations and other intrusive cognitions (such as those

experienced in OCD), differ not only with regard to the appraisal of source and content,

but also in terms of the nature of the dysfunction in inhibitory control.

The aim of the current study was to clarify the critical component(s) of

inhibitory control specifically related to hallucination predisposition. Harnishfeger

(1995) developed a taxonomy of inhibition that categorises inhibitory processes

according to three dimensions: (1) intentional (consciously suppressed) or unintentional

(automatically suppressed); (2) cognitive (controlling mental processes) or behavioural

(controlling motor responses or impulses); and (3) inhibition (an active suppression

process operating in working memory) or resistance to interference (a gating

mechanism that prevents irrelevant information from entering working memory). Based

on this taxonomy, Waters and colleagues (2003, 2006) have argued that auditory

hallucinations are specifically associated with impairments in intentional cognitive

inhibition, and indeed have found empirical evidence of this relationship in individuals

with schizophrenia. Importantly, Paulik, Badcock and Maybery (2007) recently

extended these findings to show similar difficulties in healthy, young adults

(undergraduates) predisposed to hallucinations. However, a potential weakness of these

studies is the failure to systematically investigate the separable dimensions of inhibitory

control involved, namely intentionality and inhibition/resistance to interference2.

In showing that hallucination predisposed individuals perform poorly on a task

assessing intentional cognitive inhibition, Paulik et al. (2007) leave open several

possibilities, that is, that those predisposed to hallucinations may have difficulties (a) in

any cognitive control process intentional in nature (irrespective of whether it involves

inhibition or resistance to interference), (b) in any process involving inhibition rather

than interference control (irrespective of whether it is intentional or unintentional in

nature), or (c) more selectively, in only those processes that are both intentional and

involve inhibition. Therefore, the current study employed two cognitive inhibition tasks,

one that demands intentional resistance to interference (the directed ignoring task; DI,

2 Given that hallucinations are a cognitive experience, it appears reasonable to assume that the

inhibitory difficulties involved in their production are occurring on a cognitive – as opposed to a

behavioural – level.

Chapter 4

104

Connelly, Hasher, & Zacks, 1991) and one that demands unintentional inhibition (the

Brown-Peterson variant task; B-P, Kane & Engle, 2000), and administered them to the

same sample as tested by Paulik et al. (2007). This sample comprised groups of high

and low scoring participants on a measure of hallucination predisposition (the Launay-

Slade Hallucination Scale-Revised [LSHS-R], Bentall & Slade, 1985). Thus, if

intentionality is the key dimension involved in the development of hallucinations, then

the high LSHS-R group should perform worse than the low LSHS-R group on the DI

task but not the B–P task. Alternatively, if the critical dimension concerns inhibition of

irrelevant information (impartial to whether this operates on an intentional or

unintentional level), then performance of the high LSHS-R group should be worse than

the low LSHS-R group on the B-P task but not on the DI task. However, if it is the

specific combination of intentional inhibition that is integral to the experience of

hallucinations, as Waters and colleagues propose, then the high LSHS-R group should

not be impaired on either task. Finally, in order to investigate the specificity of these

predicted inhibitory difficulties to hallucination predisposition, we also examined

associations with anxiety, sub-clinical delusional ideation and negative schizotypal

traits.

METHOD

Participants

The participants recruited in the current study were the same as those recruited

in Paulik et al. (2007). Five hundred and eighty nine undergraduate psychology students

completed the 12-item LSHS-R. To obtain a high (n = 28) and low (n = 25) LSHS-R

group, a random sample of students from the upper (scores above 26) and lower (scores

below 6) deciles of the undergraduate sample was invited to take part in the second

phase of the study. The exclusion criteria included a personal history of psychosis, poor

English, poor visual acuity, head injury or neurological disorders resulting in marked

cognitive dysfunction, and an IQ below 85. Accordingly, two participants from the high

LSHS-R group were excluded from analysis, and one participant’s data (from the high

LSHS-R group) on the directed ignoring task was deleted due to visual discrimination

difficulties. Of the remaining 51 participants, there were 18 females and seven males in

the low LSHS-R group (mean age = 19.08, SD = 2.63), and 17 females and nine males

in the high LSHS-R group (mean age = 19.65, SD = 3.55).

Chapter 4

105

Measures

Directed Ignoring (DI; Connelly, Hasher, & Zacks, 1991)

In this task, participants read aloud ten short stories (two practice and eight test

stories) printed in italics (20-point Arial). Half the stories were for the distractor

condition and half for the control condition. In the distractor condition, four distractor

words (which were semantically or thematically related to the story) printed in regular

(non-italicised) font appeared 15 times each, interspersed among the words in the story

(a total of 60 distractors per story). The stories were matched on distractor word length

(4-8 characters) and frequency (Kucera & Francis, 1967) and target passage length (125

words, comprising between 7 and 10 sentences). Participants were asked to read out

loud only the words printed in italics. In the control condition no distractor items were

included in the text, though 60 blank spaces matching the average length of distractor

items were inserted into the passages to control visual scanning requirements between

conditions. Four multiple-choice questions followed each story (on a separate screen) to

assess comprehension, each with four alternative answers, all of which were plausible,

although only one was correct. Each multiple-choice question had one of the distractor

items as a plausible, but incorrect, response choice (a foil). The condition (distractor or

control) paired with each story and the order in which the stories were presented were

counterbalanced across participants. Reading time, the number of distractor items read

aloud (intrusions), and the number of foils chosen on the multiple-choice questions were

used to index intentional control of interference. Accuracy on the multiple-choice

questions was used to assess text comprehension.

Brown-Peterson Variant (B-P; Kane & Engle, 2000).

This task is thought to measure a specific type of unintentional inhibition named

proactive inhibition, which is the ability to automatically inhibit memory intrusions of

previously learnt – and no longer relevant – information when recalling new

information belonging to the same category (Solso, 1995). In each of the five blocks of

this task, participants viewed, read aloud, and attempted to recall three lists, each

comprising ten serially presented words (see Kane & Engle, 2000, for details). All lists

within a block were comprised of words from the same semantic category, and all lists

Chapter 4

106

(within and between blocks) were matched for average word length (maximum length

of 10 letters) and frequency (Battig & Montague, 1969). The categories selected were

four-footed animals, vehicles, occupations/professions, fruits, and sports. After each list

was presented (at a rate of one word every 2 s) a distractor task was performed for 15 s.

Participants were required to count backwards by two’s from a number presented on the

screen (which disappeared after 1500 ms), at a pace that was set by the sounding of

beeps (played every 1500 ms). A green screen with the word "Recall" centred on it then

appeared for 20 s, during which the participant was asked to recall aloud as many words

from the previous list as possible in any order. A beep and red screen with the word

"Stop" centred on it appeared for 2 s to prompt the participant to stop recall before the

next list of words was presented. To ensure that participants were not actively

rehearsing items during the distractor task, responses to this task were recorded and

participants’ results were excluded from analysis if their accuracy rate was less than

75% (all participants managed to attain this accuracy level). In this proactive inhibition

task, the cognitive overflow of previously - but not currently - relevant items from the

same category increases from list one (when there is no overflow to inhibit) to list three.

Thus, the recall of each of the three lists summated across blocks (which we expect to

decrease from list 1 to 3), and the number of intrusions (items recalled from previous

lists) were used to measure inhibition.

Additional Measures

The LSHS-R (Bentall & Slade, 1985) was used to confirm the identification of

individuals predisposed to hallucinations. The 12 LSHS-R items are rated on a 5-point

scale (0 = certainly does not apply to me, 4 = certainly does apply to me), yielding a

total score of 0 to 48 (for an evaluation of this scale, see Paulik et al., 2006). IQ was

estimated from the Wechsler Abbreviated Scale of Intelligence (WASI) vocabulary and

matrix reasoning subtests (Wechsler, 1999). The 7-item anxiety subscale of the short

form of the Depression Anxiety Stress Scales (DASS; Lovibond & Lovibond, 1995)

assessed state anxiety (score range 0-42). The 40-item Peters Delusions Inventory (PDI;

Peters, Joseph, & Garety, 1999) measured delusional thinking (total score range 0-40).

The 27-item introvertive anhedonia subscale of the Oxford-Liverpool Inventory of

Feelings and Experiences (O-LIFE; Mason, Claridge, & Jackson, 1995) assessed

schizotypal personality features that closely correspond to negative schizophrenic

symptomatology (score range 0-27).

Chapter 4

107

Procedure

Ethics approval for the project was obtained from the University of Western

Australia Human Research Ethics Committee and written informed consent was

obtained from each participant prior to testing. The tasks reported on in the current

study were administered along with the cognitive inhibition task reported in Paulik et al.

(2007). The order of the tasks was counterbalanced across participants. Participants

were tested individually and offered course credit points or $20 reimbursement for

time/expenses.

RESULTS


Participants’ scores on single measures were excluded if they were identified to

be three or more SDs away from their respective LSHS-R group mean. Four single data

points were deleted from the data file accordingly (one from each of the following

variables: OLIFE, B-P errors, DI intrusions, and DI control RT). The data were scanned

for multivariate outliers using Cook’s distance, and no cases were identified. An alpha

level of .05 was used throughout the analyses.

A summary of the two LSHS-R groups’ performance on the additional measures

is presented in Table 1. As expected, substantial group separation was obtained on the

LSHS-R. There was also a significant group difference on WASI IQ scores favouring

the high LSHS-R group. Consequently, to control for these differences in intellectual

ability, IQ scores were entered into the subsequent analyses as a covariate. The high

LSHS-R group also obtained significantly higher scores than the low LSHS-R group on

the PDI and DASS-Anxiety subscale but there was no significant group difference on

the O-LIFE introvertive anhedonia subscale. Thus, where significant effects were found

on key measures, PDI and DASS-Anxiety scores were used as additional covariates to

test the specificity of the results.

Chapter 4

108

Table 1


Low LSHS-R Group

(n = 25)

High LSHS-R Group

(n = 26)

Mean SD Mean SD t

LSHS-R 2.80 1.71 31.69 2.74 44.99*

WASI 112.32 8.71 119.15 7.34 3.04*

PDI 4.72 3.45 16.04 6.56 7.67*

DASS-Anxiety 4.32 4.61 10.77 6.88 3.92*

O-LIFE introvertive

anhedonia

3.32 2.93 5.44 4.65 1.93

* p < .05

Directed Ignoring Task

Reading Time

Mean reading times were submitted to a 2 (LSHS-R Group: high, low) x 2

(Story condition: control, distractor) ANCOVA. The Story condition main effect was

significant (F(1,46) = 28.33, MSE = 44.21, p < .05), and as expected all participants

took longer to read the distractor stories than the control stories. The Group main effect

was not significant, though the Group x Story condition interaction effect was

significant (F(1,46) = 4.50, MSE = 44.21, p < .05), with simple effect analyses showing

that the high LSHS-R group was significantly slower at reading the distractor stories

than the low LSHS-R group (F(1,48) = 3.95, MSE = 158.22, p < .05), whilst there was

no significant group difference for reading time of control stories (see Table 2 for group

means and SEs). When PDI and DASS-Anxiety scores were entered separately into the

analysis as additional covariates, the Group x Story condition interaction effect was no

longer significant.

To investigate whether these two additional variables independently relate to

intentional resistance to interference, hierarchical multiple regression analyses were

performed on the data. The dependent variable was constructed by subtracting control

RT from distractor RT. The first set of independent variables entered into the analyses

was LSHS-R group (as a binary variable) and WASI-IQ, and together they significantly

contributed to the prediction of the dependent variable (R2 = .305, p < .05). While

DASS-Anxiety made a significant additional contribution to the variance accounted for

Chapter 4

109

when it was entered next into the equation (R2 change = .061, p < .05), delusional

ideation (PDI) did not (R2 change = .042, p > .05). Thus, it appears that while anxiety

makes a modest unique contribution to resistance to interference (in addition to any

effect shared with hallucination predisposition), the relationship that sub-clinical

delusional ideation may have with this form of cognitive control is shared with


Table 2

LSHS-R Group Means and Standard Errors (Adjusted for Group Differences in IQ) on

the Measures of Cognitive Control

Low LSHS-R Group

(n = 25)

High LSHS-R Group

(n = 26)

Mean SE Mean SE

Directed Ignoring

Reading time (s) – control stories 41.53 1.11 41.91 1.14

Reading time (s) – distractor stories 60.25 2.59 66.90 2.65

Intrusions 2.68 0.62 4.95 0.61

Foil errors 1.37 0.23 1.35 0.24

Brown-Peterson variant

Words recalled a – list 1 28.31 1.06 31.32 1.04

Words recalled – list 2 22.80 1.10 24.00 1.07

Words recalled – list 3 17.23 1.00 19.01 0.98

Total intrusions b 4.08 0.65 3.85 0.64

Note. a Total number of words correctly recalled (5 blocks of 10 words summed).

bNumber of previous list items incorrectly recalled (lists 2 and 3 summed).

Intrusions

When an ANCOVA with the single factor of LSHS-R group was conducted on

the number of intrusions recorded from the distractor condition, it showed that the high

LSHS-R group read out loud significantly more of the distractor items than did the low

LSHS-R group, F(1,49) = 6.32, MSE = 8.44, p < .05 (see Table 2 for group means and

SEs). When DASS-Anxiety or PDI scores were entered into the analysis as an additional

covariate, the Group effect no longer reached significance. Hierarchical regression

analyses were used to investigate whether these additional variables independently

Chapter 4

110

relate to this index of intentional resistance to interference. The first set of independent

variables entered into the analyses was LSHS-R group and WASI-IQ, and together they

made a significant, but modest contribution to the prediction of the dependent variable

(R2 = .123, p < .05). Neither DASS-Anxiety (R

2 change = .010, p > .05) nor PDI (R

2

change = .041, p > .05) significantly contributed to the variance accounted for when

either were subsequently entered into the regression equation. The number of intrusions

significantly correlated with reading time for distractor stories (r = .308, p < .05, N =

49) – but not control stories (r = .034, p > .05, N = 48) – and also correlated with the

number of foil errors in the multiple choice comprehension questions (r = .287, p < .05,

N = 49), supporting its validity as an index of interference.

Multiple-choice Questions: Foil Errors and Accuracy

There was no significant group difference in the total number of distractor items

chosen as the correct response (foil errors) on the multiple choice questions of the

distractor stories, F(1,49) = 0.001, MSE = 1.24, p > .05 (see Table 2 for group means

and SEs). To assess story comprehension, participant’s overall accuracy (percent of

answers correct) was calculated for each story condition. When a 2 (LSHS-R group:

high, low) x 2 (Story condition: control, distractor) ANCOVA was performed, no

significant main or interaction effects were found, indicating that story comprehension

was not influenced by the presence of distractors for either LSHS-R group. Over-all

accuracy (percentage correct) was high for both the high (M = 89.59, SD = 6.36) and

low (M = 89.71, SD = 4.91) LSHS-R groups, indicating that both groups had good

comprehension of the passages.

Brown-Peterson Variant Task

Word Recall

The number of words correctly recalled in each list (summed across the 5

blocks) was recorded for each participant. A 2 (LSHS-R Group: high, low) x 3 (List: 1,

2, 3) ANCOVA showed a significant List main effect, F(2,49) = 3.34, MSE = 9.87, p <

.05, with post hoc pair-wise comparisons revealing a significant difference in recall

between all three lists, with the number of items correctly recalled progressively

decreasing from lists 1 to 3 (see Table 2 for group means and SEs). Neither the Group

Chapter 4

111

main effect nor the List x Group interaction effect was significant. An identical pattern

of results was obtained when 2 (LSHS-R Group: high, low) x 2 (List: 1, 2; or 1, 3)

ANCOVAs were conducted as suggested by Friedman and Miyake (2004).

Intrusions in Recall

The number of words incorrectly recalled from the previous within-block lists

was recorded for each participant (thus only recall errors in lists 2 and 3 were of

interest). When a 2 (LSHS-R Group: high, low) x 2 (List: 2, 3) ANCOVA was

performed, no significant main or interaction effects were found (see Table 2 for

summated means and SEs).

DISCUSSION

The main findings of the current research are consistent with the proposal that

deficits of intentional (i.e. voluntary) cognitive control play an important role in the

production of hallucinations. ‘The distinction between an action that is intentional and

one that is not seems to have something to do with the consciousness of the goal of the

actions’ (Brown, 1989, p. 113). In line with this view, the current data from the B-P

task shows that when the requirement to inhibit is unintentional (automatic), no LSHS-

R group differences in performance are found. Rather, as expected, all participants show

a steady decrease in ability to recall words from the same category across consecutive

lists. One previous study by Peters, Pickering and Hemsley (1994) reported a correlation

between LSHS total scores (not specifically selecting high and low scorers) and

unintentional inhibition, however, the specific task used (a negative priming task) fails

to correlate with more established measures of unintentional inhibition (Friedman &

Miyake, 2004), and additionally, the sample size (N = 28) in their study may not have

been large enough to generate a full range of LSHS scores. Furthermore, Peters and

colleagues (2000) did not find a significant correlation between the frequency of

auditory hallucinations and unintentional inhibition in individuals with schizophrenia

using this same negative priming task.

In contrast, when the task requires deliberate (i.e. intentional) control of

interference from concurrent distractors – as in the DI task – the high LSHS-R group

had distinct difficulties; showing increased intrusions and reading times on distractor

stories despite equivalent text comprehension and reading time of control stories.

Chapter 4

112

Waters et al. (2003) and Paulik et al. (2007) have previously argued that auditory

hallucinations in schizophrenia and healthy young adults arise as a result of failures of

intentional cognitive inhibition specifically. The current results support and refine this

proposal. Our findings suggest that in addition to the difficulties with active suppression

(intentional ‘inhibition’, as found in Paulik et al., 2007), individuals predisposed to

hallucinations also have difficulty with gating external information (intentional

‘interference control’, as measured on the DI task). However, LSHS-R group

differences on the measure of interference control were no longer significant once

variation in state anxiety or sub-clinical delusional ideation were controlled for.

Regression analyses were subsequently conducted to investigate whether anxiety and

sub-clinical delusional ideation uniquely contributed to variance in intentional

resistance to interference, over and above the variance that hallucination predisposition

accounted for. These results showed that anxiety made a modest, but significant unique

contribution to resistance to interference – as measured by RTs (but not intrusions) – in

addition to any contribution shared with hallucination predisposition. Thus, anxiety may

serve to exacerbate existing intentional resistance to interference difficulties in

individuals prone to hallucinations and/or delusional ideation. This supposition is

supported by the findings that problems gating concurrent, distracting information are

common in high anxious samples (found using the DI task; Chong, 2003; Hopko,

Ashcraft, Gute, Ruggiero, & Lewis, 1998). The regression analyses, however, revealed

that sub-clinical delusional ideation (PDI) did not make a unique contribution to

intentional resistance to interference, and thus, it seems that the relationships that

hallucination proneness and sub-clinical delusional ideation have with intentional

resistance to interference are interrelated. For instance, a problem in resistance to

interference might be a precursor to both hallucinations and delusional ideation, with

each symptom having additional specific precursors (e.g., impairments in intentional

inhibition for hallucinations). Indeed, Paulik et al. (2007) demonstrated a specific

difficulty with the intentional inhibition of previously relevant distractors in

hallucination predisposed individuals using the same sample as the current study even

when differences in sub-clinical delusional ideation and anxiety were controlled for.

Taken together, these findings suggest that both sub-clinical and clinical (as

demonstrated by Waters et al., 2003) hallucinatory experiences involve a similar

mechanism, that is, a difficulty with intentionally suppressing unwanted cognitions

already held in working memory. However, further research is needed to examine in

greater detail the two different forms of intentional control discussed here, especially

Chapter 4

113

since no published studies (to our knowledge) have investigated the relationship

between intentional resistance to interference and schizophrenia-related symptoms in a

clinical sample.

The clinical implications of the finding that cognitive control difficulties in

hallucination-prone individuals (and possibly hallucinating individuals with

schizophrenia) are operating at an intentional level are two-fold. Difficulties with

intentional inhibition may lead to – at least in some individuals – greater intentional

efforts to suppress unwanted mental intrusions (termed ‘thought suppression’), which

has been shown to lead to paradoxical effects of increased availability – and thus,

increased frequency – of the unwanted cognition (thought, memory, image, etc.)

(Wegner & Zanakos, 1994). Therefore, interventions aimed at teaching hallucination-

prone and actively hallucinating individuals more effective cognitive control strategies

(to replace ‘thought suppression’), such as active-acceptance and distraction-based

strategies (Farhall & Gehrke, 1997; Morrison & Wells, 2000), may help to reduce the

availability and frequency of unwanted mental intrusions entering working memory.

It should be noted that the findings reported in the current study are based on an

undergraduate psychology student sample, and thus may not be representative of the

healthy population at large. In addition, it is possible that the absence of a significant

group difference on foil errors on the DI comprehension task may have occurred

because the questions were not difficult enough for an undergraduate sample (accuracy

was close to ceiling), or because recognition was assessed using an explicit memory

test, which previous researchers have claimed under-represents attention paid to

irrelevant stimuli (Connelly, Hasher, & Zacks, 1991). Finally, it should be noted that

studies using the DI task have not traditionally included intrusions as a measure of

interference control. Although this intrusion measure correlated significantly with the

other key measures on this task, it is possible that it is also measuring another form of

inhibitory control (namely, behavioural, or pre-potent-response inhibition; Friedman &

Miyake, 2004), which may explain the inconsistency between the outcomes of the two

regression analyses (namely, why hallucination predisposition accounted for less of the

variance in this measure than the reading time variable, and why anxiety did not make

an independent contribution to its prediction). To further understand the cognitive

mechanisms underpinning unwanted mental intrusions, it will be important for future

research to investigate the dissociable components of inhibitory control specifically

related to different types of cognitive intrusions (i.e. flashbacks, intrusive thoughts,

Chapter 4

114

impulses, etc.) and different clinical disorders characterised by unwanted mental

intrusions, such as OCD, GAD, PTSD and schizophrenia.

Chapter 4

115

ACKNOWLEDGEMENTS


funding from the Ron and Peggy Bell Foundation. We also thank Matt Huitson for his

help with task programming.

Chapter 4

116

REFERENCES







Bak, M., Myin-Germeys, I., Delespaul, P., Vollebergh, W., de Graaf, R., & van Os, J.

(2005). Do different psychotic experiences differentially predict need for care in

the general population? Comprehensive Psychiatry, 46, 192-199.

Battig, W. F., & Montague, W. E. (1969). Category norms for verbal items in 56

categories: A replication and extension of the connecticut category norms.

Journal of Experimental Psychology Monograph, 80, 1-46.



527-529.

Brown, J. W. (1989). The nature of voluntary action. Brain and Cognition, 10, 105-120.

Chong, J. L. Y. (2003). Anxiety and working memory: An investigation and

reconceptualisation of the processing efficiency theory. The University of

Western Australia, Perth.








Farhall, J., & Gehrke, M. (1997). Coping with hallucinations: Exploring stress and

coping framework. British Journal of Clinical Psychology, 36, 259-261.






Chapter 4

117


Academic Press.












Kucera, H., & Francis, W. N. (1967). Computational analysis of present-day English.

Providence, RI: Brown University Press.





McGee, R., Williams, S., & Poulton, R. (2000). Hallucinations in nonpsychotic

children. Journal of the American Academy of Child and Adolescent Psychiatry,

39, 12-13.

Morrison, A. P. (2001). The interpretation of intrusions in psychosis: An integrative

cognitive approach to hallucinations and delusions. Behavioural and Cognitive

Psychotherapy, 29, 257-276.




Morrison, A. P., & Wells, A. (2000). Thought control strategies in schizophrenia: A

comparison with non-patients. Behaviour Research and Therapy, 38, 1205-

1209.





Chapter 4

118




Paulik, G., Badcock, J. C., & Maybery, M. T. (2007). Poor intentional inhibition in

individuals predisposed to hallucinations. Cognitive Neuropsychiatry, 12, 457-

470.

Peters, E. R., Joseph, S. A., & Garety, P. A. (1999). Measurement of delusional ideation

in the normal population: Introducing the PDI (Peters et al. Delusions

Inventory). Schizophrenia Bulletin, 25, 553-576.

Peters, E. R., Pickering, A. D., & Hemsley, D. R. (1994). 'Cognitive inhibition' and

positive symptomatology in schizotypy. British Journal of Clinical Psychology,

33, 33-48.

Peters, E. R., Pickering, A. D., Kent, A., Glasper, A., Irani, M., David, A. S., et al.

(2000). The relationship between cognitive inhibition and psychotic symptoms.

Journal of Abnormal Psychology, 109, 386-395.

Purdon, C., & Clark, D. A. (1993). Obsessive intrusive thoughts in nonclinical subjects.

Part I. Content and relation with depressive, anxious and obsessional symptoms.


Solso, R. L. (1995). Cognitive Psychology (4th ed.). Needham Heights, MA: Simon &

Schuster.



Vasterling, J., Brailey, K., Constans, J., & Sutker, P. (1998). Attention and memory

dysfunction in post-traumatic stress disorder. Neuropsychology, 1, 125-133.



Research, 62, 275-280.








119

ANXIETY, INHIBITION, AND

HALLUCINATION PREDISPOSITION

120


121


The results presented in Chapter 3 and 4 identified that the cognitive control

difficulties specific to hallucination predisposition (not shared with other schizophrenia-

related symptoms) is intentional cognitive inhibition. The results of the second study

presented in Chapter 2 identified that state anxiety – but not depression or stress – is

consistently related with all components of hallucination predisposition. It was

speculated that the one feature common to all three of the hallucination predisposition

components is intrusiveness. Similar to hallucinatory-type experiences, everyday

intrusive cognitions have been empirically linked to failures of inhibitory control

(Friedman & Miyake, 2004; Kramer, Humphrey, Larish, Logan, & Strayer, 1994), and

what is more, anxiety has been empirically linked to both increased intrusive cognitions

and poor inhibitory control (e.g., Amir, Coles, & Foa, 2002; Badcock, Waters, &

Maybery, 2007; Hackmann, Surawy, & Clark, 1998; Hopko, Ashcraft, Gute, Ruggiero,

& Lewis, 1998; Wood, Mathews, & Dalgleish, 2001). Although the findings reported

in Chapter 3 suggest that the intentional inhibition difficulties found in hallucination

predisposition exist independent of state anxiety, it remains possible that anxiety may

exacerbate these existing inhibition difficulties, since the degree of variation in state

anxiety in the previous study may not have been high enough to influence (impair)

inhibitory ability.

The aim of Chapter 5 was to examine the direct effects of anxiety on intentional

inhibitory performance in healthy individuals, and to also investigate whether

hallucination predisposed individuals are more susceptible to the cognitive effects of

anxiety than most. A music mood induction paradigm was employed to sequentially

induce, in separate phases, an anxious and a neutral mood state in high and low

hallucination predisposed individuals, and compare inhibitory performance following

each form of induction. Since the duration of mood induction effects is restricted, it was

only possible to administer one cognitive task following each mood induction phase.

The Inhibition of Currently Irrelevant Memories (ICIM) task employed in Chapter 3

was selected, since the findings from the two previous chapters suggest that intentional

inhibition difficulties are most consistently – and specifically – related to hallucination

predisposition. Trait anxiety was also investigated in Chapter 5, since there is some

evidence that trait and state anxiety have different effects on – or relationships with –

cognitive processes (e.g., Heinrich & Spielberger, 1982; Puliafico & Kendall, 2006).


122

REFERENCES













Heinrich, D. L., & Spielberger, C. D. (1982). Anxiety and complex learning. In I. G.

Sarason & C. D. Spielberger (Eds.), Stress and anxiety (series in clinical and

community psychology) (Vol. 4, pp. 145-165). New York: Wiley & Sons.







Puliafico, A. C., & Kendall, P. C. (2006). Threat-related attentional bias in anxious

youth: A review. Clinical Child and Family Psychology Review, 9, 162-180.


Emotion, 1, 166-181.

Chapter 5

123

Chapter 5

Effects of anxiety on the intentional inhibition of currently

irrelevant memories: A hallucination predisposition study 1

ABSTRACT

Anxiety has been strongly implicated in the onset of hallucinatory episodes.

Both hallucinatory experiences (in schizophrenia and hallucination predisposition) and

anxiety disorders have been empirically linked to difficulties intentionally suppressing

unwanted cognitions. The current study had three aims: (1) to replicate the finding of

intentional inhibition difficulties in healthy individuals predisposed to hallucinations;

(2) to investigate the impact of anxiety on intentional inhibitory performance; and (3) to

examine a possible interaction between anxiety and intentional inhibition in high- and

low hallucination-predisposed individuals. In this study, undergraduate students

psychometrically identified as having a high (N = 28) or low (N = 33) hallucination

predisposition were compared on an intentional inhibition task both when in an anxious

and when in a neutral mood state, using a music mood induction procedure. The results

replicated previous findings that hallucination predisposed individuals have intentional

inhibition difficulties. There were no significant overall or between group differences on

intentional inhibition in the anxious and neutral mood conditions. These results suggest

that state anxiety in non-clinical individuals does not impair intentional inhibition.

However, whilst the mood induction procedure was shown to be effective, the size and

duration of the effects were modest. Consequently, either more marked or longer lasting

changes in anxiety may impair inhibition performance. Consistent with this

interpretation, trait anxiety was found to correlate significantly with intentional

inhibition, even when controlling for state anxiety and hallucination predisposition.

Keywords: Hallucination predisposition; Hallucinations; Anxiety; Mood induction;

Intentional inhibition


(2008). Effects of anxiety on the intentional inhibition of currently irrelevant memories: A

hallucination predisposition study. Unpublished manuscript, University of Western Australia.

Chapter 5

124

You hear a voice saying “pick up that knife, you idiot”. It‟s a young man‟s

voice, he sounds angry and he seems to be close by. You start to reply, then look

around. No one is there.

Auditory hallucinations (AHs) are complex, cognitive intrusions. They arise

with a compelling sense of reality but in the absence of corresponding external

stimulation. They are predominantly negative in content, and are typically experienced

as uncontrollable, unwanted and intrusive (Nayani & David, 1996; Slade & Bentall,

1988). The impact on a person‟s wellbeing can be devastating, with the severity of AHs

being associated with anxiety, depression, anger, fear, stress, low self-esteem, and a

heightened risk of suicide (e.g., Alpert & Silvers, 1970; Close & Garety, 1998; Hustig

& Hafner, 1990; Walsh et al., 1999). However, anxiety in particular, has not only been

found to accompany the experience of AHs, but to also precede hallucinatory episodes,

suggesting that emotional disturbance may play a direct causal role in the onset of AHs

(e.g., Delespaul, deVries, & van Os, 2002). Strengthening this conjecture, Slade (1972,

1973) showed that by effectively reducing anxiety in individuals with schizophrenia

through behavioural intervention, the frequency of AHs was also significantly reduced.

Although AHs are traditionally associated with schizophrenia, recent studies

have shown that as many as 10-25% of healthy individuals will experience an AH at

some stage during their lives (Tien, 1991). This has prompted the study of

hallucinatory-type experiences in the general population (Choong, Hunter, & Woodruff,

2007). This type of research permits the study of hallucinatory experiences in the

absence of the possible confounding variables associated with schizophrenia, such as

other schizophrenia-related symptoms, medications, institutionalisation, and general

cognitive decline. The most commonly used measure of hallucination predisposition is

the revised Launay-Slade Hallucination Scale (LSHS-R: Bentall & Slade, 1985a;

Launay & Slade, 1981). Studies employing this instrument have found that similar

features define the hallucinatory experience in both healthy individuals predisposed to

hallucinations and individuals with schizophrenia (Serper, Dill, Chang, Kot, & Elliot,

2005). For example, in one of our previous studies (Paulik, Badcock, & Maybery, 2006)

we found that anxiety, depression and stress were all related to hallucination

predisposition and, similar to the hallucinatory experiences of individuals with

schizophrenia (Norman, Malla, Cortese, & Diaz, 1998), anxiety was most strongly and

consistently related to hallucination predisposition.

Auditory hallucinations in schizophrenia and hallucination predisposition have

been linked to difficulties with intentional cognitive inhibition, that is, difficulties

Chapter 5

125

intentionally suppressing previously relevant information held in working memory. In

two related papers, Badcock and colleagues (Badcock, Waters, Maybery, & Michie,

2005; Waters, Badcock, Maybery, & Michie, 2003) reported that this inhibitory

impairment is not a general feature of schizophrenia but is associated with increased

severity of AHs specifically. More recently, we showed a similar, though somewhat

milder, difficulty of intentional inhibition in healthy young adults (undergraduates) with

high scores on the LSHS-R (Paulik, Badcock, & Maybery, 2007). Importantly, given

the evidence that anxiety has also been linked to numerous forms of inhibitory control

(e.g., Amir, Coles, & Foa, 2002; Badcock, Waters, & Maybery, 2007; Dorahy,

McCusker, Loewenstein, Colbert, & Mulholland, 2006; Enright & Beech, 1993; Hopko,

Ashcraft, Gute, Ruggiero, & Lewis, 1998; Wood, Mathews, & Dalgleish, 2001), it is

interesting to note that this difficulty remained even when controlling for state anxiety.

