not until the stage of exhaustion and effusion sets in that the pupils dilate. If, then, the enlarged pupil of B. were a symptom of the state of the brain induced by it, that state should be precisely the opposite of what it really is.

Secondly, Christison has put on record a case of poisoning by opium and B. conjointly, in which the cerebral symptoms were those of the former, while the pupils were "excessively dilated and not contractile." Here, as the author observes, the opium "prevented the delirium induced by B. in the early stage; while on the other hand the B. prevented the usual effect of opium on the pupils, and actually produced the opposite action." That is, the cerebral influence of the B. was neutralized and superseded by that of the opium; but its mydriatic power was fully exerted. If, now, the dilated pupil of B. were symptomatic of the condition of the brain induced by the drug, we should have in this instance a contradiction of the axiomatic law, causa sublata tollitur effectus.

Thirdly, it has been ascertained by experience that the mydriatic action of A., even when exerted through the constitution, is a peripheral one, and independent of the nervous centres. A full account of the observations which establish this view is given by Dr. H. C. Wood. That it holds good when the drug is locally applied it is easy to believe; and it suffices to say that the effect may be produced after section of the trigeminus and the cervical sympathetic, and even after extirpation of the ciliary ganglion-in frogs after removal of the eye from the body. But the case from the same author given as A. II., is still more decisive.

11,

We must conclude, then, that the dilatation of the pupil induced by B. is the result of a local and peripheral action of the drug, and altogether independent of its effect on the central nervous system.

We have yet to inquire by what means B. exerts this local action which we have found it to possess. It has been shown that the pupil may be dilated either by the depression of the influence of the third nerve, or by excitement of that of the sympathetic. The old conception of B. as a "narcotic," and, later, the ascertained power of A., locally applied, to paralyse the accommodatory action of the eye (of which more anon), has made it generally assumed that the mydriasis which occurs under its influence is due to paresis of

the oculo-motorius, causing a relaxation of the circular fibres of the iris analogous to that of the sphincters of the rectum and bladder. There are, however, grave objections to this view as a complete account of the phenomena, the most serious of which is that in complete paralysis of the third nerve (or after section of it in animals) the mydriasis is much less than that which results from A., and may be considerably increased by the use of the drug. Dr. Harley, too, aptly points out the difference between the effects of conium (which undoubtedly paralyzes the oculo-motorius) and those of B. on the eye.

This physician, with Wharton Jones, Benjamin Bell, Allen Thompson, and (formerly) myself, have maintained that the mydriasis of A. is dependent entirely upon sympathetic excitation. That it does produce this ef fect generally is shown by the contraction of the arterioles which it induces; and that it exerts the same action upon the eyes is evident from the widely open, staring and protruded appearance they present under its influence, this group of symptoms concurring with dilatation of the pupils when the sympathetic is galvanized in the neck. Vulpian, moreover, has observed that in poisoning by curare, as long as galvanization of the cervical plexus occasions dilatation, however slight, of the pupil, so long B. also will determine it. Again, it is evident (as Dr. Wood justly states) the dilatation produced by the drug is "not merely a passive movement of relaxation, but is active, capable of tearing up inflammatory adhesions, even when of some firmness." I cannot doubt, therefore, that to excitation of the radiating fibres of the iris through the sympathetic, the mydriasis of B. is largely due. At the same time, as there is good evidence, from the failure of accommodatory power, that the ciliary branches of the third are paralyzed under full atropism, relaxation of the circular fibres may also be a factor in the result.

Is the pupil ever contracted under the influence of B., and, if so, what explanation can be given of it? Such a symptom is noted by four of Hahnemann's provers, and by himself (H. 245-9). Dr. Harley, too, has observed that just before the mydriasis of the drug has set in, the influence of light will cause the pupil to contract more closely than under similar circumstances before the ingestion of the drug. "This contraction has persisted for several minutes, when all at once the pu

pil has given way, and become broadly dila. ted." Dr. Sharp, who finds that he can induce slight contraction of his own pupils with one-fifth solution of the mother tincture of B., and Rossbach and Frölich, who have obtained similar results in animals with very minute quantities of A. (from about gr. .00005 to .0001), believe the difference to be a question of dose. I am not prepared to pronounce upon the question; but from the somewhat parallel action of gelsemium, I am rather inclined to think that any contraction of the pupil which B. can effect is a symptom of commencing hyperæmia, either in the eye itself or in the brain. In the one symptom of this nature supplied by Hahnemann it was associated with rather severe frontal headache (comp. H. 245 and 96.)

(To be continued.)

TRAUMATIC NEURITIS.

BY F. R. DAY, M. D.

CHICAGO.

(Read before the Ill. Hom. Med. Association.)

