eases of hyperpyrexia we, therefore, regard as of neurotic origin—as due to some cause which exercises a paralyzing influence on the heat-inhibiting function. Pyrexia may result either from in creased production or from defective inhibition, but hyperpyrexia is clue only to defective inhibition.
In the cases instanced there has been a direct lesion of the nervous centres to explain the paralysis of inhibition. Other cases there are in which hyperpyrexia is as marked, but in which the sequence of events by which it is brought about is not so apparent. Rheumatic hyperpyrexia is a case iu point. Another is heat apoplexy ; and it will lead to a clearer understanding of the whole subject if we premise what we have to say regarding rheumatic hyperpyrexia by a brief consideration of the process by which heat apoplexy is brought about.
That continued exposure to a high temperature is likely, in a native of a temperate climate unaccustomed to such exposure, to cause disturbance of the thermal apparatus there can be no doubt.
Heat is an excretory product requiring to be eliminated; its chief seat of formation is the muscles ; its main channel of elimination is the skin; a high temperature of the atmosphere necessarily inter feres with such elimination, because in such an atmosphere heat can not readily be thrown off. Heat-elimination being thus checked and heat-production continuing as usual, heat must accumulate in the system, unless some agency steps in either to increase elimination or diminish formation. Under ordinary circumstances nature provides the remedy; for the same atmosphere which makes heat-elimination difficult causes also increased activity of the skin, and so meets the difficulty which itself creates ; while the general influence of residence in a hot climate leads to habits of life which diminish tissue metabo lism and heat-production; thus the risk of beat-accumulation is dim inished at both ends. But circumstances every now and then arise which break through these habits. Such circumstances are those which call for exposure and muscular effort during the heat of the day, as in the case of soldiers on the, march. Tissue metabolism and heat-production are stimulated, while the body is exposed to a temperature which makes a corresponding increase in heat elimina tion difficult. Nature guards against this danger by restraining heat production. This she does by increased activity of the heat-inhibiting function. The difficulty in the present case is the throwing off of the heat in consequence of the high temperature of the surrounding atmo sphere. This difficulty only creates a necessity for more vigorous ef
forts on the part of the heat-inhibiting centre; this centre continues to work at high pressure, and struggles to keep the temperature down till over-stimulation leads to exhaustion; the struggle is too much for it, its efforts become feebler, it gets more and more unfit to cope with the difficulty, and ultimately, overcome by fatigue, it ceases to act. Thus is removed the last safeguard, heat-production goes on apace, heat rapidly accumulates in the system, and heat apoplexy with its attendant hyperpyrexia results. What takes place in the thermic centre in such circumstances is the counterpart of what takes place in the respiratory centre, when an excess of carbonic acid in the at mosphere, by the ordinary laws of diffusion, prevents the due elimin ation of that gas from the blood. The first effect of an increase of carbonic acid in the blood is to stimulate the respiratory centre, and cause increased force and frequency of the respiration. If the amount of gas in the atmosphere be so great as to make its due elimination impossible, that gas accumulates more and more in the blood; the respiratory centre gets fatigued, its efforts become feebler, the res pirations become slower, the interval between them longer, and finally they cease. The cause of their cessation is paralysis of the respira tory centre induced by over-stimulation and fatigue; and the cause of this is not the taking in of carbonic acid from without, but the im possibility of eliminating in an atmosphere of that gas the carbonic acid which is formed in the system. So in heat apoplexy, it is not the heat of the surrounding atmosphere which raises the temperature of the body ; but in such an atmosphere heat cannot be properly eliminated, it tends to accumulate in the blood, and the only way to prevent disas ter is to limit heat-production. With this object the heat-inhibiting centre is stimulated to make unusual efforts. In most cases it suc ceeds, and the only evidence of the struggle is excessive perspiration and a sense of exhaustion. But the effort may be too much for it, it gets fatigued, its efforts become feebler, production goes on apace, inhibition is in abeyance, the reins are cast loose, and hyperpyrexia results. Thus is explained the hyperpyrexia of heat apoplexy.