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Psychosomatic Medicine 63:476-486 (2001)
© 2001 American Psychosomatic Society

ORIGINAL ARTICLES

Mechanisms and Mediators of Psychological Stress-Induced Rise in Core Temperature

Takakazu Oka, MD, PhD, Kae Oka, MD, PhD and Tetsuro Hori, MD,PhD

From the Departments of Psychosomatic Medicine (T.O.) and Integrative Physiology (T.O., K.O., T.H.), Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan; and the Department of Neurology (T.O., K.O.), Beth Israel Deaconess Medical Center and Harvard Medical School, Harvard Institutes of Medicine, Boston, Massachusetts.

Address reprint requests to: Takakazu Oka, MD, PhD, Harvard Institutes of Medicine 819, 77 Avenue Louis Pasteur, Boston, MA 02115. Email: toka{at}caregroup.harvard.edu

OBJECTIVE: Despite numerous case reports on "psychogenic fever," it remains uncertain how psychological stress raises core temperature and whether the rise in core temperature is a real fever or a hyperthermia. This article reviews studies on the psychological stress–induced rise in core temperature (PSRCT) in animals with the aim to facilitate studies on the mechanisms of so-called psychogenic fever in humans.

METHODS: To address this question, we reviewed the mechanisms and mediators of the PSRCT and classic conditioning of the fever response in animals.

RESULTS: The PSRCT is not due to the increased locomotor activity during stress, and the magnitude of the PSRCT is the same in warm and cold environments, indicating that it is a centrally regulated rise in temperature due to an elevated thermoregulatory "set point." The PSRCT caused by conventional psychological stress models, such as open-field stress, is attenuated by cyclooxygenase inhibitors, which block prostaglandin synthesis. On the other hand, the PSRCT elicited by an "anticipatory anxiety stress" is not inhibited by cyclooxygenase inhibitors but by benzodiazepines and serotonin Type 1A receptor agonists. The febrile response can be conditioned to neutral stimuli after paired presentation with unconditioned stimuli such as injection of lipopolysaccharide, a typical pyrogen.

CONCLUSIONS: Most findings indicate that the PSRCT is a fever, a rise in the thermoregulatory set point. The PSRCT may occur through prostaglandin E2–dependent mechanisms and prostaglandin E2–independent, 5-HT–mediated mechanisms. The febrile response can be conditioned. Thus, these mechanisms might be involved in psychogenic fever in humans.

Key Words: psychogenic fever • emotional hyperthermia • stress-induced hyperthermia • stress • fever • fever of unknown origin.

Abbreviations: CRF = corticotropin-releasing factor; GABA = {gamma}-aminobutyric acid; 5-HT = serotonin; ICV = intracerebroventricular; IL-1 = interleukin-1; IL-6 = interleukin-6; IFN = interferon; IM = intramuscular; IP = intraperitoneal; IV = intravenous; LPS = lipopolysaccharide; MIP-1 = macrophage inflammatory protein-1; {alpha}-MSH = {alpha}-melanocyte-stimulating hormone; PGE2 = prostaglandin E2; PO = per os (by mouth); POA = preoptic area of the hypothalamus; PSRCT = psychological stress–induced rise in core temperature; SC = subcutaneous; Tco = core temperature; TNF = tumor necrosis factor.




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