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Roswell P. Flower Library
THE GIFT OF
ROSWELL P. FLOWER
FOR THE USEOF
THE N. Y. STATE VETERINARY COLLEGE.
1897

 
AW 209.021 1698
Rheumatoid arthriti

Ii ic

Bae

 
RHEUMATOID ARTHRITIS:

ITS PATHOLOGY, MORBID ANATOMY,

AND

TREATMENT.

 

BY

GILBERT A. BANNATYNE, M.D. Glas., M.R.C.P. Ed.,

Fon. Physician to the Royal United Hospital, and to the Royal
: Mineral Water Hospital, Bath.

 

SECOND EDITION.—ILLUSTRATED.

 

ye

BRISTOL: JOHN WRIGHT & CO.
LONDON: SIMPKIN, MARSHALL, HAMILTON, KENT & CO., Liv.

1898.
§
No 120%

JOUN WRIGHT AND CO..
PRINTERS AND PUBLISHERS, BRISTOL.

Fec

267
52
(878
PREFACE TO SECOND EDITION.

In response to many suggestions I now give my
more matured ‘ideas'as to the. nature and origin
of Rheumatoid Arthritis, and it will be noticed
that further experience and observation have led
me, as well as others, to believe yet more firmly.
in the bacterial theory as to the origin of the
disorder, and have also caused me to conclude
that there are at least two separate forms of
disease at present classed under the term rheu-
matoid arthritis—the one acute and undoubtedly
microbic in character, the other chronic and
probably degenerative, As far as possible I have
tried to point out the clinical differences, so that
those called upon to treat either condition may
appreciate fully the requisite essentials and indi-
_ cations necessary to insure a successful result.

» Barz, April, 1898.
PREFACE TO FIRST EDITION.

THE writing of a treatise on Rheumatoid Arthritis
involves much labour, not only on account of the
mass of literature which has to be traced and
classified, but, also, and more especially in my
case, from the recent discovery of micro-organisms,
implying, in consequence, the rewriting of all its
pathology, morbid anatomy, and_ treatment.
Such an upheaval cannot be accomplished in a
day, and this small work is only intended to be an
introduction to further and more perfect investi-
gation. Many parts of it will, probably, in the
near future require revision, but it has been my
ambition to avoid, as far as possible, making any
statement unsupported by facts or by logical —
deductions therefrom. I have here utilized the
discovery of Dr. Wohlmann and myself of the
micro-organisms which we believe to be specific
to the disease, and. the latter's life history and
peculiarities, as worked out and elucidated by
Dr. Blaxall. To them both my sincere thanks are
due. In the light of our discovery I have been
vi PREFACE.

 

led to enquire into the nature of two complaints
which have been hitherto classed as only
variations of one and the same disorder. This,
for reasons given later on, I do not consider to
be correct, and I propose to study and, keep’
distinct Senile Arthritis from the more general-.
ized disease Rheumatoid Arthritis.

Barn, 1896.
CONTENTS.

CHAPTER I.

INTRODUCTORY AND HISTORICAL - 1

Nomenclature—Evidence of its Antiquity—Landré Beau-
vais—Heberden— Haygarth — Cruveilhier— Adams— Fuller—
Charcot—Deville— Broca—-Key— Senator— Garrod— Virchow
ere pacer le Individuality—Its Frequency,
etc. é

‘CHAPTER II.
ETIOLOGY AND PATHOLOGY 14

Micro-organisms a cause—Charcot—French Views—Pye-
Smith—Hutchinson—Forsbrooke—Trophic Impulses—Motor
Cells —-Neuritis—Reflex Action—Functional Depression—
Toxic Action—Joint Changes in Tabes—Stewart—Biumler—
Muscular Atrophy—Bacteria a Cause—Arguments in Favour
of this Theory—Nerve Symptoms—Chvostek’s Views—Selec-
tive Actions—Primary and Secondary Symptoms—Toxemia
—Motor-ganglion cells—Reaction of degeneration—Muscular
Atrophy—Pigmentation—Anemia—Prédisposing causes, ete.

’
,

CHAPTER III.
PATHOLOGICAL ANATOMY AND BACTERIOLOGY 55

Degenerative Character of Changes—Point of Origin—How
the Bacteria gain Access—Naked Eye Appearances—Changes
in -Synovial Membrane—Loose bodies—Ligaments—Charac-
ters of Synovia—Changes in the Cartilages—Cornil and
Ranvier’s Views—Erosion—Pyroliferation—Lipping—Changes
in Bones—Rarefication — Osteo-sclerosis — Volkmann —
Changes in the Muscles—Central Nerve Changes—Peripheral
Nerves—Cardiac Changes—Kidney—Blood—Glands—Fibrous
Nodules—-Heberden’s Nodes—Situation and mode of Growth
—Gout as 4 Cause—Their Nature—Various Observers’ Views
-— Bacteriology.
vill CONTENTS.

 

CHAPTER IV.
PAGE

VARIETIES AND DIAGNOSIS - 86

Errors in Diagnosis—Acute Rheumatoid Arthritis—Osteo-
Arthritis—Charcot’s Classification—Post-Rheumatic, Gonor-
rheal and Gouty forms—Acute Rheumatoid Arthritis—In-
fantile Arthritis—In Children—In Adults—Symptoms—
Appearances of Joints—Chronic Rheumatoid Arthritis—Age— -
Appearances—Bony Changes—Diagnosis between it and
Nerve Diseases—Charcot’s Disease—Rheumatism—Gout—
Chronic Rheumatism, etc.

CHAPTER J.

SYMPTOMS AND PROGNOSIS’ 100

Premonitory Symptoms—Spender—Primary Symptoms due
to Micro-organisms—Appearance of Joints—Heat of Skin—
Arthrite Séche—Synovial Pouches—Joints first affected—.
Symmetry — Ankylosis— Deformities— Dislocations — Osteo-
phytic Out-growths—Forms of the Deformities—In the Hands
and Knees—Its Causes—Difference in Acute and Chronic
Cases — Cardiac Symptoms — Endocarditis — Pericarditis—
Changes in the Glands—Secondary Symptoms—Muscular
Atrophy—Its Characters—Selective Power—Myotatic Irrita-
bility—Fever—Pulse Rate—Tachycardia—Tension—Anemia
— Hemorrhages — Purpura—Neuritis — Its Frequency —
Trophic Phenomena—Skin Changes—Glossy Skin—Loss of
Hair—Atrophy—Downy Growth of Hair—Pigmentation—
Sweating—Dyspepsia—-Kidney—Cardiac troubles—Prognosis.

‘

CHAPTER VI.

TREATMENT 130

Preliminary considerations — Antitoxin — Causes — Diet—
Clothing —Exercise — Drugs—Creasote — Guaiacol— Guaiacol
Carbonate—Benzosol— Phenols —6-Naphthol—Betol—Salol—
Action of Creasote—Hudeod—Douglas Powell—Intestinal
Antiseptics — Iron — Arsenic — Iodides — Salicylates— Actea
Racemosa—Ichthyol —Hyoscyamus— Relief of pain — Dr.
Spender’s treatment—Guaiacol externally—Carbolic Acid
applications—Electricity—Thermal treatment—Alkaline and
Sulphur Waters—Bath—Aachen—<Action of Bath Waters—
Bath treatment—Aix treatment -- Hot Air Baths—Sea Voyages
—Extension—Excision—Summary.
 

CONTENTS. ix

 

CHAPTER VII.

SENILE ARTHRITIS * - 1859

Morbus Coxe Senilis—Senile Arthritis— Monarticular
Rheumatoid Arthritis—In whom seen—Symptoms—Morbid .
cee in the Bones—Trophic Phenomena—
Treatment :

APPENDIX 163
LIST OF AUTHORITIES 172

INDEX 177

 
LIST OF ILLUSTRATIONS.

 

PLATE I, Page 78.
Skiagraph of bones of hand in Rheumatoid Arthritis.

PLATE II, Page 90.
Photograph showing swellings in joints, etc.; swellings being
soft and doughy; also atrophy of right hand.

PLATE III, Page 92.
Another case with swellings and general emaciation.

_ PLATE IV, Page 93.

Fig, A.—Spindle shaped enlargement of joints with atrophy.
Fig. B.— Pulpy swelling of joints.

PLATE V, Page 102.

ig. A,—Shows deflection of left hand.
Fig. B.—Shows spindle shaped swelling of phalangeal joints.

PLATE VI, Page 104.

Fig. A,--Eulargements of the heads of bones, synovial swellings
and atrophy. ;

Fig. B.—Ulnar deflection in a chronic case.

PLATE VII, Page 109.

rig. A.—Dislocation backwards of index finger.
iy, B.--Ulnar deflection.

PLATE VIII, Page 123.

Fig. A.—Fusiform deformity of index finger.
Fig. B.— Hemorrhage under nails.
xii LIST OF ILLUSTRATIONS.

x

WOOD ENGRAVINGS.

PAGE

Fig. 1.--Bone from an acute case of Rheumatoid disease - 58
Fig. 2.—Osteophytes, eburnated bone, grooves on articu-
lating surfaces - - 59
Fig. 3. -Connective tissue showing micro-organisms 62
fig. 4.--Sections through diseased cartilage 66
Fig. 5. -—Metacarpal bone, showing apreaplyres - 68
Fig. 6, —Osteoclast eating bone - 70
Fig. 7.—Multipolar ganglion cells from anterior cornua 71
Fig. 8.—Portion of nerve, showing neuritis 499

ig. 9.—Head of femur from case of morbus coxe senilig 161

'
RHEUMATOID ARTHRITIS :

Irs ParHotocy, Morsrp ANATOMY, AND TREATMENT.

 

CHAPTER I.

INTRODUCTORY AND HISTORICAL.

ERRATA.

 

~ Page 387, line 11, for “ Oster” read ‘ Osler.”
Page 103, line 1, for * Plate III,” read “ Plate IV.”

TENE VNU ee
;

 

back as any other known form of disease, but it was not
until the beginning of this century, or the end of the
last, that it came to be recognised and differentiated from
the allied disorders, gout and rheumatism. Indeed, I am
not certain that in some countries it is even yet recog-
nised as a separate form of disease, for in France and
Germany some still hold it to be only a form of chronic
rheumatism. This is curious, as one of the best works
ever written on the subject was penned by that great
observer, Charcot. Much of the difficulty surrounding |
the disorder is, I am sure, caused by the ambiguity of
1
xii

‘
«

Bh
LIST OF ILLUSTRATIONS.

wens

WOOD ENGRAVINGS.

Fig. 1.--Bone from an acute case of Rheumatoid disease

Pig

Fig
Lig
Fug.

fig.

 
 

. 2.—Osteophytes, eburnated bone, grooves on articu-
. lating surfaces .

. 8. - Connective tissue showing micro-organisms.
. 4.--Sections through diseased cartilage

. 5.-Metacarpal bone, showing osteophytes

 
 

PAGE

58
RHEUMATOID ARTHRITIS :

Irs PatnoLtocy, Morpip ANATOMY, AND TREATMENT.

 

CHAPTER I.
INTRODUCTORY AND HISTORICAL.

Nomenclature—Evidence of its Antiquity—Landré Beauvais —
Heberden—Haygarth—Cruveilhier—Adams—Fuller—- Charcot
—Deville—Broca—Key—Senator-—Garrod— Virchow —Hutch-
inson—Spender—Its Individuality -—Its Frequency, etc.

ITHERTO, the disease which we call Rheumatoid
Arthritis has not only been known by different
names, but different diseases have been classed

under this heading—the number and diversity of the
terms employed corresponding in a certain sense with
the number and diversity of the views advanced with
regard to its etiology and. pathology. It is undoubtedly
a disease per se, and has probably existed as such as far
back as any other known form of disease, but it was not
until the beginning of this century, or the end of the
last, that it came to be recognised and differentiated from
the allied disorders, gout and rheumatism. Indeed, I am
not certain that in some countries it is even yet recog-
nised as a separate form of disease, for in France and
Germany some still hold it to be only a form of chronic
rheumatism. This is curious, as one of the best works
ever written on the subject was penned by that great
observer, Charcot. Much of the difficulty surrounding
the disorder is, I am sure, caused by the ambiguity of
1
2 RHEUMATOID ARTARITIS.

the various terms which have, at’ one time or another,
been applied to it, none of which seem exactly to
describe its characteristics, but leave much to the
imagination of the individual observer. Of recent years ©
the principal terms employed to designate it have been
those of rheumatoid arthritis, and osteo-arthritis. Now
how much better would it be had we been content with one
name only, even if that one did not actually describe the
condition with perfect accuracy? What an amount of
confusion might have been saved! This want of exacti-
tude in nomenclature would soon have been compensated
for by the increased knowledge which we would have
been enabled to store up and note for comparison about
a complaint, the study of which, and the disentangle-
ment of whose literature and prevailing impressions, are
enough to appal even the boldest. Many and various
are the theories which, at one time or another, have
been advanced to explain the congeries of symptoms
called rheumatoid arthritis; and many and various are
the diseases which, at one time or another, have come
under our notice labelled rheumatoid arthritis, osteo-
arthritis, rheumatic gout, etc., these terms being, as a
rule, quite indiscriminately apportioned. No wonder
confusion has reigned supreme. It is, therefore, with
fear and trembling that I now endeavour, as far as our
still limited knowledge renders possible, to throw a ray
of light into the obscurity surrounding the etiology and
pathology of the disease, with the hope that it will, in
the near future, enable us to walk with surer footsteps.

Of the many names used to designate the acute or
destructive form of the disorder, I have here assumed
that that of rheumatoid arthritis is the one best known
to the largest number, and, therefore, the one best suited
to be used permanently. It, in my opinion, is the one
fulfilling to the greatest extent the requirements of
INTRODUCTORY AND HISTORICAL. 3

science. This term was first applied by Garrod, and
although it hardly gives one the best mental idea of
what the disease is, yet I think, from many points of
view, it is the most suitable. It has been objected that
the word Rheumatoid, which means, freely- translated,
like rheumatism, is misleading; so it is, to a certain
extent. Yet no one will deny that while quite separate
and distinct, it, to a certain extent, in outward appear-
ance at least, does resemble some forms of rheumatism.
It is a much more suitable term than any of those which
include Rheumatic as part and parcel of their being.
Rheumatic applies to a totally different condition, and
to bring it in leads to endless confusion. Osteo-arthritis
is a term implying a condition much more marked in
the chronic forms of the disease, and which I would keep
for those chronic osteo-sclerotic cases so often seen in
the later stages. Some have objected to the use of
arthritis at all, as they hold that the inflammatory
changes in the joints are merely secondary to nutritional
changes elsewhere ; were it not for this, the term most
commonly used in Germany, arthritis deformans, would
have become much more popular. This objection to
arthritis can hardly be sustained, especially in con-
sequence of our newer light on the origin of the disease.
The late Dr. Brabazon suggested pernicious arthritis
as a suitable term, while the French occasionally now use
the expression, rhumatisme chronique infectieux. Both
these really describe the condition better than most of
the others, but as the term rheumatoid arthritis is dis-
tinctive, I see no really urgent reason why we should
adopt a new term, which is bound to lead only to renewed
confusion and to provide yet another term for our already.
overcrowded nomenclature.

The following is a lis§ of the terms which have, at one
time or another, been applied to the disease :—
4 RHEUMAI1OID ARTHRITIS.

1. “ Goutte Asthenique Primitif,” by Landré Beau-
vais, in 1800.1

2. ‘ Digitoram Nodi,’”’ by Heberden, in 1804.?

8. ‘ Nodosity of the Joints,” by Haygarth, in 1805.3

4. “ Chronic Rheumatism of the Joints,” by Todd, in
1843.4

5. ‘ Arthrite Séche,” by Deville and Broca, in 1848
and 1850.5°"76

6. “Rheumatic Gout,” by Fuller, in 1852.”

7. “‘Rhumatisme Chronique Primitif,” by Charcot
and Vidal, in 1853 and 1855.8

8. ‘ Usure des Cartilages Articulaire,” by Cruveilhier
in 1858.9

9. “Chronic Rheumatic Arthritis,’ by Adams, in
1857.

10. ‘“‘Rhumatisme Noueux,’” by Trousseau, in 1860.4

11. “ Arthritis Deformans,” by Virchow, in 1869.2

12. ‘Rheumatoid Arthritis,’ by Garrod (Sir A.), in
1876."

18. “ Osteo-arthritis,”’ by Spender, in 1888.

14. “ Pernicious Arthritis,’ by Brabazon, in 1896.

15. ‘“‘Rhumatisme Chronique Infectieux,” by Chauf-
fard and Ramond, in 1896.%

From this list we see that, even from the beginning,
there has been a difference of opinion as to what is, and
what is not rheumatoid arthritis, as well as an uncer-
‘tainty as to the nature of the morbid process; somé
ascribing the changes to rheumatism, whereas others have
thought they were gouty. in nature; some, in their
writings, describing typically rheumatoid cases, and
others as typically what are not rheumatoid.

Turning to the history of the complaint, we find its
characteristic changes have been found in the bones of
its victims in times which, if rot quite prehistoric, are
practically so. As far as I can learn, the oldest bones
INTRODUCTORY AND HISTORICAL. 5

showing these changes are those found by Mr. Page
May” in Egypt, then those found in lower Egypt by
Mr. Petrie,” who suggests as a probable date 1300 B.C.
Next come those discovered by Mr. Eve,'* also in Egypt,
and probably referable to the Ptolemaic period (second
century B.C.); and following on these are those of a
Norse Viking, found in the Christiania Fjord; those
found in Pompeii, by Chiaje; those in the Convent of
Marienthon in Pomerania, by Virchow ”; those in the
Roman Sarcophagus at Smithfield, — Dr. Norman
Moore %!; those in the Catacombs of Paris, found by
Lebert 2 all showing distinct traces of bony rheu-
matoid, or osteo-arthritic change. Coming down to
more recent times, we find the disease was first des-
cribed by Sydenham,” from a clinical point of view, in
the year 1683, as a modification of rheumatism. In
1708 it is referred to in the writings of Musgrave *; in
1764 and 1768 in those of Haller” and De Sauvages,”®
respectively. In those writings one can trace references
to the disease, but it was not actually described as a
disease per se until the year 1800, when Landré Beau-
vais*” published his Thesis on ‘“‘ Goutte Asthenique
Primitif,’” which condition we now recognise as one of
rheumatoid arthritis. Amongst the other features to
which he drew attention was the special liability of
women to its attacks, its chronic nature, its destruction
of the cartilages, and its enlargement and deformity of
the affected joints. He recognised that it could not be
due to gout, thus differentiating for the first time be-
tween that disease and rheumatoid arthritis. In 1804
Beauvais’ opinion received the support of Heberden,*
who, however, went further, and differentiated between
it. and rheumatism. He mentioned that there was
little or no fever, no redness of the skin, no great
pain, but swelling of the affected part; that the
6 RHEUMATOID ARTHRITIS.

disease was not particularly apt to begin in the foot,
but if so, it soon left it and attacked other joints,
several of which, one after the other, became the seat
of the distemper after the first onset; that it was very
crippling ; and that one attack caused more weakness of
the limbs than would have been produced by gout in
many years. He mentioned that the wrists and the
fingers were specially liable to the disease, and that once
attacked it tended to remain permanently in these joints.
He also described what have ever since been known as
Heberden’s nodes, as occurring on the terminal phal-
anges of the fingers.

In 1805 Haygarth * published his clinical ‘‘ History
of Diseases,’ which gives the clinical appearance of
rheumatoid arthritis, describing it fully, and also differ-
entiating between it and rheumatism. In 1813 Chomel®
alluded to Landré Beauvais’ thesis, but believed that the
disease referred to by the latter belonged to a rheumatic
type. In 1827 Scudamore*! mentioned that he had
seldom seen such cases as are described by Haygarth,
except secondary to gout and rheumatism. In 1833
Brodie,” in his work on “Diseases. of the Joints,”
called attention to its being quite distinct from both
rheumatism and gout; and during the years 1829 to
1840 Cruveilhier * wrote mentioning the necessity of
observing its clinical characteristics, and gave it the
name, ‘‘ Usure des cartilages articulaire.”” He pointed
out that true bony ankylosis may occur. During this
period also it was studied and commented upon by
Lobstein ** (1888), Key ** (1883), Robert Smith *° (1885),
Canton *? (1848), Deville ** (1848), Broca ® (1850), and
Adams “’ (1857) in this country and France; whilst in
Germany, Meyer ** (1849), Weber # (1858), and Leis #
wrote explaining the rationale of the various phenomena,
observed. These observations were subsequently con-
INTRODUCTORY AND HISTORICAL. 7

firmed by Cornil,** Vergely* (1858), and Ranvier *°
(1865). Deville and Broca gave it the name “ Arthrite
Séche,” and Adams that of ‘‘ Chronic Rheumatic
Arthritis.” Robert Smith and Adams both pointed out
that many cases of disease of the hip joint, resulting
from injury, were of the nature of rheumatoid arthritis,
and thereby have caused confusion with regard to the
difference between it and malum coxe senile, Adams
gave many beautiful illustrations of the morbid anatomy.
He said Sandifort,*’ of Leyden, was the first to notice
the disease, in the hip joint, in the post mortem room.
Adams also corroborated Cruveilhier’s observation about
the occurrence of true bony ankylosis, and he mentioned
that the polyarticular cases were usually preceded by
acute rheumatism. Moreover, he drew attention to the
relationship between the monarticular cases and injury.
Colles, in 1889—1857, remarked that two different pro-
cesses were at work, one absorbing, and one forming
fresh bone. In 1843 Todd * called it ‘‘ Chronic Rheu-
matism of the Joints,” and considered the changes to be
more of an irritative than inflammatory nature. In
1849 Redfern *® gave some good illustrations of the
disease, and showed the nature of the cartilaginous
changes. In 1852 Fuller, in his work on “ Rheu-
matism and Allied Disorders,” called it ‘‘ Rheumatic
Gout.” He said that although it was in some respects
closely allied to rheumatism, yet he considered it more
of a gouty nature; at the same time he thought it was
not a compound of the two disorders, but a distinct
disease. In 1853 Charcot and Trastour™ published
their thesis. As Charcot’s views have been more largely
received and criticised than any other, his opinions will
come under consideration later on, and as they crop up.
In 1855 Vidal *? followed Charcot with his thesis. They
all three gave it the name ‘‘ Rhumatisme Chronique
3 RHEUMATOID ARTHRITIS.

Primitif,”’ and they all held that it was only a form of
chronic rheumatism. This view is still held in France
by many, as may be seen from Charcot’s later writings,
‘and also from those of Besnier,*? Homolle,** Lacaze-
Dori, and Mathieu.** In England, America, and Ger-

many, this is not the view held by most writers on the
subject, many of them being of the opinion that Heber-
den and Haygarth were right in regarding it as a disease
per se, and that although it presents many outward
appearances resembling both gout and rheumatism, yet
.it differs entirely in essentials, and that it is evidently
a distinct disorder. Adams and Fuller, who did much
work in the elucidation of the characteristics of the
disease, held this view, and coming down to more recent
times we find that Sir A. Garrod * showed unmistakably
that the excess of uric acid, present in gout, was entirely
absent in rheumatoid arthritis. It was classed by him
under three headings, namely, acute, chronic, and ir-
regular. The chronic form he further subdivided into
general and local. Since then many have written on
the subject, and their studies have brought about a pro-
found change in the prevailing views as to its nature.
Senator *® described it under the name of “ Arthritis
Deformans,” a name which had previously been given to
it by Virchow,®® and he believed that it was a true con-
stitutional disease. Hutchinson looked on it as the
result of a rheumatic diathesis, caused by the blending
of the elements of gout and rheumatism, now the one
and now the other element predominating. In 1884 Sir
‘Dyce Duckworth ® gave it the name of ‘“‘ Chronic Rheu-
matic Arthritis,’ and thought it was a form of true
rheumatism. Lane® (A.), in 1884, thought that the
changes in the joints were caused simply by wear and
tear; and Ord,® in 1885, considered it to be purely of
reflex nervous origin. Spender,® in 1888, pointed out
INTRODUCTORY AND HISTORICAL. 9

some of the early nerve phenomena under the name of
osteo-arthritis. In 1890 Dr. A. E. Garrod,® calling it
‘Rheumatoid Arthritis,’ wrote a treatise on fhe
subject; also in that year Lane (H.) and Griffiths ©
pointed out the differences between rheumatoid arthritis,
chronic rheumatic arthritis, and osteo-arthritis ; while
in 1893 Forsbrooke ® brought out his dissertation, and
advanced the view that it was anemia to which it and
all the vaso-motor and trophic changes were due; the
joint changes he considered being due to trophic mal-
nutrition ; and quite recently Dr. Brabazon” suggested
that. it might be called ‘“‘ Pernicious Arthritis,” refer-
ring more especially to the symptoms. In May, 1896,
Chauffard and Ramond™® drew attention to the occur-
rence of enlarged glands in certain cases, and also re-
corded the fact that in one case they succeeded in finding
a small diplo-bacillus in the synovia. This diplo-bacillus
differs from the micro-organisms found by Schiiller,®
but in many respects closely resembles those previously
found by Dr. Wohlmann and myself. In 1897, Prof.
Baumler opened a discussion on the disease at the Berlin
Congress for Internal Medicine,” and the following con-
clusions were arrived at: (1,) That the name ‘ Rheu-
matism” should be limited to acute rheumatism and
certain variations of that disease; (2,) That a special
form of disease, of poly-articular nature, distinguished by
its chronic course, by having no tendency to heart disease,
by not being readily influenced by the salicylic prepara-
tions, but one which quickly Jeads to malformations, and
ultimately to destruction of the joint tissues, should be
called arthritis, or better, poly-arthritis deformans; (3,)
That the cause of the disease is not known with certainty
inasmuch as many conditions predispose to it, such as
insufficient food, nerve exhaustion, and other previous
joint affections, there being also a special tendency to the
10 RHEUMATOID ARTARITIS.

disease in women, and apparently in connection with
their sexual organs. It is not more common in the poor
than in the rich; (4,) That no special connection with-
organic or functional nerve disorders, either of a central
or reflex origin, can be established; (5,) That it is not
unlikely, and the more recent bacteriological researches
give this idea a certain basis, that we are dealing with
an infective disease ; and (6,) That it should not be lost
sight of that there may be several causes and infections at
work at one and the same time. At the British Medical
. Association Meeting in Montreal, in August, 1897, Prof.
Stewart 7 opened a discussion on the disease, but more
especially with reference to the relationship between it
and diseases of the nervous system, tuberculosis and
rheumatism. Little new knowledge was brought for-
ward, but the infective nature of the disease seemed to
be gaining ground and to be generally accepted as best
explaining the various phenomena of the disease.

Such are the main points in the history of the disease,
and one wonders that, with such a mass of literature
having direct bearing on the subject, we should have
been so long.in the dark, both with regard to its
pathology and its etiology, and, Iam sorry to say, also
with regard to its morbid anatomy. Yet such is the
case. If it is granted that we are dealing with a disease
by itself, one would look for some salient symptom or
symptoms, without which we would have no rheumatoid
arthritis. This we find in the joints and nervous sys-
tem. The joint symptoms are always the primary ones,
the nerve phenomena being purely secondary, but their
presence, in one. shape or another, is so persistent that
one can regard them as essential elements only. The
conjunction of symptoms is such as we find in no other
morbid process. It is not merely occasional joint
troubles, associated with nerve lesions, or vice versd, but
INTRODUCTORY AND ATISTORICAL. II

it is a constant conjunction of certain symptoms, in a
well marked sequence, referable on the one hand to the
joints, and on the other to the nervous system. We
are therefore forced to the inevitable conclusion, that
we are dealing with a disease per se, and one in which
the primary lesion is in the joints.

Turning to the frequency with which it is met, I may
say that it is a common form of disease occurring, as
one observer states (Haygarth), as often as 1 in every
310 patients, giving a percentage of 032. During the
years 1898 to 1897 there were admitted to the Bath
Royal Mineral Water Hospital 4,744 patients, of whom
1,061 suffered from rheumatoid arthritis, 2,470 from
rheumatism, and 602 from gout. It is more common in
the poor and badly nourished, and is also more common
in the cold damp parts of the globe than in either the
dry cold or hot damp. :

 

REFERENCES.

Landré Beauvais.—* Goutte Asthenique Primitif,”’ 1800.

Heberden.—* Commentaries,” 1804.

Haygarth.—“ Clinical History of Diseases,” 1805.

Todd.—“ On Gout and Rheumatism,” 1843.

Deville.—“ Bull. de la Soc. Anatom.,” xxii. and xxiii., 1848.

Broca.-- “ Bull. de la Soc. Anatom.,” xxv., 1850.

Fuller.‘ Rheumatism, Rheumatic Gout, and Sciatica,”
1852.

Charcot.—“ Thése de Paris,” 1853.

Cruveilbier.—“ Anat. Pathologique.” Liv. ix.

10. Adams.-—‘‘ On Rheumatic Gout,” 1857, and 8rd edit. 1873.

11. Trousseau.—‘ Clinique Médicale.”

12. Virchow.—“ Virchow’s Archiv.,” xlvii., 1869. .

13. Garrod, Sir A.—‘‘ Gout and Rheumatic Gout,”’ 1876. s

14. Spender.—“ Osteo-arthritis,” 1888.

15. Brabazon.— British Medical Journal,” vol. i. 1896, p. 7238.

16. Chauffard and Ramond.—-“ Revue de Médecine,’ May 10,

1896.

17. Petrie._-Museum, Royal College of Surgeons, 1891.

18. Eve.—‘ Brit. Med. Journal,” vol. i., 1890.

19. Chiaje.-—‘‘ Arthritis Deformans from Pompeii.”

oo Nou oO Pr
12

20.
21,
22.
23.
24.
25.

27.
28.
29,
30.

31.
32.
33.
34.
35.
36.

37.
38.
39.
40.
41.
42.
43.

44,

45.
46.
47.
48.
49,
50.
51.
52.
53.

54.

55.
56,
57.
58.
59.
60.
61.
62.
63.

‘RHEUMATOID ARTHRITIS.

Virchow.—Loc. cit., p. 298.

Moore.—“ Path. Soc. Trans.,” 1883, Xxxiv., p. 226.

Lebert.—“ Handbuch der Pract. Med.,” 1859, ii., p. 874.

Sydenham.—“ Opera,” Sec. vi., cap. v.

Musgrave.—‘ De. Arthritide Symptomatica,” p. 24.

Haller.—* Elementa Physiologica,” vi., p. 9.

De Sauvages.-—‘ Nosolgia Methodica,” “class vii., order i.

Landré Beauvais.—Loc. cit.

Heberden.—-Loc. cit., chap. xxviii.

Haygarth.—Loc. cit.

Chomel.-—“‘ Essai sur le Rhumatisme ; ;: Thése de Paris,
1813,

Scudamore.— On Rheumatism,”’ p. 487, 1827.

Brodie.—‘ Diseases of the Joints,” 1833.

Cruveilhier.-—Loc. cit.

Lobstein.—“ Anat. Pathologique,” 1883, ii., p. 348, 1833.

Key.—“ Med. Chir. Trans.,” 1833, xviii., p. 208.

Robert Smith.—‘ Dublin Journal Med. "Sciences, ” 1835, vi.,
p. 208.

Canton.—‘‘ London Med. Gazette,” N.S., 1848, vi., p. 410.

Deville.—Loc. cit., 1848, xxii., p. 272, xxiii., p. 141.

Broca.—Loce. cit., 1850, xxv., p. 435.

Adams.—Loc. cit., 1857.

Meyer.—“ Miiller’s Archiv.,” 1849.

Weber.—“ Virchow’s Archiv., ” Jan. 1858, p. 74.

Leis.—Quoted Charcot “ Syd. Soc. Trans. ,’ “ Maladies des
Vieillards,” p. 139. ;

Cornil.-_‘ Niemeyer’s Internal Pathologie,” vol. ii., p. 556,
(transl.).

