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12 APHASIAS AND RELATED DISORDERS

12 APHASIAS AND RELATED DISORDERS
Harrison’s Manual of Medicine

12

APHASIAS AND RELATED DISORDERS

Global Aphasia
Broca’s Aphasia (Motor or Nonfluent Aphasia)
Wernicke’s Aphasia (Sensory or Fluent Aphasia)
Conduction Aphasia
Pure Word Deafness
Pure Word Blindness
Isolation of Speech Area
Laboratory Studies in Aphasia
Bibliography

Aphasias are disturbances in the comprehension or production of spoken or written language. Aphasias may be classified based on their clinical manifestations, the anatomic location of the underlying lesion, their etiology, and associated clinical symptoms (Table 12-1).

Table 12-1 Clinical Features of Aphasias and Related Conditions

Global Aphasia
ETIOLOGY   Occlusion of internal carotid artery (ICA) or middle cerebral artery (MCA) supplying dominant hemisphere (less commonly hemorrhage, trauma, or tumor), resulting in a large lesion of frontal, parietal, and superior temporal lobes.
CLINICAL MANIFESTATIONS   All aspects of speech and language are impaired. Patient cannot read, write, or repeat and has poor auditory comprehension. Speech output is minimal and nonfluent. Usually hemiplegia, hemisensory loss, and homonymous hemianopia are present.
Broca’s Aphasia (Motor or Nonfluent Aphasia)
ETIOLOGY   Core lesion involves dominant inferior frontal convolution (Broca’s area), although cortical and subcortical areas along superior sylvian fissure and insula are often involved. Commonly caused by vascular lesions involving the superior division of the MCA; less commonly due to tumor, abscess, metastasis, subdural hematoma, encephalitis.
CLINICAL MANIFESTATIONS   Speech output is sparse, slow, effortful, dysmelodic, poorly articulated, and telegraphic. Most patients have severe writing impairment. Comprehension of written and spoken language is relatively preserved. Patient is often aware of and visibly frustrated by deficit. With large lesions, a dense hemiparesis may occur, and the eyes may deviate toward side of lesion. More commonly, lesser degrees of contralateral face and arm weakness are present. Sensory loss is rarely found, and visual fields are intact. Buccolingual apraxia is common, with difficulty imitating movements with tongue and lips or performing these movements on command. An apraxia involving the ipsilateral hand may occur due to involvement of fibers in the corpus callosum.
Wernicke’s Aphasia (Sensory or Fluent Aphasia)
ETIOLOGY   Embolic occlusion of inferior division of dominant MCA (less commonly hemorrhage, tumor, encephalitis, or abscess) involving posterior perisylvian region.
CLINICAL MANIFESTATIONS   Although speech sounds grammatical, melodic, and effortless (“fluent”), it is often virtually incomprehensible due to errors in word usage, structure, and tense and the presence of neologisms and paraphasia. Comprehension of written and spoken material is severely impaired, as are reading, writing, and repetition. The patient usually seems unaware of the deficit. Associated clinical symptoms can include parietal lobe sensory deficits and homonymous hemianopia. Motor disturbances are rare.
Conduction Aphasia
Comprehension of speech and writing is largely intact, and speech output is fluent, although paraphasia is common. Repetition is severely affected. Most cases are due to lesions involving supramarginal gyrus of dominant parietal lobe, dominant superior temporal lobe, or arcuate fasciculus. Lesions are typically due to an embolus to either the ascending parietal or posterior temporal branch of the dominant MCA. Associated symptoms include contralateral hemisensory loss and hemianopia.
Pure Word Deafness
Almost total lack of auditory comprehension with inability to repeat or write to dictation and relatively preserved spoken language and spontaneous writing. Comprehension of visual or written material is superior to that of auditory information. The lesion(s) are typically in or near the primary auditory cortex (Heschl’s gyrus) in the superior temporal gyrus. Causes are infarction, hemorrhage, or tumor.
Pure Word Blindness
Inability to read and often to name colors with preserved speech fluency, language comprehension, repetition, and writing to dictation (alexia without agraphia). Lesion usually involves left occipitostriate cortex and visual association areas as well as fibers in splenium of corpus callosum connecting right and left visual association areas. Most patients have an associated right homonymous hemianopia, hemisensory deficit, and memory disturbance due to vascular lesions involving the left posterior cerebral artery (PCA) territory. Rarely, tumor or hemorrhage may be the cause.
Isolation of Speech Area
Hypotension, ischemia, or hypoxia may result in borderzone infarctions between the anterior cerebral–MCA–PCA territories that spare the sylvian region of the MCA. Pts are severely brain damaged and have parrot-like repetition of spoken words (echolalia) with little or no spontaneous speech or comprehension.
Laboratory Studies in Aphasia
CT scan or MRI usually identifies the location and nature of the causative lesion. Angiography helps in accurate definition of specific vascular syndromes.

TREATMENT
Speech therapy may be helpful in treatment of certain types of aphasia.

Bibliography

For a more detailed discussion, see Mesulam M-M: Aphasias and Other Focal Cerebral Disorders, Chap. 25, p. 140, in HPIM-15.

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