Deliberate
hyperthermia has been used clinically as
experimental therapy for neoplastic and
infectious diseases. Several case fatalities have occurred with this form of treatment, but most were attributable to systemic complications rather than central nervous system toxicity. Nonetheless, demyelating
peripheral neuropathy and neurological symptoms of
nausea,
delirium, apathy, stupor, and
coma have been reported. Temperatures exceeding 40 degrees C cause transient vasoparalysis in humans, resulting in cerebral metabolic uncoupling and loss of pressure-flow autoregulation. These findings may be related to the development of
brain edema,
intracerebral hemorrhage, and
intracranial hypertension observed after prolonged
therapeutic hyperthermia. Furthermore, deliberate
hyperthermia critically worsens the extent of histopathological damage in animal models of traumatic, ischemic, and hypoxic
brain injury. However, it is unknown whether these findings translate to episodes of spontaneous
fever in neurologically injured patients. In a clinical setting
fever is a strong prognostic marker of a patient's primary degree of neuronal damage, and a causal relation with long-term functional neurological outcome has not been established for most types of
brain injury. Furthermore, in the neurosurgical intensive-care unit
fever is extremely common whereas
antipyretic therapy is only poorly effective. Therefore maintaining strict normothermia may be an impossible goal in many patients. Although there are several physiological arguments for avoiding exogenous
hyperthermia in neurologically injured patients, there is no evidence that aggressive attempts at controlling spontaneous
fever can improve clinical outcome.