Next after these gross mechanical lesions of the nerves are certain poisons to be named as productive of glycosuria; these are carbonic oxide, carbon disulphide, curare, morphine, strychnine, 'nitrobenzol, of amyl, and others. Asphyxiation, profuse hemorrhage, and intravenous injections of dilute salt solutions are frequently pro ductive of the same result.
Whenever under such and similar conditions glycosuria is pro duced, an abundant supply of glycogen must be presumed to be pres ent in the liver; in badly nourished, glycogen-poor individuals this result is not observed. In any case the duration of the glycosuria is measured by hours only.
There can hardly be any doubt that all the above-named injuries, and others similar to them, act in the main in the same way as the puncture at the floor of the fourth ventricle, viz., they lead to a dis charge from its reservoir of the previously formed glycogen, either by a direct influence upon the liver itself or indirectly through the intervention of the nervous system. Since the liver enters especially into consideration here, I have called all these forms of glycosuria " hepatogenous." 2. Clinical Forms (Alimentary G-lycosuria complicating other Dis eases).'--Possibly some of these experiments may have a bearing also upon true diabetes mellitus in man, but that is a point that cannot be considered here. We have primarily to determine how far these facts throw light upon glycosuria occurring in the course of other diseases, a condition to be clearly differentiated from true diabetes. The facts teach us that, under certain conditions, the glycogen reser voirs become, as it were, too narrow to hold large amounts of this sub stance. Does this storage insufficiency play any clinical role? In studying this question the attention of clinicians will be directed espe cially to diseases of the nerves, muscles, and diver, disturbances of the circulation (passive congestion of the liver), and poisoning. Indeed, we are already in possession of a series of facts in human pathology • which are so closely related to the results of animal experimentation that we can scarcely doubt that we have to do with identical processes.
In this category belong the rare transitory glycosurias following concussion of the brain (A. Fischer), cerebral apoplexy (011ivier,
von Frerichs, 'Schutz, Loeb, and others, and three personal observa tions of the author), severe neuralgia, and disturbance of the mental balance. In these cases the glycosuria lasts usually a few hours only, or at most a few days. It is nevertheless in just these cases that it is difficult to draw the line between transitory glycosuria and dia betes mellitug, for, in the first place, many of these acute neuroge nous forms of glycosuria pass over into chronic diabetes (Frerichs), and secondly, many instances are ou record in which individuals had suffered from temporary glycosuria following the influences above mentioned, and then subsequently, sometimes years later, acquired unmistakable diabetes mellitus. In these individuals apparently a latent diabetic disposition slumbered for a long time, to be awakened—at first only temporarily —by nervous influ ences. The whole history of acute neurogenous glycosuria and daily repeated experiences teach us that individuals react in very varying degree to the above-mentioned influences. The individual predisposi tion appears to be of more importance than the special form of lesion inflicted.
In this group belong also the acute forms of glycosuria, almost always disappearing iu a few hours, which follow poisoning by cer tain substances, such as morphine, hydrocyanic acid, mineral acids (rarely), nitrite of amyl, carbonic oxide, chloralamid, nitrobeuzol, anilin, ergotin (one case observed by the writer), etc. Here also are to be mentioned the rare instances of acute glycosuria described by Gans and Finkler as occurring during an attack of biliary colic. This form finds its analogy in the experiment of ligating the bile duct, which is followed by a rapid discharge of glycogen from the liver.
In view of the rare occurrences of spontaneous glycosuria in or ganic disease, the attempt has often been made to gather data relat ing to the sufficiency or insufficiency of the glycogen depot in various affections, by the exhibition of large amounts of sugar. As a rule grape sugar has been selected, in doses of from 150 to 200 grams— not more, since with larger doses even in healthy individuals a tran sitory glycosuria is produced (see page 43).