Vergely. —“« Thase de Paris,” 1858.

Ranvier.—‘* Thése de Paris,’’ 1865.

Sandifort.—‘‘ Museum Anatomicum,”’ 1798.

Todd.—Loc. ‘cit.

Redfern.—‘ Edin. Monthly Journal,” 1849.

Fuller.--Loc. cit.

Charcot & Trastour.—‘“‘ Thése de Paris.”’

Vidal.—‘ Thése de Paris,” 1855.

Besnier.—“ Dict. Encyclop. des Sciences .Méd.,” 1876, p.
155.

Homolle.—“ Dict. de Med. et Chir. Prat.” ; Article, ‘ Rhu-
‘matisme,” 1882.

Lacaze-Dori.—‘‘ Thése de Paris,” 1882.

Mathieu.—“ Thése de Paris,” 1884.

Garrod, Sir A.—Loc. cit., 1862—1876.

Senator.—“ Ziemssen’s Handbuch,” 1875 and 1879.

Virchow.—Loc. cit.

Hutchinson.-—“ Pedigree of Disease,” 1884, p. 126.

Duckworth.“ Heath’s Dict. Prac. Surg. ” 1886, i., p. 293.

Lane, A..—‘‘ Path. Soc. Trans.,” 1884 and 1886.

Ord.—“ Brit. Med. Journal,” "1884, ii., p. 268, and “ Trans.
Clin. Soc.,’”’ 1879.

% ag
64.
65.

66.
67.
68.
69.
70.

71.
72.

INTRODUCTORY AND HISTORICAL. 13

Spender.—“ Osteo-arthritis,” 1888.
Garrod, A. E.—“ Treatise on Rheumatism and Rheumatoid
Arthritis. »* 1890.

‘Lane & Griffiths.—“ The Rheumatic Diseases ” (so-called),

1890.
Forsbrooke.—“ Dissertation on Osteo-arthritis,” 1898.
Schiiller. —“Chir. Mitth. iiber die chron. -rheum. Gelen. k.- |
Entziind.,” and “ Langenbeck’s Arch.,” Bd. 45, 1892, and *
“ Berl. klin. Woch.,” Sept. 3, 1893.
Bannatyne & Wohlmann.—“ Lancet,” April 25, 1896.
Baumler.—-‘‘ Verhandlungen des xv. Congresses fiir Innere
Médicin zu Berlin,” 1897.
Stewart.—‘ Brit. Med. Journal,” Oct. 30, 1897, p. 1224.
May.—“ Brit. Med. Journal,” vol. ii., 1897, p. 1631.

 
14

CHAPTER II.

ETIOLOGY AND PATHOLOGY.

Micro-organisms a Cause—Charcot—French Views—Pye-Smith
—Hutchinson—F orsbrooke—Trophic Impulses— Motor Cells—
Neuritis—Reflex Action—Functional Depression—Toxic Ac-
tion—Joint Changes. in Tabes—Stewart—Baumler—Muscular
Atrophy—Bacteria a Cause—Arguments in Favour of this
Theory— Nerve Symptoms—Chvostek’s Views— Selective
Actions—Primary and Secondary Symptoms—Toxemia—
Motor-ganglion Cells—Reaction of Degeneration—Muscular
Atrophy—Pigmentation—Anzemia—Predisposing causes, etc.

Part I.

From the discovery made by Dr. Wohlmann and my-
self, no doubt remains, in my mind, that rheumatoid |
arthritis is caused by the micro-organisms which we
found to exist in the joint fluids and tissues, and which
we therefore look upon as specific. Unfortunately we
have not succeeded in proving beyond cavil that these
micro-organisms are the cause par excellence, as we have
failed:to reproduce the disease in animals. This remark
applies also to the micro-organisms found by Schiiller,1
and Ramond and Chauffard.?? Whether our failure
arises from the insusceptibility of the animals experi-
mented on, or from some failure in technique, I cannot
say: yet the fact remains that we have not reproduced
the disease, and therefore it devolves on us to bring
forward such other evidence as bears on the subject,
so that an unbiassed opinion may be formed as to the
probability of the disease being an infective process, and
as to the probability of our bacillus being the specific
ETIOLOGY AND PATHOLOGY. 1S

cause. To clear the ground, I will state and shortly
criticise such theories as have been advanced from time
to time as to its pathology.

i.—According to Charcot, and many foreign observers,
rheumatoid arthritis is only a secondary form of rheu-
matism, but as, in the majority of cases, the disease
arises as a primary one, there can be no ground for this
belief. It, undoubtedly, may arise as a sequela of acute
rheumatism, or in fact of any acute arthritis; but to say
it is only a form of rheumatism is, I think, grossly
misrepresenting the disease and its characteristics.
One has only to look at its clinical characters, quite
apart from its morbid anatomy, to perceive the differ-
ence. In this country it has always been regarded as a
disease per se, at least ever since its peculiarities were
thoroughly appreciated, and, I think, it is hardly
necessary for me here to point out each individual
difference, but will take it for granted that, in this
country at least, this individuality is admitted.

iii—Dr. Pye Smith? holds that the disease is of a
senile character. This is not often the case in true
rheumatoid, and something more than senility must
exist, in the acute cases, as they mostly arise in the
young or comparatively young. It is probable that Dy.
Pye Smith referred to certain cases which I class as
Senile Arthritis, a disorder which I regard as purely
degenerative and altogether different from the acute and
specific disease we are now studying.

iiii—Hutchinson * looks upon it as simply a result of
the combined action of the rheumatic and gouty processes,
now the one and now the other element predominating.
He believes in a basie Rheumatic diathesis, capable of
subdivision into off-shoots. In many ways such a theory
is supported by facts; but we must regard this basic
diathesis as only a diathesis. The poison of gout is as
16 RHEUMATOID ARTHRITIS.

different from that of rheumatism as they are both from
that of rheumatoid arthritis. It is positively certain,
however, that a certain form of diathesis does predispose
to arthritic changes, but what these changes will be will
probably depend on local conditions.
. iv._Forsbrooke® holds that the anzmia, which is
present in this disease, is responsible for the jomt and
other changes. He states that at first, owing to a
daficiency of oxygen in the blood, the vaso-motor centre
in the medulla is stimulated, and by consequent con-
striction of the minute vessels supplying the joints and
smaller nerves, the nutrition of these parts is interfered
with. This deprivation of blood, which although at first
functional. in nature, may give rise to organic change.
The stimulation of the vaso-motor centre, if prolonged,
ends in exhaustion, followed by dilatation of the joint
vessels and inflammation. Ingenious as this theory is, it
rests on the assumption that anemia is present before
any of the joint or nerve troubles. This has not been
found to be the case, so how can it. be the cause?
Personally, although I have noticed anemia in a large
proportion of cases, it has not been invariably present,
and it has certainly not been the first symptom. It is
more likely that the anemia is caused by the poison
generating the disease; and is therefore only a sequela,
not a cause. The anemia of rheumatoid arthritis has
all the characteristics of a toxemic anemia, and is more
fully considered elsewhere.

v.—Remak,® Senator,’ Ord,® Sir Dyee Duekworth, ®
and many. others, have all been of the opinion that
the disease is due to some abnormal nerve condition,
although they differ as to its being a primary lesion of:
the nervous system, or only secondary to a lesion else-
where. The majority hold that it originates through
abnormal trophic impulses, and probably in a similar
ETIOLOGY AND PATHOLOGY. 17

manner to the joint changes arising in tabes dorsalis,
syringo-myelia, etc. The abnormal trophic impulses are
usually stated to arise from changes in the spinal cord,
but it appears to me this theory is based on quite insuf-
ficient grounds, and it is difficult to see how it became
so generally accepted. If we examine it, two questions
arise (1,) Have any gross or other lesions sufficient to
account for the abnormal impulses been found? and (2,)
Can trophic impulses produce such changes as we find
in this disease ?

(1,) What are the conditions which might give rise to
the abnormal trophic impulses ?

We would expect to find some gross lesion either in
the central nervous system (a), or in the peripheral
nerves (b); or else some reflex (c), nutritional (d) or
toxic (¢) condition might exist which could give rise to
the necessary abnormal impulses.

(a,) If due to a gross change in the central nervous
system the lesion will, of necessity, be so extensive that
we can think of no condition which could possibly give
rise to it, unless it be a blood one. A poison circulating
in the blood is the most likely agent to affect the exten-
sive area necessarily involved: for we must remember
that the trophic influences which govern the nutrition of
the joints, bones, and skin are under the control of the
cord, the centre being probably situated in the inter-
mediate grey matter, whilst that of the muscles is con-
trolled by the anterior grey matter (probably the motor
nerve cells). As the nerve endings have a structural
continuity with the tissues, the nutrition of the tissue
molecules depends on the nutritional condition of the
nerve and nerve centres. So far no gross organic change
has been detected in the central nervous system, except
in three cases in which Folli !° discovered an atrophic
condition in the cells of the anterior cornua. Klippel,”

, = v
18 RHEUMATOID ARTHRITIS.

according to Massolongo, observed somewhat similar
changes, and in one case I have also observed alterations
in the condition of the ganglion cells. These conditions
are, however, so altogether inextensive, and have been
entirely confined to the motor ganglion cells, that one
must reject the idea that they can originate such a wide-
spread disorder.

(b,) If due to a gross lesion in the nerves themselves
we would expect to find symptoms of nerve degeneration
in all and every case of rheumatoid disease—but this is
not the case. In only a certain number is an unmis-
takable neuritis present, and this so often markedly.
follows the arthritis that there can be no doubt it is
secondary in its nature. This neuritis may be caused by
the existing joint inflammatory process, or else it may
be due to the action of toxins circulating in the blood.
It is undoubted that toxins may thus give rise to such
a condition, thereby showing not only a selective action
in the parts acted on, but also a peculiarity in the acting
virus. MM. Pitrés and Vailliard have found a well- °
marked neuritis in several cases, and they believe that
there is a distinct relationship between the presence of
this neuritis and the development of the trophic changes.
It must be noted that although finding marked changes
in the nerves supplying the wasted muscles yet they
found none in those supplying the articulations. On the
other hand Duplay and Cazin® found an inflammatory
condition of the nerves supplying the affected joints. As
will be seen, the results of such examinations have
hitherto been so uncertain and contradictory that one
must assume there is no constant occurrence of a
neuritis. This agrees well with all clinical experience,
and with what. one would expect from the nature of the
disease.

(c,) Dr. Ord’s™ view of the disease is that it is entirely
ETIOLOGY AND PATHOLOGY. 19

caused by reflex action set up by some uterine or other
visceral derangement. He believes that the irritation
engendered in the uterus causes impulses to be conveyed
to the central nervous system, which in turn give rise
to other morbid impulses which are conveyed, by the
peripheral nerves, to the joints, etc., and there cause
the changes which we know by the name of rheumatoid |
arthritis. Admitting that reflex influences may cause
trophic changes in the skin and muscles, and apart from
the fact that the disease occurs in men free from genital
irritation in a proportion of one to eight women, one can-
not believe that the acute organic changes in the joints
can be set up by any such reflex action. Trophic lesions
have been traced to injuries of the nerve centres, and of
the nerves leading to the part, but not to reflex irritation,
and there is no evidence that reflex irritation can give
rise to such lesions of the nerves or nerve centres.
Although denying that such impulses can cause organic
mischief, yet I admit that, by causing debility and
anemia, they may so lessen the natural defences of the
joints that these may readily become the prey of the
poison, which causes rheumatoid disease. They must
therefore be borne in mind as potent predisposing
causes.

(d,) Is this disease then, as we cannot explain it other-
wise, due to a functional depression of certain areas of
the cord or of some of the peripheral nerves? It is pos-
sible to conceive that deficient nutrition of certain areas
might set up trophie changes, and as this condition is
likely to occur in all debilitating states we would look for
it as a sequela of acute illness, or else in those who are
congenitally weak. Dr. Garrod™ states that out of 500
cases of rheumatoid arthritis he traced a family history
of arthritic trouble in 216. Rheumatoid disease prac-
tically only occurs in debilitated people, and is often a
20 RHEUMA TOID ARTARITIS.

sequela of some acute condition which has left impair-
ment or enfeeblement of the nutritional state, both of
the body generally and of the nervous system locally.
This, however, may be said of any disease, and is only
therefore of negative value; what is of more importance is
the fact that it would be against all experience to find
permanent symptoms, such as are seen in this disease,
arise without some slight change in the ultimate nerve
elements, which might be recognisable on microscopic
examination. If due to nutritional changes we would
look for some alteration in the medulla as being that
portion of the motor path which has the least nutritional
stability. Could we explain the joint symptoms by,
‘other means, we might readily conceive how nutritional
changes might be set up.which would account for the
trophic and vaso-motor symptoms.

(e,) With regard to the toxie action of bacterial poisons
on the nervous system, it is of importance to note that
nutritional, as well as actual organic change may result.
The nerves under these circumstances are usually more
liable to be affected than the spinal cord; but there are
many diseases in which it is obvious that it is the cen-
tral nerve centres which are affected, as for example in
syphilis, tetanus, etc. Toxic agents, however, often
exhibit a remarkable selective action, and as yet we do
not know what are the influences which determine such
susceptibility. For example, take the case of alcohol,
which being itself the result of the growth of organisms,
and being almost as low in the scale as the bacterial
‘toxic agents, gives rise to many and diverse nerve
conditions. Again the question arises, Can it be possible
that the action of toxic products is limited to certain
cells or groups of cells? Buzzard’® says there are
reasons for believing that this is quite possible, and as
instances he quotes various epidemics of infantile and.
ETIOLOGY AND PATHOLOGY. 21

spinal paralysis which it is impossible to doubt were due
to an infective origin. To admit the action of toxic
poisons on the nerve system and exclude that of their
originators on the local joint structures would be
illogical.

(2,) Apart from the question of finding gross lesions
the question is, Can trophic abnormal impulses produce
such lesions as we find in the diseased joints? I hold
that they cannot. They can, and undoubtedly do, pro-
duce muscle, integumentary, and , other nutritional
changes. But that they can bring about such acute
conditions as exist in rheumatoid arthritis I cannot
believe. In tabes the joint changes are altogether
' different in nature and appearance, and depend on a
definite nerve lesion. In syringo-myelia they are also
different. In ataxic paraplegia, and many other forms
of nerve disease, we also see arthritic changes, but, on
the one hand, they are all accompanied by definite nerve
lesions, and on the other they seldom present more than
swelling, and effusion into the joint. A wasting, with
some slight reparative change, one might possibly get;
but it appears to me inconceivable that such extensive
inflammatory lesions could arise without some sure and
certain guide to a nerve lesion, easily recognisable on
either macro- or microscopic examination. Marie,” *"4'*
one of our most accurate observers, says the patho-
logical anatomy of tabes and rheumatoid arthritis is
quite distinct, and that although points of difference
might be mentioned, in his eyes this is not necessary.
But let us study this point more carefully. As has been
said, in tabes, syringo-myelia, progressive muscular
atrophy, hemiplegia, ataxic paraplegia, etc., we occa-
sionally find arthritic lesions, and, as a type, let us take
tabes. In this disease we may have arthritic changes
either of an atrophic or hypertrophic form, or a mixture
22 RHEUMATOID ARTHRITIS.

of both forms may occur. The joint changes usually
appear suddenly with no pain and affect chiefly the
larger joints, such as the knee, and are characterized by
effusion into the synovial sac followed by destruction of
the cartilages and general disorganisation of all the joint
structures. The bones’ may waste, or bony out-growths
may appear. Such are the clinical features as seen
in nerve arthropathies, and it will be noticed that they
differ very considerably from what we see in rheumatoid
arthritis. Two theories have been advanced as to the
occurrence of these changes, neither of which exactly
fits the case of rheumatoid arthritis. One is, that the
function of the so-called trophic centres for the joints
in the cord is interfered with, thereby implying some
central lesion; the other, which is probably the true
one, is that owing to lessened or disturbed sensation
traumatic influences, which pass unnoticed, set up the
inflammatory joint changes. It is obvious that in rheu-
matoid arthritis we have neither central nerve iesions
nor have we a disturbance of sensation. Stewart,’9
speaking on the subject, says there are very strong
_ grounds for believing that the joint changes in rheu-
-matoid disease are not due to disease in the spinal cord,
as should such changes be brought about in that way we
would expect some evidence on examination of these
changes in the cord. The strong presumption is there-
fore that the joint changes do not arise in consequence of
« nerve lesion.

Having thus disposed of the more common views, let
us now consider some other arguments which have, from
time to time, been advanced to prove that rheumatoid
arthritis is due to a nerve disorder. We find Dr. Garrod”
quoting several cases where the disease developed after
a shock to the nervous system. As Baumler” says, this
can only be regarded as pre-disposing and not as the
ETIOLOGY AND PATHOLOGY. 23

exciting cause. Again, Dr. Spender ” mentions various
nerve phenomena which he has noticed occurring soon
after the onset of the joint lesions. He mentions such
symptoms as pigmentation of the skin, local sweatings,
neuralgia, tachycardia, etc. He also mentions cases
where “bulbar warnings’? were noticed quite early
in the disease, °°? and which progressed only to
terminate with the death of the patient. He maintains
that the arthritis is not the cause of muscular atrophy,
and that which is called ‘‘ arthritic muscular atrophy ”
does not arise in a similar way to that of rheumatoid
arthritis. He says the muscular atrophy of rheumatic
arthritis is a reflex tropho-neurosis, a pure irritation
of the articulay nerves, causing atrophy through the
anterior cornua of the cord, whilst that of rheumatoid
arthritis is an integral part of the disease, and the cause
of the arthritis is the cause of the atrophy. The most
difficult point to explain in rheumatoid arthritis is cer-
tainly this museular atrophy. It is one of the most im-
portant and earliest symptoms, and is usually, from the
very first, well marked. It extends to the whole of a
muscle, and not only to that part which is in contact with
the joint, or distal to it; and it follows so closely on the
first appearance of the joint-trouble as to preclude the
possibility of extension of inflammation to the nerves.
It is found that the extensors are principally affected,
but not exclusively so. The selective character of the
atrophy is a sufficient proof that the changes in the
muscles cannot be set down to mere disuse. It has
usually been attributed to some reflex nerve influence
having its origin in the peripheral nerves of the affected
joints. This has been suggested by Paget, Vulpian,”*
Charcot, and others. They argue that, assuming a
derangement in the nutrition of the motor.cells of the
cord, determined by the morbid impulses from the joint-
24 RHEUMATOID. ARTHRITIS.

nerves, the influences from the motor cells will, in all
probability, determine the alterations in the muscle
nutrition. This theory, they hold, is supported by the
fact that by the previous division of the posterior spinal
roots,” "46 wasting of the muscles can be prevented in
arthritis of the knee-joint artificially produced. Such an
argument cannot be admitted to apply to the atrophy of
rheumatoid arthritis, the one being an experimental
arthritis in a healthy animal, the other being the
evidence of a diseased condition. It is known that
disease in a joint may set up spinal trouble,” e.g.,
primary spastic paraplegia, and from this we gather that
influences from the joint nerves act on the controlling
’ structure of the muscle reflex centre. The muscle reflex
centres seem also to be under the influence of other
centres, because if there be disease higher up they may
also pass into a condition of increased activity, the path
. which determines their activity being the pyramidal
tract. At the same time, we must remember that |
_ atrophy takes place in all forms of chronic arthritis and
even in subacute cases such as are seen in syphilitic,
tuberculous, or hemophylic disease. No matter what
the cause is then, the first lesion is in the joints, and not
in the spinal cord. Another theory is that the atrophy
is caused by reflex vaso-motor spasm: this view was
advanced by Brown-Séquard; whilst Striimpell * sug-
gested that the inflammation might have spread from the
joints to the muscles, setting up a myositis; and in one
class of cases it has been noted by Sabourin™ that
inflammation had spread from a joint, and affected the
nerves as well as the muscles, giving rise to an ascending
neuritis. If neuritis has occurred the muscle fibres will,
be found to be narrowed, and the connective tissue to
have undergone proliferation. Vallat ® noticed such a
change in the muscle fibres, but he found that the
ETIOLOGY AND PATHOLOGY. 25

motor nerves were normal. These changes were all
microscopical.

We are now face to face with a dilemma. We must
either admit that the disease is one depending entirely
on an abnormal nerve condition, or else we must formu-
late a new theory as to its causation. The nerve theory
is quite unsatisfactory and unsatisfying. Could we
account for the joint changes in some other way the
nerve theory explains many of the symptoms, more
especially the skin changes, and the muscular atrophy ;
but it does not explain the joint conditions. Owing to
our want of knowledge as to the morbid processes
which govern the vaso-motor and trophic impulses, we
are unable to closely criticise any theory advanced with
regard to their method and mode of action, especially in
cases where only some abnormal disturbance of their
functional activity exists, but so far no evidence has
been produced which would give countenance to this
theory. Without the joint lesions we should have no
rheumatoid arthritis, and therefore unless a theory can
explain this fact we have no right to consider it perfect.
It has been mentioned already that many observers hold
the changes to be similar to those which occur in tabes.
To me they appear not to be so—they differ in appearance,
in minute anatomy, and also in clinical history. In tabes
the joint changes are due to a descending degeneration
of the nerves, a change always found when looked for,
and therefore their origin differs essentially from any-
thing found in rheumatoid disease. To my mind this
fact invalidates the whole argument. How, then, do we
account for the disease? The theory which I advance
and believe in is, that the disorder is due to a micro-
organism which has as habitat the joints, and which
there gives rise to soluble products which, when absorbed,
pass to the central nervous system, giving rise to the
nerve symptoms so common in this disease.
26 RHEUMA TOID ARTHRKI/IS.

The arguments I would advance in favour of this
view, apart from the actual bacteriological evidence, are
shortly as follows :—

(1,) The frequent occurrence of this disease as a
sequel to other forms of known infective disease. About
55 per cent. of my cases in which a definite cause is
assigned, arise, I find, as the sequel of some infective
antecedent disease, such as rheumatism, gonorrhea,
influenza, tonsillitis, typhoid fever, etc. In another 25
per cent. we find a history of disease of the female organs
of generation, in 20 per cent. catarrhs of the gastro-
intestinal and respiratory mucous membranes, chills and
getting wet, and in 5 per cent. a history of direct injury.
Stewart found 50 per cent. of his cases had suffered
from previous infective diseases such as gonorrhea,
otitis media, subcutaneous abscesses, etc. Now while
some of the above disorders obviously can act only as
predisposing the soil to inroads of bacteria, others would
supply the actual lesion through which the bacteria
could gain access to the circulation. In this class would
be tonsillitis, gastro-intestinal, respiratory and genito-
urinary catarrhs, etc. A catarrh of the mucous
membranes acts by producing mucous abrasions upon
which organisms can settle; by weakening the epi-
thelial cells in favour of the parasite; and by weaken-
ing the nutrition and vital energy of the body generally.
With such conditions it is easy to see there will be
little difficulty in gaining access to the circulation,
and .once having obtained a footing they will pass
readily to all the tissues of the body.

(2,) Its numerous nerve symptoms for which no
adequate nerve lesion has been found. This in my mind
is one of the strongest arguments. Were the disease due
to nerve troubles there can be no doubt adequate lesions
would exist in the central nervous system. But there
ETIOLOGY AND PATAOLOGY. 27

is no evidence of their existence, and sufficient search
has been made to render their existence impossible of
remaining undiscovered. Yet, as the nerve symptoms do
exist, we can only conclude that they are due to toxic
action, and the probability is that the toxic products are
produced by bacteria in the body and are not due to
autc-formation.

(8,) The occurrence during the course of the disease
of such disorders as pneumonia, pleurisy, pericarditis,
endocarditis, etc., must necessarily imply an infective
process. I find that about 3 per cent. of my cases
developed either pneumonia or pleurisy during the
time they were under my care, and about 17 per cent.
developed endocardial or pericardial conditions after
the onset of the disease.

(4,) Its polyarticular character, as Professor Biumler
says, is sufficient to suggest its infective nature.

(5,) Its course and nature also point this way. A
disease marked by distinct and persistent swellings,
showing periodic exacerbations, has all the characters of
an infective trouble.

(6,) The presence of enlarged glands proximal to. the
affected joints must surely be caused by an infective
materies morbi.

(7,) The result of treatment by guaiacol, salophen,
ete., also surely points to a disease whose symptoms are
mainly caused by bacterial products, for is not the
principal action of these drugs to free the system of the
albuminous products elaborated by micro-organisms by
way of the kidneys ?

This theory is the one which has recently been largely
accepted both at the Congress for Internal Medicine at
Berlin, and at the British Medical Association Meeting
at Montreal. Professor Baumler’ says the possibility
that a joint disease can be produced by lesions of
28 RHEUMATOID ARTARITIS.

the mucous membranes of the genito-urinary apparatus,
especially in females, or of the respiratory or gastro-
intestinal tracts, suggests the probability of its infective
character, and also explains its frequency in women who
suffer from such disorders, as well as explains its appear-
ance at, or about, the period of child-birth, or of the
climacteric. It would also explain better what influence
injury to the central nerve system has on its occur-
rence. He says the mere fact of its polyarticular char-
acter is enough to lead one to suppose we are dealing
' with an infective disease, the materies morbi of which
circulating in the blood is carried to the synovial sacs,
and to which they would appear to be specially suscep-
tible. It is for this reason Waldman ® desired to class
the disease as. an infective form of rheumatism, and
which leads various French observers to describe it
as ‘‘infecteux.’’ Riva,3! of Parma, in a recent paper,
suggests the infective nature of the disease, and Prof.
Stewart © and others at the British Medical Meeting at
Montreal also adopt this view. Dr. Shingleton Smith %*
there stated that he considered it likely to be due to
some infective agent, that it bore no relation to either
tubercle or syphilis, but that its close pathological
association with post-gonorrheal arthritis renders it
likely that some such parasitic organism as that des-
eribed by Bannatyne, Wohlmann and Blaxall, was the
infective agent of the disease, and that all the other
numerous etiological factors commonly described might
be swept away. He pointed out the differences between
the early and the late stages of the disease and thought
it probable that the parasitic stage was of limited
duration, and that the later phenomena were all the
. sequele of the arthritis, in which perhaps mixed and
secondary infections might play a part. On the other
hand, Chvostek 3 at the Berlin discussion said there was
ETIOLOGY AND PATHOLOGY. 29

no ground for supposing that chronic rheumatism (the
discussion was on Rheumatoid Arthritis, which the
Germans call one of the forms of chronic rheumatism)
was a disease of bacterial origin. He said the great
variety in the course of the disease was opposed to any
such view; the only two characteristic features of the
disease being the joint swellings and the transitory
nature of these. He said the most satisfactory view of
the disease was to regard it as due to toxins, produced in
the body but not by micro-organisms. He also stated
that a bacterial invasion gave rise to a very different
kind of joint inflammation, characterized by its long
duration, and the large amount of swelling which
accompanied it. It seems to me he cannot have been
talking of rheumatoid disease, for what joint disease has
less transitory or more marked swellings? His argu-
ments tell strongly in favour of a bacterial origin. So
far, therefore, the balance of opinion is in favour of my
view. Buzzard points. out that frequent and more or
less prolonged periods of remission of symptoms, and
the occurrence from time to time of fresh outbursts in a
disease, point mainly to an infective origin, and remind
one clearly of what occurs in syphilis, a typically
infective disease.1° Assuming this theory is accepted,
we know that the chief lesions must be due, not to the
mechanical presence of the micro-organisms themselves,
but to their metabolic products. We have therefore an
infection followed by an intoxication.

The infection consists in the micro-organisms selecting
a suitable nidus in which they may grow and propagate,
and, like all other pathogenic bacteria, they exhibit a
selective power in their choice of a habitat, which never
varies. In the joints, Dr. Wohlmann and I found —
positive proof that the micro-organisms grow and
propagate, for their presence can be demonstrated in _
30 RHEUMATOID ARTHRITIS.

the joint fluids by staining, and in the tissues on section.
What governs this selective power we know not; but it
appears curious, that out of all the sites to which. they
obtain access, they should, as far as we at present know,
only choose the joints. We know, that in relation to
different causes of disease, the various tissues of the body
exercise the most markedly different influences, even
though the cells constituting these various tissues have
originally sprung from the same:cell. This difference is
not limited to the various tissues of the same species of
animal, for, when we compare different species, we find
that even the same organ or form of tissue may present
the most marked differences in relation to the factors
giving rise to disease. For example, we see how in man
the liver is an inhospitable host to the bacillus of
tubercle. But it is not so with the liver of the ox or
he guinea-pig. Of similar import is the fact, that. if
we examine every one of the pathogenic microbes, we
will find different species of animals presenting very
varying degrees of susceptibility. ven in the case of
such a disorder as anthrax, there are all varieties
amongst the various species, from immunity in the frog,
to extreme susceptibility, as in the mouse and guinea-
pig. This variation in susceptibility applies not only to
species, but to varieties and races of animals and men.
It is well known that the white rat presents an almost
complete immunity to anthrax, and that the Algerian
sheep are much less susceptible than other breeds. A
similar fact is observed in. man in this respect, that
negroes are, as compared with white men, singularly in-
susceptible to yellow fever. Again it may be noted that
joints are specially liable to bacterial infection, ¢.g., such
diseases as pyemia and gonorrhcea, and if, as seems
likely, acute rheumatism is due to bacteria, or their pro-
ducts, we have yet further proof of this peculiar liability.
ETIOLOGY AND PATHOLOGY. 31

In rheumatoid arthritis, as in acute rheumatism,
ulcerative endocarditis, etc., it is possible that the
bacteria grow also on the endocardium and pericardium,
as otherwise it is difficult to account for certain of the
symptoms. It is probable that they grow freely in the
lesions through which they gain entrance, and possibly
also in other localities. But having no proof one way
or another on this point, we must leave it for future
consideration. On the other hand, in the joints them-
selves we have positive proof that the organisms grow
and propagate freely, doing so not only in the synovial
fluid and membrane, but also in the ligamentous, cartil-
aginous, and, to a less extent, in the bony structures.
Their presence gives rise to acute inflammatory changes
leading to ulceration, erosion, and destruction of the
hard as well as of the soft tissues. This process varies
in intensity and, usually as the disease progresses, is
accompanied by a coincident, but varying amount of re-
parative change which may end in a general hardening
and thickening of bones, cartilage and ligaments. This
change appears to occur either when the bacteria have
exhausted the pabulum on which they exist or else it is
an attempt on the part of nature to limit and shut off
the disease. ‘Possibly the production pf toxic products
may play some part in the matter. The joint symptoms,
which are due to the local action of the micro-organisms
and their products, may therefore be regarded as primary
or essential; whilst those which are due to their indirect
action, by the absorption of their products, may be
regarded as secondary or symptomatic. Although these
latter vary in every case, not only in intensity and in
nature, yet they would appear to have a common
toxemic origin; and some symptom of this toxemia is
invariably present.

The effects of the intoxication are principally seen by
4
32 RHEUMATOID ARTHRITIS.

their action on the nervous system, and to explain this
picking out of certain areas, besides the toxic theory we
must add a supplementary hypothesis of ‘ susceptibility
of parts.” Edinger ** accounts for this susceptibility
on the theory that those parts first degenerate which
suffer the heaviest demands upon their function. With
regard to the severity of the toxic effects, Van Geisen *
says that the nerve degeneration is in direct ratio
to the duration of the action of the poison. Changes
produced by acute poisoning may be recovered from,
although the degeneration may be profound, but

prolonged toxic action destroys the cell, and the.

integrity is irremediable. The whole course, dura-
tion, and termination of toxic disease depends upon
the course of parenchymatous degeneration, con-
trolled by the duration and intensity factors of the
poison.

