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APHASIA Dr V B Kasyapa J GM I year Date: 20/09/16

Aphasia in brief - Dr. Kasyapa

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Page 1: Aphasia in brief - Dr. Kasyapa

APHASIADr V B Kasyapa J

GM I yearDate: 20/09/16

Page 2: Aphasia in brief - Dr. Kasyapa

Definitions

• Phonation: Production of vocal sounds without word formation.– Function of Larynx

• Vocalisation: Sound made by the vibration of the vocal cords and modified by vocal tract.– Symbolise & communicates ideas and thoughts– Function of Vocal tract

Page 3: Aphasia in brief - Dr. Kasyapa

Definitions

• Articulation: Enunciation of words and phrases.– Function of organs & musculature innervated by

brainstem.• Language: Mechanism for expressing thoughts &

ideas– By speech (auditory symbols)– By writing (motor symbols)

(or)Any means of expressing or communicating a feeling or thought using a system of symbols.- Function of Cerebral cortex.

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Definitions

• Grammar/ Syntax: Set of rules for organizing the symbols to enhance their meaning.

• Symbols of language: – Sounds– Marks– Gestures, etc…

• Semantics : the study of meaning in language• Prosody : the patterns of stress and intonation in

a language

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Linguistic communicationMotor acts necessary for execution

Reception

Interpretation of auditory & visual images

Retention

Recall Visualisation of symbols

Association of motor centres that control expression

Motor elements of expression

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Slurred speech/ Difficulty in speechDysarthria Aphasia

Disorder of motor production (or) articulation

Disorder of language

Normal Language Language is abnormal

Unable to coordinate muscles of speech Unable to comprehend or express the speech

Associated with other bulbar abnormalities (dysphagia/ brain stem lesions)

Associated with other language functions like reading, writing,…

May not be a brain disease Always due to a brain disease

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APHASIA - Definition

• A disorder of language, including various combinations of impairment in the ability to spontaneously produce, understand and repeat speech, as well as defects in the ability to read and write.

or• Disorders of previously intact language abilities

due to brain damage; not due to paralysis or disability of the organs of speech or of muscles governing other forms of expressions.

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HistoryScientist Contribution

Dax (1836) Relationship between aphasia and lesions of left hemisphere

Broca (1861) Loss of speech with lesions of left inferior frontal convolution

Trousseu (1862) First used term ‘Aphasia’

Wernicke (1874) Loss of speech comprehension (word deafness) from lesion of left superior temporal gyrus (LSTG)

Lesion posterior to LSTG (region of Angular gyrus) is associated with word blindness (inability to comprehend written words)

Conduction aphasia description

Lichtheim (1885) Subcortical aphasia

Wernicke-Lichtheim model of cortical speech areas

Bason, Geschwind Wernicke-Geschwind model of cortical speech areas

H Jackson Affected language function may not necessarily related to the location of lesion

Page 9: Aphasia in brief - Dr. Kasyapa

Cortical level of language comprehension

• Level of arrival : perceived language symbols, seen/ heard.– No further differentiation of impulses– Primary cortical reception areas

• Level of Knowing : Recognition of impulses– Formulation of engrams for recall of stimuli revisualisation

• Level of Expression : Recognition of symbols in forms of words.– Higher elaboration and association of learned symbols as

language

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Levels of Motor speech function

• Emotional Level : Most primitive– Response to painful stimuli

• Automatic level : automatic speech– Yes or no; counting days

• Proportional level : vocalisation on volition, symbolic or intellectual language– Communication of thoughts, ideas, feelings and

judgement using words, syntax, semantics and rules of conversation.

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ANATOMY OF SPEECH AREAS

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• Language functions are not discretely localised in brain as vision/ elemental senses.

• But more localised than intelligence/ judgement/ creativity

• Primary cortex effected – focal deficits• Association cortex effected – higher cortical

malfunction

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• Mainly located in peri-sylvian areas of language dominant hemisphere

Pre Rolandic/ Anterior areas Post Rolandic/ Posterior areas

Para sylvian inferior frontal(PIF) areas Para sylvian superior temporal(PST) areas

