The short- and long-term effects of ultraviolet irradiation on the exposed cat cerebrum: Light-microscopic, enzyme-histochemical and fine-structural observations

Abstract

Light-microscopic, enzyme-histochemical and electron-microscopic findings are reported in 20 cats following local exposure of the cerebral cortex to ultraviolet irradiation. The observations ranged from 3 hr to 1 year after injury. The acute lesion (3 and 24 hr after irradiation) is characterized by focal cortical necrosis, associated with vasogenic edema of the adjacent cortex and underlying white matter. In the cortex, most of the edema is intracellular, while in the white matter it is extracellular, and accompanied by swelling of the astrocytes. In the area of maximal injury, extracellular edema is also found in the cortex, associated with an extracellular exudation of plasma fluid and fibrin. Vascular changes include increased pinocytotic activity in the endothelial cells, widening of the capillary basement membranes, and a decrease of ATP-ase and other cyto-membrane enzyme activity in the vessel walls. The subsequent stages are characterized by a proliferative vascular and cellular response. Increase of ATP-ase and other cyto-membrane enzyme activity is found in the proliferating blood vessels. The astrocytic response is characterized by an increase of glycogen rosettes, usually in the cortical astrocytes, increased glial-filament formation, and increased tetrazolium reductase activity. In the late stages (6–12 months after irradiation), intense fibrillary gliosis is found beneath the old cortical scar. The tetrazolium reductase activity of the white matter astrocytes becomes reduced, but a conspicuous increase of ATP-ase and other cytomembrane enzyme activity is demonstrated in the area of fibrillary gliosis. Marked thickening and convolution of the capillary basement membranes persist in places, especially in the area of old injury. A focal increase in extracellular space in the white matter is still present 1 year after irradiation. The correlation of these structural changes with impairment of the blood-brain barrier function is discussed.