ADULT LANGUAGE DISORDERS

Week 4Feb 3rd, 2011

Review

According to Luria, Posterior cortex is responsible for perception, recognition, and integration of sensory information (T/F)

Diffused lesions are spread throughout the brain (T/F)

Lesions in anterior left hemisphere produce ____nonfluent________ aphsias

Aphasia is an impairment of language processing (T/F)

Defective auditory comprehension, poor self-monitoring, fluent paraphasic speech, and defective repetition skills are characteristics of _wernickes_ aphasia.

• Functional reorganization of language after stroke

• Recovery of function in Wernicke’s aphasia may be accompanied by a redistribution of activity within both cerebral hemispheres.

• fMRI data suggests that clinical recovery is associated with a redistribution of function to the right hemisphere (Thurlborn et al., 1999; Cherney & Robey, 2001)

Wernicke’s aphasia

Comprehension deficit

Fluent but paraphasic speech

Reading comprehension deficits: Aphasic Alexia Oral reading versus reading

comprehension

Writing deficits

Wernicke’s aphasia:Differentiating features

Ancillary behaviors: Depression: 37% (cumulative)

▪ Major post stroke depression▪ Reactive post stroke depression

▪ Sadness, dependency and indecisiveness

Lesion causing Wernicke’s symptomatology may go unnoticed.

Wernicke’s Aphasia

1. Locus of lesion is parietal operculum or arcuate fasciculus although controversy exists over lesion site• Left hemisphere supramarginal gyrus and arcuate

fasciculus• The insula, and underlying white matter of left

hemisphere• Small lesions of Wernicke’s area• More anterior and inferior lesions (anterior

supramarginal gyrus, underlying white matter, angular gyrus, and insular cortex) are deemed responsible for phonologic output problems

Conduction Aphasia

▪ 2. breakdown in transmission of information from posterior to anterior regions

▪ 3. relatively good auditory comprehension

▪ 4. verbal expression consists of ▪ Fluent, preserved melody, variety and complexity of syntactic structures▪ word finding problems, ▪ paraphasias with much higher incidence of phonemic than verbal paraphasias; ▪ hallmark feature of disorder is severe repetition deficit, especially for functions

and numbers

▪ 5. much more aware of errors and more interested in correcting errors than Wernicke’s patients probably due to better comprehension

▪ 6. visual comprehension is relatively intact and writing skills mirror verbal output

Conduction Aphasia

Disconnection Model Conduction aphasia

as disconnection between the auditory “comprehension” region and the speech “production” region.

Repetition, which requires interaction between two centers is imapired

Many have challenged the rigid disconnection model of conduction aphasia

Conduction Aphasia

The Bimodal distribution model: damage along the continuum extending from Wernicke’s area to Broca’s area.

Researchers have reported variability in the degree of fluency with the less fluent patients exhibiting more anterior lesions; those with higher fluency scores had more posterior lesions (Kertesz et al., 1977)

Conduction Aphasia

The “Two” Conduction Aphasias Two disorders with distinct pathophysiologic

mechanism (Nadeau, 2001)▪ Repetition conduction aphasia: deficit in auditory

short-term memory, disturbance only of verbal repetition tasks

▪ Reproduction conduction aphasia: more general language impairment affecting phonologic output process▪ Deficits in word production across verbal tasks including

conversation, naming, and oral reading as well as repetition.

▪ These two types of difficulties arise from lesions in functionally distinct but anatomically adjacent areas in temporoparietal region

Conduction Aphasia

Primary criteria for diagnosis Fluent, paraphasic conversational speech

No significant difficulty in comprehension of normal conversation

Significant verbal repetition disturbance

A preponderance of phonemic paraphasias Simmons-Mackie (2005)

Conduction Aphasia

Differentiating features (text book, pg 156)

Conduction Aphasia

Broca’s Aphasia/ AOS Conduction Aphasia

Nonfluent Fluent (100-200 WPM)

Dysprosody Intact prosody

Agrammatic Preserved grammer or paragrammatic

Comprehension relatively good

Comprehension relatively good

Repetition impaired proportionate to other verbal tasks

Repetition disproportionally impaired

Error recognition Error recognition

Probably anomic Probably anomic

More description of salient features:• Fluency

▪ Fluent but not as fluent as Wernicke’s aphasics

• Word finding (content words): Some variability • Paraphasias: phonemic paraphasias

▪ produce more errors on a forced choice of specific target words

• Error recognition• Repetition

▪ Difficulties appear more on phrases, short sentences, poly syllabic words

• Auditory comprehension• Reading

Conduction apahsia

Favorable spontaneous recovery pattern

Conduction aphasics show significant or even complete recovery

Sometimes they “evolve” from classifications such as “jargon or Wernicke’s aphasia

They perform well in situations that do not require single-word accuracy or specific responses.