How then do we apply these facts to what we find in
rheumatoid arthritis ? Let us first take the case of the
muscular atrophy which is one of the most constant
symptoms of the disease. Apart from true rheumatoid
atrophy, we must remember that atrophy may occur as
a consequence of a secondary neuritis. Such a condition
has been described by Sabourin,** Vallat,° Striimpell,”®
Duplay and Cazin," and is of less interest than the true
rheumatoidal atrophy, and can be: easily distinguished,
as it presents all the characters of ordinary muscular
atrophy in the re-action of degeneration and alteration
in the muscle structure, etc. This is absent in the true
form, in which the extensors are principally, but not
exclusively affected. The selective character of the
atrophy is sufficient proof that the changes cannot be
set down to mere disuse. The atrophy therefore, is in
all probability, due to an abnormal condition of the
multipolar nerve cells in the anterior cornua depending
1

ETIOLOGY AND PATHOLOGY. 33

on toxic poisoning.* For it is reasonable to suppose
that, given a soluble poison circulating in the blood,
some areas in the central nerve system should be
affected, and these all the more, especially as they may
be predisposed to it by reflex irritation from the joints.
The areas to be affected will be those which have the
heaviest demands on their function. That such a reflex
irritation does occur has been stated by many observers,
and has been even said to be sufficient to cause the
atrophy itself (Paget, Vulpian,’* Charcot, and others).
It has been argued that, assuming a derangement of
the motor cells of the cord determined by the morbid
impulses from the joint nerves, the influences from the
motor cells will determine the alterations in the muscle
nutrition. In the light of the discovery of the micro-
organisms, and of recent observations with regard to
the action of toxins on the nerve system, we may
disregard this reflex irritation except in so far as only to
regard it as a predisposing cause. On turning again to
the cells themselves, we find, according to Ferrier, that
the cell body with its nucleus is primarily concerned in
the nutrition of the motor nerve, and its correlated
muscular fibre, while the dendritic processes serve to
convey incitations to functional activity. He also states
that lesions of these processes may cause paralysis with all
the symptoms of a spinal paralysis, but with no muscular
degeneration. If such a condition can exist, might we
not consider it possible that by the action of a toxic body,

 

* The path of motor innervation is composed of two portions,
fa) the pyramidal cell with its dendritic processes, and centri-
fugal or axis cylinder process which courses along the pyramidal
tract, and (b) the spinal multipolar cell with its processes, and
axis cylinder process ending in the muscle fibre. It has been
shown by Golgi’s 7 method of staining that the pyramidal axis
cylinder ends in an arborescence which merely comes into contact
with the spinal cell or interlaces with its dendritic processes, and
there is no actual continuity.

: 3
34 RHEUMATOID ARTHRITIS.

the cell’s action might by itself be so lowered or held in
abeyance that nutritional changes in the muscles would
ensue without much disturbance of the conductive faculty.
of the processes, and also without any degeneration of
the muscle beyond wasting? Any disease attacking the
central nervous system and causing actual change, never
attacks the cells alone, or the fibres alone; for the neuron
(the compound of cell, axis cylinder, and terminal:
branching) is one coherent entity. So the lesion in this
case must consist of a depression of the function of
cértain cells, for if we compare the clinical characters of
the atrophy with that of progressive muscular atrophy
we will see that no actual lesion can exist. In progres-
sive muscular atrophy, of which Buzzard’ says some
mode of infection would best explain the clinical features
and the pathological anatomy, we have a slowly
progressive lesion of the ganglion cells and their
prolongation in the axis cylinders of the nerve fibres. In
this disease, where the atrophy is marked by the
_ reaction of degeneration, there are actual degeneration
changes in the cord, whilst in rheumatoid arthritis, with
no reaction of degeneration, there are no changes in the
cord. No theory will account for this unless it be as I
have said. The cell’s vitality must be lowered. In
one class of cases, of which those mentioned by Dr.
Spender *® may be taken as typical examples, we must
assume that the action on the cells has been so great as
actually to give rise to a distinct lesion, and this spread-
ing upwards in the pyramidal tract has finally come to
affect the bulbar neuclei. Folli’s !° discovery of atrophy
of the motor cells, goes a long way to confirm this theory.
What was probably only at first a depression of func-
tion due to the changes set up by the rheumatoid
toxin had apparently, in the long run, become actual
organic change. Miller,*° speaking of the muscular
ETIOLOGY AND PATHOLOGY. 35

wasting seen in phthisis, says it is due to a vaso-
contraction affecting certain centres of the cord; the
vaso-contraction being caused by the products of the
-bacilli, just as the products of pyogenic organisms cause
vaso-dilatation and diapedesis.

With regard to the selective site of the muscular
atrophy, and apart from Edinger’s theory (see p. 82),
we find Dr. Ferrier saying, ‘It is not unreason-
able to suppose that the degree of representation, and
therefore the trophic strength, of the extensors in the
anterior cornua is less than that of the flexors, while
such extensors as have the most numerous connections
with the spinal segments would have a greater vital
resistance than those whose segments are fewest.”’ From
this we may deduct that those muscles with the lowest
trophic representation will be those which are first, and
most affected, in any disease which lowers the vitality of
the nerves and nerve centres. Duplay and Cazin”
have suggested that it is due to the anatomical rela-
tionship between the nerves which supply the joint
corpuscles, and those which supply the affected muscles.
This does not explain it all, however, and Dr. Ferrier’s
explanation seems the more probable, and the more
easily understood, especially if we add that reflex im-
pulses may possibly help in the selection.

It has been proved that certain toxins have the power
of producing changes in the vaso-motor system, and also
in the trophic condition of the skin. It is thus that we
account for the local sweatings and pigmentation. We
know that normal pigment is formed from a particular '
product of metabolism of the cutis, being formed both in
the ordinary epithelial cells and in the connective tissue
-cells. These connective tissue pigment cells are the
regulators of the metabolic process, as they consume the
surplus pigment-forming substance. The abnormal pig-
30 RHEUMATOID ARTHRITIS.

mentation of rheumatoid arthritis is probably due to a
local increase in the formation of the normal pigment,
consequent upon some abnormal innervation, and to
a deficient consumption of the surplus by the con-
nective tissue cells. The vaso-motor ehanges are in
all probability due to the centre situated in the inter-
medio-lateral tract, being affected in a similar fashion
to those in the anterior cornua.

One of the greatest points of interest is the tachyeardia. .
Bezangon *! states that tachycardia may in some cases
be due to pressure on the vagus, but he suggests: that
more often it is due to the absorption of certain toxins.
He cites the case of the bacillus tuberculosis, and also of
certain staphylococci, streptococci, etc., of the secondary
‘ purulent infection so common in phthisis. Bouchard
obtained from tuberculin a substance to which he gave

the name ectasine, which had the property of producing - c

dilatation of the vessels. Toxins, with similar powers,
have been obtained from the product of the bacillus
pyocyaneus by Charrin and Gley; and from those of the
staphylococcus aureus by Arloing. By acting as vaso-
dilators these substances would tend to produce tachy-
cardia, since the heart tends to act more rapidly as the
peripheral friction diminishes. In other cases the toxins,
by giving rise to a neuritis of the vagus may cause it.
Vierordt in a case of phthisis found such a neuritis, as '
evidenced by a great number of vagus fibres having
undergone degeneration and atrophy. With regard to the
local sweating, it is probably due to paresis, caused by the
toxin acting on the sudoriferous, and vaso-motor centre of
the bulb. Similar action is seen in influenza (Semmola*’). :

Anemia in many cases is marked. Now it has
been found by Hunter“ that, in all probability, per-.
nicious anemia is caused by the presence of bacterial
poisons, just as it has been found to occur from the
ETIOLOGY AND PATHOLOGY. 37

presence of cadaveric poisons, and analogous ferments.
Such being the case it requires little imagination to
conceive that a similar process may occur in rheu-
matoid arthritis. These bacterial poisons would seem to
act by a hemolytic process which is specially limited
in its action to the portal blood. There are some special
points of interest in the anemia of rheumatoid arthritis.
These are the diminution of the hemoglobin value of the
red cells and the increase in the number of the white.
Forsbrooke also notes this diminution of the hemoglobin.
According to Oster we have three classes of anemia :—
(1,) Those in which the percentage of hemoglobin in
_each corpuscle remains the same, and the percentage of
colouring matter corresponds to the percentage of the
corpuscles. This is usually seen in anemia due to
hemorrhage, or arising from some organic disease. It
may be noted that Laker “ and Mackenzie “ both point
out that in malignant disease the hemoglobin value is
decreased. The former states that from this fact alone
one can diagnose the nature of the tumour, at least in
so far as to say it is malignant or benign.

(2,) Those in which the hemoglobin is reduced out of
all proportion to the reduction of the corpuscles, so that
the individual value of each red cell in colouring matter
may be greatly lowered. Chlorosis is the typical example
of this class. .

(83,) Those in which the percentage of hemoglobin is
increased, and in which, therefore, the anemia is not so
great as the reduction would appear to indicate. This is
seen most markedly in pernicious anemia.

In rheumatoid arthritis, then, we have to do with an
anemia belonging to the second class—in fact an
oligochromemia.

We have now to ask ourselves. why, in one form of
anemia, the hemoglobin value should be lessened, and
38 RHEUMATOID ARTHRITIS.

in another increased? Where it remains constant it is
probably due to a loss of blood as a whole, whereas, in
the other cases, it must be due to some abnormal con-
dition having a direct influence on the blood cells or
their contents. We know that anemia implies a want
in the adjustment between the gains and the losses of
the blood—defective hemogenesis or excessive hemolysis,
the former depending upon deficiencies in quantity
or quality of the food, insanitary surroundings or
mode of life, inherited or acquired defect in the hemo-
poietic viscera etc., and the latter on the processes of
fever and inflammation, or to the presence of deleterious
substances in the blood. With the former condition we
have nothing to do. It would appear as if most forms
of anemia in which destruction of the red cells and their
contents is the typical feature, must depend, for their

* occurrence, on some substance, harmful to their existence, ~

~ circulating throughout the system. Dr. Hunter “ says
that blood destruction is of two kinds— (a) passive,
which is the ultimate destiny of the red corpuscles, and
which being a process of natural decay is evidenced by
the presence of pigment in the spleen, liver and bone- |
marrow; and (b) aetive, in which the hemoglobin
escapes from the corpuscles into the plasma, and is in
great part excreted by the liver as bile pigment. In
health no trace of this breaking up and excretion of free
hemoglobin is found, but in such a disease as pernicious
anemia there is abundant evidence of it in the liver cells.
This has been found not only in pernicious anemia, but
also in malaria, and as the result of certain poisons
which destroy the blood. Now, this destruction of the
blood would not appear to take place so much in the liver
as one would expect, as in the spleen and to a less extent in
the gastro-intestinal capillaries. This Hunter has demon-
strated by many beautiful experiments. He found that
ETIOLOGY AND PATHOLOGY. 39

almost all hemolytic process was stopped by removal of
the spleen, whilst experimenting with toluylenediamin.
The chief function of the liver would, therefore, appear
to be the disposal of the products of hemolysis. He goes
on further to show that certain substances, such as
toluylenediamin, act on the blood indirectly and depend
for their effect on the action of certain cells and especially
of those of the spleen; whereas such substances as pyro-
gallic acid, glycerine, distilled water, etc., act directly,
and depend on the quantity injected for their effect.

This, however, does not help us much in solving the
question as to why, in one case, the same class of poison
should produce an increase in the hemoglobin value,
whilst in another it diminishes it. Are we to suppose
that each individual poison possesses a selective action,
and that it has the power of picking out one constituent
only, of the blood, for special attention? This is possible
from what we know of the action of bacterial poisons,
but it is hardly probable. It appears to me more likely
that the different classes of bacterial poisons will have
different effects—-thus the toxic albumens may have the
power of dissolving out the hemoglobin without destroy-
ing the cell (see the action of snake poison and that of
malaria) and the ptomaines may be more destructive to
the life of a corpuscle than to its contents.

In rheumatism we have an acute disease which is most
probably due to an infective organism (Newsholme),“
and in which Dr. Garrod * finds a loss of the red
corpuscles with a corresponding loss of hemoglobin—the
corpuscular value remaining constant. In some cases,
during the course of the disease, there is, however, a
tendency to a decrease in the corpuscle value of a tran-
sitory nature, but which may become more permanent
during convalescence, producing a more or less chronic
anemia. In malaria, a disease due to an infective
4o RHE UMA TOID ARTHRITIS.

protozoa in all respects peseniblinws bacterial iitoution: #
we have, according to many: observers (see Mannaberg,”
Evans,” etc.), a reduction in the hemoglobin value,
especially after the paroxysms. Mannaberg says that
‘for several days after the last paroxysm of fever the
proportion of hemoglobin still fell.” _He gives as explan-
ation of this the supposition that the hemoglobin is
dissolved out by the parasitic poison circulating in the
liquor sanguinis. Evans! notes a reduction in the
number of the red corpuscles, and also of the hemo-
globin—the loss of the latter exceeding that of the
former. He found no change in the number of the white
corpuscles. Finally, in pernicious anemia, Dr. Hunter
maintains that the anemia is due to the presence of
bacterial poisons acting on the blood in the portal capil-
‘laries, thus causing an anemia in which there is an
increase in the hemoglobin value of the individual cells.
I take it that in the first disease, as there is no
increase in the number of the white corpuscles, we are
dealing with a pure toxemia—the bacteria themselves
. not entering into the blood. And in the second we have
a mixed cause—the parasite not only destroying the cells
and their contents by their presence, but their toxins,
by dissolving out the hemoglobin, produce a diminished
hemoglobin value. And in the last case we are probably
dealing with an alkaloidal. poison absorbed from the
intestinal canal. According to Cohnheim * certain sub-
stances, of which snake poison is one, has the effect, of
dissolving the blood corpuscles, and Maragliano ® states
that there are certain pathological conditions in which
the blood serum exercises a destructive influence upon
the red cells, which causes them to give up their hemo-
globin to the menstruum, and that it then disappears
from the blood. In the present state of our knowledge
one does not like to dogmatise, but it would appear to
ETIOLOGY AND PATHOLOGY. 41

me as if the two classes of bacterial poisons (ptomaines
and albumoses) had each distinctive actions. In rheuma-
toid arthritis we are dealing with a disease in which the
micro-organisms exist in the blood, but they, as far as
I know, do not seem to destroy it as do the malarial
' parasites,.and that probably, therefore, the anemia is
to a great extent due to the action of their toxic pro-
ducts, dissolved and circulating in the blood.

The increase in the number of white corpuscles is of
‘interest as it is found in most infective conditions, and
according to Hunter * the increase is roughly propor-
tional to the severity of the disease. Habershon® says

_he has noticed an increase, not only after the introduc-
tion of alkaline carbonates, but also from the presence
of toxins in the blood. Should bacteria themselves be
present, the destruction of the red cells will probably be
greater and occur sooner than where their products only
exist. .
re Parr IL
Assumina that the disease is of an infectious nature, we
find the predisposing causes are all those which, by
some means ox other, lower ‘the constitutional state.
The tissues, in health, being able to resist the inroads
of disease it is only among such influences as would
bring the body generally into a condition of lowered
vitality, that we look for. predisposing causes., Of
these causes the principal are :— ,

1. Heredity.—It is difficult to prove direct inheritance,
not only on account of the difficulty in the diagnosis, but
also on account of the confusion which exists as to what
form of disease the term rheumatoid arthritis should be
strictly applied to. It may happen likewise, even
although the proper nomenclature is understood in the:
42 RHEUMATOID ARTARITIS.

individual cases, that the disease may have passed over one
or more generations. It may be described as occurring
sporadically ; and that, out of a family of brothers and
sisters, some are affected, but others escape. Heredity,
therefore, is very hard to trace. It is known besides
that an inherited tendency to disease does not in all
cases manifest itself in an exact reproduction of the
morbid peculiarity of the parent in the child, but may
tend to give rise to allied conditions. Thus, it may
happen, that in those inheriting an arthritic diathesis, in
some rheumatoid arthritis may develop, in others gout,.
and in others rheumatism. Statistics go to prove that.
a certain diathetic predisposition to arthritic disease
does exist. By this we mean a diathesis in general,
not in special, and in all cases it is easier to trace and
to prove this inheritance of a diathesis than of a disease
itself. One member of a family may have gout, one
rheumatism, whilst yet another rheumatoid arthritis.
In the case of gout and rheumatism heredity has been
clearly proved, and this is probably due to the fact that
they are both diseases well known and have been read-
ily recognised for ages, whereas rheumatoid arthritis.
has not. By some it has been said also, to be peculiarly
liable to occur in those inheriting a tendency to phthisis. ,
This is as one would expect, but there is nothing in com-
mon between the two diseases, except that a tuberculous.
tendency may, by lowering the resistance, tend to bring
about rheumatoid changes, and it is only in this connec-
tion that there can be any association between the two
disorders. The rheumatoid materies morbi would, in
such cases, find a system weakened and unprepared to
resist its inroads, and would therefore in all probability
fall an easy prey.

As a cause, heredity was recognised early in the
history of the complaint, for we find that Heberden,®
ETIOLOGY AND PATHOLOGY. 3

Adams” and Fuller,** amongst the early observers, all
mention it. Coming down to more recent times we find
a history of heredity was obtained in 11 out of 41 cases
by Charcot,® and in 10 out of 45 by Trastour. These
statistics are quite unreliable, however, as these observers
only regarded rheumatoid arthritis as one of the many
forms of rheumatism, and as such the family history
was taken. Garrod® traced in 84 out of 500 a direct
descent, givihg a percentage of 16°8. The average per-
centage of heredity, in rheumatism (taking the results
of Fuller, Syers, Pye-Smith, Garrod, etc.), is 23-9.
When we consider the inheritance of other forms of
arthritic disease, in rheumatoid arthritis the percentage
is much greater. Garrod® gives a percentage of 43-2.
On further analysis he mentions that there was a history
of gout in 20 per cent., whilst only 12°8 gave one of
rheumatism. This is very remarkable, and I have quite
failed to verify it. Sir A. Garrod and Sir Dyce Duck-
worth point .out that the disease is most common in
female members of gouty families. My statistics do
not bear this out, for taking three years at the Bath
Royal Mineral Water Hospital (1894-1897), I had 293
patients suffering from rheumatoid arthritis, and of
‘these only 15 gave a history of direct inheritance. In
-only a very few could gout be clearly traced. In several
there was a history of rheumatism affecting a brother or
sister, and in 36 affecting a father or mother. Heredity
does not seem to render a patient more liable to be
attacked in early life, but it does seem to affect the acute-
ness of the disorder.

2. Sex.—There can be no doubt that the disease is
much more common in women than in men. Out of 293
cases 41 were in men, and the rest in women (13°9 and
861 per cent.). Gout affects men more commonly,
whereas rheumatism does so in nearly equal propor-
44 RHEUMATOID ARTHRITIS.

tions. Haygarth “ found 1 man to 34 affected, and
Garrod ™ found that it occurred in 411 females to 89
males (82°2 and 17°8 per cent.). As was pointed out by
Adams, Senator, and others, the joints most affected in
men, are the larger ones, such as the hip or shoulder,
and in women, the smaller ones. Charcot, Trousseau,®
Duckworth, and others, have also observed it to be more
common in women. This frequency in women is almost’
certainly due to'the frequency of some genito-urinary
derangement, some abnormal condition of which readily
enables the micro-organisms to obtain access to the
blood, and thence to the joints. In the case of children
rheumatoid arthritis is more common in boys than in
 girls—the younger the child the greater the proportion
of males. As puberty is approached this diminishes
until the proportion of females equals, and finally
greatly exceeds that of males. .
8. Age.—-Much has been written about the age at
which the disease most commonly commences. By
most it is held to be essentially a disease of the early,
degenerative period. According to my experience many
of the acutest cases occur, however, in young adults,
and ‘often even in children. Dr. A. E. Garrod” shows
that the commencement of the disease in females
steadily increases with each five-yearly period, until
the one from 45 to 50 is reached, after which the num-
bers rapidly. fall. In males, on the other hand, the
decrease does not occur until 70 has been reached
and in them also there is no steady increase, but two
maxima exist, one between 30 and 33, and the other
between 50 and 55. The special liability of women
between the ages of 40 and 50, is probably due to. the
occurrence of the climacteric. In women there are two
great periods of life—the period of puberty, and that of
the climacteric, The former is a time of great strain, both
ETIOLOGY AND PATHOLOGY. 45.

mentally and physically, not only on account of the new
conditions which the reproductive organs have taken on,

but also on aecount of the general bodily conditions
induced thereby. It is a period attended by a general
aptitude for disease, as there seems to be a special con-
nection between the physiological processes going on,
and the general bodily health. At the same time
women seem liable to attacks of disease for which no
reason can be assigned. The period of the climacterie
is at the other end of life, answering in many respects to
the period of puberty in being a time in which the whole
system is in a state of unrest, unstable and ready to.
develop unhealthy tendencies. Unfortunately it is a.
degenerative process, and, from its very nature, we
would expect to find it the more productive of mischief,
The sudden fallin the number of cases occurring after
the menopause is’ probably due to the fact that, all.
uterine activity having ceased, there are fewer roads by
which micro-organisms can gain access to the system.
It is almost certain that a climacteric occurs in men
in a similar fashion, but it is not so marked, and
probably occurs later in life. The following is an
analysis of 293: cases :—

 

 

AGES OF FIRST OCCURRENCE. & FEMALES. MALES.
— 7
Between 10 and 20. ‘f 14 5
20 4. 88. 54 5
5 380 ,, 40. 78 8
*3 40 ,, 50. 50 11
5 50 ,, 60. 45 9
35 60 ,, over jl 3

 

Totals ... ba 2 252 41

 

4. Catarrh of the Mucous Membranes.—How far a.
46 RHEUMATOID ARTHRITIS.

catarrh of the mucous membranes of the respiratory,
-gastro-intestinal, or genito-urinary systems acts as a
predisposing cause, it is hard to say; but that it is
through its agency that the micro-organisms finally
gain a footing is almost undoubted. I have traced
the onset of the disease in several cases, almost with
absolute certainty, to chronic catarrhal tonsillitis ;
several to the onset of dyspeptic conditions, and a
still larger number to the onset of genito-urinary
troubles. It is a frequent sequela of confinements,
and, more rarely, begins during pregnancy. Uterine
‘derangements are responsible for the onset of many
disorders, but none more markedly so than rheuma-
toid disease; and how can we wonder at it, when
we find, as a consequence of some local irregularity,
women ina state of worry and anxiety, sleepless.
with much pain and nerve exhaustion, their mental
and physical powers being both at their lowest ebb?
Dr. Ord laid special stress upon this fact, and I think
it is well merited, though my reasons are different. He
noticed that, in certain instances, the disease in the
joints was limited to one side; and in these cases there
was ovarian pain, and tenderness on the same side as
the joint lesions. He also noticed paroxysms of pain
occurred with the monthly periods. He considered these
uterine and ovarian derangements to be the cause of
the disease, through reflex action. To my mind, it is
more probable that the ovarian and uterine derange-
ments act only by affording a lesion through which
the micro-organisms may reach the circulation; and,
by the induced irritation and debility, render the
system so lowered and impaired as readily to fall a victim.

In 298 cases, 18 occurred after confinements ; 2 dur-
ing pregnancy; 2 after a miscarriage; and one after
marriage.
ETIOLOGY AND PATHOLOGY. 47

In a large number there was irregularity in the
monthly functions, but I rarely could trace a case
directly to these disorders. Garrod says that 105 out of
176 were normal in their menstruation. Five occurred
soon after a confinement, 3 after miscarriages, and 8
during pregnancy.

5. Emotional Causes.—The influence of these is not
confined to the period immediately preceding the onset
of the disease, but they also to a certain extent influence
the progress of the disorder. Over and over again do we
find patients say they are worse after any anxiety or
worry, and it has been known even to arise after a period
of prolonged worry; but in such cases worry probably
only acts by lowering the tone of the constitution.
Stewart ® mentions 4 cases as having been caused by
worry. Other mental causes assigned are sudden shock
and fright. Both Kohts® and Leyden ® mention cases
in which severe shock was the cause—the shock arising
from shells bursting in time of war.

6. Atmospheric Conditions.—-Rheumatoid arthritis is
most commonly met with under those influences most
favourable to the prevalence of catarrhal and inflam-

.matory affections of the air and digestive tracts, that
is, on cold and damp soils with a variable temperature,
and, as we know, at those seasons of the year—the spring
and autumn—-when these conditions are most likely to
prevail. Professor Charcot regarded a combination of
damp and cold as the most potent cause. He was of the
opinion that exposure to such influences must be pro-
longed, and that articular lesions did not necessarily arise
until some time had elapsed. Many sufferers corroborate
this and ascribe the onset of their complaint to damp-
ness, and there is no doubt that cold and damp often
markedly increase the misery of the wretched patients.
The disease is more common in Ireland than in
48 RHEUMATOID ARTHRITIS.

. England, and this is accounted for by the prevalence of
damp in the former country, and. Adams” has pointed
out that it is specially common in Holland. Stewart
points out that it is very rare in Canada. This one would
expect in a country with such a dry air. Although a
dry climate is least favourable to its development, it is
not unknown in any locality. In this respect we are apt
to confound, and itis difficult to avoid confounding, its
indirect effects as predisposing agents with its direct
effects as exciting cause. Further, when we would test
the relative influences of atmospheric conditions, our
endeavours to arrive at a just conclusion are seriously
hampered by the co-existence with them (but partly no
doubt arising out of them) of peculiarities of habit, and
modes of life, and other special conditions of unhealthi-
ness. Out of 298 cases, 26 developed after getting wet,
or after a chill.

7. Injury.—Injury, as traumatism pure and simple,
has not a marked effect on the occurrence of acute rheu-
matoid arthritis. Only a few cases have I been able to

, trace to this, but if we look at the term in its wider
sense it comes to have a much more important bearing.
A direct injury, in its immediate consequences, may
appear so trifling as to merit little or no attention, yet
it may, in its ultimate consequences, end in the crippling
and loss of the use of an important member of the body.
Orth and Wysokowitsch’! have shown that traumatic
lesions will cause a. local predisposition to infective
processes. Occasionally, but more rarely, it appears to
follow on some injury which has set up some acute
inflammatory condition. In one case I found it occur
subsequent to fracture of a patella, and whilst the
patient was in the recumbent position in consequence of
this fracture. A history of such direct injury, and. its
consequences, is rare. One more often hears of injury
ETIOLOGY AND PATHOLOGY. 49

after the joints are diseased, and then the question of
effect and cause comes to be a difficult one. Looking
at it from a broader point of view our idea of the im-
portance of injury, as a cause, alters. In 293 cases 46
occurred after acute or chronic rheumatism. I here
regard the injury caused to a joint, when caused by
rheumatism, gout, gonorrhea, or any other form of
arthritis which may so frequently precede a rheumatoid
onset as having more or less the nature of a direct
injury. That rheumatoid disease frequently follows
attacks of such diseases is not to be wondered at, when
we remember the injury they do to a joint, and when we
consider that rheumatism, and most other forms of acute
arthritis, are probably caused by micro-organisms or
their products—at least, at present there seems to be
good ground for believing that such is the case (7? and ). °
Just as one form of micro-organism or its poison can
inhibit the growth of another so does the converse occur.
Roger ™* has shown that rabbits which are naturally im-
mune will succumb to quarter-evil if simultaneously
the chemical products of the bacillus prodigiosus, proteus
vulgaris, or staphylococcus be injected. Other vegetable
bodies, such as the vegetable ferments, have the same
effect. Klein’ and others have shown that the simul-
taneous injection of the bacillus prodigiosus and various
pyogenic germs with the bacillus of tetanus will render
animals capable of resisting a simple infection of the
tetanus bacillus extremely susceptible. Again, the viru-
lence of the bacillus diphtherie may be greatly increased
by the inoculation of the bacillus pyocyaneus. But we
must remember that while certain diseases render the
tissues more susceptible to the attacks of other diseases,
yet certain micro-organisms lose their virulence when
confined in closed cavities such as a joint, possibly from
the action of their own products.” What the effect of
4
50 RHEUMATOID: ARTHRITIS.

rheumatism and its allied disorders is we do not know,
and it is a moot point, whether they act by reducing the
resistant power which normally exists in all tissues, but
in this case more especially in the joints, or else of the
blood. But we do know, as has been stated by Ewing ”
and Fodor,’® that anything which reduces the blood’s
alkalinity reduces its germicidal power. Ewing found
that normal blood serum is a powerful protective agent.
against the inroads of bacterial infection, and that
toxins act harmfully, not merely by their direct effect,
but also because they lower the resistant power of the
blood against secondary infections. He found that
snake poison, which in its nature belongs to the same
class of poisons as those formed by bacteria, greatly
lessens the blood’s germicidal power. Fodor records a
number of experiments showing the influence of the
_ alkalinity of the blood on diseases produced by micro-
organisms. Four series of experiments on animals
are first reported which show clearly that, by the
administration of alkalies (sodium bicarbonate by the
mouth or by subcutaneous injection), the power of
resistance against infection with cultures of. anthrax
bacilli is greatly increased. The normal alkalinity of
the blood was determined by the examination of seventy-
six healthy rabbits, and four experiments are reported
showing the increase in the alkalinity of the blood which
occurs after the administration of sodium bicarbonate.
He then records the results of a large number of
observations on the alkalinity of the blood in rabbits
after infection with the bacilli of anthrax, cholera,
typhoid fever, tuberculosis, and erysipelas. These
observations show that in the living organism, after
infection with certain bacilli, there.is first an increase
of the alkalinity of the blood and then a diminution of
the same, more or less. If the infection is fatal, the
ETIOLOGY AND PATHOLOGY. 51

diminution of the alkalinity is marked and progressive ;
if not fatal, the diminution is slight, and is followed by
an increase of the same, in consequence of which the
alkalinity of the blood becomes permanently higher than
before the infection. Thus there exists a connection
between the pathological action of certain bacteria and’
the alkalinity of the blood. Those rabbits which have the
greater alkalinity of the blood, as well as those in which
the alkalinity of the blood is increased to a greater
extent alter infection, have greater power of resistance
against certain infectious organisms (anthrax bacilli)
than the rabbits in which the alkalinity of the blood
is less. It appears, therefore, that the degree of
alkalinity of the blood, as well as the power of the
organism to increase this alkalinity with corresponding
intensity after infection, is of essential influence upon’
immunity.

Although we are still in the dark as to their mode of
action there is no doubt as to the frequency with which
rheumatoid arthritis follows on infective processes affect-
ing one or more joints. Stewart says 50 per cent. of
his cases had suffered from previous infective diseases,
more especially gonorrhcea or gonorrheal arthritis, and
it is worthy of remark that although the gonorrheal
arthritis was confined to one joint yet the subsequent
rheumatoid arthritis attack was poly-articular. He con-
cludes that a mono-joint infection may predispose to a
general joint affection. Chvostek” says thatin consider-
ing’ joint invasions we must bear in mind as causative
factors, not only toxins of those micro-organisms which
we believe to be infective, but also those chemico-toxic
substances produced by indirect bacterial activity.

Such then are the more common predisposing causes,
and herewith I append a list of those assigned in 132
cases out of 293 :—
§2

‘RHEUMATOID ARTHRITIS.

After confinement - - 18
» wmoiscarriage - 3
4) Marriage - 1

During pregnancy - 2

After acute rheumatism” 41
5, chronic rheumatism 6
» diphtheria j Y
» influenza 11
»  tonsillitis 7
» typhoid fever 2
» dyspepsia 2
» injury 6
» concussion of the spine e = 1
» necrosis of the jaw from caries of teeth 1
» hard work 4
» getting wet or from a chill 25

132

The other 161 cases gave histories too unreliable, or
could give no cause.