I. On the importance of the early recog nition of neuritis.

Many acute diseases are self-limited. After a certain run, they end spontaneously, having few or no sequelæ. It matters little what treatment is employed--the course is essentially the same. The patient gets sick-the patient gets well. The same is true of many injuries. Nature repairs the damage in her own mysterious way, and in her own selected time.

On the other hand, there is a tendency on the part of some acute diseases to lapse into a chronic condition, which is difficult of control. These cases demand skillful treatment and constant attention, in order that they may result favorably.

This is especially true of inflammation of the nerves. When these delicate structures become acutely inflamed, either idiopathically, symptomatically or traumatically, chronic inflammation, or, possibly, a state of sclerosis, is apt to follow, which often baffles every effort of the specialist. Furthermore, the tendency of inflammation in a nerve is to extend-centrally-along the nerve-fibers, to involve the neighboring plexus and its branches, and, possibly, to reach the spinal cord, or even the brain itself.

The acute stage is of short duration, and is

a precious time for active treatment, in order to avoid the unfortunate results enumerated. It is, therefore, of paramount importance that neuritis should be recognized early, and the proper treatment at once instituted.

II. On the diagnosis of neuritis.

It has been my privilege to see, in dispensary and private practice, a number of cases of acute and chronic neuritis, and the remarkable uniformity with which the symptoms were misinterpreted by other physicians, convinced me that these diseases are but little understood by the majority of practitioners. One was called hysterical joint; another, muscular rheumatism; others went as sprains, neuralgia, congestion of the brain, and even as writer's- cramp.

The symptoms are clear and well-defined, and when once understood the diagnosis is easy.

Most cases of acute neuritis follow injuries, such as blows, cuts, gun-shot wounds, fractures, compression, etc. From four to seven days after the receipt of an injury, the patient becomes feverish, and complains of pain along the course of the affected nerve. This pain, the most important symptom to the patient, soon becomes continuous a constant ache, attended with burning. Patients it is like the toothache, and is very trying to their disposition, making them irritable and fretful. Some become hysterical. At times the paroxysms of pain are almost unbearable. During the night the pain is greatly increased, interfering with sleep and rest. Movement of the affected part, or pressure on the nerve, add greatly to the suffering.

say

The pain gradually extends up the nervefibres to the neighboring plexus, and thence radiates outward along the other branches, particularly along those that are distributed to the joints. At first this pain is a neuralgia, and not dependent upon any inflammatory condition of the plexus. The nerve is thickened under the pathological processes, and we can feel it, as we might a cord, under the finger-tips-a condition which becomes more and more marked as the disease progresses.

The functions of the nerve are gradually interfered with. If a mixed nerve is injured, there will be disturbances of motion and sensation. The muscles supplied by it become more and more paretic, and cut off from voluntary stimuli, while involuntary

twitching and cramps of these same muscles are of frequent occurence, and accompanied by more or less pain. The disturbances of sensation are variable, but, as a rule, are at first paræsthetic, and later anæsthetic. Patients complain of peculiar sensations, such as burning, crawling, tingling and pricking, and occasionally of exaggerated sensibility to touch. But these usually give place, in the course of a week or ten days, to incomplete anæsthesia. This may be said to mark the beginning of the sub-acute stage, which is characterized by changes in the nutrition of the parts supplied by the injured nerve-trophic changes which, in the course of time, affect all the tissues, from the softest to the hardest. The muscles begin to atrophy, and may show the reactions of degeneration when examined with electricity.

The

The skin becomes puffy, and takes on a glossy appearance, which is quite characteristic of this stage of the disease. The circulation is changed, and there is a mottled, congested look about the hand or foot. sense of touch is not entirely gone, but is blunted, and when examined by the æsthesiometer, patients cannot distinguish the two points until they are far apart.

By the time these conditions are well established-which takes about two months the disease may be said to have run into the chronic state.

The symptoms remain about the same. The pains are still continuous, but duller than during the acute stage. There are occasional exacerbations, and also short intervals during which the pain is entirely gone.

The trophic changes progress, and the harder tissues show alterations. The muscles continue to atrophy, the nails become clubbed and brittle, the bones begin to show trophic changes, and cause more or less deformity, and the member is as useless as in a case of paralysis. This stage is of indefinite duration, and may last for years.

At any time during this period the pathological process may extend from its original location, toward the central organs. It gradually invades the healthy portions of the nerve, and causes more extensive muscular paresis and atrophy. If it reaches the spinal cord it may set up degenerative changes there, and then the case presents many of the characteristics of progressive muscular atrophy. III. On the treatment of neuritis.

As has been said, the acute stage is the

time for energetic treatment, in order that the trouble shall not run into the chronic stage. We can hardly hope to avoid the sub-acute, for there are very few cases of acute neuritis that do not become sub-acute before recovery.

