Marked Protection by Moderate Hypothermia after Experimental Traumatic Brain Injury

These experiments examined the effects of moderate hypothermia on mortality and neurological deficits observed after experimental traumatic brain injury (TBI) in the rat. Brain temperature was measured continuously in all experiments by intraparenchymal probes. Brain cooling was induced by partial immersion (skin protected by a plastic barrier) in a water bath (0°C) under general anesthesia (1.5% halothane/70% nitrous oxide/30% oxygen). In experiment I, we examined the effects of moderate hypothermia induced prior to injury on mortality following fluid percussion TBI. Rats were cooled to 36°C ( n = 16), 33°C ( n = 17), or 30°C ( n = 11) prior to injury and maintained at their target temperature for 1 h after injury. There was a significant (p < 0.04) reduction in mortality by a brain temperature of 30°C. The mortality rate at 36°C was 37.5%, at 33°C was 41%, and at 30°C was 9.1%. In experiment II, we examined the effects of mod erate hypothermia or hyperthermia initiated after TBI or long-term behavioral deficits. Rats were cooled to 36°C ( n = 10), 33°C ( n = 10), or 30°C ( n = 10) or warmed to 38°C ( n = 10) or 40°C ( n = 12) starting at 5 min after injury and maintained at their target temperatures for 1 h. Hypothermia-treated rats had significantly less beam-walking beam-balance, and body weight loss deficits compared to normothermic (38°C) rats. The greatest protection was observed in the 30°C hypothermia group. Since a temperature of 30°C can be induced in humans by surface cooling without coagulopathy or ventricular fibrillation, hypothermia to 30°C may have potential clinical value for treatment of human brain injury.