 

* With regard to acute rheumatism being assigned as a cause,
some confusion must arise from a primary attack of rheumatoid
arthritis being described as one of acute rheumatism. Many
such cases are pure acute rheumatoidal attacks, and statistics on
this point, therefore, are apt to be unreliable and misleading.

a
ES SiS ore

won
go BS

et et
Sou ¢

 

REFERENCES.

Schtiller.—“ Gelen. k-Entziind v. Langenbeck’s Arch.,” Bd.
45, 1892, and ‘ Berliner klin. Woch.,” Sept. 4, 1898.

Chauffard & Ramond.— Revue de Médicin,” May 10, 1896.

Pye Smith.—“ Guy’s Hospital reports,” 1874, xix.

Hutchinson.—“ Pedigree of Diseases.”

Forsbrooke.—“ Dissertation on Osteo-arthritis.”

Remak.—“ Deutsche Klin.,” 1863 ; ‘‘ Med. Centralzt.’’ 1861.

Senator.—* Ziemssen’s Handbuch,” 1875 and 1879.

Ord.— Brit. Med. Journal,” vol. ii., 1884, p. 268.

Duckworth.-—« Brit. Med. Journal,” vol. ii., 1884, p. 268.

Follii—*TI] Policlinico,” December, 1894.

Klippel quoted Massolongo.—“ Riforma Medica,” vol.. ii.,

1893, p. 159.

Pitrés & Vailliard.—“ Rev. de Médicin,” No. 6, 1887.
Duplay & Cazin.—‘ Arch. Générales,” January, 1891.

Ord.—-Loce. cit.

Garrod.— Treatise on Rheumatism, etc.,” p. 239.
Buzzard.— Clin. Soc. Transl.,” vol. xxi., p. 59.
17.
18.

19.
20.
21.
22.
23.
24.
25.

27.
28.
29,
30.
31.
382.

33.
34,
35.

36.

38.
39.
40.
41.
42.

43.

44,

46.
47.
48.
49.

50.
51.
52.

53.
54.
55.
56.
57.
58.
59.

ETIOLOGY AND PATHOLOGY. 53

Marie, P.—‘*Lectures on Diseases of the Spinal Cord” (Syd.
Soc.), p. 236. ,

Marie, P.—Quoted Souza Leite in thesis on ‘‘ Acromegaly ”
(Syd. Soc.), p. 77.

Stewart.—“ Brit. Med. Journal,” Oct. 30, 1897, p. 1225.

Garrod.—Loc. cit., p. 287.

Biumler.—‘ Congress f. Innere Médicin,” Berlin, 1887.

Spender.—“ Karly symptoms of Osteo-arthritis.”

Spender.—“ Brit. Med. Journal,” vol. i., 1894.

Vulpian.—‘ Lecons sur l’Appareil Vaso-moteur,” 1875.

Raymond.—* Rev. de Médicin,” 1890, p. 3.4.

Hoffa.— Volkmann Klin. Vortrage,” 1892.

Gowers. —“‘ Diseases of the Nervous System,” p. 443.

Striimpell.—* Munchener Med. Wochensch,” 1888.

Sabourin.—“ Thése de Paris,” 1873.

Vallat.—“ Arch. Générales,” 1877.

Riva.-—Quoted Stewart, “Brit. Med. Journal,” Oct. 30, 1897.

Smith-Shingleton.—‘ brist. Med. Chir. Journal,” Dec., 1897,
p. 828.

Chvostek.—“ Congress f. Innere Médicin,” Berlin, 1897.

Edinger, see Brown.—“ Lancet,” Nov. 6, 1897, p. 1187.

Van Geisen.——“ State Hospital Bull,” New York, vol. i., Nos.
2 and 4,

Sabourin.—“ Thésede Paris,” 1873.

Golgi quoted Schiffer. —“ Brain,” vol. xvi., p. 147.

Ferrier.—‘ Brit. Med. Journal,” 1898, vol. ii.

Spender.—“ Brit. Med. Journal,” 1893. :

Miller.—* Edin. Med. Journal,” Sept., 1896, p. 225.

Bezancon.—‘‘ Rev. de Médicin,” January, 1894.

Semmola,— Transl. of the Académie de Médicin,” 1891—
1892.

Hunter.— Practitioner,” 1890 and ’89, and ‘“ Brit. Med.
Journal,” vol. ii., 1892.

Laker.—“ Centralb. f. d. Med. Woch.,” 1887, p. 405.

Mackenzie.— Brit. Med. Journal,” 1891, vol. i.

Hunter.— Brit. Med. Journal,’’ 1889, vol. ii.

Newsholme.-—Loc. cit.

Garrod.— Brit. Med. Journal,”’ 1892, vol. i., p. 385 and 1189.

Mannaberg.—“‘ Malarial Parasites” (Syd. Soc. transl.), p.
389.

Mannaberg.-—Loc. cit., p. 385.

Evans.—“ Brit. Med. Journal,’ 1891, vol i., p. 759.

Cohnheim.—“ Lecture on General Pathology” (Syd. Soc.
transl.), vol. i., p. 474.

Maragliano.—“ Berlin klin. Woch.,” August 1, 1892.

Hunter.—Loce. cit., 1892, vol. i., p. 1189.

Habershon.—“ Brit. Med. Journal,” 1892, vol. i., p. 1189.

Heberden.—‘ Commentaries,” Appendix, p. 417.

Adams.—“ On Rheumatic Gout.”

Fuller.—‘ Rheumatic Gout and Sciatica,” note, p. 335.

Charcot.—‘ Maladies des Vieillards,” 2nd Ed., p. 228.
60.
61.
62.
63.
64,
65.
67.
68.
69.
70.
71.
72.
73.
74.
75.

76.
77.
78.
79.
80.

RHEUMATOID ARTHRITIS.

Trastour.—“ Du Rhumatisme,’’ 1853.

Garrod.—‘‘ Rheumatism and Rheumatoid arthritis,” p. 238.

Garrod.—Loc. cit., p.239.

Haygarth.—-‘‘ Clin. History of Diseases,” 1805.

Garrod.—Loce. cit., p. 240.

Trousseau.— Clin. Méd.,” 1865 (Syd. Soc. transl.).

Garrod.—Loc. cit., p. 241.

Kohts.—‘ Berlin klin. Wochenschr.,” 1873, p. 304.

Leyden.—“ Klinik. der Riickenmarks-krankheiten,” 1874.

Adams.—Loc. cit., p. 15. ‘

Orth & Wysokowitsch.—‘ Allbut’s Med.,” p. 547, vol. i.

Sahli.—-“ Deutches Arch. fiir Innere Médicin,” 1893.

Newsholme.—‘ Lancet,” vol. i., 1895, p. 661.

Roger.—“ Rey. de Médicin,” 1891.

Klein.—“ Annual Report Local Government Board Suppl.,”’
1892—1893.

Kiefer.—‘ Centralb. f. Gynak. Leipsig,” 1896, No. 42.

Ewing.—“‘ Lancet,” vol. 1., 1894, p. 1886.

Fodor.—‘‘ Centralb. f. Bakt. u. Parasitenk,” Feb. 28, 1895.

Chvostek.—Quoted ‘‘ Clin. Sketches,” Feb., 1896.

Waldman.—'' Volkmann’s Samml. klin. Vortr.,” No. 238,
1884.
5S

CHAPTER III. .

PATHOLOGICAL ANATOMY AND
BACTERIOLOGY.

Degenerative Character of Changes—Point of Origin—How the
Bacteria gain Access—Naked Eye Appearances—Changes in
Synovial Membrane—Loose bodies—Ligaments—Characters
of Synovia—Changes in the Cartilages—Cornil and Ranvier’s
Views—Erosion—Pyroliferation—-Lipping —Changes in Bones—
Rarefication — Osteo-sclerosis — Volkmann — Changes in the
Muscles—Central Nerve Changes—Peripheral Nerves —Cardiac
Changes -— Kidney — Blood -— Glands — Fibrous Nodules —
Heberden’s Nodes—Situation and mode of Growth—Gout as
a Cause—Their Nature—Various Observers’ Views—Bacteri-

ology.

On examining after death the changes in rheumatoid
arthritis, we are at once struck by the extensive and
degenerative character of the lesions. Much has ‘been
written about these, but owing to the scarcity of
post-mortem material, until the acute stages at least
are past, few observers agree. Colles' and Todd? held |
that the disease was not inflammatory in nature, whilst
Adams,? Brodie,* and Cruveilhier,® did; Fuller® looked
upon it as a disorder of nutrition, rather than the result
of inflammation ; and Senator’ regarded the changes as
partly inflammatory, and partly degenerative, whilst
Garrod also held this view. Rindfleisch® stated that the
disease was essentially one of those lingering inflam-
matory conditions which accompany the decay of the
organism, like atheromatous disease of the internal coat
of the arteries. He said that the inflammation, not
being powerful enough to cause suppuration, sets up a
56 RHEUMATOID ARTARITIS.

hyper-plastic overgrowth. Trousseau,’® in his clinical
lectures, says “‘ the synovial membrane demonstrates its
inflammatory origin.” From what we know of the
disease its changes must be inflammatory in origin, and
they probably begin in’ the synovial membrane, and
spread from thence to the cartilage and deeper structures.
In acute rheumatoid arthritis the changes are, of course,
principally destructive in character; but as the disease
progresses and becomes more chronic, more and more
reparative change occurs, leading to cartilaginous, osteo-
phytic and ligamentous hardening and overgrowth. As
I have said, in the acute cases the inflammatory and
destructive element is in excess, whilst in the chronic or
osteo-arthritic, the fibroid or sclerotic is.

Brodie, Adams, and others, thought that the disease
commenced in the synovial membrane, whilst Volkmann,
Billroth #4 and Garrod consider it starts in the cartilages.
Given a micro-organism circulating in the blood, I think
it probable that the synovial membrane will be the
first to suffer, and after gaining access to the joint
fluid, one would expect it to spread rapidly and affect
almost simultaneously, by dissemination, the whole of the
internal surface of the synovial cavity. The question
is, How do the micro-organisms gain access to the joint.
cavity in the first instance? The probability is that
they do so by setting up an endarteritis in one of the small
vessels on the surface of the synovial membrane, with a
diffuse cell exudation, and this, by extension and rupture,
breaking into the joint cavity, liberates them for further
mischief. As regards this point the experiments by
Chvostek * are of interest as they show: (1,) That the
walls of blood-vessels, not evidently altered anatomically,
are permeable to bacteria; (2,) That the anatomical
structure of the synovia and its vessels is an obstacle,
and bacteria enter the joints considerably later than they
PATHOLOGICAL ANATOMY. 57

do'the kidneys through the renal vessels; (8,) That the
exit of bacteria depends on (a,) their kind—thus staphy-
lococci pass most readily, then streptococci, and lastly
the bacteria coli. This is probably due to the relative
virulence of each micro-organism for each individual
animal, and also to certain tissues being more suscep-
tible to certain bacilli than others. (b,) Their virulence—
in this connection the action of toxins must be con-
sidered ; (c,) other factors, chiefly nervous—for instance,
section of a nerve hastens the exit of. bacteria. If this
theory be correct it, of course, makes the synovial mem-
brane far more likely to be primarily affected than the
cartilages. However, I do not think one can lay much
stress on which portion is primarily affected, nor is it of
vital importance.

1. General appearance of the joint.—To the eye we
find an affected joint presents the following general
characteristics: It is. swollen’ and increased in size,
usually, in the acute stages, in a characteristic ovoid

anner ; but which, in the more chronic stages, becomes
lesszarked and more irregular. In the chronic forms
ee ee ea produced, partly by out-growth
from the cartilages or bones, and partly by twisting or
distortion of the joint; the deformity may be due to
both or either of these causes. On opening the joint
we probably find some fluid, certainly in the earlier,
and acuter cases almost always. Trousseau remarks
that the joint is often distended by hydrarthrosis. This
presence of synovial fluid during life is often deceptive,
and the doughy or pulpy synovial membrane produces
a feeling difficult to differentiate from that of fluid.
The synovial membrane we notice is thickened—in acute
cases this thickening being soft and pulpy, whilst in
the chronic stages it is hard and dense, the ligaments
being affected in a similar way, and, in very chronic
58 RHEUMATOID ARTHRITIS.

cases, may present cartilaginous or even bony deposits.
The imner surface of the synovial membrane is injected,
often intensely so, and is granular in appearance, readily
breaking down on pressure and being easily torn. Here
and there small abrasions may be noticed, but they are
seldom of any depth. In chronic cases the villi are
thickened, and more prominent than usual ; this is easily
demonstrable by placing a piece in water, when the villi
float up, showing their character beautifully. The peri-
articular cellular tissue is affected in a similar fashion
to its neighbours. All the soft tissues undergo great
development of new formed tissue, and the subsequent
contraction and adhesion of which, with the surrounding
parts, give rise to stiffness and limitation of the joint
movements, and finally to fibrous ankylosis. These
adhesions and contractions play a great part in the
development of deformities.
On turning to the articular
surfaces, we find the carti-
lage in the acute cases
soft, with here and there
an erosion, which may or
may not reach the bone.
In more chronic cases, be-
sides erosions the cartilage
itself may present a velvety

 

IG. 1.—This bone is from an acute case

of rheumatoid disease. ‘The ligaments and appearance, said to be

peri-articular tissue were much thickened,
the synovial membrane was red and in- asec Sai
fected, softened, thickened and pulpy and char acteristic. In the bone

readily broke down on handling. ‘The S Ps ve
cartilage as a ener was softened, and on 1 places will be seen small

the surface there was a small erosion about

one-third of the whole of the articulating or large erosions, according
surface. There was no corresponding at
erosion on other cartilage. Underneath, to the severity of the case.
the bone was eroded, red and soft, even
extending beyond the margins of the ulcer. In the acute cases, the
Débris filled the floor of ulcer. : a

bone is red, rarefied, vas-
cular and soft, but later on becomes sclerosed, hard,
dense and almost of an ivory consistency, and now there

 
PATHOLOGICAL ANATOMY. 59

may also possibly be some lipping or growth of new carti-
lage and bone round the edges of the articulating surfaces.
Beneath the cartilage the bone presents, as a rule, a
normal appearance, showing that where protected it does
not undergo change. This, however, is not invariably the
case, aS we now and then see changes going on in
bone protected by cartilage. Such are the appearances:
en masse, so now let us study the
individual elements separately.
2. Changes in the synovial mem-
brane and surrounding parts.—
The synovial membrane, as we
have already mentioned, presents
at first a bright red appearance
from the injection of its vessels,
is soft and pliable, but in the
later stages it becomes duller,
granular and hypertrophied ; and,
as a whole, much _ thickened.
Lebert® mentions a. varicose
condition of the vessels of the aie aap sipaitaes on
synovial membrane, but probably cbumated bone; C, Grooves on
ulating surfaces (after B:
he refers to a congested con- 70th).
dition. In the later stages the villi become
prominent and hypertrophied; they may undergo fatty
or cartilaginous degeneration, so that the appear-
ance may be that of a number of pedunculated fatty
polypi, or else of a quantity of dendritic vegetations,
villi, or fingers, some fatty, and some cartilaginous.
The polypi arise from the budding and growth of the
normal villi. In the normal state we know that the
synovial membrane is edged by fringes and villi, and
that these have appendages; and it is from these
fringes that the polypi and other vegetations arise.
These fringes look highly vascular, and have a soft

 
60 RHEUMATOID ARTARITIS.

velvet-like feel Under the microscope we see that the
synovial cells have undergone proliferation, and that
large numbers of newly formed blood-vessels exist, some
full of blood, but all with thickened walls. Scattered
throughout are numbers of small round cells. M.M.
Cornil and Ranvier’* state that the cartilage may
be formed in the synovial fringes as follows: ‘‘ The
normal fat cells in the fringes or villi undergo degener-
ation, and are replaced by embryonic cells, and whilst
those in the centre form cartilage, those at the periphery
form fibrous tissue.’’ According to Kélliker,” in. the
normal state, cartilage cells exist in the synovial fringes,
and it is more reasonable to suppose that the cartilage
is developed from these, than in the method suggested
by M.M. Cornil and Ranvier. Rindfleisch torrobor-
ates the evidence with regard to the presence of:
pedunculated polypi, vegetations, villi, and fringes. As
a rule these only become prominent in the chronic
stages, and this specjally refers to the cases where
cartilaginous degeneration has occurred. The pedicles
which fasten those nodules of cartilage to the synovial
membrane, are apt to become stretched, and may in
the end break off, giving rise.to loose bodies which lie
free in the cavity of the joint. In very chronic cases,
these cartilaginous bodies may still further undergo
change, and become ossified. It has also been stated that
loose cartilaginous bodies are found in various burse.

The loose bodies found in rheumatoid arthritis may
be classified into: (a,) Melon-seed-like bodies, and
masses of coagulated fibrin, derived from the synovial
surfaces; (b,) Loose bodies derived from the synovial
membrane, consisting of fully formed tissues, such as
cartilage and bone ; and (c,) Loose bodies derived from the
articular end of the bones, being detached ecchondroses |
and osteophytes.
PATHOLOGICAL ANATOMY. 61

(a,) Melon-seed-like bodies.—Rokitansky % refers to
bodies of this kind, and mentions cases in which he has
seen fibrous or fibroid small bodies, varying in size and
shape, projecting from the surface of the synovial
membrane, and which he says can quite conceivably
become detached. Again, it is stated that fibrinous
exudation gives rise to both melon-seed bodies, and
to fibrinous masses. A case of the latter is mentioned
by Dr. Logan Turner. On microscopical examination
the fibrinous mass was found to'consist of fibrin with a
large number of cells, resembling jensonytes, entangled
in its meshes.

(b,) Loose bodies derived from the synovial membrane,
consisting of fully formed bone or cartilage.—Most of
the loose bodies found in rheumatoid joints undoubtedly
arise from abnormal development of the fringes, which
normally exist at the margins of the articular cartilages.
These increase in size and vascularity, giving rise to
sessile and pedunculated bodies, varying in number and
size. During this process the membrane itself undergoes
change, and the connective tissue cells develop into
fibrous tissue, fibro-cartilage, cartilage, and bone. As
time goes on, the connecting pedicle of the peduncu-
lated bodies grows thinner, and finally the body may
drop off, in some cases after a slight sprain or wrench,
but in others during some natural movement of the
joint. These bodies, examined microscopically, present
the character of hyaline cartilage, with here and there
cells undergoing proliferation.

(c,) Loose bodies derived from the articular ends of
the bones, being detached ecehondroses and osteophytes.—
In rheumatoid joints formative changes are constantly
taking place at the periphery, giving rise to nodular
outgrowths of cartilage, and finally by deposition of
lime salts or ossification they become bony. These
62 RHEUMATOID ARTHRITIS.

nodules may become detached possibly by injury, and
thus lead to such a body existing loose in the joint.
In one ‘such case the body was found to consist of
hyaline cartilage irregularly arranged. In some places it
was proliferating, and in others ossification had begun.

The ligaments which form part of the affected joints
become swollen and inflamed, and finally undergo
absorption, or are so replaced by newly formed connective
tissue, that it is impossible to trace them on the most
careful dissection. Owing to the cellular tissue under-
going great development, and from the formation of
new connective tissue, adhesions are formed with the
surrounding parts which lead to stiffness and difficulty
in moving the joint, and finally even to fibrous
ankylosis.

Under the microscope the synovial membrane is seen
to be infiltrated with newly formed connective tissue cells,
the blood-vessels are dilated, and their walls thickened,
and here and there are small collections of leucocytes
surrounding them. On proper staining, micro-organisms

are discovered scattered
' throughout the mem-
brane, but moreespecially
wherever there are any
collections of round cells.

Similar changes are
nena Si ceienmats sete oteanaetse noted in the soft peri:
mee articular connective tis-
sue. In the ligamentous structures, during the acute
stages, the intercellular spaces seem to be increased in
size and number, and a few round cells present them-
selves ; whereas, in the chronic stage, they are replaced
and converted into a mass of dense connective tissue, in
which little or no structure can be traced.

Ii has. often been stated that in rheumatoid arthritis

 

 

 

 
PATHOLOGICAL ANATOMY. 63

there is no effusion. This, however, is quite incorrect,
as again and again have I definitely proved its presence
by tapping a joint. It certainly is present in the most
acute cases, and often in considerable quantities. It is
most often noticed in the knees, wrists, and phalangeal
joints. In these latter joints it often forms small, tense,
. synovial protrusions, which give the impression of small
elastic bags full of fluid. Brodie, Adams, Fuller, Garrod,
Trousseau and others, have recognised the presence of
fluid, whilst Besnier,’® Senator, and Homolle,” deny it.
On examining the fluid, Hoppe Seyler ® found that it
contained the following ingredients :—

 

Mucin 18°19 per thousand.
Albuminous Substances 20°92 55
Etherial Extracts - ‘93 sf
Alcoholic ‘i 1:30 43
Watery 5 65 48
Acetic i. 1:53
Inorganic Substances - 8°79 5
Es
Total Solids 62°31 “a
Water 947-69 a

The etherial extracts were cholesterin, lecithin, and,
traces of fat. I have found the fluid to be a straw
coloured viscid fluid, with a dash of reddish colouration
(trace of blood), and moderately alkaline.

Under the microscope (on cold stage) large numbers.
of multinuclear granular corpuscles are seen, very
little, if any, larger than red-blood discs. Most of the
round cells are quiescent, but a considerable number
of irregular ones show active amceboid movements.
There are a few rouleaux of red corpuscles, and a
few scattered individual red discs. Also indistinctly
seen are numerous small round bodies, some highly
refractile, and with them a few bodies (very faint),
apparently micro-organisms. On staining these latter,
they prove to be bacteria in large numbers.
64 RHEUMATOID ARTHRITIS:

Normal synovial fluid is found to contain in addition
to fat molecules, a few ameeboid corpuscles, as well as
cells similar to those which occur on the projections of
the membrane.” We thus see that, beyond the micro-
organisms, this fluid differs also in the number of cells
present, both amceboid and granular. The presence of
blood is probably accidental. Dr. Goodhart, as men-
tioned by Dr. Fagge, on one occasion found blood
effused into a rheumatoid joint.

It is very rare to have suppuration, and, in fact, I
know of no case in which it has occurred. Dr. Mansel
Moullin,” however, reports three such cases. He believes
that the bacteria which caused it reached the joint by
the blood. The disease in all cases began in the soft
parts, and spread from thence to the bones, cartilages, and.
ligaments. Dr. J. R. Lunn also reports one such case.**

3. Changes in the eartilages—Many believe that
the first changes begin in the cartilages, but I am not
inclined to agree with them. I think, however, that the
cartilage must be involved at a very early stage. Post-
mortem, we usually find that the whole surface of the
cartilage has suffered, but, if seen early, it is also not
uncommon to find the disease limited to one or more
small patches. Rindfleisch says the cartilage undergoes
a perfectly homologous proliferation, beginning in the
outermost or superficial layers, and gradually extending
to the deeper; that the cells divide, and group them-
selves into rows of eight to twenty, and go on growing
until the matrix has disappeared, and a tissue made up
of cells or large vesicles results. Billroth says the
intercellulayysubstance does not soften as in inflamma-
tion but that it breaks up into filaments. He says the
changes commence in the cartilage, and spread from
thence to the synovial membrane, and then to the bone
and periosteum.
PATHOLOGICAL ANATOMY. 65

To the naked eye the first change is a loss of natural
polish, and it comes to present an appearance which has
been likened to velvet, and is softer than in the
normal condition. As the disease spreads and becomes
more developed, the central parts of the affected
areas break down, and erosions occur which, gradually
extending and deepening, cause the whole of the cartilage
to be absorbed, and the heads of the bones exposed.
As the erosion goes on a new formation of cartilage may
take place round the edge, giving rise to the lipping or
heaping up so often seen in the advanced cases. A sort
of pseudo-lipping may be observed when the central
portions are erosed down to the bone, whilst the
marginal portions are nearly, if not quite, unaffected.
Close investigation is necessary to distinguish between
these conditions. When true lipping does occur, it does
not do so in very regular sequence, but rather does so
in nodules, and it is from this circumstance that the
name ‘‘Rhumatisme Noueux,”’ by which it was long .
known, wasderived. Under the microscope, we find that
the process of disease consists in a proliferation of the
cartilage cells, beginning in the outermost or superficial
layers, gradually extending to the deeper. This
process was first described by M.M. Cornil and Ranvier.
They show how the cells undergo multiplication, and
form groups of from eight to twenty cells surrounded
by capsules, and that in some cases large mother cells
develop, and within these other and smaller daughter
cells. Of these latter some may have their own capsules
whilst others would appear to be without them.

Cornil and Ranvier show how it can be ‘demonstrated,
by staining with iodine, that these cells are not true
cartilage cells, as their capsules only stain very faintly, if
atall. According to them the superficial layer of capsules
swells, and, becoming globular, burst, and discharge

5
66 RHEUMATOID ARTARITIS.

their contents into the joint cavity. The capsules in
the next and succeeding rows, being only able to grow
perpendicularly, open into the more superficial rows,
forming parallel tubules, and, as time goes on, these
burst in turn into the joint, leaving the tubules empty
(Rindfleisch and Weber”), whilst the ground substance
or matrix lying between them becomes separated into
filaments, giving rise to its fibrillated and velvety
appearance. According to Rindfleisch, mucous degener-.
ation of the fibrils occurs, causing them to disappear
the more easily, and thus also explaining the presence
of mucin in the joint fluid. Ihave never been able to
verify this description.

In sections I have seen proliferation of the cartilage
cells, -but never any arrangement into tubules as
described by Cornil and Ranvier. Did it occur, one
would expect to find cartilage cells in the joint
fluids. I have never done so with certainty, and I
have examined many cases in the hope of finding them.
Of course, the cells may have undergone so much degen-
eration, and alteration, that they would be unrecogniz-
able. What I have seen under the microscope is, round
an erosion, a large number of round cells which penetrate
for some distance into the substance of the cartilage.

 

Fic. 4.—Sections through diseased cartilage; A, proliferating cartilage cells;
B, round celled tissue; C, periarticular loose connective tissue.

In this area the cartilage cells are seen to be proliferat-
ing freely, and the matrix to be disappearing, being
PATHOLOGICAL ANATOMY. 67

eaten away, partly by the round cells, and partly
replaced by the newly formed cartilage cells. Deeper
down the proliferation still continues, but in a less
marked way. With regard to the fibrillation of
the matrix, the use of reagents rather interferes
with one’s results, so on that point I can make no
definite statement, but I can emphatically state that
I have never seen anything at all approaching the
drawings which illustrate most of our text-books. The
process is one resembling, I take it, all other erosions,
and inflammatory conditions of cartilage. A few
micro-organisms J have always found in the superficial
layers, mixed up with the round celled tissue, also in the
layer of proliferating cartilage.

. The cells, at the edges of the cartilage, proliferate in
a similar manner. Cornil and Ranvier ascribe the mar-
ginal overgrowth to the fact that the cartilages, at their
margins, are overlapped by a layer of synovial membrane
which prevents the escape of the cellular contents into
the cavity of the joint. The cartilaginous overgrowth
may become converted into osseous tissue, the change
beginning as shown by Volkmann in the layer nearest
the original bone. As a rule, even when seen in the late
stages of the disease, these osteophytes have still a
covering of cartilage. The lipping which is seen in gout
differs from that just described. According to Dr. Wynne
the outgrowths in the latter disease are a sprouting of
the cancellous tissue of the epiphysis, carrying with it
the cartilage, which, however, only covers it as far as
its summit—the rest being covered by fibrous tissue
continuous with that of the periosteum, and synovial
membrane. In ossifying arthritis the lipping differs
from that of rheumatoid, in that the outgrowths arise
independently of the articular surfaces, and are not
covered by the articular cartilages.”
68 RHEUMATOID ARTHRITIS.

4, Changes in the bones,—As the cartilage erodes,
and leaves bare the bone underneath, we have certain
changes occurring. In the acute stages, when the
‘disease involves the bone, it presents a red and vas-
cular appearance. It is soft, and readily breaks down:
as the bony constituents are absorbed. These are
replaced by a red, semi-fluid material differing greatly —
from the normal marrow; and is, under the micro-'
scope, found to consist largely of giant cells, with
many nuclei (osteoclasts), in a mass of round cells.
As the disease becomes chronic we find the bone.
presents a hard, white, polished, ivory-like surface,
to which the term “eburnation” has been applied.
This hard dense layer is thin, and erosions through
it, showing the cancellous tissue beneath, presenting |
features as above, are not uncommon.

On the surface of the exposed bone, as it hardens, we
see grooves and strie, which are found to correspond
with the eminences, and protuberances,
on the opposing articulating surface (see
) Fig. 2). As the result of the processes
of destruction and new growth, the bones.
often present amushroom-like appearance.

Volkmann ™ described such a condition,

saying that they looked as if they had
been moulded whilst in a softened con-
dition.
} True bony ankylosis rarely occurs,
pee §.-Motacrpl except in the spinal column (Bowlby).
phytes(afterBilroth). Adams noticed occasionally hypertrophy
of the shafts, whilst Broca™ described this as being
chiefly confined to the epiphysis.

Various theories have been advanced to explain the
eburnation. It is, probably, one of Nature’s safeguards
to prevent further inroads of the disease. Zeigler *

 
PATHOLOGICAL ANATOMY. 69

states that, whilst the superficial layers of the cartilage
are proliferating, and becoming fibrillated, a softening
process is going on, in the deeper layers, which leads to
the formation of cavities; and these becoming filled,
later on, with the vascular medullary substance which
grows into them from the bone, give rise to ossification.
Cornil and Ranvier believe the eburnation to be due to
the discharge into the adjacent medullary spaces of the
contents of the most deeply seated cartilage capsules,
which, as they enlarge, cause the bone to be absorbed ;
and these cells from the capsules, by a process of osteo-
sclerosis, give rise to the hardened surface. In some
cases they attribute it to the extension of inflammatory
processee to the most superficial layers of. the bone.
Some think local osteitis is the principal cause, and
others that it is due entirely to mechanical means, i.e.,
the rubbing of the bones one upon another. The bony
structure of the epiphysis may also be altered.

Volkmann, whose theory is probably correct, has —
pointed out that the changes are caused, to his mind, by
a rarefying osteitis followed by an osteosclerosis. That
the wasting of the bone is not purely mechanical is
proved by the fact that the change sometimes goes on in
parts protected by cartilage.

On examining sections of bone, and also of the medul-
lary tissue, it is evident that the nature of the process is a
rarefying osteitis ;"but a process of sclerosis or hardening
will be seen as the case passes from an acute to a chronic
condition.

I have failed to find micro-organisms in the soft
medullary tissue, but I have no doubt they exist. I find
Gwilt 2° mentions that, in this disease, he noticed the
medullary tissue was a great deal more vascular with
proliferation of the corpuscles than in the normal. This
has also been noticed by Husse”” and Kussmaul.* If we
70 RHEUMATOID ARTHRITIS

compare the medullary substance with that found in
morbus coxe senilis, we see that, in the latter disease,
which is due almost entirely to a process of absorption,
the bony interstices are filled with a yellow fatty sub-
stance, quite different from the red vascular substance
of rheumatoid disease.

To recapitulate, I would say, we have an acute’
inflammatory disease set
up by micro-organisms
starting in the synovial
membrane, spreading
thence to the cartilage,
bones, and ligaments,
causing in the cartilage
and hones at first an ulcerative or eroding process,
followed, as the disease becomes less acute, by harden-
ing and thickening. This is following most other types
of disease, and ‘explains all the post-mortem appearances
as well as all the clinical symptoms.

Before leaving this division of the subject, let us con-
sider some other points of interest.

