prove that there probably is some such internal secretion present. This is somewhat similar to the fact that we know that certain diseases are infectious and due to some micro-organism long before that organism has been discovered. One fact which goes to prove the above, is the following: Stimulation of the sympathetic branches which supply the pupil causes a dilatation of the pupil. If we cut the autonomic branches supplying the pupil we get a constant dilatation of the pupil which is due to a constant stimulation of the sympathetic system, which now has no inhibition. So it is probable that these two systems are under constant stimulation of certain internal secretions and that one system antagonizes the other in such a way that normally the action of the two systems just balances. In some individuals however, the balance does not keep even so that some lean more toward stimulation of the sympathetic system. and some more toward that of the autonomic system, that is, in some people more adrenalin is being secreted and in some more pilocarpoid secretion is being produced. If the above is true, individuals who lean toward the autonomic system, ought to react less to a subcutaneous injection of adrenalin than those who lean more toward the sympathetic system, and this fact has been proven to be true by experiments on a large number of cases. Stimulation of the vagus causes a slow heart. It also causes contraction of the bronchial muscle, increases gastric secretion, increases peristalsis, etc. Therefore, if people lean more toward the autonomic system, they ought to present some of the above named symptoms and it is found that they do. To this class of people who lean more toward the stimulation of the enlarged vagus system, Eppinger applies the name of vagotonikers. It is known that atropine paralyzes the vagus and if the above is due to a greater stimulation of the greater vagus system, then an injection of atropine should relieve the above named symptoms at least for a time and it does, as can easily be shown by the action of atropine in relieving the bronchial spasm in an asthmatic attack. According to this theory, asthmatics belong to the above class of vagotonikers, who have an increase stimulation of the autonomic or enlarged vagus system, which the pilocarpoid secretion stimulates. This increased secretion causes at times a bronchial spasm and hence an attack of asthma. As before stated, asthmatics usually have an eosinophilia and an eosinophilia is usually found in people belonging to the class of vagotonikers. It has further been shown that these vagotonikers are people in whom anaphylaxis is more liable to occur. Strumpell is more inclined to attribute the cause of bronchial asthma to a swelling of the bronchial mucosa, with an increase of the bronchial secretion and he also points out that this secretion neurosis is found in other parts of the body of the same person, such as a colica mucosa and also points out that they are very liable to urticaria and eczemas, so he places the people under a type which Czerny of Strassburg classifies as having the exudative diathesis. Sometime ago, Carmalt Jones claimed that the dyspnoea of bronchial asthma was caused by a specific bacterial toxin. In a case of bronchial asthma, a bacillus was found in the sputum in almost pure culture. It was insolated and seemed to be a short immotile rod with rounded ends. The bacillus grew readily on ordinary culture media and did not ferment sugar. A vaccine was prepared and the dyspnoea stopped after the injection of 20-30 million bacilli. At the end of three months the symptoms returned but yielded to a repetition of the vaccine treatment. Up to the time of his report, 52 cases had been treated with satisfactory results. I have not heard or seen anything in the literature of late years about the above, so this treatment in all probability was found not to be all it was hoped for by the author. That asthma is due to many reflex conditions of nose, etc., is known by you all, so I will no longer take your time by explaining the same. It can readily be seen that individuals classified as having the exudative diathesis of Czerny and as Vagotonikers by Eppinger, are especially liable to anaphylaxis and it is along these lines that I believe the etiology of at least some cases of bronchial asthma can be best explained. LITERATURE. Lancet, October 22, 1910, G. Billard. Medical Record, August 5, 1911, Editorial. New York Medical Journal, January 7, 1911, Moschcowitz. Vagotonie (pamphlet), Eppinger. Spezielle Pathologie und Therapie, Grumpell. Allergie, Von Pirquet. Journal Medical Research, April, 1910, Bladwin. Archives Int. Med., June 15, 1909, Weaver. Archives Int. Med., June 15, 1909, Anderson and Rosenau. Journal A. M. A., September 17, 1910, Meltzer. Journal A. M. A., December 2, 1911, Herrick. Journal A. M. A., January 20, 1912, Grinnan. New York Medical Journal, January 21, 1911, Barach. Wiener Klin Wochenshrift, November 11, 1910, Kraus. St. Petersburger Med. Woch., XXXIV, 1910, Carnalt Jones. Medical Reviews. Management of Toxaemia of Pregnancy. By A. B. SOMERS, M. D., Omaha. Pernicious vomiting and eclampsia are in a degree unfortunate terms, in that they give only a single symptom which in no way explains the underlying condition back of these symptoms, and in case of eclampsia the condition may be absolutely alarming and not recognized until the occurrence of the convulsive seizure. The term toxaemia refers to an underlying pathological condition that is operative in both vomiting and eclampsia, and if not identical in both instances, is amenable, in a large degree, to the same plan of treatment The arterial symptoms are not identical, for with vomiting there is often a condition of hypo-tension, while in eclampsia there is a condition of hyper-tension. Notwithstanding these conditions the importance of dilution of toxines and eliminative treatment is practically the