A

SYSTEM

OF

PRACTICAL MEDICINE.

BY

AMERICAN AUTHORS.

EDITED BY

WILLIAM PEPPER, M.D., LL.D.,

ASSISTED BY

LOUIS STARR, M.D.,

VOLUME II.

GENERAL DISEASES (CONTINUED)

DISEASES OF THE DIGESTIVE SYSTEM.

PHILADELPHIA:
LEA BROTHERS & CO.
1885.

CONTENTS OF VOLUME II.

GENERAL DISEASES (CONTINUED).

RHEUMATISM. By R. PALMER HOWARD, M.D.

GOUT. By W. H. DRAPER, M.D.

RACHITIS. By ABRAHAM JACOBI, M.D.

SCURVY. By PHILIP S. WALES, M.D.

PURPURA. By I. EDMONDSON ATKINSON, M.D.

DIABETES MELLITUS. By JAMES TYSON, A.M., M.D.

SCROFULA. By JOHN S. LYNCH, M.D.

HEREDITARY SYPHILIS. By J. WILLIAM WHITE, M.D.

DISEASES OF THE DIGESTIVE SYSTEM.

DISEASES OF THE MOUTH AND TONGUE. By J. SOLIS COHEN, M.D.

DISEASES OF THE TONSILS. By J. SOLIS COHEN, M.D.

DISEASES OF THE PHARYNX. By J. SOLIS COHEN, M.D.

DISEASES OF THE OESOPHAGUS. By J. SOLIS COHEN, M.D.

FUNCTIONAL AND INFLAMMATORY DISEASES OF THE STOMACH. By SAMUEL G. ARMOR, M.D., LL.D.

SIMPLE ULCER OF THE STOMACH. By W. H. WELCH, M.D.

CANCER OF THE STOMACH. By W. H. WELCH, M.D.

HEMORRHAGE FROM THE STOMACH. By W. H. WELCH, M.D.

DILATATION OF THE STOMACH. By W. H. WELCH, M.D.

MINOR ORGANIC AFFECTIONS OF THE STOMACH (Cirrhosis; Hypertrophic Stenosis of Pylorus; Atrophy; Anomalies in the Form and the Position of the Stomach; Rupture; Gastromalacia). By W. H. WELCH, M.D.

INTESTINAL INDIGESTION. By W. W. JOHNSTON, M.D.

CONSTIPATION. By W. W. JOHNSTON, M.D.

ENTERALGIA (INTESTINAL COLIC). By W. W. JOHNSTON, M.D.

ACUTE INTESTINAL CATARRH (DUODENITIS, JEJUNITIS, ILEITIS, COLITIS, PROCTITIS). By W. W. JOHNSTON, M.D.

CHRONIC INTESTINAL CATARRH. By W. W. JOHNSTON, M.D.

CHOLERA MORBUS. By W. W. JOHNSTON, M.D.

INTESTINAL AFFECTIONS OF CHILDREN IN HOT WEATHER. By J. LEWIS SMITH, M.D.

PSEUDO-MEMBRANOUS ENTERITIS. By PHILIP S. WALES, M.D.

DYSENTERY. By JAMES T. WHITTAKER, A.M., M.D.

TYPHLITIS, PERITYPHLITIS, AND PARATYPHLITIS. By JAMES T. WHITTAKER, A.M., M.D.

INTESTINAL ULCER. By JAMES T. WHITTAKER, A.M., M.D.

HEMORRHAGE OF THE BOWELS. By JAMES T. WHITTAKER, A.M., M.D.

INTESTINAL OBSTRUCTION. By HUNTER MCGUIRE, M.D.

CANCER AND LARDACEOUS DEGENERATION OF THE INTESTINES. By I. EDMONSON ATKINSON, M.D.

DISEASES OF THE RECTUM AND ANUS. By THOMAS G. MORTON, M.D., and HENRY M. WETHERILL, JR., M.D., PH.G.

INTESTINAL WORMS. By JOSEPH LEIDY, M.D., LL.D.

DISEASES OF THE LIVER. By ROBERTS BARTHOLOW, A.M., M.D., LL.D.

DISEASES OF THE PANCREAS. By LOUIS STARR, M.D.

PERITONITIS. By ALONZO CLARK, M.D., LL.D.

DISEASES OF THE ABDOMINAL GLANDS (TABES MESENTERICA). By SAMUEL C. BUSEY, M.D.

