On a theoretical background, hypothermia surmounts pharmacological neuroprotection by providing simultaneous effects on several mechanisms potentially relevant in the postischemic maturation of the damage. Measurements of the infarct size in animal models reveal that mild hypothermia is probably one of the most effective and documented neuroprotective intervention, both in focal and global ischemia models. As expected, hypothermia is more effective, and the results more consistent, when the time window for initiation of treatment is shorter than 6 h, with an apparent correlation between effect size and time window in the range of 0–6 h. There seems to be also an inverse relationship between temperature depth and reduction in infarct size. Mild hypothermia, such as cooling by 1°C or 2°C, is still associated with a noteworthy 20%–30% infarct size reduction. A few controlled studies in patients with ischemic stroke show feasibility and safety of cooling to a target temperature of 33°C–34°C, for 12 or 24 h, associated with antishivering pharmacological treatment. Hypothermia can be safely induced in acute stroke patients by infusion of iced saline, and the target temperature can be obtained and maintained by either surface or endovascular cooling, followed by controlled rewarming. Multicenter, randomized, phase III trials are ongoing to test the efficacy of the procedure.
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|Titolo:||Therapeutic hypothermia for acute stroke|
|Data di pubblicazione:||2014|
|Appare nella tipologia:||02a Capitolo, Articolo o Contributo|