A 64-year-old lady, on physical examination exhibits symptoms suggestive of a movement disorder with associated speech deficits.
This clinical presentation is classified as ‘hypokinetic dysarthria’ by her neurologist. It is associated with:
A. The answer is Parkinson’s disease. Bradykinesia or hypokinesia is a motor feature of Parkinson’s disease. Dysarthria is a deficit in the motor aspect of speech. It is usually secondary to a motor neurological deficit. Dysarthria can affect not only articulation, but also phonation, breathing, or prosody (emotional tone) of speech. Total loss of ability to articulate is called anarthria, whereas dysarthria usually involves the distortion of consonant sounds. The Mayo Clinic classification of dysarthria divides dysarthria into six basic types, each one corresponding to a predominant motor disorder: flaccid (lower motor neurone disorders), spastic (upper motor neurone disorders), ataxic (cerebellar lesions), hypokinetic (parkinsonian), hyperkinetic (choreiform/tic disorders), and mixed. Mixed dysarthrias are seen in conditions with multiple motor lesions, for example mixed spastic–ataxia of multiple sclerosis or mixed spastic–flaccidity of amyotrophic lateral sclerosis. Speech therapy may be of substantial benefit to many dysarthric patients.
A 32-year-old man is diagnosed with a right-sided hemiparesis. On examination, his speech shows non-fluent aphasia.
His comprehension is intact, but repetition is impaired. He is most likely to have:
D. Testing a person’s speech is usually done in three steps. The first step is to test for the fluency of speech. Non-fluent output is characterized by a paucity of verbal output (usually 10–50 words per minute), whereas fluent aphasics have a normal or even exaggerated verbal output (up to 200 words or more per minute). Lesions of the motor (Broca’s) area produce a non-fluent aphasia. Assessment of language comprehension is the second step. Patients with focal lesions limited to the left frontal lobe (Broca’s area) will have preserved comprehension (Broca’s and transcortical motor aphasia). Patients with left posterior temporal or parietal involvement will show impaired comprehension (Wernicke’s, global, transcortical sensory, and isolation aphasias). The third step is to evaluate repetition. Transcortical aphasias usually have an intact repetition. Patients with Broca’s, Wernicke’s, or conduction aphasia typically show impaired repetition. In conduction aphasia, speech is fluent (as in Wernicke’s aphasia) but comprehension is intact (unlike Wernicke’s aphasia).
A patient presents with features suggestive of Gerstmann’s syndrome. He also has aphasia.
Which of the following is the most likely type of aphasia with which he may present?
A. Transcortical sensory aphasia is similar to Wernicke,s aphasia but is distinguished by the retained ability to repeat. Lesions causing transcortical aphasias do not disrupt the perisylvian language circuit from Wernicke’s area through the arcuate fasciculus to Broca’s area. Instead, they interrupt connections from other cortical centres into the language circuit (hence the name transcortical). These areas include the dominant angular gyrus, posterior middle temporal gyrus, and periventricular white matter pathways of the temporal isthmus underlying these cortical areas. When this results from involvement of the angular gyrus, it is frequently accompanied by Gerstmann’s syndrome, constructional apraxia, and other evidence of the angular gyrus syndrome.
Regarding aphasia, which of the following statements is true?
C. Paragrammatism is seen in Wernicke’s aphasia. Speech is characterized by being empty of meaning, containing verbal paraphasias, neologisms, and jargon productions. Most patients with Wernicke’s aphasia have no elementary motor or sensory deficits. A right homonymous hemianopia may be present. Patients may be unaware of the deficit and may present with paranoia, as they do not realize why others do not understand them. The presence of paragrammatism may be difficult to distinguish from formal thought disorder in schizophrenia. In contrast, Broca’s aphasia shows agrammatism. In this case, the speech pattern is non-fluent; on examination, the patient speaks hesitantly, often producing the principal, meaning-containing nouns and verbs but omitting small grammatical words and morphemes. This pattern is called agrammatism or telegraphic speech, for example: ‘I go home’ or ‘wife here morning’. Reading is often impaired in Broca’s aphasia despite preserved auditory comprehension. Broca’s aphasia is associated with right hemiparesis, hemisensory loss, and apraxia of the non-paralysed left limbs. Due to the awareness of the deficit, patients with Broca’s aphasia may be more prone to depression. Pure word deafness is a syndrome of isolated loss of auditory comprehension and repetition, without any abnormality of speech, naming, reading, or writing. It is caused by bilateral, or sometimes a unilateral, lesion, isolating Wernicke’s area from input from both Heschl’s gyri. A lesion representing most of the territory of the left middle cerebral (not posterior circulation) artery leads to a global aphasia.
Which of the following is true regarding acquired defects in reading and writing?
E. Pure alexia without agraphia is associated with left posterior cerebral artery stroke, with infarction of the medial occipital lobe, often the splenium of the corpus callosum, and often the medial temporal lobe. Alexia is the acquired inability to read. Patients with alexia without agraphia can write but cannot read their own writing. Alexia with agraphia is sometimes called acquired illiteracy. Alexia with agraphia is seen in angular gyrus lesions and is associated with Gerstmann’s syndrome. It is seen in stroke of the angular branch of the middle cerebral artery. Transcortical aphasias are analogues to the syndromes of global, Broca’s, and Wernicke’s aphasias, with intact repetition. Lesions producing transcortical aphasias disrupt connections from other cortical centres into the language circuit. Lesions to the arcuate fasciculus (usually in either the superior temporal or inferior parietal regions) present with conduction aphasia.
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