INDEX

CONTRIBUTORS TO VOLUME II.

ARMOR, SAMUEL G., M.D., LL.D.,

Brooklyn.

ATKINSON, I. EDMONDSON, M.D.,

Professor of Pathology and Clinical Medicine and Clinical Professor of Dermatology in the University of Maryland, Baltimore.

BARTHOLOW, ROBERTS, A.M., M.D., LL.D.,

Professor of Materia Medica, General Therapeutics, and Hygiene in the Jefferson Medical College, Philadelphia.

BUSEY, SAMUEL C., M.D.,

An Attending Physician and Chairman of the Board of Hospital Administration of the Children's Hospital, Washington, D.C.

CLARK, ALONZO, M.D., LL.D.,

Late Professor of Pathology and Practical Medicine in the College of Physicians and Surgeons, New York.

COHEN, J. SOLIS, M.D.,

Professor in Diseases of the Throat and Chest in the Philadelphia Polyclinic; Physician to the German Hospital, Philadelphia.

DRAPER, W. H., M.D.,

Attending Physician to the New York and Roosevelt Hospitals, New York.

HOWARD, R. PALMER, M.D.,

Professor of Theory and Practice of Medicine in McGill University, Montreal; Consulting Physician to Montreal General Hospital, Canada.

JACOBI, ABRAHAM, M.D.,

Clinical Professor of Diseases of Children in the College of Physicians and Surgeons, New York, etc.

JOHNSTON, W. W., M.D.,

Professor of Theory and Practice of Medicine in the Columbian University, Washington.

LEIDY, JOSEPH, M.D., LL.D.,

Professor of Anatomy in the University of Pennsylvania, Philadelphia.

LYNCH, JOHN S., M.D.,

Professor of Principles and Practice of Medicine in the College of Physicians and Surgeons, Baltimore.

MORTON, THOMAS G., M.D.,

Surgeon to the Pennsylvania Hospital, Philadelphia.

MCGUIRE, HUNTER, M.D.,

Richmond, Va.

SMITH, J. LEWIS, M.D.,

Clinical Professor of Diseases of Children in the Bellevue Hospital Medical College, New York.

STARR, LOUIS, M.D.,

Clinical Professor of Diseases of Children in the Hospital of the University of Pennsylvania, Philadelphia.

TYSON, JAMES, A.M., M.D.,

Professor of General Pathology and Morbid Anatomy in the University of Pennsylvania, Philadelphia.

WALES, PHILIP S., M.D.,

Washington.

WELCH, WILLIAM H., M.D.,

Professor of Pathology in Johns Hopkins University, Baltimore.

WETHERILL, HENRY M., JR., M.D.,

Assistant Physician to the Pennsylvania Hospital for the Insane, Philadelphia.

WHITE, J. WILLIAM, M.D.,

Surgeon to the Philadelphia Hospital; Assistant Surgeon to the University Hospital; Demonstrator of Surgery and Lecturer on Venereal Diseases and Operative Surgery in the University of Pennsylvania, Philadelphia.

WHITTAKER, JAMES T., M.D.,

Professor of Theory and Practice of Medicine in the Medical College of Ohio, Cincinnati.

ILLUSTRATIONS TO VOLUME II.

GENERAL DISEASES

RHEUMATISM.

Acute Articular Rheumatism.

SYNONYMS AND DEFINITION.—Acute Rheumatism, Acute Rheumatic Polyarthritis, Rheumarthritis, Rheumatic Fever, Polyarthritis Synovialis Acuta (Heuter).

Acute articular rheumatism is a general non-contagious, febrile affection, attended with multiple inflammations, pre-eminently of the large joints and very frequently of the heart, but also of many other organs; these inflammations observing no order in their invasion, succession, or localization, but when affecting the articulations tending to be temporary, erratic, and non-suppurating; when involving the internal organs proving more abiding, and often producing suppuration in serous membranes. It is probably connected with a diathesis—the arthritic—which may be inherited or acquired. It may present such modifications of its ordinary characters as to justify being called (2d) subacute articular rheumatism, and it may sometimes pass into the (3d) chronic form.

