Abstract
Although the first studies on the therapeutic effects of deep hypothermia during surgical procedures and after acute central nervous system injury were published more than 40 years ago, the importance of relatively small variations in ischémic brain temperature was discovered in the late 1980s [1–4]. In experimental studies of transient cerebral ischemia, mild to moderate variations in intrais-chemic brain temperature dramatically altered histopathologic outcome in selectively vulnerable brain regions. Although a decrease in ischémic brain temperature was shown to be neuroprotective, mild temperature elevations worsened outcome. Experimental data have also demonstrated that several pharmacologie agents protect the postischemic brain by temperature-dependent mechanisms [5, 6]. This fact has complicated the interpretation of pharmacologie studies directed at ischemic protection.