פרק 22 Chapter 22 Disorders of Speech and Language Flashcards

1
Q

איזה איזור אינו משתתף ב-repetition?
א. Superior parietal lobule
ב. Heschl
ג. Supramarginal
ד. Angular

A

superior parietal lobule

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2
Q

Table 22-1THE MAIN APHASIC SYNDROMES
(10)

A
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3
Q

תיאור של מטופל שלא מצליח לקרוא אבל מצליח לכתוב אך לא מבין את מה שכתוב
1. אנגולר+קלרקריין קורטקס
2. סופרה-מרגינל
3. אונה טמפורלית

A

Angular/ Calcarine cortex=
alexia without agraphia

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4
Q

מטופל שהגיע עם תיאור של כאב ראש, לא יכול לקרוא, מצליח לכתוב, קוואדרנטופיה עליונה מימין והפרעה בזיהוי צבעים. איפה הפגיעה?
1. broca’s area
2. wernike’s area
3. splenium of corpus callosum
4. supramarginal gyrus

A

splenium of corpus callosum

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5
Q

מטופל בן 50 שלפתע לא מצליח לנקוב בשמות ילדיו, הפרעה בשיום עם פאראפזיות פונטיות וסמנטיות, שטף תקין, הבנה שמורה, חזרה תקינה. מה עוד יהיה חלק מהתמונה הקלינית?
1. חולשת יד ופנים מימין
2. קוואדריאנופיה עליונה קונטראלטרלית
3. סינדרום תחושתי דמוי תלמוס

A

ANOMIC APHASIA

קוודאדריאנופיה עליונה קונטראלטרלית

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6
Q

20- בן 69 עם יתר לחץ דם, התקבל בשל הפרעת דיבור. בבדיקה דיברו ספונטני שוטף, הבנה מופרעת בצורה קלה, הפרעה קשה בחזרה (Repetition).
מהו מקום הפגיעה:

  1. Supramarginal gyrus
  2. Thalamus
  3. Splenium corpus callosum
  4. Sup. Temporal gyrus
  5. Frontal suprasylvian
A

no repetition= conduction aphasia= supramarginal gyrus or insula

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7
Q

מה מתאר חולה עם אפזיה שמתבטאת בשטף תקין, הבנה שמורה, שלא מצליח לחזור על משפט?
א. Broca aphasia
ב. Conduction aphasia
ג. Global aphasia
ד. Transcortical aphasia

A

Conduction aphasia=
no repetition= supramarginal gyrus or insula.
the patient is fluent, comprehension may be slightly impaired, cannot repeat
——–
more types of aphasia:
Transcortical The identifying feature of these language disturbances is a preservation of the ability to repeat. Destruction of the vascular border zones between anterior, middle, and posterior cerebral arteries, usually as a result of prolonged hypotension, carbon monoxide poisoning, or other forms
of anoxic-ischemic injury; may effectively isolate the intact motor and sensory language areas, all or in part, from the rest of the cortex of the same hemisphere.
* Transcortical Sensory- In transcortical sensory aphasia the patient suffers a deficit of auditory and visual word comprehension, making writing and reading impossible, in every way conforming to Wernicke’s aphasia**. Speech remains **fluent, with marked paraphasia, anomia, and empty circumlocutions**. However, unlike the deficit in Wernicke’s and conduction aphasias, **the ability to repeat the spoken word is preserved**.
* **Transcortical Motor**-In transcortical motor aphasia, the patient is **unable to initiate conversational speech, producing only a few grunts or syllables as in Broca-type aphasia**. Comprehension is relatively preserved, but **repetition is strikingly intact
, distinguishing this syndrome from pure word mutism. Transcortical motor aphasia occurs in two clinical contexts: (1) in a mild or partially recovered Broca’s aphasia in which repetition remains superior to conversational
speech (repeating and reading aloud are generally easier than self-generated speech) and (2) in states of abulia and akinetic mutism with frontal lobe damage.