ETIOLOGY.—There is a general consensus of opinion that acute articular rheumatism belongs especially to temperate climates, and that it is exceedingly rare in polar regions; but respecting its prevalence in the tropics contradictory statements are made. Saint-Vel declares that it is not a disease of hot climates; Rufz de Levison saw only four cases of acute articular rheumatism, and not one of chorea, in Martinique during twenty years' practice; while Pruner Bey says it is common in Egypt, and Webb remarks the same for the East Indies. Even in temperate climates, like those of the Isle of Wight, Guernsey, Cornwall, some parts of Belgium (Hirsch), the disease is very rare—a circumstance not to be satisfactorily explained at present.

Acute articular rheumatism is never absent; it occurs at all seasons of the year, although subject to moderate variations depending mainly upon atmospheric conditions. It is the general opinion that it prevails most during the cold and variable months of spring, but this is not true of every place, nor invariably of the same place. Indeed, Besnier,¹ after a long and special observation of the disease in Paris, concludes that there it is most frequent in summer and in spring. In Montreal, during ten years, the largest number of cases of acute rheumatism admitted to the General Hospital obtained in the spring months (March to June inclusive), when they averaged 51 a month; 33 was the average for all the other months, except October and November, when 26½ was the average. The statistics of Copenhagen, Berlin, and Zurich show a minimum prevalence in summer or in summer and autumn.

¹ Dictionnaire Encyclopédique des Sciences Méd., Troisième Serie, t. iv.

Occupations involving muscular fatigue or exposure to sudden and extreme changes of temperature, especially during active bodily exertion, predispose to acute articular rheumatism; hence its frequency amongst cooks, maid-servants, washerwomen, smiths, coachmen, bakers, soldiers, sailors, and laborers generally.

While no age is exempt from acute articular rheumatism, it is, par excellence, an affection of early adult life, the largest number of cases occurring between fifteen and twenty-five years of age, and the next probably between twenty-five and thirty-five. A marked decline in its frequency takes place after the age of thirty-five, and a still greater after forty-five. It is not uncommon in children between five and ten, and especially between ten and fifteen, but is very rare under five, although now and then one meets with an example of the disease in children three or four years of age. While the acute articular affections observed in sucklings are, as a general rule, either syphilitic or pyæmic, some authentic instances of rheumatic polyarthritis are recorded. Kauchfuss's two cases among 15,000 infants at the breast, Widerhofer's case, only twenty-three days old, Stager's, four weeks old, and others, are cited by Senator.²

² Ziemssen's Cyclop. of Pract. Med., xvi. 17.

An analysis of 4908 cases of acute rheumatism admitted to St. Bartholomew's Hospital, London,³ during fifteen years, and of 456 treated in the Montreal General Hospital during ten years,⁴ gives the following percentages at given periods of life:

The close correspondence existing in the two tables for all the periods of life above fifteen is very striking: the disparity between them below the age of fifteen may, I believe, be explained by the circumstance that the pauper population of Montreal is, when compared with that of London, relatively very small, and by the further fact that the practice of sending children into hospitals hardly obtains here.

³ St. Bartholomew's Hospital Reports, xiv. 4.

⁴ Dr. James Bell, in Montreal General Hospital Reports, i. 350.

No doubt the above tables do not correctly represent the liability of children to acute articular rheumatism, but they are probably a fair statement of the relative frequency of the disease in the adult hospital populations of London and Montreal. If primary attacks of the disease only were tabulated, the influence of youth would be more evident, for it is scarcely possible to find on record an authentic instance of the disease showing itself for the first time after sixty. Dr. Pye-Smith⁵ has done this in 365 cases, and the results prove the great proclivity of very young persons to acute rheumatism: Between five and ten years, 6 per cent. occurred; between eleven and twenty, 49 per cent.; from twenty-one to thirty, 32.3 per cent.; from thirty-one to forty, 9.5 per cent.; from forty-one to fifty, 2.2 per cent.; and from fifty-one to sixty-one, 1.1 per cent. The same author has also shown that secondary attacks are most common in the young; so that advancing age not only renders a first attack of the disease improbable, but lessens the risk of a recurrence of it. The influence of age upon acute rheumatism is further shown in the fact that the disease is less severe, and less apt to invade the heart, in elderly than in young persons.

⁵ Guy's Hospital Reports, 3d Series, xix. 317.

