suddenly at the end of a few hours by polyuria and profuse sweating, when the patient recovered. Attacks of tachycardia might follow each other at intervals of a few days, or there might be very long respites.

The diagnosis, said Dr. Silva, was established by the abruptness of the paroxysms, which were not accompanied by sounds of organic lesions of the heart. This abruptness of the symptoms, which broke out and disappeared suddenly without leaving behind them any alteration in the general health, was also a guide to the clinician in distinguishing tachycardia from the true endocarditis; and in angina pectoris arhythmia, which was generally absent in tachycardia, was present.

Regarding the pathogeny of this affection, Dr. Silva said that many theories had been advanced. According to certain authors, it was an excitation of the great sympathetic; according to others, it was, on the contrary, an ephemeral paralysis of the pneumogastric nerve which caused the attack. Debove and Courtois-Suffit thought it was a bulbar neurosis; Fräntzel thought it was an undiscovered lesion of the myocardium. The speaker thought that the beginning of the attack depended upon the pneumogastric nerve, and that later this attack was kept up by the poisons produced by the excessive work of the heart.

Regarding bradycardia, or the slow pulse of Charcot, the author continued, this syndrome was manifested especially in old persons. The patient was attacked suddenly with malaise, the face became pale, and he fell to the ground in a condition of trembling and profuse sweating. The pulse slackened and did not reach more than from seven to ten beats. Soon the patient recovered consciousness himself, and all the alarming symptoms disappeared at the end of a few minutes. The attacks might break out without any apparent cause or after emotion, anger, etc. The patient might succumb after the first attack. More frequently the attacks occurred every two weeks or every month; in the interval the patient, who might live many years, was very well.

Dr. Silva stated that the diagnosis of bradycardia was very easy and the prognosis very grave.

Charcot and Caracretti had thought it was a circulatory or functional anatomical lesion of innervation, but Dr. Silva thought, on the contrary, that bradycardia depended sometimes upon a lesion of the centre of the pneumogastric nerve, sometimes upon arterio-sclerosis, and at other times upon a lesion of the myocardium.

The two affections, he thought, should be treated in the same way that is, with hydrotherapy, electricity, thoracic massage, and climatic treatment.

EPILEPSY AND AUTO-INTOXICATION.-Dr. C. Agostini has followed up the researches of Voisin and Mirto, who have shown (Journal of Medical Science, July, 1897) that the urine of epileptics possesses a special toxicity (and those of a number of other observers have demonstrated that true epileptic fits can be produced as the result of auto-intoxication by abnormal products developed in the gastro-intestinal canal), and has made an investigation into the composition and toxicity of the gastric fluid and urine in epileptic insanity at various periods in relation to fits. He finds that in the intervals between the fits the gastric juice is in most cases normal as far as can be recognized by mere chemical analysis with, however, a tendency to hyperacidity and especially excess of hydrochloric acid. For a short time previous to a fit and for some time afterwards, there are changes indicating a condition of transitory dyspepsia. An epileptic convulsion in proportion to its duration and intensity greatly disturbs the whole digestive functions of the stomach, increasing the secretion of hydrochloric acid and mucus, favoring the development of abnormal fermentation products leading to the appearance of biliary acids, lowering the peptic action and diminishing the sensibility, motility and absorbing power of the organ. In the intervals between the fits the toxicity of the gastric juice (tested upon rabbits) is not necessarily greater than in healthy individuals provided the patient is not suffering from chronic gastric catarrh. In the prodromal period in relation to a convulsive seizure, and especialy in those cases in which there is chronic gastric catarrh, the stomach wash displays energetic and constant toxic properties.

After a convulsion this toxicity is still further increased. Attacks of petit mal increase the gastro-toxic power in a similar manner. The toxic principles appear to be of the nature of leucomaines and are probably the same as those that are found in the gastric fluid of dyspeptics in general. Examination of the urine shows that in the intervals between the fits the tissue metabolism of epileptics is below normal as evidenced by the elimination of azotised substances (urea, uric acid and creatinin) phosphoric acid and chlorides. The excretion of azotised products is further diminished in the prodromal period. After a violent motor fit there is an increase in the density and acidity of the urine and in the elimination of all the ordinary products of tissue change except.chlorides. None of the abnormal constituents of the urine that may appear after a fit do so regularly or constantly. The urine of epileptics has always a greater toxicity than that of the normal individual. This toxicity is increased in that period immediately preceding a fit. After a convulsion the urine is hyper-toxic and remains so for more than twenty-four hours. The toxicity is always proportionate to the gravity of the gastro-intestinal disturbance associated with the fits. It is probably the products that have the general reaction of leucomaines. The administration of bromides distinctly diminishes the toxicity of the urine.

