APPROACH TO LANGUAGE AND SPEECH DISORDERSSURENDRA KHOSYADM NEUROLOGY IHBAS DELHI

Focus Questions

Does the patient possess a speech or language impairment?

Is this impairment aphasia?

If it is aphasia, what is its type and severity?

Clinical courseA 52-year-old woman was brought to the emergency service with severe headache and brief loss of consciousness. She was lethargic and had slight nuchal rigidity on neurological examination. Motor and sensory findings were normal. Initial CT of the brain revealed subarachnoid hemorrhage (SAH), more prominent in the right Sylvian fissure. There were no findings suggestive of an ischemic insult She was hospitalised with a diagnosis of subarachnoid hemorrhage. She had no known developmental or childhood neurological disorders. Upon admission, a TCD revealed a mean middle cerebral artery (MCA) velocity of 82 cm/sec on the right and 65cm/sec on the left side. A cerebral angiogram showed an MCA bifurcation aneurysm. Her neurological examination was normal and TCD values were within normal limits for the next two days. On the third day of her admission, she developed non-fluent aphasia characterized by reduced verbal output, word-finding disturbances and phonemic paraphasias in both oral and written language. Left hemianopsia and spatial neglect were found on confrontation testing. She also had left hemiparesis and hemihypoesthesia. Cranial CT and electroencephalographic study were normal. Mean MCA velocities were elevated to 185 cm/sec on the right and 90 cm/sec on the left side. Post-SAH vasospasm-related ischemia and crossed Wernicke’s aphasia were diagnosed. She was followed up with intravenous fluid administration, hemodilution and hypertension. In the meantime, TCD values gradually returned to normal levels. SPECT findings were also consistent with right parieto-temporal and fronto-parietal ischemia with crossed cerebellar diaschisis on the right cerebellum . A diagnosis of crossed aphasia was confirmed

Language and Speech Disorders  :  Aphasia and Aphasic SyndromesAphasia is defined as a disorder of language acquired secondary to brain damage.  Alexander and Benson (1997).Aphasia is a disorder of language rather than speech. Speech is the articulation and phonation of language sounds.Aphasia is different from motor speech disorders,dysarthria,dysphonia (voice disorders), stuttering, and speech apraxia. Dysarthrias disorders of articulation of single sounds; tongue or larynx and dysfunction of the muscles, neuromuscular junction, cranial nerves, bulbar anterior horn cells, corticobulbar tracts, cerebellar connections, or basal ganglia. Apraxia of speech is a syndrome of misarticulation of phonemes, especially consonant sounds. Aphasia is distinguished from disorders of thought.

5 COMPONENTS OF LANGUAGE

Phonology

Morphology

Syntax

Form

Semantics

Content word

meanings

Pragmatics

Function

STRUCTURE OF LANGUAGE

Phonology = rules regarding how sounds can be used and combined.

Syntax = the way sequences of words are combined into phrases and sentences.

Morphology = the form and internal structure of words.

Semantics = the understanding of language.

Pragmatics = rules that govern the reasons for communication as well as the choice of codes to be used when communicating.

From Kertesz A, Lesk D, McCabe P: Arch Neural 34:590

From Kertesz A, Lesk D, McCabe P: Arch Neural 34:590

From Kertesz A, Lesk D, McCabe P: Arch Neural 34:590

From Kertesz A, Lesk D, McCabe P: Arch Neural 34:590

From Kertesz A, Lesk D, McCabe P: Arch Neural 34:590

Aphaisal Battery

Mostly used 3 test batteries: MTDDA, PICA & Boston.

They differ in their orientation with respect to 3 major goals of testing stated by Goodglass & Kaplan (1972).

These objectives are

(1) assessment of assets and liabilities of patient in all language areas as a guide to therapy.

(2) measurement of the level of performance over a wide range, for both initial determination and detection of change over time.

(3) diagnosis of presence and type of aphasic syndrome, leading to inferences concerning cerebral localization.

Classification test:

WAB – Western aphasia batteryBDAE – Boston diagnostic Aphasia Examination

Non-classification test:

MTDDA – Minnesota Test for differential diagnosis of aphasiaPICA Porch Index of Communicative Ability

Tests that make a prognostic statement:MTDDA or PICA

Porch Index of Communicative Ability (PICA) -

PICA second goal of evaluation, which providing measurement of degree of deficit and amount of recovery.

PICA consists of 18 subtests of 4 language modalities.

