Abstract
In the 1980s, the brain-protecting effet of mild hypothermia therapy in which the brain temperature was maintained at 33-35°C was demonstrated using a global brain ischemic model or traumatic brain injury model, and this technique is currently being applied clinically. In the 1990s, reports providing confirmation of the brain-protecting effect of mild hypothermia above 30°C in focal brain ischemic models have been published, reaching a total of 19 reports to date. Eleven experimental groups among these studies were classified into a transient middle cerebral arterial occlusion (MCAO) group and the other 11 into a permanent MCAO group. In the transient MCAO group, the duration of MCA occlusion was 1 to 3 hours. The brain or body temperature during hypothermia was 30-34°C and the duration of hypothermia was from the start until within 1 hour after ischemia in most cases. Evaluations were performed by comparing the infarct volume after 1 day with that up to after 1 week. The CBF, SEP, T1-T2 relaxation time, development of cortical spreading depression and NO synthesis were also assessed in some studies. In the transient MCAO group, the effectiveness of hypothermia was confirmed by all of the authors, whereas in the permanent occlusion group, effectiveness was confirmed in 8 studies out of 11, and no brain-protecting effect was noted in the remaining 3. These findings clarified that when mild hypothermia was commenced during ischemia or within 1 hour after focal brain ischemia, the infarct volume was reduced in most experiments, mainly with rodents. Howerve, it is unclear whether or not this effect is continuously observable at the chronic stage such as several months after ischemia. In the present review, we discuss the efficacy and the problems of mild hypothermia therapy for human focal brain ischemia.
