liver for their explanation. They are explained satisfactorily by that defect in the assimilative process by which the conversion of amylaceous and saccharine food is checked; the series of changes by which the non-nitrogenous elements of our food are ultimately converted into CO, and water is interrupted at the formation of glucose. This is the old chemical theory of Bouchardat, and one which is certainly in accordance with the facts observed in the class of cases to which we have alluded. Again, if glycosuria was the necessary result of the excessive formation of animal sugar by the liver, is it not strange that morbid anatomy should not present us with some constant lesion of the liver as the result of the long-continued hyperæmia to which the organ must have been subjected? It is well known that the most diverse lesions have been found in this disease in the lungs, liver, kidneys, and alimentary canal, and that excepting the nerve-lesions, which have been found in a few cases, pathological anatomy has furnished no clue to the seat of the disease.

It is, moreover, worthy of mention that the records of cases of lesion of the floor of the fourth ventricle, the locality in which it is claimed irritation gives rise to glycogenesis, do not uniformly present the symptom of glycosuria in their clinical history. My friend, Dr. Seguin, has furnished me with four such cases, in which nothing is said of the occurrence of glycosuria, though in all there was extensive lesion involving the ventricle and the upper part of the medulla. Again, it may be objected that the experiments upon which the reflex origin of diabetes mellitus is predicated prove more than the exclusive hepatic origin of the disease. Dr. Harley, in his excellent monograph upon diabetes, likens the production of sugar in the liver from reflex irritation to the muscular contractions which result in the frog's limbs from the application of the galvanic current to the sensory motor circuit. In the glycogenic function of the liver, he says, "The pneumogastric is the analogue of the sensory, and the spinal cord and splanchnic of the motory nerves of the frog's limbs, so that an irritation applied to any portion of the branches of the preumogastric nerves, spinal

cord, or sympathetic reflex glycogenic circuit, is as effectually followed by a secretion of sugar as the application of galvanism to the sciatic nerves of the frog's limbs is followed by muscular contraction." Thus, he continues, "Diabetes can be artificially established by applying the irritation to the extremities of the pneumogastric in the liver, as when stimulants are injected into the portal vein; or by irritating the pulmonary branches distributed in the lungs, as when chloroform is inhaled; or by applying galvanism to the cervical portion of the nerves, or by irritating their roots, as when injury is applied to the floor of the fourth ventricle; or by acting on the downward chain, as, e. g., when the splanchnics are divided." Now, this analogy is not quite so plain as it at first appears. The pneumogastric is a peculiar nerve, not only in the extensive distribution to some of the most important vital organs, the heart, lungs, liver, and stomach, but in its endowment with a specific sensibility, by which it plays an important part in the maintenance of the vital functions, so that an irritation applied anywhere in its course, or in the course of its numerous and complicated connections, may be followed by a variety of effects; and it seems just as possible that the glycosuria, which is said to be produced through the irritation of its pulmonary, hepatic, or gastric branches, is the result, in some cases at least, of a disturbance of the pulmonary or gastric functions, as of the hepatic; and this leads us to speak of the second point to which we wish briefly to call attention, viz., the interpretation of the neurotie element in the etiology of diabetes. The generally accepted explanation of the experimental production of glycogenesis through nerve irritation is, that it produces dilatation of the hepatic blood-vessels, a consequent hyperæmia of the liver, thus increasing its glycogenic function. Dr. Dalton, in the succinct and clear review which he gave at the last meeting of the Academy of the subject of hepatic glycogenesis, described the numerous and diverse conclusions which have been drawn by different experimenters in this field of inquiry. Admitting, however, what seems to be established by satisfactory evidence,

that sugar is formed in the liver, are we, therefore, justified in referring glycosuria in all cases to an exaggeration of this function?

