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of grey hair so often seen in cases of cranial neuralgia and headache.

The presence of diacetic acid in the urine-which gave a very strong diacetic acid reaction--at a time when the patient was being fed solely by nutrient enemas, is worth noting. Rolleston and Tabbs* found diaceturia in nearly all cases of chronic gastric ulcer in women which were treated by starvation; in patients with severe or persistent vomiting there was usually an especially well-marked reaction; the administration of nutrient enemata did not diminish the diaceturia; it disappeared sooner or later after the return to mouth feeding, but in those patients who could be fed by the mouth, even in small quantities, it did not make its appearance.

Parotitis occurred in this case, as it does so often in cases which are treated by rectal alimentation alone, and that although great care had been taken of the mouth from the first, and an antiseptic mouth-wash had been used. Of course, it was impossible, with the patient in such a condition, to ensure absolute cleanliness, much less asepticity of the mouth, so that one cannot be sure that it was not produced by direct infection through Stenson's duct. If, as is suggested, it is produced by indirect infection through the blood or lymph, the predisposing cause being the inactivity of the gland, it would seem to be advisable to give such patients some pungent substance to chew, so as to keep the gland in action.

Perhaps the point of greatest interest in the case was the occurrence of the perforation although the patient had taken no solid food for at least two weeks, had been confiend to bed for eight days, had had nothing by the mouth for twentyfour hours but whey, barley water, and a little Valentine's meat juice by the teaspoonful at a time, and before that had been absolutely starved. One thought suggests itself: During the last twenty-four hours before death We had been giving gr. xx. of bicarbonate of soda every four hours instead of lime-water as at first; did that help to cause it? One is reminded of a remark of Sir Lauder

*Brit. Med. Jour., July 16, 1904

Brunton's that once, when he was treating a case of gastric ulcer in this way, hemorrhage came on, and he had suspected that the soda had conduced to it by softening the mucous membrane; perhaps it removed a protective coat of mucus. The liberation of CO, in the stomach may have had something to do with it.

The presence of a second ulcer, whose base was perilously thin, is worth remembering. Had the patient recovered from the operation, a second perforation might have taken place, causing a recurrence of urgent symptoms, the meaning of which might easily then have been mistaken. To operate at once again would have been the right treatment, and the chances of success would probably have been just as good as at the first operation. Noteworthy, too, was the complete relief from pain which the operation gave, though it did not save the patient's life.

Last of all, it is perhaps worth while to enquire how it happened that the occurrence of perforation had apparently not been suspected, much less diagnosed, by my house physician, although, when I first saw the patient next morning, the evidence of it was unmistakable, and it would seem to have occurred some seventeen hours earlier. My house physician at the time was a man who was acting as locum tenens for a month; he was a Cambridge graduate, and an able man. He had been qualified some fifteen months; his medical knowledge was extensive, and he had had twelve, months' practical experience as resident medical officer at a children's hospital. was very keen about his work, and, curiously enough, was especially keen about gastric cases, for he was actually working upon the occurrence of tetany in gastric cases for his graduation thesis. He was certainly watching the case with the utmost care, and had a special nurse always at the bedside. Notwithstanding all this, he failed to spot the occurrence of the perforation. It is hard to account for it; I can only think that men are taught too much detail and are apt to be overwhelmed by it; they are not trained sufficiently to take wide views, to look for the big things, to grasp each of their cases as a whole.

He

ABSTRACTS.

ADAMS-STOKES DISEASE.

PERSISTENT SLOW PULSE WITH EPILEPTIFORM ATTACKS.

INTEREST has lately been revived in this symptom-group, which was first described by two Dublin physicians-Robert Adams in 1827, and W. Stokest in 1846. Adams described the case of a man, aged sixty-eight, who had for a long time. been incapable of exercise and subject to dyspnoea and cough. He was seen when recovering from an apoplectic attack which had occurred three days before. He was then able to go about the house, but had a constant tendency to sleep and a troublesome cough. But what most attracted Adams's attention was "the irregularity of his breathing and the remarkable slowness of his pulse, which generally ranged at the rate of 30 a minute." The patient had had at least twenty apoplectic attacks in the last seven years, preceded for a day or two by vertigo and loss of memory. During the fits the pulse would become even slower than usual." Death occurred six months afterwards, and at the necropsy fatty degeneration of the heart was found.