5. Changes in the muscles.—The principal change is a
well marked atrophy of the muscle substance which
affects the whole of the muscle, and not only a part of it.
There-is no diminution in the number of the fibres, but
each fibre is found to be decreased in size. As a whole
the muscle presents, what Debove ” calls, the colour of
dead leaves. In a few cases degeneration of the muscles
has been found, showing itself by Jongitudinal striation
with proliferation of the sheath nuclei, and increase of
the interstitial tissue (Vallat).®” This change, probably,
only occurs in those cases in which inflammatory
changes have spread from the joint to the muscles,
nerves, or central nerve system.

6. Changes in the central nerve system.—The only

 

Fic. 6.—Osteoclast eating bone.
PATHOLOGICAL ANATOMY. 71

‘changes hitherto noticed havé been an atrophy of the
motor cells in the anterior cornua in a few isolated cases,
described by Folli.®! I have only been successful in
obtaining specimens from a degenerated nervous system
in one case. In this one, on examining the spinal cord,
degeneration was found with
vacuolation % *"* 53 of the
ganglion cells of the anterior
cornua. The vacuolation of
nerve cells consists in the
appearance, within thenerve
cell, of oval or perfectly
spheroidal bodies of high
refractile power quite un-
affected by any staining
reagent, colourless, but
lustrous. In many cases
this quality is wanting, and
it is then evident that the
spheroidal outline is of a
genuine cavity or vacuole
from which the former con-
tents have escaped by rup-
ture. The removal of the
contents of such vacuoles
may be effected during life
by absorption by the lymph
connective system. The fie. 7.—-Mvxrirocar Ganetion Crris
: FRoM ANTERIOR CorNnua.
protoplasm surrounding the (1 , Cell ewollen with bright trans-
vacuoles is, more or less, in x 350), Aye assented
a state of granular degen- cell; B, Granular degeneration.
e . 8and 4 show vacuolation, seen
eration. The degeneration, ,, m»| also in
and the feeble staining, Penola Gaeceeal
indicate a fatty change in the cell protoplasm. The
significance of this is understood when we realize that

 
72 RHEUMATOID ARTHRITIS.

fatty degeneration and vacuolation indicate a state of
defective oxygenation, probably arising from some
change in the blood corpuscles. We see examples of
this in chronic pulmonary affections, alcoholic states,
and from the effect of certain poisons (arsenic, phos-
phorus, etc.), or any of the many circumstances which
restrict the supply of oxygen to the tissues. Those
elements naturally suffer earliest, and most, whose nutri-
tion is carried on at the greatest disadvantage. The
exact importance of this occurrence cannot at present
be accurately estimated.

Massolongo * refers to changes in the anterior cornua
observed by Klippel, but does not particularise them.

7. Changes in the nerves.—In a certain number of
cases peripheral neuritis has been noticed, but in so few
as to negative any idea that
this is the cause of the disease.
It is almost certain that when .
it does occur it is caused by
an extension of the inflam-
mation of the joint. Pitrés
and Vailliard*> report some
cases where they found such
a condition of the nerves, but
they express the opinion that
these changes cannot be the
cause of the joint lesions. In
other cases again we find that
the spinal cord and nerve roots
there “way neuritis; A, thuckene acon have been affected by a spinal
bundles, greatly diminished in size; 6, @¢thritis, probably by com-
blood-vessels with thickened walls. pression and narrowing of
the foramina. In these cases we may have a descending -
neuritis. I have been fortunate enough to obtain sections
from the nerves, in a case of rheumatoid disease which

 

 

 

 
PATHOLOGICAL ANATOMY. 73

had undoubtedly given rise to a secondary neuritis.
__ There could be no doubt that it was secondary in nature.
" Under the microscope there was an infiltration of small
round cells in the nerve sheath, around the vessels, and
amongst the nerve fibres themselves, especially in the
neighbourhood of the sheath. Thickening of the endo-
neural septa, and of the interfibrillary substance, was
also seen; and there was a thickening of the intima of the
blood-vessels, which encroached upon the lumen of the
vessel.

8. Changes in the heart.—Lesions of the endocardium -
and pericardium are comparatively rare, but not
so rare as is thought. MM. Charcot and Cornil
mention numerous cases in which changes were present,
and with no rheumatic history, and in which the lesions
developed after rheumatoid joint troubles. Any valve
may be affected, but my experience has been that the
disease is almost entirely confined to the mitral valves.
I have had few opportunities of examining such cases post-
mortem, but other writers state that the affected areas
present a hardening, and thickening, with vascularity,
and small vegetations arise from their surfaces. Peri-
carditis has been seen in several instances. __

9. Changes in the kidneys.—-Charcot and Trousseau
lay special stress on the occurrence of chronic albuminous
nephritis, but I think it is a much rarer complication
than they would lead one to suppose, at least in this
country.

10. Changes in the blood.—In almost 95 per cent. do
we find anemia exists in a greater or lesser degree. The
blood, under these circumstances, presents the following
characters. There is a slight, but well marked diminu-
tion in the number of red blood corpuscles, a marked
diminution in the hemoglobin, and a slight increase in
the number of the white corpuscles. The percentage of
74 RHEUMATOID ARTHRITIS.

the diminution of the red corpuscles. ranges from'85 to
56 per cent.; whereas that of the hemoglobin does se
from 80 to 45 per cent. It is thus-evident that the
hemoglobin value of each corpuscle is lessened. The
percentage increase of the white corpuscles is small.
The blood shows red corpuscles of varying size and vary-
ing shapes, but does not present any microcytes nor yet.
any nucleated corpuscles. The hemoglobin appears to
be less in quantity in each cell, as well as in a less stable
union with the cell stroma. It crystallizes out. more
readily and is more easily acted upon by such substances
as common salt, acetic acid and sulphate. of soda in
solution. There is a difficulty sometimes in distinguishing
between a swollen red cell with its hemoglobin dissolved
out and a white cell. This might account for the
variability in the estimation of the number of the latter. .

11. Changes in the glands.—As one would expect, we
find in the glands of the arm and leg, some enlargement,
but there is none of the spleen. This enlargement is
such as is found in other bacterial diseases, and consists
of a chronic hyperplasia. Chauffard and Ramond*
report 7 cases in which they found enlargement of the
lymphatic glands. On section these were found to be
normal in appearance, except for an overgrowth of the
connective tissue causing compression of the lymphoid
tissue. Still,*” describing a form of rheumatoid arthritis’
in children, mentions that both the lymphatics and spleen
were affected. In adults I have not come across enlarge-
ment of the spleen, although I have seen it in children.
In these cases, however, there were. other causes which
might have accounted for it, and at. present I -do not
think much stress can be laid on this point.

12. Fibrous nodules, although more common in. acute
or chronic rheumatism, are not unknown. They consist
of round celled tissue which, probably, originates in an
PATHOLOGICAL ANATOMY. 75:

endarteritis. Dr. Pitt 9° describes such a condition, and
mentions that this endarteritis may account for the cold
extremities so often seen in this disease. Nepven*
describes a nodule formed round a vessel with small
disintegrating clots, whilst Cavafy “ mentions that the
nodules are probably vascular in origin.

A subject now crops up of much interest, namely, the:
relationship between chronic rheumatoid arthritis, and
what are known as ‘Heberden’s nodes. These are small
enlargements or osteophytic outgrowths from the normal.
nodules, round the articular surfaces of the bones of the:
hand. They were first described by Heberden‘*! who.
gave it as his opinion that they had nothing whatever to:
do with gout. This has been, and still is, a much vexed.
question, and as these nodes may occur in the more:
chronic forms of polyarticular rheumatoid arthritis we
have to ask ourselves what their relationship to this.
disease may be.

They occur, as I have said, as small rounded nodular
growths, usually arising from the third phalanges, but.
sometimes from the second. They are practically pain-
less, and have no tendency to ulcerate, and though they
somewhat interfere with the movements of the fingers,
yet they are more disfiguring than painful. The nodes.
may be the only symptom of disease present, but they
are more usually associated with a generalised disease,.
and they may precede or follow such a disease. On exam-.
ination they are found to consist of an outgrowth from.
the bony tissue, and are covered by a hernial process or
projection of the synovial membrane, forming a pouch or-
bag, which, as a rule, contains fluid, and acts much as.
a bursa. On microscopical examination, they are found
to be formed of true bone. It is found that these nodes,
usually, as Heberden says, present themselves in elderly
people of the female sex, above 60 years of age; but L
76 RHEUMATOID ARTHRITIS.

have seen them well developed in patients of 40. At

first, we find that the third joint of a finger is enlarged,
and as a whole, and not only on one aspect. On the
dorsum the furrows which mark the normal joint are
seen to have disappeared, and are replaced by an
elevation—the whole joint forming a distinct thickening.
This can be detected on the palmar aspect as well. The
enlargement of the bones is not confined always to one
phalanx, but both of the opposing phalanges may be
_ affected. This enlargement goes on until we have a small

tumour, obviously growing from the bone, about the size-

of a pea, over which glides, possibly, a bursa or synovial
pouch. The development of these nodes is accompanied
by peculiar sensations in the fingers, such as numbness,
and they are often accompanied by pain on pressure, or
on movement. They may, however, be quite painless,
and even if not so, the pain is never severe. When
they become quiescent the pain goes completely. If the
disease is not arrested, the movements of the joints
become much interfered with, and ankylosis may finally
result. When nodes are present in rheumatoid arthritis
we find that deformities seem to develop specially early,
and to be more persistent. The usual deformity is de-
flection of the terminal phalanges towards the radial
side, and this is rendered more conspicuous by the
deflection of the finger, as a whole, to the ulnar side.
Are these growths then the ordinary osteophytic out-
growths, so common in rheumatoid arthritis, or are they
something different? Some assert that they are true
gouty formations, and others that they have nothing
whatever to do with gout, but are by nature a form of
rheumatoid arthritis. Heberden, as I have said, main-
tained that they were not gouty, as he had seen them in
people who had never been affected with gout. Begbie *?
differed from him entirely, and said they were intimately

ke te ee
PATHOLOGICAL ANATOMY. 77

connected with gout. He stated that he had watched
their development from the first, being sometimes the
result of an inflammatory affection, more or less acute,
and attended with the constitutional disturbance which
marks the fit of gout ; but more commonly they were the
consequence of a slow and chronic gouty disorder. He
also said he had never seen them except in those suffering
from gout or from the gouty diathesis. Charcot, on the
other hand, agreed with Heberden, and denied that they
had any connection whatever with gout. He stated that
it was a form of rheumatoid arthritis, and that the ana-
tomical changes were those of this disease. Sir. A. B.
Garrod“ stated that he had seldom seen them in patients
suffering from true gout, and agreed with Heberden’s view
with regard to them. Dr. A. E. Garrod was of the same
opinion, but said he had seen them in cases with clear
histories of gout, and no other arthritic affection. Duck-
worth“ believed that they were of a true gouty nature, and
said that the changes found by Charcot were frequently
of an undoubted gouty nature. In gout he had seen true
ankylosis result from the deposit of urates, and exostoses
may also be caused thereby. Lecorché * also took this
view. Pfeiffer maintained that they were a symptom of
true gout, as he had seen them arise in cases of gout, and
in cases where uratic deposits existed, but he admitted that.
he had also found them in people in whom there was no
gout. Personally, I have seen these nodes most frequently
in chronic rheumatoid arthritis, never in the acute forms;.
but I have also seen them in true gout. Is it not possible
that they may be common to both diseases? They are
unquestionably the result of some irritation giving rise
to an increased, and morbid growth in the normal
nodules ; so why should not this irritation have its origin
as much in the poison of one disease as in the other? I
have seen a considerable number of such cases, and 1
78 RHEUMATOID ARTHRITIS.

have in no instance found any deposit of gouty material
in the.nodules. They have always been of pure bony
‘substance, but this, of course, does not invalidate the
argument that the gouty poison may have originally
‘started the morbid process.

The accompanying skiagraph (Plate I) was taken
by J. W. Gifford, Esq., of Chard, the patient being
-an inmate of the Bath Royal Mineral Waters Hos-
pital, and through whose kindness I am permitted to
publish it.

The patient, a lad of 20, was the subject of acute rheu-
matoid arthritis—the synovial swellings being marked.
A small sesamoid bone can be distinguished on the
inner side of the first metacarpo-phalangeal joint.
What is of special interest, however, is the fact,
‘that in the acute stages no bony outgrowth occurs.
Indeed, as this skiagraph shows, there is, if anything,
a diminution in the size of the bone, as may be seen in
the heads of the metacarpals-—which have a rounded off
appearance not often seen in a normal bone. This is
specially noticeable in the second metacarpal at its ulnar
side, the disease in this joint being specially acute.
‘The thickened condition of the soft tissues in the neigh-
bourhood of all the phalangeal joints should also be noted.
‘The deformity of the little finger was due to contraction
-of the flexor tendons, with atony of the extensors.

Since the introduction of the X rays much has been
done to show that there is no bony enlargement in the
acute forms of the disease, but, as Barjon *® shows, in the
‘chronic. stages bony excrescences are the rule. Oudin,
Barthélemy, Béclére,® Baumler 4 and others have all
‘studied the disease from this standpoint, and their results
are as various as the conditions examined. Most of the
-evidence goes to show, however, that in the acute stages
no bony enlargement exists, and also that there is a
PLATE I,

 

 

 

SWiyaype

  

Skiagraph of the Bones of the hand in a case of Rheumatoid Arthritis,

 
BACTERIOLOGY. 79

difference’ between a skiagraph of a tabetic knee and one
of a rheumatoid knee.

BacrerioLoey.

For some time before the actual discovery of the micro-
organisms, Dr. Wohlmann and I, looking at the clinical

nature of the disease, and at the course of the symptoms,
' suspected that the disease was microbic in character.
The absence of post-mortem material hindered us in
obtaining any definite proof until we decided to obtain
what specimens we could from the living subject. In
this way we were led to aspirate affected joints, and
examine the fluids so obtained microscopically and by
cultivation. NowI wish it to be clearly understood in
what class of case this micro-organism hag been found.
It has been found in only the acute polyarticular cases
with soft synovial enlargements of the joints accom-
panied by muscular atrophy, by cold sweating palms, by
pigmentary changes, by marked cachexia, by a rise in
temperature, and possibly by some enlargement of the
glands. I have not found it in the chronic cases with
outgrowth of bone and lipping, and in fact the question
arises whether we are dealing with one or two diseases.
I am rather inclined to think that the name rheumatoid
arthritis includes two quite distinct disorders, but for the
moment I will leave this question in abeyance, as long
as it is clearly understood that it was from the acute
and from the acute cases only that we obtained the
micro-organisms. From the joints then of acute cases
we obtained some synovia, on staining which we were
readily successful in determining a micro-organism
was present, but at the same time were troubled with
the difficulty in staining it properly, and getting the
cover-glass free from precipitate. However, we, to a
certain extent, overcame these difficulties, and got
1

80 RHEUMATOID ARTHRITIS.

. fairly good results with carbo-fuchsin and methyl-
blue, sufficiently so to satisfy ourselves that it was a
micro-organism, and always the same micro-organism, we
were dealing with. Our first culture attempts utterly
failed, but by degrees we got fair results. Our apparatus
and media being deficient, led in most instances to the
growths dying out in the course of from three to four
weeks’ time. However, in the long run we succeeded in
obtaining growths on blood-serum, agar-agar, and in beef
bouillon. The bacillus—for to us it appeared to be a
dumb-bell shaped bacillus—was found to be about 2u
long, the ends staining deeply, the connecting portion
not at all. In fact in many cases it resembled a diplo-
coccus. It appears to grow more freely when it has a
plentiful supply of air, possibly pointing to a greater
need of oxygen. It has also been found in pieces of
synovial membrane obtained during aspiration and in the
cartilages, synovial membrane, and periarticular tissues
in the few sections we have been fortunate enough to
obtain. On Dr. Blaxall’s suggestion the blood in some
of the acute cases has been examined, and in several
the micro-organism has been found, but never so
characteristically as to warrant one in diagnosing the.
disease from that alone.

The following is a synopsis of our present knowledge

of the appearance, method of staining, mode'of growth,
etc., of the micro-organism :—

(1,) The micro-organism is very minute, appearing at
first sight to be a diplococcus. The two ends of the
bacillus stain deeply, but there is an intervening portion
which never stains. Dr. Blaxall, after careful observa-
tion, came to the conclusion that it was a bacillus from
the fact that the intervening portion is as broad as the
diameter of the stained extremities, and that it has
parallel contours. The average length is 24 and the
BACTERIOLOGY. 81

average breadth ‘64, varying considerably according to
the intensity of the staining. Under the microscope it
always appears smaller than the measurements would
lead one to suppose.

(2,) The micro-organism has been found in the
synovial fluid, synovial membrane, cartilage and bony
debris in erosions as well as occasionally in the blood.

(3,) It may be stained with gentian violet, methyl
violet or carbolic fuchsin. It is found, however, that
these stains, if allowed to evaporate at all, deposit on the
cover-glass in a manner which so closely resembles the
organism that it is by no means easy to recognise which
is which. The most useful stain is probably aniline-
methylene blue. After fixing in the usual way the
cover-plass is immersed in dilute acetic acid for about
two minutes, well washed and dried, and then placed
film side down on a watch-glassful of stain, and the whole
placed, for three to five days in a moist chamber in the
dark. It is then washed in gently running water, dried
and mounted. The prolonged staining deeply colours
the organism, whilst the moist chamber prevents the
evaporation of the dye and precipitation on the cover-
glass. A still better method, and one used by Dr.
Blaxall, is to mix a drop of the specimen to be examined
(which I here presume is fluid) with a few drops of stain
on a cover-glass, and rub out with a platinum needle.
The cover-glass, with stain and synovia, is then dried
slowly and passed through the flame of a burner, after-
wards being freely washed, dried and mounted. It
may also be detected in a hanging drop specimen. The
organism very readily gives up its stain when treated
with acids and other decolourising agents; by Gram’s
method it is completely decolourised.

(4,) On cultivation it grows best in litre or half-litre
flasks of peptone beef broth which have been filtered

6
82 RHEUMA TOID ARTHRITIS.

repeatedly until they are perfectly bright and clear. The
flasks having been sterilized and proved to be so are
inoculated with a drop or two of synovial fluid, and are
then incubated at blood heat. During the first three
days no growth appears, but on the fourth small minute :
particles may be seen floating in the clear fluid, giving
rise to an appearance resembling ‘‘gold dust.’”’ At times
the growth appears to stop at this stage, but in others it
may become slightly flocculent. It never becomes turbid. .
A culture displays the organism, on microscopic examina-
tion, in considerable numbers either as discrete indi-
viduals or as zooglea masses. They are non-mobile, but
have a marked oscillatory movement, as may be seen in
the hanging drop specimen. Dr. Blaxall was thus
enabled to watch their mode of subdivision.

It also grows on nutrient agar-agar, appearing in
about three days, if kept at blood heat, as a fine trans-
parent film, which under a lens resolves itself into
minute colonies, perfectly transparent. On Loffler’s
serum it grows as minute points difficult to observe
unless where the condensation water has washed off the
cholesterin. It grows in milk without causing curdling
or precipitation of the casein, but it does not grow in
nutrient gelatine either at a temperature of 22° C. or
37° C.

(5,) On inoculation, experiments have been unsatis-
factory. Dr. Blaxall inoculated mice, guinea-pigs and
rabbits but got no fatal results, but in rabbits he sus-
pected some joint trouble. The experiments were few -
in number, and as these animals do not suffer from

rheumatoid arthritis naturally one would hardly expect. —

an artificial disease to be set up. This negative result
only proves that this organism is not pathogenic to the
animals experimented on.

(6,) This micro-organism has not been found in any ©
BACTERIOLOGY. 83

other disease of the joints. I have examined many
cases of different diseases and have failed to find it, and
Dr. Blaxall examined synovia from chronic synovitis,
gonorrheeal and tubercular affections, and also failed to
find it.

Now with reference to the discoveries of others we have
first Schuller,” who in 1893 described a bacillus 2°6u
long by 75-995 broad which exhibited polar staining,
and which was easily stained by the ordinary methods,
especially carbolic fuchsin, but was very easily decolour-
ised. Growing readily on gelatine at 25° C., as small white
knobs, it soon liquefied it to such an extent that the whole
mass became opaque white. On agar-agar it grew
as ereyish-white flecks or films. It is obvious from its
manner of growth that this is an entirely different
organism to the one discovered by Dr. Wohlmann and
myself. Bouchard and Charrin™ described certain
cases of apparent rheumatoid disease, to the French
Association for Science in 1894, due to a staphylococcus,
and finally, in May, 1896, Chauffard and Ramond *
found in one case a small bacillus (diplo-bacille), short
and thin, and having much the appearance of a diplo-
coccus. It was very easily stained by all the ordinary
methods, but was not decolourised by Gram’s method.
All cultivation experiments failed except in synovial
fluid, where it grew freely. On inoculation into pigeons,
rabbits, mice and guinea-pigs, they all appeared to be
immune. Such is the bacteriology as it at present
stands, and until definite proof can be given that the
organism, found by Dr. Wohilmann and myself, can
reproduce the disease, its réle in the disease must remain
to a certain extent conjectural. Its presence is certain,

‘but its significance is another matter.*

 

* Dr. Blaxall’s report is embodied as an appendix.
oo
&

OR Co NEY

Bee Pe ~
PHO PSO Or

e
or

15a.

16.
17.
18.
19.

21.

22.
_ 28.
24.
25.
26.
27.

29.
30.
31.
32.
33.

34,
35.
36.
37.
38.
39.

40.

RHEUMATOID ARTHRITIS.

REFERENCES.

Colles—Quoted Garrod, “Rheumatism and Rheumatoid
Arthritis,” p. 274.

Todd.—‘ On Gout and Rheumatism,’ 1843.

Adams.—“ On Rheumatic Gout,” 1873.

Brodie.—“‘ Diseases of the Joints,” 1833.

Cruveilheir.—“ Anat. Pathologique, ” Leg. ix.

Fuller.—‘ Rheumatism, Rheumatic Gout and Sciatica, gi
1852.

Senator.— Ziemsson’s Handbuch.”’
Garrod.—“ Treatise on Rheumatism and Rheumatoid
Arthritis.”

Rindfleisch.—“ Pathological Histology.”’

Trousseau.—‘ Lect. on Clinical Medicine” (Syd. Soc. transl.).

Billroth.-—‘‘Gen. Surgical Pathology and Therapeutics,”
(transl.).

Chvostek.—‘ Wien. klin. Wochenschrift,” June 27, 1895.

Lebert.—‘‘ Handbuch der Pract. Med.,” 1859, ii.

Cornil and Ranvier.—‘‘ Manual of Pathological Histology,”
vol. i., 1892.

Kélliker.—“ Elements of Human Histology.”

Rokitansky.—“‘ Path. Anatomy,” Sydenham Society, vol.
iii., p. 289.

Besnier.— ‘‘ Dict. Encyclop. des Sciences Méd.,” 1876, p. 155.

Homolle.—“ Dict. de Méd. and Chir. Prat.,” 1882.

Hoppe Seyler.—“ Virchow’s Arch.,” 1872.

“‘ Quain’s Anatomy,” 9th edit., p. 219.

Moulin, M.—* Lancet,” 1891, vol. ii., p. 125.

Weber.—“ Journal of Nervous and Mental Dis.,” New York,
1884.

Griffiths.—“ Journal of Pathology,” June, 1897, p. 482.

Volkmann.—“ Handbuch der Chirurgie,” Band ii., p. 555.

Broca.—‘‘ Bull. de la Soc. Anatom.,’” xxv., 1850.

Zeigler.—‘ Virchow’s Archiv.,” 1877, lxx., p. 592.

Gwilt.—‘‘ Handbuch der Path. Anat.,” p. 1000.

Husse.—“ Zeitschrift fiir Rat. Med.,” vol. v., p. 192.

Kussmaul.—‘ Arch. fiir Physiolog. Heilkunde,” vol. xi., 1852.

Debove.—“ Prog. Méd.,” 1880, p. 1011. ‘

Vallat.—-‘‘ Arch. Générales de Méd.,” 1877.

Folli.— Il Policlinico,’ December, 1894.

Voit and Bauer.—“‘ Zeitschrift fiir Biologie,” vii.

Trzebinskii—‘‘ Arch. fiir Path. Anat. u. Physiolog. u. fiir
Klin. Med.,” Bd. cvii., Heft 1.

Massolongo. —“ Riforma Medica,” 1898, vol. ii., p. 159.

Pitrés and Vailliard.—* Revue de Méd.,” 1887, No. 6.

Chauffard and Ramond.—“ Rev. de Méd., ie May 10, 1896.

Still.—“ Med. Chir. Trans,” 1896.

Pitt.—“ Clin. Soc. Trans.,’’ vol. xxvii., 1894, p. 54.

Nepven.—*‘ Comptes rendus de Soc. de biologie,” Paris,
1890, vol. ii., p. 328

‘Cavafy.—* Path. Trans.,” 1883, p. 41.
41,
42,
43.
44,

45.

46.
47.
48,
49,
50.

51.
52.
53.

54.
55.

BACTERIOLOGY. 85

Heberden.—* Commentaries,” 1804.

Begbie.—Contrib. to “‘ Practical Medicine,” 1862, p. 28.

Charcot.-—‘‘Giuvres Complétes,” tome vii., 1889, p. 217.

a Sir A. B.—‘‘ Gout and Rheumatic Gout,” 1876, p.
503.

Garrod, Dr. A. E.—‘‘ Rheumatism and Rheumatoid
Arthritis,” 1890, p. 266.

Duckworth, Sir Dyce.—“ Treatise on Gout,’ 1889, p. 71.

Lecorché.-—‘‘ Traité de la Goutte,” 1884, p. 122.

Pfeiffer.—‘ Lancet,” vol. i., 1891, p. 819.

Barjon.—‘‘ La Radrographic Appliquée,” Paris, 1897.

Oudin, Barthélemy, et Béclére.— Soc. Méd. des Hépit.,”
280, 1897, and “‘ Sem. Méd.,” 1897, No. 268, s. 208.

Baumler.—‘‘ Congress fiir Innere Medicin,” Berlin, 1897.

Schiiller.—* Berlin Klin. Wochenschrift,” Sept. 4, 1893.

Bouchard and Charrin.—Assoc. Francais pour l’avan. des
Sciences, Caen, 1894.

Lunn.-—‘‘ Lancet,” vol. i., 1896, p. 294.

Turner.— Edin. Hosp. Reports,” vol. iii., p. 627.

 
86

CHAPTER IV.
VARIETIES AND DIAGNOSIS.

Errors in. Diagnosis-— Acute Rheumatoid Arthritis — Osteo-
Arthritis—Charcot’s Classification—Post-Rheumatic, Gonor-
rheal and Gouty forms—Acute and Sub-acute Rheumatoid
Arthritis — Infantile Arthritis —In Children —In Adults —
Differences — Symptoms — Appearances of Joints — Chronic
Rheumatoid Arthritis—Age—Appearances—Bony Changes—
Diagnosis between it and Nerve Diseases—Charcot’s Disease—
Rheumatism—Gout—Chronic Rheumatism, etc.

‘

1.—VARIETIES.

Propasty Rheumatoid Arthritis is responsible for more
errors in diagnosis than almost any, other form of
known disease. This not only arises from the difficulty
in recognising the disease from certain forms of rheu-
matism and gout, but also because under the name
rheumatoid arthritis several forms of disease have been,
and still are classified. A further differentiation is greatly
to be desired, not only on account of the treatment to
be pursued, but likewise for prognostic purposes. It has
been my lot to see annually a large number of cases _.
sent to Bath for treatment, and to which, in the greater
proportion of cases, the wrong name is given. Most
confusion arises apparently between what is, and what
is not chronic rheumatism, the larger proportion of
cases thus designated being cases of rheumatoid
disease; and, again, there often is confusion between
rheumatoid arthritis, and some forms of chronic gout.
With care one can usually differentiate between these
conditions, but it is not always easy to do so straight
off.
VARIETIES. 87

' Even having settled what is recognized at present as
rheumatoid arthritis a new difficulty arises, for it is not
only possible, but probable, that there are at least two
forms of disease included in this term. It is not quite
certain that the acute polyarticular disease is the sameas _
the chronic osteophytic and possibly monarticular one.
That the later and chronic stages of the acute form
closely resemble those chronic from the outset I do not
doubt, yet there is a something which makes me doubt
their identity. An acute case may pass into a chronic
stage having most of the characteristics of one chronic
from the first, but to my mind the term rheumatoid
arthritis should be limited entirely to the acute poly-
articular inflammatory disease, with marked wasting and
trophic nerve troubles, and with no bony or cartilaginous
outgrowths. When these occur the disease has invariably
become chronic. For this reason it is my intention to
divide the disease into two sections. In one: (a,)I will class
all the acute and sub-acute cases characterized by inflam-
matory changesin the joints, and by ulceration and erosion
of the cartilages and bones, by muscular atrophy, by nerve
and trophic phenomena, and by glandular enlargement,
etc.; and, in the other (0,) all the chronic cases character-
ized by a slowly progressive thickening and hardening of
all the joint structures, by the development of deformities,
by the formation of osteophytes, and by the lipping of
cartilage, ete. Owing to the bony changes and to the
general thickened character of the joints, it is to this
form of the disease, rather than to the acuter, that I
would more especially confine the term osteo-arthritis.
The disease may arise as a primary disease, or else
secondary to such diseases as rheumatism, gout, gonor-
rhea, ete. When it arises subsequent to rheumatism some
observers hold that the rheumatoidal attack is merely the
continuation of the rheumatic changes; but, of recent
88 RHEUMATOID ARTHRITIS.

years, other views have been advanced and accepted. We
have come to understand how any acute arthritic attack
lays the joint tissues open to a subsequent attack of the
same disease, and also to one of some other disease. But
. What is curious is, that a disease originally limited to one
joint should render the patient liable to a generalised
disease—yet such is the case. This rather points to some
blood condition, than to one entirely dependent on a local
joint state. McArdle? points this out, and I have often
proved the truth of his observation. If we believe, as
I do,, that both rheumatism and rheumatoid arthritis
are caused by infective organisms, or by their elaborated
poisons, we can more readily understand, and appre-
ciate, the significance of this rather remarkable fact.
Schiller 2? goes the length of stating that the rheumatic
poison renders the joints and constituticn more liable
to be affected by rheumatoid arthritis. In post-rheumatic
forms, we find an increased tendency to the occurrence
of visceral lesions. As a sequela of gout Hutchinson *
mentions cases as proof of his theory, as to the nature
and origin of the disease. ‘Garrod supports the view that
it is a common sequela, but Sir Dyce Duckworth disagrees
with it entirely. The latter holds that all deformities
and distortions, met with in uratic arthritis, are due
entirely to gout. With regard to their clinical features,
he says, they in many ways resemble those of.
rheumatoid arthritis. I have failed to find any positive
evidence of the onset of rheumatoid arthritis after an
attack of gout, but it undoubtedly is seen in those with
hereditary gouty tendencies, and who may have had
obscure arthritic attacks, which may, or may not, have
been .outy—more probably though they were slight but
unsuspected rheumatoid warnings. The occurrence of
rheumatoid changes, after a gonorrhcal arthritis, is
naturally much rarer than that following a rheumatic
VARIETIES. 89

attack. It, however, does occur, and has been mentioned
in the writings of Charcot, Lorain‘ (who gave it the
name Rhumatisme blenorrhagique 4 forme noueux), Sir
Alfred Garrod, Dr. A. E. Garrod, Prof. Stewart, and
others. ;

The disease having arisen either primarily or secondary
to some other trouble, is found to occur in the following
sub-divisions.

I. Acute Rheumatoid Arthritis, and

II. Chronic Rheumatoid or Osteo-Arthritis.

For a moment, let us glance at the other forms
of classification hitherto adopted—most of them being
based on that of Charcot. His was as follows :—

1. Rhumatisme Articulaire Chronique primitif général-
isé ou progressif (the Rhumatisme Noueux of others).—
This group included cases having a tendency to become
general, the small joints of the extremities, such as
those of the hand, and especially of the metacarpo-
phalangeal, being symmetrically affected, and also
characterized by the fact, that during the progress of the
disease, most of the other joints are successively attacked
in a definite order, and for the most part the mischief
is irreparable.