Motor/ expressive aspects Sensory/ perceptive aspects

By Superior division of MCA By Inferior division of MCA

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Area Location function

Broca’s Inferior frontal gyrus Motor association area

Just anterior to primary motor areas for the lips, tongue and face

Executive area for language function

Left precentral gyrus of Insula

Cortical area beneath frontal and temporal lobes

Motor planning of speech

Wernicke’s Superior temporal gyrus Sensory association cortex

Posterior to primary auditory cortex

Arcuate faciculus

Deep white matter tract Connection between association areas

From Wernicke’s area -> around posterior end of sylvian fissure -> sub cortical white matter of insula -> to Broca’s

? Relay station in pre motor/ motor area

Additional fibres from subcortical white matter of insula

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Area Location Function

Angular gyrus

Inferior parietal lobule Reading and similar non verbal language function

Caps posterior ramus of sylvian fissure

Between Wernicke’s and visual cortex

Supra marginal gyrus

Between visual cortex and posterior peri sylvian language areas

Visual language function

Exner’s writing centre

In middle frontal gyrus of language dominant frontal lobe

Writing

Near frontal eye field ? Connections with Wernicke’s through white matter tracts

Anterior to primary motor cortex of hand

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Classification of Aphasia

• Difficult to classify.• Frequently mixed• Lesions similar in size & location on imaging

studies may be associated with different aphasic syndromes even in persons with identical cerebral dominance for speech.

• Pure forms are uncommon• Sometimes, there may be no peri-sylvian lesion.

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• Crude classification :– Expressive aphasia vs. Receptive Aphasia (Speech defect vs. Understanding defect)– Non fluent vs. Fluent– Motor vs. Sensory– Anterior vs. Posterior– Central vs. Para-central(Involves peri-sylvian vs. Watershed area infarction)(Loss of repetition vs. Normal repetition)

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BROCA’s APHASIA

• Lesion : Anterior peri-sylvian speech areas in PIF region.

• Speech : Laboured– Non fluent spontaneous speech– Decrease amount of linguistic output• Few words• Short sentences• Poor grammar

– Telegraphic (without linking words)

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– Para/ Agrammatism (misuse of words & defective syntax)

– May preserve emotional & automatic speech (may even possible to sing)

– Unable to repeat what they heard/ unable to read aloud

– Monophasia (recurrent utterances)• Able to comprehend (may seem inability with

difficult material; grammar > semantics)

BROCA’s APHASIA

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• Self aware and frustrated.• If writing involves -> non paretic left hand may

also involves

• If writing spared -> Verbal apraxia

• Milder form: occasional errors in word formation, word finding difficulty on rapid fire manner

BROCA’s APHASIA

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• Associated with

– Contralateral hemiparesis/ facio-brachial paresis

vision is spared

– Buccofacial apraxia -> Dysarthria

– Alexia (third alexia of dejerine) - inability to

recognize or read written words or letters

BROCA’s APHASIA

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Apraxia of speech/ mini-Broca/ baby-Broca/ Cortical dysarthria

• Lesion : only Broca’s area involved• Speech : Forgets how to make sounds of speech– Only speech is effected– Prosody is impaired -> shuttering quality (like foreign

language)– Normal grammar with correct language– Syllable transposition (“pasghetti”)

• Defective control without weakening vocal tract• Normal comprehension• Normal writing

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Pure word mutism/ Aphemia/ Pure motor aphasia of Dejerine

• Inability to speak

• Normal auditory comprehension

• Normal reading and writing

• Lesion : small lesion in PIF area

Page 24: Aphasia in brief - Dr. Kasyapa

Wernicke’s Aphasia

• Lesion : PST region (Auditory association cortex, Angular gyri & Supramarginal gyri)

• Speech : Fluent, Effortless– Normal prosody, sentence length & phrase– Word deafness (unable to understand speech)– Word blindness (unable to read)– Normal/ Increased word output (logorrhoea/

hyperlalia)– Naming & Repetition defects (from poor

comprehension)

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Wernicke’s Aphasia– Paraphasic errors– Neologism (new words)– Agrammatism– No meaning with gibberish utterances– May also evolve from a state of mutism

• Not able to understand what he is speaking -> agitated -> gibberish talk (like psychotics)

• Dissociation between comprehension deficits for spoken and written languages may be seen

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Wernicke’s Aphasia

• Mini-Wernicke’s : mild paraphasia– Minimal difficulty in understanding grammatically

complex material• Jagron aphasia/ Word salad : Plentiful words

wrongly used• Association with larger areas of involvement– Visual disturbances– No hemiparesis

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Global Aphasia

• Lesion : large sized in entire peri-sylvian language centre

Or separate lesions involving PIF & PST

• Mostly due to occlusion of ICA or proximal MCA.