However, it is feasible that the degree of variation in state anxiety during this study was

not high enough to influence (impair) inhibitory ability, thus leaving open the

possibility that heightened levels of anxiety may exacerbate performance difficulties.

The first aim of the current study was to replicate the finding of intentional

inhibition difficulties in healthy individuals predisposed to hallucinations on the

Inhibition of Currently Irrelevant Memories task. The second aim was to examine

whether higher levels of state anxiety may impair this particular form of inhibition in

non-clinical healthy individuals, since the only previous study which investigated, and

found evidence for, a relationship between anxiety and intentional inhibition tested a

clinical sample – specifically, obsessive-compulsive disorder (Badcock et al., 2007).

The third aim of the current study was to investigate whether high hallucination

predisposed individuals are more susceptible to the effects of anxiety on intentional

inhibitory performance than low hallucination predisposed individuals. To achieve these

aims, a music mood induction procedure was adopted to experimentally manipulate

anxious and neutral moods, rather than relying on natural and often minor fluctuations

in mood state. Mood induction procedures have been effectively employed to

investigate the effects of anxiety on cognitive processes and can clearly indicate a

causal role of anxiety on inhibitory impairment, if present (e.g., Gray, 2001; Shackman

et al., 2006; Shapiro & Lim, 1989). The relationship(s) between trait (dispositional)

anxiety and the key variables will also be investigated.

Chapter 5

126

METHOD

Participants

Nine hundred and eighty five undergraduate psychology students completed the

LSHS-R (Bentall & Slade, 1985b) as part of their course requirements. Twenty nine

participants from the upper 15% (scores ≥ 24), and 33 participants from and lower 15%

(scores ≤ 7) of the distribution responded to an invitation to take part in the current

study, which formed the high and low LSHS-R groups, respectively. Exclusion criteria

included a personal history of psychosis, bipolar disorder or ADHD2, poor English, poor

visual acuity, head injury or neurological disorder resulting in marked cognitive

dysfunction, or an IQ below 85. Accordingly, one participant from the high LSHS-R

group was excluded from the analysis. This yielded a final high LSHS-R subgroup

comprised of 16 females and 12 males (mean age = 18.68, SD = 2.06) and a low LSHS-

R subgroup comprised of 18 females and 15 males (mean age = 19.03, SD = 2.16).

Measures

Inhibition of Currently Irrelevant Memories (ICIM) Task

The ICIM task (Schnider, Valenza, Morand, & Michel, 2002) is a repeated

continuous recognition task, which we have previously examined in individuals with

schizophrenia (Waters et al., 2003) and in hallucination predisposition (Paulik et al.,

2007). The task was presented in two blocks: one following each mood induction (see

the Procedure section). Each block consisted of two runs (separated by a 30 s break),

each involving the sequential presentation of 85 black and white line drawings on a

computer screen (Snodgrass & Vanderwart, 1980; Szekely et al., 2003). Twenty-eight

pictures occurred only once in a run, whilst six occurred twice, and 15 occurred three

times, yielding 49 first presentations in a run (distractors), 21 second presentations, and

15 third presentations (36 targets in total). Different pictures were used in each of the

two blocks, however, the blocks were matched on picture frequency, visual complexity,

name agreement, recognition response times, and the number of different categories the

2 A current diagnosis (self report) of ADHD was included as an exclusion criteria, since

empirical studies have reported cognitive inhibition deficits in individuals with ADHD (e.g.,

Barkley, 1997) and stimulant medications used to treat ADHD may interfere with the RT data.

Chapter 5

127

pictures were drawn from (Szekely et al., 2004). Each picture was presented in the

centre of a computer screen for 2 s, with a 700 ms interstimulus interval. In each run,

the participants‟ task was to indicate as quickly and accurately as possible (by pressing

„yes‟ or „no‟ keys) whether they had already seen each picture within the current run.

The second run used the same picture set as the first run, however, the presentation

order and pictures selected to be targets changed. On this run, participants were

explicitly asked to forget the pictures they had seen on the first run. Thus, the first run

required the learning and recognition of novel items, while the second run also required

participants to intentionally inhibit the memory of pictures that had been seen on the

previous run. The dependent variables were the number of false alarms (FA: incorrectly

selecting a distractor) and Hits (correct detection of a target), together with the response

times (RTs) for correct responses to targets (Hits) and distractors (correct rejections,

CR) for both runs. The number of FAs on run 2 specifically is assumed to reflect the

failure to inhibit memories of pictures that are currently irrelevant.

Mood Induction Procedure

A music mood induction procedure was selected based on previous

demonstrations that music has a significant and enduring effect on mood state in both

males and females (Albersnagel, 1988; Clark, 1983). Two seven-minute excerpts were

taken from two pieces of classical music, Stravinsky‟s „The Rite of Spring (Part 2: The

Sacrifice)‟ and Fauré‟s „Opus 19‟, which have been used in previous research and found

to be effective in engendering anxious and neutral mood states, respectively

(Albersnagel, 1988; Shapiro & Lim, 1989; Stober, 1997). An additional two-minute

excerpt was taken from Fauré‟s „Opus 19‟ to restore mood state back to a neutral state

following the anxiety induction procedure.

Mood Measures

Two visual analogue mood scales (VAMS) – each using an18 cm line marked 0

to 30 – were used to assess momentary anxiety (with the words „anxious‟ and „relaxed‟

as anchor points) and momentary depression (with the words „depressed‟ and „happy‟ as

anchor points). Visual analogue mood scales are less likely to interfere with mood

induction effects than longer scales, have a high test-retest reliability (e.g., Kreindler,

Levitt, Woolridge, & Lumsden, 2003), and moderate to high concurrent validity when

Chapter 5

128

compared to more extensive mood scales (e.g., Cella & Perry, 1986). Trait anxiety was

measured using the relevant subscale of the short form Depression, Anxiety and Stress

Scales (DASS; Lovibond & Lovibond, 1995). This subscale has seven items, which are

rated (“in a typical week in the past 12 months”) on a four point scale (0 = “Did not

apply to me at all”, 3 = “Applied to me very much, or most of the time”), which are

multiplied by two, yielding a score range of 0 to 42. The trait version of the DASS is

shown to have moderate long-term (3-8 year) re-test reliability (Lovibond, 1998).

Additional Measures

The LSHS-R (Bentall & Slade, 1985b) was re-administered at time of testing to

confirm the reliability of group allocation to high and low LSHS-R subgroups. The 12

LSHS-R items are rated on a 5-point scale (0 = certainly does not apply to me, 4 =

certainly does apply to me), yielding a total score of 0 to 48. Intelligence was estimated

from the Wechsler Abbreviated Scale of Intelligence (WASI) vocabulary and matrix

reasoning subtests (Wechsler, 1999). The short 21-item version of the Peters Delusions

Inventory (PDI-21; Peters, Joseph, Day, & Garety, 2004) measured delusional thinking

(total score range 0-21), while the introvertive anhedonia subscale of the Oxford-

Liverpool Inventory of Feelings and Experiences (O-LIFE; Mason, Claridge, &

Jackson, 1995) assessed schizotypal personality features that closely correspond to

negative schizophrenic symptomotology (score range 0-27).

Procedure

Ethics approval was obtained from the University of Western Australia Human

Research Ethics Committee and written informed consent was obtained from each

participant prior to testing. Participants were tested individually and offered course

credit points or $20 reimbursement for time/expenses.

Each participant underwent both the anxious and the neutral mood induction

procedures. At the start of the testing session, participants completed the trait-anxiety,

delusional thinking, and schizotypy questionnaires. The WASI subtests were

administered in between the two mood induction phases. Following each of the mood

induction procedures, participants immediately completed one block of the ICIM task.

Both the order of the mood induction conditions and the assignment of the ICIM blocks

to the mood induction conditions were counterbalanced across participants. Participants

Chapter 5

129

rated their state anxiety and depression six times using the VAMS: immediately prior to

each mood induction, immediately following each mood induction, and immediately

after each ICIM block. Participants were asked to listen to a two-minute excerpt from

the neutral-mood music after completing the ICIM task that followed the anxiety mood

induction in order to restore mood back to a neutral mood state. At the end of the testing

session, participants were also offered (only one accepted) to watch a 30 minute episode

of a comical television show – Mr Bean – if they were still feeling anxious.

RESULTS


Twelve univariate outliers (single data points more than 3 SDs from the

participants‟ respective LSHS-R group mean) and three multivariate outliers

(Mahalanobis distance, p < .001) were identified and removed prior to analysis of the

data. Table 1 presents LSHS-R group means together with questionnaire and IQ results.

As expected, substantial group separation was obtained on LSHS-R scores collected at

the time of experimental testing. The high LSHS-R group also obtained significantly

higher scores on the PDI and the DASS-trait anxiety, but there was no significant group

difference on WASI-IQ or the O-LIFE introvertive anhedonia subscale.

Table 1


Low LSHS-R group

(N = 33)

High LSHS-R group

(N = 28)

Mean SD Mean SD t

LSHS-R total a 3.67 1.93 33.03 3.65 40.15*

WASI IQ 109.42 10.14 111.14 10.34 0.65

DASS anxiety 2.94 3.09 14.21 9.28 6.49*

PDI total 4.19 2.52 11.25 2.88 10.14*

OLIFE introvertive

anhedonia

5.66 5.61 7.46 5.10 1.30

* p < .05

Note. a The LSHS-R scores presented are the scores obtained at time of testing.

Chapter 5

130

Efficacy of Mood Induction Procedure

For both mood induction conditions, a 2 (LSHS-R Group: low, high) x 3

(Induction Phase: pre-induction, post-induction, post-ICIM completion) x 2 (Rated

Mood: anxiety, depression) ANOVA was conducted using VAMS ratings (see Figures

1a and 1b for overall means and SEs). When Mood Order (anxiety induction versus

neutral induction administered first) was entered into the analyses of VAMS mood

ratings as an additional between subjects variable, no main or interaction effects

involving Mood Order were significant, consequently, this factor was not included in

subsequent analyses.

As seen in Figure 1a, in the analysis of data from the anxiety mood induction

condition, the main effects of Rated Mood (F (1,57) = 6.40, MSE = 21.54, p < .05) and

Induction Phase (F (2,57) = 28.93, MSE = 12.37, p < .05) were significant. The

Induction Phase x Rated Mood interaction effect was also significant (F (2,57) = 14.68,

MSE = 5.29, p < .05), with post hoc paired t-tests showing that for both anxiety and

depression ratings, negative affect was significantly higher both immediately following

the anxiety mood induction and after the proceeding ICIM task than at the pre-induction

phase, although anxiety ratings – but not depression ratings – had significantly

decreased from the post-induction to the post-ICIM task phase (although as seen in

Figure 1a, anxiety ratings at the post-ICIM task phase still remained higher than

depression ratings). No effects involving LSHS-R Group were significant. These results

show that the anxiety mood induction was equally effective for both LSHS-R groups,

had a greater effect on anxiety than depression, and that the effects were partially

maintained until the end of the ICIM task.

As seen in Figure 1b, in the analysis of data from the neutral mood induction

condition, there was a significant Induction Phase main effect (F (2,56) = 12.31, MSE =

15.75, p < .05. In addition, there was also a significant LSHS-R Group x Induction

Phase x Rated Mood interaction effect (F (2,56) = 3.21, MSE = 8.16, p < .05). Post hoc

paired t-tests – conducted separately for the high and low LSHS-R groups – showed that

for both groups, anxiety ratings were significantly lower following the neutral mood

induction (but not at the post-ICIM task phase) than at the pre-induction phase, although

the low – but not the high – LSHS-R group‟s anxiety ratings had significantly increased

from the post-induction phase to the post-ICIM task phase (returning to pre-induction

levels). For the depression ratings, the post hoc paired t-tests showed that while there

Chapter 5

131

were no significant differences in ratings across the induction phases for the low LSHS-

R group, the high LSHS-R group‟s depression ratings were also reduced following the

neutral mood induction. This LSHS-R group difference may be attributable to the high

LSHS-R group‟s significantly higher pre-induction depression ratings than the low

LSHS-R group (t (58) = 3.02, p < .05). These findings indicate that the neutral mood

induction was effective; anxiety ratings were significantly reduced following the neutral

mood induction for both LSHS-R groups (although the duration of the mood induction

was limited), and the reduction was specific to anxiety – rather than reducing negative

affect more generally – for the low LSHS-R group.

(a) (b)

Figure 1. Entire sample mean anxiety and depression VAMS ratings across the three

induction phases for (a) the anxiety mood induction condition, and (b) the neutral mood

induction condition (error bars represent one SE of the mean).

Intentional Inhibition and Hallucination Predisposition

A one-tailed (planned comparison) t-test was employed to test the prediction

that healthy individuals highly predisposed to hallucinations exhibit poorer intentional

inhibition than individuals with lower predisposition. The results confirmed that the

high LSHS-R group made significantly more FAs on run 2 (mean = 9.18, SD = 4.94)

than the low LSHS-R group (mean = 7.03, SD = 4.53), t (57) = 1.74, p < .05,

successfully replicating the findings reported by Paulik et al. (2007).

15

16

17

18

19

20

21

22

23

24

25

Pre-Induction Post-Induction Post-ICIM task

Induction Phase

Rel

axed

A

nxio

us

g

Anxiety Rating Depression Rating

15

16

17

18

19

20

21

22

23

24

25

Pre-Induction Post-Induction Post-ICIM task

Induction Phase

Rel

axed

A

nxio

us

g

Anxiety Rating Depression Rating

Chapter 5

132

Effects of Anxiety on ICIM Task performance

Encoding and Recognition

Performance on run 1 requires the learning and recognition of novel pictures.

The effect of mood induction on FAs in run 1 was examined using a 2 (LSHS-R Group:

high, low) x 2 (Mood Induction: neutral, anxiety) ANOVA (see Table 2 for means and

SDs). No effects were significant. When the same analysis was conducted using run 1

Hits (target detection), again no effects were significant. These findings suggest that

neither anxious mood nor hallucination predisposition affects the ability to learn and

recognise new targets in memory.

Table 2

LSHS-R Group Means and SDs for FAs, Hits, and Reaction Times (ms) for Correct

Responses on the ICIM Task for the Anxiety and Neutral Mood Conditions

Low LSHS-R Group

(N = 33)

High LSHS-R Group

(N = 28)

Mean SD Mean SD

Anxiety – FA Run 1 1.52 1.52 1.37 1.33

Neutral – FA Run 1 1.22 1.13 1.82 1.52

Anxiety – FA Run 2 3.94 3.10 4.93 2.98

Neutral – FA Run 2 3.31 2.19 4.25 2.80

Anxiety – Hit Run 1 33.22 1.91 33.37 2.51

Neutral – Hit Run 1 33.50 1.83 33.48 2.61

Anxiety – Hit Run 2 30.82 3.61 32.74 2.31

Neutral – Hit Run 2 32.25 2.50 32.48 2.78

Anxiety – CR RT Run1 732.61 87.36 747.50 99.93

Neutral – CR RT Run 1 718.77 93.68 722.79 91.31

Anxiety – Hit RT Run 1 736.21 73.87 713.27 89.16

Neutral – Hit RT Run 1 736.85 85.88 710.41 76.49

Anxiety – CR RT Run 2 787.58 91.08 755.39 68.18

Neutral – CR RT Run 2 786.80 97.33 775.13 94.12

Anxiety – Hit RT Run 2 764.61 74.16 728.29 75.70

Neutral – Hit RT Run 2 765.47 90.29 732.29 90.80

Chapter 5

133

Intentional Inhibition and Target Detection in Run 2

Unlike run 1 performance, run 2 requires participants to intentionally inhibit

memories of previous-run pictures. As predicted, the number of FAs made on run 2 was

somewhat higher following anxious mood induction (mean = 4.31, SD = 2.99)

compared to neutral mood induction (mean = 3.75, SD = 2.54), however, a 2 (LSHS-R

Group: high, low) x 2 (Mood Induction: neutral, anxiety) ANOVA showed that this

difference was not statistically significant, F (1,57) = 2.41, MSE = 3.89, p = .126. Note

that the main effect of LSHS-R group in this analysis is in essence the same test as the

one-tailed t-test reported in the Intentional Inhibition and Hallucination Predisposition

section above, and thus, will not be repeated again here. The interaction of mood

induction and LSHS-R group was non-significant, suggesting that anxious mood did not

differentially affect the high and low LSHS-R groups‟ inhibitory performance on the

ICIM task (see Table 2 for details). A 2 (LSHS-R Group: high, low) x 2 (Mood

Induction: neutral, anxiety) ANOVA on the number of Hits made on run 2 revealed no

significant effects, indicating that target detection was similar in both LSHS-R groups

and not differentially affected by mood induction (see Table 2 for group means).


To investigate the effects of mood induction on RTs for encoding and

recognition of novel neutral pictures, a 2 x (LSHS-R Group: high, low) x 2 (Mood

Induction: neutral, anxiety) x 2 (Response: CR, Hit) ANOVA was conducted using

participants‟ median RTs for correct responses on run 1 (see Table 2 for details). No

main effects were significant, however, the LSHS-R Group x Response interaction

effect was significant, F (1,59) = 6.14, MSE = 2875.67, p < .05. Post-hoc t-tests

conducted within each group showed that there was a significant difference between CR

and Hit RTs for the high LSHS-R group only, with this group making Hits significantly

faster than CRs, F (1,27) = 7.09, MSE = 2144.22, p < .05. Furthermore, the Mood

Induction x Response interaction effect was also significant, F (1,59) = 5.17, MSE =

967.18, p < .05. Post hoc paired t-tests showed that RTs for CR were slower during the

anxious (mean = 739.44, SD = 92.85) than the neutral (mean = 720.61, SD = 91.85)

mood induction, whilst the mood induction conditions did not have significantly

different effects on RTs for Hits. Given the significant LSHS-R group differences on

Chapter 5

134

PDI and DASS-trait Anxiety scores, to test the specificity of these findings, the main

analysis was repeated with these scores included as covariates. When DASS-trait

Anxiety was included as a covariate, the results did not change. However, when PDI

scores were added as a covariate, the Mood Induction x Response interaction effect was

no longer significant (all other effects remained unchanged).


To investigate the effects of mood induction on RTs when inhibition demands

were introduced to the task, a 2 x (LSHS-R Group: high, low) x 2 (Mood Induction:

neutral, anxiety) x 2 (Response: CR, Hit) ANOVA was conducted using participants‟

median RTs for correct responses on run 2 (LSHS-R group means and SDs are reported

in Table 2). As expected, given the introduced inhibition demands, the Response main

effect was significant (F (1,58) = 13.55, MSE = 3376.90, p < .05), with participants

responding slower to make a CR (mean = 777.12, SD = 81.43) than a Hit (mean =

747.28, SD = 75.50) overall. No other effects were significant.

Trait Anxiety and Intentional Inhibition in Run 2

DASS-trait anxiety was significantly correlated with the number of FAs made

on run 2 of the ICIM task (r = .34, p < .05, N = 59) but not run 1 (r = .08, p > .05, N =

59) following anxious mood induction, though not following neutral mood induction

(FA run 2 r = .16, p > .05, N = 59; FA run 1 r = .10, p > .05, N = 59). This correlation

remained significant when controlling for current state anxiety (VAMS post-anxiety

induction rating; partial r = .36, p < .05, N = 55). Interestingly, this correlation also

remained significant when LSHS-R scores were controlled for (partial r = .30, p < .05,

N = 55), suggesting that hallucination predisposition and trait anxiety have independent

relationships with intentional inhibition.

DISCUSSION

The current study successfully replicated the primary finding reported by Paulik

et al. (2007) of intentional inhibition difficulties in hallucination predisposed

individuals. Overall, the high LSHS-R group made significantly more FAs on the

inhibitory run – but not on run 1 – than the low LSHS-R group. However, there were

Chapter 5

135

several differences of note regarding the additional inhibition-related indices between

the current study and our previous predisposition study. Although all participants were

slower to correctly reject distractors than to correctly identify targets (Hits) on the

inhibitory run in the current study, unlike in our previous study (Paulik et al., 2007), this

was not unique to the high LSHS-R group, and furthermore the high LSHS-R group was

not significantly slower to make a CR on the inhibitory run than the low LSHS-R group,

both of which we would expect if intentional inhibition difficulties also slow inhibition

(when successful) in hallucination predisposed individuals. These discrepancies in

findings may be attributable to the reduction in the number of runs from 3 (in Paulik et

al., 2007) to 2 (in the present study), which was done to permit two administrations and

so that the task would be short enough not to outlive the duration of the mood

manipulation effects. This modification may have decreased the sensitivity of the task to

individual differences in inhibitory ability, since the amount of exposure to – and thus

salience of – each item increases across the runs.

The present study also utilized a mood induction procedure in order to examine

whether high levels of anxiety caused a reduction in the intentional inhibitory ability of

healthy non-clinical individuals, and whether this effect is similar for high- and low

hallucination predisposed individuals. The music mood induction procedure was found

to be reasonably effective in engendering anxious and neutral mood states: both LSHS-

R groups were equally sensitive to the procedure, and the effects were specific to

anxiety (not negative affect in general). However, it must be noted that the duration and

magnitude of the mood induction effects were modest – a common problem with mood

induction designs – which limits the conclusions which can be drawn from the results.

The current study did not find any strong evidence that state anxiety impairs

intentional inhibition in healthy individuals, irrespective of their hallucination

predisposition. Specifically, participants did not make significantly more FAs and were

not significantly slower to make CRs on run 2 in the anxious condition than in the

neutral condition. Given the modest magnitude and limited duration of the mood

manipulation, these findings must be taken with caution. In particular, it must be noted

that the pattern of FA means was in the predicted direction for both LSHS-R groups,

leaving open the possibility that much higher levels of anxiety may have led to impaired

inhibitory performance.

With respect to the third aim of the current study, the absence of a significant

interaction between LSHS-R group and mood induction condition in the analysis of FA

run 2 data suggests that individuals who are predisposed to hallucinatory-type

Chapter 5

136

experiences are no more susceptible to the influence that anxiety has on intentional

inhibition (if any) than non-predisposed individuals. Despite the absence of significant

effects involving mood state on cognitive performance, it will be important for future

research to investigate whether anxiety influences other cognitive processes found to be

involved in AHs, such as context memory (Anderson & Shimamura, 2005; Waters,

Badcock, & Maybery, 2006) and reasoning (Allen et al., 2005), since studies have

clearly shown state anxiety to be involved – at some level – in the onset of AHs (e.g.,

Delespaul et al., 2002).

Somewhat surprisingly, the most interesting findings concerning anxiety arose

from the analysis of trait anxiety. Trait anxiety was found to correlate significantly with

FAs made on the inhibitory run (but not run 1) of the anxious mood condition. This

relationship was independent of state anxiety. Indeed, the majority of studies that have

documented a link between anxiety and inhibitory impairments have compared high and

low trait anxious individuals, or clinically anxious and control participants (e.g., Amir,

Coles, Brigidi, & Foa, 2001; Amir et al., 2002; Badcock et al., 2007; Enright & Beech,

1993; Hopko et al., 1998; Wood et al., 2001). The current study‟s finding suggests that

the inhibition impairments previously documented in clinically anxious individuals may

be related to their anxious disposition, rather than their characteristically high levels of

state anxiety, potentially explaining the absence of significant mood related effects on

the ICIM task in the current study. High trait anxious individuals are said to be

characterised by the propensity to believe that intrusive cognitions (varying from

reoccurring unwanted thoughts to AHs) should and must be controlled, and thus, make

intentional efforts to suppress them (Wells & Carter, 2001). However, it has been well

established that most intentional efforts to suppress unwanted cognitions are

unsuccessful; paradoxically, such intentional efforts often increase the availability – and

thus, frequency – of the unwanted cognition (Wegner & Zanakos, 1994). This may

explain the relationship between trait anxiety and intentional inhibition found in the

current study. We make no speculation however as to which may arise first – the

anxious predisposition (and accompanying beliefs about the necessity to control

intrusive cognitions) or poor intentional inhibitory control – since the relationship is

most likely bi-directional, both maintaining the other. Finally, the correlation between

trait anxiety and intentional inhibition remained significant when controlling for

hallucination predisposition, suggesting that hallucination predisposition and trait

anxiety have independent relationships with intentional inhibition. Thus, it may be that

individuals with a high anxious disposition are characterised by poor inhibitory control,

Chapter 5

137

which, when coupled with additional impairments such as context memory binding

(Waters, Badcock, Michie, & Maybery, 2006), may lead to an increased risk of

hallucinatory experiences. However, the independent nature of these relationships

suggests that the inhibitory difficulties experienced by hallucination predisposed

individuals are not always linked to an anxious predisposition, and vice versa.

The current study has several limitations to note. A limitation that has already

been highlighted is that the duration and magnitude of the mood induction effects were

modest, and thus, the level of arousal required to have an effect on cognition may not

have reached a critical threshold (especially near the end of the task). Indeed, previous

mood induction studies have found that the effects of mood on cognition are most

prominent for the individuals for whom the mood induction elicits the highest level of

anxiety (e.g., Gray, 2001). Finally, the ICIM task may not have been challenging

enough to detect anxiety‟s effect on inhibitory performance. Wood, Mathews and

Dalgleish (2001) found that high trait anxious individuals had difficulties resisting

interference from distracting information, but only when there was an increase in mental

load due to dual processing demands. However, the second run of the ICIM does

require multiple cognitive operations, since the participants are explicitly instructed to

forget the previous-run items while simultaneously having to perform the continuous

recognition task.

Although more research is required to establish the role of state and trait anxiety

in the onset and maintenance of hallucinatory experiences, the clinical implications

from the current study‟s findings should not be overlooked. The current study did not

find evidence that state anxiety impairs intentional inhibition, suggesting that state

anxiety does not substantially contribute to hallucinatory-type experiences in the

healthy population by causing or exacerbating inhibitory control difficulties. This

suggests that anxiety must be influencing the predisposition for hallucinatory

experiences through additional neuro-cognitive mechanisms, and thus, interventions for

voice hearers may be most effective if both anxiety management and cognitive control

strategies (to replace unhelpful compensatory coping strategies, such as suppression) are

targeted. It will be important for further research to investigate the relationships

between hallucinatory experiences, inhibition, and anxiety in individuals with

schizophrenia, since the operational relations between these three variables may differ

in individuals who have developed full blown psychotic symptoms.

Chapter 5

138

ACKNOWLEDGEMENTS


funding from the Ron and Peggy Bell Foundation. We also thank Sophie Dosvik and

Dana Sidoruk for their help with the testing of participants, Prof. Colin MacLeod for his

contribution to the interpretation of the mood induction outcomes, Matt Huitson for his

help with task programming, and Joyce Chong for providing the music excerpts.

Chapter 5

139

REFERENCES

Albersnagel, F. A. (1988). Velten and musical mood induction procedures: A

comparison with accessibility of thought associations. Behaviour Research and

Therapy, 26, 79-96.





Alpert, M., & Silvers, K. N. (1970). Perceptual characteristics distinguishing auditory

hallucinations in schizophrenia and acute alcoholic psychoses. American








Anderson, L., & Shimamura, A. P. (2005). Influences of emotion on context memory

while viewing film clips. American Journal of Psychology, 118, 323-337.







Barkley, R. A. (1997). Behavioral inhibition, sustained attention, and executive

functions: Constructing a unifying theory of ADHD. Psychological Bulletin,

121, 65-94.

Bentall, R. P., & Slade, P. D. (1985a). Reality testing and auditory hallucinations: A

signal detection analysis. British Journal of Clinical Psychology, 24, 159-169.

Bentall, R. P., & Slade, P. D. (1985b). Reliability of a scale measuring disposition


527-529.

Chapter 5

140

Cella, D. F., & Perry, S. W. (1986). Reliability and concurrent validity of three visual-

analogue mood scales. Psychology Report, 59, 827-833.



9, 206-212.

Clark, D. M. (1983). On the induction of depressed mood in the Laboratory: Evaluation

and comparison of the Velten and musical procedures. Advances in Behaviour

Research and Therapy, 5, 27-49.



Psychology, 37 173-188.




Dorahy, M. J., McCusker, C. G., Loewenstein, R. J., Colbert, K., & Mulholland, C.

(2006). Cognitive inhibition and interference in dissociative identity disorder:

The effects of anxiety on specific executive functions. Behaviour Research and

Therapy, 44, 749-764.


compulsive disorder. British Journal of Clinical Psychology, 32, 67-74.

Gray, J. R. (2001). Emotional modulation of cognitive control: Approach-withdrawal

states double-dissociate spatial from verbal two-back task performance. Journal

of Experimental Psychology: General, 130, 436-452.




Hustig, H. H., & Hafner, R. J. (1990). Persistent auditory hallucinations and their

relationship to delusions and mood. Journal of Nervous and Mental Disease,

178, 264-267.

Kreindler, D., Levitt, A., Woolridge, N., & Lumsden, C. J. (2003). Portable mood

mapping: The validity and reliability of analog scale displays for mood

assessment via hand-held computer. Psychiatry Research, 120, 165-177.



Chapter 5

141

Lovibond, P. F. (1998). Long-term stability of depression, anxiety, and stress

syndromes. Journal of Abnormal Psychology, 107, 520-526.





Nayani, T. H., & David, A. S. (1996). The auditory hallucination: A phenomenological

survey. Psychological Medicine, 26, 177-189.








470.

Peters, E., Joseph, S., Day, S., & Garety, P. (2004). Measuring delusional ideation: The

21-item Peters et al. Delusions Inventory (PDI). Schizophrenia Bulletin, 30,

1005-1022.







265-272.

Shackman, A. J., Sarinopoulos, I., Maxwell, J. S., Pizzagalli, D. A., Lavric, A., &

Davidson, R. J. (2006). Anxiety selectively disrupts visuospatial working

memory. Emotion, 6, 40-61.

Shapiro, K. L., & Lim, A. (1989). The impact of anxiety on visual attention to central

and peripheral events. Behaviour Research and Therapy, 27, 345-351.

Slade, P. D. (1972). The effects of systematic desensitisation on auditory hallucinations.


Chapter 5

142

Slade, P. D. (1973). The psychological investigation and treatment of auditory

hallucinations: A second case report. British Journal of Medical Psychology, 46,

293-296.






215.

Stober, J. (1997). Trait anxiety and pessimistic appraisal of risk and chance. Personality

and Individual Differences, 22, 465-476.

Szekely, A., D'Amico, S., Devescovi, A., Federmeier, K., Herron, D., Iyer, G., et al.

(2003). Timed picture naming: Extended norms and validation against previous

studies. Behavior Research Methods Instruments and Computers, 35, 621-633.

Szekely, A., Jacobsen, T., D'Amico, S., Devescovi, A., Andonova, E., Herron, D., et al.

(2004). A new on-line resource for psycholinguistic studies. Journal of Memory

and Language, 51, 247-250.



Walsh, E., Harvey, K., White, I., Manley, C., Fraser, J., Stanbridge, S., et al. (1999).

Prevalence and predictors of parasuicide in chronic psychosis. UK700 group.


Waters, F. A. V., Badcock, J. C., & Maybery, M. T. (2006). The 'who' and 'when' of





Research, 62, 275-280.








Chapter 5

143

Wells, A., & Carter, K. (2001). Further tests of a cognitive model of generalized anxiety

disorder: Metacognitions and worry in GAD, panic disorder, social phobia,

depression, and nonpatients. Behavior Therapy, 32, 85-102.


Emotion, 1, 166-181.

Chapter 5

144

145

AUDITORY HALLUCINATIONS, INHIBITION

AND ANXIETY IN SCHIZOPHRENIA

146


147


So far, the results of our previous investigations have identified that healthy

individuals predisposed to hallucinations have difficulties with intentional, but not

unintentional, forms of inhibitory control, with intentional inhibition being the only

form of inhibitory control uniquely related to hallucination predisposition. Anxiety has

been empirically linked to inhibitory control difficulties in the literature (e.g., Badcock,

Waters, & Maybery, 2007; Hopko, Ashcraft, Gute, Ruggiero, & Lewis, 1998; Wood,

Mathews, & Dalgleish, 2001), and consistent with this, the findings from Chapter 5

revealed a significant relationship between intentional inhibition and trait anxiety (and a

non-significant pattern of effects of state anxiety on intentional inhibitory control).

Although Badcock and colleagues have already documented a relationship between

intentional inhibition difficulties and auditory hallucinations (AH) in schizophrenia


2003), the relationships between AHs, other forms of cognitive control and anxiety have

not yet been investigated in this clinical population.

Chapter 6 investigates the relationships between different forms of cognitive

control (using the same measures employed in Chapter 3 and 4), anxiety, and

schizophrenia-related symptoms (including AHs) in individuals with schizophrenia. The

cognitive task performance of schizophrenia and control participants was also

compared. Furthermore, the findings from this study permitted speculation regarding

the continuity of cognitive and affective dysfunction across the hallucination

continuum, through the (non-statistical) comparison of the results obtained in Chapter 6

with those reported in previous chapters. This comparison is elaborated on in the

General Discussion.

