approach to Language dysfunction and speech disorder


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  • Magnetic resonance imaging study of the brain of a patient with Broca aphasia. In this patient, the cortical Broca area, subcortical white matter, and the insula all were involved in the infarction. The patient made a good recovery.  
  • approach to Language dysfunction and speech disorder

    2. 2. 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?
    3. 3. Clinical course A 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
    4. 4. Language and Speech Disorders : Aphasia and Aphasic Syndromes Aphasia 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. 5. 5 COMPONENTS OF LANGUAGE Phonology Morphology Syntax Form Semantics Content word meanings Pragmatics Function
    6. 6. 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.
    7. 7. From Kertesz A, Lesk D, McCabe P: Arch Neural 34:590
    8. 8. From Kertesz A, Lesk D, McCabe P: Arch Neural 34:590
    9. 9. From Kertesz A, Lesk D, McCabe P: Arch Neural 34:590
    10. 10. From Kertesz A, Lesk D, McCabe P: Arch Neural 34:590
    11. 11. From Kertesz A, Lesk D, McCabe P: Arch Neural 34:590
    12. 12. 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.
    13. 13. Classification test: WAB – Western aphasia battery BDAE – Boston diagnostic Aphasia Examination Non-classification test: MTDDA – Minnesota Test for differential diagnosis of aphasia PICA Porch Index of Communicative Ability Tests that make a prognostic statement: MTDDA or PICA
    14. 14. 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.
    15. 15. 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 Disturbances oVisual and Reading Disturbances oSpeech and language disturbances oVisuomotor and writing disturbances oDisturbances of numerical relations and arithmetic processes
    16. 16. 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)
    17. 17. 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
    18. 18. 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
    19. 19. 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.
    20. 20. 2. Auditory Comprehension Word 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.
    21. 21. 3. Naming Responsive 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.
    22. 22. 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).
    23. 23. 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.
    24. 24. 6. Automatic speech Automatized 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.
    25. 25. 7. Reading Comprehension Symbol 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.
    26. 26. 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).
    27. 27. 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
    28. 28. BOSTON APHASIA CLASSIFICATION SYSTEM 5. Transcortical Motor Aphasia 6. Transcortical Sensory Aphasia 7. Isolated Aphasia 8. Anomic Aphasia
    29. 29. 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
    30. 30. Feature Syndrome Spontaneous speech Intact Naming ± Impaired, especially colors Comprehension Intact Repetition 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 Agraphia Acquired 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
    31. 31. Feature Syndrome Spontaneous speech Fluent, often some paraphasia Naming ± Impaired Comprehension Intact or less impaired than reading Repetition Intact Reading Severely impaired Writing Severely impaired Associated signs Right hemianopia Motor, sensory signs usually absent Features of Alexia with Agraphia This 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.
    32. 32. Lesion analysis of language production deficits in aphasia Aphasiology Volume 28, Issue 3, 2014 Abstract 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
    33. 33. Improving quality of life in aphasia—Evidence for the effectiveness of the biographic- narrative approachAphasiology Volume 28, Issue 4, 2014 Abstract Background: 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
    34. 34. 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
    35. 35. 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
    36. 36. 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)
    37. 37. 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.
    38. 38. RECOVERY  Global aphasia to Broca aphasia  Wernicke aphasia to conduction or anomic aphasia
    39. 39. BIOLOGICALAPPROACHES 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): 443–450 Herein, 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
    40. 40. Transcranial Magnetic Stimulation (TMS): Potential Progress for Language Improvement in Aphasia Stroke.2011; 42: 409-415 Abstract Aphasia 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.
    42. 42. 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? .
    43. 43. 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 .
    44. 44. 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
    45. 45. Dysarthrias Dysarthrias 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.
    46. 46. Type Localization Auditory Signs Characteristic Disease(s) Flaccid Lower motor neuron Breathy, nasal voice, imprecise consonants Stroke, myasthenia gravis Spastic Bilateral motor neuron Strain-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 Cerebellum Irregular articulatory breakdowns, excessive and equal stress Stroke, degenerative disease Hypokinetic Extrapyramidal Rapid rate, reduced loudness, monopitch and monoloudness PD Hyperkinetic Extrapyramidal Prolonged 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
    47. 47. 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
    48. 48. 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)
    49. 49. 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 primar motor cortex and perhaps the Broca area, whereas apraxia of speech may be localized to the insula
    50. 50. 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
    51. 51. 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
    52. 52. 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.
    53. 53. WERNICKE-GESCHWIND MODEL 2. 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)