learn the exact way in which these poisons act. There are a few drugs which cause the same result, but they have never been studied with this point in view. Here might be included the vertigo from alcohol and tobacco. In the vascular cases it is not easy to differentiate between local auto-intoxication and the beginning tendency to lethal decay. It would always seem to be secondary to some lesion cutting off proper blood supply. This may be an embolus, or the swelling of a thrombosis when neither of them go on to actual softening. A different cause, still vascular, is hemorrhage when there is the pressure of a foreign body intruded into the brain, and the same may be said of a tumor, one being sudden in its onset and the other gradual. We cannot be so sure of the immediate cause of vertigo in meningitis, as it often occurs before pressure symptoms are manifest. In auditory vertigo there may be a reflex condition as where the disease is in the middle ear (this is not certain, however). In Meniere's disease the trouble is immediately in the vertiginous apparatus, but not at its cerebral centre; it can hardly be termed reflex, as by that term we expect a secondary set of neurones, physiologically related, to be occupied. In Meniere's the labarynthine impulses seem to be sent directly to their own centre or centres in the cortex without the intervention of any secondary or auxiliary neurone.

In passing to the more practical feature of this subject, namely, the treatment, I wish to announce my old-fashioned belief in the efficacy of drug remedies, and that the closer their symptoms correspond to those of the disease the more likely they are to assist in a cure. As experienced homoeopathists you hardly need prompting in the matter of drug pathogenesy. All remedies given for conditions causing, or including vertigo, should cover that symptom, and in most instances this can readily be attained. Those cases which are likely to be the most trying, are those which as far as we can see are purely nervous,-functional vertigo. Here we have but few objective symptoms to guide us, or else we find such a host of inconsequential ones that apart from the vertigo we are quite in the dark. Most authors state that neurasthenic vertigo is particularly worse on first rising in the morning. My observation does not correspond to this statement, as the patients have the vertigo, or have it worse, just in proportion as they are fatigued, which is mostly in the latter part of the day. In hysterical vertigo the exacerbation may be at any hour of the day, and is mostly controlled by emotion or excitement.

Just a word here regarding the paroxysms of attack. From many observations it has seemed to me that it is owing to changes in the vaso-motor control in the cerebral circulation. From various causes there may be either a spasm or a paresis in the cerebral vessels, either local or general. Of the exciting causes we yet have much to learn. They may be psychic, reflex or toxic. In hysteria they are probably psychic; in neurasthenia, asthenic (from fatigue), and in migraine, and general epilepsy (non-focal), from toxemia. There are undoubtedly other causes for these irregular

ebbs and floods in the brain about which we know absolutely nothing, but, what is most important, we know there are remedies corresponding to the phenomena.

It would ill become me to attempt to instruct members of this Club in drug pathogenesy, as you have spent your lives in that study. A few suggestions, however, as to the one symptom may be admissible. Conium has as one of its results, objective vertigo, and there seem to be but few of our remedies in which the vertiginous symptom is objective. Tabacum also has this particular form, as all of you will recall if you remember your first cigar. Granatum has both subjective and objective dizziness. It is strange that so little stress is laid on this symptom in our works on materia medica. My attention was first called to the symptom several years ago, when I noticed that in giving the active principle. in cases of tapeworm my patients were all obliged to take their bed for two or three hours on account of the intense vertigo. This could not have been on account of the primary irritation of the parasite, as the result was the same where I made a mistake in the diagnosis and there was no parasite present. While I had a service in the hospital there seemed to be at one time a regular epidemic of vertigo, without other constitutional symptoms, and all recovered in a satisfactorily short time under the administration of only Granatum. Lachesis has been of great service in those attacks of vertigo which accompany the hot flashes of the climacteric in women. Probably the most resistant forms are those depending upon arterio-sclerosis, or accompanying brain lesions. such as embolism, or a hæmorrhagic clot. In these cases but little aid can be expected from remedies, although in sclerosis a prolonged treatment will usually in the end bring relief, due attention being paid to diet and the use of electricity. Here the barium salts have a beneficial effect on the connective tissue proliferation and on the disordered heart action.

