Human brain temperature: regulation, measurement and relationship with cerebral trauma: Part 1

Temperature has a major effect on survival in all animal species. Despite wide variations in climate, organ temperature is regulated ‘tightly’ by homeostatic mechanisms controlling heat production and conservation, as well as heat loss. Although less is known about the temperature of the healthy or injured human brain, mammalian brain homeothermy involves interplay between neural metabolic heat production, cerebral blood flow and the temperature of incoming arterial blood. Recent advances in invasive and non-invasive thermometry have allowed measurement of brain temperature to be made in man. In health, small differences only exist between local brain and body core temperature. Large (negative) brain–body temperature dissociation, observed in some patients after severe brain damage, does not appear to be a feature of cerebral homeothermy in healthy people. The extent to which changes in brain temperature reflect, or ‘drive’, secondary cerebral pathology remains uncertain in patients with traumatic brain injury (TBI). Raised temperature may be due to a regulated readjustment in the hypothalamic ‘set-point’ in response to inflammation and infection, or it may occur as a consequence of damage to the hypothalamus and/or its pathways. Diagnosis of the mechanism of raised temperature; fever v. neurogenic hyperthermia (regulated v. unregulated temperature rise) is difficult to make clinically. Whatever the cause, a 1–2°C rise in brain or body temperature, especially when it develops early after injury, is widely regarded as harmful. There is no clear evidence that fever per se leads directly to worsened neurological damage or poor outcome, nor evidence that antipyretic treatments (pharmacological or cold-induced therapies) preserve damaged brain tissue or result in a better outcome. Part 2 follows part one with a detailed analysis of the evidence for the significance of raised temperature on outcome after TBI.