Due to unforeseeable circumstances, the testing phases of Chapters 5 and 6

overlapped, and thus, the decision of which measures to include in Chapter 6 was based

on previous chapter findings and an analysis of a preliminary data set from the study

reported in Chapter 5 (which unfortunately did not match the final outcomes of the

study). Thus, a measure of state (not trait) anxiety was administered. This decision was

also made with the knowledge that state anxiety has been found to increase immediately

prior to the onset of a hallucinatory episode, implicating a role in AH production

(Delespaul, deVries, & van Os, 2002).


148

REFERENCES















Research, 62, 275-280.


Emotion, 1, 166-181.

Chapter 6

149

Chapter 6

Inhibitory dysfunction, anxiety and auditory hallucinations 1

ABSTRACT

Intentional inhibition impairments have been associated with auditory

hallucinations (AHs) in schizophrenia and hallucination predisposition in healthy

individuals and may explain their intrusive/uncontrollable nature. Anxiety has been

strongly linked to intrusive cognitions and may contribute to this impairment. The aims

of this study were to dissociate the critical component(s) of inhibitory control

specifically related to AHs and to investigate the role of anxiety in these difficulties.

Two measures of intentional control and one measure of automatic inhibition were

administered to schizophrenia (N = 61) and healthy control (N = 34) participants.

Schizophrenia participants were impaired on intentional resistance to interference but

not intentional or unintentional inhibition. However, AH severity (but not delusions or

negative symptoms) specifically correlated with intentional inhibition. Anxiety was

positively correlated with both AH severity and intentional inhibition. These findings

support a specific deficit of intentional inhibition underlying AHs in schizophrenia. The

data also provides evidence that anxiety may exacerbate (though cannot entirely account

for) impairments in intentional inhibition. Finally, the findings suggest that anxiety also

contributes to AH severity via a separate, as yet unknown, mechanism.

Keywords: Schizophrenia; Auditory hallucinations; Cognitive inhibition; Anxiety


(2007). Inhibitory dysfunction, anxiety and auditory hallucinations. Manuscript submitted for

publication (October 2007).

Chapter 6

150

By definition, auditory hallucinations (AHs) are intrusive, unwanted, and

uncontrollable mental events that interrupt ongoing reality (Morrison, 2005). In this

regard, they can be conceptualised as a type of unwanted mental intrusion. However,

one thing that differentiates AHs from both other types of intrusive cognitions (which

include thoughts, images or impulses) experienced by healthy non-clinical individuals

as well as the unwanted intrusions characteristic of particular clinical populations (such

as posttraumatic-stress disorder (PTSD) and obsessive-compulsive disorder (OCD);

Clark & Rhyno, 2005), is that they are perceived as being of non-self origin (Morrison,

2005). Nevertheless, given the commonalities, it seems plausible that the cognitive

mechanism/dysfunction underpinning everyday unwanted mental events may also

contribute to the experience of AHs. Empirical findings suggest that both clinical and

everyday intrusive cognitions are a product of poor inhibitory control (Amir, Coles, &

Foa, 2002; Badcock, Waters, & Maybery, 2007; Friedman & Miyake, 2004; Kramer,

Humphrey, Larish, Logan, & Strayer, 1994; Schnider & Ptak, 1999). It is interesting to

note therefore that recent empirical studies have also provided evidence tying

intentional inhibitory impairments to an increase in severity of hallucinations in

schizophrenia (Badcock, Waters, Maybery, & Michie, 2005; Waters, Badcock,

Maybery, & Michie, 2003) and heightened predisposition to hallucinations in healthy

individuals (Paulik, Badcock, & Maybery, 2007).

Badcock and colleagues recently developed - and have provided empirical

support for - a dual-deficit model of AHs (Badcock et al., 2005; Waters, Badcock,

Michie, & Maybery, 2006), which contends that at least two cognitive deficits are

critical to experiencing AHs: an intentional inhibition deficit (Badcock et al., 2005;

Waters et al., 2003) and a deficit in binding of contextual memory (Waters, Maybery,

Badcock, & Michie, 2004). This model posits that a failure to intentionally inhibit

irrelevant thoughts and memories results in this information intruding into

consciousness, which may explain the shared features of AHs and other types of

intrusive cognitions. According to the model, these intrusive cognitions are

subsequently misidentified as being of non-self origin because the contextual

information that is required for correct recognition and identification is incomplete due

to a deficit in contextual binding, accounting for the source attribution difference

between AHs and other intrusive cognitions (Badcock et al., 2007). According to this

model, the cognitive control difficulties involved in producing AHs operate on a

strategic, intentional level, which, according to the inhibition taxonomy developed by

Harnishfeger (1995), is defined as ‘cognitive intentional inhibition’. According to

Chapter 6

151

Harnishfeger’s (1995) taxonomy, inhibitory processes can be categorised according to

three dimensions: (1) cognitive (controlling mental processes) or behavioural

(controlling impulses or motor responses); (2) intentional (consciously suppressed) or

unintentional (automatically suppressed); and (3) inhibition (an active suppression

process operating in working memory) or resistance to interference (a gating

mechanism that prevents irrelevant information from entering working memory).

Two of our most recent studies aimed to dissociate the components of

inhibitory control that are related to hallucination predisposition (Paulik et al., 2007;

Paulik, Badcock, & Maybery, 2008).We found that healthy individuals highly

predisposed to hallucinatory-like experiences exhibited a similar difficulty to

hallucinating individuals with schizophrenia on the Inhibition of Currently Irrelevant

Memories (ICIM) task, which requires the intentional inhibition of previously – but not

currently – relevant items (Paulik et al., 2007). Paulik et al (2008) then examined

whether this intentional inhibition impairment was rooted in difficulties with (a) any

intentional cognitive control process (irrespective of whether it involves inhibition or

resistance to interference), (b) any process involving inhibition rather than interference

control (irrespective of whether it is intentional or unintentional in nature), or (c) only

those processes that are both intentional and involve inhibition. This was achieved by

administering two cognitive tasks that differentially measured intentional resistance to

interference (directed ignoring [DI] task) and unintentional inhibition (Brown-Peterson

[B-P] task; Kane & Engle, 2000) to the same sample of high and low hallucination

predisposed participants tested on the intentional inhibition (ICIM) task (as reported in

Paulik et al., 2007). Whilst there was evidence that poor intentional resistance to

interference is linked to positive symptoms of psychosis in general, the main conclusion

was that hallucination predisposition is related to cognitive control difficulties that are

both intentional and involve inhibition (Paulik et al., 2008). Such an approach has not

yet been attempted in the investigation of schizophrenia. Consequently the current study

was designed to test the notion that the severity of hallucinations in individuals with

schizophrenia is linked to impaired intentional inhibition but is not related to

unintentional inhibition, by using the same range of cognitive control measures used in

our previous studies of hallucination predisposition.

Chapter 6

152

Anxiety and Inhibitory Control

High levels of anxiety have been shown to increase task-irrelevant unintentional

intrusive cognitions (e.g., Freeston et al., 1994; Hackmann, Surawy, & Clark, 1998),

and several of the anxiety disorders are characterised by intrusive cognitions. For

example, PTSD is characterised by intrusive recollections and flashbacks of the

experienced trauma (including thoughts, images and perceptions), and OCD is

characterised by intrusive and persistent thoughts, impulses, and/or images (World

Health Organization [WHO], 1993). Consequently, it is not surprising that these

disorders, and anxiety in general, have also been linked to impaired inhibitory control.

However, anxiety has not been found to relate to all types of inhibitory processes.

Anxiety has been empirically linked to both intentional resistance to interference (e.g.,

Amir et al., 2002; Hopko, Ashcraft, Gute, Ruggiero, & Lewis, 1998; Wood, Mathews,

& Dalgleish, 2001) and intentional inhibition (Badcock et al., 2007) - although the latter

has only been investigated in a sample of OCD participants, and thus it remains

unknown whether anxiety relates to this form of inhibitory control in individuals

without an anxiety disorder. In contrast, unintentional forms of inhibitory control have

not been empirically linked to anxiety (e.g., Heinrichs & Hofmann, 2004). Therefore,

any examination of the proposed link between intentional cognitive control and the

severity of auditory hallucinations must investigate the influence of variations in

anxiety. This is particularly important in view of the substantial evidence directly

linking anxiety and auditory hallucinations (Freeman & Garety, 2003).

Anxiety and Auditory Hallucinations

It has been consistently reported in the literature that heightened levels of

anxiety are common in hallucinating individuals with schizophrenia (e.g., Norman,

Malla, Cortese, & Diaz, 1998), and in fact anxiety has even been found to predict the

development of schizophrenia and the onset of hallucinations in at-risk individuals (e.g.,

Tien & Eaton, 1992). Furthermore, a recent time-sampling study found that

hallucinating individuals with schizophrenia reported a rise in their anxiety levels

immediately prior to the onset of a hallucinatory episode, with anxiety returning to a

baseline level shortly after the cessation of the episode (Delespaul, deVries, & van Os,

2002). Whilst it is generally accepted that heightened anxiety is not necessary for

Chapter 6

153

hallucinations to occur, such findings suggest that it may play an important role in the

onset and/or maintenance of hallucinatory experiences. Based on the studies reviewed

above, it seems plausible that anxiety may affect the severity of AHs by exacerbating

existing cognitive control difficulties. Thus, the second aim of the current study is to

investigate the relationship that anxiety has with inhibitory processes and schizophrenia

symptomatology.

Hypotheses

The current study was designed to test the hypotheses that (a) schizophrenia

participants will perform more poorly than control participants on intentional – but not

unintentional - cognitive control measures due to the high prevalence of positive

symptoms (which are linked to these cognitive control difficulties); (b) within the

schizophrenia group, intentional inhibition (as measured by the ICIM task) will

correlate positively with the severity of AHs, but not delusions or negative symptoms;

(c) within the schizophrenia group, intentional resistance to interference (as measured

by the DI task) will correlate positively with both positive symptom scores (namely,

AHs and delusions), but not negative symptoms; and (d) within the schizophrenia

group, unintentional inhibition (as measured by the B-P task) will not correlate with any

of the schizophrenia symptom measures. With regard to the second aim of the study we

hypothesize that (a) anxiety will correlate positively with intentional – but not

unintentional – cognitive control measures; and (b) anxiety will also correlate positively

with the severity of AHs, but not delusions or negative symptoms. Furthermore, we

intend to explore the interrelationships between anxiety, cognitive control, and

schizophrenia-related symptoms.

METHOD

Participants

Sixty nine individuals meeting International Classification of Diseases (ICD-10;

WHO, 1993) criteria for schizophrenia (n = 57) or schizoaffective disorder (n = 12)

were recruited through the Centre for Clinical Research in Neuropsychiatry (CCRN)

from Graylands Hospital and related outpatient clinics and hostels in Perth, Western

Australia. Two schizophrenia participants were subsequently excluded because the

Chapter 6

154

diagnosis provided by their treating psychiatrist was not confirmed at interview

(according to ICD-10 criteria) at the time of testing. Control participants were 39

healthy individuals who had participated in previous research at CCRN, and were

initially recruited from the Perth community via a random telephone recruitment

screening procedure set up at CCRN. Inclusion criteria for all participants included

fluency in English (attended an English speaking school since age 6), and being aged 18

– 60 years. The exclusion criteria for all participants included hospital admission for a

drug or alcohol rehabilitation program within the past 12 months, poor visual acuity

(compromising task performance), neurological disorders, serious head injury, and a

pre-morbid full-scale IQ (estimated from the National Adult Reading Test – 2nd

edition

[NART]; Nelson & Willison, 1991) below 75. Additional exclusion criteria for control

participants included a personal or family history of bipolar disorder or any form of

psychosis, a current diagnosis of OCD, PTSD (ascertained at interview), or Attention-

Deficit Hyperactivity Disorder (self-report)2. Participants were not excluded for other

unrelated psychological disorders. Based on these criteria, six schizophrenia participants

and five control participants were excluded from the study. Of the remaining

participants, there were 12 females and 49 males in the schizophrenia group (47 right

handed, 7 left handed, 7 ambidextrous), and six females and 28 males in the control

group (26 right handed, 3 left handed, 5 ambidextrous). Of the schizophrenia

participants, 88.5% were taking antipsychotic medications (69% atypicals only, 8%

typicals only, and 11.5% typicals and atypicals) and 84% were out-patients at the time

of testing.

Measures

Inhibition of Currently Irrelevant Memories (ICIM) Task (Schnider, Valenza, Morand,

& Michel, 2002)

The ICIM task is a repeated continuous recognition memory task involving three

runs in the current version (Paulik et al., 2007). In each run, 85 black and white line

drawings (Snodgrass & Vanderwart, 1980) were presented serially on a computer screen

2 Empirical studies have reported cognitive inhibition deficits in samples of ADHD, OCD and

PTSD individuals (e.g., Amir et al., 2002; Badcock et al., 2007; Barkley, 1997); thus, to reduce

the noise in the control group, this was included as an exclusion criteria. There were no

incidents reported in case notes of current ADHD, OCD or PTSD in the schizophrenia group.

Chapter 6

155

from which the participant had to detect those pictures that were repeated (targets).

Repeated presentation is assumed to increase the strength of activation of the internal

representation (memory trace). Each picture was presented for 2 s, with a 700 ms

interstimulus interval. Some of the pictures were shown only once (28), and others were

shown two (6) or three times (15) in a run; yielding 49 distractors (first presentations)

and 36 targets (21 second presentations and 15 third presentations) in each run.

Participants responded as accurately and rapidly as possible (by pressing keys marked

‘yes’ or ‘no’) whether each picture had or had not already been presented within the

current run. There was a 30 s break between runs 1 and 2, and a 5 minute break

between runs 2 and 3. The second and third runs consisted of the same set of pictures

used in run 1, however the pictures selected as targets and the order changed. On the

second and third runs participants were explicitly asked to forget that they had already

seen the pictures and to identify repeated pictures within the current run only. Thus,

performance on run 1 requires encoding and recognition only, whilst runs 2 and 3 also

demand the intentional suppression of responses to targets from previous runs.

Intentional inhibition is reflected in the number of false positive responses (false alarms:

FAs) made on runs 2 and 3, that is, the number of first presentations on the current run

mistaken as targets. However, FAs on run 1 were also examined, since they reflect

recognition ability. General recognition was measured by the number of correctly

identified targets (Hits) made on all three runs.

Directed Ignoring (DI) Task (Connelly, Hasher, & Zacks, 1991)

In our modified version of the conventional DI task, participants read aloud 14

short stories (two practice and 12 test stories), with or without distractor text. There

were three conditions (four test stories in each): control, distractor-new, and distractor-

old. The two distractor conditions were developed to examine whether the previous

relevance of the to-be-ignored text differentially impacted on schizophrenia and control

participants’ ability to resist interference. In each condition, participants were instructed

to read aloud only target text - printed in italicised font (20-point Arial). In the distractor

conditions, an unrelated story printed in regular (non-italicised) font was interwoven

into the target story passage, such that the flow of target text was disrupted by the

insertion of a segment of distractor text, with the first word of distracting text fitting

with the sentence flow of target text. In the distractor-old condition, the distractor story

was the story that had been read (target) in the previous passage. Half of the distractor-

Chapter 6

156

old stories followed stories read in the control condition, and half followed stories read

in the distractor-new condition. In the distractor-new condition, the distracting story had

never been read before. In the control condition, blank spaces matching the average

length of a distracting text section were inserted into the passages to control visual

scanning requirements between conditions. Target and distractor stories were matched

on length (125 words, comprising between 7 and 10 sentences), and sections of target

and distractor text were 3-9 words in length. After each story, participants were

presented with two multiple-choice questions to assess comprehension, each with four

alternative answers (all plausible, though only one correct). Each comprehension

question had part of the distractor story’s content as a plausible, but incorrect, response

choice (a foil). The order in which the stories were presented was counterbalanced

across participants. The indices of intentional resistance to interference were reading

time (control and distractor stories) and reading time interference (RT-Interference: the

difference between distractor reading time and control reading time), intrusions (the

number of distractor text sections read aloud on each distractor story, including sections

that were only partially read aloud, summated across stories), and the percentage of foils

(of the total incorrect responses) chosen on the multiple-choice questions. Overall

accuracy on the multiple-choice questions was used to assess text comprehension.

Brown-Peterson Variant (B-P) Task (Kane & Engle, 2000)

This task was included as a measure of unintentional inhibition. In this task,

participants read aloud and attempted to recall three lists of words, each list comprising

of ten serially presented words (at a rate of one word every 2 s) on a computer screen

(see Paulik et al., 2008, for details). All lists within a block were comprised of words

from the same semantic category (either four-footed animals, occupations, or fruits),

and all lists were matched for average word length and frequency (Battig & Montague,

1969). After each list, a distractor task was performed for 15 s. Participants were

required to count backwards by two’s from a number presented on the screen, at a pace

set by an auditory signal every 1500 ms. Participants were then asked to recall aloud as

many words from the previous list as possible in any order in 20 s. To ensure that

participants were not actively rehearsing items during the distractor task, participants

with a counting accuracy rate of less than 70% were excluded. Four schizophrenia

participants’ results were excluded from the analysis of this task accordingly. In this

type of unintentional inhibition task, the participant must automatically inhibit memory

Chapter 6

157

intrusions of previously learnt – but no longer relevant – items (from previous lists)

when recalling new items belonging to the same category (Solso, 1995). Thus, the

cognitive overflow of [within block] previous list items increases from list one (no

overflow) to list three (maximum overflow). Inhibition was measured by the summated

accuracy of recall (across blocks) of each of the three lists (which we expect to decrease

from list 1 to 3) in the analyses directed at group comparisons and list 1 recall minus list

3 recall (which we had termed B-P Inhibition) in correlational analyses.

Clinical Interviews

Diagnosis for the schizophrenia group was confirmed using the Diagnostic

Interview for Psychosis (DIP; Castle et al., 2006). Items from the DIP were compiled to

obtain a current delusion score with a score range of 0 – 8 (items included in this score

were Thought Insertion, Thought Broadcast, Thought Withdrawal, Delusions of

Passivity, Delusions of Influence/Reference, Grandiose Delusions, and Bizarre

Delusions), and a current negative symptom score with a score range of 0 – 6 (items

included in this score were Restricted Affect, Blunted Affect, Rapport Difficult to

Establish, Thought Blocking, Poverty of Speech, and Restricted Quantity of Speech).

The auditory hallucinations (AH) subscale from the Psychotic Symptom Rating Scales

(PSYRATS; Haddock, McCarron, Tarrier, & Faragher, 1999) is an 11-item interview

(each item is rated on a 5-point rating scale, from 0 to 4) from which an AH severity

score (based on frequency, duration and loudness) was obtained (Haddock et al., 1999)

for those participants who reported hearing voices during the past four weeks (which is

the time frame stipulated by the PSYRATS). Haddock et al’s (1999) previous factor

analysis study showed that each item on the AH severity scale had a high factor loading

(.53 to .78) and excellent inter-rater reliability (0.98 to 1). The short version of the Mini

International Neuropsychiatric Interview (MINI; Sheehan et al., 1997) was administered

to control participants to screen for psychological disorders, including schizophrenia.

Additional Measures

Pre-morbid full-scale IQ was estimated from the NART (Nelson & Willison,

1991). The Digit Span subtest of the Wechsler Adult Intelligence Scale – 3rd

edition

(WAIS-III; Wechsler, 1997) was used as a measure of working memory. State anxiety

Chapter 6

158

was measured with the 7-item anxiety subscale of the Hospital Anxiety Depression

Scale (HADS; Zigmond & Snaith, 1983), which has a score range of 0 - 21.

Procedure

Ethics approval for the project was obtained from the North Metropolitan Area

Mental Health Service Ethics Committee. The DI task was administered last in the

cognitive testing session because some participants found the task difficult and/or tiring,

which occasionally resulted in task non-completion. Testing took approximately 2 hours

for control participants and 3 hours for schizophrenia participants. Control participants

were offered $20 and schizophrenia participants $25 for reimbursement of

time/expenses.

Data Analysis

The design and approach to data analysis adopted in the current study follows

the analyses carried out in Waters et al.’s (2003) schizophrenia study. The first round of

analyses focused on group level comparisons (schizophrenia vs. control) on the three

cognitive control tasks in order to investigate whether inhibitory difficulties were

present in the schizophrenia sample. Interrelationships between anxiety (measured using

HADS) and the various inhibition indices were investigated across the entire sample

using Pearson’s correlation coefficients. Subsequent to this, correlations between

HADS-Anxiety and symptom scores (PSYRATS-AH and DIP sub-scores) were

computed. The final and most important stage of the data analysis was the investigation

of the relationships between the inhibition indices and the symptom scores, again using

correlations. The latter two correlational analyses were performed within the sample of

actively hallucinating schizophrenia participants (N = 34). This subgroup was used to

maintain sample consistency across all correlations involving schizophrenia-related

symptom scores, since only those schizophrenia participants who reported hearing

voices over the past four weeks could be administered the PSYRATS-AH.

Schizophrenia participants with and without hallucinations did not differ significantly

on any of the variables reported in Table 1, or with regard to antipsychotic medications,

in- versus out-patient status, or DIP symptom scores.

Chapter 6

159

RESULTS


Fifteen single data points were identified as univariate outliers (≥ 3 SDs away

from their respective group mean) and deleted from the data file. The data were scanned

for multivariate outliers using Cook’s distance, and two cases from the schizophrenia

group were identified and subsequently excluded from the analyses that included both

these variables (variables: DIP negative symptom score and ICIM FAs on both runs 2

and 3).

As seen in Table 1, there was no significant difference between the control and

schizophrenia participants on age, however the schizophrenia group had a significantly

lower mean level of education, lower pre-morbid IQ (NART), poorer working memory

(WAIS-III Digit Span), and higher levels of state anxiety (HADS-Anxiety) than the

control group. Consequently, in the following group comparisons where significant

effects were found, these variables were entered into the analyses separately as

covariates to examine any possible confounding effects.

Table 1

Group Means, SDs, and T-tests for the Demographic Characteristics and Additional

Measures

Controls (N = 34) Schizophrenia (N = 61)

t-tests Mean SD Mean SD

Age (yrs) 41.35 11.85 38.00 10.01 1.46

Education a (yrs) 12.56 1.99 11.40 1.88 2.77*

Length of illness (yrs) 15.67 9.23 -

Age of Illness Onset (yrs) 22.33 6.20 -

NART-IQ 109.65 8.80 98.18 10.49 5.38*

Digit Span scaled score 11.62 2.77 8.59 2.43 5.53*

HADS-Anxiety 4.21 3.07 8.77 4.43 5.33*

* p < .05

Note. NART-IQ = full scale WAIS-III IQ estimated from the National Adult Reading

Test; HADS = Hospitalised Anxiety and Depression Scale. a Highest level of education

completed (secondary and tertiary education only).

Chapter 6

160

Schizophrenia- and Control Group Comparisons

ICIM Task Performance

One control participant and four schizophrenia participants did not complete the

ICIM task. As in previous studies, run 1 was analysed separately from the inhibitory

runs (run 2 and 3) (Paulik et al., 2007; Waters et al., 2003). Group means and SDs for

FAs and Hits are presented in Table 2.

Intentional Inhibition (False Alarms: FA)

When a univarite ANOVA was performed on run 1 FAs, no significant group

differences were found, indicating that the schizophrenia and control participants were

equally able to identify and correctly reject novel pictures. A repeated measures

ANOVA performed on FAs made on runs 2 and 3 revealed a significant Run main

effect only (F(1, 83) = 21.36, p < .05), with more FAs being made on run 2 than run 3 in

general. The absence of any significant Group effects indicates that poor intentional

inhibition is not related to schizophrenia in general.

Target Detection (Hits)

When a univarite ANOVA was performed on run 1 Hits, there was a significant

Group main effect (F(1, 88) = 8.89, p < .05), with controls having a higher Hit rate than

individuals with schizophrenia. The effect remained significant when any of the

additional measures were entered separately into the analysis as covariates. Similarly,

repeated measures ANOVA on runs 2 and 3 Hit data also produced a significant Group

main effect (F(1, 85) = 12.03, p < .05), suggesting that overall the schizophrenia

participants had poorer recognition of repeated pictures than the control participants. No

other effects were significant. This Group main effect remained significant when the

additional measures were entered separately into the analysis as covariates.

Chapter 6

161

Table 2

Group Means, SDs, and T-tests for the Performance Indices of the Cognitive Inhibition

Tasks

Controls (N = 34) Schizophrenia (N = 61)

Mean SD Mean SD

ICIM FA Run 1 1.38 1.43 1.43 1.30

ICIM FA Run 2 5.38 2.76 5.91 4.46

ICIM FA Run 3 3.64 2.73 4.87 4.48

ICIM Hit Run 1 a 34.61 1.95 32.96 2.78

ICIM Hit Run 2 31.55 2.77 28.20 3.82

ICIM Hit Run 3 30.73 3.68 28.53 4.85

DI Control RT (s) 43.34 5.41 55.48 10.65

DI Distractor RT (s) 80.54 22.71 112.36 32.70

DI Intrusions 4.88 3.54 15.38 12.19

DI Control Errors b

12.50 9.23 16.08 9.45

DI Distractor Errors b

7.17 8.45 18.69 17.38

DI Foil Errors c 24.07 28.47 25.64 25.55

B-P List 1 Recall 5.99 1.29 4.58 1.28

B-P List 2 Recall 4.13 1.14 2.79 1.07

B-P List 3 Recall 3.26 1.19 1.92 0.91

* p < .05

Note. ICIM = Inhibition of Currently Irrelevant Memories task; B-P = Brown-Peterson

variant task; DI = Directed Ignoring task. a

Maximum number of hits in each run is 36.

bPercentage of incorrect responses on comprehension questions.

c Percentage of foil

errors of total incorrect responses on comprehension questions.

DI Task Performance

Preliminary analyses of the two different distractor story conditions (distractor-

new and distractor-old) showed there was no significant differences between these

conditions on any of the outcome variables, thus, the data from these conditions were

combined in the following analyses. Seven schizophrenia participants did not complete

the DI task.

Chapter 6

162

Reading Time (RT)

Repeated measures ANOVA was used to compare the groups on their reading

time of control and distractor stories. As expected, there was a significant Story main

effect (F(1, 82) = 299.10, p < .05), with all participants taking longer to read the

distractor stories than the control stories, and a significant Group main effect (F(1, 82) =

35.31, p < .05), with schizophrenia patients’ reading times slower than controls’. There

was also a significant Group x Story interaction (F(1, 82) = 16.62, p < .05); examination

of the data showed that whilst schizophrenia participants were significantly slower than

control participants on both story conditions, this difference was greater on the

distractor condition (see Table 2), suggesting that schizophrenia participants were more

sensitive than control participants to the adverse effects of distracting information on

RT. The pattern of results remained the same when any of the additional measures were

entered separately into the analysis as covariates.

Intrusions

A univariate ANOVA conducted on the number of distracting excerpts read

aloud (intrusions), revealed that the schizophrenia participants made more intrusions

than the control participants overall (F(1, 81) = 22.45, p < .05), which remained

significant when the additional variables were entered into the analysis separately as

covariates.

Comprehension

A repeated measures ANOVA comparing the two groups on the percentage of

incorrect responses on the comprehension questions for the control and distractor

conditions, revealed a significant Group main effect (F(1, 82) = 13.86, p < .05), and

Story x Group interaction effect (F(1, 82) = 4.20, p < .05). Post-hoc t-test revealed that

the schizophrenia participants only made significantly more comprehension errors than

the control participants on the distractor stories, suggesting that the two groups’

comprehension was comparable for stories read free of distraction, while the presence

of distracting text compromised the schizophrenia participants’ comprehension more so

than the control participants’. The group main effect remained significant, while the

interaction effect did not, when the additional variables were entered into the analysis

separately as covariates. A univariate ANOVA of foil errors revealed no significant

differences between the groups.

Chapter 6

163

B-P Task Performance

As expected, when a repeated measures ANOVA was conducted on correct list

recall (lists 1- 3), there was a significant List main effect (F(2, 178) = 291.50, p < .05),

with post hoc tests showing that recall progressively decreased across each list,

reflecting the build up of same-category intrusions across lists. As reported in Table 2,

the control participants also correctly recalled significantly more items per list overall

than the schizophrenia participants, F(1, 89) = 42.60, p < .05. The absence of a

significant List x Group interaction effect suggests that schizophrenia participants did

not have unintentional inhibition difficulties relative to control participants. The pattern

of results remained the same when any of the additional measures were entered into the

analysis as covariates.

Correlations between Anxiety and Inhibition Indices

Within the entire sample, HADS-Anxiety correlated significantly with FAs

made on run 3 (r = .24, p < .05, N = 88), but not run 1 (r = .00, p > .05, N = 86) or run 2

(r = .10, p > .05, N = 86) of the ICIM task, suggesting that anxiety relates to intentional

inhibition of previously relevant items, but only when the items are highly salient, since

the number of previous presentations of each item increases across the runs. On the DI

task, HADS-Anxiety was significantly correlated both with RT-Interference (r = .26, p

< .05, N = 84) and the number of intrusions made on the distractor stories (r = .29, p <

.05, N = 82), but not the percentage of foil errors (r = -.03, p > .05, N = 85). On the B-P

task, HADS-Anxiety did not significantly correlate with B-P Inhibition (r = -.13, p >

.05, N = 91). These findings confirm that anxiety is related to intentional, but not

unintentional, forms of cognitive control.

Correlations between Anxiety and Schizophrenia-Related Symptoms

To rule out the possible effects of antipsychotic medication on task performance

in the correlational analyses only involving schizophrenia participants, a

chlorpromazine equivalent dosage score was calculated for each schizophrenia

participant and correlated with all the measures included (British National Formulary,

1995; Woods, 2003). The only significant correlation was found with intrusions made

on the DI task; thus, where correlations involving intrusions were significant, this

Chapter 6

164

dosage was controlled for using partial correlations. The mean score on the severity

component of the PSYRATS-AH was 6.49 (SD = 2.42).

Within the actively hallucinating schizophrenia group, HADS-Anxiety

correlated significantly with the PSYRATS-AH severity score (r = .45, p < .05, N = 34),

and thus, where significant correlations were obtained between AH severity and

inhibition indices below, partial correlations were computed controlling for HADS-

Anxiety. In contrast, HADS-Anxiety did not significantly correlate with either the

delusions symptom score (r = -.04, p >.05, N = 34) or the negative symptoms score (r =

.29, p >.05, N = 34), highlighting the unique relationship between anxiety and auditory

hallucinations.

Correlations between Schizophrenia-Related Symptoms and Inhibition Indices

As reported in Table 3, within the actively hallucinating schizophrenia group,

AH severity correlated significantly with FAs on run 3, but not with FAs on run 1 or run

2 on the ICIM task. This correlation remained significant when partialling out the

effects of HADS Anxiety (partial r = .37 p < .05, N = 29), suggesting that the

relationship between intentional inhibition and hallucination severity is independent of

the relationship these variables have with anxiety. Furthermore, the correlation between

anxiety and AH severity remained significant when controlling for FAs on run 3 (partial

r = .45 p < .05, N = 29), suggesting that anxiety must influence the severity of auditory

hallucinations through additional mechanisms other than intentional inhibition. FAs (on

any of the runs) did not correlate with any other symptom score (see Table 3).

On the DI task, neither RT-Interference, the number of intrusions, nor the

percentage of foil errors correlated significantly with the PSYRATS-AH severity score

or the DIP symptom scores (see Table 3). As reported in Table 3, B-P Inhibition did not

significantly correlate with the PSYRATS-AH severity score or either of the DIP

symptom scores.

Chapter 6

165

Table 3

Pearson Correlations for PSYRATS-AH Severity Score and DIP Symptom Scores and

Inhibition Indices on the Cognitive Inhibition Tasks (N = 33)

AH severity Delusions Negative Symptoms

ICIM FA Run 1 .00 .23 .04

ICIM FA Run 2 .21 -.02 .28

ICIM FA Run 3 .37* -.06 .29

DI RT-Interference a .07 .11 -.05

DI Intrusions -.29 -.04 -.08

DI Foil Errors b -.24 -.14 .11

B-P Inhibition c -.18 -.16 .09

* p < .05

Note. ICIM = Inhibition of Currently Irrelevant Memories task; B-P = Brown-Peterson

variant task; DI = Directed Ignoring task. a Distractor RT minus Control RT.

bPercentage of foil errors of total incorrect responses on comprehension questions.

c B-P

List 1 recall minus List 3 recall.

DISCUSSION

Auditory hallucinations are perceived as being intrusive, unwanted and

uncontrollable (Morrison, 2005). Furthermore, such experiences are typically

accompanied by high levels of anxiety and distress (Norman et al., 1998). Needless to

say, the costs of AHs to the individual can be enormous. The current study aimed to

delineate the cognitive control processes theorised to underpin these features of AHs,

and to investigate how anxiety may relate to these variables.

