That some such economy is carried on within the organism in certain abnormal state, is to my mind out of question. On the one hand we find that in all cases of dyspnoea in consequence of deficient oxygen, the body temperature lowered; and when dyspnoea increases to such an extent as to cause clonic convulsions, the mercury column of the thermometer falls lower still, although under ordinary circumstances muscular contractions are invariably accompanied by increase of temperature. On the other hand in tetanus caused by strychnine, where respiration is often impeded, in consequences of a tetanic state of the respiratory muscles and where the blood is made at the same time unfit to absorb the usual amount of oxygen, in consequence of the direct toxic action of the poison-even in such a case we find a rise of temperature of 3 degree to 4 degree F. We find asphyctic convulsions have then a lowering effect upon body temperature while tetanic convulsions have the opposite effect. There must then be some particular arrangement which in a case of threatened asphyxia keeps the body temperature low inspite of the spasms. And the only way to explain it appears to me to be this: The heat evolved in the course of tissue metamorphosis is all converted into mechanical muscular work-into muscular contraction. But once granted that there is such a heat-moderating agency in some abnormal state of the organism, we are driven to admit that a similar agency must necessarily exist in the healthy body, as a physiological institution, so to say; for Virchow has proved long ago that pathological and physiological processes are the same in kind, varying only in degree and relativeness according to varying conditions of life.
The difference between tetanus and asphyctic convulsions as far as caloric evolution is concerned, would then, according as I understand it, consist in this, that in the former the proportion of energy liberated by muscular combustion is largely in favour of heat production, while in the latter, almost the whole of the energy developed by muscular and tissue combustion in general is employed in favour of the work of contraction giving rise to an actual caloric deficit.
I need not tell you that what has just been said with regard to asphyctic convulsions may be made applicable to the spasms- tonic or clonic-of cholera. This is especially the case in the spasmodic variety of cholera, where part of the spasms are really, as we have seen before, of asphyctic nature. In the non- spasmodic variety the origin of the spasms is different. They do not start from the medulla oblongata, but set in gradually in the measure as vomiting and purging are proceeding, partly in consequence of the increasing venosity of the blood, known as it is that the flow of venous blood through a muscle causes it to contract; and partly in consequence of irritation of the motor nerves brought on by their being deprived of water. Thus the spasms in the extremities are, to all appearance, primarily due to the venosity of the blood. They manifest themselves first in the parts most remote from the heart- in the fingers and toes-where the stagnation in the flow of blood is first felt. Later on there is the additional element of nervous irritation as already mentioned. The spasms on the other hand of the blood-vessels on the right side of the heart and of the vaso-motor nerves in general, appear to be of nervous origin from the very onset; they are due to the specific action of the cholera poison, and originate most likely within the vaso-motor centres. Of whatever nature and origin the spasms of the non-spasmodic variety of cholera may however be, they have this in common with the asphyctic convulsions, that they are carried on, at the cost of the scanty heat yet produced in the system so long as there is life-heat being actually converted into mechanical muscular work -into muscular contraction. As to the agency which presides over this economic process, I have already mentioned is to be, according to my opinion, a part of the function of the heat- regulating provision existing within our organism, and known by the name of caloric centre. The general idea with respect to the function of the caloric centre is this, that it regulates tissue metamorphosis and the combustion connected there with; irritation of the centre being supposed to inhibit metamorphosis. The caloric centre would accordingly stand in close connexion with the process of nutrition, or with the trophic nerves. According to my view on the subject, however, the caloric regulation stands in close connexion, not with the hearth of combustion, but with those tissues that are chiefly concerned with the expenditure of heat-the muscular system. Let us now inquire what facts have to say on the subject; let us go back to the experiments of Ferrier. He defined on the surface of the brain of cats, dogs, rabbits and monkeys, the different centres from which various movements of the limbs, face, and mouth and tongue, eyes and ears, etc., could be definitely excited. This gives us an idea in how far spasms may be cerebral in their origin. Since Ferrier`s discovery it has been found by Hitzig, Eulenberg and Landois that the ablation or destruction of regions ion close proximity to Ferrier`s motor centres is followed by exaltation of temperature in the opposite hind legs; on the other hand electrical stimulation of the same region lowered the temperature of the limbs of the opposite side. It would then appear that the cerebral heat regulating apparatus, is in fact, closely connected with the organs of locomotion, and not with the organ of nutrition. It is further evident, that the seat of that heat- regulating apparatus is not one caloric centre as was all along suspected, but could none the less never be localised; but that its seat is moreover to be looked for in the vicinity of the various motor centres, in other words that there is no caloric but many caloric centres, as many as these motor centres. It would further appear that in tetanus the motor centres are directly or reflexly excited, while the neighbouring parts are not; consequently there is unusual muscular contraction uninfluenced by any extraordinary inhibition on the parts of the corresponding caloric centres; and we have muscular contraction along with high temperature. In the case of asphyctic convulsions where the cause is haematic and therefore general in its operation, the irritation sets up in the motor centres of the brain in consequence of the venosity of the blood, naturally spreads to their vicinity, so that the very agencies that generate convulsions, stimulate the caloric centres, thereby causing them to exert their full inhibitory power and prevent a wasteful evolution of heat.
The regulation of heat is affected by nerve centres. Both the production and elimination of heat have, each of them their own regulating process. The thermotaxic control is, however, one that governs them both and connects their respective processes so as to result in a constant temperature. Trambe ascribed fever to retention of heat in consequence of irritation of the vaso-motor centres and consequent contraction and therefore diminution of blood circulation of the cutaneous capillary vessels. Experiments have, however, shown that pyrexia is accompanied by increased discharge of heat. It is even not true that the cutaneous vessels of fever patients are constantly contracted they vary, while heat is constantly discharged. Nor is the heat of fever patient constant, it varies. In fact febrile temperature is both inconstant and unstable-thermotaxis is impaired. Liebermaster thinks in pyrexia the index of the heat regulating machine is altogether changed, from being 98.4 in health, it becomes 102, 103, etc., and this irrespective of all other changes as to the amount of heat production or loss.
According to Dr. Burdon Sanderson excessive combustion cannot fully account for the excessive fever heat. There are, it is true, increased exhalation of carbonic acid and excretion of urea, but after calculation they do not represent a source of heat sufficient to cause the increased temperature of the body. We must, however, compare heat production in health with heat production in fever, under like circumstances-that is to say under like diet. Increase of food in health increases heat production; the fever patient on a a low diet, according to Dr. Sanderson, produces 50 Percent more heat than a man on full diet.
In the year 1885 Drs. Aronson and Sachs of Berlin exhibited on the occasion of the Berlin Medical Congress the following series of experiments. When a puncture wit a fine needle is made through the brain of a rabbit in such wise as to pass vertically through the medical side of the corpus striatum near the nodus cursorius of Nothnagel the temperature in the muscles and in the rectum promptly rises from 1/2 to 2 1/2 C, or say 2 1/2 to 4 1/2 F and remains high for many hours, returning ultimately to the normal again. The animal appears to be but little affected by th operation, and eats and moves about gaily…… The sensitive region is of no great extent and can be defined with considerable precision……By a highly ingenious method they succeeded in passing a weak electric current through the sensitive region, with out exciting any of the neighbouring parts, so as to make sure that it was stimulation of the nervous element and not destruction that causes the rise of temperature.
