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POWERS, CHARLES A., Denver, Col. SUTTON, RICHARD LIGHTBURN, AMERICAN CLIMATOLOGICAL As-
PRICE, A. F., U. S. Navy.
Washington, D. C.

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SCHROEDER, HENRY H., New York. SCHROEDER, J. HENRY, Cincinnati, Ohio.

Scott, G. S., Lampoc, Cal.
SENN, NICHOLAS, Chicago.
SHELDON, JOHN G., Telluride, Col.
SHRADY, GEORGE F., New York.
SHULTZ, R. C., Los Angeles, Cal.
SPOONER, HENRY G., New York.
SPRATLING, WILLIAM P., Sonyea,
N. Y.

SQUIRES, G. W., East Avon, N. Y.
STARR, M. ALLEN, New York.
STEDMAN, CHESTER J., Newport,
R. I.

STEDMAN, THOMAS L., New York. STEERS, WILLIAM H., Brooklyn,

N. Y.

STEVENS, GEORGE T., New York.
STEWART, DOUGLAS H., New York.
STONE, WILLARD J., Gloversville,
N. Y.

STONER, A. P., Des Moines Iowa.
STRASSER, AUGUST ADRIAN, Ar-
lington, N. J.
STUBBERT, EDWARD, New York.
STURMDORF, ARTHUR, New York.

WARD, GEORGE GRAY, JR., New York.

WARD, NATHAN G., Philadelphia. WARFIELD, LOUIS M., Savannah, Ga.

SOCIATION.

AMERICAN DERMATOLOGICAL AS

SOCIATION.

AMERICAN ELECTROTHERAPEUTIC

ASSOCIATION.

AMERICAN LANRYNOLOGICAL AS

SOCIATION.

AMERICAN LARYNGOLOGICAL,
RHINOLOGICAL, AND OTOLOG-
ICAL SOCIETY.
AMERICAN MEDICAL ASSOCIATION.
AMERICAN NEUROLOGICAL ASSOCI-

ATION.

AMERICAN ORTHOPEDIC ASSOCIA

TION.

AMERICAN PUBLIC HEALTH As

SOCIATION.

BRITISH MEDICAL ASSOCIATION.
CANADIAN MEDICAL ASSOCIATION.
CONFERENCE OF STATE AND PRO-
VINCIAL BOARDS OF HEALTH
OF NORTH AMERICA.
MEDICAL SOCIETY OF NEW JERSEY.
MEDICAL SOCIETY OF THE COUNTY

OF NEW YORK.

WATKINS, I. L., Montgomery, Ala.
WAYSON, JAMES T., Honolulu.
WEBER, LEONARD, New York.
WEEKS, JOHN E., New York.
WHITE, J. HUTCHINS, Muskogee,
I. T.
WILSON, B. CLIFF, Powellsville, MEDICAL SOCIETY OF THE STATE
Ohio.
OF PENNSYLVANIA.

MEDICAL SOCIETY OF THE STATE OF NEW YORK.

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Vol. 64, No. 1... Whole No. 1704.

A Weekly Journal of Medicine and Surgery

NEW YORK, JULY 4, 1903.

Original Articles.

ARTERIAL SCLEROSIS AS A CAUSE OF NERVOUS DISEASE.

By M. ALLEN STARR, M.D., LL.D.,

PROFESSOR OF DISEASES OF THE MIND AND NERVOUS SYSTEM, COLLEGE OF PHYSICIANS AND SURGEONS, NEW YORK.

It

I. THE rôle that is played in the etiology of nervous diseases by endarteritis is becoming more and more widely recognized. It has, of course, long been known that disease of the arteries is the primary affection in the ordinary type of hemiplegia; whether due to a rupture of the vessel and hemorrhage, or to a stoppage of the blood current by thrombosis or embolism. Ever since the classical studies of Heubner upon syphilitic endarteritis this cause has been recognized in those cases of apoplexy which are so common among syphilitics in early life. is not, however, a matter of general knowledge that a very large number of the cases of hemiplegia occurring in childhood and in infancy are also to be traced to vascular disease. It is true that the infantile hemiplegias are, in many cases, of traumatic origin; injuries at birth producing a rupture of the blood vessels and consequent destruction of the brain tissue, which subsequently prevents its proper development. But there are a large number of cases of infantile hemiplegia that are not traceable to this cause, in which the attack has developed during the first or second year of life, possibly as a sequel to some reflex convulsion and possibly without apparent ascertainable cause. Recent investigations have proven that obliterating endarteritis may be the result of inherited syphilis, and hence it becomes evident that disease of the blood vessels is a factor in the causation of infantile cerebral palsies.

