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The heat-dissipating mechanisms of the body, notably vasodilation and sweating, are impaired This effect has followed operations or other trauma in the region of the oor 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 remains at that level until death some hours or days later, or it 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 rare, and unexplained fever of moderate degree should not be attributed to a putative brain lesion Hyperthermia is also part of the malignant hyperthermia syndrome, in which, in a small number of cases, there is an inherited (autosomal dominant) susceptibility to develop hyperthermia and muscle rigidity in response to inhalation anesthetics and skeletal muscle relaxants (page 1272) It has been found to be due in these few instances to a defective ryanodine receptor Closely related is the neuroleptic malignant syndrome, which is the result of an idiosyncratic reaction to neuroleptic drugs (page 1025) 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; ie, they often produce hypothermia (a persistent temperature of 35 C 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 rst described by Gowers, has been found in association with a cholesteatoma of the third ventricle (Pen eld) and with agenesis of the corpus callosum (Noel et al) Episodically, there are symptoms of autonomic disturbance salivation, nausea and vomiting, vasodilation, sweating, lacrimation, and bradycardia; the rectal temperature may fall to 30 C and seizures may occur Pen eld referred to these attacks incorrectly as diencephalic epilepsy (page 466) 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 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 Cardiovascular Disorders with Hypothalamic Lesions Ranson demonstrated a number of autonomic effects upon stimulation of the hypothalamus; these effects as well as hypertension were recorded in Pen eld s case of diencephalic epilepsy, mentioned above Since Byer and colleagues description of large, upright T waves and prolonged QT intervals in patients with stroke, it has been appreciated that acute lesions of the brain particularly sub-.

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arachnoid hemorrhage and head trauma may be accompanied by changes in the electrocardiogram (ECG) as well as by supraventricular tachycardia, ectopic ventricular beats, and ventricular brillation Most of the same effects can be induced by very high levels of circulating norepinephrine and corticosteroids Considering the numerous catastrophic lesions of the brain as well as extreme emotional states that can provoke arrhythmias and other changes in the ECG, the hypothalamus, with its limbic connections and ability to mount a massive sympathoadrenal discharge, is the likely source of these autonomic changes Cropp and Manning found that the changes seen in the ECG, particularly cerebral T waves and other reversible repolarization abnormalities, could occur almost instantaneously (too quickly for attribution to circulating factors) during surgery for a cerebral aneurysm Again, the hypothalamus is implicated, but as yet no direct evidence links this structure to direct cardiac control Gastric Hemorrhage In experimental animals, lesions placed in or near the tuberal nuclei induce super cial erosions or ulcerations of the gastric mucosa in the absence of hyperacidity (Cushing ulcers) Gastric lesions of similar type are seen in patients with several types of acute intracranial disease (particularly subdural hematoma and other effects of head injury, cerebral hemorrhages, and tumors) In seeking causative lesions, as in patients dying with cardiac changes, one searches in vain for a lesion in the various hypothalamic nuclei A functional disorder in this region is nonetheless suspected Neurogenic Pulmonary Edema Following the original observations by Maire and Patton in humans, numerous cases of massive and often fatal pulmonary edema have been described in relation to catastrophic intracranial lesions head injury, subarachnoid and intracerebral hemorrhage, bacterial meningitis, and status epilepticus being the usual ones A sudden elevation in intracranial pressure is involved in most cases, usually accompanied by a brief bout of extreme systemic hypertension but without obvious left ventricular failure which is one reason the pulmonary edema has been attributed to a neurogenic rather than a cardiogenic cause Also, it has been shown that experimental lesions in the caudal hypothalamus are capable of producing this type of pulmonary edema, but almost always with the interposed event of brief and extreme systemic hypertension Both the pulmonary edema and hypertensive response can be prevented by sympathetic blockade at any level, suggesting that the adrenergic discharge and the hypertension it causes are essential for the development of pulmonary edema The rapid rise in vascular resistance and systemic blood pressure is similar to the pressor reaction obtained by destruction of the nucleus of the tractus solitarius, as described in Chap 26, making understandable the few instances of neurogenic edema that have followed acute lesions in the medullary tegmentum [as was seen in one of our patients (Brown et al)] At issue is whether the hypothalamus exerts a direct sympathetic in uence on the pulmonary vasculature, allowing a leakage of protein-rich edema uid, or if the edema is the result of sudden and massive overloading of the pulmonary circulation by a shift of uid from the systemic vasculature The latter theory, essentially one of momentary right heart failure, is currently favored but does not explain all aspects of the syndrome Likewise, the role of circulating catecholamines and adrenal steroids has not been fully elucidated These issues have been summarized in the text on neurologic intensive care by Ropper and colleagues.