Consistent with the first set of hypotheses, the schizophrenia group had

difficulty on at least one form of intentional control, namely intentional resistance to

interference (DI task), and were not significantly different from controls on the measure

of unintentional inhibition (BP task). These findings suggest that difficulties in

intentional resistance to interference may play an important role in schizophrenia, which

is broadly consistent with extensive evidence of deficits in executive/volitional

behaviour in this disorder (e.g., Merlotti, Piegari, & Galderisi, 2005; Zec, 1995), whilst

automatic cognitive control processes, including automatic resistance to interference,

appear to remain relatively intact (e.g., Fleming, Goldberg, Gold, & Weinberger, 1995;

Kopp, Mattler, & Rist, 1994; Randolph, Gold, Carpenter, Goldberg, & et al., 1992).

Chapter 6

166

Somewhat surprisingly, no group differences were obtained on the intentional

inhibition (ICIM) task, which is inconsistent with the findings reported by Waters et al.

(2003). This inconsistency is likely to be attributable to the lower number of target

repetitions employed in the version of the task employed in the current study. The

salience (strength of activation of internal representation) of each item in the ICIM task

is assumed to be largely determined by the number of repeated presentations of each

item (Schnider et al., 2002). Since Waters et al. (2003) repeated targets eight times

within each run (whereas targets were repeated a maximum of three times in the current

study)3, their version of the ICIM task would be expected to yield a higher level of

internal activation for target items, which would make previous run targets more

difficult to inhibit. Nonetheless, consistent with our second set of predictions, AH

severity within the schizophrenia group was significantly and positively correlated with

difficulties in intentional inhibition, but was unrelated to difficulties with either

unintentional inhibition or intentional resistance to interference. Specifically, AH

severity was significantly associated with FAs on run 3 of the ICIM task – when item

repetition and associated inhibitory demand is presumed to be at a maximum in this

version of the task. However, a recent study by Badcock and colleagues (2005) tested –

and found support for – the premise that poor intentional cognitive inhibition is not a

general feature of schizophrenia, but rather, is linked to hallucinations specifically. The

current findings lend further support to this idea.

These results suggest that the cognitive control difficulties experienced by

schizophrenia individuals who experience AHs are both intentional (rather than

unintentional) and inhibitory (as opposed to involving resistance to interference) in

nature. The same conclusions were recently reported by us in a study examining

varieties of inhibitory control in healthy young adults predisposed to hallucinations

(Paulik et al., 2007, 2008). Together these findings are consistent with the notion of a

continuum of hallucinatory experiences linked to a common and specific impairment in

3 In our predisposition study (Paulik et al., 2007), we chose to employ the version of the ICIM

task which has fewer target repetitions but more individual targets, since Schnider’s group

(consistent with Waters et al., 2003) found that the former version was too easy for healthy

control participants, and thus, not sensitive to modest individual or group differences within a

non-clinical sample (Schnider et al., 2002). To permit direct comparisons between the findings

obtained from our earlier predisposition study and the current study on the ICIM task, we

decided to also employ this version of the ICIM task.

Chapter 6

167

intentional inhibition, which is not shared with other schizophrenia-related symptoms,

or explained by the co-occurrence of anxiety.

Paulik et al. (2008) reported that increased difficulty with intentional resistance

to interference (as measured by the DI task) was related to sub-clinical positive

symptoms (namely, hallucination-like experiences and delusional beliefs) in healthy

individuals. However, this predicted relationship was not present in the schizophrenia

group in the current study. One possible explanation for this discrepancy may be that

some (though not all) of the cognitive processes leading to clinical and sub-clinical

positive symptoms may be different. However, it is also viable that this discrepancy is

due to the changes made in the DI task stimuli. In our earlier study (Paulik et al., 2008),

distractor text was thematically related to the target text. The current study aimed to

manipulate the previous relevance of the distracting text by using the previous story’s

target text as the distracting text on half of the distractor conditions. This change was

made to make the DI task more similar - and thus comparable - to both the B-P and

ICIM tasks. However, the trade off entailed in this change was that the distractor text

was unrelated thematically to the target passage in the current study. Previous studies

have shown that some populations who experience difficulty with this task (such as the

elderly) have more pronounced difficulty with distracting text that is related to the target

text than that which is unrelated (e.g., Connelly et al., 1991). Thus, it remains possible

that a relationship between positive symptoms and intentional interference control may

be evident if the distractor interference is semantically related to the competing goal-

relevant information.

Inhibitory control aside, it is important to note that the schizophrenia group

made significantly fewer Hits on all runs of the ICIM task and had significantly poorer

recall on all lists of the B-P task than the control group. This is consistent with general

recognition (required for ICIM performance), recall (required for B-P performance) and

working memory difficulties that have been widely documented in the schizophrenia

research literature (see Aleman, Hijman, de Haan, & Kahn, 1999, for review) and is

consistent with the findings of previous schizophrenia studies employing these tasks

(e.g., Badcock et al., 2005; Fleming et al., 1995; Randolph et al., 1992; Waters et al.,

2003). The presence of these memory-based difficulties in the schizophrenia group, in

the absence of inhibition difficulties, highlights the independence of inhibitory

performance from memory functioning on the ICIM and B-P tasks in this sample.

The second aim of the current study was to investigate the relationship that

anxiety has with the other variables of interest. As predicted, it was found that for the

Chapter 6

168

entire sample anxiety was related to intentional inhibition and intentional resistance to

interference – but not unintentional inhibition. In concordance with the general findings

in the anxiety literature (e.g., Badcock et al., 2007; Hopko et al., 1998), the direction of

this relationship was such that individuals with higher levels of self-reported anxiety

had poorer intentional cognitive control than those with lower levels of anxiety. As

expected, anxiety was also significantly correlated with AH severity in schizophrenia

participants with active hallucinations, but not with other symptom scores. Although

anxiety has been linked to positive symptoms in general - but not negative symptoms -

in the schizophrenia literature (e.g., Norman et al., 1998), the few studies that have

separated the different types of positive symptoms have largely reported that the most

robust relationship exists between anxiety and AHs (e.g., Guillem, Pampoulova, Stip,

Lalonde, & Todorov, 2005). Similar to the pattern of relationships found in

hallucination predisposed individuals (Paulik et al., 2007), the relationship between AH

severity and intentional inhibition (reported above) remained significant when the

effects of anxiety were statistically controlled. It is clear that not all individuals who

experience AHs report heightened levels of anxiety immediately prior to a hallucinatory

episode (Delespaul et al., 2002; Freeman & Garety, 2003). However, when present,

anxiety’s functional role (or one of) may be to exacerbate existing deficits of intentional

inhibition, perhaps by driving the inhibitory difficulties over some form of threshold.

Interestingly, the current study also found that the association between anxiety and AH

severity remained significant when controlling for variation in intentional inhibition,

suggesting that anxiety must be contributing to AH severity through other underlying

neuro-cognitive processes, such as context memory (Sison & Mather, 2007), which

have not yet been investigated. This will be an important avenue for future research.

There are potential limitations of the current study. Firstly, as discussed, the DI

task was modified to increase its commonalities with the other cognitive control tasks;

however this has restricted our ability to make comparisons between the current

schizophrenia study and our previous hallucination predisposition study (Paulik et al.,

2008). However, it seems unlikely that group differences seen on the DI task are due to

the greater difficulty of this task. Recognition memory was clearly impaired in the

schizophrenia group on the ICIM task, suggesting that this task was more difficult for

schizophrenia than control participants, yet no differences in FAs occurred. Rather, the

emergence of group differences appears to be determined by the specific underlying

cognitive processes involved. In addition, as in our earlier studies we employed a

measure of state – rather than trait - anxiety since state anxiety has been shown to

Chapter 6

169

increase immediately prior to the onset of a hallucinatory episode, implicating a role in

AH production (Delespaul et al., 2002). However, the majority of studies that have

documented a link between anxiety and inhibitory impairments have compared high and

low trait anxious participants or individuals with clinical anxiety disorders and healthy

controls (e.g., Amir et al., 2002; Badcock et al., 2007; Hopko et al., 1998; Wood et al.,

2001). Future studies should therefore examine that the influence of trait anxiety on the

cognitive control processes involved in auditory hallucinations.

In summary, we have provided further evidence for impaired intentional

inhibition linked to the severity of AHs. Further, we show that anxiety should be

included as an important contributory factor in multifactorial models of hallucination

development. Importantly, we have identified at least one mechanism by which anxiety

exerts its effects; namely, by adding to the existing impairment of intentional inhibition.

Our findings have important clinical implications. In particular, it is clear that treatment

programs targeting hallucinatory-type experiences would be most effective if both

anxiety management and intentional cognitive control strategies were to be targeted.

Furthermore, inclusion into such treatment programs should not discriminate between

individuals who do and do not meet diagnostic criteria for schizophrenia, since our

current and previous findings (Paulik et al., 2007, 2008) suggest that at least some of the

principal cognitive and affective mechanisms underlying hallucinatory-type experiences

span across the continuum. This treatment combination may, therefore, be particularly

important in designing interventions for high risk populations, who commonly exhibit

increased anxiety and isolated symptoms, such as hallucinations, but have not yet

developed fully fledged psychosis.

Summary

Schizophrenia participants overall showed a slective difficulty intentionally resisting

external distractor interference (on the DI task), however overall they did not have

difficulties inhibiting internal cognitions (on either the ICIM or B-P task).

AH severity correlated significantly with the intentional inhibition (ICIM) task, but

not the unintentional inhibition (B-P) task or the intentional resusiatnce to interference

(DI) task. Thus, AHs are linked to cognitive control difficulties that are both

intentional (not unintentional) and inhibitory (not resistance to interference) in nature,

supporting the Badcock et al. model.

This association between AH severity and intentional inhibition was independent of

anxiety and unique to AHs (that is, intentional inhibition was unrelated to

schizophrenia overall or other schizophrenia-related symptoms).

Chapter 6

170

Anxiety correlated significantly with both AH severity and intentional inhibition,

suggesting that anxiety may exacerbate intentional inhibition deficits in hallucinating

individuals. However, anxiety remained significantly associated with AH severity

when controlling for intentional inhibition, suggesting that anxiety must influence

additional mechanisms involved in AH production, such as context memory.

This pattern of associations is similar to that found in hallucination predisposed

individuals (Paulik et al., 2007, 2008), supporting a continuum approach to AHs.

Chapter 6

171

ACKNOWLEDGEMENTS


funding from the Ron and Peggy Bell Foundation. We also thank Sarah Howell, Alan

Bland and Christina Read for assistance with participant recruitment, John Dean for the

on-going DIP training he provided, Matt Huitson for his help with task programming,

and the Western Australia Family Schizophrenia Study for providing NART scores for

participants.

Chapter 6

172

REFERENCES



1366.












121, 65-94.




British National Formulary (1995). British National Formulary. London: British

Medical Association and the Royal Pharmaceutical Society of Great Britain.

Castle, D., Jablensky, A., McGrath, J., Carr, V., Morgan, V., Watterreus, A., et al.

(2006). The Diagnostic Interview for Psychoses (DIP): Development, reliability

and applications. Psychological Medicine, 36, 69-80.









Chapter 6

173

Fleming, K., Goldberg, T. E., Gold, J. M., & Weinberger, D. R. (1995). Verbal working

memory dysfunction in schizophrenia: Use of a Brown-Peterson paradigm.

Psychiatry Research, 56, 155-161.



Therapy, 41, 923-947.


(1994). Health-related intrusive thoughts. Journal of Psychosomatic Research,

38, 203-215.




Guillem, F., Pampoulova, T., Stip, E., Lalonde, P., & Todorov, C. (2005). The

relationships between symptom dimensions and dysphoria in schizophrenia.











Academic Press.









Kopp, B., Mattler, U., & Rist, F. (1994). Selective attention and response competition in

schizophrenic-patients. Psychiatry Research, 53, 129-139.

Chapter 6

174









Nelson, H. E., & Willison, J. R. (1991). National Adult Reading Test manual (2nd ed.).

Windsor, UK: NFER-Nelson Publishing Company.





470.

Paulik, G., Badcock, J., & Maybery, M. (2008). Dissociating the components of



Randolph, C., Gold, J. M., Carpenter, C. J., Goldberg, T. E., & et al. (1992). Release

from proactive interference: Determinants of performance and

neuropsychological correlates. Journal of Clinical and Experimental

Neuropsychology, 14, 785-800.






Sheehan, D. V., Lecrubier, Y., Sheehan, K. H., Janavs, J., Weiller, E., Keskiner, A., et

al. (1997). The validity of the Mini International Neuropsychiatric Interview

(MINI) according to the SCID-P and its reliability. European Psychiatry, 12,

232-241.

Sison, J. A., & Mather, M. (2007). Does remembering emotional items impair recall of

same-emotion items? Psychonomic Bulletin and Review, 14, 282-287.



Chapter 6

175


215.


Schuster.






Research, 62, 275-280.




Waters, F. A. V., Maybery, M. T., Badcock, J. C., & Michie, P. T. (2004). Context

memory and binding in schizophrenia. Schizophrenia Research, 68, 119-125.

Wechsler, D. (1997). Wechsler Adult Intelligence Scale - Third Edition. San Antonio,

USA: Psychological Corporation.


Emotion, 1, 166-181.

Woods, S. W. (2003). Chlorpromazine equivalent doses for the newer atypical

antipsychotics. Journal of Clinical Psychiatry, 64, 663-667.

World Health Organisation. (1993). The ICD-10 classification of mental and

behavioural disorders: Diagnositic criteria for research (10th ed. Vol. 1).

Geneva: World Health Organisation.

Zec, R. F. (1995). Neuropsychology of schizophrenia according to Kraepelin: Disorders

of volition and executive functioning. European Archives of Psychiatry and


Zigmond, A. S., & Snaith, R. P. (1983). The hospital anxiety and depression scale. Acta


176

177

GENERAL DISCUSSION

178

Chapter 7

179

Chapter 7

General Discussion

In this chapter, the main findings pertaining to the three central aims of this

thesis are reviewed in turn. Since cognitive processes are complex and invariably

interact with additional cognitive and perceptual processes to some degree, possible

alternative interpretations of the findings pertaining to each of the three central aims

will be critiqued in the respective sections. The methodological strengths and

limitations of the completed research, suggestions for future research, and clinical

implications will also be discussed.

REVIEW OF THESIS AIMS

Auditory hallucinations (AHs) are intrusive and often distressing cognitive

experiences. Despite the pressing need for effective treatments targeting these

perturbing symptoms, the progress in treatment development has been curtailed by the

immaturity of understanding of the complex interactions between cognitive and

affective processes contributing to their production. Thus, the overall aim of this thesis

was to contribute to the collective understanding of the processes involved in AHs. This

was actuated by the empirical investigation of three central aims. The first aim was to

dissociate the particular components of cognitive control related to AHs in both

hallucination predisposition and schizophrenia. The components of cognitive control

were defined using Harnishfeger‟s (1995) inhibition taxonomy which categorises

inhibitory-related processes along three dimensions: intentional (consciously

suppressed) versus unintentional (automatically suppressed); cognitive (suppression of

cognitive contents and processes) versus behavioural (suppression of motor actions and

impulses); and inhibition (active suppression operating on the content of working

memory) versus resistance to interference (the gating of information prior to entering

working memory). This aim was formulated to test the conjecture posited by the

Badcock et al. dual-deficit model of AHs, that a specific deficit in intentional cognitive

inhibition is responsible for the intrusive and unintentional aspects of AHs (Waters,

Badcock, Michie, & Maybery, 2006). The second aim of this thesis was to investigate

Chapter 7

180

the role of negative affect (chiefly anxiety) in AHs, specifically in relation to the

cognitive control processes under investigation. The third aim was to investigate the

continuum approach to hallucinatory-type experiences with respect to the key

constructs. The continuum approach assumes that similar cognitive and affective

disturbances contribute to the production of hallucinatory-type experiences in both

healthy individuals predisposed to hallucinations and individuals with schizophrenia.

Each chapter of this thesis empirically addressed one or more of the central

thesis aims. Chapter 2 aimed to clarify the different features of hallucination

predisposition and to subsequently examine the shared and unique relationships that

anxiety, depression and stress have with these different features. The findings reported

in this chapter permitted speculation on the continuity of affective associations with

AHs across the continuum, and provided (speculative) insight into the possible

processes involved in AH production that these affective states may influence.

Together, Chapters 3 and 4 aimed to dissociate the critical components of cognitive

control specifically related to hallucination predisposition, independent of other

schizophrenia-related symptoms and anxiety. Chapter 5 investigated the relationships

between anxiety (state and trait), intentional inhibition, and hallucination predisposition.

Specifically, this study examined the effects of state anxiety on the intentional

inhibitory performance of healthy individuals with either a low or high hallucination

predisposition using a mood induction procedure. Finally, Chapter 6 aimed to dissociate

the critical components of cognitive control specifically related to AHs, and the

involvement of anxiety in the examined relationships, in schizophrenia. The same

cognitive control tasks used in Chapter 3 and 4 were employed in Chapter 6 to permit

comparison of findings in hallucination predisposition and schizophrenia, allowing

speculation regarding the continuity of cognitive and affective processes involved in the

production of hallucinatory experiences across the symptom continuum.

COGNITIVE CONTROL AND HALLUCINATORY EXPERIENCES

Summary of Findings and Interpretation

Each of the empirical chapters contributed in some way towards discerning the

particular components of cognitive control related to AHs across the continuum.

Chapter 2 (study 1) confirmed that hallucination predisposition (as measured by the

Chapter 7

181

Launay-Slade Hallucination Scale; LSHS-R; Bentall & Slade, 1985) is a

multidimensional construct. Whilst the individual dimensions differed in some aspects

(namely, content/themes and source attribution), all dimensions described intrusive

mental events. These findings were interpreted as providing indirect evidence of

inhibitory-related difficulties in hallucination predisposition, since empirical studies

have attributed everyday intrusive mental events to poor cognitive inhibitory control

(Friedman & Miyake, 2004; Kramer, Humphrey, Larish, Logan, & Strayer, 1994;

Schnider & Ptak, 1999).

The study reported in Chapter 3 directly examined intentional cognitive

inhibitory ability of psychometrically identified high and low hallucination predisposed

healthy individuals using the LSHS-R. Intentional inhibition was measured using a

modified three-run version of the Inhibition of Currently Irrelevant Memories (ICIM)

task (Schnider & Ptak, 1999; Schnider, Valenza, Morand, & Michel, 2002) employed

previously by Badcock and colleagues to examine intentional inhibitory impairments

and AHs in schizophrenia (Badcock, Waters, Maybery, & Michie, 2005; Waters,

Badcock, Maybery, & Michie, 2003). The results showed that the high hallucination

predisposed participants mistook more previous-run items as having already been seen

on the current run (false alarms; FAs) than did low hallucination predisposed

participants. This finding was interpreted as evidence of intentional inhibition

difficulties in hallucination predisposed individuals, and was replicated using a two-run

version of the ICIM task in the study reported in Chapter 5. In addition, Chapter 3 also

revealed evidence of slowing of inhibitory processes (that is, when inhibition was

executed successfully), since the high predisposed group were slower to correctly reject

previous-run items on the inhibitory runs than the low predisposed group, and were

slower to make a correct rejection than a correct identification (Hit) on the inhibitory

runs. This slowing of inhibition was not replicated in Chapter 5, however, as noted in

the Discussion section of Chapter 5, this difference may have been due to the reduction

in the number of runs, and thus item saliency. Importantly, the reported intentional

inhibition difficulties could not be explained by group differences in general cognitive

or recognition ability (since no group differences on FAs or Hits were found for run 1,

which does not require inhibition), or anxiety or other schizophrenia-related symptoms

(since the effects remained significant even when controlling for these additional

variables).

Chapter 4 sought to determine whether the inhibitory difficulties related to

hallucination predisposition are restricted to those cognitive control processes that are

Chapter 7

182

both intentional (as opposed to unintentional) and inhibitory (as opposed to resistance to

interference) in nature, through the administration of an unintentional inhibition task

(Brown-Peterson [B-P] variant task; Kane & Engle, 2000) and an intentional resistance

to interference task (directed ignoring task [DI] task; Connelly, Hasher, & Zacks, 1991)

to high and low hallucination predisposed participants. The study found no evidence of

unintentional inhibition difficulties in hallucination predisposed individuals.

Conversely, the study showed that the high hallucination predisposed individuals had

difficulty intentionally resisting interference from goal-competing external distractors;

taking longer to read passages when distractors were presented concurrently, and

reading more of these distractors aloud, than low hallucination predisposed individuals.

However, unlike the intentional inhibition difficulties reported in Chapter 3, these

difficulties did not remain significant when controlling for either delusional ideation or

anxiety, with follow-up regression analyses suggesting that difficulties with intentional

resistance to interference may be a common mechanism underlying sub-clinical positive

schizophrenia symptoms more generally (i.e., not unique to hallucination predisposition

specifically), as well as anxiety.

Chapter 6 used the same set of cognitive tasks employed in the predisposition

studies (namely, the ICIM, B-P, and DI tasks) to examine the components of cognitive

control related specifically to AHs in individuals with schizophrenia. The study found

that, as a group, schizophrenia participants were not impaired on either the intentional

or unintentional inhibition tasks, however they were impaired on the intentional

resistance to interference (DI) task relative to healthy control participants (specifically,

they had slower reading times on distractor passages and read more distractors aloud).

This finding is consistent with the extensive evidence of deficits in executive/volitional

behaviour in schizophrenia1 (Merlotti, Piegari, & Galderisi, 2005; Zec, 1995), whilst

automatic cognitive control processes, including automatic resistance to interference,

remain relatively intact (Fleming, Goldberg, Gold, & Weinberger, 1995; Kopp, Mattler,

& Rist, 1994; Randolph, Gold, Carpenter, Goldberg, & et al., 1992). However, at the

symptom level, the only form of cognitive control found to specifically correlate with

AH severity was intentional inhibitory control (specifically, FAs on the inhibitory run of

the ICIM task). Importantly, intentional inhibition was not related to delusions or

negative symptoms, demonstrating the specificity of this deficit to AHs. Furthermore

1 See the Discussion section of Chapter 6 for an outline of the likely reasons why the

schizophrenia group did not perform more poorly than the control group on the other intentional

cognitive control task (the ICIM task).

Chapter 7

183

the correlation with AH severity remained significant when controlling for anxiety,

confirming that anxiety does not cause – though may exacerbate – intentional inhibition

deficits associated with AHs. These findings are consistent with the Badcock et al. dual-

deficit model of AHs (Badcock et al., 2005), replicating and extending their previous

findings linking AH severity to impaired intentional inhibition using the ICIM task in

schizophrenia (Waters et al., 2003).

The finding that deficits of intentional inhibitory control underlie AHs

implicates the involvement of the frontal lobes in AHs, since prior neuroimaging studies

have linked various forms of inhibitory control to the activation of numerous regions of

the frontal lobe (e.g., Aron, Robbins, & Poldrack, 2004; Fuster, 1999; Konishi et al.,

1999; Wyland, Kelley, Macrae, Gordon, & Heatherton, 2003) – possibly subserved by a

series of frontal-loops (Miller & Cohen, 2001) – with the orbitofrontal cortex (OFC)

found to be specifically involved in intentional inhibition, as measured with the ICIM

task (Schnider, Treyer, & Buck, 2000). This challenges more traditional

conceptualisations of the neural origins of positive and negative symptoms, with frontal

lobe dysfunction traditionally linked exclusively to negative symptoms, and positive

symptoms primarily linked to temporal lobe dysfunction (e.g., Mattson, Berk, & Lucas,

1997; Norman, Malla, Morrison-Stewart, et al., 1997; Wible et al., 2001; Wolkin et al.,

2003; Zemishlany, Alexander, Prohovnik, et al., 1996).

Critical Examination of Findings

There are additional possible interpretations of the findings reviewed in the

previous section that must be considered. For instance, Badcock and colleagues‟

propose that, in addition to an intentional inhibition deficit, impaired binding of

contextual information (e.g., temporal and spatial information) to memories contributes

to the production of AHs (Waters, Badcock, & Maybery, 2006). Since the intentional

inhibition (ICIM) task employed in Chapters 3, 5 and 6 required participants to inhibit

memory traces of pictures presented on previous runs, an alternative interpretation of

the findings may be that individuals who experience AHs make more FAs on the latter

runs due to difficulties accessing or monitoring temporal contextual information for the

stimuli (possibly due to deficits in contextual binding). Whilst the task does require

some degree of temporal monitoring, neuroimaging and electrophysiological studies

have shown that the underlying deficit in suppressing irrelevant memories can be

distinguished from deficits in source memory or temporal order. For example,

Chapter 7

184

performance on the inhibition runs of the ICIM task involves neural regions found to be

specifically involved in cognitive inhibition, such as the OFC (Aron et al., 2004; Dias,

Robbins, & Roberts, 1997; Schnider & Ptak, 1999; Schnider et al., 2000; Treyer, Buck,

& Schnider, 2003) which has also been linked to AHs (Silbersweig et al., 1995).

Furthermore, the neural regions involved in temporal monitoring are not activated

during performance, or related to FAs, on the inhibitory runs of the ICIM task (Cabeza

et al., 1997; Schnider et al., 2000). However, future studies investigating inhibitory

control in relation to AHs would benefit from using measures which minimise the

involvement of additional processes thought to contribute to the production of AHs,

such as context memory.

Kapur (2003; Kapur, Mizrahi, & Li, 2005) proposed that hallucinations are the

direct experience of dopamine-driven aberrantly salient cognitions, such as memory

traces (see the Dopamine Theories section of Chapter 1 for a more in-depth discussion).

Accordingly, it may be argued that the association between hallucinatory experiences

and increased FAs made on the inhibitory runs of the ICIM task is due to heightened

salience of memory traces of previously seen items, making the items more difficult to

inhibit and potentially influencing their perceived current relevance. Following Kapur‟s

proposal, one would expect that individuals with hallucinations would exhibit a

recognition advantage as well as an inhibition disadvantage since dopamine-driven

salience would affect all memory traces. The results from the three chapters employing

the ICIM task are inconsistent in their pattern of recognition (Hit) data: with some

evidence of a recognition advantage in hallucination predisposed participants on later

runs, though not the first run, of the ICIM task reported in Chapter 3; no evidence of a

recognition advantage in the hallucination predisposition study reported in Chapter 5;

and although not reported in Chapter 6, there were no significant positive correlations

between Hits and AHs severity in the schizophrenia study. In addition, if all memory

traces are aberrantly salient, an association between AHs and B-P task performance

could also be expected, since this task also requires the inhibition of previously relevant

– currently irrelevant – memory traces. No such association was found in either Chapter

4 or 6. Thus, the most plausible cause of difference in findings on the B-P task and the

ICIM task is the intentionality of the inhibitory processes involved, since this is the

primary feature distinguishing the two tasks. In sum, the findings from this thesis

provide limited support for an aberrant salience explanation of the inhibition results.

However, future research might aim to experimentally manipulate variation in memory

salience in order to examine the effect on inhibitory performance. It is also clear that

Chapter 7

185

many current cognitive models of AHs, including the Badcock et al. dual-deficit model,

do not adequately specify the mechanism(s) driving the activation of the intrusive

cognitions that become AHs. Recent biologically based studies suggest that such

activation arises from the spontaneous activation of auditory cortex (Hunter et al., 2006)

and/or dopaminergic modulation of spontaneous activation (Pihan, Gutbrod, Baas, &

Schnider, 2004). Whilst such endogenous activation of neural circuits may be critical to

the initial activation of intrusive cognitions, the current thesis highlights the possibility

that subsequent cognitive mechanisms may ironically increase the activation of

representations due to repeated efforts to suppress unwanted intrusive thoughts

(Baumeister, Vohs, & Tice, 2007; Wegner & Zanakos, 1994; see the Discussion section

of Chapter 4). Such effects may represent a cognitive “kindling” of specific memories,

possibly explaining the common repetition in content of AHs.

The three cognitive control tasks employed in this thesis were not identical in all

respects besides the type of cognitive control involved. However, it seems unlikely that

these differences could explain the selective association between intentional inhibition

(measured using the ICIM task) and hallucinatory experiences. For example, the tasks

differed in the modality of the to-be-inhibited stimuli. Namely, the ICIM task presents

pictures, while both of the other tasks present printed verbal information which

participants read aloud – words for the B-P task and sentences for the DI task. However,

the mode of stimulus presentation need not have a significant effect on one‟s ability to

exert cognitive control over the to-be-inhibited stimuli, since (1) the inhibition tasks do

not require the suppression of the external stimuli themselves, but rather the suppression

of the internal representation of the stimuli, the process of which is amodal (Anderson,

Qin, Jung, & Carter, 2007; Murray et al., 2004), (2) the literature shows that participants

often sub-vocalise pictorial stimuli on visual recognition tasks, introducing a verbal

component (e.g., Prinz, 1978; Whitehouse, Maybery, & Durkin, 2006), and (3)

theoretically, one may expect that cognitive control difficulties would be more

pronounced on auditory/verbal tasks, consistent with the modality of AHs. In sum, the

significant association between impaired performance on a non-verbal task of

intentional inhibition and AHs, strongly suggests that this deficit is not restricted to the

modality of the hallucinatory experience it underlies, namely audition. The cognitive

control tasks also differed with regard to the previous relevance of the to-be-ignored

stimuli: namely, the to-be-inhibited stimuli on both the ICIM and B-P task were

previously relevant, while the distractor items of the original DI task (the version used

in Chapter 4) were novel. To investigate whether this had any effect on participants‟

Chapter 7

186

ability to intentionally resist interference, the previous relevance of distractor items was

experimentally manipulated in Chapter 6, such that on half of the distractor trials the

distracting text was the target text in the previous trial, and on half the trials the

distracting text was novel. The study found no effects involving previous relevance,

eliminating this as a confounding variable.

As reviewed in Chapter 1, two of the most widely debated cognitive accounts of

AHs are the mental imagery and inner speech theories. The findings pertaining to the

ICIM task could not be easily explained by increased auditory mental imagery, since

this would also be expected to be associated with (1) difficulties on the B-P task as well

as the ICIM task, and (2) increased recognition facilitation in addition to increased

inhibition difficulties on the ICIM task (assuming auditory/verbal mental imagery in

this task arises from sub-vocalization of picture names). However, neither of these

outcomes predicted by the increased auditory mental imagery account was obtained.

Similarly, the reduced visual mental imagery account also has difficulties explaining the

findings, since one would expect reduced Hits on all runs of the ICIM task to be

associated with AHs, which was not found on any of the studies. Since participants have

been found to sub-vocalise the names of items on visual recognition tasks, the inner

speech explanation of AHs (and thus the ICIM task findings) can not necessarily be

eliminated on the basis that the ICIM task does not involve inner speech. As previously

asserted, we do not dispel the notion that AHs may be both misidentified memories and

inner speech/thoughts, however, we argue that the primary mechanism leading to their

intrusion into consciousness is failed intentional inhibition, rather than a failure of inner

speech monitoring mechanisms per se. Consistent with this, neuroimaging studies have

shown that AHs can occur in the absence of activation of the neural substrate involved

in inner speech, suggesting other cognitive contents (i.e. memories) and processes (i.e.

inhibition) must be involved in AH production (Stephane, Barton, & Boutros, 2001).

Strengths, Limitations and Implications for Future Research

The cognitive control tasks employed were selected on the basis that they have

been utilised as cognitive control measures in multiple research domains and – unlike

cognitive control measures such as the Stroop task and negative priming tasks (Berens

& Eling, 2003; Friedman & Miyake, 2004; MacLeod, 1991) – there has been minimal

debate over the key cognitive processes involved in the tasks (e.g., ICIM task: Schnider

& Ptak, 1999; Schnider et al., 2000; Schnider et al., 2002; Treyer et al., 2003; Waters et

Chapter 7

187

al., 2003; B-P task: Burns, 2004; Friedman & Miyake, 2004; Laming, 1992; Randolph

et al., 1992; DI task: Connelly et al., 1991; Hopko, Ashcraft, Gute, Ruggiero, & Lewis,

1998; Kipp, Pope, & Digby, 1998; Phillips & Lesperance, 2003). However, there was

limited information regarding the discriminant power of each of the cognitive control

tasks employed available, leaving open the possibility that one of the tasks may have

had greater discriminant power than the others. Confirmation of the findings reported in

this thesis through the comparision of cognitive controls tasks with known and

comparable discriminant power would be of merit.

There were some minor costs associated with the methodological choices made.

For instance, the version of the ICIM task employed in this thesis was a modified

version of the ICIM task used by Badcock and colleagues in their schizophrenia studies

(Badcock et al., 2005; Waters et al., 2003). This was because the original version was

found not to be sensitive enough to detect individual differences in inhibitory ability in

healthy (non-clinical) participants. Thus, so that modest effects could be detected in the

hallucination predisposition studies, we employed a modified version of the ICIM task

developed by Schnider and colleagues (2002) for use in a non-clinical sample (see the

Measures section of Chapter 3 for modification details). The same version of the task

was used in the schizophrenia study (Chapter 6) to permit discussion of the continuity

of cognitive difficulties across the AH continuum. However, the drawback of this

decision is that any differences in outcomes between the schizophrenia study reported in

Chapter 6 and the Waters et al. (2003) study are likely – though cannot be confirmed –

to have arisen due to the changes in the number of target repetitions, and thus target

salience (see the Discussion section of Chapter 6 for a more detailed discussion).