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A careful study of two hundred consecutive cases of apoplexy in private practice of which I have records has shown that in 80 per cent. of these cases there have been distinct prodromata of the apoplectic attack. For months, or even years, before the occurrence of the rupture or occlusion of the blood vessel the patients have complained of various symptoms which have usually been designated as neurasthenic. These symptoms all point to disturbance of function in the brain, chiefly in the cortical activity. The symptoms are very numerous and variable. Those that are the most commonly observed are a disturbance of mental action which the patients complain of as a dulness and hebetude, difficulty of clear thinking, difficulty in remembering events of recent occurrence, a sense of perplexity in regard to matters which should be clear; a sense of difficulty in the management of affairs which should be easy; and an irritability of temper and lack of control over emotions, that become a source of annoyance both to themselves and to the members of their family. Other patients complain of temporary sensations of numbness in one limb, or in one side of the body; of irregular darting pains through the head; of ringing in the ears, or of sounds in the head; of slight uncertainties of vision, occasional sudden dimness being not un

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common, and of vertigo. These symptoms occur with such uniformity as a preliminary to apoplectic attacks that they cannot be considered as merely of neurasthenic origin but must be traced to the malnutrition of the neurones consequent upon the original arterial disease. As all the processes of nutrition in brain cells and fibers must be carried on primarily by a process of osmosis through the vessel walls, it stands to reason that the earliest evidence of disease in these walls will be imperfect function consequent upon malnutrition.

The practical outcome of these observations is to warn the practitioner against dismissing a middleaged person who complains of these symptoms with the mere diagnosis of neurasthenia. In every such case the condition of the blood vessels should be investigated, attention being paid not merely to the nervous manifestations, but also to the condition of the heart, the possible existence of an accentuated second sound of the heart, the tension of the arteries, not merely in one wrist but in various parts of the body, especially in the temple, and the condition of the kidneys. If these factors be recognized and the condition of arterial sclerosis be made the object of treatment, the so-called neurasthenia will be much more likely to yield to treatment than if attention be merely concentrated upon remedies directed to the nervous system. I do not wish to have it supposed that all cases of neurasthenia have this origin. The large majority of such cases are due to malnutrition and auto-intoxication.' But in persons in middle life or beginning old age arterial disease may be a cause.

II. The facts hitherto mentioned are a matter of common knowledge and will be recognized by every physician. It is not as commonly known that the majority of diseases of the spinal cord are equally traceable to disease in the vessel wall. Williamson of Manchester' was the first to call attention to this fact; and here and there articles have appeared confirmatory of his position. But even in recent textbooks there is a lack of clear statement of the rôle which arterial sclerosis plays in the production of spinal paralysis. I may mention a few of the diseases in which it enters as an important etiological factor:

First: Anterior poliomyelitis, bulbar paralysis and ophthalmoplegia, that are diseases of homologous motor neurones of the cord and cerebral axis, are now known to fall into two categories, according to their origin. The majority of the cases are clearly infectious. This is proven in the case of anterior poliomyelitis by the occurrence of the disease in epidemics. But there is quite a proportion of the cases of anterior poliomyelitis which occur without the febrile movement characteristic of infectious disease. Recent pathological observations, especially of Mott, have demonstrated the lesion to be a rupture in some cases, a thrombosis in other cases, of some branch of the anterior spinal artery supplying the anterior gray horns of the spinal cord. And what is true of anterior poliomyelitis has also been found true of bulbar palsy and ophthalmoplegia, for in a number of cases of this affection Siemerling

and others have found vascular disease as the basis of the lesion.

Second: Myelitis whether of disseminated or transverse variety is also traceable either to infection or to a rupture of a blood vessel, in the latter case occurring as does cerebral hemiplegia without febrile symptoms. Investigation of Savage' and of Allan have proven the existence of arterial changes in many cases of this disease.

