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(Stroke. 2003;34:1051.)
© 2003 American Heart Association, Inc.
Emerging Therapies |
From the Departments of Neurological Surgery (W.D.D.), Neurology (W.D.D.), and Pediatrics (J.W.K.), University of Miami School of Medicine, Miami, Fla.
Correspondence to W. Dalton Dietrich III, PhD, Scientific Director, The Miami Project to Cure Paralysis, University of Miami School of Medicine, Lois Pope LIFE Center, 1095 NW 14th Terr (R-48), Miami, FL 33136-1060. E-mail ddietrich@miami.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Therapeutic hypothermia as a potential treatment for stroke, cerebral ischemia, and other neurological diseases has gained momentum since the initial discovery that relatively small differences in intraischemic brain temperature critically determine ischemic neuronal vulnerability.1 Since that time, laboratories throughout the world have investigated the potential use of mild-to-moderate hypothermia in many ischemia models.2,3 Various studies have also investigated potential mechanisms contributing to hypothermic protection. Pathomechanisms sensitive to intra- and postischemic temperature reductions and elevations include glutamate release, stabilization of the blood-brain barrier, oxygen radical production, intracellular signal conduction, protein synthesis, ischemic depolarization, reduced cerebral metabolism, membrane stabilization, inflammation, activation of protein kinases, cytoskeletal breakdown, and early gene expression.2,4 Because the pathophysiology of ischemic brain injury is complex, the fact that many injury mechanisms have been reported to be temperature sensitive may account for the dramatic effects of temperature on ischemic outcome. Thus, therapeutic hypothermia has the necessary support from preclinical data to initiate well-designed clinical studies targeting various patient populations.
In a recent issue of The New England Journal of Medicine, the results of 2 randomized clinical trials showed clearly that mild hypothermia improves neurologic outcome and reduces overall mortality in survivors of out-of-hospitalwitnessed cardiac arrest.5,6 In the study from Australia, a total of 77 patients who remained comatose after the return of spontaneous circulation (ROSC) were randomized to receive 12 hours of hypothermia or standard normothermic temperature management.5 In that study, surface cooling was begun in the field and the target temperature of 32°C to 34°C was reached
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