Stokes described three similar cases, but these earlier descriptions appear to have attracted but little attention, as Dr. Bristowe,§ in an address in 1893, on the influence of extreme slowness of the pulse in the causation of epileptiform convulsions, refers the earliest recorded case to 1885. Bristowe relates the history of five cases, and since then the condition has been recognised clinically in this country, France, and America, but has only recently obtained special notice in Germany.

*Dublin Hosp. Rep. Vol. IV., p. 396. § Trans. Med. Soc. London. Vol. XVII.

+ Dublin Quar. Jour. of Med. Sci., 1846. St. George Mivart, Lancet, Jan. 3, 1885.

A brief account of two recent cases will serve to describe the clinical phenomena. Percy Kidd's* patient was a woman of fifty-eight years, who had been ill for about four years. She complained of dyspnoea, especially on exertion, and of fainting fits brought on by exertion or excitement. The first fit occurred five years ago, and since she has been unable to go out alone in consequence. There is no warning to the fits; they have always the same character, and last from two or three minutes to half an hour. She may have five or six in a day, though they may be absent for weeks. She also complains of sharp pains in the region of the heart. The pain may be present without the fits, though at times it comes on as the fits are passing off. The pulse varied from 25 to 28, of moderate tension, and the artery not thickened. The cardiac dulness was slightly increased outwards, the impulse was not felt, and a faint systolic murmur, loudest at the mid-sternum at the level of the third rib, was heard. Vomiting occurred occasionally, usually after food, but sometimes in the morning or as a fit was passing off. The following is a description of a fit which occurred while under observation "The patient suddenly cried out, her head was retracted, the pupils were widely dilated, the face was cyanosed, and the pulse was imperceptible for forty seconds. She was quite unconscious, her whole body being rigid and extended. Incontinence of urine occurred, and, as she recovered, retching took place. On recovery the pulse rose to 52. The whole fit lasted for five minutes. In another fit a few days later, the pulse ceased for ninety seconds, and this fit lasted for three minutes."

Jacquet describes the case of a man of thirty years of age. For several years he had easily become tired with very slight exertion; this had been worse the last year. The first attack of loss of consciousness occurred one year before admission, and during it the pulse rate was 17 per minute. He had a similar attack the next day, but then remained free until a short time before entering hospital. There was a doubtful history of syphilis. He was very anæmic, with a

* Lancet, Feb. 13, 1904.

Deutsches Arch. f. klin Med., Bund. LXXII.

slow, regular pulse, 24 to 32. The heart was enlarged transversely, and the impulse was heaving. There was a soft systolic murmur at the apex. During the pause one or two low tones were heard, not accompanied by a perceptible pulsation. The jugular veins pulsated two or three times more frequently than the arteries. The arteries were not thickened nor tortuous. During an attack he lost consciousness, became very pale, the pulse was absent for a short time, and the sounds of the heart were very feeble. pulse was irregular and unequal after the attack. lasted for about ten minutes. There were never convulsive movements, but there was often involuntary micturition, and at times an aura. The patient died ten months later. At the necropsy there was no evidence of arterio-sclerosis, but fragmentation of the muscle of the left ventricle was found. The medulla oblongata was normal.

The

The attack

Bradycardia as a synonym for slow pulse is perhaps an unnecessary addition to medical terminology. Clifford Allbutt* pours out considerable scorn upon the word: "It hoodwinks the student who does not rid himself of the false prepossession that in so large a word must lie a specific meaning; he does not realise its emptiness. . . . With the word 'tachycardia we introduce a new conception; with bradycardia we introduce nothing; the word is but wind." Similarly the Stokes-Adams syndrome must not be raised to the dignity of a disease; it is not a clinical entity, but the more or less chance association of two or three functional disturbances, which are by no means due to a single pathological lesion. In the heart may be found fatty degeneration, fibroid degeneration, arterio-sclerosis of the coronaries alone or with disease of the cerebral vessels. Uramic poisoning may be the cause, and also lesions of the medulla and vagus. Gilliest has recently written a full summary of our present knowledge of the group. The cardinal symptoms are three(1) slow pulse, (2) apoplectiform or epileptiform attacks, (3) disturbances of respiration.

(1) The slow pulse may be permanent or transitory, and is often very obstinate. The rate is not influenced by posi

System of Medicine, Vol. V.,

p. 832.

+ Montreal Med. Jour., June, 1904,

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