Third: The condition of spastic paralysis commonly known as Erb's syphilitic paraplegia is now recognized as due to malnutrition of the dorsal region of the spinal cord with consequent descend

in a slowly progressing paralysis of the legs with imperfect control of the bladder, and of the rectum, with atrophy of the muscles, and with irregular and indefinite sensory disturbances, chiefly of the nature of numbness and not attended by pain. This condition appearing as a rule after the age of sixty is prone to advance slowly, and finally becomes a complete paraplegia. It has been classed as the feebleness of old age and has been thought to be due to senile atrophy of the neurones, but, as a matter of fact, Dana showed some time ago and recent autopsies have proven that the disease of the nervous system in these cases is traceable to the obliteration

[graphic][subsumed][subsumed]

Group of atheromatous arteries (cerebral) seen under a low power. The walls are thickened (endarteritis) and degeneration is present in the thickened areas.

ing degeneration in the lateral columns.' The origin of the malnutrition of the dorsal region of the cord is the syphilitic endarteritis which obliterates the spinal blood vessels, especially on the posterior and lateral surfaces of the cord,

and hence produces a state of malnutrition in the white columns. The endarteritis is of the ordi

nary obliterating type and is clearly of syphilitic origin, though it must be stated that there is no pathological distinction to be made between obliterating endarteritis which is specific and one which is non-specific.

Fourth: There are numerous cases that have been hitherto classed together as senile paraplegia, in which a gradually advancing weakness culminates

of the blood vessels, to the thickening of their walls, and to the consequent malnutrition of the part.

Fifth: Combined sclerosis, which is a compara-.

tively rare but easily recognized form of paraplegia,

presenting a combination of the symptoms of

spastic paralysis with the unsteady gait of loco

motor ataxia, and which was named by Gowers ataxic paraplegia, has been recently shown by Marie to be due to malnutrition of the posterior and lateral columns of the cord consequent upon arterial disease. Marie's specimens show a thickening of the arteries and a degeneration in the cord that follows the distribution of the spinal blood vessels.

Thus we see that many forms of spinal-cord disease can be traced to arterial degeneration.

III. Diseases of the peripheral nerves are also occasionally due to endarteritis in the small vessels which accompany them. It is well known that in cases of chronic alcoholism sudden severe attacks of brachial or sciatic neuritis are observed. These differ from the ordinary alcoholic neuritis in being localized on one side. Some years ago Klumpke saw in one such case an extensive hemorrhage in the posterior cord of the brachial plexus, and described the condition as an apoplectic type of neuritis. Since that observation many others have been published of the same character, and hence we must regard it as probable that in a few cases in which a very sudden onset of either sciatic or brachial neuritis occurs without the ordinary cause of cold, or strain, to explain them, we have to deal with a rupture of a vessel in the nerve trunk. These cases are slow in their course, the symptoms are very intense and last for several weeks, and the case not infrequently becomes a chronic one, owing probably to the formation of a connective tissue scar within the nerve sheath, which constantly produces pres

sure.

IV. The facts already cited with regard to the occurrence of prodromata in cases of apoplexy traceable to malnutrition in the brain due to arterial disease and mistaken for cerebral neurasthenia, awakens the suspicion that some minor nervous symptoms, both of spinal cord and of nerve disease, may also be due to this same factor. We have a spinal type of neurasthenia characterized by pain in the back, by irregular sensations of numbness and tingling, by irregular pains in the body, twitching of the muscles and feelings of weakness in the limbs, and possibly irregular action of the bladder, and chronic constipation. In these cases it is not sufficient to make the diagnosis of a spinal neurasthenia. Attention must be paid to a possible underlying cause, namely, endarteritis.

V. Various forms of neuralgia may be brought into the same etiological category. It is now well recognized, from the lesions found in the Gasserian ganglion after extirpation for the relief of trigeminal neuralgia, that the origin of neuralgia may be a hemorrhage into the ganglion. Years ago Kaposi showed that hemorrhage into the posterior spinal ganglia was capable of producing both herpes and intercostal neuralgia. Such hemorrhages, of course, imply an affection of the vessel-wall as a predisposing cause, and therefore we are justified in tracing some cases of neuralgia, especially a neuralgia occurring in old age, to arterial degeneration. showed that neuralgia in old persons is often due to sclerosis in the small arteries accompanying the nerve, and applied this fact in the treatment by using nitroglycerin in such cases with success.