It is not needed to direct your attention to the various toxic vertigos, with which you are familiar. There is one toxemia which does not seem to have the attention which it deserves, the error in metabolism which results in the formation of oxalic acid which with many other symptoms causes vertigo. In this condition I have found no remedy to act as well as Kali nitricum, although I confess my knowledge of this special action is almost wholly from clinical sources. Therefore, vertigo must like other conditions be treated with the concomitants when such can be discovered, as often these concomitants are the disease, and the vertigo of secondary importance, but never negligible.

My present practice brings me more in contact with vertigo connected with gross spinal and cerebral diseases, but a consideration of that subject demands a special discussion of the diseases. themselves, and would too far extend this paper.

A CONTRIBUTION OF THE SPINAL CORD SCLEROSIS DUE TO THE ANAEMIAS

BY WILLIAM F. BAKER, M.D., PHILADELPHIA, PA.

The spinal cord sclerosis due to the anæmias, of which much has been written lately, are special forms of nervous conditions, and in reality they differ very little in symptomatology from the organic lesions. We must remember that these form a very small percentage of cases and occur quite infrequently in comparison with the well known organic lesions.

The philosophy of these conditions is one of nutritional change. It has been established beyond a doubt that there is a mutual relation of the trophic functions and those which have to do with the manifestations of irritability. In the neurone world there can be no such thing as repose. Hodge has demonstrated increases in the cell element and cell shape by excessive exercise of their physiological elements. He showed that prolonged faradic irritation of a peripheral of sensory nerve in a cat leads to distinct alteration in the cells of the corresponding spinal ganglia and later he was enabled to demonstrate similar changes in the nerve cells of other animals after a hard day's exercise.

On comparison of the non-fatigued cells (in the case of faradic stimulation the cells of the spinal ganglia on the other side not stimulated in other instances, the cells of animals captured in the morning) with these artificially or normally fatigued, he found alterations in the latter both in protoplasm and nucleus.

The nuclei of the tired cells were diminished in size; they presented a zigzag border and stained more intensely than did normal nuclei. The protoplasm was often shrunken and stained more feebly than in the cells not fatigued. The alteration disappeared within about twenty-five hours after cessation of electrical stimulation, which lasted five hours; and, in the case of the working animals, after a night's rest.

By an analysis of this neurone philosophy one can readly account for any of the symptoms which are presented and are to be diagnosed. We have the same affection complete of the upper neurone track. We know as yet of no diseases in which the tracks which lead to the cerebellum or originate from it are alone affected. Such pure neurone diseases of the cerebellum cannot arise independently, because the cerebellar tracts are most intimately connected both anatomically and functionally with other spinal and cerebral fibre systems, and in pathologic cases all must be affected.

There is, however, a disease which indicates a definite cerebellar tract:- namely, that situated in the periphery of the lateral column tracts of the spinal cord. This disease is Friedreich's ataxia. It is hereditary, and manifests itself by marked. ataxia disturbances, yet, even when the patella reflexes are absent, sensation is not decidedly impaired.

Anatomically, this disease produces degeneration in three different columnar systems. We find destruction of fibres in the posterior columns (but not in the roots or in their course), in the pyramidal tracts, and in the posterior columns it takes place in the area of the association tracts, the course of which we know to be shorter. As has been stated, the posterior roots and their zone of entrance are normal, probably also their entire course.

The disease in the course of the pyramidal tracts apparently does not affect the motor fibres since muscular spasms and increased reflexes constantly appear here. It is still a mooted question, which must be settled by further researches, which fibre tract is destroyed. Attention must be called to Monakow's tract which unites with the pyramidal tracts and descends into the lateral columns. There is certainly degeneration of the cerebellar lateral column tracts and the cells of Clark's column which form their origin. Since various authors believe in a primary implication (congenital atrophy) of the cerebellum, we may assume diseases of the tract of the cerebellum. We may hope that, in the future, thorough histologic investigations of this rare disease may give us more accurate information as to the origin and relation of the cells connected with the degenerate fibres.

