him in the wards, but this was difficult to make out clearly. He feels painful sensations, and can tell the difference between heat and cold. His limbs are not wasted.

He has some incontinence of urine, and has some trouble with his bowels, thinking they are never moved, which may be a delusion, or may be due to anesthesia of the rectum, which may not respond to sensory stimuli. He has no optic neuritis.

Summarizing, the chief symptoms referable to a spinal cause are abdominal pain and constriction, rapid loss of power in the limbs, with accompanying partial loss of sensation, excitable reflexes, a tendency to constant spasticity, with attacks of extreme spasm in the legs on every attempt at movement, and incontinence of urine. His legs are not wasted, and electrical changes have not occurred.

Everything in this case points, as in the other cases, to a lesion of the thoracic cord, but one differing in character from those we have considered. The dominating symptoms are those of compression and irritation. It might be a case of compression-myelitis from a rapidly developing extra-medullary tumor or an inflammation of the cord substance. It is most probably a case of compression-myelitis associated with rapidly developing caries of one or more of the thoracic vertebræ. The lesions causing compression of the spinal cord are usually fractures, growths, aneurisms, pachymeningitis, and caries; the last probably occurring oftener than any of the others. In caries, inflammation of the bone and its surroundings is present, and pachymeningitis often develops, and sooner or later mechanical compression from giving way of the bones. The attack of explosive spasticity in this man's case is to be explained by the irritation of the nerve-roots by an inflammatory process; most of the other symptoms by compression, although some may be due to limited destruction.1

Independently of his history, his symptoms will scarcely bear any other translation. This man, without atrophic disorder of the muscles which are supplied by the nerves of the lumbar enlargement, has lost cerebral control over his limbs,-a loss which is due to the breaking of connection between his brain and the parts of the spinal cord which supply the lower limbs.

It is now several months since the delivery of this lecture. This man soon became entirely bedridden, and recently died in the wards of my colleague Dr. J. H. Lloyd, having developed shortly before his death cauda-equinal symptoms in addition to those just related. Autopsy revealed dorsal caries and its usual accompaniments, much as anticipated in the lecture, and also invasion from a trophic eschar of the equinal region.

What else could this be except transverse myelitis, from compression or other cause? He may have a brain lesion, as he had convulsions, which are probably cerebral in origin; but no single cerebral or intracranial lesion could produce symptoms such as we have observed here. A small growth in a very unusual position in the pons might give many of the phenomena present; but it is inconceivable that you would then have uniform paralysis of the two extremities and uniform spastic phenomena, and that his arms and the upper part of his body should also be involved. He might have a double lesion of the cerebral hemispheres, involving only the cortical centres for the legs, but it is not probable; or a tumor in the longitudinal fissure pressing in both directions on the leg centres of both hemispheres, but that also is improbable. We have no evidence of caries of the vertebræ, and as a result localized pachymeningitis and compression-myelitis.

The convulsions and his mental state may be accidental concomitants, or a spinal affection may be superimposed upon a past cerebral state. It is true that in certain acute diseases of the spinal cord we occasionally have convulsions at the onset of the disorder. In one case reported three general convulsions, with unconsciousness, accompanied the onset of an acute myelitis. I have had one or two similar cases. I have in mind a patient who was attacked with myelitis and neuritis, and had almost universal convulsions in the very early stages of the disease, before it had rendered her incapable of using the limbs. So you see that we may have occasionally a history of convulsions with acute spinal disease. It is more probable in this case, however, that the patient had convulsions which had no connection with the disease we are particularly studying.

For the acute stages of any form of myelitis the treatment would be practically the same. First, let me again emphasize the fact that it is most important to recognize that the case is one of transverse myelitis. Nine out of ten cases probably are not recognized at first. They may be supposed to be simply cases of weakness, or of rheumatism, or of hysteria; or-which is most likely-they may not be diagnosticated until the patients are off their legs and much central mischief has been done. Later, the mistake is made too often of supposing the case to be necessarily hopeless. As soon as you suspect that a patient has beginning inflammation of the spinal cord, put him to bed, and keep him there. Even the position in bed is important. Put him on or towards his face, or on his side, arranging this, if possible, so that he will not be on a strain. The legs may be made dependent below the level of the bed. If you simply place the patient on his side he will

not stay there; he needs more support, which can be had with a board, which should be padded. Keep him absolutely still. Use counterirritation to his back; and probably the best way to do this is by the alternate application of water at the temperature of 115° F. and icecold water, ten or fifteen minutes at a time, two or three times daily. Use either dry or wet cups, and have the bowels opened in such a way that it will not be necessary to move the patient much.