Dana

I do not wish to be understood as laying too much stress upon this factor in nervous disease. I have no desire to trace all nervous affections, including both neurasthenia and serious types of paralysis, to arterial disease, yet I cannot but feel that it is a factor in the production of many forms of nervous disease, and that it should receive more attention in the management of these cases.

And when we consider the forms of treatment which appear to be of most benefit both in neurasthenia, in neuralgias, in spinal paralysis, and in hemiplegia, we find that they include methods. which have as a result the establishment of an equable circulation. Thus life in the open air without exposure to great changes of climate; the use of tepid baths of considerable duration, or alternate

douches of hot water, long continued, followed by a quick cool douche of short duration; a diet free from alcohol and rich forms of food; moderate exercise, sufficient to produce a mild perspiration, but not sufficient to cause exhaustion and not attended by any great degree of effort; and massage, -are of considerable service.

It has not seemed to me that the ordinary treatment of arterial sclerosis by drugs was very satisfactory. From unknown causes of internal origin a very great variation in the tension of the pulse is commonly observed. Thus a patient with marked degeneration of the arteries will at one time have a very high tension pulse and at another time a soft pulse without high tension. It is, of course, possible by the use of iodide of potassium in 5 or 10grain doses 3 times a day, or of chloral in 5-grain doses every three hours, of nitroglycerin in varying doses from up to 6 of a grain every three hours, and of nitrite of sodium 1 to 4 grains every three hours, to produce immediate softening in a hard pulse. Yet in a condition in which spontaneous changes in the pulse tension are possible, it is manifestly improper to keep up such remedies constantly. It has seemed to me that there must be some agent within the body which regulates the pulse tension. If that agent is in excess the tension is abnormally low; if that agent is wanting the tension is abnormally high. It has been my observation in the treatment of Basedow's disease that a patient suffering from this condition never has a high-tension pulse. In fact, a low tension is noticeable in this condition.

We cannot but believe that many of the symptoms of Basedow's disease are due to an excess of thyroid secretion in the blood, and it is undoubtedly owing to the presence of this secretion in excess that the low tension of the pulse is due in this affection. This is proven by the therapeutic effects of thyroid obesity, or in acromegaly. In all of these diseases extract when administered in myxedema, or for I have watched the effect of thyroid extract very carefully, and have uniformly found that it reduced the arterial tension very markedly. It has seemed to me probable, therefore, that in some cases of arterial sclerosis, and in many cases of temporary high-tension pulse, there may be a permanent or temporary defect or arrest of secretion of the thyroid gland. Thus in migraine, in which the sudden attack of sick headache is almost always attended by a very great increase in the arterial tension, there is, as a rule, during the attack a remarkable dryness of the skin, pallor, and coldness of the skin, not unlike that observed in myxedema. And this is quite suggestive of a sudden arrest of secretion of the thyroid gland as a partial cause of the attack of migraine. But aside from theoretical considerations, which may or may not be correct, the practical effect of the administriation of thyroid extract in conditions of arterial disease is decided. Thus in conditions of temporary high-tension pulse I have found the administration of thyroid extract of very great benefit. And whatever the underlying cause of the increase of arterial tension may be, it is markedly relaxed by the administration of this remedy. Thus in migraine, which has just been mentioned, it is quite capable in many cases of arresting the attack, and in those conditions of vertigo, headache, and confusion of mind which attend a high-tension pulse, and which are associated very often with a lithæmic state, the addition of thyroid extract to other remedies will give marked relief. In conditions of chronic or permanent arterial sclerosis' when the pulse tension is constantly high, I have also seen a certain amount

of benefit from its use, and for this reason I much prefer it to the continued use of nitroglycerin.

