3. Goat.—The frequent coincidence of gout and diabetes has been often remarked upon. In Germany, where gout is not common, the opportunity for observations of this kind is not often presented, and it is, therefore, not to be wondered at that we have to look for illus trations of this relationship to English and French authors espe cially. Their writings are rich in observation of this kind. Among Englishmen, Front, Bence Jones, Lauder Brunton and Sir Dyce Duckworth have especially emphasised this point; of the French writers we may mention Claude Bernard, Brongniart, Charcot, Bouchardat and Bouchard.
The connection declares itself in various ways. Often typical gout occurs in middle life ; later the attacks cease and glycosuria ap pears. Again cases are observed in which attacks of gout alternate with glycosuria (diabetes alternans). In a third group gouty symp toms and glycosuria are present at the same time. Most of the cases of this kind reported were of slight gravity, interfering little or not at all with nutrition, and not incompatible with a long life. Less benign were those in which diabetes existed first, the gouty symp toms appearing later (Bouehardat).
It has been previously remarked that sufferers from diabetes not uncommonly present an ancestral history of gout (hereditary alter nating gout).
An insight into the intimate relation between gout and diabetes has not been vouchsafed us. Our knowledge on this point is much less certain than on the connection between obesity and diabetes, and very naturally, since we know almost nothing of the true nature of gout. We are ignorant of the chemical processes which lead to an increased formation and excretion of uric acid, and the many tomes which have been written on this subject contain only the smallest fragments of real knowledge, the rest being pure hypothesis. Any further study of the intimate connection existing between diabetes and gout would therefore be unprofitable.
4. Nervous Diseases.—Diabetes is so often observed in individuals suffering from disease of the nervous system that a relationship of cause and effect cannot be gainsaid, but there is much discrepancy among writers as to the extent to which this relationship exists. Naturally every anomaly of the nervous system in diabetics is not to be regarded as the exciting cause of the glycosuria; for commonly enough the case is reversed, diabetes being the primary, and the ner vous affection (for example neuralgia, neuritis, or neurasthenia) the secondary condition. But even when this is carefully kept in view, every physician who has had many cases of diabetes in his practice can call to mind a number of instances in which the diabetes has made its appearance during the course of some nervous malady.
But when we go further and attempt to trace a connection between diabetes and any special lesions of the nervous system, we tread at once upon uncertain ground. There is little that can be said on this point. Glycosuria, as a chronic affection, follows cerebral lesions much more frequently than it does spinal or peripheral alteration. Among functional nervous diseases neurasthenia leads in an etiologi cal sense, hysteria being far behind. Diabetes occurs also in the' insane, yet the statistics of asylums show a smaller percentage of dia betics than do those of general hospitals. From a comparison of the statistics of the Charite Hospital in Berlin I gather the following : During the years 1890-1893, 23,825 patients were treated in the four medical divisions, among whom were 67 diabetics, or one diabetic for every 355 patients ; during the same period, in the psychiatric clinic of the Charite, out of 2,535 patients not one suffering from diabetes was found. These figures are large enough to deserve
attention.
If now we turn from this general survey to a consideration of the more important details, we find most worthy of note those cases in which diabetes has followed immediately upon an injury or concus sion of the brain. Cases of this kind are always most striking and belong to those against which objections can least often be urged. As regards the clinical forms of the disease so occurring, we find every grade of transition, from an insignificant glycosuria lasting only a few days or hours up to a disease presenting a complete picture of chronic diabetes mellitus.
We are fortunately in position to arrive, through the results of experiments, at an understanding of those cases of temporary glyco suria which follow an acute brain injury, whether this have been pro duced by external violence, by intracranial embolism, or by rupture of a vessel. We must recall Claude Bernard's pigiire, and also the fact that the same result has been observed to follow other acute in juries of the most varied character to the nervous system in animals. The reference to these experimental results is certainly justifiable, and all authors admit it. We have to assume that a centrifugal irritation passes from the injured portions of the central nervous system to the liver, causing this organ to give up its stores of glycogen. As then the consumption of sugar does not keep pace with the over-saturation of the blood, acute temporary hyperglycemia and glycosuria result.
Possibly now we are also warranted in assuming that, following upon a sudden injury of this sort, a permanent irritation proceeds, directly or reflexly, under certain circumstances from the organically injured or functionally diseased portions of the nervous system, and is transmitted to the glycogen-storing organs (muscles, liver, and other glands) and these exert a continuous opposing influence to the accu mulation of glycogen. This disturbance leads further to hyper glycdemia and glycosuria.
I must not neglect to mention that the participation of the pancreas is alleged even in neurogenous diabetes. In accordance with this doctrine we must assume that influences of either a restricting or a stimulating character are reflexly transmitted to the pancreas from the diseased nervous area, and these cause a disturbance of function. Opposed to this conception, however, is the fact that even in the most marked lesions of the nervous plexus surrounding the pancreas, only transitory glycosuria at the most, never permanent diabetes, is produced. This objection is, of course, not absolutely conclusive, but all explanations of what actually takes place in neurogenous dia betes must be regarded as yet as purely theoretical.
F. A. Hoffmann" has endeavored, from the study of a rich collec tion of clinical material, to form a picture of the peculiarities of neu rogenous diabetes. In this form of diabetes, he maintains, obesity is never developed. He gives further the following differential table: