Summary: These experiments examined the effects of moderate hypothermia on mortality and neurological def icits observed after experimental traumatic brain injury (TBI) in the rat. Brain temperature was measured contin uously in all experiments by intraparenchymal probes, Brain cooling was induced by partial immersion (skin pro tected by a plastic barrier) in a water bath (OOe) under general anesthesia (1.5% halothane170% nitrous oxide/ 30% oxygen). In experiment I, we examined the effects of moderate hypothermia induced prior to injury on mortal ity following fluid percussion TBI. Rats were cooled to 36°e (n = 16), 33°e (n = 17), or 300e (n = II) prior to injury and maintained at their target temperature for I h after injury. There was a significant (p < 0.04) reduction in mortality by a brain temperature of 30oe. The mortality rate at 36°e was 37.5%, at 33°e was 41 %, and at 300e wasThe cerebral protective effects of profound hypo thermia «18°C) have been known for many years. As early as 1950, reports of cerebral protection from global ischemia by profound hypothermia in animals stimulated clinical interest (Mohri and Me rendino, 1969). By 1955, 100 cardiac surgical cases had been performed under deep hypothermia with cardiac arrest (Mohri and Merendino, 1969). As pump oxygenators became more efficient, deep hy pothermia and cardiac arrest were only occasion ally used in adult cardiac surgery (Crawford and Saleh, 1981). In pediatric cardiac surgery, however, conditions were encountered routinely where total cessation of circulation at temperatures of 17-20°C Abbreviations used: ANOYA, analysis of variance; TB1, trau matic brain injury, 114 9.1 %. In experiment II, we examined the effects of mod erate hypothermia or hyperthermia initiated after TBI 01 long-term behavioral deficits. Rats were cooled to 36°e (I = 10), 33°e (n = 10), or 300e (n = 10) or warmed to 38°( (n = 10) or 400e (n = 12) starting at 5 min after injury an( maintained at their target temperatures for I h. Hypother mia-treated rats had significantly less beam-walking beam-balance, and body weight loss deficits compared t( normothermic (38°C) rats. The greatest protection wa: observed in the 300e hypothermia group, Since a temper ature of 300e can be induced in humans by surface cool ing without coagulopathy or ventricular fibrillation, hy pothermia to 300e may have potential clinical value fOJ treatment of human brain injury.