Object manipulation, visual matching, and copying abstract forms.

Minnesota Test for Differential Diagnosis of Aphasia (MTDDA) - Of the 3 goals of examination.MTDDA Aims include differential diagnosis and prediction of recovery.

Differential diagnosis refers to whether patient has aphasia or aphasia plus perceptual disorders, apraxia, dysarthria, or some other brain damage.

MTDDA is the most comprehensive of the tests for aphasia, it takes 2 to 6 hours to administer, 3 hours on the average. It consists of 46 subtests divided into 5 sections:

oAuditory DisturbancesoVisual and Reading DisturbancesoSpeech and language disturbancesoVisuomotor and writing disturbancesoDisturbances of numerical relations and arithmetic processes

Boston Diagnostic Aphasia Examination (BDAE)The Boston oriented toward the presence and type of aphasia. leading to location of brain damage (Goodglass & Kaplan, 1972).

The BDAE designed for language behaviors and identification of aphasic syndromes.

Its include auditory comprehension, self initiated and conversational speech, word retrieval, and repetition.

"A short form contains select items from 21 select subtests of the standard form" (Brookshire, 2007, pg.219)

The BDAE provides an objective basis for the identification of aphasic syndromes

They include profiles of a prototypical case and of range of performance for Broca's, Wernicke's, conduction and anomic aphasias

Items and scoring:Items and scoring on the BDAE is as follows (Goodglass & Kaplan, 1972):The BDAE is comprised of 8 subscales:•Fluency•Auditory comprehension•Naming•Oral reading•Repetition•Automatic speech•Reading comprehension•Writing

1. Fluency:Melodic line: The examiner should observe the intonational pattern in the entire sentence. Phrase length: The examiner should observe the length of uninterrupted runs of words. Articulatory agility: The examiner should observe how the client articulates phonemic sequences. Grammatical form: The examiner should observe the variety of grammatical construction. Paraphasia in running speech: The examiner should observe substitutions or insertions of semantically erroneous words in running conversation. Word-finding: The examiner should observe the client's capacity to evoke needed concept names and informational content in the sentences. All features are scored on a 7-point scale where 1 is the maximum abnormality and 7 the minimum abnormality.

2. Auditory ComprehensionWord discrimination: Consists of a multiple choice task and samples six categories of words: objects, geometric forms, letters, actions, numbers and colors. 

Body-part identification: Includes 24 items, the first 18 are related to body part names, and the remaining 8 with right-left comprehension.

Commands: The client is requested to carry out commands. The score in this subscale ranges from 0 to 15. 

Complex ideational material: In this section the examiner asks general questions such as "will a stone sink in water?" and the client is required to understand and express agreement or disagreement

Score ranges from 0 to 10.

3. NamingResponsive naming: The examiner asks the client a question containing a key word associated with the expected answer. Then the client should answer the question using the following words: nouns (watch, scissors, match, drugstore); colors (green, black), verbs (shave, wash, write) and a number (twelve)

Visual Confrontation: The client should name the images presented by the examiner. The visual stimulus items are from cards 2 and 3 and represent objects, geometric forms, letters, actions, numbers, colors and body parts.

Animal naming: The first word "dog" is provided by the examiner to stimulate the client. Then the client should provide all animals name that he/she knows within 60 seconds.

Body part naming: The examiner points to 10 body parts to be named on him/her.

4. Oral Reading

Word reading: The examiner indicates a word from card 5 that should be read by the client. Three points are given when the word is read within 3 seconds, 2 points within 3 to 10 seconds, 1 point within 10 to 30 seconds, and 0 if the client provides the wrong answer. Maximum score is 30. 

Oral sentence: Ten sentences should be read from cards 6 and 7. The sentences are scored as pass (score of 1) or fail (score of 0).

5. Repetition

Words: A wide sampling of word types is presented, including a grammatical function word, objects, colors, a letter, numbers, an abstract verb of three syllables and a tongue twister. An item is scored correct if all phonemes are in correct order and recognizable. One point is allowed per item for a total of 10. 

High and low probability sentences: The sentences should be repeated by the client, alternating between a high- and a low-probability item. One point is given for each sentence correctly repeated and high- and low- probability sections are scored separately from 0 to 8.

