With occlusion of penetrating branches of the ACA, typified by occlusion of Heubner’s artery, the anterior limb of the internal capsule and caudate is usually involved. In a series of 18 cases of unilateral caudate region infarcts collected by Caplan and associates, a transient hemiparesis was present in 13. Dysarthria and either abulia or agitation and hyperactivity were also common. Stuttering and language difficulty occurred with two of the left-sided lesions and visuospatial neglect with three of the right-sided ones. Alexander and Schmitt cited cases in which occlusions of the proximal artery (ACA), which included the Heubner artery, resulted in right hemiplegia (predominant in the leg) with grasping and groping responses of the right hand and buccofacial apraxia that were accompanied by a diminution or absence of spontaneous speech, agraphia, and a limited ability to name objects and compose word lists but with a striking preservation of the ability to repeat spoken and written sentences (i.e., transcortical motor aphasia). With bilateral caudate infarctions, a syndrome of inattentiveness, abulia, forgetfulness, and sometimes agitation and psychosis was observed. Transitory choreoathetosis and other dyskinesias (we have seen two cases of ballismus) have also been attributed to ischemia of the caudate and anterior basal ganglia, occurring sometimes under conditions of prolonged standing and exercise (Caplan and Sergay; Margolin and Marsden).
This is a long, narrow artery that springs from the internal carotid, just distal to the origin of the posterior communicating artery. It supplies the internal segment of the globus pallidus and posterior limb of the internal capsule and several contiguous structures including (in most patients) the optic tract (Figs. 33-6 and 33-9). It then penetrates the temporal horn of the lateral ventricle, where it supplies the choroid plexus and anastomoses with the posterior choroidal artery. This being a small caliber branch, most strokes in this territory are due to in situ atherosclerosis of the type that occurs in diabetics but occlusion of the orifice of the vessel by an embolus is possible and it is a known complication of clipping of an aneurysm at the upper reaches of the carotid artery.
Only a few complete clinicopathologic studies have been made of the distinctive syndrome caused by occlusion of this artery. It was found by Foix and colleagues to consist of contralateral hemiplegia, hemihypesthesia, and homonymous sectorial hemianopia as a result of involvement of the posterior limb of the internal capsule and white matter posterolateral to it, through which the geniculocalcarine tract passes, and the lateral geniculate nucleus. There has been considerable discussion regarding the vascular anatomy supply of the lateral geniculate; several authors have suggested that the anterior choroidal artery supplies the lateral and medial portions of the nucleus and a lesion there causes a homonymous quandrantopias in the upper and lower fields but sparing a sector that lies along the equator (cleverly called “quadruple quadrantanopia”). The complimentary stroke in the lateral geniculate is one from occlusion of the posterior (lateral) choroidal artery, which supplies the middle segment of the nucleus and gives rise a sectorial defect lying along the equatorial visual field (see Frisen et al, and Osborne et al). This combination of extensive unilateral motor, sensory, and visual impairment in an individual with well-preserved language and cognition distinguishes this stroke syndrome from the more common ones involving the major cerebral arteries. Decroix and colleagues reported 16 cases (identified by CT) in which the lesion appeared to lie in the vascular territory of this artery. In most of their cases, the clinical syndrome fell short of what was expected on anatomic grounds or had additional features.