Motor speech disorders, both severe Broca aphasia and the more restricted and transient types, are most often a result of vascular lesions. Embolic stroke in the territory of the upper (rolandic, superior) division of the middle cerebral artery is the most frequent type and results in an abrupt onset of aphasia. Small strokes may give way to rapid improvement (hours to days); contrariwise, infarctions that extend beyond the central Broca region at times produce a more severe clinical syndrome than might be anticipated from the size of the lesion. It is these latter strokes, especially if the underlying frontal white matter is damaged, that tend to cause lasting speech difficulty. Because of the territory that is supplied by the superior branch of the middle cerebral artery, strokes that cause Broca aphasia are usually associated with right-sided brachiofacial paresis (face, proximal arm, and hand) as described earlier, and sometimes with a left-sided manual-brachial apraxia (sympathetic apraxia as described in Chap. 3). Atherosclerotic thrombosis, primary or metastatic tumor, subcortical hypertensive, traumatic, or anticoagulant-induced hemorrhage, and seizure, should they involve the appropriate parts of the motor language cortex, may also declare themselves by a Broca aphasia.
A closely related syndrome, pure word mutism (aphemia), causes the patient to be wordless (mute) but leaves inner speech intact and writing undisturbed. Anatomically, this is believed to be in the nature of a disconnection of the motor cortex (Broca area) for speech from lower centers and is described with the dissociative speech syndromes discussed further on in this chapter.
This syndrome comprises two main elements: (1) impairment in the comprehension of speech—basically an inability to perceive word elements, both spoken and written, and (2) a relatively fluent but paraphasic speech (further defined in the following text). The first of these grossly affects the internal stream of conversation and its attendant manipulation of symbolic language and causes a restricted form of confusion. The defect in language is manifest further by a variable inability to repeat spoken and written words. The location of the lesion in cases of Wernicke aphasia is the left superior lateral temporal lobe near the primary auditory cortex. The involvement of visual association areas or their separation from the primary visual cortices is a common accompaniment that is reflected in an inability to read (alexia).