6. Automatic speechAutomatized sequences: Four sequences are tested: days of the week, months of the year, number from one to twenty-one and the alphabet. Two points maximum are given for complete recitation of any series and 1 point is given for unaided runs of 4 consecutive words when reciting days, 5 consecutive words when reciting months, 8 consecutive words when reciting numbers and 7 consecutive words when reciting the alphabet. Reciting: Several nursery rhymes are suggested to elicit completion responses. A score of 0 is given if the client is unable to recite, 1 for impaired recitation and 2 for good recitation.

7. Reading ComprehensionSymbol discrimination: Cards 8 and 9 contain 10 items each. The examiner shows the word or letter centered above the five multiple-choice responses and asks the client to select the equivalent. One point is given to each correct item. Word recognition: Using cards 10 and 11 the client is requested to identify the one word, out of 5, which matches the word said previously by the examiner. This task is repeated another 7 times and a score of 1 point is given to each correct answer. Oral spelling: The client should recognize 8 words spelled by the examiner. One point is given for each correct recognition. Word-picture matching: Ten words are selected from card 5 to be identified on cards 2 and 3. One point is given for each correct recognition. Sentences and paragraphs: The examiner reads 10 sentences from cards 12 to 16. The client is requested to complete the ending of a sentence with a four multiple choice options. One point is given for each correct sentence.

8. Writing Mechanics: The client is requested to write his/her name and address with the stronger hand. In case he/she is not able to do so, then the examiner can write the sentence and the client should then transcribe it. Score ranges from 0 to 3 according to performance level. Serial writing: The client should write the alphabet and numbers from 1 to 21. The score is the total number of different, correct letters and numbers, combined for a maximum score of 47. Primer-level dictation: The client should write the letters, numbers and primer words that are dictated by the examiner. A score is given by adding the number of correct words. Spelling to dictation: The client should write the words dictated by the examiner. Score is based on the amount of correct words written by the client. Written confrontation naming: The patient should write the name of the figure that is shown from cards 2 and 3 by the examiner. The examiner should show 10 figures. One point is given for each correctly spelled response. Sentences to dictation: The client should write the three sentences dictated by the examiner. Scores for each sentence range from 0 to 4. Narrative writing: Card 1 has a picture of a cookie theft which is shown to the client who must then write as much as he/she can about what he/she sees in the picture. The client should be encouraged to keep writing for 2 minutes. Scores for this section range from 0 (no relevant writing) to 4 (full description in grammatical sentences).

BOSTON APHASIA CLASSIFICATION SYSTEM

Major Classification System (Benson, 1979) Recognises eight subtypes of aphasia Assess: Boston Diagnostic Aphasia Examination

1. Broca’s Aphasia. Lesion of the expressive speech area

2. Wernicke’s Aphasia. Lesion of the receptive speech area

3. Conduction Aphasia. Disconnection of the expressive and receptive areas

4. Global Aphasia. Extensive lesion involving both expressive and receptive areas

BOSTON APHASIA CLASSIFICATION SYSTEM

5. Transcortical Motor Aphasia6. Transcortical Sensory Aphasia7. Isolated Aphasia8. Anomic Aphasia

Clinical Features of Aphasias and Related Conditions

  Comprehension Repetition of Spoken Language

Naming Fluency

Wernicke's Impaired Impaired Impaired Preserved or increased

Broca's Preserved (except grammar)

Impaired Impaired Decreased

Global Impaired Impaired Impaired Decreased

Conduction Preserved Impaired Impaired Preserved

Nonfluent (motor) transcortical

Preserved Preserved Impaired Impaired

Fluent (sensory) transcortical

Impaired Preserved Impaired Preserved

Isolation Impaired Echolalia Impaired No purposeful speech

Anomic Preserved Preserved Impaired Preserved except for word-finding pauses

Pure word deafness Impaired only for spoken language

Impaired Preserved Preserved

Pure alexia Impaired only for reading

Preserved Preserved Preserved

Feature Syndrome

Spontaneous speech IntactNaming ± Impaired, especially colorsComprehension IntactRepetition Intact

Reading Impaired (some sparing of single letters)

Writing Intact

Associated signs Right hemianopia or superior quadrantanopia

  Short-term memory loss

  Motor, sensory signs usually absent

 

Features of Pure Alexia without AgraphiaAcquired inability to read.The lesion in pure alexia is nearly always a stroke in the territory of the left posterior cerebral artery, with infarction of the medial occipital lobe, often the splenium of the corpus callosum, and often the medial temporal lobe

Feature Syndrome

Spontaneous speech Fluent, often some paraphasia

Naming ± Impaired

Comprehension Intact or less impaired than reading

Repetition IntactReading Severely impairedWriting Severely impairedAssociated signs Right hemianopia

  Motor, sensory signs usually absent

Features of Alexia with AgraphiaThis overlaps Wernicke aphasia, reading is more impaired than auditory comprehension. Associated deficits right hemianopia and elements of the Gerstmann syndrome: agraphia, acalculia, right-left disorientation, and finger agnosia.The lesions in the inferior parietal lobule, especially the angular gyrus. Etiologic strokes in the territory of the angular branch of the left middle cerebral artery and mass lesions in the same region.