Another potential limitation was that the highest and lowest scoring participants

on the LSHS-R were selected for comparison in Chapters 3 – 5 in order to maximise the

difference in hallucination predisposition between our comparison groups, and thus

maximise any associated cognitive differences between the groups. Although this

approach is used throughout the LSHS-R literature, the limitation of this approach is

that the group which formed the comparison for the high LSHS-R group was also on an

„extreme‟ end of the normal LSHS-R distribution, and thus it is possible that this group

may have had superior intentional inhibition, in addition to the high LSHS-R group

having inferior intentional inhibition. However, it is unlikely that the group differences

on the ICIM task reported in Chapters 3 and 5 were due to atypical performance of the

low LSHR-R group, since the low LSHS-R groups mean FA and Hit rates were

comparable to those reported from a random undergraduate sample previously tested on

Chapter 7

188

this same version of the ICIM task (Schnider et al., 2002). Nevertheless, future studies

would benefit from the inclusion of a mid scoring LSHS-R group to eliminate this

possibility. Another minor drawback is that substabce use was not screened for in the

undergraduate studies (Chapters 3 – 5). Long-term substance use has been linked to

cognitive impairments (Yucel, Lubman, Solowij & Brewer, 2007) however, previous

research that has examined the LSHS-R and substance use reported that only 8% of

undergraduate students report any association between their substance use and

experiences rated on the LSHS-R (Laroi & Van Der Linden, 2005). Furthermore, one

would expect that if substance use was higher in the high LSHS-R group (compared to

the low LSHS-R group) in the current studies, and was having an negative impact on

cognitive ability one would expect to see impaired performance across all tasks in that

group – which was not the case.

The cognitive underpinnings of hallucinations in other modalities (such as

visual, tactile, olfactory and gustatory) warrant further research. Similarly, the role of

intentional inhibition in hallucinations experienced in other clinical populations (e.g.,

Alzheimer‟s disease) also merits further investigation. In addition, future schizophrenia

studies may benefit from including a measure of disorganised symptoms, since several

schizophrenia taxonomies have grouped disorganised symptoms into a third symptom

category (e.g., Peralta & Cuesta, 2001), and interestingly, disorganised symptoms have

been previously linked to difficulties with unintentional forms of cognitive control (e.g.,

Guillem et al., 2001).

Finally, the association reported in this thesis between AHs and inhibitory

control further supports the conceptualisation of AHs as a type of cognitive intrusion

(Morrison, 2005), since everyday cognitive intrusions are also thought to be a product

of impaired cognitive control (Friedman & Miyake, 2004). However, it is possible that

other forms of cognitive intrusions – such as flashbacks (experienced in posttraumatic-

stress disorder [PTSD]), obsessive thoughts and compulsions (experienced in obsessive-

compulsive disorder [OCD]) – may be due to failure of different forms of cognitive

control. While Badcock and colleagues showed intentional inhibition difficulties (using

the ICIM task) in OCD participants relative to healthy control participants, they noted

that the pattern of performance difficulties was qualitatively different to the pattern

found for hallucinating individuals with schizophrenia, implicating both unique and

shared underlying mechanisms (Badcock, Waters, & Maybery, 2007). Future studies

should examine the different components of cognitive control related to different types

of cognitive intrusions, in both the healthy population and in different clinical disorders

Chapter 7

189

characterised by cognitive intrusions, such as schizophrenia, OCD, PTSD, and

generalised anxiety disorder. This research may assist the development of more

effective and individually tailored therapeutic interventions.

Clinical Implications

The clinical implications of the findings pertaining to the first aim of the thesis

are patent. Interventions aimed at reducing the severity of hallucinatory-type

experiences of individuals with schizophrenia and healthy hallucination predisposed

individuals should target intentional forms of inhibitory control. Direct cognitive

remediation may appear to be the most obvious approach given the intentional nature of

the impairments, however, given the paradoxical increase in unwanted cognitive

intrusions associated with repeated attempts to suppress unwanted cognitions (Wegner

& Zanakos, 1994), such an approach may be unwise. An alternative option may be to

modify maladaptive cognitive coping strategies, which may be further impairing – or

relying heavily upon – intentional inhibitory ability, such as replacing suppression-

based coping strategies with more effective coping strategies for intrusive cognitions,

such as active acceptance (Farhall & Gehrke, 1997) or distraction (Morrison & Wells,

2000). Consistent with this proposal, treatment outcome studies have shown that the

effectiveness of socio-psychological interventions for AHs, such as cognitive-behaviour

therapy, is significantly increased by the inclusion of coping training (e.g., Jenner, van

de Willige, & Wiersma, 1998; Wiersma, Jenner, van de Willige, Spakman, & Nienhuis,

2001).

Intentional inhibition deficits have also been documented in other clinical

disorders characterised by intrusive cognitions, such as OCD (Badcock et al., 2007).

While the development of effective treatments for AHs is still in its infancy, several

different socio-psychological interventions targeting intrusive obsessions and

compulsions in OCD have been developed and found to be efficacious in reducing

intrusion severity and frequency, as well as associated distress and impairment

(Abramowitz, Brigidi, & Roche, 2001; O'Connor et al., 2005). Thus, socio-

psychological treatment programs for AHs may benefit from borrowing and adapting

intervention strategies utilised in the treatment of OCD symptoms.

Chapter 7

190

Summary

In summary, the findings pertaining to the first aim of this thesis implicate the

specific involvement of intentional inhibition in the development and/or maintenance of

hallucinatory-type experiences across the symptom continuum. Furthermore, the

findings suggest that this cognitive control impairment cannot be explained by the

presence of other schizophrenia related symptoms or anxiety. This impairment may be

responsible for the intrusion of auditory mental representations into ongoing

consciousness, contributing to the perceived intrusiveness and uncontrollability of AHs,

as hypothesized in Badcock and colleague‟s dual-deficit model of AHs (Badcock et al.,

2005).

The aggregated findings suggest that unintentional inhibition is unrelated to AHs

in hallucination predisposition and schizophrenia. In contrast, the findings reported in

this thesis suggest that difficulties with intentional resistance to interference may be

related to the predisposition to positive symptoms and schizophrenia more generally,

however, such difficulties are not uniquely related to the experience of AHs. Finally, the

current findings emphasise the importance of dissociating (or at least specifying) the

cognitive control processes in all studies examining „inhibition‟, since the findings from

this thesis further illustrate that inhibition is not a unitary construct.

ANXIETY AND HALLUCINATORY EXPERIENCES


The second aim of the current thesis was to examine the relationships between

negative affect (anxiety in particular), dissociable forms of cognitive control, and

hallucinatory experiences across the symptom continuum. Indeed, examining the

possibility that anxiety contributes to the production of AHs through its effects on

cognitive control has not previously been investigated, and represents a novel

contribution to the literature.

The second study presented in Chapter 2 examined the shared and unique

relationships of state anxiety, depression and stress with the three components of

hallucination predisposition. Anxiety was the only affective variable to consistently

relate to all three hallucination predisposition components, even when eliminating the

Chapter 7

191

shared variance accounted for by the other affective constructs. This finding

complements the previous literature on hallucination predisposition (Allen et al., 2005),

AH onset (Delespaul, deVries, & van Os, 2002; Tien & Eaton, 1992), and reality

distortion in schizophrenia (Norman, Malla, Cortese, & Diaz, 1998). This led to the

narrowing of focus to the role of anxiety in the onset of AHs in the remaining chapters

of the thesis. The findings of Chapter 2 led to the speculation that anxiety may

contribute to the intrusive nature of AHs. Consistent with this conjecture, anxiety has

been found to increase task-irrelevant intrusive cognitions, and what is more, most

anxiety disorders are characterised by different forms of cognitive intrusions, such as

flashbacks in PTSD, and obsessional thoughts and compulsions in OCD (American

Psychiatric Association, 2000; Freeston et al., 1994; Hackmann, Surawy, & Clark,

1998; Seibert & Ellis, 1991; Wegner & Zanakos, 1994). As previously noted, intrusive

cognitions, including AHs, have been found to be the product of failed cognitive

inhibition (Badcock et al., 2005; Friedman & Miyake, 2004; Kramer et al., 1994;

Schnider & Ptak, 1999; Waters et al., 2003). However, in contrast to the current thesis,

few, if any, studies have attempted to delineate the specific variety of cognitive control

adversely affected by anxiety or in different anxiety disordered populations. This

observation is important since anxiety may influence different forms of cognitive

control in different ways.

Consistent with Chapter 2, the studies presented in Chapters 3, 4, and 5 showed

significantly higher levels of anxiety in the high than the low hallucination predisposed

individuals, and although not reported in Chapters 3 or 4, anxiety was significantly

correlated with LSHS-R scores (r = .51, p < .05, N = 51). Similarly, the study presented

in Chapter 6 showed higher levels of anxiety in schizophrenia than control participants,

and moreover, showed that anxiety was significantly correlated with AH severity, but

not delusions or negative symptoms. These findings further highlight the specific

relationship between anxiety and AHs across the symptom continuum.

This thesis was specifically interested in the relationship between anxiety and

cognitive control in the production of AHs. Where effects involving LSHS-R group

differences were significant in the analysis of cognitive control tasks in Chapters 3 and

4, state anxiety was controlled for to examine whether these effects were mediated by

anxiety. The intentional inhibition difficulties exhibited by the high hallucination

predisposed participants in Chapter 3 remained significant when controlling for

variance in anxiety, suggesting that these intentional inhibition difficulties do exist

independently of anxiety. This finding was expected given that anxiety is not invariably

Chapter 7

192

present prior to the occurrence of AHs, though does not rule out the possibility that

anxiety may exacerbate existing intentional inhibition difficulties. In contrast, as

reported in Chapter 4, the link between poor intentional resistance to interference

(measured using the DI task) and hallucination predisposition did not remain significant

when controlling for anxiety, and follow-up regression analyses showed that anxiety

independently contributed to the prediction of intentional resistance to interference

ability, above the variance shared with sub-clinical positive symptoms. This finding is

consistent with previous studies which have shown problems gating concurrent

distracting information in highly anxious samples (e.g., found using the DI task; Hopko

et al., 1998).

Together, the findings presented in Chapters 3 and 4 linked hallucination

predisposition to specific difficulties with intentional inhibition, thus, Chapter 5 aimed

to examine the possible involvement of anxiety in this relationship. A music mood

induction procedure was employed to compare ICIM task performance immediately

following an anxious mood induction and following a neutral mood induction.

Although participants made more FAs on inhibitory runs on the anxious than the neutral

mood condition, this effect of mood was not significant, possibly due to the modest

magnitude and duration of the induced mood states (a common problem with mood

induction designs). In line with this interpretation, the study revealed a significant

relationship between intentional inhibition and trait anxiety. Interestingly most of the

previous studies that have linked anxiety to cognitive impairments have compared high

and low trait anxious participants, or clinically anxious and control participants (e.g.,

Amir, Coles, Brigidi, & Foa, 2001; Amir, Coles, & Foa, 2002; Badcock et al., 2007;

Enright & Beech, 1993; Hopko et al., 1998; Wood, Mathews, & Dalgleish, 2001). This

significant association allows the possibility that more severe or longer lasting changes

in anxiety may indeed exacerbate difficulties with intentional inhibition. Evidence of a

significant correlation between state anxiety and intentional inhibition across all

participants reported in Chapter 6 supports this conjecture. However, it is equally

possible that the relationship between trait anxiety and intentional inhibition (Chapter 5)

signifies a shared common cognitive vulnerability underlying anxious (pre)disposition

and hallucination predisposition: poor intentional inhibition. Importantly, this

relationship between trait anxiety and intentional inhibition was found to be largely

independent of hallucination predisposition. Thus, although individuals with high trait

anxiety are likely to be at a heightened risk of experiencing AHs if contextual memory

Chapter 7

193

difficulties are also present (Waters, Badcock, & Maybery, 2006), high trait anxiety

alone does not equate to hallucination predisposition.

Consistent with the findings reported in Chapters 4 and 5, the schizophrenia

study reported in Chapter 6 showed that anxiety was significantly correlated with both

intentional inhibition and intentional resistance to interference across the entire sample,

but not with unintentional inhibition. This pattern of associations is consistent with the

existing literature that has linked poor intentional – but not unintentional – cognitive

control to heightened anxiety (i.e., using the ICIM task: Badcock et al., 2007; using the

DI task: Hopko et al., 1998; using the B-P task: Heinrichs & Hofmann, 2004). Since

anxiety, intentional inhibition and AH severity were all found to significantly correlate

with one another, partial correlations were used to investigate the independence of these

relationships. Similar to the findings presented in Chapter 3, the results showed that in

the schizophrenia sample, the relationship between AH severity and intentional

inhibition remained significant when controlling for anxiety, suggesting that the

intentional inhibition deficits present in schizophrenia individuals who hallucinate

(Badcock et al., 2005) are not dependent on the presence of anxiety. Interestingly, the

correlation between AH severity and anxiety also remained significant when controlling

for intentional inhibition, suggesting that anxiety must contribute to the development of

AHs through other (i.e., additional) underlying cognitive processes, such as context

memory binding (Anderson & Shimamura, 2005; Sison & Mather, 2007; Steel, Fowler,

& Holmes, 2005; Waters, Badcock, & Maybery, 2006) or reasoning (Allen et al., 2005).

Future research should therefore examine the influence of anxiety on other cognitive

processes linked to AHs.


Neural network (or “connectionist”) models have often been used to explain the

intrusive cognitive symptoms characteristic of anxiety disorders (e.g., Stein &

Hollander, 1994; Stein & Ludik, 2000; Tryon, 1998). These models are similar to

Kapur‟s notion of aberrant salience; they posit that biological processes, such as the

dysregulation of the neurotransmitters dopamine and serotonin, can lead to the

spontaneous spread of activation of mood-congruent internal representations (i.e.,

memories and self-schemas), resulting in cognitive intrusions (Stein & Ludik, 2000;

Tryon, 1998). Semantic network models specifically propose that emotion will activate

– or maintain activation of – internal representations consistent with the emotion that

Chapter 7

194

has triggered it (Tryon, 1998). These accounts have been used to explain the link

between anxiety and selective attention to, and difficulty inhibiting, threat-related

stimuli (Matthews & Harley, 1996; Stein & Ludik, 2000). However, similar lines of

reasoning do not sufficiently explain the relationship between anxiety and intentional

control reported in this thesis, since the to-be-inhibited stimuli were neutral in both

tasks. Likewise, many previous studies have reported general (not threat specific)

cognitive difficulties in anxiety disordered samples (e.g., Amir et al., 2002; Amir, Foa,

& Coles, 1998; Hopko et al., 1998; Wood et al., 2001), such as the intentional inhibition

deficits in OCD reported by Badcock and colleagues (2007) using the ICIM task.

Furthermore, while we do not dispute that anxiety can automatically trigger the

activation of emotion-congruent internal representations, we argue that anxiety must

also interfere with intentional inhibition ability, since sufficient inhibitory ability should

prevent these automatically activated internal representations from intruding into

consciousness.

An alternative interpretation of the findings presented in this thesis is that

anxiety leads to a reduction in cognitive resources. As the name suggests, „limited

resource‟ theories of anxiety propose that many of the cognitive anomalies associated

with anxiety can be attributed to a reduction in the cognitive resources available during

a state of heightened anxiety. Evidence for these theories stem from the findings that

differences in the cognitive performance of high and low anxious individuals often

(though not always) become evident once a second concurrent operation is introduced to

a task (Eysenck, 1992; Wood et al., 2001). This theory emerged as an explanation of the

well documented selective attention to threat-related information associated with

anxiety. However, other theorists have hypothesised that this selective attention occurs

because of an anxiety-induced difficulty with the inhibition of cognitive processes and

contents that are goal irrelevant, especially if the distracting information is consistent

with current concerns (Fox, 1994). If the anxiety findings reported in this thesis were

due to limited cognitive resources compromising task performance, a significant

negative correlation between anxiety and recognition (Hits) on the ICIM task would

have been expected, since the impairing effects of scant availability of resources is

unlikely to be selective as to which process it impairs. Consistent with the impaired

inhibition account, the correlations between anxiety and recognition on the ICIM task

(in all relevant chapters) were not significant.

Chapter 7

195


Anxiety has been found to rise immediately prior to the onset of hallucinatory

episodes, implicating the involvement of state anxiety in the onset of AHs (Delespaul et

al., 2002). While it was hypothesised that anxiety may contribute to the development of

AHs through its influence on cognitive control, previous empirical studies linking

anxiety to poor inhibition however, have predominantly studied clinically anxious or

high trait anxious individuals. Thus, it remained unclear from the previous research

whether these cognitive control impairments are caused by fluctuations in anxiety, or

are instead an underlying cause of anxiety. Thus, one of the additional aims, and a key

strength of this thesis was to examine the relationship between state anxiety and

different forms of cognitive control in non-clinically anxious individuals. However, the

drawback of this approach was that within group variance and intensity of state anxiety

(including in the mood induction study) may not have been sufficient to capture the

effects (if any) of state anxiety on cognitive control.

As is the case with all domains of psychology, the direction of causation of

effects cannot be determined through the use of traditional correlational or between-

group designs, unless the independent variable is experimentally manipulated.

Experimental manipulation of state anxiety in the study of cognitive control processes

linked to AH has not been reported in the literature. To overcome this limitation, a

mood induction procedure was utilised in Chapter 5 to examine the direct effects of

induced anxiety on intentional inhibition performance – the method of which has been

effectively employed in other sub-fields of the anxiety and cognition literature (e.g.,

Gray, 2001; Shackman et al., 2006; Shapiro & Lim, 1989). However, a common

limitation of these procedures is that the degree of mood change elicited may not be

large, thus making it difficult to detect modest effects. Consistent with this, the size and

duration of the induced mood states in Chapter 5 were limited, leaving open the

possibility that state anxiety impairs intentional inhibition, especially given the (non-

significant) pattern of mood effects on inhibitory ability reported in Chapter 5, and the

significant correlation between state anxiety and intentional inhibition reported in

Chapter 6. Further research is required to tease apart these effects, which may be

possible if shorter cognitive control tasks are employed when using a mood induction

design, to ensure the mood induction effects outlive the duration of the task. Treatment

studies can also provide insight into the direction of causation, since one would expect

that if anxiety is causing the cognitive control impairments found in clinically anxious

Chapter 7

196

individuals, successful treatment (reduction) of anxiety would also lead to an

improvement in cognitive control ability.

Since state anxiety was chosen as the primary affective construct under

investigation in this thesis, trait anxiety was not measured in all chapters of the thesis.

Trait anxiety was measured in the mood induction study because interactions between

trait and state measures of anxiety have been reported previously in the mood induction

literature (e.g., Broadbent & Broadbent, 1988).2 Due to unforeseeable circumstances,

the testing phases of the experiments reported in Chapter 5 and 6 overlapped, and thus,

consistent with earlier chapters, only a measure of state anxiety was included in the

schizophrenia study presented in Chapter 6. However, given the association between

trait anxiety and intentional inhibition reported in Chapter 5, follow-up studies might

usefully investigate trait anxiety in a schizophrenia sample.

It is essential that further research be conducted into the numerous roles that

negative affective states, in particular anxiety and depression, play in an hallucinatory

event. Negative affect has been implicated as a trigger, a maintenance mechanism, a

determinant of content, and a by-product of AHs (Freeman & Garety, 2003). As

reviewed in Chapter 1, our overall understanding of the multifaceted and reciprocal

relationship between negative affect and AHs is still largely immature, particularly with

regard to the onset and maintenance of AHs, which has the greatest implications for

treatment and prevention. Whilst our investigations have focused exclusively on the

involvement of anxiety (subsequent to Chapter 2), previous studies have linked

depression most closely to the transition into psychosis in healthy individuals who

already experience AHs (Krabbendam, Myin-Germeys, Bak, & van Os, 2005;

Krabbendam, Myin-Germeys, Hanssen et al., 2005; Krabbendam & van Os, 2005).

While not investigated in the current thesis, further research regarding the involvement

of depression in psychosis transition is critically important, and will undoubtedly

provide further important clinical implications regarding the prevention and treatment of

psychosis, especially for healthy individuals already experiencing AHs. Finally, the

findings from this thesis also suggest that anxiety must have additional influences on the

production of AHs other than through its effects on cognitive control. Thus, a fertile

avenue for further research will be the involvement of anxiety in the initial activation of

intrusive cognitions (as hypothesised by Nayani & David, 1996), as well as its possible

2 Although not reported on in the manuscript presented in Chapter 5, there were no significant

interactions involving trait anxiety in the Efficacy of Mood Induction Procedure analyses or in

the Effects of Anxiety on ICIM Task Performance analyses.

Chapter 7

197

influence on the cognitive processes leading to source misattribution, such as in context

memory binding (Steel et al., 2005; Waters, Badcock, & Maybery, 2006).


The pattern of findings involving anxiety obtained from this thesis has important

clinical implications which should not be overlooked. Although relationships were

found between anxiety, intentional inhibition, and AHs in schizophrenia and

hallucination predisposition, these relationships were independent of one another. Thus,

while anxiety may exacerbate existing intentional inhibition deficits in individuals who

experience AHs, anxiety must be influencing additional processes involved in the onset

of AHs. Thus, treatment programs targeting AHs are likely to be most effective if both

anxiety management and inhibition remediation strategies are included. Consistent with

this view, there is some evidence to suggest that the combination of cognitive

remediation and socio-psychological therapies addressing affective disturbance is more

effective at treating the symptoms of schizophrenia than either strategy alone (Penades

et al., 2006).

Summary

In summary, the findings pertaining to the second aim of this thesis confirm the

well documented association between anxiety and hallucinatory experiences across the

symptom continuum, as well as the association between anxiety and intentional forms

of cognitive control. However, the findings suggest that the intentional inhibition

difficulties present in individuals who experience AHs are not reliant on (i.e., mediated

by) the presence of anxiety, although anxiety may serve to further exacerbate intentional

cognitive control difficulties, and thus, contribute to the maintenance of AHs. Finally,

the results also suggest that anxiety must contribute to the production of AHs through

mechanisms other than intentional inhibition. This latter finding emphasises the need

for further research into the involvement of anxiety in AH production, and also

highlights the importance of treating anxiety in addition to the remediation of

intentional inhibitory impairments in treatment programs targeting AHs.

Chapter 7

198

THE HALLUCINATION CONTINUUM


A continuum approach to AHs predicts that similar, though possibly less severe,

cognitive and affective anomalies underlying AHs in schizophrenia will be found in

healthy individuals predisposed to experiencing AHs. The third aim of the current thesis

was to test the continuum hypothesis with regard to the cognitive and affective variables

under investigation. This section will discuss the similarities and differences in the

results obtained in this thesis from healthy young adults predisposed to hallucinations

(Chapters 2, 3, 4 and 5) and schizophrenia individuals with hallucinations (Chapter 6) 3,

while also incorporating previous findings reported in the research literature.

There were striking similarities between hallucination predisposition (as

measured using the LSHS-R) and the experience of AHs in schizophrenia. The factor

structure of the LSHS-R in healthy individuals (reported in Chapter 2) was similar to

that previously obtained from hallucinating and non-hallucinating individuals with

schizophrenia (Serper, Dill, Chang, Kot, & Elliot, 2005), and appeared to parallel two of

the key defining features of AHs in schizophrenia, namely, intrusiveness and external

source attribution (Slade & Bentall, 1988). Finally, both in Chapter 2 and in previous

schizophrenia studies, religiously themed AHs have been linked to lower levels of

associated affective distress than most non-religious AHs (Davies, Griffin, & Vice,

2001; Peters, Day, McKenna, & Orbach, 1999). These findings are consistent with the

continuum approach to AHs since the characteristic features of the experience appear to

be similar in both patients and non-patients.

Of central importance, hallucination predisposition and AH severity in

schizophrenia were both specifically linked to impaired intentional inhibition (ICIM

task: Chapters 3, 5 and 6), but not uniquely related to intentional resistance to

interference (DI task) or unintentional inhibition (B-P task) (Chapters 4 and 6). In both

samples, these documented intentional inhibition difficulties were not related to

delusions or negative symptoms (Chapters 3 and 6). All chapters documented high

levels of anxiety associated with hallucinatory-type experiences, and in individuals

predisposed to hallucinations this association was stronger and more consistent for

3 It should be noted that the type of data analyses performed to inspect the data in the

hallucination predisposition and schizophrenia samples was not identical.

Chapter 7

199

anxiety than either depression or stress (Chapter 2), which is consistent with the

previous schizophrenia literature (Delespaul et al., 2002; Norman et al., 1998; Tien &

Eaton, 1992). Finally, despite significant relationships between anxiety and intentional

inhibition (reported in both Chapters 5 and 6), the relationship between intentional

inhibition and hallucination predisposition (Chapter 3) and AH severity in

schizophrenia (Chapter 6) remained significant when controlling for anxiety, showing

that, across the symptom continuum, the intentional inhibition difficulties that underlie

AHs are independent of anxiety.

The one major difference between the hallucination predisposition and

schizophrenia studies in this thesis of note, was that intentional resistance to

interference (as measured by the DI task) was related to sub-clinical positive symptoms

(namely, hallucinatory experiences and delusional beliefs) in healthy individuals

(Chapter 4), but was unrelated to either AH severity or delusions in individual with

schizophrenia (Chapter 6). It is possible, therefore, that there is a discrepancy between

some (but not all) of the cognitive processes leading to clinical and sub-clinical positive

symptoms. However, there are two other possible explanations for this incongruity.

Firstly, changes to the semantic relatedness of DI task stimuli (see Chapter 6,

Discussion) may have inadvertently lowered the task difficulty in the schizophrenia

study. Thus, poor resistance to interference may be related to the positive symptoms of

schizophrenia, but only when goal-relevant and goal-irrelevant information are related.

Secondly, it is possible that the found association between DI task performance and

sub-clinical positive symptoms in healthy individuals actually reflects a vulnerability to

schizophrenia more generally (i.e. schizotypy). This proposal is consistent with the

findings reported in Chapter 6, since schizophrenia participants (overall) performed

more poorly than control participants on the DI task interference indices. In further

support of this interpretation, additional correlational analyses revealed a significant

association between DI intrusions and all three sub-clinical symptom measures

administered in Chapter 4, including introvertive anhedonia (r = .36, p < .05, N = 48;

LSHS-R: r = .29, p < .05, N = 49; Peter‟s delusion inventory: r = .35, p < .05, N = 49).4

4 The relationship between the cognitive control measures and introvertive anhedonia were not

investigated in either Chapter 3 or 4, since the high and low LSHS-R groups did not differ

significantly on this measure. As a side point, the introvertive anhedonia scale did not correlate

significantly with any of the inhibition indices on either the ICIM or the B-P task.

Chapter 7

200


As with all studies based on psychometric identification of individuals

considered to be at heightened risk for a symptom or disorder, it is necessary to consider

exactly what high scorers are at risk of. Specifically, it could be argued that the high

hallucination predisposed participants tested in Chapters 3, 4 and 5 may have been

predisposed to schizophrenia more generally (i.e., high schizotypy), rather than

hallucinations more specifically. If this were the case, the findings reported in these

studies may signify cognitive and affective vulnerability markers for schizophrenia

more generally, rather than hallucination predisposition per se, since a between-group

data analysis design was adopted, rather than examining symptom correlations.

Although there is some overlap between hallucination predisposition and schizotypy

(and indeed, using additional follow-up analyses we argued that this overlap may have

been responsible for the group effects on the DI task reported in Chapter 4), there are

several important points which refute this alternative conjecture with regard to the

intentional inhibition findings. Firstly, as reported in Chapters 3, 4 and 5, there was no

significant difference between the high and low LSHS-R groups on the measure of

introvertive anhedonia, which would be expected if this group as a whole were

vulnerable to schizophrenia (Mason & Claridge, 2006; Yung & McGorry, 1996).

Secondly, although the high LSHS-R participants had higher delusion ratings than the

low LSHS-R participants, this was expected, since AHs and delusions are found to co-

occur even in healthy individuals without psychosis (van Os, Hanssen, Bijl, & Ravelli,

2000). Thirdly, and most importantly, the LSHS-R group differences on the ICIM task

remained significant when controlling for delusional ideation, highlighting the

specificity of intentional inhibition difficulties linked to hallucination predisposition,

consistent with the schizophrenia study findings (Chapter 6).


Until recently, the empirical examination of AHs has almost exclusively been

conducted in schizophrenia samples. The finding that similar affective and cognitive

disturbances are associated with hallucinatory experiences in the general population as

are found in schizophrenia, suggests that these disturbances found in schizophrenia may

not [only] be the product of the clinical symptoms themselves (i.e. distress caused by

AHs), or features associated with schizophrenia (i.e. inhibition deficits due to general

Chapter 7

201

cognitive decline), since many individuals identified through the LSHS-R as being

predisposed to hallucinations are not experiencing full-blown psychotic symptoms. This

implies that these cognitive and affective disturbances are directly involved in the

development of hallucinatory-type experiences. Likewise, support for the continuum

approach to AHs is extremely valuable, since it further validates the study of psychosis

at the symptom level, which is especially important in schizophrenia because of the

heterogeneity of its genotypic and phenotypic presentation, and the consequent ongoing

debate over diagnostic criteria and sub-grouping (Harris, Gordon, Bahramali, & Slewa-

Younan, 1999; Keefe & Fenton, 2007; Liddle, 1987; Peralta & Cuesta, 2001).

Furthermore, studying AHs in a healthy population overcomes the ethical and

methodological issues of over-testing clinical samples, and also avoids the confounding

variables often associated with testing a schizophrenia sample, such as the influence of

other symptoms, global cognitive decline, and the effects of medication and

institutionalisation.

Clearly the findings reported in the hallucination predisposition studies

(Chapters 2, 3, 4 and 5) were based on undergraduate psychology student samples, and

thus may not be representative of the healthy population at large, since undergraduate

samples typically have a higher mean IQ (or „cognitive reserve‟) than the general

population, as well as a more restricted range of ages, socio-demographic

characteristics, and educational experiences. However, this is not a major limitation for

several reasons. Firstly, one would expect, if anything, that cognitive disturbances

associated with hallucination predisposition would be reduced in a student sample

compared to a general population sample, given their higher than average IQ or

„cognitive reserve‟ that may protect them from cognitive disturbances. Secondly, it is

important to note that studies have reported similar occurrence rates of hallucinations in

student populations as in the general population (Barrett & Etheridge, 1992; Johns,

Nazroo, Bebbington, & Kuipers, 1998). To overcome this limitation, future research

should examine the relationships between hallucination predisposition, anxiety and

inhibitory control in the general population to ensure the representation validity of these

findings. In addition, the different statistical analyses employed in each of the studies

limited our ability to make direct comparisons across studies. The statistical approach

adopted in each study was chosen to address the specific aim of that study and to fit

with, or to replicate (in instance of the schizophrenia study; Waters et al., 2003), the

existing literature. Finally, the range of experimental measures selected for analysis

varied occasionally across each of the studies, again limiting some comparisons. For

Chapter 7

202

example, reaction times on the ICIM task were not reported in the schizophrenia study

(Chapter 6). The reason for this decision was that speed of cognitive processing and

motor response speed impairments have been well documented in schizophrenia,

making reaction time a less sensitive measure of inhibitory control (e.g., Badcock,

Williams, Anderson, & Jablensky, 2004; Gale & Holzman, 2000). In contrast, reaction

times have been found to be particularly sensitive measures of inhibitory control on the

ICIM task in healthy participants (Schnider et al., 2002), and thus were included in the

predisposition studies (Chapters 3 and 5).

The methodological obstacles faced in the experiments presented in this thesis

provide promising avenues for future research. The ability to generalise the findings to

hallucinatory experiences occurring in modalities other than the auditory modality

warrants further research. The LSHS-R was used to measure hallucination

predisposition in Chapters 2 to 5 to ensure consistency with the existing hallucination

predisposition research literature. However, the LSHS-R includes items that describe

visual hallucinatory-type experiences, and thus is not strictly a measure of

predisposition to AHs (although it should be noted that of the 12 items, only one is

visual and one does not specify a modality). Conversely, the measure of hallucinations

in the schizophrenia study was restricted to AHs, since AHs are by far the most

common type of hallucination, and consequently, severity measures of hallucinations

are largely restricted to auditory experiences (e.g., Haddock, McCarron, Tarrier, &

Faragher, 1999). However, it is possible that similar cognitive and affective

mechanisms may underlie both forms of hallucinations, since auditory and visual items

on the LSHS-R scale did not group into separate components in the factor analysis

reported in Chapter 2, and furthermore, the risk of experiencing visual hallucinations is

increased in individuals who experience AHs in both schizophrenia and the general

population (Johns et al., 2004; Liddle, 1987; Ohayon, 2000). Consistent with this,

Badcock and Maybery (2005) have mapped the Badcock et al. dual-deficit model of

AHs onto a recent dual-deficit model of visual hallucinations proposed by Collerton and

colleagues (Collerton, Perry, & McKeith, 2005). Finally, in this thesis, the separable

relationships between the different hallucination predisposition components (i.e., those

identified in Chapter 2) and the cognitive variables under investigation were not

examined, since this thesis aimed to investigate the cognitive difficulties thought to

underpin the „intrusive‟ feature of hallucinatory-type experiences, which all three

LSHS-R components shared. Similarly, anxiety was found to relate to all three LSHS-R

components, making this style of investigation unnecessary. However, future studies

Chapter 7

203

may wish to separate the LSHS-R components in the investigation and analysis of the

cognitive deficits thought to underlie the source misattribution feature of AHs (Laroi &

Woodward, 2007), such as deficits in contextual memory binding.