CASE 1. Mr. P., aged 46, was perfectly well until eight years ago. At that time began to complain of pains in the feet and inability to use both lower extremities. These came on gradually and was particularly noticed when walking in the dark. Was totally unable to go upstairs unassisted. The patient grew steadily worse until a complete paralysis of both lower limbs resulted, and the patient was confined to the hospital.

At this time very severe pains developed, sharp and shooting in character. The physical examination showed that the patellar reflexes were exaggerated. Complete reduction in the muscular strength. The limbs were spastic to the ankle; clonus was very marked. The anæmia of this patient was very pronounced. The blood examination showed red cells 2,500,000; white 8,500; hæmoglobin 76 per cent. Red cells were poorly nourished and irregularly shaped.

Examination of Lung. Expiratory murmur prolonged, especially at R apex.

Soft blowing hæmic murmur at base of heart.

During our observation of the anæmias and of the spinal symptoms attending these anæmias there were represented many conditions simulating the cases which have been observed as true spinal cord lesions. The limit of conditions that can be observed in the spinal cord following upon or incident to either primary or secondary anæmia is perhaps never reached. Another notable condition is cited below, showing the following:

CASE 2. Middle-aged man. An examination with the patient in the recumbent posture revealed ataxia. Slow and uniform movements are impossible or they are performed paroxsymally, or interruptedly; even the mere raising of the leg is done in an

irregular, zigzag way, the raised leg falls at a spot more or less remote from the place intended. A given object can be touched with the great toe only after very irregular, secondary movements; instead of describing a circle with the tip of the foot the figures become angular and often irregular. Touching the knee with the heel of the opposite foot "the knee-heel test" is only possible by means of the awkward contractions which often cause the foot to shoot far beyond the mark; the heel can be slowly moved along the tibia of the other leg only with the utmost difficulty. Here it is evident that the ataxia, especially the irregularity of movement, becomes more distinct when these maneuvers are performed with the eyes closed, but only when noteworthý disturbances of the socalled muscular sense are simultaneously present if these are absent, the closure of the eyes has but little affect upon the ataxia, and it is also evident that, if well marked, the ataxia is not prevented by the careful use of the eyes, but at most is merely decreased.

In the most extreme grades of ataxia, walking and standing finally become impossible, the legs lose their hold, are projected in all directions. If left to himself the patient falls, and even if supported upon both sides or carried, the legs wobble about wildly. Spasmodic and paroxysmal movements invariably appear, and the patient can no longer assume the position necessary for standing or walking. Yet course power may be quite well retained, although the patients may have become entirely helpless, and are confined to their beds or to rolling chairs.

Ataxia usually appears much later in the upper extremities, only the cases of tabes superior being exceptions to this rule. Ataxia, of course, interferes with all of the finer movements for which the hands are constantly used, such as buttoning the coat, tying a cravat, embroidering, cutting, writing, drawing, piano playing, etc. The movements become uncertain, spasmodic, awkward, zigzag-like, etc., particularly if they are performed without the aid of the eyes (buttoning the suspenders at the back). Ataxia becomes distinctly evident when the patient tries to touch with his fingers the tip of his nose or an object held in front of him, or if the fingers of both hands, being some distance apart, are gradually approximated at their tips ("index finger test"). When they attempt to grasp an object held in front of them, the fingers are drawn apart and awkward grabbing is noted, as well as when they try to describe figures in the air with a finger, such as circles, numerals, etc., and in writing and piano playing all movements are irregular, aimless, jerky and angular.

Finally, the hands become useless for the purposes of daily life; the patient can no longer eat nor dress without assistance, can hold nothing in the hands, and, in fact, is quite helpless.

Ataxia may also appear in the muscles of the trunk. The harmonious action of the muscles necessary to maintain the equilibrium in standing, sitting and in many movements, becomes dis