The neuropathology of stroke

Abstract

Vascular-circulatory derangements affecting the function of the central nervous system may result in parenchymal lesions that are hemorrhagic, ischemic, or mixed. Most nontraumatic intraparenchymal brain hemorrhages are found in association with cerebral arteriolar sclerosis and other stigmata of hypertensive disease, such as hypertrophy of the left cardiac ventricle and granular kidneys. Global temporary ischemia, the type that exists during severe and transient hypotension, results in a wide variety of parenchymal lesions that may be bilateral, unilateral, supratenorial, or infratentorial. The cerebral and cerebellar cortices, white matter, basal ganglia, brain stem, and spinal cord may be involved simultaneously or there may be isolated, focal lesions that are confined occasionally to any one of these areas. Regional ischemia, the type induced through the occlusion of a major intracranial artery, evolves through a stage of acute encephalomalacia, during which the morphologic change consists of alternating cellular swelling and shrinkage. This is followed by leukocytic inflammation at three to four days and the beginning of resolution at about the tenth day after arterial occlusion. In the evolution of this form of abnormal circulation, after a few minutes, some neurons in the most distal arterial territories show the first recognizable changes. In these neurons the mitochondria swell massively. Astrocytes and neurites in the same foci are selectively swollen, whereas oligodendrocytes and capillaries remain structurally unchanged during the initial stages of ischemic injury.