The collective finding that similar cognitive and affective processes underlie

hallucinatory experiences in healthy hallucination predisposed individuals and

individuals with schizophrenia suggests that treatment programs targeting hallucinatory

experiences need not include diagnostic label in the inclusion criteria. Already,

worldwide organisations, such as the Hearing Voices Network (also known as

Intervoice), sponsor therapeutic group programs that are attended by both individuals

with and without a psychotic illness (James, 2001; Romme & Escher, 2000). This

organisation strongly advocates for this within-group diversity to reduce stigma and to

promote a sharing of coping skills and advice between people who have and have not

yet learnt to cope with their „voices‟. In addition, the previously suggested treatment

combination (namely, anxiety management and treatments targeting intentional

inhibition) may be particularly useful in the prevention of psychosis onset in ultra high-

risk individuals, since these individuals often exhibit affective disturbance and isolated

symptoms, such as AHs (Mason et al., 2004). However, further research is required to

investigate whether untra high-risk individuals are characterised by similar cognitive

and affective dysfunctions, as the continuum model predicts.

Summary

Together the current findings support the continuum approach to AHs, and

suggest that there are both shared and unique mechanisms contributing to the experience

of hallucinations at different points along the AH continuum. The findings from the

studies presented in this thesis generally show more similarities than differences

between the pattern of associated cognitive and affective difficulties in healthy

hallucination predisposed individuals and hallucinating individuals with schizophrenia.

Specifically, the findings suggest that hallucinatory experiences across the continuum

are critically related to intentional inhibitory impairments (which are unrelated to other

schizophrenia-related symptoms) and heightened levels of anxiety (more so than

depression or stress). The intentional inhibition difficulties found to underpin

Chapter 7

204

hallucinatory experiences were found to occur independently from anxiety across the

symptom continuum. However, the findings confirmed the previously documented

association between anxiety and poor intentional cognitive control, suggesting that

anxiety may exacerbate existing intentional inhibition difficulties in hallucinating

individuals across the continuum.

FINAL COMMENTS

Badcock and colleague‟s cognitive model of AHs began with the proposition

that at least two cognitive deficits are integral to the production of AHs in

schizophrenia: an intentional cognitive inhibition deficit, hypothesised to contribute to

the unintended and intrusive nature of AHs, and a contextual memory binding deficit,

hypothesised to contribute to the source misattribution aspect of AHs (Badcock &

Maybery, 2005; Badcock et al., 2007; Badcock et al., 2005; Waters, Badcock, &

Maybery, 2006; Waters et al., 2003; Waters, Badcock, Michie et al., 2006). The

findings reported in this thesis compliment and extend this model, highlighting a third

component connected to the experience of AHs: anxiety. Undoubtedly this model will

continue to evolve, with future research likely to expose additional processes involved

in the production of AHs, such as the mechanisms leading to the initial activation of the

cognitions prior to their intrusion into consciousness.

Importantly, the findings reported in this thesis have shed light on the cognitive

and affective underpinnings of AHs. However, clarification is undoubtedly required

concerning the ways in which the profile of deficits advocated by the Badcock et al.

model maps from the cognitive level onto the neural level in individuals who experience

AHs. Ultimately, to achieve a full understanding of how these multiple

deficits/dysfunctions might emerge and interact during the development of AHs, the

amalgamation of unique insights gained from different methodological approaches (e.g.,

cross-sectional and longitudinal designs) will be required, as well as the integration of

information at the levels of genetics, neurobiology, cognition and behaviour.

To conclude, it is clear that understanding the mechanisms involved in the

production and maintenance of AHs is one of the most important challenges facing

schizophrenia researchers, since the experience of AHs is often frightening and

disabling, and is associated with a need for care (Bak et al., 2005). The burden of these

emotional and financial consequences of AHs to the individual, their families, and the

community at large is tremendous. While it is acknowledged that a multidimensional

Chapter 7

205

understanding of AHs is only just emerging from its infancy, it is hoped that the

concepts and findings presented in this thesis have not only offered further insights into

the underpinnings of AHs, but provided a solid base upon which future research – and

ultimately, clinical interventions – can build.

Chapter 7

206

REFERENCES

Abramowitz, J. S., Brigidi, B. D., & Roche, K. R. (2001). Cognitive-behavioral therapy

for obsessive-compulsive disorder: A review of the treatment literature.

Research on Social Work Practice, 11, 357-372.





American Psychiatric Association. (2000). Diagnostic and Statistical Manual of Mental

Disorders (DSM-IV-TR) (4th ed.). Washington DC: American Psychiatric

Association.







Amir, N., Foa, E. B., & Coles, M. E. (1998). Automatic activation and strategic

avoidance of threat-relevant information in social phobia. Journal of Abnormal


Anderson, J. R., Qin, Y., Jung, K.-J., & Carter, C. S. (2007). Information-processing

modules and their relative modality specificity. Cognitive Psychology, 54, 185-

217.

Anderson, L., & Shimamura, A. P. (2005). Influences of emotion on context memory

while viewing film clips. American Journal of Psychology, 118, 323-337.



Badcock, J. C., & Maybery, M. T. (2005). Common or distinct deficits for auditory and

visual hallucinations? [Open Peer Commentary]. Behavioral and Brain

Sciences, 28, 757-758.




Chapter 7

207




Badcock, J. C., Williams, R. J., Anderson, M., & Jablensky, A. (2004). Speed of

processing and individual differences in IQ in schizophrenia: General or specific

cognitive deficits? Cognitive Neuropsychiatry, 9, 233-247.

Bak, M., Myin-Germeys, I., Delespaul, P., Vollebergh, W., de Graaf, R., & van Os, J.

(2005). Do different psychotic experiences differentially predict need for care in

the general population? Comprehensive Psychiatry, 46, 192-199.

Barrett, T. R., & Etheridge, J. B. (1992). Verbal hallucinations in normals: I. People

who hear "voices." Applied Cognitive Psychology, 6, 379-387.

Baumeister, R. F., Vohs, K. D., & Tice, D. M. (2007). The strength model of self-

control. Current Directions in Psychological Science, 16, 351-355.



527-529.

Berens, G., & Eling, P. (2003). The Stroop color-word test measures more than you

think. Nederlands Tijdschrift voor de Psychologie en haar Grensgebieden, 58,

115-121.

Broadbent, D., & Broadbent, M. (1988). Anxiety and attentional bias: State and trait.

Cognition and Emotion, 2, 165-183.

Burns, D. J. (2004). The simultaneous acquisition effect: Simultaneous task learning

inhibits memory for order. American Journal of Psychology, 117, 229-248.




Collerton, D., Perry, E., & McKeith, I. (2005). Why people see things that are not there:

A novel perception and attention deficit model for recurrent complex visual

hallucinations. Behavioral and Brain Sciences, 28, 737-794.



Davies, M. F., Griffin, M., & Vice, S. (2001). Affective reactions to auditory

hallucinations in psychotic, evangelical and control groups. British Journal of


Chapter 7

208









compulsive disorder. British Journal of Clinical Psychology, 32, 67-74.

Eysenck, M. W. (1992). Anxiety: The cognitive perspective. Hove, UK: Erlbaum.



Fleming, K., Goldberg, T. E., Gold, J. M., & Weinberger, D. R. (1995). Verbal working

memory dysfunction in schizophrenia: Use of a Brown-Peterson paradigm.

Psychiatry Research, 56, 155-161.

Fox, E. (1994). Attentional bias in anxiety: A defective inhibition hypothesis. Cognition

and Emotion, 8, 165-195.



Therapy, 41, 923-947.


(1994). Health-related intrusive thoughts. Journal of Psychosomatic Research,

38, 203-215.




Fuster, J. M. (1999). Synopsis of function and dysfunction of the frontal lobe. Acta

Psychiatrica Scandinavia, 395, 51-57.

Gale, H. J., & Holzman, P. S. (2000). A new look at reaction time in schizophrenia.


Gray, J. R. (2001). Emotional modulation of cognitive control: Approach-withdrawal

states double-dissociate spatial from verbal two-back task performance. Journal

of Experimental Psychology: General, 130, 436-452.

Guillem, F., Bicu, M., Bloom, D., Wolf, M. A., Desautels, R., Lalinec, M., et al. (2001).

Neuropsychological impairments in the syndrome of schizophrenia: A

Chapter 7

209

comparison between different dimensional models. Brain and Cognition, 46,

153-159.










Academic Press.

Harris, A. W. F., Gordon, L. W., Bahramali, H., & Slewa-Younan, S. (1999). Different

psychopathological models and quantified EEG in schizophrenia. Psychological

Medicine, 29, 1175-1181.






Hunter, M. D., Eickhoff, S. B., Miller, T. W. R., Farrow, T. F. D., Wilkinson, I. D., &

Woodruff, P. W. R. (2006). Neural activity in speech-sensitive auditory cortex

during silence. Proceedings of the National Academy of Sciences, 103, 189-194.

James, A. (2001). Raising our voices: An account of the hearing voices movement.

London: Handsell Publishing.

Jenner, J. A., van de Willige, G., & Wiersma, D. (1998). Effectiveness of cognitive

therapy with coping training for persistent auditory hallucinations: A

retrospective study of attenders of a psychiatric out-patient department. Acta


Johns, L. C., Cannon, M., Singleton, N., Murray, R. M., Farrell, M., Brugha, T., et al.

(2004). Prevalence and correlates of self-reported psychotic symptoms in the

British population. British Journal of Psychiatry, 185, 298-305.



Chapter 7

210







Kapur, S., Mizrahi, R., & Li, M. (2005). From dopamine to salience to psychosis -

linking biology, pharmacology and phenomenology of psychosis. Schizophrenia

Research, 79, 59-68.



Kipp, K., Pope, S., & Digby, S. E. (1998). The development of cognitive inhibition in a

reading comprehension task. European Review of Applied Psychology, 48, 19-

25.

Konishi, S., Nakajima, K., Uchida, I., Kikyo, H., Kameyama, M., & Miyashita, Y.

(1999). Common inhibitory mechanism in human inferior prefrontal cortex

revealed by event-related functional MRI. Brain, 122, 981-991.



Krabbendam, L., Myin-Germeys, I., Bak, M., & van Os, J. (2005). Explaining

transitions over the hypothesized psychosis continuum. Australian and New

Zealand Journal of Psychiatry, 39, 180-186.

Krabbendam, L., Myin-Germeys, I., Hanssen, M., de Graaf, R., Vollebergh, W., Bak,

M., et al. (2005). Development of depressed mood predicts onset of psychotic

disorder in individuals who report hallucinatory experiences. British Journal of




185-189.




Laming, D. (1992). Analysis of short-term retention: Models for Brown-Peterson

experiments. Journal of Experimental Psychology: Learning, Memory, and

Cognition, 18, 1342-1365.

Chapter 7

211

Laroi, F., & Van Der Linden, M. (2005). Nonclinical participants' reports of

hallucinatory experiences. Canadian Journal of Behavioural Science, 37, 33-43.

Laroi, F., & Woodward, T. S. (2007). Hallucinations from a cognitive perspective.

Harvard Review of Psychiatry, 15, 109-117.



MacLeod, C. M. (1991). Half a century of research on the Stroop effect: An integrative

review. Psychological Bulletin, 109, 163-203.

Mason, O., & Claridge, G. (2006). The Oxford-Liverpool Inventory of Feelings and

Experiences (O-LIFE): Further description and extended norms. Schizophrenia

Research, 82, 203-211.

Mason, O., Startup, M., Halpin, S., Schall, U., Conrad, A., & Carr, V. (2004). Risk

factors for transition to first episode psychosis among individuals with 'at-risk

mental states'. Schizophrenia Research, 71, 227-237.

Matthews, G., & Harley, T. A. (1996). Connectionist models of emotional distress and

attentional bias. Cognition and Emotion, 10, 561-600.

Mattson, D. T., Berk, M., & Lucas, M. D. (1997). A neuropsychological study of

prefrontal lobe function in the positive and negative subtypes of schizophrenia.

Journal of Genetic Psychology, 158, 487-494.



Miller, E. K., & Cohen, J. D. (2001). An integrative theory of prefrontal cortex function.

Annual Review of Neuroscience, 24, 167-202.






1209.

Murray, M. M., Michel, C. M., Grave de Peralta, R., Ortigue, S., Brunet, D., Gonzalez

Andino, S., et al. (2004). Rapid discrimination of visual and multisensory

memories revealed by electrical neuroimaging. Neuroimage, 21, 125-135.



Chapter 7

212





Norman, R. M., Malla, A. K., Morrison-Stewart, S. L., Helmes, E., Williamson, P. C.,

Thomas, J., et al. (1997). Neuropsychological correlates of syndromes in

schizophrenia. British Journal of Psychiatry, 170, 134-139.

O'Connor, K., Aardema, F., Bouthillier, D., Fournier, S., Guay, S., Robillard, S., et al.

(2005). Evaluation of an inference-based approach to treating obsessive-

compulsive disorder. Cognitive Behaviour Therapy, 32, 148-163.

Ohayon, M. M. (2000). Prevalence of hallucinations and their pathological associations

in the general population. Psychiatry Research, 97, 153-164.

Penades, R., Catalan, R., Salamero, M., Boget, T., Puig, O., Guarch, J., et al. (2006).

Cognitive Remediation Therapy for outpatients with chronic schizophrenia: A

controlled and randomized study. Schizophrenia Research, 87, 323-331.




Peters, E., Day, S., McKenna, J., & Orbach, G. (1999). Delusional ideation in religious

and psychotic populations. British Journal of Clinical Psychology, 38, 83-96.

Phillips, N. A., & Lesperance, D. (2003). Breaking the waves: Age differences in

electrical brain activity when reading text with distractors. Psychology and

Aging, 18, 126-139.

Pihan, H., Gutbrod, K., Baas, U., & Schnider, A. (2004). Dopamine inhibition and the

adaptation of behavior to ongoing reality. Neuroreport: For Rapid

Communication of Neuroscience Research, 15, 709-712.

Prinz, W. (1978). Aural and oral interference of visual search processes. Zeitschrift fur

Experimentelle und Angewandte Psychologie, 25, 441-455.





Romme, M., & Escher, S. (2000). Making sense of voices: A guide for professionals

who work with voice hearers. London: Mind.

Chapter 7

213





5880-5884.




Seibert, P. S., & Ellis, H. C. (1991). Irrelevant thoughts, emotional mood states, and

cognitive task performance. Memory and Cognition, 19, 507-513.




265-272.

Shackman, A. J., Sarinopoulos, I., Maxwell, J. S., Pizzagalli, D. A., Lavric, A., &

Davidson, R. J. (2006). Anxiety selectively disrupts visuospatial working

memory. Emotion, 6, 40-61.

Shapiro, K. L., & Lim, A. (1989). The impact of anxiety on visual attention to central

and peripheral events. Behaviour Research and Therapy, 27, 345-351.

Silbersweig, D. A., Stern, E., Frith, C., Cahill, C., Holmes, A., Grootoonk, S., et al.

(1995). A functional neuroanatomy of hallucinations in schizophrenia. Nature,

378, 176-179.

Sison, J. A., & Mather, M. (2007). Does remembering emotional items impair recall of

same-emotion items? Psychonomic Bulletin and Review, 14, 282-287.



Steel, C., Fowler, D., & Holmes, E. A. (2005). Trauma-related intrusions and psychosis:

An information processing account. Behavioural and Cognitive Psychotherapy,

33, 139-152.

Stein, D. J., & Hollander, E. (1994). A neural network approach to obsessive-

compulsive disorder. Journal of Mind and Behavior, 15, 223-237.

Stein, D. J., & Ludik, J. (2000). A neural network of obsessive- compulsive disorder:

Modelling cognitive disinhibition and neurotransmitter dysfunction. Medical

Hypotheses, 55, 168-176.

Chapter 7

214

Stephane, M., Barton, S., & Boutros, N. N. (2001). Auditory verbal hallucinations and

dysfunction of the neural substrates of speech. Schizophrenia Research, 50, 61-

78.






610-618.

Tryon, W. W. (1998). A neural network explanation of posttraumatic stress disorder.

Journal of Anxiety Disorders, 12, 373-385.

van Os, J., Hanssen, M., Bijl, R. V., & Ravelli, A. (2000). Strauss (1969) revisited: A

psychosis continuum in the general population? Schizophrenia Research, 45, 11-

20.






Research, 62, 275-280.






Whitehouse, A. J. O., Maybery, M. T., & Durkin, K. (2006). The development of the

picture superiority effect. British Journal of Developmental Psychology, 24,

767-773.

Wible, C. G., Anderson, J., Shenton, M. E., Kricun, A., Hirayasu, Y., Tanaka, S., et al.

(2001). Prefrontal cortex, negative symptoms, and schizophrenia: An MRI

study. Psychiatry Research: Neuroimaging, 108, 65-78.

Wiersma, D., Jenner, J. A., van de Willige, G., Spakman, M., & Nienhuis, F. J. (2001).

Cognitive behaviour therapy with coping training for persistent auditory

hallucinations in schizophrenia: A naturalistic follow-up study of the durability

of effects. Acta Psychiatrica Scandinavica, 103, 393-399.

Chapter 7

215

Wolkin, A., Choi, S. J., Szilagyi, S., Sanfilipo, M., Rotrosen, J. P., & Lim, K. O. (2003).

Inferior frontal white matter anisotropy and negative symptoms of

schizophrenia: A diffusion tensor imaging study. American Journal of



Emotion, 1, 166-181.

Wyland, C. L., Kelley, W. M., Macrae, C. N., Gordon, H. L., & Heatherton, T. F.

(2003). Neural correlates of thought suppression. Neuropsychologia, 41, 1863-

1867.

Yucel, M., Lubman, D. I., Solowij, N., & Brewer, W. J. (2007). Understanding drug

addiction: A neuropsychological perspective. Australian and New Zealand


Yung, A. R., & McGorry, P. D. (1996). The prodromal phase of first-episode

psychosis: Past and current conceptualizations. Schizophrenia Bulletin, 22, 353-

370.




Zemishlany, Z., Alexander, G. E., Prohovnik, I., Goldman, R. G., Mukherjee, S., &

Sackeim, H. (1996). Cortical blood flow and negative symptoms in

schizophrenia. Neuropsychobiology, 33, 127-131.

216

Appendices

217

APPENDICES

Appendices

218

APPENDIX A

Words Used in the Brown-Peterson Variant Task (Chapter 4 and 6)

Note. Categories and items taken from Battig, W. F., & Montague, W. E. (1969).

Category norms for verbal items in 56 categories: A replication and extension of the

Connecticut Category Norms. Journal of Experimental Psychology Monograph, 80, 1-

46. a The categories included in Chapter 6 (all five categories were used in Chapter 4).

A four-footed animal a

List 1 List 2 List 3

lion elephant tiger

sheep bear mouse

goat giraffe deer

squirrel rabbit leopard

donkey fox bull

buffalo moose antelope

camel lamb monkey

panther raccoon llama

rat zebra wolf

beaver rhinoceros mule

Mean Frequency (SD) 69.80 (62.75) 66.80 (51.92) 67.00 (57.42)

Mean Letters (SD) 5.50 (1.58) 5.90 (2.13) 5.20 (1.40)

Appendices

219

A name applied to a person to indicate his occupation or profession a


doctor lawyer teacher

plumber engineer dentist

policeman salesman professor

merchant scientist nurse

banker labourer accountant

physicist chemist clerk

fireman executive farmer

mechanic judge manager

architect pharmacist secretary

president minister bricklayer


Mean Letters (SD) 7.70 (1.25) 6.80 (1.49) 7.50 (1.9)

A fruit a


banana peach grape

apricot grapefruit plum

pineapple tomato lime

strawberry prunes watermelon

blueberry cantaloupe raspberry

mango fig avocado

raisin coconut nectarine

melon berry kumquat

lemon cherry tangerine

date blackberry papaya


Mean Letters (SD) 6.50 (1.90) 6.80 (2.44) 7.00 (2.21)

Appendices

220

A type of vehicle


train bus airplane

bicycle boat scooter

ship tricycle bike

tractor taxi cart

trailer jet jeep

cab skates helicopter

subway motorbike tank

carriage horse rocket

sled truck wagon

automobile van trolley


Mean Letters (SD) 6.00 (2.05) 5.00 (2.11) 5.90 (2.08)

A sport


golf swimming tennis

hockey soccer track

lacrosse skiing archery

volleyball ping-pong softball

fencing boxing handball

fishing rugby hunting

polo gymnastics racing

sailing squash diving

bowling boating wrestling

surfing pool skating


Mean Letters (SD) 6.70 (1.77) 6.60 (1.71) 6.90 (1.20)

Appendices

221

APPENDIX B

Stories and Comprehension Questions Used in the Directed Ignoring Task (Chapter 4)

Note. * = correct response; # = foil error (distractor intrusion)

Practice trial 1 (no distractors)

Target Passage

The Bank

Derek went to the bank early in the morning to avoid a queue. He wanted to open a new

account to save money. Even though it was early in the morning, there were already

several other people there waiting in line. Derek waited for twenty minutes before

being served. He wanted to open a savings account, and had to fill out several forms

before queuing in another line. The pen leaked, and Derek ended up with ink all over

his hands. By this time, it was shortly after noon. Derek spent another half an hour

waiting in line before being served again. When he finally opened the account, it was

already early in the afternoon. Derek decided to take the rest of the day off.

Comprehension Questions

1. Derek went to the bank to…

a. apply for a loan c. obtain a cheque book

b. open a savings account * d. change his personal details

2. When Derek got to the bank…

a. other people were already waiting in line * c. he ran into his friend

b. he was the first one there d. he was all hot and bothered

3. After the bank, Derek decided to…

a. go back to work c. eat breakfast

b. go back to university d. take the rest of the day off *

4. When did Derek go to the bank?

a. In the afternoon c. Early in the morning *

b. On Tuesday d. On Friday

Appendices

222

Practice trial 2 – with Distractors

Target Passage

The New Baby

Fred Wilson and his friend Ivan Southmore walked quickly down the white walkways

of the hospital. Fred was excited to be there that day. His enthusiasm was

understandable since this was the birth of his first child and he wanted to show his new

daughter off to his friend. As they arrived at the nursery window Fred gave his friend a

nudge and pointed to a small bundle right near the window. Fred pressed his face right

up against the glass and began to fog it up. “Isn‟t she absolutely beautiful?” Fred said to

his pal, “She‟s got her Daddy‟s brown eyes.” Ivan agreed and after about half an hour

of staring they decided to go and see the newborn‟s mother and share her joy.

Distractors

Frequency Letters

cousin 51 6

nurse 17 5

corridor 17 8

features 37 8

30.5 6.75

Appendices

223

Example of Target Passage with Distractors

The New Baby

Fred Wilson and his nurse cousin friend Ivan Southmore walked quickly down corridor

features the white walkways cousin features of the hospital. Fred was nurse corridor

excited to be there cousin nurse cousin that day. His enthusiasm was features nurse

understandable since this features corridor was the birth of his first cousin corridor

child and he wanted to nurse features show his new daughter off to corridor cousin his

friend. As they arrived at the corridor nurse nursery window cousin corridor Fred gave

his nurse features friend a corridor nudge and pointed to features cousin a small bundle

cousin right near the corridor nurse window. Fred pressed his cousin features face right

up against the nurse corridor glass and began to cousin features fog it up. "Isn't

features nurse she absolutely beautiful cousin?" Fred said to his nurse corridor pal,

"She's got cousin corridor her Daddy's features brown eyes." Ivan agreed and nurse

features after about half an corridor cousin hour of staring nurse they decided to go

corridor features and see the cousin newborn's nurse features mother and corridor share

her features nurse joy.


1. Fred arrived at the hospital with…

a. the ambulance c. his friend *

b. his family d. his cousin #

2. Fred walked down the hospital…

a. walkways # c. corridors *

b. sadly d. passages

3. When they arrived at the nursery window, Fred…

a. smiled at the baby c. pointed to a small bundle *

b. felt embarrassed d. saw the nurse #

4. The baby had her Daddy‟s…

a. nose c. ears

b. features # d. eyes *

Appendices

224

Test trials (each story was presented in the distractor/control condition 50% of the time)

Target Passage

Going Walking

Jeremy lived near a eucalyptus forest. One crisp morning, he decided to take a walk in

the forest. It would be a nice short trip for that day. He packed a small bag with his

lunch and his thermos that was filled with black coffee, and set off. He loved the local

flora and fauna, and would often spend hours admiring them. As he walked through the

forest, the smell of the eucalyptus trees filled the air, and he could hear the crickets in

the distance. After a few hours, Jeremy stopped to have lunch. As he rested on the

ground, he poured coffee from his thermos. Jeremy felt instantly refreshed after sipping

his coffee. Following lunch, he continued on his tour of the forest.

Distractors

Frequency Letters

birds 31 5

tea 28 3

bush 14 4

lake 54 4

31.75 4


1. Where did Jeremy decide to walk?

a. In a swamp c. In the bush #

b. In the park d. In the eucalyptus forest *

2. Jeremy filled his thermos with…

a. coffee * c. tea #

b. soup d. hot chocolate

3. What could he hear in the distance?

a. Frogs c. Lions

b. Crickets * d. Birds #

4. Where did he have lunch?

a. Under a pine tree c. By the lake #

b. On the ground * d. Next to the river

Appendices

225

Target Passage

The Art Gallery

Bertha McKee brushed off the droplets of water that had fallen on her as she walked

through the sprinklers to get to the art gallery. She worked there as a volunteer at the

information booth. She took her seat at the information booth and waited for the days

art viewers to arrive. Bertha loved art, and this job allowed her to see all of the different

types of art. She picked up a box of pamphlets that told of upcoming displays. When

she looked through one of the pamphlets, she became very excited. The Mona Lisa was

soon to arrive, and „Sunflowers‟, by Vincent Van Gogh, was also arriving in a few

months. Bertha could not wait for the exhibits to show at the gallery.

Distractors

Frequency Letters

museum 32 6

sculpture 11 9

paint 37 5

talent 40 6

30 6.5


1. Bertha McKee…

a. worked at the museum # c. was looking for work

b. wasn‟t able to work d. worked at the art gallery *

2. Bertha had just walked through…

a. sprinklers * c. mud

b. a construction site d. paint #

3. When it came to art, Bertha…

a. had talent # c. preferred Rembrandt

b. loved different types of art * d. liked Monet

4. What did Bertha read about in the pamphlet?

a. Job vacancies c. Upcoming displays *

b. A sculpture exhibition # d. Art history

Appendices

226

Target Passage

The Basketball Match

Glen Taylor got two tickets to the basketball match. He took along his cousin Andrew,

who was a big fan of basketball. It was the first time that Glen had been to a match,

and he wondered how different it would be to watching it on television. When Glen

and Andrew arrived at the stadium, they found their seats. They were near the front,

and close enough to get a good look at the players on the team. The atmosphere in the

stadium was electric, as everyone cheered excitedly for the team. Glen and Andrew

joined in the cheering when their team made the shot. It was even more fantastic than

Glen had imagined, and it was far better than watching the match on television.

Distractors

Frequency Letters

mate 21 4

loud 20 4

football 36 8

winning 31 7

27 5.75


1. Glen took along his…

a. mate # c. uncle

b. cousin * d. sister

2. Andrew was a big fan of…

a. sports c. basketball *

b. football # d. hotdogs

3. The atmosphere in the stadium was…

a. loud # c. sombre

b. boring d. electric *

4. Glen and Andrew joined in the cheering when their team…

a. made a shot * c. argued with the umpire

b. got a penalty shot d. were winning #

Appendices

227

Target Passage

The Birthday Celebration

Rebecca was soon turning nineteen, but she had not yet decided how to celebrate it. All

she wanted was a place for everyone to have a good time and enjoy good food. She did

not know which of her friends she was going to invite. She was unsure about this as her

work friends did not get along with her friends she plays netball with. She thought it

best to have several small gatherings with these different groups of friends. She would

have one gathering with her friends from work at her favourite coffee shop near work.

As for the other gathering, Rebecca‟s friend from netball suggested that she have a

small gathering down at the pub. Rebecca liked the sound of both those options.

Distractors

Frequency Letters

thirty 59 6

dancing 43 7

cafe 20 4

associates 15 10

34.25 6.75


1. How old was Rebecca turning?

a. Nineteen * c. Thirty #

b. Seventeen d. Twenty

2. Rebecca‟s friends…

a. were all best friends c. were all very busy

b. were all business associates # d. did not get along with one another *

3. In the end, she decided to…

a. throw one big gathering c. hold two separate gatherings *

b. go dancing # d. stay at home

4. Rebecca‟s celebration with her work friends was at…

a. her house c. a nightclub

b. a coffee shop near work * d. a café #

Appendices

228

Target Passage

The Market

Every Sunday morning, Angela Cameron went to the markets and this Sunday was no

exception. Angela enjoyed going to the markets, as there were many things to see there.

Her first stop was to shop for groceries and she liked that there were several fruit and

vegetable stalls where she could pick up some supplies for the coming week. She

bought some peaches, and bananas, as well as carrots and tomatoes. Angela then

looked for a housewarming present for her friend. She could not decide between a nice

set of fluffy towels and big comfortable cushions for her friend‟s couch. In the end, she

bought the cushions for her friend, and towels for her own place. She then went home

to have a leisurely lunch.

Distractors

Frequency Letters

Friday 60 6

Supper 37 6

Fish 35 4

Flowers 23 7

38.75 5.75


1. Angela went to the market every…

a. Friday # c. Sunday *

b. Saturday d. Monday

2. Her first stop was to shop for…

a. groceries * c. a housewarming present

b. fish # d. clothing

3. What did Angela end up buying her friend?

a. Teapot and cups c. Flowers #

b. A jumper d. Cushions *

4. What did Angela go home for?

a. Dinner c. Breakfast

b. Lunch * d. Supper #

Appendices

229

Target Passage

The Music Fan

Jason always wanted to be a rock star. He is a big fan of heavy metal music, and has

many heavy metal albums. He has been collecting albums since he was thirteen, when

he bought an ACDC album. At this age, he would lie in bed with the radio turned up

loud, and play air guitar to all the songs on the album. He dreamt of being famous and

playing guitar on stage in front of thousands of adoring fans. Jason‟s taste in music has

since matured, but he still wonders what it would be like to be a famous rock star.

Sometimes, when he thinks no one is looking, he puts ACDC on and plays air guitar

like he did when he was thirteen.

Distractors

Frequency Letters

Musician 23 8

Piano 38 5

Tapes 35 5

Concerts 39 8

33.75 6.5


1. Jason is a big fan of…

a. jazz c. pop music

b. concerts # d. heavy metal music *

2. Since John was thirteen he has been collecting…

a. Metallica records c. music tapes #

b. rock posters d. albums *

3. When he was younger, Jason wanted to be a…

a. rock star * c. songwriter

b. musician # d. jazz musician

4. When he thinks no one is looking, he…

a. plays piano # c. dances around in the room

b. play air guitar * d. plays the drums

Appendices

230

Target Passage

The Trip

It was Charlie‟s first trip to Europe. He had been looking forward to it for a year, and

had spent the last few months planning where he would visit. Most of all, Charlie

looked forward to visiting France, and hoped to see the Eiffel Tower in Paris. He had

spent the last ten months learning to speak French, and took along his English-French

dictionary with him. When he arrived in Paris, his good friend Marc met him at the bus

terminal. Marc was French and would show Charlie around the sights of Paris. Charlie

had arrived in spring, but the weather was unexpectedly chilly for that time of year. It

was a good thing he wore his scarf and gloves to keep him warm.

Distractors

Frequency Letters

Ireland 13 7

camera 36 6

Autumn 22 6

airport 19 7

22.5 6.5


1. Where was Charlie most looking forward to travelling to?

a. Italy c. Germany

b. Ireland # d. France *

2. What did Charlie take on the plane with him?

a Camera # c. English-French dictionary *

b. French thesaurus d. Travel guide

3. Which season was it?

a. Summer c. Autumn #

b. Spring * d. Winter

4. Charlies good friend Mark met him at…

a. midday c. the airport #

b. Notre Dame d. the bus terminal *

Appendices

231

Target Passage

The Outdoor Cinema

Space Out, a movie about aliens from Jupiter, was showing at the outdoor cinema.

