Forty Three Flashcards
What is the difference between dysarthria/anarthria and dysphasia/aphasia? Which sounds are created by which cranial nerves?
I. Speech versus Language:
A. Dysarthria/Anarthria (disturbance in the production of sounds): motor deficit of
the musculature of face, tongue, throat, resulting in the abnormal production of
speech. Language itself is not impaired. The impairment leading to slurred
speech can be evaluated by having the subject make different sounds (“MA” sound impaired by facial paralysis, “TA” sound impaired by tongue paralysis, “KA” sound impaired by paralysis of pharynx.
B. Dysphasia/Aphasia (disturbance of language function): a disorder of language
involving an impairment of comprehension and/or expression of the spoken and
written words used in communication.
Which hemisphere mediates language? What are the critical areas, where are they located, and what is their function? What regulates the emotional aspect of language?
- Language is mediated by the dominant hemisphere (usually the left hemisphere).
a) Brodmann’s areas 44 and 45, or Broca’s area, coordinates expressive functions.
b) Posterior part of Brodmann’s areas 22, or Wernicke’s area, coordinates language comprehension.
c) A white matter tract called the arcuate fasciculus connects the two language centers
d) Prosody of language (emotional expression) is mediated by the non-dominant hemisphere in the corresponding areas.
What are two types of language deficits? What will be impaired in all aphasias affecting primary language areas?
b) Language deficits are usually characterized as expressive or receptive,
although many patients have a mixture of both components.
c) All aphasias affecting primary language areas (i.e. the perisylvian region) have impaired repetition.
Describe the 3 characteristics of wernickes aphasia with examples.
a) Fluent or receptive aphasia (Wernicke’s aphasia):
(1) Comprehension of spoken and written words marked diminished. Thus reading, following commands and repetition are markedly impaired.
(2) Speech output (words per minute) is normal or increased, but content is characterized by frequent paraphasic errors (word salad or jargon speech).
(a) Semantic paraphasic errors: Substitute one word for another (i.e. watch instead of clock)
(b) Phonemic paraphasic errors: Substitute one syllable for another (i.e. dock instead of clock)
(3) The patient can comprehend the emotional content of language, and can generate speech with emotional content and inflections and cadence which sound normal.
Describe 3 characteristics of broca’s aphasia with examples.
b) Non-fluent or expressive aphasia (Broca’s aphasia):
(1) Output of spontaneous speech is markedly diminished. Written and spoken language is characterized by loss of articles of speech (a, and, the), loss of normal grammatical structure (agrammatical speech) and may be limited to expostulations.
(2) Syllabic perseveration: only one sound can be produced, and is used in all efforts to communicate
(3) Interjectional speech: latency very prolonged, and the words produced emerge under pressure, as exclamations.
What is conduction aphasia? What causes it? Same questions for global aphasia.
c) Conduction aphasia: comprehension preserved, output fluent, but naming and repetition impaired (damage to arcuate tract)
d) Global aphasia: All aspects of language function are impaired. (Damage to all of it)
What is anomic aphasia? Where is it usually located? What are transcortical aphasias? What causes them? What are 2 types? What are their characteristics?
a) Anomic aphasia: Isolated impairment of naming. Lesion usually located at junction of occipital and temporal lobe.
b) Transcortical aphasias: Also called isolation aphasias. Considered to be due to separation of the speech centers from other brain areas.
(1) Transcortical sensory aphasia: poor naming and comprehension, but repetition is intact. Usually due to lesion posterior to Wernicke’s area.
(2) Transcortical motor aphasia: can name and repeat, but has decreased spontaneous speech. Lesion usually anterior to Broca’s area.
Describe various lesions in the visual system and the resulting clinical presentation.
- Testing the visual fields allow one to explore for pathology in large area of the brain.
- Lesions in the eye, retina or optic nerve cause unilateral vision loss.
- Lesions in the optic chiasm can lead to bitemporal visual field loss
- Lesions in the optic tract, lateral geniculate body or occipital cortex usually cause a visual field loss on the contralateral side (homonymous hemianopia).
- Lesion in the optic radiation coursing through the temporal lobe (Meyer’s loop) leads to a superior field cut (pie in the sky).
- Lesion in the optic radiation coursing through the parietal lobe lead to an inferior field cut (pie on the floor).
- The upper bank of the calcarine cortex relates to the contralateral inferior visual quadrant, and the lower to the upper quadrant. Often lesions affect both upper and lower bank leading to a homonymous hemianopia.
- The macula is represented at the very pole of the occipital lobe and may be spared in ischemic lesions affecting the occipital lobe.
Where is the lesion in anton’s syndrome? What is the result? Same questions for alexia without agraphia.
a) Anton’s syndrome: Results from bilateral occipital lesion leading to total cortical blindness. Patients often are unaware of blindness. Pupillary light reaction intact. Exam shows normal retinas, extra ocular movements, pupillary responses, but no recognition of objects by sight, and strong confabulations of vision.
b) Alexia without Agraphia: Lesion of the dominant occipital lobe and deep white matter, including splenium (posterior part) of corpus callosum. In this syndrome the patient has a congruous right homonymous hemianopia, is able to write but not read. The right visual cortex (which is not damaged) is disconnected from the language areas in the left hemisphere because of destruction of the posterior corpus callosum.
What are visual neglect and visual extinction and what causes them? What are alexia, prosopagnosia, and achromatopsia, and constructional apraxia, and where is the damage located? Where is the lesion in balint’s syndrome and what are the results?
a) Parietal lesions result in derangement of cells sensitive to both unilateral and bilateral visual influences leading to visual neglect (ignoring visual stimulation from one side) or extinction (ignoring one side when other side has visual stimulation)
b) Trouble reading (alexia), trouble with face recognition (prosopagnosia), trouble recognizing colors (achromatopsia) and trouble copying a design (constructional apraxia) are also associated with parietal lobe lesions.
c) Balint’s syndrome: Bilateral parietal-occipital lobe lesion can lead to difficulty with integrating visual input, and fixating to visual stimuli. Thus patients literally “cannot see the forest for the trees” (simultagnosia). They also have difficulty moving the eyes to visual target (optic apraxia) or reaching for a visual target (optic ataxia)
What is anosmia and what are some causes?
C. The most frequent cause of anosmia is seen with nasal congestion. Rare
inflammatory damage can occur with meningitis. Head trauma that results in
laceration or avulsion of the nerve at the cribriform plate can affect sense of
smell in up to 7% of victims. In such cases, recovery of olfaction is rare.
Some degenerative disease can cause anosmia (Parkinson’s disease,
Alzheimer’s disease).
What is visual agnosia? What is neglect/body agnosia? What What is gerstmann’s syndrome? What is anosognosia?
- Visual agnosia: in spite of normal visual acuity or field, the patient cannot recognize an object’s character or meaning by sight, but must use some other sensory modality to identify it.
- Neglect/Body agnosia: impaired integration of cortical sensory modalities leads to a failure to recognize body parts as belonging to the self, or that there is a difference between body and environment. (e.g. alien limb syndrome)
- Gerstmann’s syndrome: finger agnosia, right/left differentiation deficit, acalculia, and agraphia.
- Anosognosia: a failure to recognize a deficit. A severe impediment to rehabilitation.
