There has been recent interest in a role for the cerebellum in language function, based partly on observations in the Williams syndrome, in which cognitive impairment is associated with a preservation of language skills that is sometimes striking in degree (see Chap. 38). In this disease, the cerebellum is spared in the face of greatly diminished volume of the cerebral hemispheres (see Leiner et al). Some studies of cerebral blood flow also implicate the cerebellum in various language functions; based on our clinical experience, however, we would judge any language deficits from cerebellar disease to be subtle or nonexistent. Dysarthria, of course, is common with cerebellar disease.
In the investigation of aphasia, it is first necessary to inquire into the patient’s native language, handedness, and previous level of literacy and education. It has been surmised that following the onset of aphasia, individuals who had been fluent in more than one language (polyglots) improved more quickly in their native language than in a subsequently acquired one (a derivative of the Ribot law of retained distant memory). This rule seems to hold if the patient is not truly fluent in the more recently acquired language or has not used it for a long time. More often, the language most used before the onset of the aphasia will recover first (Pitres law). Usually, if adequate testing is possible, more or less the same aphasic abnormalities are found in both the first and the more recently acquired language. Dementing illnesses such as Alzheimer disease, however, do cause increasing use of the first acquired language.
Many naturally left-handed children are trained to use the right hand for writing; therefore, in determining handedness, one must ask which hand is preferred for throwing a ball, threading a needle, sewing, or using a tennis racket or hammer, and which eye is used for sighting a target with a rifle or other instrument. It is important, before beginning the examination, to determine whether the patient is alert and can participate reliably in testing, as accurate assessment of language depends on these factors.
One should quickly ascertain whether the patient has other gross signs of a cerebral lesion such as hemiplegia, facial weakness, homonymous hemianopia, or cortical sensory loss. When a constellation of these major neurologic signs is present, the aphasic disorder is usually of the total (global) type. A right brachiofacial paralysis aligns with Broca’s aphasia; in contrast, a restricted right hemianopia or quadrantanopia is a common accompaniment of Wernicke aphasia, and hemiparesis is absent. Dyspraxia of limbs and speech musculature in response to spoken commands or to visual mimicry is generally associated with Broca aphasia, but sometimes with Wernicke aphasia. Homonymous hemianopia without motor weakness tends often to be linked to pure word blindness, to alexia with or without agraphia, and to anomic aphasia.
The bedside analysis of aphasic disorders that we find most useful entails the systematic testing of six aspects of language function: conversational speech, comprehension, repetition, reading, writing, and naming. Simply engaging the patient in conversation permits assessment of the motor aspects of speech (praxis and prosody), fluency, and language formulation. If the disability consists mainly of sparse, laborious, nonfluent speech, it suggests, of course, Broca aphasia, and this possibility can be pursued further by tests of repeating from dictation and by special tests of praxis of the oropharyngeal muscles. Fluent but empty paraphasic speech with impaired comprehension is indicative of Wernicke aphasia. Impaired comprehension but perfectly normal formulated speech and intact ability to read suggest the rare syndrome of pure word deafness.