same. This difference of tension is noticeable only in the early stages of pregnancy, there being no difference so far as my observation extends in the pulse of vomiting or eclampsia during the latter months of pregnancy. While the pathologists are discussing the ultimate cause of eclampsia, if there be one, aside from the existence of pregnancy-doubtless there are more than one-the clinician is obtaining fairly satisfactory results from therapeutic resources that are in a degree familiar to all of us. In discussing this question it might be well to eliminate nephritis, diabetes, serious heart lesions, pernicious anemia or other serious organic disturbances afflicting the pregnant woman. Tweedy, of the Rotunda Hospital, holds that eclampsia is a general toxaemia, due to increased metabolism and increased elimination caused by the presence and demands of the foetus on the maternal organism. In this theory the severe headaches, pernicious vomiting and albuminuria are classified with eclampsia and regarded as having a common origin. There is a curious resemblance between diabetic coma, uremia, yellow fever and phosphorus poisoning to eclampsia in their pathology and clinical symptoms. Alterations in the liver, acute hepatitis, necrosis and cloudy swelling or fatty degeneration are common to both groups. The increased viscidity of the blood, its decreased alkalinity in diabetic coma and the socalled acid intoxications, are present in the advanced stages of eclampsia. Headache, lethargy, pruritus, loss of appetite, nausea, flashes of light, tremor, etc. are common symptoms of eclampsia as well as of the toxaemias of the non-pregnantTweedy lays emphasis on the difficulty of differentiating between the convulsions of eclampsia and those of other toxaemias, and the comparative ease with which they can be differentiated from epilepsy." The following factors, according to J. S. Lawrence, Journal Surg. and Obstet., are considered to contribute to the sup port of this theory. First. Eclampsia occurs more frequently in multiple than in single pregnancies. Second. In England and Ireland it tends to occur when the weather is damp and cold. Third. The birth of the child or its death in utero improves the maternal condition. Fourth. Albuminuria accompanies eclampsia. Fifth. The kidney diseases subside and do not tend to recur in subsequent pregnancies. The treatment is eliminative because it is claimed that when the waste products can be eliminated and the nitrogenous intake can be reduced recovery is insured. It would appear that we know enough about the ultimate causes of pernicious vomiting and eclampsia to know that they are due to pregnancy complicated by toxaemia, the toxaemia being due to a variety of causes. These facts furnish us with sufficient knowledge to establish a reasonable working hypothesis in the management of these cases. Knowing the danger that threatens every pregnant woman, and the means of prevention, it is fair to state that the number of cases of eclampsia that will occur in the experience of any practitioner will depend largely upon his "eternal vigilance" in the application of these principles of treatment from earliest pregnancy, through labor and the early days of the puerperium; for occasionally convulsions will occur several days after confinement. Prevention then is a question of vital importance and there are three points in the way of prophylaxis that should be emphatically impressed on the mind of every pregnant woman. First-An abundant amount of exercise in the open air. Second-The ingestion of large quantities, one quart or more daily, of pure water between meals. Third-Keep the bowels in an open condition by fruits, vegetables and if need be, laxatives, the alkaline salts or mineral water being preferable for this purpose, owing to the tendency to acidosis. The application of these three simple rules would practically prevent the occurrence of pernicious vomiting and puerperal eclampsia. Regarding the treatment of eclampsia I choose to consider it under three heads: First-Management during the convulsive seizure. Second-Dilution of toxines and promotion of secretion and elimination. Third-Emptying of uterus. I am fully aware that the general concensus of opinion would place emptying the uterus in advance of promotion of elimination, but there are some notable exceptions to this opinion and it is well to remember that emptying the uterus does not remove the toxaemia which, after all may be said and done, is a very fundamental cause, and while this may be a good rule for the surgical experts inside institutions, I believe it to be a poor rule for the every day practitioner in general practice. The facts are that women die of toxaemia after delivery, and women frequently have their first convulsions after delivery. The first eclampsia I ever saw the convulsive seizure came on shortly after completion of the third stage of labor. Another point to be considered is that convulsions are often precipitated by the shock of labor and the shock of any operative procedure may result in bringing on a convulsion or increasing the attacks if they have already begun, unless the patient be under the influence of an anesthetic, so that in case of an eclamptic condition without actual convulsions I believe it poor management to resort to operative procedures on account of this danger; for it is a well established fact that convulsive seizures of themselves are exceedingly dangerous to both mother and child. Shock, as an excitant of convulsive seizures, is worthy of our most serious consideration. In eclamptic conditions without convulsive seizures what we most desire is time to quiet nervous disturbance, relieve tension and pulse frequency, dilute toxines and promote elimination, and the operator that disregards these essentials and proceeds to bring on labor or delivery by the ordinary methods makes a mistake. I remember a case that went into her first |