Aphasias/LOC

Question 0

Transcortical Motor Aphasia

Answer 0

A nonfluent aphasia with preserved repetition.
Brain damage for TCMA is usually in the dorsal lateral frontal cortex
Can affect association fibers. The areas of white matter that connect the central regions of the language center to the areas outside of it have been severed
AKA: Isolation Syndrome
Characterized by a notable decrease of spontaneous verbal output
Can have a perseverative utterance
Utterances may be started but not finished
Comprehension can be functional, well enough for day to day activities, for conversation
They may show an inability to initiate any response, but this can be complicated by a significant apathy
TCMA pts seem distant and difficult to engage in conversation
Not emotional, just upset or angry
They show little interest in using language

Question 1

Transcortical Aphasia

Answer 1

Some patients with aphasia show an ability to repeat that is much better than their other language abilities
Aphasia with good repetition almost always indicates pathology outside of the perisylvian area
The damage is in the boarder zone or watershed areas
Much of the cortical damage in these cases has occurred in the watershed arterial zone
Three different types of cortical aphasias

Question 2

Transcortical Sensory Aphasia

Answer 2

A fluent aphasia with preserved repetition

• Usually associated with damage to the angular gyrus
• Conversational speech is fluent and filled with neologistic or semantic jargon
• This type of aphasia isolates Wernicke’s aphasia, this is different because these pts are able to repeat. Affects the watershed regions of the upper parietal lobe.
• Their ability to repeat words accurately is surprising in this context.
• No press of speech like in Wernicke’s aphasia
• Comprehension of spoken language is severely disturbed
• when they do repeat words, they do not seem to understand what they are saying
• Naming is always a problem (serious anomia)

Question 3

Transcortical Mixed Aphasia

Answer 3

A global aphasia with (relatively) preserved repetition.
Damage associated with TCMA involves both anterior and posterior portions of the watershed area.
Stenosis: partial occlusion or blockage of the internal carotid artery. When there is a blockage the blood cannot get to the watershed areas so cells start to die.

Question 4

Primary Progressive Aphasia

Duffy

Answer 4

“A language deficit of insidious (unknown, gradual worsening) onset, gradual progression, and prolonged course, in the absence of generalized cognitive impairments ( at least for a substantial period of time), due to a degenerative condition, predominately and presumably involving the left Perisylvian region of the brain “ (Duffy, 1987).

• Cognition usually remains intact, affects language, gets worse over time and for some it will morph into something else.

Question 5

Clinical Presentation of Primary Progressive Aphasia

Answer 5

> Speech and language complaints are similar to those seen in aphasia
PPA pts rarely deny their deficits, pts know that something is going on
The pt usually initiates the search for a diagnosis and management
PPA pts and family members do not observe memory disturbances unrelated to verbal functions
Personality changes are generally not reported
Job performance may be unchanged if their occupation is not demanding verbally
The initial presentation of the PPA pts can be strikingly different for that of pts showing early dementia who are often referred because of the family’s concern about memory, personality, orientation, and occupational disabilities.

Question 6

Demographics of PPA

Answer 6

> Basic demographics: from the review of 54 cases by Duffy and Peterson (1992)
Age: Range 40-75 with a mean of 59.3 years
Sex: 37 males and 17 females
Duration of isolated syndromes: mean 5.3 years. About half the group eventually developed nonaphasic signs of cognitive decline, either on neuropsychological testing, activities of daily living, or both
Mean age at spread of cognitive impairments: 59.5
Autopsy Findings (14 of 54 cases):
Picks Disease
Creutzfeldt-Jakob disease
Alzheimer’s Disease
Focal spongiform degeneration in L-hemisphere
Nonspecific cellular changes

Question 7

Language of Confusion

Answer 7

This is a language impairment that is usually caused by diffuse bilateral trauma to the brain such as from head injury, toxic conditions, post-surgical stress, or related events
> Will damage the brain tissue all over
>Typically, pts show normal syntax, semantics, and phonology, but the context of their language is confused and confabulatory
>In most cases, the onset is sudden

Question 8

Language of Confusion

Answer 8

> A good distinction between aphasia and LOC is that pts with LOC have language abilities that are better than their ability to communicate
In pts with aphasia, their language abilities are worse than their abilities to communicate
This is not an aphasia, this is a language characteristic that can follow TBI

Question 9

Subcortical Aphasia

Answer 9

> There is evidence that pts with damage to subcortical structures can demonstrate aphasic-like language disturbances
Thalamic aphasia
Aphasia associated with damage to the basal ganglia
Aphasia associated with damage to subcortical white matter
There is controversy about whether subcortical structures like the thalamus have a direct role in our language abilities
Nevertheless, language deficits have been associated with subcortical brain damage