By the time that a patient with an acute neurologic injury is admitted to the neurocritical care unit, the primary damage has already occurred and the major focus of intervention shifts to that of preventing secondary injury. The brain accounts for only 2% of the body's mass, yet it utilizes 25% of the body's energy stores and receives 15-20% of the total cardiac output. It is exquisitely sensitive to even the briefest period of anoxia, with the latter frequently resulting in dire consequences.

Brain temperature plays a major role in modulating the effects of ischemia and anoxia. The potential life-saving effects of hypothermia have been evident ever since early people first noted that individuals who became immersed in ice-cold water and drowned were able to be revived with no apparent neurologic injury. Cold-water immersion was recognized as having life-preserving effects; however, the mechanisms by which this occurred remained largely unknown. Although early physicians such as Hippocrates understood that cold water or ice had tissue-preserving and anti-inflammatory effects, its application to preserving the brain tissue took severalcenturies of medical advancement to be realized.

Induced hypothermia was first used as a modern neurologic therapeutic tool by Dr. Temple Fay, who reported cooling 124 patients with severe head injury in the 1940s. This then led Bigelow et al. to use hypothermia as a neuroprotective agent during cardiac surgery that required cardiac arrest (CA), causing global cerebral ischemia.