Therapeutic hypothermia (TH) has been employed as a neuroprotective strategy for a wide array of clinical problems since the late 1940s. Animal studies have determined that the neuroprotective effect of hypothermia is pleiotropic, impacting many steps in both the ischemic cascade and reperfusion injury. Interest in the neuroprotective effects of TH for ischemic brain injury has been resurgent, fueled by both recent positive and negative clinical trials. A review of preclinical and clinical reports on TH in adult patients is provided in this article.
Animal data and several large clinical studies of mild to moderate TH (32°C–34°C) for global cerebral ischemia describe favorable neurologic outcomes, with few adverse effects. However, clinical implementation for global ischemia remains poor. Some animal data support a role for TH in focal cerebral ischemia, if instituted soon after the onset of ischemia, and in the setting of reperfusion. Clinical studies of TH for focal cerebral ischemia have so far been equivocal. The available data suggest that, despite sharing some common components in the ischemic cascade, focal and global cerebral ischemia are pathophysiologically disparate, and may respond to different neuroprotective strategies.
TH is a safe, effective neuroprotective strategy for global cerebral ischemia. Because of the neuroprotective efficacy of TH in adult comatose survivors of cardiac arrest, neurologists should advocate the implementation of this strategy. TH for focal ischemia is a promising therapeutic option, but requires more basic and clinical investigation.
From the *Departments of *Neurology and †Anesthesiology and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland.
Supported in part by NIH grants R44-NS-38016 and RO1-HL-EB-71568 (to R.G.G.).
Reprints: Robert E. Hoesch, MD, PhD, 600 North Wolfe Street, Pathology 509, Baltimore, MD 21287. E-mail: firstname.lastname@example.org.