Although the brain accounts for only 2% of the body's mass, it utilizes 25% of the body's energy and stores and receives 15% to 20% of the total cardiac output. Given these high demands, it makes intuitive sense that even brief periods of anoxia have dire consequences. Cerebral ischemia can be considered either a focal or global process. Focal ischemia is classically exemplified by the syndrome of acute ischemic stroke, whereas global ischemia is most often the consequence of cardiopulmonary arrest (usually due to a malignant cardiac dysrhythmia). The consequences of focal and global ischemia can be profound, ranging from partial to complete disability or death.

The potential lifesaving effects of hypothermia have been evident since early observations that individuals (particularly children) who became immersed in ice-cold water and drowned were able to be resuscitated with no apparent neurologic injury. Although it was understood that the cold water had life-preserving effects, the mechanisms involved remained largely unknown. Certainly, such early physicians as Hippocrates understood that cold water or ice had tissue-preserving and anti-inflammatory effects; however, their beneficial role in preserving brain tissue took several centuries of medical advancement to be realized.

Induced hypothermia as a modern neurologic therapeutic tool dates to the 1940s, when Dr. Temple Fay first reported cooling 124 patients with severe head injury (1). Ten years later, hypothermia was used as a neuroprotective agent during cardiac surgery that required cardiac arrest, which caused global cerebral ischemia (2). Then, in one of the earliest preclinical reports, it was shown that a drop in brain temperature as little as a 2°C to 5°C resulted in marked protection against global ischemia (3). This finding led to the reintroduction of the concept of therapeutic hypothermia for neuroprotection.

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