Internally, many remedies of questionable value have been used. Ergot is one of these, and reports differ as to the results obtained, although theoretically it should be of value. One of the best combinations of drugs in the early stages is probably that of the iodides, bromides, and ergot. Mercury is usually recommended, and seems to do good at times. If mercury is used, it should be in the form of inunction, or of calomel, kept up for some time.

Remedies such as salicylic acid, the salicylates, phenacetin, antipyrin, etc., which have been found so useful in neuritis, should also be tried in myelitis,—at least in its early stages,—although but little use has been made of them for this affection.

In transverse dorsal or lumbar myelitis serious accidents may arise. The tendency in myelitis of a certain type and of certain severity will be paralysis or paresis of the bladder walls, and perhaps of the sphincter. If of the bladder walls, there will be more or less retention of urine, and these patients also dribble sometimes; the bladder gets nearly full and dribbles over, but a certain amount is left, which decomposes and sets up cystitis. The necessity of making careful examinations and catheterizing is apparent, or in a week or two you may have secondary myelitis or other constitutional conditions from infection. In catheterizing, of course, you should be careful to see that the instrument is perfectly clean. It may be necessary in certain instances to keep the bladder washed out with antiseptic solutions or benzoic acid, and to give morphine, with camphor water and belladonna, internally. Be on the watch for bed-sores, which may be of two kinds,—that is, from pressure, or trophic due to the cord disease. If the patient suffers much from the first variety of these, it will be your fault; but, in spite of all you can do, trophic sores may appear. Everything should be done to prevent this, as by the use of air-cushions and water-beds, and of peroxide of hydrogen in washing out the sores, and of iodoform or a mild galvanic current to stimulate.

If, in spite of this treatment, the case goes on to a paralytic condition, the treatment will be different. The patient should not, however, be put on his feet too soon, and you should not give up all

hope of improvement even if he shows no signs of it for weeks or months. Keep him in bed from five to ten weeks, until you are sure no further improvement from enforcing quiet will take place. Now use tonics, as strychnine, and everything to improve the nutrition of the patient; and alteratives, such as hydriodic acid, may prove useful. He should be treated at intervals with the galvanic current, but too strong currents should not be used. Massage is useful, and should be applied Strychnine may be used hypodermically. In compression-myelitis attention should, of course, at first be given to the source of the compression. If spinal caries is suspected, it is of great importance, and may save the patient, to put him in bed at the right time and treat him carefully by extension and other measures called for in this affection. In fractures and fracture-dislocations, extension and operation must be always carefully considered.

skilfully and at first gently.

Professor of Diseases of the Mind and Nervous System, College of Physicians and Surgeons, New York.

GENTLEMEN,-Here is a man who shows the peculiar condition of sweating of the whole of one side of the head. As I touch him I can feel a very perceptible difference between the two sides, one side being moist, whereas the other is dry. Unilateral sweating is a rather uncommon affection. The sweating here cannot be ascribed to a paralysis of the vaso-motor nerves, as it can be in many cases. You can very well see that the man might have dilatation of the vessels and increased secretion as a result of that. You know that increased secretion of saliva is accompanied by great functional hyperæmia of the vessels in the glands. A paralysis of the vaso-constrictors will lead to dilatation of the arteries, and consequently to increased circulation in the skin at large, and, of course, in the sweat glands pertaining to the skin. We find such cases, but this does not belong to that category, because there is no apparent difference in the color of the two sides of the face. The ears are of exactly the same color that they have always been. Here then is a unilateral sweating of one side of the head, which cannot be attributed to paralysis of the vaso-motor nerves. We have to think, therefore, of those nerves that govern the secretion of sweat. There are such nerves; their existence has never been doubted, although they cannot be distinguished from other nerves under the microscope. You know very well that sudden fright will throw one into a tremendous perspiration, and you know very well that anxiety well that anxiety or grief is capable of drying up the sweat entirely. Abnormalities in the secretion of perspiration occur frequently in neurasthenia. So there must be some mechanism governing this secretion that is capable of being affected