Body temperature regulation, which is tightly controlled by several mechanisms in healthy individuals, is often altered after an acute brain injury (ABI) because of either non-infectious (i.e. tissue damage, systemic or cerebral inflammation, vascular injury, hemorrhagic lesions, deep venous thrombosis) and/or infectious causes. As such, ABI patients often experience fever (variously defined as a body temperature exceeding 37.5 to 38.5 °C), regardless of the type of brain disease and site of temperature measurement. In both experimental and human studies, fever has been associated with exacerbated ischemic injury, cerebral edema, intracranial hypertension and with temporary neuro-worsening; moreover, ABI patients experiencing fever had also an increased risk of mortality and of poor neurological outcome. Preventing and/ or treating fever is therefore currently implemented and considered standard of care in the clinical management of ABI patients. Moreover, lowering body tempera- ture below normal ranges (i.e. hypothermia) can reduce intracranial pressure and provide some neuro-protective effects, although its benefits in clinical studies remains highly controversial. The term “targeted tempera- ture management” (TTM) encompasses these different approaches; however, the optimal method to provide optimal TTM is unknown
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