2. Rhumatisme Articulaire Chronique Primitif fixe ou
partial—In this group were placed those cases in which
the disease is localized to one or two of the larger
joints, producing deep-seated mischief. It is sometimes
called arthrite séehe or morbus coxe senilis.

3. Nodosities d’ Heberden. — This group contained
those cases usually classed amongst gouty affections, and
confined either to the extreme joints of the fingers, or
else to the next row, leaving, as a rule, the metacarpo-

_phalangeal joints free. | “

More recently, Dr. Garrod® has qualified this classi-

fication by adding a fourth group of cases which: occur
9° RHEUMATOID ARTHRITIS.

_ subsequently to attacks of acute rheumatism, gout, or
= gonorrheeal arthritis. These two classifications form
the basis of all subsequent ones, and for all practical
purposes are efficient, but on one pointI dissent from both
writers, and in fact from all English authors, and this is
with regard to Morbus Coxe Senilis. This form of

disease, I hold, is not true rheumatoidal, and, therefore, _

I have omitted it from my classification. In this view I

am supported by such an authority as Waldman,’ who
regards it as a purely senile change of the tissues of the
joints and bone.

1.—Acutz Ruevumatorip ARtTHRItis.

In this division come all cases, seen alike in the young

and in the grown up, occurring either as a primary ©

disease, or secondary to some other form of arthritis, or
to injury. In these forms it is always poly-articular.
Although occurring at any period of life, the acuteness of
the disorder varies largely with the age of the individual
attacked. In children it rarely is chronic, but tends to
assume a rapidly progressive character, only differing
‘from the acute form seen in adults by its more frequent
fatal termination. In young adults it also is usually
acute. In elderly people acuteness is rarely seen, but, in
this respect, it makes up by its intractableness. In
children, we must carefully distinguish it from those cases
of multiple nerve arthropathies—a few of which have

been recorded. These are so similar to what one would © *:

expect in rheumatoid disease, that I am almost tempted!

to believe that they are cases of this disorder, only
occurring in a somewhat unusual manner. Pasteur ®

mentions such a case, in which there was no enlarge---

ment of the ends of the bones, but there was arthritis,
accompanied by a hide-bound condition of the skin.
Barlow ° reports another such case, in which there were

SS
Lene
PLATE II,

 
VARIETIES. or

subcutaneous nodules. One must remember that
arthritis has been known to arise in scleroderma, and
scleroderma in rheumatoid arthritis. Jaccoud ” mentions
a class of cases somewhat similar, under the name of
Rhumatisme fibreux. Wagner ™ also has described
similar cases. From examinations, these joints show
little change in the cartilages, but fibrous bands develop
across the joints, and greatly restrict their movements,
as well as lead, by slow contraction, to great deformity.
There is always great doubt as to what we are dealing
' with in such cases, but one must always bear in mind
that arthritic changes are fairly common as the result
of spinal degenerative changes. Such being the case,
great care is not only necessary in the diagnosis, but in
the treatment. Dr. Still,” in Clifford Allbutt’s Medicine,
says there is in children a disease which presents
important differences both in its clinical symptoms and
morbid anatomy, as well as one which is clinically
analogous to the rheumatoid arthritis of adults. The
first type of disease is characterized by chronic pro-
gressive enlargement of the joints, with enlarged glands
and spleen. The onset is acute with pyrexia, and the
joint thickening affects the tissues round the joints, rather
than the bones or cartilages, and there is also muscular
wasting. Enlargement of the glands is a constant
symptom, and in 9 out of 12 cases the spleen was also
enlarged. Post-mortem, the synovial membrane was
thickened and vascular, and there was some pitting of
the cartilage, but there was no osteophytic change. The
pure rheumatoid arthritis in children he considers to be
characterized by bony thickening and lipping about the
joints, and by the presence of bony grating and the ab-
sence of enlargement of the glands and spleen. Now his
description of the first class corresponds to my description
of what we see in adults in the acute form of the disease,
92 RHEUMATOID ARTHRITIS.

and also his second with the chronic form. To me he
appears to be considering just the self same forms of the |
disease. Ido not believe that the first form he describes.
as peculiar to children differs in any respect from the
acute form in adults except in the splenic enlargement,
which may have been an accidental occurrence so
common in children; but of course the question still
remains, Are there two diseases both in adults and in
children? Dr. Still’s idea of what is pure rheumatoid
arthritis is the popular one, that there must be bony
enlargement. This, I would strongly urge on my readers,
is not the case, at least, not in the forms we most
frequently see it. in in Bath. The youngest child
I have seen affected was a boy, aged four, the next,
also a boy, aged seven (Plate IT), and the next a girl, aged
eight (Plate IIT). Undoubted cases have been recorded
by Sir Alfred Garrod,® Lecaze Dori,‘ Monocoro,” Dr.
A. E. Garrod, Lloyd Davies, etc. In his “ Diseases
of Children,” Dr. Money” mentions that rheumatoid
arthritis is seen in children, and that it may follow
on an acute attack of rheumatism: that it may affect
both the feet and hands, and resemble the multiple
joint affection of middle-aged women, rather than the
arthritis sicca of the old. The propensity, he says,
to deformities and ankylosis in awkward positions is
rather great. Henoch, in his book on ‘“ Diseases of Chil-
dren,” also mentions certain cases of apparent rheuma-
toid disease, but he, like many foreign observers, does

not. differentiate between it and chronic rheumatic .”

arthritis.

Turning to the consideration of the acute form as seen
in adults we find Fuller "8 was the first to point out its
characteristics and subsequently Garrod drew attention
to it, pointing out various things to be noted in the
differential diagnosis between it and acute rheumatism.
PLATE III,

 

This shows well the swellings in fingers, wrists, knees,

 
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yurof yo Suyjeas Adiug—_ */ “Aydorye payxareur YZ syutol yo yuewIeSa«vp~ue padeys atpuridg— pF “Ary

  

 
 

‘AL HLV'Td
VARIETIES. 93

Both he and Fuller draw attention to its obstinacy, to
the character of its articular swellings, and to the liability
of certain joints to be involved. Some deny that this
form exists, holding that it is only a modification of acute
rheumatism, but, although, if care ‘be not exercised
it lends itself to much confusion, yet, to one who has
studied the two diseases, no confusion is possible. In
rheumatoid arthritis the disease involves the bones,
cartilages, synovial membrane, and ligaments, and is
accompanied by well marked atrophy, trophic, vaso-
motor, and other nerve phenomena, which render it quite
distinctive and characteristic.

It is undoubtedly more important from the clinical
standpoint than the average chronic case, and what
makes these cases so specially interesting is the
age at which they occur, children and young adults
being for the most part affected. We find it usually com-
mences in one joint, probably one of the metacarpo-
phalangeal ones, but it does not remain long confined to
this one joint, but spreads like wild-fire to most of the
other joints of the body. It shows a -wonderful
symmetry not only in the joints affected, but, to a less.
extent in the degree. Symmetry is also seen in the
other phenomena present. The joints are swollen,
presenting a characteristic, ovoid or spindle-shaped
enlargement, painful and tender to the touch, and hot.
On palpation, they either feel resistant and elastic (Plate
IV, Fig. A), with distinct fluctuation, or else they feel
as if they had undergone maceration. The ligaments
and other joint structures being soft, and doughy, and
admitting of a finger tip being sunk between the
heads of the bones; and they at times feel as if they
would drop apart (Plate IV, Fig. B). The second con-
dition is the more advanced stage of a rapidly
pregressive disease—the cartilages, and other joint
94 RHEUMATOID ARTHRITIS.

structures, being destroyed by, the acute inflammatory
process which is at work. Later on the joints will
become harder again as cicatrisation and condensation
occur. This feeling, and that of tense resistance, are
quite. characteristic. Along with this the extremities.
feel cold, and look blue, being bathed in a cold clammy
perspiration, although the body temperature is raised
generally. Recent pigmentations, and other integu-
mentary abnormalities, develop on the face, body, and
forearms, etc., and enlargement of the glands is seen,
whilst all the time a progressive muscular atrophy
is occurring. The affected muscles are not merely
those in the immediate neighbourhood of the diseased
joints, or even distal to them, but may be situated on
the proximal side as well. A characteristic selection of
the muscles is observed, the atrophy is accompanied by
cramps, and fibrillary twitchings, with, sometimes,
increase of the reflexes, but, unless peripheral neuritis
has been set up, no reaction of degeneration. As the
case progresses the pain becomes greater, worse probably
at night, and on movement of the joint; the movement
also gradually becomes more and more limited. No sleep
may be obtainable, except by the use of powerful hyp-
notics, and the disease becomes more and more distressing
to watch and to treat. Cardiac abnormalities are fairly
common, whilst pleurisy, pneumonia, or pericarditis
may add their quota of distress to an already overtaxed
system.

II.—Curonic Rusumatorp AgtHritris on Osts0-ARTHRITIS.

In this form it may be only the later stages of an
acute attack, or it may arise per se, and be always
chronic ; or it may follow on some other form of arthri-
tis; or as the result of injury. It may affect many
joints, or it may be confined to only one or two. Asa
DIAGNOSIS. 95

primary disease it is most often seen in middle-aged
and elderly women. It is characterized by great
hardening and thickening of the joint tissues, both
soft and hard; by eburnation of bone; by erosion of '
the cartilages; by osteophytic deposits ; by cartilaginous
overgrowths and new deposits; by lipping, etc. There
is consequently much deformity, distortion, and stiffness.
This latter varies, as in one case it may be of the
slightest, whilst in another it may resist all treatment,
and end in ankylosis. Pain as a rule is not acute,
being more of a constant, gnawing, or wearying charac-
ter. One joint only may be affected, and in which it
may remain, or it may advance steadily from joint to
joint, causing great crippling, not only from deformity,
but from fixing and ankylosis. One marked feature is
the absence of fever, of almost all heat in the joints,
and by the absence of the trophic and gland changes.
It looks as if the sclerosis or condensation of the bones
and tissues, so peculiar to this condition, had given them
power to resist not only the inroads of the micro-
organisms, but the absorption of their toxins. We
must in these cases discount all the trophic and nerve
abnormalities of the acuter stages and those arising

' from disuse. In many respects in rheumatoid arthritis

one sees resemblances to phthisis, but in none more so
than between the acute and chronic forms, for, have we
not an almost analogous condition between phthisis and
fibroid phthisis ?

2.—DIAGNOSIS.

From Chareot’s Joint Disease it may be distinguished
clinically, by the absence of the nerve symptoms so well
marked in that disease, especially the muscular inco-
ordination, etc., and by the fact that the joint changes in
tabes are marked by the suddenness of the onset; by
96 RHEUMATOID! ARTHRITIS.

the absence of pain; by the large quantity of fluid in
the joint; by the fact that the joint changes at first are
always atrophic, although they may later on become
hypertrophic, and by the increased mobility.

From other nerve arthropathies by the absence in
them of pain, and by the presence of well marked nerve
symptoms. :

From Syringomyelia, by the formation of new bone
in rheumatoid arthritis being confined to the interior
of the joint capsule, while in syringomyelia and other
spinal arthropathies there may be extreme ossification
of the periarticular soft parts (Volkmann). This cannot
be relied upon, however, as in the chronic cases of
rheumatoid arthritis there may be considerable formation
of bone in the adjacent tendons, ligaments, bursa, etc.,
but the paralysis, ocular and bulbar, should, if carefully
noted, render the diagnosis fairly easy.

From Pulmonary Hypertrophic Osteo-arthropathy, by
the presence of pulmonary troubles in that disease, and
by the changes being almost entirely confined to the
bones, more especially their shafts, but until more is
known of this disease we are not in a favourable position
to lay down strict, laws with regard to its differential
diagnosis.

From Aeute Rheumatism there is little difficulty in
making a diagnosis, except in those rare cases of rheu-
‘matoid arthritis, where several joints become acutely
inflamed at one time. The whole history of the case
is otherwise different. Its preponderating frequency in
women is a point of importance. Apart from this, the
general clinical features of the arthritis are quite
different; while acute rheumatism begins in the medium
sized joints and spreads-to the smaller, rheumatoid
arthritis begins in the smaller and spreads to the
larger. The former, too, is migratory and uncertain in
DIAGNOSIS. 97

its extension; the latter is slowly progressive, with a
greater tendency to symmetry. The pyrexia of acute
rheumatism, the perspiration, the greater liability to
cardiac complications, are all characteristic. The real
difficulties arise in chronic cases, when the joint must be
minutely examined so as to make out that the stiffness,
swelling, and deformity, depend upon a general thicken-
ing of the textures about the joints, and not on destruc-
tive changes in the joint.

From Chronie Gout the distinction is made by noting
the previous history, and by careful examination of the
joints. Besides the fact of its greater frequency in men
in middle life, whose habits and mode of life contribute
to bring it on, there is usually an account of previous
acute attacks in the joints, mostly the great toe, and, while
in the course of time other joints are affected, the disease
cannot be said to have the same progressive character
and symmetrical spread. The joint changes too are
different. Urate of soda deposits may be noticed in, or
about the joint, as well as elsewhere, as in the ears, etc.
What is quite certain is that the destruction of inter-
articular cartilage, and alterations in the ends of the
bones in rheumatoid disease, are not due to previous
gouty deposits.

A point to be noted in diagnosis is the muscular
atrophy, which presents. in rheumatoid arthritis the
following peculiar and typical features :—

1. It is most marked in the muscles in the immediate
neighbourhood of the joints (interossei, etc.).

2. It is not infrequently found to have affected
muscles beyond this region (trapezius, deltoid pec-
torals, etc.).

8. It improves, and tends to disappear if the joint
trouble ceases, although it would seem to persist at

times long afterwards. :
7
98 RHEUMATOID ARTHRITIS.

4. It is sometimes accompanied by changes in the
electrical excitability of the muscles.

In all cases also the teeth should be examined. In
gout they are almost invariably ground down—even in
women, whilst in rheumatoid arthritis this is never seen
unless in people with a gouty inheritance.

 

REFERENCES.

1. McArdle.—‘‘ Dublin Med. Journal,” 1885, lxix., p. 490, and
lxx., p. 898.
2. Schiiller.— “ Med. Record,” Sept. 23, 1893. an
8. Hutchinson.—* Med. Times and Gaz.,” 1881, vol. i.
4. Lorain.—“ Union Médicale,” 1866, xxxii., p. 617.
5. Charcot.—‘‘ Maladies des Vieillards.”’ mS
6. Garrod.—‘t Rheumatism and Rheumatoid Arthritis,” p. 236. Hi “i
7. Waldmann.— Arthritis def. u. Chron. Gel. Rheum.”; :
“Volkmann’s Samml. Klin. Vortr.,” No. 238, 1884.
8. Pasteur.—‘‘ Clin. Soc. Trans.,” vol. xxii.
9. Barlow.---Quoted Garrod, loc. cit., p. 247.
10 Be hies —‘Legons de Clin. Méd.,” 1867, lecon, xxili., p.
59
11. Wagner.--‘‘ Miinchener Med. Wochenschr.,” 1888.
12. Still.—‘ Allbutt’s Medicine,” vol. iii., p. 102.
18. Garrod, Sir. A.--‘‘ Rheumatism and Rheumatic Gout.”
14. Lecaze "Dori..— Thése de Paris,” 1882. at
15. Monocoro. — “Rhumatisme Chronique Noueux des Cy,
Enfants,” 1880. ee
16. Lloyd Davies.-—“ Lancet,” vol. ii., 18938, p. 928.
17. Money.—“ Diseases of Children, ” p. 130.
18. ce Rheumatism, Rheumatic Gout and Sciatica,”
85

 

 
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DIAGNOSIS.

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100

CHAPTER V.
SYMPTOMS AND PROGNOSIS.

Premonitory Symptoms—Spender—Primary Symptoms due to
Micro-organisms—Appearance of Joints—Heat of Skin—-Ar-
thrite Séche—Synovial Pouches-—Joints first affected —Sym-
metry — Ankylosis — Deformities — Dislocations—Osteophytic
Out-growths—Forms of the Deformities—In the Hands and~
Knees—Its Causes—Difference in Acute and Chronic Cases—
Cardiac Symptoms—Endocarditis—Pericarditis—Changes in
the Glands—Secondary Symptoms—Muscular Atrophy—Its
Characters—Selective Power—Myotatic Irritability—Fever—
Pulse Rate—Tachycardia-—Tension—Anemia—Hemorrhages
--Purpura—Neuritis—Its Frequency—Trophic Phenomena—~
Skin Changes—Glossy Skin-—Loss of Hair—Atrophy— Downy
growth of Hair—Pigmentation—Sweating—Dyspepsia—Kid-
ney—Cardiac troubles—Prognosis.

 

1.—Symproms.

As a rule, in every illness we find some salient, constant
and characteristic abnormalities which may be taken to
represent an individual disorder. It is so in rheumatoid
arthritis. In this disease the joint symptoms are charac-
teristic and constant, and the character and number of
them, with the number of the structures attacked, all
suggest a systemic disease.

The symptoms may be divided into

A.—Premonitory Symptoms ;

B.—Primary Symptoms, and

C.—Seeondary Symptoms, being those more especially
due to the absorption of the bacterial products.

A.—The Premonitory Symptoms.

The disease, in many cases, has no premonitory
symptoms, the first indication of anything being wrong

‘being slight pain in a joint with some swelling, and
SYMPTOMS. IcI

tenderness on pressure, or on movement. Should, how-
ever, premonitory symptoms be present, they usually
present themselves in the form of numbness, tingling, or
other abnormal nerve sensation of the extremities.
Howard,' Homolle,? and Garrod,? all mention such cases.
Howard compares them with the abnormal sensations
noticed in spinal disease. Garrod quotes cases in which
there was a sensation of pins and needles in the arms
and hands, and growing pains in the bones. In my
experience I have never been able to get a really reliable
history of any such premonitory symptom. I have had
patients say they have felt. abnormal sensations, but on
further investigation there has almost invariably been
some antecedent trouble which has caused such confusion
as to render the evidence quite unreliable. Patients
naturally pay more attention to slight abnormal nerve
sensations than they do to a trivial pain or swelling of a
finger joint or knuckle. I think, therefore, little reliance
can be placed on the occurrence of premonitory symptoms.
Before leaving the subject, however, I would mention the
symptoms described by Dr. Spender,‘ which, according to
him, if not actually premonitory, occur very early after
the onset of the disease. The symptoms referred to are
various vaso-motor and trophic disturbances, which will
be discussed more fully later on, andpain. The pain on
which he lays such stress is one occurring in the ball of
the thumb, and on the inner side of the wrist. He
considers it to be of great importance, and almost patho-
gnomonic, and it may be accompanied by a feeling,
described by patients, as of being ‘‘ parboiled, scalded,
stung all over with nettles,” etc., the pains themselves
being various in character, but those of a neuralgic
character being most common and characteristic. They
are more often referred to the bones than to the joints
themselves.
102 RHEUMATOID ARTHRITIS.

Given then a disease ushered in by the foregoing pre-
monitory sensations, or by neuralgic pains, it is not long
before we find evidence of the disease in the joints
themselves ; and, following on the joint symptoms, come
atrophy of the muscles, with, at shorter or longer
intervals, certain other symptoms due, for the most.
part, to derangement of the nerve and vaso-motor
systems. The occurrence of certain changes in the joints, »
with or without these other symptoms, then, constitutes
the disease called rheumatoid arthritis. Of the local
symptoms, of course, the most important are those
referable to the joints.

B.—Primary or essential Symptoms.

1. Symptoms due to the presence of miero-organisms in
the joints.—To the eye the earliest symptom is some
enlargement of one or more joints. This may vary in
degree from the most: trivial swelling to an enormous
distension. It assumes all sorts of shapes and charac-
teristics, and the skin covering the joints may be subject
to many and various changes. Apart from trophic
changes it may be reddened, but more often presents
a bluish, asphyxiated look quite characteristic. As a
rule, the shape is more or less characteristic in so far as
the joint alone is affected, but should the tendons
or their sheaths have undergone rheumatoid change, one
can never say what the alteration may be. In an
ordinary acute case the joint will be more or less spindle-
shaped, merging gradually into the tissues above and
| below (Plate V, Fig. B, and Plate IV, Fig. A), due
either to the presence of fluid, or else to pulpy swell-
‘ing of the synovial membrane; occasionally we may find
that the swelling is not symmetrically spindle-shaped,
and there are what seem to be pseudo-depressions between
the heads of the bones, due to these latter being pushed
apart by the swollen joint tissue, and to the general
PLATE V.

 

Tig. A.—Shows deflection of left hand. There is complete dislocation of 1st
phalanx of index finger on to palmar surface of metacarpal, and partial of
2nd phalanx on to palmar surface of Ist ring finger.

 

tig. B.--Shows spindle shaped swelling of phalangeal joints.
 
SYMPTOMS. 103

softening of the ligaments and tendons (Plate IIT, Fig. B).
In chronic cases the enlargement is usually more irregular,
and may, from the. enlargement of the heads of the
bones, and from the presence of nodules of osteophytic
growth, as well as from the swelling of the synovial
membrane and presence of fluid, present an enormous
and irregular enlargement. As the disease commences
in the synovial membrane it is not until the later stages
of the acute, or in the chronic form that we see much
bony enlargement (Plate VI, Fig. A). Owing to cystic
enlargements, or burse, certain aspects of the joint
may be increased in size out of all proportion to the
rest. In many cases the mapping out of the synovial
sacs is very perfect, from the swelling being almost
entirely confined to them, and, in such cases, the enlarge-
ment is sharply demarcated from the surrounding tissues.

While the acute stage is still in progress, to the
touch the joints feel hot — the temperature often
being raised. 1°-2° Fahr. above that of the surround-
ing surfaces.

As to the eye, so to the touch, we find three con-
ditions :—

(a,) A tense, elastic, and resistant swelling with
distinct fluctuation, often with secondary sac-like
protrusions of synovial membrane—best seen in the
joints of the fingers, and evidently caused by the
presence of a considerable quantity of fluid under
some tension.

(b,) A soft flabby doughy enlargement, feeling as if
the joints, ligaments, and all the surrounding tissue
had undergone maceration. Over the joint cavity there
may be a sort of depression in the middle of the
otherwise generalised swelling, and everything feels
doughy or pulpy. There is seldom much fluid present
in such cases, but the swelling being due to the dis-
104 RHEUMATOID ARTHRITIS.

organization and pulpy synovial membrane they are
most acutely progressive. It is often a late stage of the
acute form, and shows that much destruction of the joint
has taken place.

(c,) The third condition is that described by the French
under the name, “ Arthrite Séche.’’ In these cases the
joints are enlarged and nodular, and one feels that the
heads of the bones have undergone enlargement; the
synovial membrane is doughy; there is much crepitation
on movement; movement is difficult and this even, if «
passive, causes pain; and there may be ankylosis. It is
not seen in the more acute stages.

At first, on passive movement, there may be little or
no pain, and there may be no tenderness ; but pain in the
acute forms soon becomes marked and persistent both on
movement and at rest, especially at night. On move-
ment in the drier, and more chronic forms, we get grating
on moving the heads of the bones one over another.
This may become quite a marked feature. At first it
is of a fine character, but soon passes into the coarser
varieties of crepitation, which convey the idea that
one is rubbing two erosed pieces of bone together,
and which only cease from total inability to move the
joint.

During the first stages the skin over the joints may be
reddened, and dusky in hue, with increase of pigment,
etc., whilst in the later we see various trophic changes,
such as “glossy” skin.

‘ With regard to the pouches or cysts seen either
in connection with, or in proximity to, a joint, Mr.
Morant Baker’ says that they arise from the synovial
cavities by a process of distention. The synovial fluid
on reaching a certain degree of tension finds its way out
into the tissues in the direction of least resistance. It
does so either through some normal channel, such as
PLATE VI.

 

Fig. A.—Shows cartilaginous and bony enlargements of the heads of the bones,
with considerable synovial swelling and thickening. Atrophy is marked.*§ K—Shows
thickening of wrist joint.

 

Fig, 2.—Ulnar deflection in a chronic case,
SYMPTOMS. 105

that by which a bursa communicates with a joint, or
else by the formation of a hernial projection of synovial
membrane. Finally it pushes its way into, and between,
the tissues until its boundaries come to be formed by the
/muscles and other surrounding tissues. I have often
watched such pouches gradually being pushed through the
tissues surrounding the joints, and one can readily
understand how they might have their communication
with the joint cut off either by pressure, from a rapid
enlargement of the joint, or else by a twist, or by some
inflammatory process. JI do not think that these
synovial pouches ever actually burst. On puncturing
them I have, more than once, seen the escape of all
the fluid from a joint; and, on pressure, one can make
them disappear with a temporary increase of the fluid in
the joint, thus demonstrating their intimate connection
with it.

With regard to the presence of fluid in the joints:
in almost all the acute cases it is present, often in large
amount. However, with the synovial membrane and
ligaments in a state of doughy or pulpy softening and
degeneration, it is not always easy to differentiate
between the two conditions. Hemorrhages into the
joints are rare, but not altogether unknown. Suppura-
tion is even rarer, and I have never seen it (see
p. 64).

In the acute forms of rheumatoid arthritis the
small joints of the hand are those most liable to be
affected by the rheumatoid changes. They are usually
the joints first affected, and often form the starting
point from which it spreads all over the body. It
not infrequently happens, however, that the disease
is not only confined to the fingers, but to the terminal
interphalangeal, or even one terminal interphalangeal

joint.
106 RHEUMATOID ARTHRITIS.

Charcot gives the following statistics from 45 cases, as
to its origin ® :—
25, or 53°5 per cent., started in the small joints of the hands
and feet first.
4, or 88 started in the great toe first.
7, or 17°7 55 started in the hands and feet at the same

time as in a larger joint.

9, or 20:0 $4 started in the larger joints first.

He says the arthritis, as a rule, spreads from the
periphery to the centre; the fingers first being affected,
then the elbows, and then the shoulders. In young
patients hé says it is usually general from the first, and
that it is only in the elderly or chronic cases that its .
progressive character is so well seen. Haygarth’ men-
tions that 20 out of 34 cases had the hands affected first,
and Ord ® 24 out of 88. Garrod out of 500 found that
252 commenced in the hands, 64 in the knees, and 28 in
the feet; whilst in 430, or 86 per cent., the hands were
affected at the same period of the disease.

_. In the 298 cases I take for comparison, I could only get
a reliable history in 280 with regard to the joint first
affected. Out of these, 68 per cent. began in the hands ;
16 per cent. in the ankles; 10 per cent. in the knees;
4 per cent. in the shoulders, and neck; and 2 per cent.
in the elbows and hips.

The disease rarely, or never, travels down a limb,
although it may occasionally do so from a knee or elbow
to the fingers or toes. It is noticed that the joints
. most liable to other conditions are those most liable to
be affected also in this complaint, with one exception.
This is the temporo-maxillary joint, which is rarely
affected in other disorders, but shows a peculiar liability,
almost pathognomonic, to be affected in rheumatoid
disease. It may happen that the disease in the jaws is so. -
extreme that all movement is prevented, and feeding has
to be effected through the vacant space left by the
SYMPTOMS. 107

removal of a tooth. The inability to open the jaw may
only be from stiffness and cicatricial contraction, but it
may also happen from true ankylosis.

Garrod gives a table of the joints most fre-
quently affected. For comparison, I also give my
‘results :—

Berean tas:
Out of. 293 cases 97°4 per cent. had their hands affected ... 86°0
” ” ” 84°6 ” ” elbows rr ... 25°0
” » 9» 820 ,, si neck yoo.
” » 9 20 ,, a knees yy tee 60°6
” ” ” 679 ” ” ankles ” w B44
” ” ” 67-9 ” ” jaws ” ... 25°0°
93 »s » SEO .,, ie shoulders ,, ... 25°0
” ” » 12°5 ” ” hips ” .. 146
” oO; 25, 45 sterno-clavicular »—

The centripetal order is broken at the neck and knees,
but as these joints are specially liable to arthritic trouble
we would almost expect them to be so also in this disease.
In acute rheumatism, the knees are the joints most
frequently affected. One of the most marked features of
the disorder is its symmetry: This is not only seen with
regard to the joints affected, but algo to the time of the
invasion, and, to a less extent, to the degree of severity
with which individual joints are affected. At the same
time it is usual to find one limb more affected than the
other, and the peripheral joints more than the more
central ones. This is often beautifully demonstrated.
Garrod says this symmetry is carried so far that corres-
ponding portions of the cartilages are destroyed. This
I cannot confirm. Dr. Havilland Hall * recently men-
tioned that the crico-arytenoid joint may be implicated
in this disease. Bearing in mind how generalised the
disease is, there is no reason why the arytenoid
cartilages should escape, more especially as the neigh-
bouring joint, the temporo-maxillary, is so often affected,
and Casselberry“ has recorded a case the clinical history
108 RHEUMATOID ARTHRITIS.

of which would point to the crico-arytenoid joint being
thus implicated.

When ankylosis occurs it may be from true or fibrous
ankylosis, or more rarely from interlockings of the
osteophytic out-growths. This latter is most common
in the case of the jaws. Fibrous ankylosis may usually
be diagnosed from true or bony ankylosis, by some slight
movement detected on careful examination, or the attempt
to obtain movement may cause a contraction of the
muscles which oppose it, or else pain may be induced.
Spondylitis, or disease of the vertebre, is not uncommon,
and it is confined almost entirely to the acute form.

In all cases, at one time or another, there is pain. The
pain is varied, and arises from many different causes.
That arising in the joints is, as a rule, of a gnawing
character, is made worse by movement, and often by’ the
warmth of the bed. It differs in intensity in different
cases, and from time to time. Although there may be
no actual pain in the joints, patients often complain of a
pain in the ligaments and tendons, as if the joints
were being stretched. Pain is usually less in the joints
distended with fluid, but in acute cases with comparatively
little effusion, and where the eroded cartilages rub one
on another, it is most marked. Besides this we may
have pain from cramp or spasm of the muscles, or there
may be pain referable to the bones. Again, we may have
neuralgic pains; and pain along the course of a nerve,
due to neuritis. In some cases there may be radiating
pains which, if there be spondylitis, is probably due
to irritation or compression of the nerve roots.

We now have to consider the deformities and disloeations
which may arise in chronic cases and apart from synovial
thickening. In every joint affection there is a certain
amount of deformity or distortion due to the thickening
and swelling of the joint tissues, and possibly in rhen-
PLATE VII.

 

Fig. A,—Dislocation backwards of index finger through relaxation of
ligaments and erosion of the cartilages and head of the bones; also partial
dislocation of rine finger.

 

 

vig. B.—Shows ulnar deflection.
SYMPTOMS. 109

matoid arthritis it may stop at this stage, but, on the
other hand, as the disease progresses, and as the tissues
become contracted, destroyed, or greatly weakened, there
may arise those great alterations from the normal which.
cause 80 much crippling and distortion. The disease, as
it advances, may cause an increased tonicity on the part
of certain muscles, and a weakness, or atony, on the part
of others, the result being a deformity which, although
at first readily reducible, soon becomes irreducible and
permanent. Along with the development of such
deformities we find marked wasting, and shortening of
certain muscles, which may occur to such an extent that
joints quite free from disease may actually become partially
or completely dislocated. This has also been known to
occur in such diseases as paralysis agitans, congenital
brain atrophy, etc. (Plate VII, Fig. A), where the
process is of course very slow, and chronic in its nature.
A somewhat similar condition has been described by
Jaccoud,® as occurring in his ‘‘Rhumatisme fibreux.”’
It may also occur in all chronic forms of arthritis.

