Striatocapsular infarction A number of interesting syndromes occur with deep lesions in the territory of the penetrating vessels of the MCA, collectively known as lenticulostriate, or penetrating vessels (see Figs. 33-6 and 33-8). Most, as mentioned, are attributable to emboli that lodge in the stem of the main vessel, although imaging studies may show a patent middle cerebral artery, implying that the embolus has moved on. Others are undoubtedly atherothrombotic as mentioned earlier. These lesions in the corona radiata are larger than typical lacunar infarctions (see further on) but probably have a similar pathophysiology.
Although the infarction is centered in the deep white matter, most of the syndromes include a fragment of one of the cortical stroke patterns described further on. The most common type is a large striatocapsular infarction, similar to that described by Weiller and colleagues. All of their patients had a degree of hemiparesis and one-fifth had aphasia or hemineglect. Aphasia, when it occurred, tended to be a limited form of the Broca type and is usually short-lived. With smaller deep strokes, incomplete motor syndromes affecting only the arm and hand, without language disturbance or neglect are common; these are difficult to differentiate from small embolic cortical strokes.
Homonymous hemianopia is an infrequent occurrence with posterior capsular lesions, but when it occurs, is probably a result of damage to the region of the lateral geniculate nucleus and optic radiations, but it is infrequent and must be distinguished from visual hemineglect of contralateral space. Bilateral cerebral infarctions involving mainly the insular–perisylvian (anterior opercular) regions manifest themselves by a diplegia of the face, tongue, and masseters that results in anarthria without aphasia (see Mao et al and Bakar et al).
Superior division An embolus entering the middle cerebral artery most often lodges in one of its two main branches, the superior division (supplying the rolandic and prerolandic areas) or the inferior division (supplying the lateral temporal and inferior parietal lobes), sometimes together designated as M2 segments; see Figs. 33-2 and 33-7. Atherothrombotic occlusion of these vessels is infrequent.
Complete infarction in the territory of the superior division causes a dense sensorimotor deficit in the contralateral face, arm, but, to a lesser extent the leg, as well as ipsilateral deviation of the head and eyes; that is, it differs from the MCA stem occlusion syndrome in that the leg and foot are partly spared and less involved with weakness than the arm and face (“brachiofacial,” or “chierobrachial” paralysis); there is no impairment of alertness. Less extensive strokes are more common than this archetype and the deficits are correspondingly milder. If the occlusion is long lasting (not merely transient ischemia with disintegration of the embolus) there will be slow improvement; after a few months, the patient is able to walk with a spastic leg, while the motor deficits of the arm and face may remain. The sensory deficit may be profound, resembling that of a thalamic infarct (as described in Chap. 8) but more often it is less severe than the motor deficit, taking the form of stereoanesthesia, agraphesthesia, impaired position sense, tactile localization, and two-point discrimination, as well as variable changes in touch, pain, and temperature sense (see Chap. 21). With left-sided lesions there may initially be severe aphasia to the point of mutism, or there is a predominantly nonfluent (Broca’s) aphasia, reflected by effortful, hesitant, grammatically simplified, and dysmelodic speech (see Chap. 22).