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Global Aphasia

• Speech : grossly non fluent

– Severe comprehension deficit

– Anomia, no repetition

– Severe Monophasia

• Associated with Hemiplegia and field defects

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Conduction Aphasia (Leitunsaphasie)

• Lesion : interruption the conduction between Wernicke’s and Broca’s area– Deep white matter lesion in supramarginal gyrus– Involves Arcuate Fasiculus (AF).– Embolic occlusion of a terminal branch of MCA

may cause this aphasia in cortical injury• Disconnection syndrome : dissociation

between anterior and posterior peri-sylvian language areas

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Conduction Aphasia (Leitunsaphasie)

• Speech : poor repetition– Relative preservation of other language functions– Impaired comprehension (unlike WA)– Paraphasia– Relatively fluent– Variable Naming difficulty– Difficult to read aloud– Difficulty in writing dictation

• Patient is aware and tries to correct.

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Anomic Aphasia• Definition :– Should be called only if the naming is isolated

deficit throughout the course of illness.– Any aphasia type as it develops/ recovers may

pass through a stage like this

• Also called “Non localising syndrome”• Only disease which suggests a lower temporal

lobe lesion

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Anomic Aphasia• Speech : Naming deficit

– Fluent– Normal comprehension– Able to repeat– Empty speech (due to word-finding deficits)– Paraphasias– Circumlocution

• Dysnomia : mild difficulty in naming

• May associated with wide variety of diseases– If association with Gerstmann’s syndrome, lesion may be in the

dominant Angular Gyrus.

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Trans Cortical Aphasia (TCA)

• Lesion : a disconnection of peri-sylvian area from rest of the brain– But PST & PIF with AF are intact

• It can be divided as– Mixed TCA– Trans Cortical Motor Aphasia (anterior isolation

syndrome)– Trans Cortical Sensory Aphasia (posterior isolation

syndrome)

Page 34: Aphasia in brief - Dr. Kasyapa

Trans Cortical Aphasia (TCA)

Mixed TCA (MC)

• Lesion : at BZI, both PST & PIF separated from rest of the brain

• Repetition – excellent (up to Echolalia)

• Non fluent• No comprehension

TC Motor A

• Lesion : more anterior, separation of PIF is more

• Like Broca’s• Repetition – good• Non fluent• Intact

comprehension

TC Sensory A

• Lesion : more posterior, PST isolation from word association areas in parieto, temparo occipital cortex

• Like Wernicke’s• Repetition – good• Fluent• No comprehension• Associated with

hemiparesis or other CNS symptoms

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Sub Cortical Aphasia

• Lesion : no damage to peri-sylvian cortical area in direct.– Imitates TCA– May involve• Thalamus‘• Caudate nucleus• Putamen• Peri ventricular white matter• Internal capsule of language dominant hemisphere

Page 36: Aphasia in brief - Dr. Kasyapa

Sub Cortical Aphasia

Anterior syndrome : lesion at caudate/

straito capsular area

• Non fluent• Dysarthric• Good comprehension• Poor naming• Repetition preserved• Broca’s like but Non

telegraphic

Posterior syndrome : lesion at thalamus

• Fluent• Non dysarthric• Poor comprehension• Poor naming• Repetition preserved• Wernicke’s like but

with hemiplegia

Page 37: Aphasia in brief - Dr. Kasyapa

Sub Cortical Aphasia

Proposed Mechanisms

May involve secondary dysfunction of peri-sylvian

language areas due to interruption of fibres

communicating between cortical and subcortical structures

Cortical hypo perfusion due to subcortical infarct.

Page 38: Aphasia in brief - Dr. Kasyapa

Non fluent

Good comprehension

Good repetition

Transcortical Motor Aphasia

Bad repetition

Aphasic writing

Broca’s Aphasia

Normal writing

Verbal Apraxia

Bad Comprehension

Good repetition

Mixed trans cortical Aphasia

Bad repetition

Global Aphasia

APHASIA GUIDE

Page 39: Aphasia in brief - Dr. Kasyapa

Fluent

Good comprehension

Good repetition

Anomic Aphasia

Bad repetition

Conduction Aphasia

Bad comprehension

Good repetition

Trans cortical sensory aphasia

Bad repetition

Poor reading

Wernicke’s Aphasia

Normal reading

Pure word deafness

APHASIA GUIDE

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THANK YOU

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