Lesion analysis of language production deficits in aphasiaAphasiology Volume 28, Issue 3, 2014Abstract

Background: Three aspects of language production are impaired to different degrees in individuals with post-stroke aphasia: ability to repeat words and nonwords, name pictures, and produce sentences. These impairments often persist into the chronic stages, and the neuroanatomical distribution of lesions associated with chronicity of each of these impairments is incompletely understood.Aims: The primary objective of this study was to investigate the lesion correlates of picture naming, sentence production, and nonword repetition deficits in the same participant group because most prior lesion studies have mapped single language impairments. The broader goal of this study was to investigate the extent and degree of overlap and uniqueness among lesions resulting in these deficits in order to advance the current understanding of functional subdivision of neuroanatomical regions involved in language production.Methods & Procedures: In this study, lesion-symptom mapping was used to determine if specific cortical regions are associated with nonword repetition, picture naming, and sentence production scores. Structural brain images and behavioural performance of 31 individuals with post-stroke left hemisphere lesions and a diagnosis of aphasia were used in the lesion analysis.Outcomes & Results: Each impairment was associated with mostly unique, but a few shared lesions. Overall, sentence and repetition deficits were associated with left anterior perisylvian lesions, including the pars opercularis and triangularis of the inferior frontal lobe, anterior superior temporal gyrus, anterior portions of the supramarginal gyrus, the putamen, and anterior portions of the insula. In contrast, impaired picture naming was associated with posterior perisylvian lesions including major portions of the inferior parietal lobe and middle temporal gyrus. The distribution of lesions in the insula was consistent with this antero-posterior perisylvian gradient. Significant voxels in the posterior planum temporale were associated with a combination of all three deficits.Conclusions: These findings emphasise the participation of each perisylvian region in multiple linguistic functions, suggesting a many(functions)-to-many(networks) framework while also identifying functional subdivisions within each region.

Improving quality of life in aphasia—Evidence for the effectiveness of the biographic-narrative approachAphasiologyVolume 28, Issue 4, 2014AbstractBackground: Caused by the constraints in communication, people with aphasia experience a pronounced decrease in quality of life (QoL). Beyond that identity negotiation is hindered which is crucial for QoL. This increases the severe loss of QoL. In sociocultural theories, it is postulated that identity is created through social interaction with others. In telling life stories, people build meaning and affirm identity. Biographic-narrative approaches use such life stories to support identity (re)development after disruptive events like stroke. Specific communication skills are needed for this, i.e., biographic-narrative competency. Therefore, such approaches have to be modified for the use in people with aphasia.Aims: We target on the development and evaluation of an interdisciplinary multimodal approach of biographic-narrative work. The primary aim is to improve QoL through identity renegotiation.Methods & Procedures: Five face-to-face interviews and seven group sessions were conducted in a before and after design over 10 weeks, with a follow-up assessment after three months. The intervention took place in ambulant rehabilitation units and at the Catholic University of Applied Sciences Mainz, Germany. The interviews comprise three narrative in-depth interviews, allowing participants to tell their life narration and two further semi-structured interviews to engross issues and prepare group topics. Narrations were supported by a multimodal approach, e.g., by pictures. To measure QoL, the Aachen Life Quality Inventory (ALQI), the Satisfaction with Life Scale (SWLS) and the Visual Analogue Mood Scales (VAMS) were used. Additionally, qualitative data was ascertained by semi-structured interviews with questions targeting personal growth or identity change. Seventeen participants, recruited consecutively from ambulant rehabilitation units and aphasia support groups, participated in the study. Almost all had a chronic but different type of aphasia (mean time post-stroke 40.82 months).Outcomes & Results: We found a significant improvement in health-related QoL measured by the ALQI (p < .05), which remained stable after three months without intervention. Also the self-reported mood state “happiness” grew significantly, “confused” and “tense” sank significantly (p < .05). As expected, overall life satisfaction which is a very broadly based and stable judgment did not change. According to self-reports in semi-structured interviews at the end of the intervention participants experienced a change in perspective accompanied by a change in quality of participation.Conclusions: QoL in people with aphasia can be improved by means of biographic-narrative intervention.