This certainly has not been satisfactorily proved, and it has been reasonably suggested that the appearance of sugar in the blood of the general circulation, and in the urine, may be due sometimes to a defect in the pulmonary function, through which the normal sugar production of the liver escapes oxidation. We think that a careful consideration of the physiological experiments, as well as of the pathological conditions under which glycosuria occurs, will show that quite as marked disturbances were produced in the pulmonary as in the hepatic circulation by these experiments and lesions; and, therefore, that the glycosuria may be reasonably regarded as the result, in some cases, at least, by a disturbance of the pulmonary function. Dr. Brown Sequard has recently called attention, in a short paper in the London “Lancet," to the production of hæmorrhage, anæmia, œdema, and emphysema in the lungs, by injuries to the base of the brain. He states, as the result of a large number of experiments, "that in almost all cases of injuries by crushing or section of the pons varolii, ecchymoses were found in the lungs. Sometimes the whole lung was crowded with effused blood, and real pulmonary apoplexy existed. In some instances the effusion took place in the bronchial tubes. Injuries to other parts of the base of the brain, especially the crura cerebri and the crura cerebelli, are sometimes followed by the same effects on the lung, and it is extremely probable that a slight pressure upon the pons varolii by effused blood is sufficient to produce it. Injuries to the medulla oblongata, and to the spinal cord, have but very rarely caused an effusion of blood in the lungs." He further states, "A hæmorrhage is not the only immediate effect that can be observed after an irritation of the base of the brain by crushing or cutting; an anæmic condition, œdema, and emphysema can also be produced;" and M. Ranvier, a distinguished micrographer, who assisted Dr. Brown Sequard in these experiments, found "that some small parts of

the lungs, which were found perfectly white, were absolutely deprived of blood, no doubt through a spasm of the blood-vessels having emptied them of their contents." May not this be the explanation of the so-called tubercular lesions which are found to complicate some cases of diabetes?

When we consider the fact that the sugar found in the blood of the right side of the heart disappears in the passage through the lungs, it seems reasonable to suppose that the presence of sugar in the general circulation and in the urine, may sometimes depend upon defective pulmonary function, as well as upon excessive formation in the liver. It may be objected, that if this were the case, the presence of sugar in the urine would be oftener observed, considering the great frequency of pulmonary lesions; but it is possible, as Roberts observes, that the existence of pyrexia, in which there is an excessive degree of oxidation, may account for the sugar not appearing in the urine.

Dr. Draper alluded very minutely to the large number of experiments made by the distinguished physiologist, Schiff, in which he succeeded by a variety of mechanical irritations in inducing artificial diabetes. These were mentioned because they illustrate very remarkably the numerous varied morbid conditions under which sugar may make its appearance in the urine.

It is reasonable to infer from the results of Brown Sequard's experiments, which we have quoted, that there must have been pulmonary lesions in most, if not all, the cases which Schiff describes. Those experiments, especially, in which glycosuria was produced by interference with the circulation, must have caused pulmonary engorgement, and so determined a disturbance of function which would manifest itself by the phenomena of defective oxidation; and among these the presence of sugar in the blood may surely be reckoned.

As Dr. Smith confined himself mainly to the development of the neurotic pathology of diabetes, we propose briefly to explain the hypothesis which makes the proximate cause of dia

betes the sub-oxidation of the animal and the food sugars. This hypothesis is based upon the fact, that every atom of nitrogenous or non-nitrogenous food that enters the body passes through a series of changes that terminate in the formation of urea, carbonic acid, and water—these latter being the ashes, so to speak, that leave the body when the combustion of the food, through the action of oxygen, is complete. Physiological chemistry has not yet determined the number or the nature of the links in the chain of transformation effected in the food by the action of oxygen, but they are doubtless analagous, to a certain extent, to the changes observed in the oxidation of the substances we use as food, which may be produced by artificial oxidation outside of the body. We know, e. g., that starch is convertible into sugar, and that sugar is convertible into alcohol and CO, outside of the body by a process of oxidation; and physiological experiment has demonstrated that starch, when acted upon by the saliva or pancreatic fluid, is converted into

sugar.

Now, we know that certain cases of diabetes are relieved, and in many instances cured, by a withdrawal of amylaceous. and saccharine food. The inability to convert or assimilate this kind of food seems to constitute in these cases the essential cause of the glycosuria. We are ignorant of the cause of this interruption to the complete conversion of the starch and sugar; we do not know whether it is that there is an insufficient amount of proper ferment, supposed to exist in the saliva and intestinal secretions, or whether there is, what amounts to the same thing, an excess of non-nitrogenous food, or whether there are other inexplicable conditions wanting to the thorough oxidation of this form of food. Whatever may be the cause of the failure in these cases to convert the non-nitrogenous food into its ultimate elements, the fact seems incontestable that there is a distinct variety of diabetes mellitus which is produced solely through this defect in the process of digestion, and is entirely independent of hepatic glycogenesis. But there is another class of cases in which dietetic restrictions are followed