Profoundly impressed with the difficulties that attend a purely humoral theory of gout, Cullen and many of his followers, more recently Sir Dyce Duckworth, have sought in the-nervous system a controlling influence over the manifestations of the disease. The effects of mental fatigue and violent nervous disturbance in the deter mination of an attack, the well-known nervous perturbations that ac company inflammation of the joints, the fugitive and migratory char acter of the phenomena, the intimate connection between certain arthropathies and morbid states of the central nervous system, as in tubes dorsalis, all seem to indicate that gout, if not a nervous disease, is most profoundly influenced by nervous action. A kindred disorder —arthritis deformans—has often been conjectured to be the conse quence of perverted nervous influences. If so, why may not gout, also, be a reflection of cerebro-spinal derangement? It is undoubtedly true that the nervous system does intervene most actively in all the phenomena of acute gout. Its functions are radically modified during the course of chronic, senile gout. But if we meditate upon the incipiency of the malady, as it is developed in previously healthy subjects without antecedent heredity, we shall discover that the nervous symptoms are secondary to the action of morbid causes from without. It is the unfavorable climate, the de ficient exercise, the luxurious diet, the special beverage, that is in evidence long before the manifestation of any morbid nervous phe nomena. But when the gouty constitution already exists, either as an inheritance or as an original acquisition, every function is liable to derangement, and the signs of diathetic disorder may be traced in every organ and function. A vicious circle is thus established, so that disturbance in one function excites disorder in another. The nervous system intervenes as a bond of communication between the various structures of the body, and opens its paths for the distrib a tiou of morbid movement, somewhat as the circulating fluids serve to convey morbid matter to every. part of the organism. Of any more radical or efficient participation of the nervous apparatus in the gen esis of gout, there is no satisfactory evidence.
Quite recently, Rachford, of Cincinnati, has made a number of interesting observations (Medical Xews, May 26th and Nov. 3d, 1894) on the action of paraxauthin as a factor in the etiology of migraine. He confirms the results obtained by Haig in similar cases, regard ing the increased excretion of uric acid compounds in connection with the paroxysms of headache or epileptiform convulsions that some times replace the headache. He also finds that coincidently with this evacuation of urates there is a decided increase of paraxanthin in the urine. This incompletely oxidized nitrogenous compound is
present in an almost infinitesimal quantity in ordinary urine; but, in cases of migraine and migrainous epilepsy, it and the other len comaines of the xanthin group are discoverable in relatively large quantities in the urine. According to Salomon, one litre of healthy urine contains only one milligramme of paraxanthin; while from the same quantity voided at the time of a migrainous epileptic attack, Bange and Rachford, employing the method of Salkowski and Salo mon, obtained a cubic centimetre of the substance in the form of a highly concentrated solution giving all the reactions of paraxanthin. One minim of this solution injected into the peritoneal cavity of a full-grown mouse produced great exaggeration of reflex excitability. This was followed in two minutes by tetanic contraction of all the muscles, which continued almost without intermission for three hours, until death occurred. From these experiments it is evident that, although uric-acid compounds are not poisonous, they may be accom panied by other kindred substances that are intensely lethal. Haig and Bouchard have demonstrated the excessive presence of urates iu the aggregate urine that is discharged during and after the attack of gout. also made clear the gouty affinities of hemierania. This additional research of Rachford shows that the other nitrogenous excreta of the uric-acid group are simultaneously increased when orates are redundant iu the urine. Taking into consideration their intensely poisonous character, it seems not improbable that they may exert considerable influence in determining the symptoms of the arthritic crisis. At any rate, these experiments serve to indicate the path to be followed in future researches into the physiological chem istry of gout.
We are therefore, at the conclusion of this widely extended survey, hrought to a conception of gout as a fundamental derange ment of the constitution, that may be either inherited, or acquired through a persistent course of insufficient muscular exercise, gluttony, and intoxication with highly acidulated alcoholic and etherealized beverages, causing disorder of digestion, assimilation, anabolism, and elimination, with all their attendant train of morbid symptoms, accompanied by a deposit of solidified urates infiltrating the tissues in and near the joints, culminating in violent nervous crises connected with articular inflammation, and tending to the final establishment of permanent disease, principally involving throughout the entire body the organs of locomotion, circulation, and excretion.