The middle cerebral artery (MCA) has superficial and deep hemispheral branches that together supply the largest portion of the cerebral hemisphere. Through its cortical branches, it supplies the lateral (convexity) part of the cerebral hemisphere (see Figs. 33-2 and 33-5) encompassing (1) the cortex and white matter of the lateral and inferior parts of the frontal lobe—including motor areas 4 and 6, contraversive centers for lateral gaze and the motor speech area of Broca (dominant hemisphere); (2) the cortex and white matter of the parietal lobe, including the primary and secondary sensory cortices and the angular and supramarginal gyri; and (3) the superior parts of the temporal lobe and insula, including the receptive language area of Wernicke. The deep penetrating or lenticulostriate branches of the MCA supply the putamen, a large part of the head and body of the caudate nucleus (shared with the Heubner artery, see further on), the outer globus pallidus, the posterior limb of the internal capsule, and the corona radiata (see Fig. 33-6).
The MCA may be occluded in its longitudinal portion, or the stem, that is proximal to its bifurcation (the term M1 is used to denote this portion of the vessel). An occlusion at this site blocks the flow in the small deep penetrating vessels as well as in superficial cortical branches. An occlusion at the distal end of the stem blocks only the orifices of the divisions of the artery in the sylvian sulcus but leaves unaffected the deep penetrating vessels. The idealized picture of total occlusion of the stem is one of contralateral hemiplegia (involving the face, arm, and leg as a result of infarction of the posterior limb of the internal capsule), hemianesthesia, and can include homonymous visual field deficit (because of infarction of the lateral geniculate body), with deviation of the head and eyes toward the side of the lesion. In addition, there is a variable but usually global aphasia with left hemispheric lesions and anosognosia and amorphosynthesis with right-sided lesions (see Chap. 21). Partial syndromes encompassing several parts of this ensemble are common. At the onset of the stroke, the patient may be drowsy because of an ill-defined effect of widespread paralysis of neurologic function. If there are adequate collateral vessels over the surface of the hemisphere, only those components of the stroke referable to the deep structures may be evident (mainly hemiplegia encompassing the contralateral limbs and face) as discussed below, the cortical elements of aphasia, agnosia, and apraxia then being absent or mild.
Occlusion of the stem of the MCA is usually caused by embolus and less often by a thrombus superimposed on a local atherosclerotic plaque. In the past, “middle cerebral artery thrombosis” was thought to be the most common cause of stroke, whereas studies over the years have affirmed that most carotid occlusions are thrombotic, whereas most middle cerebral occlusions are embolic (Fisher, 1975; Caplan, 1989). The emboli may lodge in the stem or, more often, drift into the cortical branches as described below; emboli infrequently enter solely the deep penetrating branches of the stem and cause a small deep infarction (lacune).
In the less-common circumstance of stenosis of the MCA with occlusion of the vessel by a superimposed thrombus, the stroke is often preceded by TIAs, producing a picture resembling that of carotid stenosis (see Caplan, 1989). Transient monocular blindness does not occur in this situation because the occlusion is distal to the ophthalmic artery. In epidemiologic studies, certain populations such as Asians are disproportionally affected by this form of intracranial atherosclerosis, as are diabetics.