The most essential element of the treatment is rest. It is indispensable. Without it every other measure will be in vain. If the nerves of the lower extremities are involved, the patient must be put to bed. If the injured member is the arm, it should be dressed in a removable splint of some kind. I find that a single splint-held in position by straps, along the posterior surface of the forearm-to be simple and satisfactory. The arm should be carried in a sling, or rested on a pillow.

Either hot or cold applications are allowable, but whichever one is adopted should be faithfully and continuously used, not at intervals, as is sometimes the case. Ice-bags or metal coils over the nerve allay the pain.

Opiates may be necessary to allay the terrible pain in this stage. Under no circumstances should they be resorted to in the other stages, since there is greater danger then of inducing the opium-habit on the part of the patient.

As soon as the disease passes into the subacute stage, the treatment is changed. Counter-irritation in the form of cantharides blisters, or applications of iodine along the course of the nerve, are of value, and the galvanic current is indispensable. Strapping the muscles with rubber adhesive plaster may be substituted for the splint, and the arm carried in a sling.

It is safe to say that if cases of acute and sub-acute neuritis receive this treatment, very few of them would run into a chronic state. The damage done would be checked at its minimum, and the process of repair could be gradually fostered by electricity and massage. But they must be used with extreme caution, and only after the pain has entirely ceased.

As to internal remedies, Aconite and Hypericum are as valuable as all others in the pharmacopoeia. But even these cannot do much without the aid of external applications.

EMBOLISM IN ACUTE ARTICULAR RHEUMATISM.

BY M. J. BLIEM, M. D.

CHICAGO.

(Read before the Ill. Hom. Med. Association.)

By the patient, this disease is to be dreaded for the agonizing pain so often attending it;

In all

by the physician, for the much more subtle, but all the more dangerous, heart trouble so frequently engendered. Acute articular rheumatism very rarely proves fatal. In uncomplicated cases the mortality is nil. cases, about 3 per cent. are fatal, and these fatal cases are mostly to be found in heart complications; the final fatality from succeeding chronic valvular disease is much greater. The number of cases developing heart lesions varies greatly, according to different statistics, all the way from 5 to 75 per cent. However, Bamberger, who has examined the subject most carefully, puts the ratio at 20 per cent. for endocarditis, and 14 per cent. for pericarditis. Myocarditis occurs

much less often. It is well known, at least, that a large majority of chronic valvular troubles have their origin in acute articular rheumatism. Were we now to discuss the cause of this frequent complication, we would enter upon uncertain and disputed ground. It does not seem a metastasis of the disease from the joints, for this usually still continues. It seems most probable that the same rheumatic agent - whatever that may be-attacks the serous membranes of the heart, as those of the joints. The endocardium, or lining membrane of the heart, is a connective tissue membrane covered with endothelial cells. It is thin in the ventricles, thicker in the auricles, and forms the valves by a reduplication. It is an inflammation of this delicate, glistening membrane that is called endocarditis. It is to be observed that this inflammation may take place in any part, but that as in other parts of the body, those which stand the greatest strain and friction are most liable to become inflamed, and therefore we find the valves of the left side most frequently implicated. We may have inflammatory patches on the surface of either auricles or ventricles without ever giving rise to any symptoms, either subjective or objective. It is the implication of the valves or their attachments that causes mischief and death. In the most common form which generally complicates acute rheumatismacute exudative endocarditis-the inflammation takes place in the superficial layers of the connective tissue, just beneath the layer of endothelium. The connective fibres themselves are inflamed; the connective tissue cells are greatly multiplied; there is exudation of a gelatinous substance into and around the fibres, which is speedily organized

into new connective tissue. As this new product of inflammation forms, it pushes upward and causes an elevation of the surface, thus forming the so-called valvular vegetations. Let us note that the exudation and resulting neoplasm are within, and not without, the endothelial layer. In a peculiar septic form of the disease these vegetations may soften and break down, forming ulcers; this is the ulcerative endocarditis, so rare, but so fatal. The softened debris is carried

away by the circulation into other organs, setting up septic processes wherever lodged. Ordinarily these vegetations accomplish their dire mission in several ways. The newlyformed connective tissue may contract, thus distorting the valves, giving rise to insufficiency; or these new growths may cause adhesions, giving rise to stenosis. Again they may become chalky; or even calcify, and thus become permanent barriers to a smooth circulation. But the last and the only immediately fatal result of these vegetations is that giving rise to the subject of this paper -embolism. We know that friction greatly facilitates the coagulation of blood; when to this we add the disordered condition of the blood in an acute fever, we need not be surprised that such deposits of coagulum should form upon the vegetation, nor that these thrombi should easily be swept from their frail moorings into the greater sea beyond. Similar thrombi may form upon the rough surface of the ulcers; rarely, too, a valve, or even the endocardium elsewhere, may be torn or fenestrated and thus give rise to thrombi.

