Hyperthermia in the immediate poststroke period is common and is associated with increased morbidity and mortality (47-51). Ironically, ischemic brain temperature tends to be higher than core body temperature (52). Hyperthermia might contribute to increased cerebral injury through several different mechanisms. First, temperature is the major determinant of the brain's metabolic rate of oxygen consumption (CMRO2). For every degree centigrade above normothermia (36.8°C), CMRO2 increases by approximately 5% to 10%; conversely, for every degree centigrade below normothermia, the CMRO2 decreases by approximately 5% to 10% (53-55). Hyperthermia is also associated with increased inflammation and an increased release of excitotoxic amino acids; conversely, hypothermia reduces the release of excitotoxic amino acids ( 56-60 ).
Hypothermia is potently neuroprotective in animal models of stroke (61-63). Anecdotal evidence suggests that hypothermia might improve outcome from malignant cerebral infarction (64). Hypothermia improves neurologic outcome in patients who experience cardiac arrest, but prospective, randomized, controlled trials of hypothermia in stroke have not yet been completed (65,66). Given the consistent relationship between hyperthermia and poor stroke outcome, it seems reasonable to target normothermia in patients with acute stroke. Until the benefit of hypothermia can be proven in a prospective, randomized, controlled trial, it should only be used in the research setting.
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