Stroke and hypothermia

July 7, 2010

Acute ischemic stroke presents a leading cause of death and disability in the industrialized world. It is characterized by large-vessel thromboembolic occlusion and other pathophysiological factors, which contribute to cellular brain tissue damage.
In the last few years, increasing interest has been focused on regulated hypothermia as a method of
cerebral protection, representing one of the most effective treatment options in reducing further deterioration of brain tissue after acute ischemic stroke, if hypothermia is induced soon after the onset of neurological symptoms and maintained for an adequately long time period.
It is well accepted (based on animal studies) that hypothermia is remarkably neuroprotective when applied during or after global or focal ischemia. Protracted hypothermia of a few ◦C (30-33 C) can provide sustained behavioral and histological neuroprotection, whereas brief or very mild hypothermia (32-35 degrees C) only delays neuronal damage.
However, there are still many questions ananswered, for instance, when and for how long the induced hypothermia should be maintained. Therefore, clinical studies are running to test its efficacy in the
treatment and prevention on stroke in humans.
For more information, consult B. Schaller, R. Graf / Pathophysiology 10 (2003) 7–35

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