Bilateral lesions in the anterior parts of the hypothalamus, specifically of temperature-sensitive neurons in the preoptic area, may result in hyperthermia. The heat-dissipating mechanisms of the body, notably vasodilatation and sweating, are impaired. This effect has followed operations or other trauma in the region of the floor of the third ventricle but we have seen it most often after massive rupture of an anterior communicating artery aneurysm. The temperature rises to 41°C (106°F) or higher and either remains at that level until death occurs or drops abruptly with recovery. Acetylsalicylic acid has little effect on central hyperthermia; the only way to control it is by active evaporative cooling of the body while administering sedation. A less-dramatic example of the loss of natural circadian temperature patterns is seen in patients with postoperative damage in the suprachiasmatic area (Cohen and Albers) and suprachiasmatic metastasis (Schwartz et al). These types of lesions are invariably associated with other disorders of intrinsic rhythmicity, including sleep and behavior. It should be emphasized, however, that instances of “central fever” are relatively rare, and unexplained fever of moderate degree should not be attributed to an existing or putative brain lesion unless other causes have been evaluated.
Hyperthermia is also part of the malignant hyperthermia syndrome, in which extreme hyperthermia and muscle rigidity occurs in response to inhalation anesthetics and skeletal muscle relaxants (also discussed in Chap. 45). In some of these instances, it has been found to be caused by a mutation in the gene encoding the ryanodine receptor. The typical inheritance pattern is autosomal dominant but penetrance is incomplete; some affected members may develop congenital central core myopathy. Closely related is the neuroleptic malignant syndrome, which is the result of an idiosyncratic reaction to neuroleptic drugs (also discussed in Chap. 41). Wolff and colleagues have described a syndrome of periodic hyperthermia, associated with vomiting, hypertension, and weight loss and accompanied by an excessive excretion of glucocorticoids; the symptoms had no apparent explanation, although there was a symptomatic response to chlorpromazine.
Lesions in the posterior part of the hypothalamus have had a different effect; that is, they often produce hypothermia (a persistent temperature of 35°C [95°F] or less) or poikilothermia (equilibration of body and environmental temperatures). The latter may pass unnoticed unless the patient’s temperature is taken after lowering and raising the room temperature. Somnolence, confusion, and hypotension may be associated. Spontaneous periodic hypothermia, probably first described by Gowers, has been found in association with a cholesteatoma of the third ventricle (Penfield) and with agenesis of the corpus callosum (Noel et al). Episodically, there are symptoms of autonomic disturbance—salivation, nausea and vomiting, vasodilatation, sweating, lacrimation, and bradycardia; the rectal temperature may fall to 30°C (86°F), and seizures may occur. Between attacks, which last a few minutes to an hour or two, neurologic abnormalities are usually not discernible and temperature regulation is normal.
Chronic hypothermia is a more familiar state than hyperthermia, being recorded in cases of severe hypothyroidism, hypoglycemia, and uremia; after prolonged immersion or exposure to cold; and in cases of intoxication with barbiturates, phenothiazines, or alcohol. It tends to be more frequent among elderly patients, who are often found to have an inadequate thermoregulatory mechanism.