Karen Dunlop arranged to meet her cousin outside the cinema before the movie. They

bought popcorn and found their seats. The aliens were new to Earth, although they had

previously been to Saturn, Mercury, and even Pluto. They had travelled much of the

solar system and wanted to learn about life on earth. The aliens came to earth on a

mission to understand how human beings function. When the movie finished, Karen

and her cousin looked around in the foyer of the cinema. There were displays on the

solar system, which were very fascinating for Karen. After admiring the displays,

Karen and her cousin left the cinema to get some dinner.

Distractors

Frequency Letters

eliminate 26 9

Mars 21 4

planet 21 6

screen 48 6

29 6.25


1. The movie was being shown…

a. At several cinemas c. On the big screen #

b. For the first time d. At the outdoor cinema *

2. The aliens were from…

a. Mars # c. Venus

b. Neptune d. Jupiter *

3. The aliens were on a mission to…

a. Understand human beings * c. Eliminate Earth #

b. Capture human beings d. Conquer Earth

4. In the foyer of the cinema, there were displays on…

a. The pyramids of Egypt c. The solar system *

b. Planets # d. The world's oceans

Appendices

232

APPENDIX C

Stories and Comprehension Questions Used in the Directed Ignoring Task (Chapter 6)

Note: * = correct response; # = foil error (distractor intrusion)

Practice 1 – Control

Target Passage

The Zoo Visit

There are many animals to see at the zoo. In the African Savannah exhibit, you can see

giraffes running alongside wild geese. There are also rhinoceros and zebras in this

section. Tigers, lions, and cheetahs form the Great Cats exhibition. They are very

graceful animals. There is also a bird enclosure. Here, there are flamingos, pelicans,

admiring them and even penguins. Children like to watch the elephants painting and

laugh at the funny expressions that the extremely playful orang-utans make. Feeding

time for the otters is also a ground great attraction at the zoo, as the otters stand up on

their hind legs patiently awaiting their food. Sometimes, the zoo is open at night, at

which time it is best to see the nocturnal animals at play.


1. In the bird enclosure, there are…

a. chickens c. doves

b. flamingos * d. trees

2. Children laugh at the…

a. elephants bathing c. playful orang-utans *

b. spiky hedgehog d. feeding lions

Appendices

233

Practice 2 – Distractor-New

Target Passage

The Music Fan

Jason always wanted to be a rock star. He is a big fan of heavy metal music, and has

many heavy metal albums. He has been collecting albums since he was thirteen, when

he bought an ACDC album. At this age, he would lie in bed with the radio turned up

loud, and play air guitar to all the songs on the album. He dreamt of being famous and

playing guitar on stage in front of thousands of adoring fans. Jason‟s taste in music

has since matured, but he still wonders what it would be like to be a famous rock star.

Sometimes, when he thinks no one is looking, he puts ACDC on and plays air guitar

like he did when he was thirteen.

Distractor Passage

Working with Computers

Tim Smith works with computers in a small local computer company. He performs a

variety of roles, but his main role is providing assistance to those who require

technical knowledge. Areas in which people often require assistance include graphic

design and web design, internet and email services, and database development. Tim

also assists with software installations, spreadsheets, and programming when the need

arises. When business is quiet, Tim will also work at the front desk. He enjoys the

interaction that this role allows him, as it is a nice change from working with

computers. He also enjoys the diversity of his job as it allows him to develop skills in

several different areas. In doing so, he is able to build on his computer training.

Appendices

234

Example of Target Passage with Distractors Passage integrated

The Music Fan

Jason always wanted Tim Smith works with computers to be a rock star in a small

local computing company. He is a big fan of heavy metal music, and he performs a

variety of roles has many heavy metal albums but his main role is providing

assistance. He has been collecting albums to those who require technical knowledge

since he was thirteen, when he bought areas in which people often require an ACDC

album. At this age, assistance include graphic design he would lie in bed and web

design with the radio turned up loud, and play internet and email services air guitar to

all the songs and database development on the album. Tim also assists with software

installations He dreamt of spreadsheets and programming being famous and when the

need arises playing guitar on stage when business is quiet in front of thousands of

adoring fans. Tim will also work at the front desk Jason’s taste in music has since

matured, he enjoys the interaction that but he still wonders what this role allows him it

would be like as it is a nice change from to be a famous rock star working with

computers. Sometimes, when he thinks he also enjoys the diversity of his job no one is

looking, as it allows him to develop skills he puts ACDC on in several different areas

and plays air guitar in doing so like he did when he is able to build on his computer

training he was thirteen.


1. Jason is a big fan of…

a. nightclubs c. rock music

b. computers # d. heavy metal music *

3. Jason sometimes…

a. plays the drums c. plays air guitar when no one is looking *

b. listens to ABBA d. works on the front desk #

Appendices

235

Control 1

Target Passage

Going Bush Walking




flora and fauna, and would often spend hours admiring them. As he walked through

the forest, the smell of the eucalyptus trees filled the air. He could hear the birds

singing in the distance. After a few hours, Jeremy stopped to have lunch. As he

rested on the ground, he poured coffee from his thermos. Jeremy felt instantly

refreshed after sipping his coffee. Following lunch, he continued on his tour of the

forest.


1. Jeremy filled his thermos with…

a. coffee * c. soup

b. milk d. hot chocolate

2. What could he hear in the distance?

a. Frogs c. Birds *

b. Crickets d. Lions

Appendices

236

Distractor-Old 1

Target Passage

The Art Gallery

Jamie McKee brushed off the droplets of water that had fallen on him as he walked

through the sprinklers to get to the art gallery. He worked there as a volunteer at the

information booth. He took his seat at the information booth and waited for the

viewers to arrive. Jamie loved art, and this job allowed him to see all different types

of art. He picked up a box of pamphlets that told of upcoming displays. When he

looked through one of the pamphlets, he became very excited. A sculpture exhibition

was coming in a few months time. He admired sculptors most of all because there

were so many different materials to work with. Secretly, he had always wished he had

studied sculpture himself.

Distractor Passage

Going Bush Walking




flora and fauna, and would often spend hours admiring them. As he walked through

the forest, the smell of the eucalyptus trees filled the air. He could hear the birds

singing in the distance. After a few hours, Jeremy stopped to have lunch. As he

rested on the ground, he poured coffee from his thermos. Jeremy felt instantly

refreshed after sipping his coffee. Following lunch, he continued on his tour of the

forest.


1. Jamie had just walked through…

a. sprinklers * c. a eucalyptus forest #

b. a construction site d. mud

2. Jamie enjoyed…

a. viewing the paintings c. apples

b. coffee # d. sculpture most of all *

Appendices

237

Distractor-New 1

Target Passage

The Bank Queue

Derek went to the bank early in the morning to avoid a queue. He wanted to open a

new account to save money. Even though it was early in the morning, there were

already several other people there waiting in line. Derek waited for twenty minutes

before being served. He wanted to open a savings account, and had to fill out several

forms before queuing in another line. The pen leaked, and Derek ended up with ink

all over his hands. By this time, it was shortly after noon. Derek spent another half an

hour waiting in line before being served again. When he finally opened the account, it

was already early in the afternoon. Derek decided to take the rest of the day off.

Distractor Passage

The Family Picnic

The Smiths were preparing for a picnic at Cook National Park. There was always

plenty of delicious food at the picnic, including sandwiches, pizza, cinnamon buns,

salad, and even a barbecue. Aunt May, Uncle Jim, and their cousins were going to

meet them at the National Park. Packing their things into their blue car, the Smiths set

off. While in the car, Sally Smith and her brothers decided to count the types of

vehicles that passed along the way. There were several station wagons and lorries, not

to mention motorbikes, scooters, and even a golf cart! Soon, the Smiths arrived at the

park. Sally and her brothers went off to play with their cousins, while their uncle and

aunt helped unpack the large picnic basket.


1. Why did Derek start his day early?

a. To pick up food for the picnic # c. To open a cheque account

b. To avoid a queue at the bank * d. To buy a new pen

2. After the bank, Derek decided to…

a. go back to work c. have a picnic #

b. go back to university d. take the rest of the day off *

Appendices

238

Distractor-Old 2

Target Passage

The Library Visit

Susan was taking her very active twins, Tommy and John, to the library for the first

time. They wanted to wear their favourite clothes. Tommy pulled out his fluffy blue

pants, and John found a bright red cape in the chest of play clothes. On the way to the

library, Susan told the toddlers about all the things they would see there. Both kids

loved the big storybooks. Tommy asked if there would be books on trains, while John

wanted books on witches. Susan was also glad to go to the library as she could

browse through some magazines and look for books on South American cooking. At

the library, the twins were amazed at all the books there were. They enjoyed

themselves very much.

Distractor Passage

The Bank Queue

Derek went to the bank early in the morning to avoid a queue. He wanted to open a

new account to save money. Even though it was early in the morning, there were

already several other people there waiting in line. Derek waited for twenty minutes

before being served. He wanted to open a savings account, and had to fill out several

forms before queuing in another line. The pen leaked, and Derek ended up with ink

all over his hands. By this time, it was shortly after noon. Derek spent another half an

hour waiting in line before being served again. When he finally opened the account, it

was already early in the afternoon. Derek decided to take the rest of the day off.


1. Susan had…

a. twins * c. to wait in line #

b. triplets d. a toothache

2. Who was going on the outing?

a. Her nieces c. Ted and Tonia

b. Derek # d. Tommy and John *

Appendices

239

Control 2

Target Passage

The Basketball Match

Glen Taylor got two tickets to the basketball match. He took along his cousin

Andrew, who was a big fan of basketball. It was the first time that Glen had been to a

match, and he wondered how different it would be to watching it on television. When

Glen and Andrew arrived at the stadium, they found their seats. They were near the

front, and close enough to get a good look at the players on the team. The atmosphere

in the stadium was electric, as everyone cheered excitedly for the team. Glen and

Andrew joined in the cheering when their team made the shot. It was even more

fantastic than Glen had imagined, and it was far better than watching the match on

television.


1. Glen took along his…

a. friend c. uncle

b. cousin * d. sister

2. The atmosphere in the stadium was…

a. boring c. sombre

b. raging d. electric *

Appendices

240

Distractor-New 2

Target Passage

The New Baby

Fred Wilson and his friend Ivan Southmore walked quickly down the white corridors


understandable since this was the birth of his first child and he wanted to show his

new daughter off to his friend. As they arrived at the nursery window Fred gave his

friend a nudge and pointed to a small bundle right near the window. Fred pressed his

face right up against the glass and began to fog it up. “Isn‟t she absolutely beautiful?”

Fred said to his pal, “She‟s got her Daddy‟s brown eyes.” Ivan agreed and after about

half an hour of staring they decided to go and see the newborn‟s mother and share her

joy.

Distractor Passage

The Fishing Adventure

Ralph Dalton was alone except for his year old dog Fletch. He was a present to him

from his wife for their first anniversary and was a male golden retriever. This was the

first time he had taken the dog on a fishing trip on the Murray River. The fish were

biting that day, and Ralph caught six of the biggest silver bream he had ever seen in

just two hours. His wife would cook some of the bream for dinner, and there would

still be enough left to give to the neighbours. Fletch began barking at a dog on the

opposite shore, rocking the boat and knocking the fish overboard. Ralph gave Fletch

an annoyed look but Fletch just looked back, wagging his tail and tongue.


1. Fred arrived at the hospital with…

a. the ambulance c. his family

b. his friend * d. Ralph #

2. After half an hour of staring, they decided to…

a. go fishing # c. go see the newborn‟s mother *

b. leave d. hold the small bundle

Appendices

241

Distractor-Old 3

Target Passage

The Overseas Trip

It was Charlie‟s first trip to Europe. He had been looking forward to it for a year, and

had spent the last few months planning where he would visit. Most of all, Charlie

looked forward to visiting France, and hoped to see the Eiffel Tower in Paris. He had

spent the last ten months learning to speak French, and took along his English-French

dictionary with him. When he arrived in Paris, his good friend Marc met him at the

airport. Marc was French and would show Charlie around the sights of Paris. Charlie

had arrived in spring, but the weather was unexpectedly chilly for that time of the

year. It was a good thing he wore his scarf and gloves to keep him warm.

Distractor Passage

The New Baby

Fred Wilson and his friend Ivan Southmore walked quickly down the white corridors


understandable since this was the birth of his first child and he wanted to show his

new daughter off to his friend. As they arrived at the nursery window Fred gave his

friend a nudge and pointed to a small bundle right near the window. Fred pressed his

face right up against the glass and began to fog it up. “Isn‟t she absolutely beautiful?”

Fred said to his pal, “She‟s got her Daddy‟s brown eyes.” Ivan agreed and after about

half an hour of staring they decided to go and see the newborn‟s mother and share her

joy.


1. What was Charlie looking forward to?

a. Buying a camera c. Going to Europe *

b. Showing off his new daughter # d. Learning a second language

2. What was the name of Charlie‟s friend?

a. Ivan # c. Maurice

b. Sophie d. Marc *

Appendices

242

Control 3

Target Passage

Gardening at Home

Today was the start of autumn, and for Nora, that meant that it was time to do some

gardening in preparation for spring. Nora used to study horticulture, and had a passion

for gardening. She loved autumn as the foliage on the trees would soon turn brown.

Her first plan was to clear her lawn of the weeds that had grown over summer. Nora‟s

next plan was to plant some rosemary, mint, and basil for an edible garden. At the

nursery, Nora selected the plants she wanted, but there were so many other plants to

admire. She decided to also plant some daffodils and tulips, and settled on a pink and

yellow colour scheme for her garden. Satisfied with her purchases, Nora then went

home.


1. Nora loved autumn because…

a. it would snow soon c. animals were preparing to hibernate

b. the weather would soon turn cold d. the foliage on the trees would soon

turn brown *

2. Nora went to the nursery to buy rosemary, mint and basil, but also bought…

a. sunflowers and roses c. daffodils and tulips *

b. a lemon tree d. gardening gloves

Appendices

243

Distractor-New 3

Target Passage

The Sunday Markets

Every Sunday morning, Angela Cameron went to the markets and this Sunday was no

exception. Angela enjoyed going to the markets, as there were many things to see

there. Her first stop was to shop for groceries and she liked that there were several

fruit and vegetable stalls where she could pick up some supplies for the coming week.

She bought some peaches, and bananas, as well as carrots and tomatoes. Angela then

looked for a housewarming present for her friend. She could not decide between a

nice set of fluffy towels and big comfortable cushions for her friend‟s couch. In the

end, she bought the cushions for her friend, and towels for herself. She then headed

back home to have a leisurely lunch.

Distractor Passage

The Outdoor Cinema

Space Out, a movie about aliens from Jupiter, was showing at the outdoor cinema.

Karen Dunlop arranged to meet her cousin outside the cinema before the movie. They

bought popcorn and found their seats. The aliens were new to Earth, although they

had previously been to Saturn, Mercury, and even Pluto. They had travelled much of

the solar system and wanted to learn about life on earth. The aliens came to earth on a

mission to understand how human beings function. When the movie finished, Karen

and her cousin looked around in the foyer of the cinema. There were displays on the

solar system, which were very fascinating for Karen. After admiring the displays,

Karen and her cousin left the cinema to get some dinner.


1. Angela‟s first stop was to…

a. shop for groceries * c. buy a housewarming present

b. see a movie about aliens # d. get lunch

2. Angela wanted to buy a present for…

a. herself c. Karen #

b. her friend * d. her mother

Appendices

244

Control 4

Target Passage

The House Project

Phillip and Gloria purchased a house and planned to make improvements to the entire

house. Most of it was in fairly good condition, but some parts required a lot of work.

They would need to get a carpenter to build shelves in the kitchen and an electrician to

do some work in the study. The bathroom also required some work, and they decided

that buying a new bath and installing new taps for the basin would improve its

appearance. The rest of the house only needed a nice coat of paint. Phillip wanted the

interior of the house to be painted red, but Gloria preferred yellow. In the end, they

compromised and decided to paint half the walls in the house red, and the other half,

yellow.


1. Where did Phillip and Gloria plan to make improvements?

a. The garden c. The bathroom

b. The entire house * d. The garage

2. What did they want done in the kitchen?

a. To get a dishwasher c. To have shelves built *

b. To put pot plants in d. To re-tile the floor

Appendices

245

Distractor-Old 4

Target Passage

The Birthday Celebration

Rebecca was soon turning nineteen, but she had not yet decided how to celebrate it.

She wanted a place for everyone to have a good time and enjoy good food. She did

not know which of her friends she was going to invite. She was unsure about this as

her work friends did not get along with her friends she plays netball with. She decided

to have several small gatherings with these different groups of friends. She would

have one gathering with her friends from work at a coffee shop. As for the other

gathering, Rebecca‟s friend from netball suggested that she have a gathering at the

pub. Rebecca looked forward to both occasions and was happy that she could

celebrate with all her friends.

Distractor Passage

The House Project

Phillip and Gloria purchased a house and planned to make improvements to the entire

house. Most of it was in fairly good condition, but some parts required a lot of work.

They would need to get a carpenter to build shelves in the kitchen and an electrician to

do some work in the study. The bathroom also required some work, and they decided

that buying a new bath and installing new taps for the basin would improve its

appearance. The rest of the house only needed a nice coat of paint. Phillip wanted the

interior of the house to be painted red, but Gloria preferred yellow. In the end, they

compromised and decided to paint half the walls in the house red, and the other half,

yellow.


2. Rebecca‟s friends…

a. did not get along * c. were all very busy

b. enjoyed going to the pub d. planned to help paint her house #

3. In the end, she decided to…

a. stay at home c. hold two separate gatherings *

b. paint half the walls red # d. throw one big gathering

Appendices

246

Distractor-New 4

Target Passage

Grandma‟s Visit

Susan woke up especially early on Saturday morning so that she could prepare for her

grandma‟s visit. Her grandma lived in the country and did not travel into the city very

often as she was getting old. She looked at her watch and saw that she had four hours

until her grandma was due to arrive. She wanted to cook a delicious roast dinner,

because this was her grandma‟s favourite meal. She took the vegetables out of the

fridge, put the oven on preheat, and began scrubbing the potatoes. Susan jumped when

she heard the doorbell ring, and saw the shadow of her grandma at the front door. She

was early! Susan decided that this was a wonderful surprise and went to greet her

grandma.

Distractor Passage

The Race

It was the day of the interschool sports carnival. Katy was both nervous and excited as

she was competing in several first division races. She had won plenty of races before,

but she had only ever raced the girls in her school, who she knew she could beat. The

girl from the other schools looked scary. Katy was happy to see the familiar faces of

her parents when she was called up for her first race. She tried to recall her coach‟s

tips, but before she knew it, the start whistle had been blown and she was off. Katy did

not win her race, but she was proud to come home with two bronze medals. She

decided she would like to compete again next year.


1. Susan wanted to…

a. go to the shops c. win a race #

b. cook a delicious roast * d. travel

2. Susan jumped when…

a. her alarm went off c. the dinner burnt

b. the start whistle blew # d. she heard the doorbell ring *

Appendices

247

APPENDIX D

Dissociating the components of inhibitory control associated

with auditory hallucinations in schizophrenia 1

ABSTRACT

Introduction: Impairments in intentional inhibition have been associated with

auditory hallucinations (AHs) in schizophrenia and with hallucination predisposition in

healthy individuals, and may explain their intrusive/uncontrollable nature. However, the

precise nature of this inhibition dysfunction has not yet been investigated in

schizophrenia. Thus, the aim of this study was to dissociate the critical component(s) of

inhibitory control specifically related to AHs in schizophrenia. Methods: Three tasks

measuring different forms of cognitive control – namely, intentional inhibition,

intentional resistance to interference, and unintentional inhibition – were administered

to schizophrenia participants with recent AHs (i.e. within the past 4 weeks; current-AH;

N = 34) or no recent AHs (i.e. not within the past 4 weeks; no-AH; N = 27), and healthy

control participants (N = 34). Results: Both current-AH and no-AH schizophrenia

participants were impaired on intentional resistance to interference but not on

intentional or unintentional inhibition compared to controls. Unexpectedly, no

significant differences occurred between the current-AH, no-AH and control groups on

intentional inhibition. However, AH severity (but not delusions or negative symptoms)

in the current-AH group significantly correlated with intentional inhibition only.

Conclusions: The results indicate that AH severity and schizophrenia more generally,

are differentially related to specific cognitive control impairments. Namely,

unintentional inhibition appears intact in schizophrenia and unrelated to AHs;

difficulties with intentional resistance to interference appear to be a more general

feature of schizophrenia, but unrelated to AHs specifically; and intentional inhibition

difficulties appear to be linked to AH severity only. Potential implications for

interventions targeting AHs are discussed.

Keywords: schizophrenia; auditory hallucinations; cognitive inhibition

1 This appendix is a revised manuscript of the study presented in Chapter 6, and has been

resubmitted for publication: Paulik, G., Badcock, J., & Maybery, M. (2007). Dissociating the

components of inhibitory control associated with auditory hallucinations in schizophrenia.

Manuscript submitted for publication to Cognitive Neuropsychiatry (May 2008).

Appendices

248

By definition, auditory hallucinations (AHs) are intrusive, uncontrollable mental events

that interrupt ongoing reality (Morrison, 2005; Slade & Bentall, 1988). In this regard,

they can be conceptualised as a type of unwanted mental intrusion. Other types of

unwanted mental intrusions, or „cognitive intrusions‟, include thoughts, images and

impulses. Although healthy non-clinical individuals also frequently experience

cognitive intrusions, they are also characteristic of particular clinical populations – such

as flashbacks typical of posttraumatic-stress disorder (PTSD), and obsessional thoughts

and impulses typical of obsessive-compulsive disorder (OCD) (Clark & Rhyno, 2005).

One primary feature that differentiates AHs from these other types of intrusive

cognitions is that AHs are perceived as being of non-self origin (Morrison, 2005).

Nevertheless, given the commonalities, it seems plausible that the cognitive

mechanism/dysfunction underpinning everyday cognitive intrusions may also contribute

to the experience of AHs. Empirical findings suggest that both clinical and everyday

intrusive cognitions are a product of poor inhibitory control (Amir, Coles, & Foa, 2002;

Badcock, Waters, & Maybery, 2007; Friedman & Miyake, 2004; Kramer, Humphrey,

Larish, Logan, & Strayer, 1994; Schnider & Ptak, 1999). It is interesting to note

therefore that recent empirical studies have also provided evidence tying intentional

inhibitory impairments to an increase in severity of hallucinations in schizophrenia


2003) and heightened predisposition to hallucinations in healthy individuals (Paulik,

Badcock, & Maybery, 2007).

Badcock and colleagues recently developed – and have provided empirical

support for – a dual-deficit model of AHs (Badcock et al., 2005; Waters, Badcock,

Michie, & Maybery, 2006), which contends that at least two cognitive deficits are

critical to experiencing AHs: an intentional inhibition deficit (Badcock et al., 2005;

Waters et al., 2003) and a deficit in binding of contextual memory (Waters, Badcock, &

Maybery, 2006). This model posits that a failure to intentionally inhibit irrelevant

thoughts and memories results in this information intruding into consciousness, which

may explain the shared features of AHs and other types of intrusive cognitions. The

second part of this model argues that these intrusive cognitions are misidentified as

being of non-self origin because the contextual information that is required for correct

recognition and identification is incomplete due to a deficit in contextual binding,

accounting for the source attribution difference between AHs and other intrusive

cognitions (Waters et al., 2006).

Appendices

249

According to the Badcock et al. model of AHs, the cognitive control difficulties

involved in producing AHs operate on a strategic, intentional level, which, according to

the inhibition taxonomy developed by Harnishfeger (1995), is defined as „cognitive

intentional inhibition‟. Harnishfeger‟s (1995) taxonomy categorises inhibitory processes

according to three dimensions: (1) cognitive (controlling mental processes) or

behavioural (controlling impulses or motor responses); (2) intentional (consciously

suppressed) or unintentional (automatically suppressed); and (3) inhibition (an active

suppression process operating in working memory) or resistance to interference (a

gating mechanism that prevents irrelevant information from entering working memory).

Validity of Harnishfeger‟s (1995) three dimensions has been supported by dissociations

reported for the different forms of inhibition using correlational designs (e.g. Earles et

al., 1997; Friedman & Miyake, 2004; Salthouse, Atkinson, & Berish, 2003; Tipper &

Baylis, 1987), clinical populations (e.g., Amieva, Phillips, Della Sala, & Henry, 2004;

Lau, Christensen, Hawley, Gemar, & Segal, 2007; Nigg, Butler, Huang-Pollock, &

Henderson, 2002), different age groups (Dempster, 1993; Harnishfeger, 1995; Hasher,

Lustig, & Zacks, 2007; Wilson & Kipp, 1998) and neuroimaging and brain lesion

studies (e.g., Dias, Robbin, & Robets, 1997; Stuss et al., 1999).

Two of our most recent studies directly compared several different types of

inhibitory control processes in healthy young adults predisposed to hallucinations

(Paulik et al., 2007; Paulik, Badcock, & Maybery, 2008). We found that healthy

individuals highly predisposed to hallucinatory-like experiences exhibited similar

difficulties to hallucinating individuals with schizophrenia (Badcock et al., 2005) on the

Inhibition of Currently Irrelevant Memories (ICIM) task, which requires the intentional

inhibition of previously – but not currently – relevant items (Paulik et al., 2007). Paulik

et al. (2008) then examined whether this intentional inhibition impairment was rooted in

difficulties with (a) any intentional cognitive control process (irrespective of whether it

involves inhibition or resistance to interference), (b) any process involving inhibition

rather than interference control (irrespective of whether it is intentional or unintentional

in nature), or (c) only those processes that are both intentional and involve inhibition.

This was achieved by administering two cognitive tasks that differentially measured

intentional resistance to interference (directed ignoring [DI] task) and unintentional

inhibition (Brown-Peterson [B-P] task; Kane & Engle, 2000) to the same sample of high

and low hallucination predisposed participants tested on the intentional inhibition

(ICIM) task (as reported in Paulik et al., 2007). Whilst there was evidence that poor

intentional resistance to interference is linked to schizotypy predisposition more

Appendices

250

generally, the main conclusion was that hallucination predisposition is related to

cognitive control difficulties that are both intentional and involve inhibition (Paulik et

al., 2008).

Given the advantages of this approach in delineating the inhibitory process(es)

specifically involved in AHs, the current study adopted the same general design in order

to determine the critical component(s) of inhibitory control underlying AHs in

schizophrenia. Thus, we administered the same range of cognitive control measures

used in our previous hallucination predisposition studies to schizophrenia participants

with recent AHs (AHs actively present during the past four weeks; „current-AH‟) or no

recent AHs (no AHs during the past four weeks; „no-AH‟), and control participants.

State anxiety was also measured and controlled for, since there is substantial evidence

directly linking anxiety and AHs (Freeman & Garety, 2003), and what is more, anxiety

has been linked to unwanted intrusive cognitions (e.g., Clark & Rhyno, 2005; Freeston

et al., 1994; Hackmann, Surawy, & Clark, 1998) and impaired cognitive control (e.g.,

Amir et al., 2002; Badcock et al., 2007; Hopko, Ashcraft, Gute, Ruggiero, & Lewis,

1998; Wood, Mathews, & Dalgleish, 2001). The presence of other schizophrenia-related

symptoms, namely delusions and negative symptoms, was also measured to test the

specificity of the relationship(s) between inhibition and AHs. Based on our previous

findings, we hypothesised that of the cognitive control measures administered, only

performance on the intentional inhibition task (ICIM) would be linked to AHs, and that

this relationship would be unique to AHs (i.e. not common to delusions or negative

symptoms). In addition, we hypothesised that schizophrenia participants overall would

perform more poorly than control participants on intentional (DI and ICIM tasks) – but

not unintentional (B-P task) – cognitive control measures, consistent with the literature

linking schizophrenia to difficulties with executive/volitional behaviour (e.g., Merlotti,

Piegari, & Galderisi, 2005; Racsmany et al., 2008; Zec, 1995).

METHOD

Participants

Sixty-nine individuals meeting International Classification of Diseases (ICD-10;

World Health Organisation, 1993) criteria for schizophrenia (n = 57) or schizoaffective

disorder (n = 12) were recruited through the Centre for Clinical Research in

Neuropsychiatry (CCRN), Graylands Hospital and related out-patient clinics and hostels

Appendices

251

in Perth, Western Australia. Two schizophrenia participants were subsequently

excluded because the diagnosis provided by their treating psychiatrist was not

confirmed on interview at the time of testing. Control participants were 39 healthy

individuals who had participated in previous research at CCRN, and were initially

recruited from the Perth community via a random telephone recruitment screening

procedure. Inclusion criteria for all participants included fluency in English (attended an

English speaking school since age 6), and being aged 18 – 60 years. The exclusion

criteria for all participants included hospital admission for a drug or alcohol

rehabilitation program within the past 12 months, poor visual acuity, neurological

disorders, serious head injury, and a pre-morbid full-scale IQ (estimated from the

National Adult Reading Test – 2nd

edition [NART]; Nelson & Willison, 1991) below

75. Additional exclusion criteria for control participants included a personal or family

history of psychosis, and a current diagnosis of Attention-Deficit Hyperactivity

Disorder (ADHD), OCD, or PTSD2. Based on these criteria, six schizophrenia

participants and five control participants were excluded from the study. Of the

remaining participants, there were 10 females and 24 males in the current-AH

schizophrenia group, two females and 25 males in the no-AH schizophrenia group, and

six females and 28 males in the control group. Of the schizophrenia participants, 88.5%

were taking antipsychotic medications (69% atypicals only, 8% typicals only, and

11.5% typicals and atypicals) and 84% were out-patients at the time of testing.

Measures

Inhibition of Currently Irrelevant Memories (ICIM) Task (Schnider, Valenza, Morand,

& Michel, 2002)

The ICIM task is a repeated continuous recognition memory task. The version of

the ICIM task used in our previous hallucination predisposition study (designed by

Schnider et al., 2002, to be sensitive enough to detect individual differences in a non-

clinical population) was employed in order to permit comparisons with these previous

findings (Paulik et al., 2007). This version has one less run, more trials per run, a greater

2 Empirical studies have reported cognitive inhibition deficits in samples of ADHD, OCD and

PTSD individuals (e.g., Amir et al., 2002; Badcock et al., 2007; Barkley, 1997); thus, to reduce

the noise in the control group, these were included in the exclusion criteria. There were no

incidents reported in case notes of current ADHD, OCD or PTSD in the schizophrenia group.

Appendices

252

number of different targets per run, and fewer repetitions per target than the original

ICIM task previously used with a schizophrenia sample (Badcock et al., 2005; Waters et

al., 2003). In each of the three runs, 85 black and white line drawings (Snodgrass &

Vanderwart, 1980) were presented serially on a computer screen. Each picture was

presented for 2 s, with a 700 ms interstimulus interval. Some of the pictures were shown

only once (28), and others were shown two (6) or three times (15) in a run; yielding 49

distractors (first presentations) and 36 targets (21 second presentations and 15 third

presentations) in each run. Participants responded as accurately and rapidly as possible

(by pressing keys marked „yes‟ or „no‟) as to whether each picture had or had not

already been presented within the current run. There was a 30 s break between runs 1

and 2, and a 5 minute break between runs 2 and 3. The second and third runs consisted

of the same set of pictures used in run 1, however the pictures selected as targets and the

order of pictures changed. On the second and third runs participants were explicitly

asked to forget that they had already seen the pictures and to identify repeated pictures

within the current run only. Thus, performance on run 1 requires encoding and

recognition only, whilst runs 2 and 3 also demand the intentional suppression of

responses to items seen only on previous runs. Intentional inhibition is reflected in the

number of false positive responses (false alarms: FAs) made on runs 2 and 3, that is, the

number of first presentations on the current run mistaken as targets. General recognition

was measured by the number of correctly identified targets (Hits) made on all three

runs. The ICIM task has been shown to have good construct validity (with AH severity

in schizophrenia participants correlating significantly with both the ICIM task and the

Haylings Sentence Completion Task, which also measures intentional inhibition; Waters

et al., 2003) and good discriminant validity (with the ICIM task not correlating

significantly with other tasks thought to measure different forms of cognitive control,

including the DI and B-P tasks3; Paulik et al., 2007, 2008). Furthermore, neuroimaging

and electrophysiological studies have shown that performance on the inhibition runs of

the ICIM task involves neural regions found to be specifically involved in cognitive

inhibition, such as the orbitofrontal cortex (Aron et al., 2004; Schnider & Ptak, 1999;

Schnider et al., 2000; Treyer, Buck, & Schnider, 2003), but not the neural regions

involved in temporal monitoring (Cabeza et al., 1997; Schnider et al., 2000).

3 These correlations were not reported in the published manuscripts (Paulik et al., 2007, 2008).

The three cognitive control measures did not correlate significantly with one another (r range =

-.01 to .18, p > .05).