In rheumatoid arthritis the principal deformities are
seen in the hands and knees. The deformities of the
hand occur in two ways. There may be deflection to
the ulnar or radial side, or there may be extension or
flexion. A combination of these two types is what we
most commonly see. The disease having commenced in
the fingers, spreads in course of time to the knuckles and
wrists. These become large and nodular, and, probably,
at the same time some deflection of the fingers occurs.
This may either be ulnar, when the whole of the finger
is involved, or else radial, when only the terminal
phalangeal joint is affected. This radial deflection of
the terminal joint has been explained, by some, as being
due to osteophytic outgrowths on the ulnar side. The
ulnar deflection only takes place from the metacarpo-
110 RHEUMATOID ARTHRITIS.

phalangeal joints, and, except for radial deflection of the
terminal joints, any deformity of the phalangeal joints
is usually confined to a fusiform enlargement arising
from synovial thickening (see Plate VII, Fig. B, and
Plate VIIT, Fig. A). When, however, the knuckles have
become affected the fingers may begin to deflect from
these joints, but always to the ulnar side. At first easily
reducible, the deformity rapidly becomes irreducible.
‘The deformities are brought about principally and .
primarily by relaxation of the ligaments and tendons.
Herringham suggests that it may be caused by atrophy
of the abductor indicis, and by the then unsupported
finger pushing the others to the ulnar side. Duckworth”
‘points out that such atrophy is not a constant feature,
and this therefore has to be discounted. Pure atrophy
alone will not cause it.

As a rule the thumb escapes, if the terminal joints alone
are affected, but it suffers if the disease becomes more
general. As the wrist enlarges the natural shape of the
arm and forearm is lost, and it comes to appear as
if the limb from the elbow to the wrist were of the same
thickness. One often notices that the burse in the neigh-
_bourhood of the olecranon are enlarged, and it is fairly
common to find that cartilaginous bodies have developed
in these burse. In the larger joints it is usually
‘impossible to find any deflection. The deformities arise
in a similar manner in the feet, but are less common.

Under the second type we find deformities of flexion
-or extension. They were first described and classified
by Charcot, who divided them into two main types,
“with several sub-varieties :—

I.—The first form is that most often met with. It is
marked by

(a,) Flexion of the terminal phalanges on the second
vat an obtuse, right, or even an acute angle.
SVMPTOMS. lil

(b,) Extension of the second phalanges on the first.

(c,) Flexion of the first phalanges on the metacarpals.

(d,) Flexion,.to a less obtuse angle, of the metacarpals
and carpals on the bones of the forearm.

(e,) Ina great many cases, inclination of all the fingers
to the ulnar border of the hand.

The sub-varieties are :—

(a,) The first and second phalanges being in the same
axis, form a single column, with the other characters as
the main type.

(b,) The terminal phalanges are extended on the
second, and the backs of the fingers appear excavated
beyond the prominent heads of the metacarpal bones.

Il.—The second type is characterized by

(a,) Eixtension of the terminals on the second phalanges.

(b,) Flexion of the second on the first phalanges.

(c,) Extension of the first phalanges on the meta-
carpals.

(d,) More or less marked flexion of the carpals on the
bones of the forearm.

(e,) In some cases deviation of all the fingers towards
the ulnar border of the hand.

The sub-varieties are :—

(a,) Flexion of all the segments of the hand, except
the terminals, on one another, so as to appear rolled
up.

(6,) Is similar, except that there is extension of the
second on the first as well.

With regard to the thumb, it is usually flexed, but
occasionally it is found extended. Combined, with these
changes there is usually flexion of the elbows, pronation
of the forearm, rigidity of the shoulder, and the upper
limb is fixed on the chest. Garrod makes the flexion or
extension of the middle joints the basis of his classifica-
tion, and which, therefore, necessitates the inclusion of
412 RHEUMATOID ARTHRITIS.

the second sub-variety of the flexion type as a sub-variety

of the extension type.

With regard to the lower limbs the hips usually remain
mobile, but the knees are flexed and fixed.

Charcot says that the chief deformities are as
follows :—

(a,) The lower end of the femur projects in front of
the head of the tibia ;

(b,) The internal condyle becomes wore prominent ;

(c,) The patella, thrown outwards, rests on the outer
condyle ;

(d,) The head of the fibula projects externally.

In the tibio-tarsal joint ankylosis is common. The
foot is, a8 a rule, abducted, and rests on its inner edge.
The big toe is turned outwards, so as to cover the other
toes. With regard to the cervical vertebre one often
sees the head thrown forwards, and bent on the sternum,
so as almost to let the chin touch it. The neck is
widened posteriorly.

If we now turn to the deformities of the knee joints,
we see that the joint is almost invariably flexed, and
mayhap slightly rotated. Can we account for this in
any way? In disease of the condyles of the femur we
know the leg always assumes a flexed position to a
greater or less extent, and that, after flexion, the foot
rotates out, and rotation increases the flexion. In
diseases of the synovial sac, unattended by disease of the
condyles, cartilages, lateral or crucial ligaments, the
entire joint remains straight. In diseases of the entire
joint, including the cartilages, the leg always flexes,
whether there is fluid present or not. I must qualify
these propositions by mentioning that certain pathological
changes may modify these deformities. But such excep-

tional deformities are always easily accounted for, as, for »

instance, that seen in Charcot’s disease, or in cases
3
SYMPTOMS 113

attended by complete destruction of either condyle of
either side of the tibia. Many have tried to account
for flexion upon the fluid hypothesis. It is true that
when the knee-joint is forcibly injected it will flex
slightly, to give the greatest possible capacity to the
capsule, but this is insufficient to explain the deformities.
The fluid hypothesis is wrong, because in, by far, the
largest percentage of cases, there is no fluid effusion, and
large serous effusions are often unaccompanied by flexion,
and after a joint is evacuated in large effusions it does
not resume the straight position. These are valid
reasons why the fluid hypothesis is incorrect. Butlet us
now examine a knee-joint. It is a hinge which, when in
the straight position, is firmly fixed, owing to the tension
of the lateral and crucial ligaments. This forces the
articular surfaces firmly together and prevents lateral
motion. The leg flexed, there is lateral motion of the
joint, which increases as the leg flexes, and not only
lateral but rotary motion takes place. This is due to the
relaxation of the crucial and lateral ligaments by flexion.
Another fact; the patella, and a portion of the capsule
anteriorly receive their nerve-supply from the obturator,
and probably from the anterior crural. The other
portion of the joint is supplied from the great sciatic.
The great sciatic supplies the flexor group, while the
obturator and anterior crural supply the extensor group.
A clinical fact is, that when the entire joint is attacked
with acute inflammation, all the muscles surrounding it
are affected by spasm. Still flexion rapidly takes place,
whereas disease of the condyles always produces great
spasm and rapid atrophy of the flexors, while the extensors
remain quiescent. Diseases limited to the patella
produce spasm and atrophy of: the quadriceps extensor
femoris.

In rheumatoid arthritis, we find certain muscles pre-

8
114 RHEUMATOID ARTHRITIS.

senting a weakness (usually to extension), resulting,
from an atrophic condition, and others (usually the
flexors) a condition of increased tonicity. The result
is naturally flexion, and, as the limb flexes, rotation
follows, and we have the deformity so commonly seen.
The increased tonicity arises probably from reflex irri-
tation from the joint, or else by the action of the toxins
on the governing nerve cells.

The question has been raised, How do the deformities,
looking at them as a whole, arise? Some have held that
they arose from an intentional desire to lessen the pain.
Trastour,2 and Beau,!® were both of this opinion.
Charcot held that they were due entirely to muscular
contraction, spasmodic if. not convulsive. These spasms
are caused according to him by a reflex action due to
irritation in the joints. This view was also taken by
Crocq. Nowadays it is recognised that they arise from
the weakness of one set of muscles being more than
overcome by the strength of another set. In the lower
leg and foot we may instance the long flexors, extensors,
and interossei as being specially affected. These latter
flex the first row of phalanges, and extend the second,
thus accounting for many of the deformities. When
they are strong we have deformities of the extensor, and,
when weak, of the flexor type. It must not be forgotten,
however, that there are accessory causes such as the
weight of the limbs, and a more or less decided laxity of
the ligaments. The deformities are not exclusively the
property of rheumatoid arthritis (and in fact are not so
very common in it in the acute form), but may occur in
gout, chronic rheumatic arthritis, paralysis agitans, etc.

Disloeations.—We find that dislocations either partial ke
or complete arise from the lengthening of certain liga-

ments, due to a softening or disorganising process, com-
bined with an increased tonicity of certain muscles; whilst

fees
SYMPTOMS. 115

the opposing ones have undergone atony. Dislocations
may also arise from severe and extensive ulceration of the
heads of the bones. We find that the most common
dislocations are those of the knees, wrists, and fingers.
In the case of the knee, the tibia is most often dislocated
backwards, the wrist either backwards or forwards, and
the fingers on to the palmar aspect, the distal bones
being displaced under the proximal ones through the
anterior ligaments giving way (see Plate V, Fig. A).

In chronic cases, the deformities are much more
marked than in the acute, and dislocations also occur
more frequently. The most usual type is dislocation of
the wrist and fingers forwards. These dislocations and
deformities become more pronounced as the disease
advances, and as contraction of the cicatricial tissue
takes place. In cases, chronic from the first, they are
less pronounced, partly owing to the osteophytic growths.
It: has been noticed that a hand which is used, up to the
last, does not develop such a regular type ‘of deformity
as another, which has been kept at rest.

2. Symptoms due to the presence of micro-organisms in
the blood.

(a,) Cardiae conditions.—I must now touch on a much
vexed question, namely, the occurrence of cardiac lesions
during the course of the disease. Personally, I am of ©
the opinion that endocarditis and pericarditis, especially
the former, are much more common complications than
one would expect. The former is fairly often seen, but the
latter much more rarely (in only about 4 to 5 per cent.).
Charcot says that they occur pretty frequently, and pre-
sent the same characters as are seen in acute rheumatism.
They are usually seen in the acute stages or during an
exacerbation. To him they appear to be less grave than
those of acute rheumatism. He gives instances of these
lesions being found' post-mortem. Romberg,* Todd,”
116 RHEUMATOID ARTHRITIS.

Trastour,!° Beau,” and Ball,?® all mention cases in which
they have found cardiac lesions with rheumatoid dis-
ease. Besnier ® took this view also, but declared that
they are rare. Sir A. Garrod ® does not believe that
they ever occur, and Dr. A. E. Garrod supports him,
although admitting that cases are seen with cardiac
lesions, due, he thinks, to some previous rheumatic
condition.

Out of 293 cases, I found 17-9 per cent. suffered from
cardiac conditions which had developed since the onset
of the rheumatoid attack.

In several others there were cardiac conditions, but
the history in these cases not being perfectly clear they
were ignored. Numerous cases occur in hospital work
in which undoubted acute endocarditis and pericarditis
have developed during the period they were under
observation. Given a micro-organism circulating in the
blood, it is of course probable that we will have symptoms
referable to their growth on the endocardium and
pericardium. AsI have said, the cardiac lesions, except
in the case of the pericardium, are seldom of a very
extensive nature, and, in the majority of cases, I have
found the mitral valve to be the one most likely to be
affected—the other valves less often. Clinically they
give rise to a booming systolic murmur rather charac-
teristic. Pericarditis is often severe and extreme.

(b,) Changes in the glands, ete.—In a considerable
number of cases we find enlargement of certain glands,
especially in children (Still, Playfair‘), most com-
monly those in the groins and armpits. In a few
rare cases I have found a chain of glands running up
from an affected joint. They invariably are found on
the proximal side of an affected joint. The glands are
usually enlarged in size, from that of a hazel nut up to-
that of a walnut, and are painful on pressure, the pain
SYMPTOMS. 117

shooting up and down the limb, but otherwise giving
rise to no symptoms. I have never, as yet, found an
enlarged spleen.

(c,) Fibroid nodules and fibrinous exudations occur in
rheumatoid disease as well as in rheumatism, syphilis,
etc. The former are seen chiefly in adults, are chronic
in nature, are often painful and tender, and vary much
in size and shape. They are found in the subcutaneous
tissues, and often close to a joint. Their occurrence has
been noted by Howard,?! Payne,*? Duckworth,* Pitt,*
etc. If we hold that these nodules consist of a central
necrotic area, surrounded by dense connective tissue and
cell exudation, there can be only one possible explanation.
The bacilli circulating in the blood must have caused an
endarteritis, with cell exudation and inflammation, which,
if severe, has ended in a local necrosis.

Extensive fibrinous exudation giving rise to a hide-
bound condition of the skin has been noted by Jaccoud
and Pitt. The exudation in these cases much resembles
granulation tissue.

C.—Secondary symptoms, or those due to the absorption
of the bacterial poisons.

1. Of these secondary symptoms, the principal may
be referred to the muscular system. In all acute cases
we have a certain amount of muscular atrophy develop-
ing sooner or later. It is one of the earliest and most
persistent of symptoms, but may vary greatly in degree.
In some it is so slight as almost to be imperceptible,
whereas in others the joint trouble seems quite secondary
to that of the muscles affected. One of its peculiarities is
a selection of the muscles affected. It is noticed, as
a rule, that the extensors and interossei are peculiarly
liable, but not invariably so. One muscle only or
a whole set of muscles may be affected, and yet the
form and extent of the disease in the joints would
118 RHEUMATOID ARTHRITIS.

appear to have little effect on this phenomenon of
selection. It is this selection, and the increase of the
tendon reflexes, which prove that the changes are not
entirely due to disuse. For we must remember that
prolonged disuse will give rise to an arthritis, combined
with muscular atrophy, having many of the symptoms
of a rheumatoidal one. Such cases have been mentioned
by Bonnet,® and Tessier.*® The selective character of
the atrophy, in rheumatoid disease, is peculiar, and this
we see when we compare it with what occurs in alcoholic
muscular atrophy, where the extensors chiefly are
affected, especially of the legs; with lead, where it is the
extensors of the fingers and wrist; and with diphtheria,
where it is the muscles of the throat, and internal |
muscles of the eye that suffer most. It is still more
remarkable that the selective power of toxic agents
should exert itself on the motor filaments only, or on the
sensory ones, as well as on them both together. Indeed,
_in some cases there is good ground for supposing that —
even the trophic and vaso-motor nerves may be specially
picked out. With regard to this point, we must bear in
mind that in the diseases mentioned, we have to do-with
a peripheral neuritis, but in rheumatoid arthritis it is
probably a central disturbance which is responsible. The
reflexes vary in different cases, but in a pure case of -
rheumatoid they are usually slightly increased. This
would rather point to some irritative lesion somewhere. It
is possible that the slight changes seen in the reaction
of degeneration indicate a difference between an intoxi-
cation and a degeneration. I am inclined to think so.
In the cases where the reflexes are absent it is almost
certain that we have to do with a neuritis, probably set
up by the joint inflammation or by toxins, or it may even
be due to a descending degeneration. In the case of a
neuritis, there will probably be pain along the course of the
SYMPTOMS. 119

affected nerve, and there will also be other characteristic
signs. The atrophy, as we see it clinically, has been said
to be of different kinds: (a,) either due to a neuritis
arising as is stated above; but (b,) more commonly it is
attributed to some reflex nerve influence having its origin
in the peripheral nerves of the affected joints; and (c,)
since the discovery of the micro-organism, I hope it will
be generally conceded that it arises more probably from
some toxic nutritional condition of the ganglion cells of the
- anterior cornua of the spinal cord. With regard to this
question Gowers” points out that the atrophy from disuse
is trifling, and tardy, and affects the muscles of the diseased
limb as a whole; and that the whole limb being affected,
precludes the possibility of the atrophy being due to any
local inflammatory change. He further points out that
the changes are such as frequently result from degenera-
tive changes in the pyramidal tracts, due to changes in the
terminations of the pyramidal fibres in the gray matter.
As a further proof that it does not arise from a local
change is the fact that the whole of a muscle is affected,
and not only that part immediately in contact with, or
distal to, the affected joint. To cause this atrophy by
peripheral means, the irritation must be intense; but I
would much rather believe that it is caused by a local
agent circulating in the blood, such as a toxin affecting
the afore-mentioned centre. The atrophy resembles that
occurring in other forms of arthritic muscular atrophy,
not only in its distribution, with its increased myotatic
irritability, but also in the absence of any reaction of de-
generation. Should any neuritis have occurred, of course
we will get the reaction of degeneration. Fibrillary
twitchings have been occasionally observed in the wasted
muscles. A tendency to spasm occurs with the increased
myotatic irritability. This spasm may exist for hours,
and give rise to the most acute pain, usually having a
120 RHEUMATOID ARTHRITIS.

cramp-like character. Ballet*® mentions cases accom-
panied by chronic spasm which occurred paroxysmally.
2. Symptoms due to changes in the eireulatory

system. By seg
The circulatory symptoms are various, and some of

them will be considered when we come to the nervous
system.

(a,) Fever.—The general body temperature seldom
shows much rise, but in the acute stages there is always
fever, usually of an irregular type. It seldom is high,
but, on one occasion, I have seen it as high as 105° Fah. |
That it rises nightly during the more progressive stages,
I have no doubt, but owing to its irregularity, and from
the fact that it is seldom high it is usually overlooked.
One reason assigned in chronic cases for the want of
fever is that owing to the condensation of the joint
tissues the absorption of the toxins is very slow, and no
great quantity is absorbed at once. This, I think, is
hardly a sufficient explanation. Most of my hospital
cases, where accurate observations are taken, present a
certain rise every evening of from one to four degrees,
and this may go on for months, as a rule, quite un-
suspected both by the patient and by the medical
attendant, unless attention be specially drawn to
it.

Amongst the other symptoms we have (b, ) Tachyeardia
or increase of the heart rate. Sir Dyce Duckworth first
pointed out that palpitation in this disease was not un-
common. An increase in the pulse rate was also pointed
out by Charcot,” but it was probably not until Spender *
drew attention to it, that any special significance was
placed on this. Spender says, that in the acute cases
the greater number are characterized, from the beginning,
by an increased velocity and tension of the heart’s action, .
and the pulse may go up at once to between 80 and 90,
SYMPTOMS. 125

and remain so for years. He says, ‘we are startled by
counting a steady pulse of much tension, varying from
90 to 110...... The pulse quickens synchronously
with the earliest sign of osteo-arthritis; there is a gradual
rise until the numerical frequency of 110, 115, or 120 is
reached, and there is scarcely any physiological variation
during day or night ....... the body is absolutely
non-pyrexial, and the icy purple coldness of the hands is
often a striking fact. There is no hemic murmur, and
there are no signs of the heart being in any way affected.
The acceleration of the circulation is not paroxysmal,
the phenomenon does not belong to that group lately
described by Dr. Bristowe,*! in which the rate of pulsa-
tion now and then suddenly increases, and as suddenly
lessens, nor is there any sign of venous engorgement or
of local cedema. It is as if the heart were running along
without check ; as if the inhibitory power of the pneu-
mogastric nerve were partially withdrawn, or partially
neutralised by a cerebral influence which cannot at
present be defined.” Such, in his own words, is the
condition which he describes. I am afraid I cannot
altogether support him in his observation. It is un-
doubted that we all see cases of rheumatoid arthritis
with an increased pulse rate, but cannot this be accounted
for by the fact that in most cases there is some pyrexia,
and by the fact that most patients with rheumatoid
disease are undoubtedly neurotic.. Sit down quietly by
the patient’s bedside, and you will find that a pulse,
going at the rate of 120, or over, will gradually subside
and diminish in frequency. Such at least has been my
experience in a large proportion of cases. But, now and
then, we undoubtedly come across cases corresponding in
all essentials to those described by Dr. Spender. They
are, however, not very common. The tachycardia prob-
ably arises from the cardiac nerves and centres having
‘

122 RHEUMATOID ARTHRITIS.

come under the same influences which affect so many of
the other portions of the nerve system.

We now turn to another class in which (c,) Anzmia
occurs. Although resembling many other anemias
in being secondary and symptomatic in nature rather
than primary or idiopathic, that of rheumatoid arthritis
is none the less interesting; and in its details may be
classed with those forms seen in various other infective
diseases. We seldom find it very marked except in
advanced and very acute cases, but in all, even the
slightest, there is, as a rule, a certain amount of blood
deficiency. Roughly speaking in about 95 per cent. of
the cases presenting themselves, in all stages, do we
find it to a greater or lesser degree. We rarely find
extreme pallor of the skin, the patients presenting more
often a sallow or brownish yellow complexion, with
moderate blanching of the mucous membranes. This
sallowness may, by degrees, pass into deeper shades,
until it insensibly merges into a distinct discolouration.
Not infrequently is it accompanied by functional cardiac
bruits and venous hums. Hemorrhages, so common in
other anemias, are rare, but not unknown. They are
very rare from the mucous membranes, being most
commonly seen as small purpuric spots on the legs. I
have seen it two or three times as hematemesis and
hemoptysis, and once under the nails of the fingers and
toes. Of course hemorrhages are rare, as they mostly
occur in cases where there is 50 per cent. or more blood
deficiency and where it depends more on a diminution of
the corpuscles than on that of the hemoglobin.

(d,) Hemorrhages.—Purpuric hemorrhages are usually
small and are usually subcutaneous. They almost never
occur from the mucous and synovial membranes. Hama-
temesis I have seen several times, and hemoptysis
once.
PEATE VIL

 

 

Fig. d.—Shows fusiform deformity of index finger.

 

ig. B.—THeemorrhage wider tiails in Rhewmatoid Arthritis.
SYMPTOMS. 123

In the course of a year I have, on an average, seen
perhaps six or eight cases where purpura was well
marked, the hemorrhagic effusions usually occurring
on the front of the legs, and more rarely on the forearms.
A very interesting case was one where it had occurred
under the nails of both hands and feet, before admission.
When first seen it was beginning to clear up, but showed
as a brownish discolouration under the nails. The ac-
companying photograph (Plate VIII, Fig. B), shows
the lesion during the process of clearing up. The
hemorrhages are almost undoubtedly due to the
rheumatoidal toxic poison inducing anemia with dila-
tation of the blood-vessels and extravasation of their
contents.

(e,) Angio-neurotie dema has been noticed in rheu-
matoid disease as occurring in patches, often near a
joint, but usually near a joint not affected by the disease.
It is usually characterized by some burning and pricking
and by itching.*8

3. Symptoms due to abnormalities of the nervous
system. Now, although strictly speaking almost all, if not
all, the secondary symptoms are due to derangement of
the nervous system, yet I have chosen for obvious reasons
to describe them separately under the various systems
in which they occur, leaving only neuritis and the more
miscellaneous trophic changes to be considered under this
heading.

(a,) Neuritis is a fairly common complication, and
usually arises from inflammation spreading from the
joint to the nerves in the proximity, more rarely from
the effect of toxins on the nerves themselves. Its most
prominent symptom is pain along the course of the nerve,
with atrophy of one or more muscles. This may become
extreme. Faradic irritability is lost, but that to voltaism is
increased in amount and often, but not always, altered in
124 RHEUMATOID ARTHRITIS.

quality. In slight cases the increase of voltaic irritability ,
may be trifling. In the nerves the irritability to both
currents lessens and is ultimately lost. There is’ a
tendency for it to spread to other branches, and nerves,
and to gradually affect nearly all the muscles of the limb.
Muscle-reflex action (myotatic irritability) is invariably
lost. The muscles in these cases are paler than normal
and smaller-in bulk. The fibres are reduced in size, and
are pale in colour; the transverse striation may be pre-
served or they may be granular; and the nuclei of their
sheaths and interstitial tissue may be increased in
number. These cases differ much from the ordinary
cases of rheumatoid arthritis, and often give rise to
difficulty in arriving at a diagnosis.

Apart from the direct spread of inflammation from the
joints to the nerves, the neuritis may be caused by the
poison generated by the micro-organisms. Recent re-
searches prove that it is these poisons, and not the
organisms themselves, that act on the nerves. The fact
of symmetry helps to prove that it is a cause acting
through the blood, and the selective action as seen is
also typical of the action of toxic agents upon various
parts of the nervous system.

(b,) Other trophie phenomena.—We best see that some
disturbance of the trophic function of the nerves has
taken place, from the symptoms due to vaso-motor
disturbance. It is probably due to this that we have
those cold clammy blue hands, evidently a local asphyxia,
with sweating of the palms, pigmentation, etc. Along
with these, but more rarely, we see local erythema and
congestion. Occasionally distinct areas of atrophy of the
skin have been observed ; perhaps one of the most marked
and most common forms being that known as “ glossy
skin.” This condition was first described by Paget, and
more recently by Mitchell. The skin, in this condition,
SYMPTOMS. 125

looks as if it had been varnished, and much resembles
a chilblain on a big scale, or else a highly polished sear.
The hairs for the most part disappear. The affected skin
is smooth, hairless, almost devoid of wrinkles, pink in
colour, and glossy. In contra-distinction to this we often
see a recent growth of downy hair, especially on the fore-
arms. Again, we may see a condition of scleroderma.
In this condition we have patches of skin, white and
ivory-like, indurated, and stiffened, and as if frozen.
The skin may be bound downto the tissues underneath,
and may impede movement, and cause deformity; the
papilla of the skin being flattened, the cutis thinner than
usual, and composed of more homogeneous connective
tissue, and the skin as a whole is less fibrous than in
the normal. The hairs gradually disappear until a con-
dition of alopecia is observed. Along with this atrophic
condition a certain amount of chronic inflammation is
seen, as evidenced by the abundant nuclei in the altered
skin, principally around the vessels, and sebaceous glands,
and in the rete Malpighii. (idema of the subcutaneous
tissues, especially of the legs, has been observed by
Vidal, 92 and Charcot,33 unaccompanied, however, by any
cause which would ordinarily give rise to it. The nails
may become brittle, and deeply ridged in the longitudinal
directions. Hadden * has described ulcerations of the
fingers, and wasting of the soft parts is pretty common.
Fagge * mentions cases in which fibrous nodules occurred
some distance away from the diseased joints, as in the
muscles of the arms and forearms. They must be dis-
tinguished from ordinary rheumatic nodules. Colombel *
also mentions various trophic changes, especially of the
skin.

4. Abnormalities of the integumentary system.

(a,) Increase in the ehromatogenous functions of the
skin. Dr. Spender® first drew attention to this.
126 RHEUMATOID ARTHRITIS.

phenomenon. The pigmentation varies from light yellow
to a deep bronze colour, ‘and it may occur in small
freckles, or in large blotches. It is most usually seen
on the forehead, temples, eyelids, hands, forearms, or
front of the legs. The freckles are round as a rule,
sharply defined from the neighbouring skin, are not
raised, but have a tendency to symmetry. When they
occur as blotches they are darker in colour, and are not so
symmetrical, except on the face, where they often sur-
round the eyes, involving the eyelids and spreading out
on to the forehead. The onset and clearing up of these
pigmentations can often be watched if the patient be kept
under careful surveillance for some period of time, and:
are of use as giving some indication of the patient’s
condition.

(b,) Sweating.—In most cases at one Pie or another
we sec abnormal sweating. It may be a mere dampness,
or else it may be so excessive as to make the skin wring-
ing wet. It may be limited to one portion of the body,
such as the palms of the hands, soles of the feet, face, or
forehead, or it may be general. Although dripping with
perspiration, yet the patient’s skin feels cold, and almost
deathlike, and they always complain of coldness of
the extremities. These are blue or of an unnatural
whiteness.

5.—The symptoms referable to the alimentary tract are
probably of less significance and are more of the nature
of a complication than those of the other systems, but
still in the large proportion of cases we find some alimen-
tary derangement. This usually takes the form of gastric
disturbance, accompanied by flatulence, and acid eructa-' ;

tions. The bowels are almost always confined, and there ’

is sometimes a tendency to vomiting. The importance

of these disorders is appreciated when we know that —
most of our treatment now-a-days is directed to improv- =
PROGNOSIS. 127

ing the patient’s general health, and to assist in the
elimination of toxic products, a thing we cannot do if
the digestive arrangements are out of order. It is also
of importance to remember that this may be the route
through which the micro-organism gains its access to
the system generally.

The urine is as a rule normal, but in some cases Money: a8
found excess of urea and uric acid, and occasionally
transitory glycosuria. This excess of uric acid is denied by
most authors, and I have never found it. Drackmann *°
noted a diminution of the phosphates excreted; Bocker
found a diminution of phosphate of calcium in the urine,
but there was four times as much found in the blood.

Apart from the cardiac conditions the principal visceral
complications are due to the occurrence of such diseases
as pneumonia, bronchitis, phthisis, interstitial nephritis,
ete. Sclerotitis, iritis, and conjunctivitis occasionally
occur. Deafness, due to the ossicles of the ear being
affected, and aphonia, due to the implication of the
arytenoid cartilages, sometimes are seen. Certain skin
affections, apart from those already mentioned, such
as psoriasis, have been described as occurring in rheuma-
toid arthritis, but their presence is probably nothing
more than an accidental occurrence.

II.—Proenosis.

With régard to prognosis little can be said of an en-
couraging nature, if we look forward to a perfect cure.
Once a joint is destroyed, as it rapidly is, we can never
make it as of old. Cases seen early may be completely
cured, but once destruction of the cartilages has occurred
I see no possibility of this occurring. One can subdue
the acute stages, but still we have left the hardening,
and thickening, the pain, stiffness, difficulty of move-
ment, and a certain amount of crippling. Still it
128 RHEUMATOID ARTHRITIS.

is marvellous what can be done, and I would never say
that any case is absolutely hopeless, for by care and
proper treatment the pain can be alleviated, and life
made more bearable both to the patients themselves and
their immediate companions. At the worst, the com-
plaint is rarely fatal to life; but what is life if one is a
total cripple, a trial to one’s self and to all about one?
On the whole I would say that the hope, to make the
joint, or joints, as good as they originally were, is futile—
it cannot be done, but we can relieve pain, subdue the
destructive elements, and leave only the actual joint —
changes to be combatted. These are no small mercies,
and, in the near future, we may hope for even greater
successes. One warning I would give, and it is, take .
the disease in time, take it in its earlier stages, and you
will reap an adequate reward in the relief you have
obtained for the sufferer, and in the knowledge that
you have subdued what has hitherto been regarded as
an altogether incurable complaint.

 

REFERENCES.

Howard.— Pepper’s Syst. of Pract. Med.,” 1885, vol. ii.,
p. 88.

Homolle.—‘ Dict. de Méd et Chir. Prat.,” 1882.

Garrod.—‘‘ Rheumatism and Rheumatoid Arthritis.”

Spender.—“ Osteo-arthritis,” 1889. /

Baker, Morant.—“ St. Barth. Hosp. Rep.,” 1885, xxi.

Charcot.—“ Thése de Paris,” 1858.

Haygarth.—“ On Nodosity of the Joints,” 1805.

Ord.—“ Trans. Clin. Soc.,” 1879, xiii, and ‘“ Brit. Med.
Journal,” 1884, vol. ii.

9. Jaccoud.—* Lecons de Clin. Méd.,” 1867, lecon xxiii.

10. Duckworth.—‘‘Treatise on Gout,” 1889.

11. Charcot.—‘‘ uvres Complétes.”

12. Trastour.—“ Thése de Paris,” 1855.

13. Beau.— Gazette des Hépitaux,” July 19, 1864.

14. Romberg.—‘ Klinische Ergebnisse,” 1846, and ‘“ Klinische

Wahrnehmungen,” 1851.
15. Todd.--“ On Gout and Rheumatism,” 1848.

PAM Rw ps
16.
17%.
18.

19.
20.
21.
22.
23.
24,
25.
26.

a7.
28.
29.
30.
al,
32.
33.
34.
35.
36.
37.
38.
39.
40.
41.
42,
43.
Ad.

PROGNOSIS. 129)

Trastour.—Loc. cit.

Beau.—Loc. cit.

Ball.—‘‘ On Rhumatisme Viceral,” ‘‘ Thése de Paris,” 1866,,
p. 121.