The general opinion that sex exercises no direct influence beyond exposing males more than females to some of the predisposing and exciting causes of acute rheumatism is perhaps true if the statement be confined to adults, to whom, indeed, most of the available statistics apply; but it should be borne in mind that a larger proportion of men than of women resort to hospitals, and there is some reason to believe that in childhood the greater liability to the disease is on the part of the female sex. Thus, the number of cases of rheumatism treated at the Children's Hospital in London from 1852 to 1868 was 478, of whom 226 were males and 252 females.⁶ Of Goodhardt's 44 cases of acute rheumatism in children, 26 were girls and 18 were boys.⁷ Of 57 examples of rheumatism in connection with chorea observed by Roger in children under fourteen, 33 were girls and 24 were boys.⁸

⁶ Vide Dr. Tuckwell's "Contributions to the Pathology of Chorea," in St. Bartholomew's Hospital Reports, v. 102.

⁷ Guy's Hospital Reports, 3d Series, xxv. 106.

⁸ Arch. Gén., vol. ii. 641, 1866, and vol. i. 54, 1867, quoted by Tuckwell.

That heredity predisposes to acute articular rheumatism is admitted by nearly all modern authorities, even Senator, while speaking of it as "a traditional belief," not venturing to deny it. The frequency of the inherited predisposition Fuller placed at 34 per cent.; Beneke, quoted by Homolle,⁹ at 34.6 per cent; Pye-Smith at 23 per cent.¹⁰ Such predisposition favors the occurrence of the disease in early life, but does not necessarily determine an attack of acute rheumatism in the absence of the other predisposing or exciting causes. That the inherited bias or mode of vital action or condition of tissue-health may be so great as, per se, to induce an attack of the disease, is held by some authorities. It is probable that not only acute articular rheumatism in the parents, but simple chronic articular rheumatism and those forms grouped under the epithet rheumatoid arthritis, may impart a predisposition to the acute as well as to the chronic varieties of articular disease just mentioned. But owing to the obscurity which still surrounds the relations existing between acute articular rheumatism and rheumatoid arthritis this point needs further investigation. In what the inherited predisposition to acute articular rheumatism consists we are ignorant; to say that it imparts to the tissues or organs a disposition to react or act according to a fixed morbid type, or that some of the nutritive processes are perverted by it, is merely to state a theory, not to explain the nature of the predisposition.

⁹ Nouv. Dict. de Méd. et de Chir., t. 31, 557.

¹⁰ Guy's Hospital Reports, 3d Series, xix. 320.

No type of bodily conformation or temperament can be described that certainly indicates a proclivity to acute articular rheumatism; nor is there any change in the constitution of the tissues or fluids of the body by which the proclivity may be recognized. We infer the existence of the inherited predisposition—the innate bias—when rheumatism is found in the family history; when acute rheumatism or cardiac disease, or chorea not produced by mental causes, occurs in childhood; when the first attack of acute articular rheumatism is succeeded by subsequent attacks; and especially when the intervals between the attacks are short. Goodhardt has recently furnished valuable, but not conclusive, evidence to prove that in children obstinate headaches, night-terrors, severe anæmia, various neuro-muscular derangements, such as torticollis, tetany, muscular tremors, stammering, incontinence of urine, recurring attacks of abdominal pain, with looseness of the bowels quickly succeeding a meal, the cutaneous affection erythema nodosum, are indications of a rheumatic bias or predisposition.¹¹

¹¹ Guy's Hospital Reports, 3d Series, xxv.

There is some basis for the opinion that residence in damp, cold dwellings predisposes somewhat to acute articular rheumatism, although not at all to the same degree that it does to the chronic articular and muscular forms. Chomel and Jaccoud especially have insisted that it will gradually create a predisposition to the disease, even if it has not been inherited. All pathologists agree that cold is the most frequent exciting cause of acute articular rheumatism, and that it is especially effective when applied while the body is perspiring freely or is overheated or fatigued by exercise. There is no necessary ratio between the degree of cold or its duration and the severity of the resulting rheumatism. A slight chilling or a momentary exposure to a current of cold air will in some act as powerfully and as certainly as a prolonged immersion in cold water or a night spent sleeping on the damp grass. This circumstance, together with the fact that cold applied in the same way may also produce a pharyngitis or a bronchitis, a pneumonia or a nephritis, etc., is held to indicate that the cold acts according to individual predisposition; and Jaccoud, Flint, and others maintain that unless a rheumatic proclivity exists cold will not produce an attack of the disease under consideration. I doubt that we are yet in a position to assert that absolutely, although the weight of argument is in its favor. Let it suffice to say, that while a prolonged residence in a cold, damp dwelling may gradually develop a predisposition to rheumatism, a short exposure to cold will be likely to induce an attack of rheumatism if the predisposition exist.