Appendices

253

Directed Ignoring (DI) Task (Connelly, Hasher, & Zacks, 1991)

In the conventional DI task, participants read aloud passages printed in italics

that either have distracting (to-be-ignored) words interspersed throughout the passage

printed in non-italic font (distractor condition) or have blank spaces interspersed

throughout the passage (control condition) (see Paulik et al., 2008 for more details). In

our modified version of the DI task, there were three conditions: control, distractor-new,

and distractor-old. The two distractor conditions were developed to examine whether

the previous relevance of the to-be-ignored text differentially impacted on schizophrenia

and control participants‟ ability to resist interference. In each condition, participants

were instructed to read aloud only target text – printed in italicised font (20-point Arial).

In the distractor conditions, an unrelated story printed in regular (non-italicised) font

was interwoven into the target story passage. In the distractor-old condition, the

distractor story was the story that had been read (target) in the previous passage. Half of

the distractor-old stories followed stories read in the control condition and half followed

those read in the distractor-new condition. In the distractor-new condition, the

distracting story had never been read before. In the control condition, blank spaces

matching the average length of a distracting text section were inserted into the passages

to control visual scanning requirements between conditions. Participants read aloud two

practice and 12 test stories (four test stories from each condition). Target and distractor

stories were matched on length (125 words), and sections of target and distractor text

were 3-9 words in length. After each story, participants were presented with two

multiple-choice questions to assess comprehension, each with four alternative answers.

Each comprehension question had part of the distractor story‟s content as a plausible,

but incorrect, response choice (a foil). The order in which the stories were presented

was counterbalanced across participants. There were three interference control indices:

(1) the difference in reading time (RT) between control and distractor stories (RT-

Interference scores were calculated for the correlational analyses by subtracting

distractor RT from control RT); (2) the number of distractor text sections read aloud,

either fully or partially („intrusions‟); and (3) the percentage of foils (of the total

incorrect responses) chosen on the multiple-choice questions. Overall accuracy on the

multiple-choice questions was used to assess text comprehension. The DI task has been

shown to have good construct validity (correlating significantly with the Stroop task,

which is also said to measure intentional interference control; Earles et al., 1997;

Salthouse et al., 2003) and good discriminant validity (e.g., Earles et al., 1997; Lau et

Appendices

254

al., 2007; Paulik et al., 2007, 2008; Radvansky & Copeland, 2006; Salthouse et al.,

2003).

Brown-Peterson Variant (B-P) Task (Kane & Engle, 2000)

This task assessed unintentional inhibition. Three blocks of stimuli were

presented (rather than five – as in Paulik et al., 2008) in order to reduce the overall test

duration. (Recall patterns from our previous study indicated that the last two blocks

provided no additional discriminate power over that obtained in the first three blocks).

In each block, participants read aloud and attempted to recall three lists of words, each

list comprising of ten words presented serially (one word every 2 s) on a computer

screen (see Paulik et al., 2008, for details). All lists within a block were comprised of

words from the same semantic category (four-footed animals, occupations, or fruits),

and lists were matched for word length and frequency (Battig & Montague, 1969). After

each list, a distractor task performed for 15 s required counting backwards by twos from

a number presented on the screen, at a pace set by an auditory signal every 1500 ms.

Participants were then asked to recall aloud as many words from the previous list as

possible in any order in 20 s. To ensure that participants were not actively rehearsing

items during the distractor task, participants with a counting accuracy rate of less than

70% were excluded. Four schizophrenia participants‟ results (all from the no-AH group)

were excluded from the analysis of this task accordingly. In this type of unintentional

inhibition task, the participant must automatically inhibit memory intrusions of

previously learnt – but no longer relevant – items (from previous lists) when recalling

new items belonging to the same category (Solso, 1995). Thus, the cognitive overflow

of within-block previous list items increases from list one (no overflow) to list three

(maximum overflow). Inhibition was measured by the difference in recall accuracy

(summated across blocks) between lists 1 and lists 2 and 3 – with poor unintentional

inhibition indicated by a steep decline in recall across successive lists (although some

decline is expected in all participants). For the correlational analyses, a B-P Inhibition

score (list 1 recall minus list 3 recall) was calculated for each participant. The B-P task

has been shown to have good construct and discriminant validity (Friedman & Miyake,

2004; Paulik et al., 2007, 2008).

Appendices

255

Clinical Interviews

Diagnosis for the schizophrenia group was confirmed using the Diagnostic

Interview for Psychosis (DIP; Castle et al., 2006). A separate interview was

administered to obtain a more comprehensive measure of AH phenomenology,

including severity, since this was the construct of greatest interest to the current study.

Accordingly, the auditory hallucinations (AH) subscale from the Psychotic Symptom

Rating Scales (PSYRATS; Haddock, McCarron, Tarrier, & Faragher, 1999), which is an

11-item interview (each item is rated on a 5-point rating scale, from 0 to 4), was

administered to those participants who reported hearing voices during the past four

weeks (which is the time frame stipulated by the PSYRATS), from which an AH

severity score (based on frequency, duration and loudness) was obtained. Haddock et al.

(1999) reported that each item on the AH severity scale had a high factor loading (.53 to

.78) and excellent inter-rater reliability (0.98 to 1). Items from the DIP were compiled to

obtain a „present state‟ (during the past 4 weeks) delusion score with a score range of 0

– 8 (types of delusions included in this score were thought insertion, thought broadcast,

thought withdrawal, delusions of passivity, delusions of influence/reference, grandiose

delusions, and bizarre delusions), and a „present state‟ negative symptom score with a

score range of 0 – 6 (symptoms included in this score were restricted affect, blunted

affect, rapport difficult to establish, thought blocking, poverty of speech, and restricted

quantity of speech). The short version of the Mini International Neuropsychiatric

Interview (MINI; Sheehan et al., 1997) was administered to control participants to

screen for psychological disorders, including schizophrenia.

Additional Measures

Pre-morbid full-scale IQ was estimated from the NART (Nelson & Willison,

1991). The Digit Span subtest of the Wechsler Adult Intelligence Scale – 3rd

edition

(WAIS-III; Wechsler, 1997) was used as a measure of working memory. State anxiety

was measured with the 7-item anxiety subscale of the Hospital Anxiety Depression

Scale (HADS; Zigmond & Snaith, 1983), which has a score range of 0 - 21.

Appendices

256

Procedure

Ethics approval for the project was obtained from the North Metropolitan Area

Mental Health Service Ethics Committee. Testing took approximately 2 hours for

control participants and 3 hours for schizophrenia participants. Control participants

were offered $20 and schizophrenia participants $25 for reimbursement of

time/expenses.

Data Analysis

The approach to data analysis adopted in the current study generally follows the

analyses carried out in the Badcock et al. (2005) and Waters et al. (2003) schizophrenia

studies. The first round of analyses compared the three groups on the three cognitive

control tasks. The second round of analyses examined the correlations between AH

severity and the inhibition indices. To examine the specificity of cognitive control

difficulties associated with AH severity, correlations between the cognitive control

measures and other schizophrenia-related symptoms (DIP delusions and negative

symptoms) were obtained. All correlational analyses were performed within the current-

AH schizophrenia group (see Table 1 for PSYRATS-AH severity mean and SD). This

subgroup was used to maintain sample consistency across all correlations involving

schizophrenia-related symptom scores, since only those schizophrenia participants who

reported hearing voices over the past four weeks could be administered the PSYRATS-

AH. Schizophrenia participants with and without hallucinations did not differ

significantly on demographic characteristics or the additional measures (as reported in

Table 1), or with regard to antipsychotic medications, in- versus out-patient status, or

DIP symptom scores.

RESULTS


One single data point from the demographic and additional measures presented

in Table 1 (specifically, the NART-IQ score of a no-AH participant) was identified as a

Appendices

257

univariate outlier (defined here, and subsequently, as a score ≥ 3 SDs away from the

respective group mean) and was deleted from the data file. As seen in Table 1, there was

no significant difference between the control group and either schizophrenia groups on

age, however the current-AH schizophrenia group had a significantly lower mean level

of education than the control group, and both schizophrenia groups had a significantly

lower pre-morbid IQ (NART), poorer working memory (WAIS-III Digit Span), and

higher levels of state anxiety (HADS-Anxiety) than the control group. Consequently, in

the following group comparisons where significant group effects were found, these

variables were entered into the analyses separately as covariates to examine any

possible confounding effects (Wildt & Olli, 1978).

To examine the possible effects of antipsychotic medication on task performance

for schizophrenia participants, a chlorpromazine equivalent dosage score was calculated

for each schizophrenia participant and correlated with all the measures included (British

National Formulary, 1995; Woods, 2003). The only significant correlation was found

with intrusions made on the DI task; thus, where significant correlations involving DI

intrusions were found, partial correlations were examined, in which dosage was

controlled.

Appendices

258

Table 1

Group Means, SDs, and T-tests for the Demographic Characteristics and Additional Measures

1. Controls

(N = 34)

2. No-AH Sz

(N = 27)

3. Current-AH Sz

(N = 34)

t-tests

Mean (SD) Mean (SD) Mean (SD) 1. vs 2. 1. vs 3 2. vs 3.

Age (yrs) 41.35 (11.85) 38.11 (10.91) 37.91 (9.40) 1.10 1.33 0.77

Education a (yrs) 12.59 (2.03) 11.67 (1.69) 11.19 (2.01) 1.86 2.85* 0.99

Length of illness (yrs) - 15.85 (10.74) 15.53 (8.00) - - 0.13

Age of Illness Onset (yrs) - 22.26 (6.02) 22.38 (6.43) - - 0.08

PSYRATS-AH severity - - 6.49 (2.42) - - -

NART-IQ 109.64 (8.80) 100.07 (11.60) 96.64 (9.38) 3.66* 5.85* 1.27

Digit Span scaled score 11.62 (2.77) 8.41 (2.42) 8.74 (2.47) 4.74* 4.53* 0.52

HADS-Anxiety 4.21 (3.07) 8.33 (4.80) 9.12 (4.15) 4.07* 5.54* 0.68

* p < .05

Note. Sz = participants with schizophrenia; PSYRATS = Psychotic Symptom Rating Scales; NART-IQ = full scale WAIS-III IQ estimated

from the National Adult Reading Test; HADS = Hospitalised Anxiety and Depression Scale. a Highest level of education completed (secondary and

tertiary education only).

Appendices

259

Group Comparisons

ICIM Task Performance

One control participant and four schizophrenia participants did not complete the

ICIM task. From the FA and Hit data, six single data points (two from each group) were

identified as univariate outliers and were deleted from the data file. As in previous

studies, run 1 was analysed separately from runs 2 and 3 (Badcock et al., 2005; Paulik et

al., 2007; Waters et al., 2003), since unlike runs 2 and 3, performance on run 1 does not

demand intentional inhibition. Group means and SDs for FAs and Hits are presented in

Table 2.

Intentional Inhibition (False Alarms: FA)

When a univarite ANOVA was performed on run 1 FAs, no significant group

differences were found, F(2, 84) = 2.03, MSE = ,2.43 p > .05, indicating that the

schizophrenia and control participants were equally able to identify and correctly reject

novel pictures. A repeated measures ANOVA performed on FAs made on runs 2 and 3

revealed a significant Run main effect only, F(1, 83) = 19.58, MSE = 4.81, p < .05, with

more FAs being made on run 2 than run 3 in general. The absence of any significant

Group effects was not expected, however it suggests that poor intentional inhibition is

not related to schizophrenia in general.

Target Detection (Hits)

When a univarite ANOVA was performed on run 1 Hits, there was a significant

Group main effect, F(2, 86) = 4.40, MSE = 6.37, p < .05, with post hoc pairwise

comparisons showing that the control group had a higher Hit rate than either of the

schizophrenia groups. The effect remained significant when any of the additional

measures were entered separately into the analysis as covariates. Similarly, repeated

measures ANOVA on runs 2 and 3 Hit data also produced a significant Group main

effect, F(2, 85) = 7.18, MSE = 25.76, p < .05, with post hoc pairwise comparisons again

showing that the control group had a higher Hit rate than either of the schizophrenia

groups, suggesting that overall the schizophrenia participants had poorer recognition of

repeated pictures than the control participants. This Group main effect remained

significant when the additional measures were entered separately into the analysis as

covariates. No other effects were significant.

Appendices

260

Table 2

Group Means and SDs for the Performance Indices of the Cognitive Inhibition Tasks

Controls

(N = 34)

No-AH Sz

(N = 27)

Current-AH Sz

(N = 34)

Mean SD Mean SD Mean SD

ICIM FA Run 1 1.38 1.43 2.04 2.16 1.23 1.06

ICIM FA Run 2 5.38 2.76 6.50 4.63 5.97 5.21

ICIM FA Run 3 3.64 2.73 4.78 3.53 4.94 5.10

ICIM Hit Run 1 a 34.61 1.95 32.92 3.08 33.00 2.59

ICIM Hit Run 2 31.55 2.77 27.67 4.61 28.19 3.87

ICIM Hit Run 3 30.73 3.68 27.54 6.39 29.29 3.11

DI Control RT (s) 43.34 5.41 55.76 10.54 55.25 10.93

DI Distractor RT (s) 80.54 22.71 116.94 36.80 108.59 29.06

DI Intrusions 4.88 3.54 14.83 11.52 17.46 15.29

DI Control Errors b

12.50 9.23 13.77 8.37 19.20 11.53

DI Distractor Errors b

7.17 8.45 14.55 18.04 22.10 16.36

DI Foil Errors c 24.07 28.47 26.12 29.37 25.24 22.49

B-P List 1 Recall 5.99 1.29 4.53 1.39 4.61 1.21

B-P List 2 Recall 4.13 1.14 2.97 1.06 2.67 1.08

B-P List 3 Recall 3.26 1.19 1.92 0.97 1.92 0.88

* p < .05

Note. Sz = participants with schizophrenia; ICIM = Inhibition of Currently Irrelevant

Memories task; B-P = Brown-Peterson variant task; DI = Directed Ignoring task. a

Maximum number of hits in each run is 36. b Percentage of incorrect responses on

comprehension questions. c

Percentage of foil errors of total incorrect responses on

comprehension questions.

DI Task Performance

Preliminary analyses of the two different distractor story conditions (distractor-

new and distractor-old) showed there were no significant differences between these

conditions on any of the outcome variables, thus, the data from these conditions were

combined in the following analyses. Three participants from the no-AH and six from the

current-AH schizophrenia groups did not complete the DI task. Three single data points

Appendices

261

(all from the control group) were identified as univariate outliers and deleted from the

data file.

Reading Time (RT)

Repeated measures ANOVA was used to compare the three groups on their

reading time of control and distractor stories. As expected, there was a significant Story

main effect, F(1, 81) = 362.20, MSE = 282575.83, p < .05, with all participants taking

longer to read the distractor stories than the control stories. There was also a significant

Group main effect, F(2, 81) = 18.03, MSE = 601293.81, p < .05, and Story x Group

interaction, F(2, 81) = 9.04, MSE = 282575.83, p < .05. Examination of the data showed

that whilst the two schizophrenia groups were significantly slower than control

participants on both story conditions, this difference was greater on the distractor

condition (see Table 2), suggesting that schizophrenia participants were more sensitive

than control participants to the adverse effects of distracting information on RT. There

were no significant RT differences between the no-AH and current-AH schizophrenia

groups. The pattern of results remained the same when any of the additional measures

were entered separately into the analysis as covariates.

Intrusions

A univariate ANOVA conducted on the number of distracting excerpts read

aloud (intrusions) revealed a significant Group main effect, F(2, 80) = 10.95, MSE =

120.30, p < .05, with post hoc pairwise comparisons showing that the no-AH and

current-AH schizophrenia groups did not significantly differ, while both schizophrenia

groups made significantly more intrusions than the control group. This effect remained


covariates.

Comprehension

A repeated measures ANOVA comparing the three groups on the percentage of

incorrect responses on the comprehension questions for the control and distractor

conditions, revealed a significant Group main effect, F(2, 82) = 11.10, MSE = 162.28, p

< .05, with post hoc pairwise comparisons showing that the current-AH schizophrenia

group made significantly more errors on the comprehension questions overall than the

control group. No other effects were significant. The Group main effect remained


Appendices

262

covariates. A univariate ANOVA of foil errors revealed no significant differences

between the groups.

B-P Task Performance

No univariate outliers were detected. As expected, when a repeated measures

ANOVA was conducted on the number of items correctly recalled on each of lists 1 to

3, there was a significant List main effect, F(2, 176) = 296.07, MSE = 0.55, p < .05,

with post hoc tests showing that recall progressively decreased across each list,

reflecting the build up of same-category intrusions across lists. There was also a

significant Group main effect, F(2, 88) = 21.12, MSE = 2.81, p < .05, with post hoc

pairwise comparisons revealing that the control group correctly recalled significantly

more items per list overall than either of the schizophrenia groups (see Table 2 for

group means and SDs). The absence of a significant List x Group interaction effect

suggests that neither of the schizophrenia groups had unintentional inhibition difficulties

relative to the comparison groups. The pattern of results remained the same when any of

the additional measures were entered into the analysis as covariates.

Correlations between Inhibition Indices, AHs and Other Schizophrenia-Related

Symptoms

The data were scanned for multivariate outliers using Cook‟s distance (>1), and

two cases were identified and subsequently excluded from the analyses that included

both these variables (variables: DIP negative symptom score and ICIM FAs on both

runs 2 and 3). AH severity (as measured using the PSYRATS) correlated significantly

with FAs on run 3 (r = .37, p < .05, N = 32), but not with FAs on run 1 (r = .00, p > .05,

N = 31) or run 2 (r = .21, p > .05, N = 31) on the ICIM task, suggesting that the severity

of AHs is related to intentional inhibition of currently irrelevant memories, but that this

relationship may be sensitive to the degree of activation of internal representations – i.e.

the salience of memory traces – which increases across runs. On the DI task, the RT-

Interference index (r = .07, p > .05, N = 28), the number of intrusions (r = -.29, p > .05,

N = 28), and percentage of foil errors (r = -.24, p > .05, N = 28) were all unrelated to

AH severity. Similarly, AH severity did not correlate significantly with the B-P

Inhibition score (r = -.18, p > .05, N = 34). Neither the DIP delusion nor negative

symptom scores correlated significantly with any of the inhibition indices (p > .05),

Appendices

263

highlighting the unique relationship between intentional inhibition difficulties and AH

severity.

DISCUSSION

Auditory hallucinations are typically perceived as being intrusive, uncontrollable

and unwanted (Morrison, 2005), and often accompanied by high levels of distress

(Norman et al., 1998). Needless to say, the costs of AHs to the individual can be

enormous. The current study aimed to delineate the cognitive control processes

theorised to underpin these features of AHs.

The principal hypothesis that AHs would be specifically linked to intentional

inhibition difficulties, and that these difficulties would not be common to other

schizophrenia-related symptoms, was supported only partially by the findings.

According to this hypothesis, one of the findings we expected was for the current-AH

schizophrenia group – but not the no-AH schizophrenia group – to perform significantly

more poorly than the control group on the ICIM task (see Badcock et al., 2005).

However, the current study showed no significant group differences on this task. This

inconsistency between current and previous findings may be attributable to differences

in the ICIM tasks used. The salience (i.e. strength of activation of internal

representation) of each item in the ICIM task is largely determined by the number of

repeated presentations of each item (Schnider et al., 2002). In previous schizophrenia

studies using this task (Badcock et al., 2005; Waters et al., 2003) targets were repeated

eight times within each run, compared with a maximum of only three times in the

current study, hence the salience of target items – and associated inhibitory demand –

was higher than in the current study. Consequently the previous version of the ICIM

task was potentially more sensitive to inhibition difficulties. Another possible reason

for the absence of group differences on the ICIM task may be the large within-group

variability in AH history: in the no-AH schizophrenia group some patients reported

never having had an AH, while others reported frequent AHs up until a month prior to

testing whilst in the current-AH schizophrenia group some reported experiencing AHs

only once a week, while others reported experiencing AHs most of every day. Since this

within-group variability would be expected to reduce the sensitivity of between-group

comparisons, correlational analyses provided further information regarding the

relationship between AHs and cognitive control.

Appendices

264

Correlational analyses provided support for the conjecture that AHs in

schizophrenia are related to difficulties in intentional inhibition. Specifically, AH

severity significantly and positively correlated with FAs on run 3 of the ICIM task –

when item salience and associated inhibitory demand is presumed to be at a maximum

in this version of the task (again highlighting the importance of item salience on the

detection of inhibition difficulties associated with AHs). Importantly, AH severity was

not related to either intentional resistance to interference (DI task) or unintentional

inhibition (B-P task), supporting the first component of the Badcock et al. model of AH,

which contends that the cognitive control difficulties underpinning AHs in

schizophrenia are both intentional and inhibitory in nature. Furthermore, intentional

inhibition (and the other forms of cognitive control) was not related to delusions or

negative symptoms, demonstrating the specificity of this deficit to AHs.

A pattern of findings similar to that reported here was recently shown in healthy

young adults predisposed to hallucinations (Paulik et al., 2007, 2008). Together these

findings are consistent with the notion of a continuum of hallucinatory experiences

linked to a common and specific impairment in intentional inhibition. This implies that

intentional inhibition disturbances are likely to be directly involved in the development

of AHs – rather than being a product of the general cognitive decline associated with

schizophrenia – since the hallucination predisposed individuals in our previous studies

were not (yet) experiencing full-blown psychotic symptoms. Support for the continuum

approach further validates the study of psychosis at the symptom level, which is

especially important in schizophrenia because of the heterogeneity of its genotypic and

phenotypic presentation, and the consequent ongoing debate over diagnostic criteria and

sub-grouping (Keefe & Fenton, 2007; Liddle, 1987; Peralta & Cuesta, 2001).

There is a large body of evidence linking schizophrenia to deficits in

executive/volitional behaviour (e.g., Merlotti et al., 2005; Racsmany et al., 2008; Zec,

1995), whilst automatic cognitive control processes, including both automatic inhibition

and automatic resistance to interference, appear to remain relatively intact (e.g.,

Fleming, Goldberg, Gold, & Weinberger, 1995; Kopp, Mattler, & Rist, 1994; Randolph,

Gold, Carpenter, et al., 1992). Consistent with this, in the current study the

schizophrenia groups had difficulty on at least one form of intentional control, namely

intentional resistance to interference (DI task), and were not significantly different from

controls on the measure of unintentional inhibition (BP task). The absence of intentional

inhibition deficits (on ICIM task) for all schizophrenia participants may also be

attributable to the reduction in item salience on this version of the task (as previously

Appendices

265

discussed). However, it is also possible that this discrepancy between the outcomes on

the two intentional tasks may be providing evidence of differential forms of

executive/volitional difficulties related to schizophrenia. This conjecture is supported by

Badcock and colleagues (2005)‟s study since they found that non-hallucinating

schizophrenia participants did not perform any more poorly on the ICIM task than

control participants, concluding that poor intentional cognitive inhibition is not a

general feature of schizophrenia. Furthermore, in our previous hallucination

predisposition studies we found that while intentional inhibition (on the ICIM task) was

uniquely related to hallucination predisposition, intentional resistance to interference

(on the DI task) was related to schizotypy predisposition more generally. Thus, it

appears that intentional resistance to interference may be related to schizophrenia more

generally, while intentional inhibition may be related to AHs more specifically.

The cognitive process of intentional resistance to interference permits an

individual to select goal-relevant stimuli from the environment whilst ignoring goal-

irrelevant stimuli. The breakdown of this process may contribute to the development

and/or maintenance of several different symptoms and features of schizophrenia. For

instance, it may contribute to the development and/or maintenance of a selective

processing bias for external stimuli that is thematically related to – or consistent with –

an individual‟s delusional beliefs (Frith, 1979). Disruption to the processing of goal-

relevant cognitions caused by the intrusion of goal-irrelevant stimuli may also

contribute to symptoms such as thought blocking, thought perseveration, disorganised

speech, and poor concentration, and may also impede other important processes – such

as reality monitoring and reality testing – thought to be involved in positive symptom

formation (Garety, Kuipers, Fowler, Freeman, & Bebbington, 2001).

Inhibitory control aside, it is important to note that the schizophrenia group

made significantly fewer Hits on all runs of the ICIM task and had significantly poorer

recall on all lists of the B-P task than the control group. This is consistent with general

recognition, recall, and working memory difficulties that have been widely documented

in schizophrenia (see Aleman, Hijman, de Haan, & Kahn, 1999, for review). The

presence of these memory-based difficulties in the schizophrenia groups, in the absence

of inhibition difficulties, highlights the independence of inhibitory performance from

memory functioning on the ICIM and B-P tasks in this sample.

There are potential limitations of the current study. Firstly, the majority of the

schizophrenia participants were medicated at the time of testing, therefore we cannot

exclude the possibility, for example, that medication selectively improved performance

Appendices

266

on the unintentional inhibition task. Secondly, the PSYRATS-AH was administered to

obtain a comprehensive measure of AH severity, since it has good psychometric

properties and has been widely used throughout the AH literature (e.g., Drake,

Haddock, Tarrier, Bentall, & Lewis, 2007; Haddock et al., 1999). The cost of using this

measure is that it can only be administered to individuals who report having

experienced AHs during the past four weeks, and thus, the correlational analyses were

limited to the current-AH sample. While it would have been ideal to include the entire

schizophrenia sample in these analyses, it should be noted that the current-AH and no-

AH schizophrenia samples did not differ from each other on any of the demographic,

cognitive or clinical variables, suggesting that the current-AH group was an adequate

representation of a schizophrenia sample. Finally, item salience was reduced in the

version of the ICIM task used here compared to the version previously used in a

schizophrenia sample (Badcock et al., 2005; Waters et al., 2003), leaving the likely –

but uncertain – possibility that this reduced salience contributed to the absence of

predicted group differences on this task. An interesting avenue for further research may

be to manipulate memory salience on the ICIM task, to help expose the mechanisms

driving, or moderating, the inhibition difficulties associated with AHs.

The current findings have important clinical implications. Interventions aimed at

reducing the severity of hallucinatory-type experiences should target intentional forms

of inhibitory control. Direct cognitive remediation may appear to be the most obvious

approach; however, given the paradoxical increase in unwanted cognitive intrusions

associated with repeated attempts to suppress unwanted cognitions (Baumeister, Vohs,

& Tice, 2007; Wegner & Zanakos, 1994), such an approach may be unwise. An

alternative option may be to modify maladaptive cognitive coping strategies, which may

be further impairing – or relying heavily upon – intentional inhibitory ability, such as

replacing suppression-based coping strategies with active acceptance (Farhall &

Gehrke, 1997) or distraction (Morrison & Wells, 2000). Furthermore, inclusion into

such treatment programs should not discriminate between individuals who do and do

not meet diagnostic criteria for schizophrenia, since our current and previous findings

(Paulik et al., 2007, 2008) suggest that at least some of the principal cognitive

mechanisms underlying hallucinatory-type experiences span across the continuum.

Appendices

267

ACKNOWLEDGEMENTS


funding from the Ron and Peggy Bell Foundation. We also thank Sarah Howell, Alan

Bland and Christina Read for assistance with participant recruitment, John Dean for the

on-going DIP training, Matt Huitson for his help with task programming, and the

Western Australia Family Schizophrenia Study for providing NART scores for

participants.

Appendices

268

REFERENCES



1366.

Amieva, H., Phillips, L. H., Della Sala, S., & Henry, J. D. (2004). Inhibitory functioning

in Alzheimer's disease. Brain, 127, 949-964.














121, 65-94.




Baumeister, R. F., Vohs, K. D., & Tice, D. M. (2007). The strength model of self-

control. Current Directions in Psychological Science, 16, 351-355.

British National Formulary (1995). British National Formulary. London: British

Medical Association and the Royal Pharmaceutical Society of Great Britain.




Castle, D., Jablensky, A., McGrath, J., Carr, V., Morgan, V., Watterreus, A., et al.

(2006). The Diagnostic Interview for Psychoses (DIP): Development, reliability

and applications. Psychological Medicine, 36, 69-80.

Appendices

269






Dempster, F. N. (1993). Resistance to interference: Developmental changes in a basic

processing mechanism. In M. L. Howe & R. Pasnak (Eds.), Emerging themes in

cognitive development (Vol. 1). New York: Springer-Verlag.





Drake, R., Haddock, G., Tarrier, N., Bentall, R., & Lewis, S. (2007). The Psychotic

Symptom Rating Scales (PSYRATS): Their usefulness and properties in first

episode psychosis. Schizophrenia Research, 89, 119-122.

Earles, J. L., Connor, L. T., Frieske, D., Park, D. C., Smith, A. D., & Zwahr, M. (1997).

Age differences in inhibition: Possible causes and consequences. Aging,

Neuropsychology, and Cognition, 4, 45 - 57.



Fleming, K., Goldberg, T. E., Gold, J. M., & Weinberger, D. R. (1995). Verbal

working memory dysfunction in schizophrenia: Use of a Brown-Peterson

paradigm. Psychiatry Research, 56, 155-161.



Therapy, 41, 923-947.


(1994). Health-related intrusive thoughts. Journal of Psychosomatic Research.




Frith, C. D. (1979). Consciousness, information processing and schizophrenia. British


Appendices

270

Garety, P. A., Kuipers, E., Fowler, D., Freeman, D., & Bebbington, P. E. (2001). A

cognitive model of the positive symptoms of psychosis. Psychological Medicine,

31, 189-195.










Academic Press.

Hasher, L., Lustig, C., & Zacks, R. (2007). Inhibitory mechanisms and the control of

attention. In A. R. A. Conway, C. Jarrold, M. J. Kane, A. Miyake & J. N. Towse

(Eds.), Variation in Working Memory. Oxford: Oxford University Press.














Lau, M. A., Christensen, B. K., Hawley, L. L., Gemar, M. S., & Segal, Z. V. (2007).

Inhibitory deficits for negative information in persons with major depressive

disorder. Psychological Medicine, 37, 1249-1259.



Appendices

271








1209.

Nelson, H. E., & Willison, J. R. (1991). National Adult Reading Test manual (2nd ed.).

Windsor, UK: NFER-Nelson Publishing Company.

Nigg, J. T., Butler, K. M., Huang-Pollock, C. L., & Henderson, J. M. (2002). Inhibitory

processes in adults with persistent childhood onset ADHD. Journal of

Consulting Clinical Psychology, 70, 153-157.





470.

Paulik, G., Badcock, J. C., & Maybery, M. T. (2008). Dissociating the components of






Radvansky, G. A., & Copeland, D. E. (2006). Memory retrieval and interference:

Working memory issues. Journal of Memory and Language, 55, 33-46.





Racsmany, M., Conway, M. A., Garab, E. A., Cimmer, C., Janka, Z., Kurimay, T., et al.

(2008). Disrupted memory inhibition in schizophrenia. Schizophrenia Research,

101, 218-224.

Appendices

272

Salthouse, T. A., Atkinson, T. M., & Berish, D. E. (2003). Executive functioning as a

potential mediator of age-related cognitive decline in normal adults. Journal of

Experimental Psychology: General, 132, 566-594.





5880-5884.




Sheehan, D. V., Lecrubier, Y., Sheehan, K. H., Janavs, J., Weiller, E., Keskiner, A., et

al. (1997). The validity of the Mini International Neuropsychiatric Interview

(MINI) according to the SCID-P and its reliability. European Psychiatry, 12,

232-241.






215.


Schuster.

Stuss, D. T., Toth, J. P., Franchi, D., Alexander, M. P., Tipper, S., & Craik, F. I. (1999).

Dissociation of attentional processes in patients with focal frontal and posterior

lesions. Neuropsychologia, 37, 1005-1027.

Tipper, S. P., & Baylis, G. C. (1987). Individual-differences in selective attention: The

relation of priming and interference to cognitive failure. Personality and




610-618.




Appendices

273



Research, 62, 275-280.




Wechsler, D. (1997). Wechsler Adult Intelligence Scale - Third Edition. San Antonio,

USA: Psychological Corporation.



Wildt, A. R., & Olli, T. A. (1978). Analysis of covariance. Quantitative Applications in

the Social Sciences (series 12). Thousand Oaks, CA: Sage Publications.

Wilson, S. P., & Kipp, K. (1998). The development of efficient inhibition: Evidence

from directed-forgetting tasks. Developmental Review, 18, 86-123.


Emotion, 1, 166-181.

Woods, S. W. (2003). Chlorpromazine equivalent doses for the newer atypical

antipsychotics. Journal of Clinical Psychiatry, 64, 663-667.

World Health Organisation (1993). The ICD-10 classification of mental and

behavioural disorders: Diagnositic criteria for research (10th ed. Vol. 1).

Geneva: World Health Organisation.




Zigmond, A. S., & Snaith, R. P. (1983). The hospital anxiety and depression scale. Acta


Documents

Inhibition, Anxiety and the Development of Auditory Hallucinations · Inhibition, Anxiety and the Development of . Auditory Hallucinations . Georgie Paulik . B.Sc. (Hons.) (Psychology)