Besides dominating heat-production the nervous centres control heat-inhibition, and by so doing keep the temperature at the normal standard in health, and in disease prevent it from passing due bounds.
Inhibition restrains and regulates functional activity, as the reins restrain and regulate the pace of a spirited horse. Slacken the reins, and he hastens his pace; let them go, and he is off at the gallop. Inhibition is an active, not a passive agency, and is in constant opera tion. This is well exemplified by the action of the vagus on the heart; stimulation of that nerve slows the heart's action, and if the stimulus be strong enough, may arrest it altogether, the arrest taking place in diastole. But the nervous system which supplies thi.: in hibiting force supplies also another, which, reaching the heart by another channel, has exactly the opposite effect: it stimulates the heart to increased activity. These two forces are in constant opera tion, and so counterbalance each other that the heart is normally kept beating at the rate of about seventy a minute.
There is no organ whose normal amount of work represents the full measure of its capacity ; there is no function whose normal state of activity represents the full possibility of its performance. Each is restrained and kept within physiological bounds by the inhibiting action of the nervous system. Tissue metabolism is no exception to the rule. Normally, tissue formation and tissue disintegration coun terbalance each other. But let the reins be slackened, let inhibition of metabolism be impaired, metabolism is necessarily increased and pyrexia results. Let the reins be cast loose, let inhibition be para lyzed, and metabolism, freed from control, is off 'at the gallop, and hyperpyrexia results. Hyperpyrexia may be defined as paralysis of inhibition of metabolism; paralysis of heat-inhibition being only part of the process.
The clearest and most undoubted cases of rise of temperature re sulting from paralysis of heat-inhibition are those in which such rise occurs as a result of a lesion of nerve centres—cerebral tumors, cere bral hemorrhage, or injury to the cervical portion of the cord.
It is impossible to regard the results of such lesions, consisting as they essentially do of pressure upon, or laceration of, a portion of the nervous centres, as other than paralytic in nature. The effect of all such mechanical lesions is not to increase, but to impair or abol ish, function—to produce more or less paralysis. The only way in
which a destructive and non-inflammatory lesion could cause tempera ture to rise is by impairing that function which normally prevents it from rising—in other words, by impairing heat-inhibition. Rise of temperature thus produced will vary according to the extent of the lesion; in slighter injuries there may be no serious damage to the nervous centres, and no greater rise of temperature than is noted in cases of cerebral hemorrhage in which the sauguineous effusion is small and does not open into the ventricles. In more extensive lesions, in which these centres are more seriously damaged (as in severe cases of cerebral hemorrhage in which the effusion is more ex tensive and tears its way into the ventricles), the temperature rises rapidly and to a much higher point; while the highest temperature of all is noted in cases of crushing of the cord, in which the heat forming parts of the body may have their connection with the heat inhibiting centres cut off more completely than is likely to be the case in any intracranial Admitting that the nervous system possesses the power to control and limit heat-formation and prevent undue rise of temperature, we have no difficulty in the maladies and injuries to which reference has been made, in attributing the increased body heat to interference with that function. The temperature rises because the reins are slackened. The sequence of events seems to admit of no other explanation. Carrying on this line of argument we cannot fail to see, not only that the rise of temperature thus induced must be directly as the extent to which heat-inhibition is impaired, but that paralysis of this function, by abolishing inhibition and leaving heat-production in uncontrolled possession of the field, must lead to hyperpyrexia. And the more we consider the pathogenesis of febrile heat, the more apparent does it become that impairment of inhibition is a much more likely cause of hyperpyrexia than is direct stimulation of heat-production. Heat inhibition remaining unimpaired, tissue metabolism could not cause those very high temperatures which characterize some cases of hyper pyrexia. Heat-inhibition being paralyzed, the temperature cannot fail to rise, and to rise rapidly, so long as tissue metabolism and heat-production continue.