Brain Hyperthermia During Physiological and Pathological Conditions: Causes, Mechanisms, and Functional Implications
Author: Kiyatkin E.A.
Source: Current Neurovascular Research, Volume 1, Number 1, January 2004 , pp. 77-90(14)
Publisher: Bentham Science Publishers
Abstract:
Although brain metabolism consumes high amounts of energy and is accompanied by intense heat production, brain temperature is usually considered a stable, tightly regulated homeostatic parameter. Current animal research, however, has shown that different forms of functional neural activation are accompanied by relatively large brain hyperthermia (2-3°C), which has an intra-brain origin; cerebral circulation plays a crucial role in dissipating this potentially dangerous metabolic heat from brain tissue. Brain hyperthermia, therefore, reflects enhanced brain metabolism and is a normal physiological phenomenon that can be enhanced by interaction with common elements of an organism's environment. There are, however, instances when brain hyperthermia becomes pathological. Both exposure to extreme environmental heat and intense physical activity in a hot, humid environment restrict heat dissipation from the brain and may push brain temperatures to the limits of physiological functions, resulting in acute life-threatening complications and destructive effects on neural cells and functions of the brain as a whole. Brain hyperthermia may also result from metabolic activation induced by various addictive drugs, such as heroin, cocaine, and meth-amphetamine (METH). In contrast to heroin and cocaine, whose stimulatory effects on brain metabolism invert with increases in dose, METH increases brain metabolism dosedependently and diminishes heat dissipation because of peripheral vasoconstriction. The thermogenic effects of this drug, moreover, are enhanced during physiological activation, resulting in pathological brain hyperthermia. Since brain hyperthermia exacerbates drug-induced toxicity and is destructive to neural cells, uncontrollable use of amphetamine-like drugs under conditions restricting heat dissipation from the brain may result both in acute lifethreatening complications and clinically latent but dangerous morphological and functional brain destruction.Keywords: brain; metabolism; cerebral blood flow; hyperthermia; metabolic neural activation; addictive drugs; emotional and physical activation; neurotoxicity
Document Type: Review article
DOI: http://dx.doi.org/10.2174/1567202043480233
Affiliations: 1: Behavioral Neuroscience Branch, National Institute on Drug Abuse - Intramural Research Program, 5500 Nathan Shock, Baltimore, Maryland 21224, USA.
Publication date: 2004-01-01
- Current Neurovascular Research (CNR) provides a cross platform for the publication of scientifically rigorous research that addresses disease mechanisms of both neuronal and vascular origins in neuroscience. The journal serves as an international forum for the publication of novel and pioneering original work as well as timely neuroscience research reviews in the disciplines of cell developmental disorders, plasticity, and degeneration that bridge the gap between basic science research and clinical discovery. CNR emphasizes the elucidation of disease mechanisms, both cellular and molecular, which can impact the development of unique therapeutic strategies for neuronal and vascular disorders.
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- In this Subject: Neurology & Psychiatry
- By this author: Kiyatkin E.A.

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