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Rheumatic Hyperpyrexia

temperature, heat, increased, nervous, rise, tissue, stimulation and symptoms

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Every now and then a case of acute rheumatism occurs which, after presenting the symptoms of the malady in the ordinary form, suddenly develops alarming nervous symptoms, with a temperature rapidly rising to 107°, 108°, 109°, or even higher, and a tendency to death by coma. Our knowledge of this condition is of recent date, and is one of the results of the more accurate clinical observation to which the use of the thermometer has led. There can be no doubt that many of the cases which our fathers described as cerebral rheu matism were cases of what we would now call hyperpyrexia.

This condition is not peculiar to acute rheumatism. It may arise in the course of any acute febrile ailment, in typhoid fever, measles, pneumonia, pycemia, etc. ; or it may be symptomatic of tumor of the brain, hemorrhage into its substance, or of other injury to nerve cen tres. We find it in its simplest and plainest form as it presents itself in heat apoplexy. Indeed the symptoms of heat apoplexy, its mode of fatal termination, and the appearances presented after death are exactly those which we find present themselves in hyperpyrexia, as it occurs in rheumatic fever, pneumonia, typhoid fever, and other febrile diseases.

Hyperpyrexia is not a disease per se; it is a morbid condition which may arise in the course of many ailments. It essentially consists in great rise of temperature, marked nervous symptoms, and a tendency to death by coma. Prominent nervous symptoms are as essential to its existence as the very high temperature to which it owes its name.

It has been supposed by some that the high temperature of the blood causes the disturbance of the nervous centres. The objections to this view are : First, that it gives no explanation of the occurrence of the high temperature; Second, that the temperature of hyperpyrexia may occur, as it not unfrequently does in relapsing fever, without causing any distur bance of the nervous system.

There can be no doubt that the process is the reverse of this and that the high temperature is a result of disturbance of nerve centres, ranking with the nervous symptoms, and like them due to the disturb ing action of some morbid agency on these centres. It is not simply aa; exaggeration of the pyrexia of ordinary febrile attacks, but a mor bid condition implanted on the pre-existing fever. How is it brought about ? The thermal apparatus of the body consists: 1. Of the tissues in which heat is formed; 2. Of the surface from which heat is eliminated; 3. Of a central controlling power in the nervous centres; 4. Of nerves connecting this with the heat-forming parts of the body; 5. Of nerves connecting it with the heat-eliminating surface.

The harmonious working of these different parts of the thermal ap paratus gives rise to the phenomena of thermogenesis, and the general result is a persistent temperature of 98.4°. Interruption of this har mony causes the temperature to rise or fall. Fall of temperature is due either to lessened formation or increased elimination of heat. Rise of temperature is produced either by increased formation or de creased elimination.

Rise of temperature due to direct stimulation of the process by which heat is formed must be brought about by an agency which increases tissue metabolism. Heat is an excretory product, a result of retrograde tissue change, and cannot be produced apart from that change. To say that heat could be directly brought about by stimu lation of a heat-producing centre, without increased tissue change, would be to place heat as a product on the same level and in the same category as volition and emotion, which is absurd. Increased heat due to direct stimulation of the heat-producing process must be due to the operation of some agency capable of causing increased activity of tissue metabolism. We can no more have increased formation of heat without increased activity of the processes during which heat is formed, than we can have increased formation of urea or increased formation of carbonic acid without increased activity of the processes during which they are formed. That the continuance of normal tissue metabolism is dependent on influences conveyed to the tissues by the trophic nerves is undoubted. And it is quite conceivable that stimu lation applied to the centres whence these trophic nerves proceed might, by causing increased activity of tissue metabolism, give rise to increased production of heat. The experiments of Messrs. Aron sohn and Sachs, in which electrical stimulation of a particular portion of the corpus striatum produced a rise of temperature varying from to 4 degrees Fahrenheit, would seem to indicate that fever may be produced by direct stimulation of a certain portion of the nervous centres; and the possibility of such a result must be kept before us in investigating the mode of production of the febrile phenomena of any given disease. But equally must it be borne in mind that such a result could be brought about only by causing increased activity of the metabolic changes by which heat is formed in the tissues. Such a nerve centre can be only one portion of the heat-producing appara tns, and it is quite possible that stimulation applied to other parts of this apparatus might cause the temperature to rise without primary stimulation of a nervous centre.

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