In this class of patients, especially in those who have suffered organic nervous changes from the effects of the arterial sclerosis, constant, skilful observation appears to be absolutely essential. It is not a difficult matter to instruct a nurse, or some member of the family, in detecting variations in the pulse tension, and even patients themselves soon come to appreciate this with a considerable degree of accuracy. Considering the great normal variations in tension, this is manifestly of importance. For it is useless to give a remedy six days in the week if a high-tension pulse only occurs on the seventh day. In these conditions, therefore, it seems unwise to keep up remedies constantly. It is far better to keep up the skilled observation of the patient and apply the remedy when it is particularly needed. Thus I have one patient who for ten years has had very extensive arterial sclerosis, and who has, about once in eight to ten weeks, without any apparent ascertainable cause, a sudden, quick rise in the arterial tension attended by pressure in the head and a sense of great alarm, and followed in the course of two hours by a general epileptiform convulsion. If in this patient at the time of the beginning of the symptoms nitroglycerin is used freely hypodermically, and chloroform is used by inhalation in moderation, the pulse tension is found to relax and the attack passes off without the onset of the convulsion. There is no object in giving this man a remedy for the relief of tension in the intervals, as at that time his pulse is as soft as possible.

It should never be overlooked that many patients who have extensive arterial disease, atheromatous arteries, and abnormally high-tension pulse, and who show symptoms traceable to these conditions, frequently live to extreme old age, and do not die from the effects of their arterial disease. It should also be remarked that many persons who present evidence of extreme arterial sclerosis live their lives without any symptoms at all. These two facts should be recollected in giving the prognosis. in this condition, for however serious the condition may appear during the attack, either of functional or organic nervous disease, we must admit that the underlying condition is one which may spontaneously subside or disappear under treatment.

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A Note on Melanoma.-C. R. Keyser states that formerly melanomata were always classified as belonging to the sarcomata or connective tissue type of tumors, and microscopically the cells often present a spindle or fusiform shape, and are arranged as in sarcomata; the pigment appears both in and between the cells. But recently it has become more and more patent that all melanotic tumors are not sarcomata, but carcinomata, for the following reasons: (1) An alveolar arrangement of the cells is not at all uncommon. (2) The cells are of an epithelioid type. (3) The tumor originates in the skin, usually in a mole. (4) The lymphatic glands are early affected.Medical Times and Hospital Gazette.

THE ANATOMY OF PORTAL ANASTOMOSIS.*

BY ROLFE FLOYD, M.D.,

NEW YORK.

THIS paper briefly describes: (1) The liver circulation in the foetus at term; (2) the changes in the liver circulation at birth; (3) the sites of anastomosis between the portal and systemic veins in the adult.

I. The liver circulation in the foetus at term.In the foetus at term the venous capillaries, although already arranged about and in the lobules, as in the adult, do not yet serve to isolate the portal from the systemic veins.

At this time the umbilical vein (Fig. 1, UM. V.), coursing from the navel in the lower edge of the suspensory ligament, enters the median groove on the under surface of the liver and there gives off small left branches (Fig. 1, L1), to the anterior part

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H.Y

L.

P.V.

UM.V.

Fig. 1.-Liver circulation prenatal condition. In this and Fig. 2 the liver is viewed from above, the vessels being seen through its substance. of the left lobe, and small right branches to the quadrate lobe (Fig. 1, Q.). Reaching the left end of the transverse fissure, it ends by dividing into three branches. One, the largest, traverses the transverse fissure and enters the right lobe (Fig. 1, R.), a second passes into the left lobe (Fig. 1, L.) while a third, continuing the direction of the parent stem for about one inch, enters the inferior vena cava, or one of the hepatic veins just before its junction with the cava (Fig. 1, D. V.). This vessel is the ductus venosus, and lies deeply buried in the ductus venosus fissure on the posterior aspect of the liver.

All the branches of the umbilical vein, except the ductus venosus, break up into smaller vessels, which finally end in the capillaries which penetrate the liver lobules.

The portal vein, bringing blood from the stomach, intestines, spleen, and pancreas, appears at this time as a comparatively small tributary, which joins the right branch of the umbilical vein where that vessel lies in the transverse fissure of the liver (Fig. 1, P. V.).

The hepatic veins (Fig. 1, H. V.) are two or three large vessels on each side, which take origin in the central veins of the lobules, and enter the inferior vena cava just before it perforates the diaphragm.

It is interesting in dissecting these vessels to note that, while the hepatic veins can be exposed by simply rubbing off the friable liver tissue, the

branches of the umbilical vein are incased in a firm, connective tissue sheath. In portal obstruction the throttling may quite as well occur in these venules of the portal canals as in the intralobular capillaries.

II. Changes in the liver circulation at birth.-At *A contribution from the Anatomical Laboratory of the College of Physicians and Surgeons.

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