There are other influences which may be regarded as auxiliaries to cold in exciting an attack, as they seem to increase the susceptibility of the patient to its operation: they establish what has been felicitously called a state of morbid opportunity. Such are all influences that reduce the resisting powers of the organs and organism, as bodily fatigue, mental exhaustion, the depressing passions, excessive venery, prolonged lactation, losses of blood, etc. It is probably in such a manner that local injuries (traumatism) sometimes appear to induce an attack of rheumatism. A blow on a finger (Cotain), the extraction of a tooth (Homolle), a hypodermic injection (ibid.), etc., may act powerfully in some persons upon and through the nervous system, and by lessening their resisting power may favor the overt manifestation of the rheumatic predisposition. But doubtless some such cases have been examples of mere coincidence.

There are certain pathological and even physiological conditions during or after which an inflammatory affection of one or several joints closely resembling acute articular rheumatism more or less frequently arises. Thus, during the early desquamating stage of scarlatina a mild inflammation of the joints of the hands and feet, and frequently of the large articulations as well, is very often seen, and it is attended with profuse perspiration, with a condition of urine like that of ordinary acute rheumatism, and occasionally with inflammation of the heart or pleura. During convalescence from dysentery an affection of a single or of several articulations resembling rheumatism has been noticed, and the two affections have even alternated in the same patient. That singular epidemic disease dengue is attended with a polyarticular affection closely resembling acute articular rheumatism, occasionally pursuing a protracted course, and not seldom leaving after it a cardiac lesion. In hæmophilia polyarticular and muscular disorders frequently arise which closely resemble, and appear to be sometimes identical with, ordinary acute articular and muscular rheumatism. Gonorrhoea too is often associated with a febrile polyarthritis, and rarely with an endocarditis at the same time. In the puerperal state an inflammation of one or several articulations is not unfrequently observed (puerperal rheumatism).

Respecting the real nature of these polyarticular inflammations very much has to be made out; and it must suffice at present to say that while many of them are of a pyæmic nature, as some examples of puerperal and scarlatinal arthritis, in which pus forms in or about the joints and in the serous cavities and viscera, some of them are no doubt examples of genuine rheumatism occurring in persons of rheumatic predisposition, which have either been induced by the lowering influence of the disease upon which they have supervened, or by the accidental coincidence of some of the other causes of acute rheumatism. There remains, however, the ordinary form of scarlatinal arthritis, which so closely resembles true acute articular rheumatism in its symptoms, course, visceral complications, and morbid anatomy that it cannot be said that the two affections are distinct and different. And much the same appears to be true of the articular affection of dengue. Yet so frequently does the articular affection accompany scarlatina and dengue respectively that it cannot logically be referred to a coexisting rheumatic predisposition, and must be a consequence of the disturbing influences of the specific poison of those zymotic affections per se.

PATHOLOGY.—The pathology of acute articular rheumatism is a very much debated question, and is not at all satisfactorily known. Hence a mere statement of the most prominent theories now held by different pathologists will be given.¹²

¹² The reader may consult with advantage Dr. Morris Longstreth's fourth chapter in his recent excellent monograph upon Rheumatism, Gout, and some Allied Disorders, New York, 1882.

The latest modification of the lactic-acid theory of Prout is founded upon the modern physiological teaching that during muscular exercise sarcolactic acid and acid phosphate of potassium are formed, and carbon dioxide set free, in the muscular tissue, and that cold, acting on the surface under such circumstances, may check the elimination of these substances and cause their accumulation in the system. This view, it is held, explains why the muscles and their associated organs, the joints and tendons, suffer first and chiefly, because the morbific influence is exerted upon them when exhausted by functional activity; and it further accounts for the visceral manifestations and the apparent excess of acid eliminated during the course of the disease. The circumstance that in three cases of diabetes (Foster,¹³ Kuelz¹⁴) the administration of lactic acid appeared to induce polyarticular rheumatism favors the idea that acid is the materies morbi in rheumatism.

¹³ Brit. Med, Jour., ii. 1871.

¹⁴ Beiträge zur Path. und Therapie des Diabetes, u. s. w., ii. 1875.

