Stroke is one of the leading causes of death in adults and also a major cause of neurological disability. Until recently, stroke has been viewed as an untreatable event and all physicians could offer a stroke victim was rehabilitation to try to regain lost functions. In an effort to reduce the damage caused by strokes, a number of treatments have been proposed. In one interventional approach, known as neuroprotectant therapy, the intent is to limit the amount of neurological damage that occurs after the initial event. Neuroprotectant approaches includes the administration of several pharmacological agents and a treatment known as mild hypothermia, or a lowering of core body temperature by 2-4 degrees Celsius. The induction of mild hypothermia has been shown to inhibit several points of the chemical cascade that cause secondary cellular death after an ischemic event and to provide broad neuroprotection.
One method of inducing mild hypothermia is through heating of the preoptic anterior hypothalamus (POAH) which is located in the lower portion of the brain adjacent to the skull. It is known that the POAH is the thermostat for sensing core body temperature and controlling thermo regulatory responses in animals. The cooling mechanisms elicited by the POAH include reduction of metabolic energy generation, vasodilatation enhancing skin cooling, and sweating. Full vasodilatation can increase the rate of heat transfer to the skin as much as eight fold. An additional one degree Celsius It is known that the POAH is the thermostat for sensing core body temperature and controlling thermo regulatory responses in animals. The cooling mechanisms elicited by the POAH include reduction of metabolic energy generation, vasodilatation enhancing skin cooling, and sweating. Full vasodilatation can increase the rate of heat transfer to the skin as much as eight fold. An additional one degree Celsius increase in body temperature can increase sweating enough to remove ten times the basal rate of heat protection.