Cabanac M, Massonnet B
Rev Neurol (Paris). 1980;136(4):285-302.
Though the same symptoms are observed in either hyper- or hypothermia, the etiology may be of four different types: 1) the thermoregulatory mechanisms may be insufficient to adapt to temperature extremes in normal subjects; 2) there may be modifications in peripheral thermoregulatory responses, when the patient compensates for the deficiency or excess by other thermoregulatory responses: the internal temperature is then not distrubed but is not stable; 3) a central lesion causing loss of ability to oppose low temperatures results in hypothermia with coma as soon as the subject is exposed to cold. Loss of ability to oppose heat is not encountered: it is superimposable on the hyperexcitation of the centers that oppose heat; 4) modifications in thermoregulatory responses are mainly evident as fever, a protective defense reaction of the organism wich should be supported rather than fought. The inverse syndrome, if it exists, is difficult to distinguish from the loss of ability to oppose cold. The term of "anapyrexia" is suggested for this latter condition. Whatever the diagnosis, measurment of rectal temperature is insufficient for diagnosis, and thermoregulatory responses have to be evaluated. Therapy for the same symptom may, in fact, be inversed depending on the etiology. It may well be that thermoregulatory function is poorly understood because of its true importance. Possessing no specific organs, it uses the various reactions that have appeared during phytogenetic development to ensure thermal homeostasis. It acts permanently through multiple, independent, regulatory loops allowing many compensatory mechanisms. This underlines, in an indirect manner, the need for the organism to maintain at all costs a constant temperature. This permanent thermal homeostasis implies that only severe disorders result in hyper- or hypothermia, that major disturbances are rapidly fatal, which emphasizes the fundamental importance of thermorgulation.