Before proceeding further it may be well to refer to the insidious development of acute endocarditis. Strange though it may seem, it is true that the severest heart lesions may develop without the patient's cognizance. There is rarely any precordial pain to inform him of new trouble. Only constant attention to the physical signs will warn the vigilant physician of the secret foe's advent. It is necessary to insist here upon the correction of a general error, that is, that the one thing necessary to establish the presence of endocarditis is a murmur. This is by no means the case. In acute rheumatism, for instance, a very low, blowing mitral murmur is frequently heard, which later entirely disappears. Nor is it ever accompanied by confirmatory signs. Such murmurs are undoubtedly caused by the unequal tension of the valves, due to

the excited action of the heart under the fever, and perhaps, also, by the peculiar condition of the blood. They are, therefore, hæmic, or blood murmurs. Probably those who report a complication of 75 per cent. have included such cases.

With the murmur there must be present confirmatory signs of disturbed circulation. With the mitral murmur-by far the most common- -there may be signs of great fulness of the pulmonary system. Consequently there will be present-first, signs of unusual fulness of the pulmonary artery, the second sound over the the pulmonary valves being strongly accentuated; and second, signs of dilatation of the right side of the heart-the area of cardiac dullness will be increased to the right.

Again I may say that even the physical signs in an exceedingly grave case may be so slight as to elude any but the most careful and skillful. The gravity of the lesion is by no means always gauged by the loudness of a murmur. At any moment the unwatchful attendant may be astonished and alarmed by the occurrence of embolism. If the clot be swept into the brain, he will not long need to wait for its effect. If, as is most common, the embolus be swept downward, and lodged in the spleen, his patient will probably have chills, an increase of temperature may follow, and he will complain of pain in the splenic region. If now he will examine the spleen, he will find it tender, swollen aud enlarged. Similar symptoms, accompanied, it may be, by hematuria, will follow the lodgment in the kidneys. The clots are usually quite small, and blocking up small arteries, hæmorrhagic infarction takes place. If it be a septic clot, as in the ulcerative form, suppurative inflammation may be set up in the vicinity, and the constitutional signs of septicemia and pyæmia will soon be developed. Otherwise the clot and wedge-shaped area of infarction may be absorbed, or may break down and form a simple abscess. In the brain, of course, embolism may cause immediate death. When the clots are large enough to shut off the circulation from a part, and the collateral circulation is insufficient to sustain the nutrition, gangrene will speedily set in. In this manner gangrene of the toes sometimes occurs.

The following case is sufficiently rare and remarkable to merit notice:

Sofer Sperl, a German, aged 28, was admitted to the Cook County Hospital, April 22,

1885. He was a man of good family history, fairly good habits, no venereal history, but subject to attacks of acute rheumatism from youth. youth. Upon admission he had been sick eight years; at that time he caught cold, had headache, and pain in the arms, which extended to the limbs, and was quite severe. There was a little swelling of the joints of both hands and arms, and a little of the feet. Cannot sleep-no appetite-bowels costiveurine normal. On examination no abnormal heart signs were noticed, nor did he give any history of previous heart trouble. His pulse ranged from 100 to 136 and was good. His highest temperature was reached on the evening of the 27th, when it was 1031 F., having been usually 102°. On the next evening, the 28th, his temperature was 951 F.

His temperature after this did not rise above 100 at any time. On the morning of the 30th he had less pain and felt better, but I noticed some livid patches on the left hand and fingers. Having ordered the left elbow wrapped in cotton, I supposed it might be caused by tight bandages, and loosened them. The next morning the arm was much worse --whole forearm livid and quite cold-sensation and motion quite gone; no radial pulse -could not detect the brachial, but the axillary was all right. In the evening careful examination detected a mitral murmur. Previous examinations had not given clear results. Sensation had returned somewhat to the whole arm and hand. Color better- radial pulse still absent. Patient does not complain.

May 2d, A. M.—Arm is apparently no better; seems to be dead; gangrenous patches forming; line of demarcation at elbow. P. M.; arm looks very badly; seems dead up to the elbow. May 3d, A. M.-About the sameears stopped up; not much pain. The arm was wrapped in cotton and kept warm.

4 A. M.-All hopes of saving the arm abandoned and it was amputated, four days after first noticing the accident. The amputation was performed through the middle of the humerus. As the patient was being anæsthetized I had my finger on the right temporal artery, when suddenly the pulse ceased. This side of the face grew cold, and remained cold and pulseless until his death, thirty-six hours later.

The brachial artery in the amputated member was dissected out; 1 inches above the