OTHER CAUSE OF APHASIA

Dialysis dementia syndrome-stuttering f/b aphasia and dementia

Creutzfeldt-jacob disease –spongiform degeneration of frontotemporal cortex

Acute encephalopathy-hyponatremia or lithium toxicity

Landau-kleffner syndrome

PROGRESSIVE APRAXIA OF SPEECH Clinicopathological and imaging correlates of

progressive aphasia and AOS– (Josephs, Duffy, Strand et. al. 2006)

Retrospective study of 17 cases who met specific inclusionary criteria Met specific published criteria for a diagnosis of PPA; PNFA; SD or AOS

  No other etiologic factors related to aphasia or AOS

Brain (2006), 129, 1385–1398

Speech Language Diagnoses Categories PPA – NOS = 7 (one of whom had a mild apraxia)  PNFA-AOS = 3 AOS = 7  Pathological Diagnoses  PSP = 6 CBD = 5 FTLD = 5  Picks Disease = 1 Major findings related to AOS All 11 patients with AOS had a diagnosis characterized by underlying tau pathology.  Initial diagnosis of AOS 5– PSP 1 – CBD 1 PiD Pathological Diagnosis of PNFA-AOS All three – CBD Pathological Diagnosis of PPA-NOS - (the one case that had some evidence of AOS – had PSP)

Localization

Nonfluent aphasia with apraxia of speech is associated with atrophy of the premotor and posterior inferior frontal cortices.

Temporal lobe atrophy is correlated with “fluent” progressive aphasia.

RECOVERY

Global aphasia to Broca aphasia Wernicke aphasia to conduction or anomic

aphasia

BIOLOGICAL APPROACHES TO APHASIA TREATMENT

Steven L. Small, M.D., Ph.D. and Daniel A. Llano, M.D., Ph.D.Current Neurology and Neuroscience Reports 2009 November; 9(6): 443–450Herein, we review the basic mechanisms neural regeneration and repair and attempt to correlate the findings from animal models of stroke recovery to clinical trials for aphasia. Several randomized, controlled clinical trials that have involved manipulation of different neurotransmitter systems, including noradrenergic, dopaminergic, cholinergic and glutamatergic systems, have shown signals of efficacy. Biological approaches such as anti-Nogo and cell-replacement therapy have shown efficacy in preclinical models, but have yet to reach proof of concept in the clinic. Finally, noninvasive cortical stimulation techniques have been used in a few small trials, and have shown promising results. It appears that the efficacy of all of these platforms can be potentiated through coupling with speech-language therapy. Given this array of potential mechanisms that exist to augment and/or stimulate neural reorganization after stroke, we are optimistic that approaches to aphasia therapy will transition from compensatory models to models where brain reorganization is the goal.

Transcranial Magnetic Stimulation (TMS): Potential Progress for Language Improvement in AphasiaStroke.2011; 42: 409-415AbstractAphasia researchers and clinicians share some basic beliefs about language recovery post stroke. Most agree there is a spontaneous recovery period and language recovery may be enhanced by participation in a behavioral therapy program. The application of biological interventions in the form of pharmaceutical treatments or brain stimulation is less well understood in the community of people who work with individuals having aphasia. The purpose of this article is to review the literature on electrical brain stimulation as an intervention to improve aphasia recovery. The article will emphasize emerging research on the use of transcranial magnetic stimulation (TMS) to accelerate stroke recovery. We will profile the current US Food and Drug Administration (FDA)–approved application to depression to introduce its potential for future application to other syndromes such as aphasia.

MOTOR SPEECH DISORDERS:APRAXIA AND DYSARTHRIA

.

FOCUS QUESTIONS What is a motor speech disorder? How are motor speech disorders classified? What are the characteristics of prevalent

types of motor speech disorders? How are motor speech disorders identified? How are motor speech disorders treated?

.

CASE STUDY #1: BOB 42-year old bilingual, married with four children,

travels, coaches soccer, involved in community activities

Diagnosed with cerebellar tumor, removed successfully, but effects from surgery…

Severely ataxic, difficulties coordinating voluntary movements, under- and over-shooting movements, and tremor

.

