Clinical Stroke Syndromes

Abstract

The main mechanism of stroke in patients who have extracranial atherosclerosis is artery to artery embolism, occasionally associated with hemodynamic disturbances. Although these mechanisms are also important in patients with intracranial atherosclerosis, branch occlusion and in-situ thrombotic occlusion play a relatively more important role in these patients. Accordingly, clinical stroke syndromes differ between extracranial atherosclerosis and intracranial atherosclerosis. In anterior circulation, middle cerebral artery atherosclerosis frequently produces subcortical infarction by way of branch occlusion. The clinical syndromes are similar to lacunar syndromes classically associated with small perforator artery diseases, although a larger size infarction can be accompanied by cortical dysfunction such as aphasia or neglect. In-situ thrombotic occlusion of the large intracranial anterior circulation arteries leads to larger infarction that results in cortical symptoms - however, parts of the cortex are usually spared due to relatively well developed collateral circulation associated with prolonged perfusion impairment. In the posterior circulation, intracranial atherosclerosis is common in the distal vertebral artery and basilar artery that often causes medullary and pontine infarction syndromes, mostly by way of branch occlusion. Posterior cerebral artery atherosclerosis produces pure midbrain or thalamic infarction through branch occlusion. Artery to artery embolisms from posterior fossa intracranial atherosclerosis lead to cortical infarction - cerebellar or temporo-occipital lobe infarction, producing ataxic syndromes, and visual field defects and associated neurobehavioral syndromes, respectively.