Occlusion of “Top of Basilar” and Posterior Cerebral Arteries

The posterior choroidal arteries originate from the posterior cerebral arteries and course forward from caudal to rostral in the thalamus. The lateral posterior choroidal arteries supply mostly the pulvinar, a portion of the lateral geniculate body, and then loop around the superior portion of the thalamus to supply the anterior nucleus. The medial arteries supply the habenula, anterior pulvinar, parts of the center median nucleus, and the paramedial nuclei. Hemianopia, hemisensory symptoms, and behavioral abnormalities may occur in patients with posterior choroidal artery territory infarcts.

POSTERIOR CEREBRAL ARTERIES

The posterior cerebral arteries are the main terminal branches of the basilar artery. Intrinsic atheromatous disease of the PCA most often affects the origin of the vessel. Most often, infarcts in the PCA territory are caused by emboli to the posterior circulation.

After giving off penetrating branches to the midbrain and thalamus, the posterior cerebral arteries supply branches to the occipital lobes and the medial and inferior portions of the temporal lobes. Infarction in the cerebral territories of the arteries most often affects vision and somatic sensation but seldom causes paralysis. The most common finding is a hemianopia caused by infarction of the striate visual cortex on the banks of the calcarine fissure or by interruption of the geniculocalcarine tract as it nears the visual cortex. If just the lower bank of the calcarine fissure is involved, the lingual gyrus, a superior quadrant-field defect, results. An inferior quadrantanopia results if the lesion affects the cuneus on the upper bank of the calcarine fissure. When infarction is restricted to the striate cortex and does not extend into the adjacent parietal cortex, the patient is fully aware of the visual field loss.

Somatosensory abnormalities are also common. The lateral thalamus is the site of the major somatosensory relay nuclei, the ventral posteromedial and lateral nuclei. Ischemia to these nuclei or white matter tracts carrying fibers from the thalamus to somatosensory cortex produces sensory symptoms and signs, usually without paralysis. Patients report paresthesias or numbness in the face, limbs, and trunk. The combination of hemisensory loss and hemianopia without paralysis is virtually diagnostic of infarction in the posterior cerebral artery territory. Rarely, occlusion of the proximal portion of the artery can cause a hemiplegia. Penetrating branches from the proximal posterior cerebral artery penetrate into the midbrain to supply the cerebral peduncle.

Cognitive and behavioral abnormalities are also common. When the left posterior cerebral artery territory is infracted, patients may lose the ability to read, although they retain the ability to write and spell. Anomic aphasia and memory loss are also common. When the right posterior cerebral artery territory is involved, disorientation to place may develop.

When the posterior cerebral artery territory is infarcted bilaterally, as may occur with emboli, the most common findings are cortical blindness, amnesia, and agitated delirium.

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