CASE STUDY #2:B

60-year old professor, likes to read, play tennis, improve the house, and play piano

Age 59, left hemisphere stroke – now slow, effortful, and inconsistently distorted speech and weakness in right side of body, including oral structures (e.g. lips)

diagnosed him with mild aphasia and mild apraxia of speech

DysarthriasDysarthrias involve the abnormal articulation of sounds or phonemes. The pathogenic mechanism in dysarthria is abnormal neuromuscular activation of the speech muscles, affecting the speed, strength, timing, range, or accuracy of movements involving speech

The Mayo Clinic classification of dysarthria six categories: (1) flaccid, (2) spastic and “unilateral upper motor neuron,” (3) ataxic, (4) hypokinetic, (5) hyperkinetic, and (6) mixed dysarthria.

Duffy, J.R., 1995. Motor Speech Disorders: Substrates, Differential Diagnosis, and Management. Mosby, St. Louis; and from Kirshner, H.S., 2002. Behavioral Neurology: Practical Science of Mind and Brain. Butterworth Heinemann, Boston.

Type Localization Auditory Signs Characteristic Disease(s)

Flaccid Lower motor neuron Breathy, nasal voice, imprecise consonants

Stroke, myasthenia gravis

Spastic Bilateral motor neuronStrain-strangle, harsh voice; slow rate; imprecise consonants

Bilateral strokes, tumors, primary lateral sclerosis

  Unilateral upper motor neuron

Consonant imprecision, slow rate, harsh voice quality

Stroke, tumor

Ataxic CerebellumIrregular articulatory breakdowns, excessive and equal stress

Stroke, degenerative disease

Hypokinetic ExtrapyramidalRapid rate, reduced loudness, monopitch and monoloudness

PD

Hyperkinetic

ExtrapyramidalProlonged phonemes, variable rate, inappropriate silences, voice stoppages

Dystonia, HD

Spastic and flaccid

Upper and lower motor neuron

Hypernasality, strain-strangle, harsh voice, slow rate, imprecise consonants

ALS, multiple strokes

 Classification of the Dysarthrias

ACQUIRED APRAXIA OF SPEECH

 Etiology most frequently is stroke  posterior inferior left frontal lobe and/or

insula may involve subcortical structures Vascular Perspective Left middle cerebral

arteries M1, M2 segments

Acquired Apraxia of Speech Can occur with: TBI Neurosurgical (tumor; AVM; SAH) degenerative disease (e.g. CBD; PSP; ALS; PPA)

A neurologic speech disorder characterized by difficulty with sequential ordering of movements in the correct spatial and temporal relationship to each other, due to impairment in planning and/or programming sensorimotor commands Language processes are not impaired (although frequently aphasia co-occurs)

APHEMIA

It is syndrome of near-muteness, with normal comprehension,

reading and writing.

Aphemia is a motor speech disorder rather than an aphasia.

Controversy whether aphemia is equivalent to apraxia of speech.

Aphemia is likely to lesions in the vicinity of the primarmotor cortex and perhaps the Broca area, whereas

apraxia ofspeech may be localized to the insula

Foreign Accent Syndrome

It is an acquired form of motor speech disorder related to the dysarthrias.

In which the patient acquires a dysfluency resembling a foreign accent, usually after a unilateral stroke.

It also occurs in multiple sclerosis, traumatic brain injury and in the degenerative disorder known as primary progressive aphasia or frontotemporal dementia

ACQUIRED STUTTERING It is associated with hesitancy in producing initial

phonemes, pauses in speech, contortions of the face, and sometimes repetition of phonemes and associated dysrhythmia of speech.

It is most often in patients with left hemisphere cortical stroke, but also reported with subcortical lesions including infarctions of the pons, basal ganglia, and subcortical white matter.

Acquired stuttering also follows traumatic brain injury and seizures, especially involving the supplementary motor area

Opercular Syndrome It is a severe form of pseudobulbar palsy in which patients with bilateral lesions of the perisylvian cortex or subcortical connections become completely mute. These patients can follow commands involving the extremities but not those mediated by the cranial nerves.

WERNICKE-GESCHWIND MODEL2. REPEATING A WRITTEN WORD

Angular gyrus is the gateway from visual cortex to Wernicke’s area

This is an oversimplification of the issue: not all patients show such predicted behavior (Howard,

1997)