1. ADULT LANGUAGE DISORDERS
Week 4
Feb 3rd, 2011

2. 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.

3. Wernicke’s 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)

4. Wernicke’s aphasia: Differentiating features
Comprehension deficit
Fluent but paraphasic speech
Reading comprehension deficits: Aphasic Alexia
Oral reading versus reading comprehension
Writing deficits
Look for patterns to diagnos wernickies aphasia

5. Wernicke’s Aphasia 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.

6. Conduction 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
Make erros in speech production…but can understand speech.

7. 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 has phonemic paraphasia. Kair for Chair. Apple bapple. Just substatuing one phoneme.
Symantic aphasia they would substitue chair for table.

8. 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

9. 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)

10. 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

11. 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)

12. Conduction Aphasia Differentiating features (text book, pg 156)
Broca’s Aphasia/ AOS
Conduction Aphasia
Nonfluent
Fluent ( WPM)
Dysprosody
Intact prosody
Agrammatic
Preserved grammer or paragrammatic
Comprehension relatively good
Repetition impaired proportionate to other verbal tasks
Repetition disproportionally impaired
Error recognition
Probably anomic

13. Conduction apahsia 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

14. Conduction Aphasia 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.

15. Anomic 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

16. 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

17. Transcortical sensory 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

18. 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

19. Fluent Aphasias Wernicke’s Conduction Transcortical sensory
Behavioral Patterns of Types of Aphasia
Wernicke’s Conduction Transcortical sensory
Auditory comprehension Severely impaired Slightly impaired Severely impaired
Repetition Impaired Impaired Intact
Speech Fluent, paraphasic Paraphasic Fluent, Paraphasic
Reading Impaired Intact Impaired
Writing Impaired Impaired Impaired

20. Nonfluent aphasias
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

21. 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

22. 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)

23. 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

24. 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)

25. 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)
Speech is very telagraphic.

26. 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.

27. 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)

28. 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

29. 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

30. 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

31. 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)

32. 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

33. 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

34. 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

35. 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

36. 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

37. 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