Conduction Aphasia

▪ Poorly localized: angular gyrus lesion and/or posterior middle gyrus

▪ Many Wernicke’s evolve into Anomic

▪ 1. Empty speech: lot of words like, thing, it, you know what I mean.. Frustrated

▪ 2. relatively good auditory comprehension

Anomic aphasia

▪ 3. verbal expression consists of predominance of word finding problems with the more salient the word, the more difficulty finding it and an absence of paraphasic errors (emptiness of substantive words in speech)

▪ 4. reading and writing skills vary from patient

to patient due to how extensive the lesion posteriorly – the more posterior the lesion, the more involved are reading and graphic impairments

Anomic aphasia

▪ 1. like severe Wernicke’s aphasia in verbal output with verbal paraphasias (both unrelated and semantic), phonemic paraphasias, neologisms, word retrieval deficits – more jargon

▪ 2. very poor auditory comprehension

Transcortical sensory aphasia

▪ 3. unlike Wernicke’s aphasia, repetition is intact as well as a preservation of memorized material

▪ 4. lesion is in posterior part of parietal lobe with sparing of Wernicke’s area and arcuate fasciculus fibers (referred to as watershed lesion)

▪ 5. written language is impaired for both reading and writing

Transcortical sensory aphasia

Fluent Aphasias

Wernicke’s Conduction Transcortical sensory

Auditory comprehension Severely impaired Slightly impaired Severely impairedRepetition Impaired Impaired IntactSpeech Fluent, paraphasic Paraphasic Fluent, ParaphasicReading Impaired Intact ImpairedWriting Impaired Impaired Impaired

Behavioral Patterns of Types of Aphasia

Nonfluent aphasias

http://video.google.com/videoplay?docid=9178936581276081395&q=broca+apahsia&total=5&start=0&num=10&so=0&type=search&plindex=0

A. Broca’s aphasia▪ Most frequently occurring aphasia syndrome▪ Non-fluent, halting verbal output▪ Incomplete and syntactically simplified sentences▪ Reduced phrase length▪ Prosodic disturbance▪ Awkward articulation▪ Concomitant apraxia of speech

Nonfluent aphasias

A. Broca’s aphasia▪ Relatively spared auditory

comprehension

▪ Impaired repetition and confrontation naming

▪ Reading and writing problems parallel auditory comprehension and verbal production respectively

▪ usually are hemiplegia or hemiparietic

Nonfluent aphasias

A. Broca’s aphasia

▪ Lesion to large frontal area including Broca’s area and/or deep to subcortical structures, including insula

▪ Small lesions in Broca’s area do not cause traditional Broca’s aphasia (Mohr et al., 1978)

▪ http://www.youtube.com/watch?v=f2IiMEbMnPM&feature=related

▪ http://www.youtube.com/watch?v=67HMx-TdAZI&feature=related

▪ http://video.google.com/videoplay?docid=-2925282641207166289&q=broca+apahsia&total=5&start=0&num=10&so=0&type=search&plindex=2

Nonfluent aphasias

A. Broca’s aphasia▪ Metter et al (1987, 1992) provided convincing

evidence that changes in the brain’s metabolic activity in regions outside of Broca’s area contribute to the pattern of language impairment seen in Broca’s aphasia.▪ Anterior internal capsule▪ lenticular nuclei

▪ http://video.google.com/videoplay?docid=7493350972829192252

▪ http://www.youtube.com/watch?v=zMm_DrHYCD0&feature=related

Nonfluent aphasias

A. Broca’s aphasia▪ Recent neuroimaging data challenges the

commonly held notion that Broca’s aphasia results from a lesion to Broca’s areas

▪ “Data support the position that a lesion to Broca’s areas is neither necessary nor sufficient to produce Broca’s aphasia” (Kearns, 2005)

Nonfluent aphasias

Theories of agrammatism: Nonlinguistic explanations Economy-of-effort explanation (Pick, 1931):

deletion of low information lexical units are due to patient’s attempt to conserve effort (compensation mechanism)

Adaptation hypothesis (Kolk et al., 1985):▪ Adaptation to reduced capacity for the temporal

computation of language▪ By opting to speak agrammatically, aphasic patients

minimize the effect of delayed processing (i.e., slowing lexical retrieval, slowing down of application of syntactic rules)

Nonfluent aphasias

Broca’s aphasia: Theories of agrammatism Stress-salience hypothesis (Goodglass and

Menn, 1985): Increased threshold for mobilizing the speech

output system Response threshold requires salient element

(affective tone, increased amplitude, stress) to overcome the elevated threshold and begin the flow of speech.

