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Mechanisms of Hypothermia, Delayed Hyperthermia and Fever Following CNS Injury
Gordon, C., L. Katz, AND L. Leon. Mechanisms of Hypothermia, Delayed Hyperthermia and Fever Following CNS Injury. Journal of Neurodegeneration and Regeneration. Weston Medical Publishing, Weston, MA, 4(1):1-19, (2012).
Central nervous system (CNS) damage is often associated with robust body temperature changes, such as hypothermia and delayed hyperthermia. Hypothermia is one of the most common body temperature changes to CNS insults in rodents and is often associated with improved outcome. Although the acute hypothermia seen in rodents is rarely observed in humans, clinical methods to induce hypothermia have shown promise for the protection against CNS damage. The hypothermic response to CNS injury is thought to provide protection against the insult by reducing metabolic demands and the generation of harmful reactive oxygen species. The most common body temperature response observed in clinical studies of CNS damage is delayed hyperthermia, which is often referred to as "fever". This elevation in body temperature may persist for several days or be recurrent and episodic in nature, but regardless of its periodicity it is typically associated with poor prognosis to a variety of CNS injuries. The tendency to refer to this response as a fever is somewhat misleading since the mechanism(s) mediating this elevation in body temperature remain poorly understood. Interestingly, hyperglycemia is another pathophysiological response associated with CNS damage that aggravates morbidity and mortality. It is thought that elevated body temperature and hyperglycemia may have synergistic actions that are deleterious for recovery, although the mechanisms responsible for these effects remain to be elucidated. This review discusses the incidence of hypothermia and delayed hyperthermia during recovery from a variety of CNS insults and proposes putative mechanisms that mediate these responses as well as the potentially deleterious interaction of high body temperature with hyperglycemia.
Recent studies have found that rodents exposed to a variety of environmental toxicants undergo a delayed fever that may persist for days. This pattern reflects what is observed clinically in humans exposed accidentally to toxicants as well as following a variety of CNS traumas such as stroke. To date, there is not review of this field. This paper endeavors to review this field of work and to propose a possible mechanism of action to explain the incidence of fever in humans and experimental animals subjected to CNS injury.
Record Details:Record Type: DOCUMENT (JOURNAL/PEER REVIEWED JOURNAL)
Organization:U.S. ENVIRONMENTAL PROTECTION AGENCY
OFFICE OF RESEARCH AND DEVELOPMENT
NATIONAL HEALTH AND ENVIRONMENTAL EFFECTS RESEARCH LAB
TOXICOLOGY ASSESSMENT DIVISION