PATHOPHYSIOLOGY OF BRAIN-SWELLING AFTER ACUTE EXPERIMENTAL BRAIN COMPRESSION AND DECOMPRESSION

GLOBAL ISCHEMIA WAS created by controlled expansion of an epidural balloon for 25 minutes in Group A (six cats) and for minutes in Group B (six cats). The alterations of intracranial pressure, arteriovenous oxygen content difference, cerebral metabolic rate of oxygen, cerebral blood flow, and electroencephalogram were observed until brain death or 24 hours' survival with normal intracranial pressure. The animals were then killed for brain histological examination. In four other cats, a 2% solution of Evans blue dye (4 mg/kg) was injected intravenously-immediately after deflation-resulting in 25 minutes of global ischemia. Two other cats received 5 minutes of global ischemia. The cats were killed 1 hour later. Abrupt swelling occurred in Group A, and no swelling was found in Group B. A transient absolute hyperemia was found immediately after deflation in both groups. The cerebral blood flow and cerebral metabolic rate of oxygen decreased markedly with low arteriovenous oxygen content difference and flat electroencephalogram in Group A, compared with gradual recovery of cerebral blood flow and cerebral metabolic rate of oxygen with high arteriovenous oxygen content difference and reappearance of electroencephalogram activity in Group B. The extravasation of Evans blue was observed on the compressed cerebral hemisphere, thalamus, hypothalamus, and brain stem in swelling animals and only on the compressed hemisphere in nonswelling animals. Histologically, the damage and congestive dilation of capillary, degeneration, and necrosis of neuronal and glial cell were found prominently on the hypothalamus and brain stem in the swelling group. There was no obvious alteration observed in the nonswelling group. This study showed that there was a close relationship between duration of compressive global ischemia and occurrence of brain swelling. it was postulated that damage of the hypothalamus and brain stem, probably caused by distortion and ischemia during brain compression, might be responsible for the vasomotor paralysis to increase cerebral blood volume. Our study suggests that, in postdecompressive acute swelling, severe cerebral ischemia is the basic feature, and damage of the control center for the vasomotor area, such as the hypothalamus and brain stem, is pathophysiological.