  • Wernicke – Fluent – but paraphasia and neologisms, no comprehension, cannot repeat
  • Broca – non fluent, comprehension intact, cannot repeat
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8
Q

בחסימה פרוקסימלית של ה
lt ant cerebral artery (ACA)
באיזה מהבאים צפויה להיות הפרעה של שפה:

  1. Broca dysphasia
  2. Wernickes dysphasia
  3. Transcortical motor
  4. Transcortical sensory
  5. Conduction
A

Transcortical motor aphasia

Transcortical The identifying feature of these language disturbances is a preservation of the ability to repeat. Destruction of the vascular border zones between anterior, middle, and posterior cerebral arteries, usually as a result of prolonged hypotension, carbon monoxide poisoning, or other forms
of anoxic-ischemic injury; may effectively isolate the intact motor and sensory language areas, all or in part, from the rest of the cortex of the same hemisphere.
* Transcortical Motor-In transcortical motor aphasia, the patient is unable to initiate conversational speech, producing only a few grunts or syllables as in Broca-type aphasia**. Comprehension is relatively preserved, but **repetition is strikingly intact, distinguishing this syndrome from pure word mutism. Transcortical motor aphasia occurs in two clinical contexts: (1) in a mild or partially recovered Broca’s aphasia in which repetition remains superior to conversational
speech (repeating and reading aloud are generally easier than self-generated speech) and (2) in *states of abulia and akinetic mutism with frontal lobe damage
.
* Transcortical Sensory- In transcortical sensory aphasia the patient suffers a deficit of auditory and visual word comprehension, making writing and reading impossible, in every way conforming to *Wernicke’s aphasia. Speech remains fluent, with marked paraphasia, anomia, and empty circumlocutions. However, unlike the deficit in Wernicke’s and conduction aphasias, the ability to repeat the spoken word is preserved.

  • Wernicke – Fluent – but paraphasia and neologisms, no comprehension, cannot repeat
  • Broca – non fluent, comprehension intact, cannot repeat
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9
Q
A

Gerstman syndrome is not a disconnection syndrome

Disconnection syndromes:
* Conduction aphasia: The Wernicke area in the temporal lobe is separated from the Broca area, presumably by a lesion in the arcuate fasciculus or external capsule or subcortical white matter. However, most often the lesion is in the supramarginal gyrus
* Sympathetic apraxia: loss of fibers that connect the left and right motor association cortices, a lesion in the more anterior parts of the corpus callosum or the subcortical white matter underlying Broca area and contiguous frontal cortex causes an apraxia of commanded movements of the left hand.
* Pure Word Deafness: loss of ability to discriminate speech sounds. Subcortical Lesion of left temporal lobe, spanning wernickes and fibers that cross corpus callosum From opposite side. Failure to activate left auditory language areas. Also in bilateral lesions of auditory cortex.
* Alexia without Agraphia: splenium of corpus callosum and left occipital lobe with loss of Connection of visual fibres to left hemisphere language areas.

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10
Q

מה מהבאים לא קשור ל
disconnection syndromes?
1. anterior commissure
2. temporo-frontal
3. temporo-parietal
4. temporo-occipital
5. parieto-occipital

A

temporo-parietal don’t cause disconnections?

Disconnection syndromes:
* Conduction aphasia: The Wernicke area in the temporal lobe is separated from the Broca area, presumably by a lesion in the arcuate fasciculus or external capsule or subcortical white matter. However, most often the lesion is in the supramarginal gyrus
* Sympathetic apraxia: loss of fibers that connect the left and right motor association cortices, a lesion in the more anterior parts of the corpus callosum or the subcortical white matter underlying Broca area and contiguous frontal cortex causes an apraxia of commanded movements of the left hand.
* Pure Word Deafness: loss of ability to discriminate speech sounds. Subcortical Lesion of left temporal lobe, spanning wernickes and fibers that cross corpus callosum From opposite side. Failure to activate left auditory language areas. Also in bilateral lesions of auditory cortex.
* Alexia without Agraphia: splenium of corpus callosum and left occipital lobe with loss of Connection of visual fibres to left hemisphere language areas.

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11
Q

Figure 22-1. Diagram of the brain showing the classic language areas, numbered according to the scheme of Brodmann. The elaboration of speech and language probably depends on a much larger area of cerebrum, indicated roughly by all the shaded zones (see text). Note that areas 41 and 42, the primary auditory receptive areas, are shown on the lateral surface of the temporal lobe but extend to its superior surface, deep within the sylvian fissure.

A
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12
Q

Figure 22-2. Cerebral structures concerned with language output and articulation. Broca area; pre- and postcentral gyri; striatum. Areas 43, 44, and 45 are Brodmann cytoarchitectonic areas. A lesion in any one of the components of this output network (B, C, or S) can produce a mild and transient Broca aphasia. Large lesions, damaging all three components, produce severe, persistent Broca aphasia with sparse, labored, agrammatic speech but well-preserved comprehension. (Illustration courtesy of Andrew Kertesz, MD, FRCP(C).)

A
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