Now it must be admitted that, as yet, no sufficient proof is forthcoming that a considerable excess of lactic acid exists in the fluids or solids of the body or in the excretions in rheumatism (it is true the point has not been sufficiently investigated). On the other hand, that acid has been found in the urine of rickets, and its excess in the system is regarded by Heitzmann and Senator¹⁵ as the cause of the peculiar osteoplastic disturbances of that disease—an affection altogether different from rheumatism. It is quite improbable that the amount of sarcolactic acid produced by over-prolonged muscular exertion, and whose elimination has been prevented by a chill or a mental emotion, is sufficient to maintain the excessive acidity of the urine and other fluids during a long rheumatic fever; and arguments can be adduced favorable to the view that excessive formation of acid is an effect rather than the cause of rheumatism: cases of that disease occur in which neither excessive muscular exertion nor exposure to chill have preceded the rheumatic outbreak. Lastly, lactic acid is not the only principle retained when the functions of the skin are arrested by cold, the usual exciting cause of rheumatism; why should not the retained acetic, formic, butyric, and other acids, for example, play their rôle in the production of the symptoms observed under such conditions?

¹⁵ Ziemssen's Cyclop., xvi. p. 177.

The same objections apply to Latham's¹⁶ hypothesis that hyperoxidation of the muscular tissue is the starting-point of acute rheumatism. He assumes, with other physiologists, the existence of a nervous centre which inhibits the chemical changes that would take place if the tissues were out of the body. If this centre be changed or weakened, the muscle, instead of absorbing and fixing the oxygen and giving out carbonic acid, disintegrates; lactic acid is formed, and, passing into the blood, may be there oxidized and produce the pyrexia of acute rheumatism. It need hardly be remarked that the existence of a chemical inhibitory centre has yet to be proved, although much may be advanced in its favor; and, secondly, the recent investigations of Zuntz render it highly probable that in all febrile affections it is the muscles chiefly, if not solely, which suffer increased oxidation, and that this is due to increased innervation—views not easily reconciled with Latham's theory.

¹⁶ Brit. Med. Jour., ii. 1880, p. 977.

The nervous theory of rheumatism and of articular diseases originated with Dr. J. K. Mitchell of Philadelphia¹⁷ in 1831, and was afterward elaborated by Froriep in 1843,¹⁸ Scott Alison¹⁹ in 1846, Constatt in 1847,²⁰ Gull in 1858, Weir Mitchell in 1864,²¹ Charcot in 1872, and by very many others since. According to present physiological doctrine, the exciting cause of rheumatism, cold, either acts directly upon the vaso-motor or the trophic (?) nerves of the articulations, and excites inflammation of them, or else it irritates the peripheral ends of the centripetal nerves, and through these excites actively the vaso-motor and trophic nerve-centres. The local lesions, on this hypothesis, are of trophic origin; the fever is due to hyperactivity of the centres supposed to control the chemical changes going on in the tissues; the excessive perspiration to stimulation of the sweat-centres; and so on. It is not held that a definite centric lesion of the nervous system exists in rheumatism, analogous to the lesions which in myelitis or locomotor ataxia develop the arthropathies of those affections, but rather a functional disturbance. One of the latest and ablest advocates of the neurosal theory of rheumatism in all its forms (simple, rheumatoid, gonorrhoeal, urethral, etc.), Jonathan Hutchinson, calls it "a catarrhal neurosis, the exposure of some tract of skin or mucous membrane to cold or irritation acting as the incident excitor influence."²²

¹⁷ Am. Jour. Med. Sci., 1831; ib., 1833.

¹⁸ Die Rheumatische Schwiele, Weimar, 1843.

¹⁹ Lancet, 1846, i. 227.

²⁰ Spec. Pathologie und Therapie, 1847, ii. p. 609.

²¹ Vide Am. Jour. Med. Sciences, April, 1875, vol. lxix. 339-348.

²² Trans. International Med. Congress, 1881, ii. 93.

In order that peripheral irritation shall thus induce inflammation of the joints and the other affections of muscles, tendons, fasciæ, etc. which are called rheumatic, he holds with the French School that the arthritic diathesis must exist, or that state of tissue-health which involves a tendency to temporary inflammation of many joints or fibrous structures at once, or to repeatedly recurrent attacks of inflammation of one joint or fibrous structure. If I understand Mr. Hutchinson correctly, he also holds that a nerve-tissue peculiarity exists which renders persons liable to rheumatism. He does not indicate either the cause or the nature of the nerve-tissue peculiarity. But modern pathology teaches that the functional conditions of the nervous centres known as neuroses, whether inherited or acquired, reveal themselves as morbid manifestations of nerve-function on the part of special portions of or the entire nervous system, and, as Dr. Dyce Duckworth has well pointed out, these neuroses may be originated, when not inherited, in various ways, as by excessive activity of the nervous system, by prolonged or habitual excesses, etc. "Thus, undue mental labor, gluttony, alcoholic intemperance, debauchery, and other indulged evil propensities in the parent come to be developed into definite neurotic taint and tendency in the offspring."

