• C T Wass and W L Lanier.
• Mayo Medical School, Rochester, Minnesota, USA.
• Int Anesthesiol Clin. 1996 Jan 1; 34 (4): 95-111.

AbstractThere is a large amount of experimental evidence that mild hypothermia in laboratory animals will protect the brain from ischemic injury. Conversely, mild hyperthermia will exacerbate injury. Supporting data in humans are limited. However, cerebral protection has consistently been demonstrated in humans subjected to complete circulatory arrest during profound hypothermia. Induced and passive mild hypothermia have become common in the management of patients at risk for ischemic neurological injury. Currently, brain temperature is managed largely by altering core temperature. Limitations of this approach are that gradients can develop between brain and core temperatures as a result of the surgical intervention, anesthetic interventions, or the patient's pathology. Further, large reductions in systemic temperature may place an undue burden on systemic physiology and, in extreme examples, systemic factors may adversely affect neurological well-being. Obviously, proper temperature management in humans at high risk for neurological injury will benefit from the following factors: First, greater evidence is needed that small changes in temperature modulate outcome in humans, commensurate with demonstrations of benefit in animals. Second, better methods are needed to monitor brain temperature during periods of risk for ischemic injury. And third, management techniques should be identified that will use brain-to-core temperature gradients to the patient's advantage, thus producing optimal alterations in brain temperature while minimally affecting systemic temperature and physiology. Before these goals can be accomplished, more research is needed, both in laboratory animals and in humans.

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