Nonfluent patients suffer from impaired prosody and can not overcome their tendency to omit grammatical morphemes.

Agrammatism

Some Linguistic Explanations Agrammatism in Broca’s aphasia is the result of a

syntactically based central language deficit (Shapiro & Thomson, 1994)

It is a manifestation of a central disruption of the syntactic parsing component of the language system. If this true, one should expect to see parallel deficits across language modalities

Against: data supports the notion of a dissociation of impairments across modalities (i.e., patients were expressively but not receptively agrammatic)

Agrammatism

Some Linguistic Explanations The mapping hypothesis: deficit in the ability to

map semantic roles onto sentence constituents (Saffran et al., 1980)

Support: Broca’s subjects able to identify grammatical violations- inconsistent with syntactic parsing account

Broca’s subjects have difficulty abstracting thematic meaning from verb roles (e.g., agent-action-object) of sentence constituents.

Unable to map sentence structure to meaning (Marshall, 1995)

Mapping therapy: mapping the thematic roles of sentence constituents onto syntax

Nonfluent aphasias

B. Global aphasia▪ 1. Lesion of entire LH language areas with specifically

large lesion of anterior part of hemisphere deep to subcortical areas

▪ 2. Very poor auditory comprehension

▪ 3. Verbal expression consists of no propositional speech with recurrent utterances (indicates damage is also subcortical), automatic serial speech (not of prognostic importance)

▪ May indicate “Yes” or ‘No” in response to questions about family members

▪ Global aphasic patients have severe, persisting deficits across all communicative modalities

Nonfluent aphasias

B. Global aphasia▪ 4. profound deficit in writing

▪ 5. reading skills vary from patient to patient depending upon extent of lesion posteriorly

▪ 6. probable accompanying apraxia of speech

▪ 7. hemiplegic

Nonfluent aphasias

C. Mixed aphasia▪ 1. show pattern of Broca’s or global aphasia

with better or worse comprehension respectively

▪ 2. have sparse verbal output (one or two word utterances with meaning)

Nonfluent aphasias

D. Transcortical motor aphasia▪ 1. lack of spontaneous speech with no

initiation of speech

▪ 2. intact repetition

▪ 3. good auditory comprehension

▪ 4. reading comprehension is fairly good

Nonfluent aphasias

D. Transcortical motor aphasia▪ 5. writing skills mirror their verbal output

▪ 6. lesion is in supplementary motor area in upper frontal lobe – affects cognitive initiation to use language

Other Patterns of Aphasias

A. Subcortical Aphasias▪ 1. Traditionally, aphasia has been considered

to result from a cortical lesion

▪ 2. May have subcortical aphasias due to lesions in structures including thalamus, caudate nucleus, putamen, and/or globus pallidus

Other Patterns of Aphasias

A. Subcortical Aphasias▪ 3. May have verbal and phonemic paraphasias,

jargon, word finding problems, naming difficulties, poor auditory comprehension

▪ 4. may have accompanying dysarthria and/or phonatory problems (weak voice)

▪ 5. depending on the site of lesion subcortically, aphasia can be fluent or nonfluent

Other Patterns of Aphasias

B. Crossed Aphasia▪ Reversed asymmetry

▪ Left – nonverbal functions

▪ Right – language functions

▪ Aphasia due to a stroke in the right hemisphere of the right-handed individuals

Evolution of Aphasias

▪ 1. If patients improve, globals evolve into mixed aphasia, then Broca’s

▪ 2. Wernicke’s evolve into conduction, conduction evolve into

anomic

▪ 3. Wernicke’s patients are typically older, Broca’s patients are typically younger

▪ http://video.google.com/videoplay?docid=3512623412231250746

http://video.google.com/videoplay?docid=2344713752476106067&total=35&start=0&num=10&so=0&type=search&plindex=9