Agostini maintains that in a large proportion of epileptics the fits are preceded by marked symptoms of gastric catarrh. In the intervals between the fits the catarrh in most cases disappears, but in many it persists, becoming aggravated about the time of the fits. In those patients who have chronic gastric catarrh the epileptic phenomena are more frequent and more severe. He believes that this chronic or transitory gastric catarrh is accompanied by putrefactive changes in the contents of the stomach and intestines and the formation of toxic substances which become absorbed and tend to accumulate in the blood giving rise to the malaise, headache and furring of the tongue which precedes the occurrence of a fit and finally determining the convulsion or series of convulsions. He has found that all measures tend

ing to the elimination of such toxic products or to the prevention of their formation, diminish the frequency of the fits or altogether prevent them. He further believes that the process of oxidation is usually deficient in epileptics. Hence leucomaines absorbed from the intestinal canal are not completely oxidized as in healthy persons. He also thinks it is probable that in epileptics on account of the morbid functioning of the nervous system, excretory processes take place with abnormal slowness so that there is a tendency to the retention in the system of products of reduction that ought to be eliminated. He fully recognizes that idiopathic epilepsy is essentially a cerebral disease and would look upon it as the result of a "polymorphic degenerate state,' the most constant and most pathognomonic feature of which is the existence of "somatic and functional asymmetry." He rejects the view of Chaslin and others, according to which epilepsy is due to a special brain sclerosis. But while admitting the existence of a cerebral abnormality that predisposes to epilepsy and often actually determines it, he contends that it is logically and experimentally proved that in many cases the determining cause of the repetition of the fits is auto-intoxication. The irritation occasioned by the toxic agents produces either hyper excitability of the psycho-motor centres or exhaustion of their inhibitory power permitting the tumultuous action of the lower automatic centres. These toxic agents need not have epileptigenetic properties. They act simply by increasing the vulnerability of the imperfect and unstable nervous system of the epileptic.

Since auto-intoxication plays so important a part in the production of epileptic fits, Agostini advocates the endeavor as far as possible to remove the factors of such intoxication. In the first place, correct gastro-intestinal catarrh when it is present, and endeavor to remove toxic substances that may have formed in the alimentary tract. As the best means of attaining this object, he recommends repeated washing out of the stomach with salt water, especially when fits are anticipated and before the occurrence of a crisis. He also advises the use of purgatives, saline enemas, diuretics (especially lactose) and the abundant administration of milk

along with salol or naphthol as intestestinal antiseptics. In the second place-endeavor to increase the activity of processes of oxidation and of normal tissue changes in general. These objects, he thinks, are best secured by the use of small doses of alcohol, careful hygiene, fresh air and moderate muscular exercise. With regard to diet he does not agree with Haig that epileptics should become vegetarians. He has found that a purely vegetable diet gives even worse results as regards the fits than a purely meat diet, a circumstance which he attributes to the fact that vegetable albumen putrefies more readily than animal albumen. He recommends a milk diet with plenty of milk. Lastly, we should endeavor to diminish the reflex activity of the cortical nerve centers, which in epileptics are in such unstable equilibrium. He believes that the only really effective drug for this purpose is potassium bromide. He recommends that it should be given in somewhat smaller doses than those generally used, and that it should be combined with salol. Its efficacy is increased by the antitoxic therapeutic measure already mentioned. If gastric catarrh appears the administration of bromides should be suspended and the attention directed to the removal of the catarrh.

CLASSIFICATION OF EPILEPTICS.-So little is known of the etiology of epilepsy that it is not possible, in the light of present knowledge, to make a satisfactory classification of its forms. The terms grand mal, petit mal, psychic and Jacksonian are largely symptomatic designations, and bear little relation to causative factors. A classification based strictly on etiology is not possible, but none will deny that such a classification would be more scientific and valuable. The classification here offered is not held to be perfect or even satisfactory, but is used as a working basis for future improvement; 1, genito-neuropathic; 2. post-paralytic; 3, traumatic; 4, hystero-epilepsy; 5, hereditary; 6, imbecilic; 7, acquired; 8, senile.-Dr. Frederick Peterson, Third Annual Report of Craig Colony of Epileptics.

PSYCHIC ANESTHESIA.-Dr. Charles W. Burr, of Philadelphia, remarks that, at the November, 1896, meeting of