But is there nothing more in acute articular rheumatism than an inflammation of certain structures, articular and visceral, lighted up in an individual of a neuro-arthritic diathesis? What do we learn from that closely-allied affection, gout, which involves especially the same organs as rheumatism, and is held by many of the ablest pathologists to belong to the same basic diathesis as it? Duckworth²³ has very ably advocated a neurotic theory of gout, but it is admitted on all hands—and by Duckworth himself—that in gout a large part of the phenomena is due to perverted relations of uric acid and sodium and to the presence of urate of soda in the blood. May we not from analogy, as well as from other evidence, infer that in that so-called other neurosis, rheumatism, a considerable part of the phenomena is due to perversions of the processes of assimilation and excretion, and to the presence of some unknown intermediate product of destructive metamorphosis—lactic or other acid? This is admitted by Maclagan and strongly advocated by Senator; and in this way the pathology of the disease may be said to embrace the humoral as well as the solidist doctrines—the resulting theory being a neuro-humoral one. No doubt pathological chemistry and clinical investigation will ere long make important discoveries respecting the pathology of acute rheumatism which shall maintain the close alliance believed to exist between that affection and gout.

²³ Brain, April, 1880.

The miasmatic theory, so ably advocated by Maclagan,²⁴ assumes that rheumatism is due to the entrance into the system from without of a miasm closely allied to, but quite distinct from, malaria. His argument on this topic is ingenious and elaborate, yet has not been favorably received by pathologists. Opposed to it are the following amongst other considerations: Heredity exercises a marked influence upon the occurrence of rheumatism; unlike malarial disease, no climate or locality is immune from rheumatism; the many indications that a diathesis plays a chief rôle in rheumatism; the remarkable influence exerted by cold and dampness in the etiology of the disease.

²⁴ Rheumatism: its Nature, Path., etc., London, 1881, pp. 60-95.

Heuter's²⁵ infective-germ theory, like the miasmatic, refers rheumatism to a principle not generated in the system, but introduced from without. A micrococcus enters the dilated orifices of the sweat-glands, and, reaching the blood, first sets up an endocarditis, and then capillary emboli produce the articular inflammations. This is a reversal of what really happens, so far as the time of invasion of the endocardium and the synovial membranes is concerned; and Fleischauer's case, in which miliary abscesses were found in the heart, lungs, and kidneys, was probably one of ulcerative endocarditis, which, after all, is a rare complication of acute articular rheumatism. Moreover, it is a gratuitous assertion to say that endocarditis exists in all cases of the disease. If, however, Heuter were content to say that acute articular rheumatism was produced by a specific germ, as held by Recklinghausen and Klebs, which on entering the system acted specially upon the joints and the fibro-serous tissues, as the poison of small-pox does upon the skin, while at the same time it sets up general disturbances of the entire economy as other zymotic poisons do, there would be nothing opposed to general pathological laws. Even the existence of a diathesis capable of favoring the action of the specific germ would be analogous to the tuberculous diathesis, which favors the action of the bacillus of tubercle; and cold, its ordinary exciting cause, might be regarded simply as a condition which renders the system more susceptible to the action of the germ, and the modus operandi of cold in doing this might be variously explained.

²⁵ Klinik der Gelenkkrankheiten, Leipzig, 1871.

SYMPTOMS.—The disease has no uniform mode of invasion. (a) Very frequently slight disorder of health, such as debility, pallor, failure of appetite, unusual sensibility to atmospheric changes, grumbling pains in the joints or limbs, or even in some muscle or fascia, precedes by one or more days the fever and general disturbance. (b) Not infrequently a mild rigor or repeated chilliness, accompanied or soon followed by moderate or high fever, ushers in the illness, and in from a few hours to one or at most two days the characteristic articular symptoms ensue. (c) In very rare cases febrile disturbance, ushered in by chills, may be followed by inflammation of the endo- or pericardium or pleura before the joints become affected.