Besnier.—‘‘ Dict. Encyclop. des Sciences Méd.,” 1876.

Garrod, Sir A.—‘‘ Gout and Rheumatic Gout,” 1876.

Howard. —“ Pepper’s System of Medicine.”

Payne.---“ Brit. Med. Journal,” 1883, vol. i., p. 622.

Duckworth, Sir D.—‘‘ Clin. Trans.,” vol. xvi., p. 52.

Pitt.—‘ Clin. Trans.,” vol. xxvii., p, 54.

Bonnet.— Traité de Maladies des Articulations.”’

Tessier.—‘‘ Memoirs sur les effets de Vimmobilité longtemps.
prolonge des Articulations.”

Gowers.—“ Diseases of the Nervous System,” vol. i., p. 498..

Ballet.—Quoted Garrod, loc. cit., p. 256.

Charcot.—Loc. cit.

Spender.—Loc. cit. Z

Bristowe.—“ Brain,” vol. x., 1888.

Vidal.—‘‘ Thése Inaugural,” 1855.

Charcot.—Loc. cit.

Hadden.-—-‘‘ Trans. Med. Soc.,”” New York, 1886.

Fagge. —“ Principles and Practice of Medicine,” vol. ii.

Colombel.—‘‘ Thése de Paris,” 1862.

_ Spender.—Loc. cit.

Money.—‘‘ Lancet,” 1887, vol. ii., and “ Brit. Med. Journal,’”
1888, vol. i.

Drackmann.—‘ Nordisht. Med. Arch.,” 1873, vol. v., p. 1.

Still.—* Allbutt’s Medicine,”’ vol. iii.

Playfair.—“ Edin. Hosp. Rep.,” 1898, p. 114. ;

Norton.—‘‘ New York Med. Journal,” Jan. 30, 1897. ba

Hall, etc.—‘‘ Brit. Med. Journal,” Feb. 20, 1897.

Casselberry.—‘‘ Centralblatt f. Laryngologie,” vol. xi., p..
255. '

 
130

CHAPTER VI.
TREATMENT.

Preliminary considerations—Antitoxin-—Causes—Diet—Clothing
—Exercise—Drugs— Creasote—Guaiacol—Guaiacol Carbonate
—Benzosol — Phenols— 6-Naphthol —Betol— Salol— Action of
Creasote-—Hudeod—Douglas Powell—Intestinal Antiseptics—
Iron — Arsenic — Iodides — Salicylates — Actzea Racemosa —

Ichthyol—Hyoscyamus -—Relief of pain—Dr. Spender’s treat-
ment—Guaiacol externally—Carbolic Acid applications—Elec- .;

tricity—Thermal treatment—Alkaline and Sulphur Waters—
Bath—Aachen—Action of Bath Waters—Bath treatment—Aix
treatment—Hot Air Baths—Sea Voyages—Extension—Excision
—Summary.

Untin quiterecently, certain forms of Rheumatoid Arthritis |

have been regarded as not only quite incurable, but also
almost impossible to alleviate. So far from this being the
case, I believe all cases, if recognised early, are curable,
and if, in the later stages, not curable, yet the attack can
be arrested, and further damage prevented. When much
disorganization of the tissues, soft and hard, of a joint
has already taken place we of course cannot renew them,
and make them as of old, but we can arrest its spread,
and we can alleviate suffering, and by improving the
general health, give greater ease and comfort—in fact,
the activity of the disease being subdued we have only
the permanent destruction and disorganization left to
deal with. This has been brought about partly by our
better comprehension of the nature of the disease, and
partly by newer methods of treatment. Now that we

know it is a parasitic disease, our way. becomes clearer,

and we have, at last, a definite aim in our methods and

aa

* beac,
TREATMENT. 131

modes of treatment. The discovery of micro-organisms
as a cause is too recent for us to have yet found aff anti-
dote, but Iam in hopes that before long one, having as
powerful an effect for good, as that of diphtheria, will be
found. As the question of immunity depends on the
neutralization of the bacterial toxins the actual destruc-
tion of the bacteria is a secondary matter to the dis-
covery of some chemical agent having neutralizing
power. Meanwhile, and until we obtain the necessary
agent, we have to content ourselves with some of the
newer drugs with antiseptic and eliminative properties :
and these in conjunction with dietetic and thermal
treatment have yielded such remarkable results that I
consider the future full of promise. I am speaking
of pure: cases of rheumatoid disease, and not of
‘“Malum coxe senilis,’’ a most important fact to re-
member.

Before considering the treatment proper, it is of impor-
tance to bear in mind that one of the first considerations
which any medical man, called upon to treat this affec-
tion, must deal with, is the cause or lesion through which
the poison has gained access to the blood. In this
respect it differs from those diseases of which diphtheria
is a type, in that, in them, the disease can be attackec
at the seat of inoculation; whereas, in intra-joint disease
the organism can only be sustained while it elaborates
its antitoxins, and marshals its leucocytes to do battle.
with the invading legions of inimical micro-organisms.
During the course of treatment one must carefully guard
against anything likely to lower or debilitate the system.
The importance of this is understood when we remem-
ber, that it is only when the general constitution is
lowered that the insidious onslaughts of micro-organisms
are likely to prove successful. And thus when we glance
at the causes which make patients liable to the disease, we
132 RHEUMA TOID ARTHRITIS.

see what a great réle debilitating agencies play, and how
it becomes of the utmost importance, by the most careful
scrutiny of the past, and of the family history, to check
those agencies before they can do, further harm. By
‘such enquiries one is usually led to an offending organ
or function, by the rectification of which, we, as far as
possible, not only improve the general health, but pre-
vent further infection.

We may now proceed to the consideration of the
principles of treatment, as we understand them,
dividing them into three sections: (I,) Diet, clothing,
etc.; (II,) Drugs; (IIT,) Thermal, electric, and surgical
treatment.

I.—Diet, CLorHine, ETC.

(a,) Diet.—No more fatal mistake can be made than to |
place a patient on what is popularly known as ‘‘low diet.”
This course was for years followed with disastrous results,
in consequence of the belief that the disease was to a
greater or lesser degree due to gout. Such we now know
not to be the case, and the diet must, as far as possible,
resemble that which one would recommend for that worst
of all wasting diseases, namely, phthisis. Of course,
where considerable febrile disturbance exists care must
be taken to give suitable liquid nourishment until the
febrile state has passed. With this proviso the diet
should be of a nourishing, as well as of a mixed character.
The practice of limiting the amount of nitrogenous food
is not beneficial—in fact, as much nitrogenous food as can
be digested should be given—care being taken to correct
any functional derangement of the digestive organs.
Fats are an important item, and above all in this class
stands eod-liver oil, which should be regarded not as a
medicine, but as a food, and should in conjunction with
maltine be given at the termination of every meal. Of
TREATMENT. 133

vegetables, Spanish onion and celery are the best.
Stimulants should be ordered, but not more than will
stimulate the secretion of the gastric juice—malt liquors
and good wines being preferred. Hach individual
case must be treated by itself, and no hard and fast
rules can be laid down—the physician must exercise
his own discretion. A good diet list is the follow-
ing :— '

May take Soups: Bouillon, mutton, chicken, oyster, turtle,
barley, rice, bean, pea.

Fish; All that agree—boiled, baked, stewed or broiled.

Meats: Beef, broiled or roast ; lamb, roast or broiled ; mutton,
roast or broiled ; poultry, roast or broiled; game; sweetbreads ;
predigested meats (beef, peptonoids, sarco-peptones, peptonized
beef-tea, essence of beef, beef jelly, etc.).

Eggs raw (and with whiskey, milk or sherry, sweetened),
poached, boiled.

Fats and Oils: Mutton, beef, butter, olive oil, cod-liver oil.

Vegetables: Greens, lettuce, celery, spinach, asparagus, cresses,
cauliflowers, onions, tomatoes, green peas, beans, lentils, and
other leguminous vegetables; rice, well cooked, sparingly ;
radishes ; potatoes, in their jackets, very sparingly.

Bread: Wheat and gluten bread, toast, milk toast. Bread
should be at least one day old, and only a small quantity.should
be taken.

Fruits, Nuts, etc.: Oranges, lemons, pears, apricots, peaches,
grapes, fresh figs, and dates ; baked apples sparingly, and avoid
them raw ; walnuts, almonds, filberts, sparingly.

Drinks: Boiled water, Apollinaris and other carbonated waters,
hot milk, cream, milk punch, egg-nog; peptonized milk, lemonade,
ginger ale, sherbet; alcoholic drinks as prescribed (brandy, whis-
key, wines, and malt liquors); malt preparations; coffee, cocoa,
chocolate, tea sparingly and weak.

It is important to take food often and at regular inter-
vals, care being taken that not more than three hours,
except during sleep, passes without food. A glass of
milk, or milk punch or liquid peptonoids, should be
placed within easy reach in case of waking during
the night.
134 RHEUMATOID ARTHRITIS.

During the day the following arrangements can be
followed :—

7.30 a.m., and while still in bed, patient should have a cup of
milk, with a dessert-spoonful of whiskey, brandy, or other stimu-
lant, or with a small quantity of tea, cocoa, and a small piece of
bread, toast, or biscuit. :

8.30-9 a.m., breakfast of milk with a little tea, coffee or cocoa,
toast or bread and butter, bacon, ham, fish, or eggs.

11 a.m., a tumblerful of milk,a cup of broth or beef-tea, or a
sandwich, and a glass of wine.

1-1.30 p.m., a substantial meal of meat, poultry, fish, or game,
with fresh vegetables, some light pudding or cooked fruit, and a
glass of wine or malt liquor.

4 p.m.,a glass of milk with a small quantity of tea, coffee, or
cocoa, and some bread and butter or a plain biscuit.

7 p.m., another substantial meal similar to the mid-day one.

9.30-10 p.m., a cup of milk or bread and milk, or milk with
some farinaceous food, such as Nestlé’s, Mellin’s, or Liebig’s, etc.

(b,) Clothing. —The body must be encased in light wool-
len garments, worn if possible next the skin, care being
taken not to over-clothe. A thin flannel vest and drawers
with a piece of wash-leather inserted inside the fabric,
next the skin, over the joints, is a most excellent plan.
The feet must be carefully guarded, especially in damp
weather. All undue exposure to damp and cold, it is
needless to say, should be avoided, and the patient must
be warned, if possible, not to expose himself during east
and north-easterly winds.

(c,) Exercise.—During an acute attack, of course the
patient should be confined to bed. As a rule this is
unnecessary during the more chronic stages, a moderate
amount of exercise being of advantage. If not able to
walk, one should be careful to see that a sufficiency of
fresh air, either by carriage-driving or in a Bath-chair is
obtained. The use of carefully regulated and graduated
gymnastics and special movements, passive exercises,

“the use of pulleys, weights, etc., are all of benefit.
TREATMENT. ; 135,

I].—Drues.

Almost every drug in the Pharmacopwia has at one
time or another been used in this most intractable com-
plaint, and all with more or less indifferent success. As.
these all, one after another, failed me, I turned to some
of the newer drugs whose properties as antiseptics.
and eliminative agents appeared to promise success..
After prolonged trial and experimenting, my results:
and deductions have led to certain facts being
ascertained.

Treatment by drugs may be divided into three
classes :—

A.—Those substances which when administered internally
are antagonistic or antidotal to micro-organisms, or to:
their products, or which enter into conjunction with
them and thereby assist in their elimination.

B.—Those substances (1) which act by improving the
general tone of the organism, and help it to resist the
inroads of micro-organisms; and (2) those whose:
action igs more or less indefinite, and which have been
given empirically, and to relieve symptoms, and

C,—Those substances which are of use when applied
externally.

A.—Those substances which are antagonistic or antidotal
to the micro-organisms or to their products, or which enter
into conjunction with them and thereby assist in their:
elimination.

In this group we have three sets of substances which
from their nature give promise of benefit in rheumatoid
arthritis. The drugs in each set enter into combination
with various organic acids, and the resulting substances.
have all more or less direct antitoxic action. Their action
varies in strength and efficiency according to the nature:
of their constituents. This is because their efficiency
136 RHEUMATOID ARTHRITIS.

‘depends on the rapidity of their decomposition after in-
gestion, and the rapidity of absorption after decomposi-
tion has occurred. Their primary action is undoubtedly
a direct local one, and they, to a greater or lesser extent,
counteract bacteria, and their products. After absorp-
tion they act more as eliminative substances entering
into combination with the toxic albumens, thus favouring
their elimination. The longer the substance takes to
decompose the greater its local action, and, in inverse
ratio, the greater the rapidity of decomposition the
greater the rapidity of absorption and _ eliminative
‘power.

The three sets of substances I have tried and experi-
mented with are :—

1. The ereasotes or guaiacols which enter into

combination with carbonic acid yielding ereasotal,
guaiacol carbonate, and with benzoic acid yielding
benzosol.

2. The phenols which enter into combination with

salicylic acid yielding salol and salophen; and

8. The naphthols whith enter into combination with
salicylic acid yielding betol, and with benzoyl chloride
yielding benzonaphthol.

I have employed these substances largely in the treat-
ment of this disease, and out of them all I have found a
few of real use; the principal being those belonging to the
ereasote and phenol groups, probably from their quicker
decomposition and greater eliminative powers. Those
belonging to the naphthol group are practically unab-
sorbed, and act almost entirely locally. From my
experience, I should say that it is the bases in all cases
which are of use, and not the acids with which they
combine. This is specially noticeable with the salicylic
acid combinations,’ which instead of being the most
useful, as one might fairly expect, are, except in the
TREATMENT. : 137

case of salophen, the most useless. The following are
of use: (1) Creasote; (2) Creasotal; (8) Guaiacol;
' (£4) Guaiacol Carbonate ; (5) Benzosol; (6) @-Naphthol;
(7) Betol; (8) Salophen, and, to a less extent,
(9) Salol.

My conclusions may be briefly summarised. The
ereasotes would appear to have a more or less specific
action on the disease ; whilst the phenols, with the ex-
ception of salophen, appear to be indifferent and useless ;
but the naphthols, by their intestinal action, apparently
are of much use in a few cases.

The question now comes to be, How do the creasotes
and their compounds act? It is supposed that they,
their compounds and derivatives, have not, more than
any other drug, any specific action on micro-organisms.
According to Hudeod! they act not as antibacillary
agents, but rather by setting up a substitutive irritation
which successfully opposes the microbic inflammation.
Dr. Douglas Powell? says that although creasote has
little direct action, yet it has an indirect germicidal
function. Others have stated that they act on the
system generally, having no direct influence, by means
of the stomach or by improving the general nutrition.
They act locally, we know, on the alimentary canal
before absorption, and afterwards by favouring the elim-
ination of the toxic aloumens with which they combine.
Whilst in the gastro-intestinal tract they act on the
mucous membrane as well as on the intestinal contents.
As absorption proceeds their virtue as local antiseptics
diminishes. It has been proved impossible to sterilize
the blood, even after large doses (Hoelscher *), so it is by
their secondary action that such drugs are more especially
valuable. This may be so, but has it not been too readily
assumed that these drugs have no direct action on the
micro-organisms themselves? May they not to a great
138 RHEUMATOID ARTARITIS.

extent impair their power-to grow and multiply if
they cannot actually destroy them? One of the argu-
ments in favour of the disease being caused by micro-
organisms, is this fact, that creasote and its allies are
of use. To be of use, fortunately for suffering humanity,
if is not necessary for a drug to destroy the micro-
organisms but only to counteract their products, as all
pernicious symptoms due to micro-organisms are pro-
duced by the deleterious effects of their products, and
not simply by the mechanical presence of the bacteria
themselves. It has been proved that the best antiseptics
for the stomach are bismuth and charcoal; for the small
intestine, salol, sodic salicylate or benzoate; and for the
larger bowel, @-naphthol and charcoal (Bates‘*). -
naphthol has proved of special value, as on it the
patient’s general health has greatly improved, as well as
the joint pains and swellings. Salol and betol appear
to be less active than their bases, and they are not so
remarkably useful as to encourage me in their further
use.

1.—The Creasotes.

The creasotes are the drugs par excellence for rheu-
matoid arthritis, and without which one would feel help- -
less indeed, and one would drift back into that. slough
of despond in which for years those much in contact
with this disease have been. Now, however, I hope a
new era is dawning, and that at last we see a ray of
light to lead us onward.

(a,) Creasote’”™ (pure beechwood creasote) may be
used in small doses, beginning with 2 drops and
gradually increasing the dose to 15 or 20 drops, divided
into three or four doses each. It may be given made
up with alcohol, with some flavouring material, with
cod-liver oil, or preferably in capsule. Creasote, although
a complex body, has for its largest constituent guaiacol,
TREATMENT. 139

and to whose agency it owes most of its efficiency. It is
strongly tasted, and has a most pungent odour. It is
liable to cause nausea, gastric irritation, and to take
away the appetite. Its use therefore is not unattended
with difficulties.

(b,) Creasotal (Creasote Carbonate).—Through the
union of creasote with carbonic acid we obtain a neutral
material of a mild, oily taste, almost odourless, and non-
caustic. It is as efficacious as creasote itself, and can be
given in larger doses than the pure creasote. At
ordinary temperature it is a thick fluid of an amber
colour, soluble in alcohol, but insoluble in water. It
may be given in doses of 15 to 20 drops daily.

(c,) Guaiacol 1° (OH. C, H,. OC,), the principal constit-
uent of creasote, has also a pungent taste and smell, and
its administration is followed by the same drawbacks as
that of creasote. Since the discovery of some of its
compounds and derivatives, it has been less frequently
used, but the benefit derived from its use is undoubted.
It is best administered in capsules, or else dissolved in
some form of tincture, in daily doses of mxx and over,
and continued steadily for months. Should it not be
bearable by the mouth, it may be administered hypoder-
mically, as is recommended in phthisis by Dr. Picot,*
of Bordeaux, and others. Administered thus it acts by
reducing the temperature, causing a profuse sweating
and allaying pain. Sciatica and supra-orbital neuralgia
have been treated so with marked success by Anders.”
He used mij of guaiacol in mx of chloroform. Cham-
ponniére?? used 10 centigramme doses dissolved in
sterilized oil, and found it acted as a local anesthetic
as well as an analgesic. I have not, as a rule, found this
hypodermic medication necessary. As an analgesic I
always obtained success when applied externally, and,
for its other properties, as its compounds are as active,
140 RHEUMATOID ARTHRITIS.

and are much more easily administered and assimilated,
when given by the mouth, one usually prefers to use
them.

(d,) Guaiacol Carbonate is an insoluble, tasteless,
odourless, white crystalline powder. It has none of the
unpleasant effects of creasote or guaiacol, which are so
‘able to irritate the stomach, and to destroy the appetite.
- It is slowly decomposed in the bowels, yielding guaiacol,

which is absorbed into the blood, and carbonic acid.
Within half to one hour after ingestion the guaiacol can
be traced in the urine. It is by far the most useful of
the whole series, but from its expense it has not been
used so generally in hospital practice as it might have
been. It is easily taken by the mouth either in powder,
in pill, or in cachet. It is the drug on which I place
most reliance, and in few cases have I found it ulfi-
mately to fail. It has now come to be my routine
treatment, and I employ it in all cases, where active
disease. exists, in doses of grs: v—x, repeated three to
four times daily. In no case have I seen any symptom
of intolerance, nor have I noticed any evil effects
produced.

Decomposition and abaorptien of the guaiacol carbon-
ate takes place throughout the entire length of the small
intestine. The process is a slow one. But the excretion
of the guaiacol after it has reached the circulation is a
rapid process. Frequently the urine shows the charac-

‘teristic guaiacol reaction within half an hour after the
ingestion of the drug; and the process continues for
hours. The amount of guaiacol in the blood at any one
time is small, and the action of the drug on the general
system is a mild one, and cannot become dangerous even
when the largest doses are given. The treatment of the
disease is, therefore, a much more intensive one than
with most other preparations, for a small quantity of
TREATMENT: 147

guaiacol is continually kept in the body fluids. The
guaiacol leaves the body as an ethereal sulphate.
Hence we may assume that during absorption the
guaiacol combines with the albuminous elements of
the blood, by means of the sulphur contained in the
albumin molecules. This union of the guaiacol with the
albumins takes place more especially with those of them
that are distinguished by their chemical reactibility.
These are of course the very poisonous albuminoids
called the “labile albumins,’’ which are caused by
bacillary life action. ’

This union of the bacillary products with guaiacol is
at once changed by the advent of oxygen. The guaiacol
with the sulphur leaves the albuminous molecule, and the
-remainder undergoes further change, and these products
are eliminated chiefly by the kidneys. Thus guaiacol
carbonate unpoisons (if one may coin a word) the blood
continuously. The body itself, freed from these poisons,
regains its liberty to devote all its energy to the destruc-
_ tion of the micro-organisms.

(e,) Benzosol (Benzoyl-Guaiacol C,, Hy, 05), is a taste-
less and odourless body which splits up into guaiacol,
and benzoic acid in the digestive tract. It was intro-
duced for use in phthisis by Dr. Walzer. It is insoluble
in water, but is so in the gastro-intestinal tract, slightly
in the stomach, but principally in the small intestines.
It is very little soluble in glacial acetic acid, but is
soluble in chloroform, ether, and hot alcohol. The dose
is grs. vj, repeated three or four times a day. It is also
of much use, but appears to be slightly less active than
the carbonate.

Owing to the nauseous taste, disagreeable eructations,
and gastric irritation set up by creasote and guaiacol,
they are now seldom used internally. More often we
use guaiacol carbonate and benzosol. The effect of any
142 RHEUMATOID ARTHRITIS.

one of the group is to improve the appetite, relieve pain,
lower the temperature, stop all inflammatory process,
and to improve the joint conditions. The patient sleeps
better, gains flesh, pigmentation and other vaso-motor .
anomalies improve, the hands are no longer cold and.
dripping with perspiration, and the patient can move
about with a great deal less pain, and more comfort.
The patients’ general appearance also undergoes change,
they are no longer anemic, anxious, and full of fancies,
but say and look as if they were on the road to
recovery. Of course such results are not obtained in
a day, and are only brought about by the most careful
combination of drugging and thermal treatment. With
regard to the drugs, benzosol. is often more immedi-
ately- followed by relief of pain; but for long continued
and severe cases, the carbonate is the more to be-
relied upon.

2.—The Phenols. ; .

(a,) Salophen, a salicylic ether of acetylpara-amido-
phenol, contains 51 per cent. of salicylic acid. It is a
crystalline, tasteless, odourless, white powder with a
neutral reaction. It is insoluble in cold water, slightly
so in hot, but dissolves readily in alkaline fluids and
fairly well in alcohol and ether. It is not changed in
the stomach, but in the intestines splits up into salicylic
acid and acetylpora-amidophenol. Its advantages over
salol are its freedom from taste and smell and its feebler
toxic action.

(b,) Salol in a few instances, combined with salicylate:
of quinine, has given good results, especially in cases
complicated by intestinal trouble. It is a valuable alter-
native drug, but cannot for routine treatment take the
place of guaiacol.

Apart from their local action in the intestinal canal
the phenols, like the guaiacols, form compounds with
TREATMENT. 143

toxic products in the blood and assist in their elimina-
tion.

3.—The Naphthols.

Betol, or Salicylate of @-naphthol, is a white,
lustrous, crystalline powder nearly inodorous, insoluble
in cold and hot water, soluble in boiling alcohol and in
warm linseed oil, decomposes in the intestines into
8-naphthol and salicylic acid. Betol is less active than
B-naphthol itself, and has therefore nothing to recom-
mend it. In all cases with intestinal disturbance,
8-Naphthol is unrivalled, and its action is certain and
safe. Given in v—x-grain doses the intestinal-canal, if
not rendered aseptic, is at least made less harmful, and
the further absorption of deleterious products prevented.
In about 5 per cent. of my hospital cases have I found
it called for, and the result has always been most
ratifying.

B.—Those substanees which act by improving the general
tone of the organism, and those whose action is more or less
indefinite.

Of this class the principal drugs are iron and arsenie.
It has not been stated even by the most ardent support-
ers of these drugs that they play any specific rdle in this
disease. On the other hand, they have only been recom-
mended as being those drugs which, from experience,
have been found most useful in so improving the general
health that the patient has been better able to with-
stand the inroads of the disease; and, as such, they are
no doubt of great use. They are best administered
combined with one another, either in the form of a pill
or else in a mixture. The best preparation to use, of
iron, is either the tincture of the perchloride, or the syrup
of the iodide. Many prefer a preparation of iron and
quinine, or of the ammoniated citrate. Arsenic may be
given as,the B.P. liquor, or as the liquor sodii arseniatis.
144 RHEUMATOID ARTARITYIS.

For the use of arsenic, we have the authority of Jenkin-
son, of Manchester, Beardsley, Charcot, Hilton Fagge,™*
etc. M. Noel Gueneau de Mussy recommended its use
externally in the form of arsenical baths. Iron alone, or
arsenic alone, is not nearly so successful as when the two
are combined.

Iodine, and the various iodides, are commonly held to
have a marked influence for good over the disease ;
iodide of iron being specially lauded as an agent of
great value. Sir A. Garrod and Dr. A. E. Garrod ® look
upon this drug as the most efficient we possess. It is,
however, probable that its usefulness depends mainly on
the iron and not upon the iodide. Whether iodide of
potassium, or even pure iodine, has any direct effect on
the course of the disease it is difficult to prove or dis-
prove, but, personally I have found little benefit from
their use. If they do act they, probably, do so by virtue
of their alterative or eliminative powers rather than by |
any direct action on the disease.

In a disease of such a nature it is no wonder we have
a large list of drugs, which have, at one time or another,
been recommended as sure and certain remedies. Of
these the following are a few: the alkalies, quinine, actzxa
racemosa, fraxinus excelsior, colehicum, etc., which have
been and still are recommended; but none of them are
of any lasting avail. Some have found benefit from the
use of the salicylates. Howard '* says that if sodii sali-
cylate is given in sufficient doses it promises well to be
.of more use, in the acute forms, or in the actively in-
flammatory periods and exacerbations, than any other
form of agent. Including See’s cases Compagnon ” has
related seveuteen cases, in many of which the pain was
relieved by its use, and its progress arrested: Actma
racemosa, according to Ringer, is of use in full doses,
especially if the uterine functions are disturbed.. Guaia-
TREATMENT. 145

eum has been recommended by many, and has occa-
sionally been found of use. Lorenze and others mention
iehthyol, but I have failed to obtain equally good results.
For the relief of painful muscular cramps, Dr. Garrod
uses hyoseyamus, with good results. Quite recently
Solis-Cohen ™ has used an extract of thyroid glands and
glycerine. The cases treated by him seemed to improve
slowly. Hyde” recommends the use of extract of joints.
I have tried this in a fairly large number of cases but
have failed to obtain any encouraging results.

C.—Those substanees which are of use when applied
externally.

These substances have been used almost entirely for
the relief of pain, and appear, except in the case of
guaiacol, methyl salicylate, and carbolic acid applica-
tions, to have little other action. Every known form of
counter-irritant has been tried, and of local applications
there is practically no end. Much of the good experi-
enced from their use has been the result of the friction
and massage associated with their application. Chili
paste; turpentine; paraffin oil; camphor; ammonia;
eajuput or eucalyptus oils; liniments of soap; ammonia;
compound camphor ; iodine ; eroton oil; turpentine; acetic
turpentine or mustard; have all been tried. Of locai
remedies for the relief of pain, the liniments of ehloro-
form, belladonna, and aconite in equal parts applied on
lint have often given ease. Dr. Spender paints a ring
of iodine one-and-a-half inches wide above and below
the joint. A eantharides blister may be tried on the
proximal side of the joint. Flannel dusted over with
flowers of sulphur is a popular remedy. Chaulmoogra oil,
cod-liver oil, oleate of mercury and morphine, unguentum-
hydrarg. eo., and others, have been used to rub into a
joint, or for strapping. All have their advocates, and all
are more or less inefficient. When articular pain is

10
146 RHEUMATOID ARTHRITIS.

severe, a local vapour bath or embedding the limb in hot

sand, as recommended by Trousseau, may give relief.

Guaiaeum plasters in the more chronic stages have been

known to relieve pain. With regard to this pain all the.
known hypnotics and analgesics have been at one time or

another employed with more or less success. Should the

local applications shortly to be mentioned not be success- ,
ful we have to fall back on the use of opium or morphia in
some of its forms, paraldehyde, chloralose, sulphonal, etc.
Opium or morphia, as being the most certain, is pre-
ferable, and one often finds that ‘after one or two good
nights the use of the hypnotic is no longer required.

The external treatment I usually follow is, either to
apply to the joints guaiacol and equal parts of olive oil;
guaiacol in the proportion of one to six of tincture of iodine,
methyl salicylate, pure or mixed with olive oil, or else
warm carbolic acid fomentations. One not only gives great
local relief, but, by absorption, the drugs have a beneficial
effect on the disease itself. Guaiaeol and methy) sali-
eylate, when applied externally, produce a numbness, a
sense of coolness and a feeling of relief. This effect
becomes more marked with every application, and the
joint condition often improves, simultaneously, in a most
unexpected fashion. But the great thing is the relief of
pain. Guaiacol was first used as an application to
painful rheumatic joints by M. Desplats. He used
equal parts of guaiacol and glycerine, and painted it on,
covering it with a dry dressing. In three cases of
arthritis deformans the results were excellent. To
mask the odour, oil of cloves is the best according
to Da Costa. Stolzeburg#® says this treatment is
accompanied by profuse sweats which it is unwise to
continue for any length of time. I have never noticed
these sweats. As arule I apply it in equal parts with
olive oil, or else with tincture of iodine, in varying propor-
TREATMENT. 147

tions, that of one to six being my most common one
(iodine 6, guaiacol 1). It increases the flow of urine, and
reduces the body temperature. Applied externally, ac-
cording to Drs. Linossier and Lanois” it is absorbed
rapidly, and can be easily detected in the urine. The
body temperature has been known to fall as much as 2°
after its application. Methyl salicylate, which must not
‘be confounded with oil of wintergreen, may be applied
pure as recommended by Sireday,” or else in varying pro-
portions with olive oil, as used by Roger.”” I usually use
it at first in the proportion of 3 to 1 of olive oil and then
pure. The preparation is applied to the skin and then
covered with gutta percha tissue with a flannel bandage
outside. Beyond a slight degree of redness it does not
appear to produce any unpleasant effects, and its
analgesic power compares favourably with that of
guaiacol. Carbolic acid I use in the strength of 1 in 40,
and apply it warm as a fomentation. This should be
renewed every two or three hours. It acts much in the
same way as guaiacol, reducing the temperature and
acting as a local anesthetic and analgesic. It is rapidly
absorbed, as can be traced in the urine. It is not quite
so efficient as guaiacol or methyl salicylate, but where
the former cannot be used, on account of their odour, it
is of use.’ It may also be tried with advantage in those
cases where they are not very successful, as occasionally
happens in acutely neurotic patients.

TII.—Euecrricat, THERMAL AND OTHER SPECIAL
Moves or TREATMENT.

4. Electrical Treatment.—The weak continuous current
(15 to 25 Leclanché cells), used twice a day, may be of
service. The sponge electrodes being well moistened in
hot salt and water, one is placed above the affected joint,
and the other over the skin at any part of the limb
148 RHEUMATOID ARTHRITIS.

distal to the joint to be operated upon. Even the induced
or interrupted current may be employed. I never use
either during the acute stages, but later on when the
disease has been subdued, and only weakness and
atrophy remain, I have found great benefit, especially
from the weak continuous current. Erb ” treated a large
number of cases by galvanism, and although having no
absolute cures he had met with occasional good results,
as far as improvement of the general state of nutrition,
and of the local troubles were concerned. He considered
it better to apply it direct to the spine than to the sympa-
thetics. When the upper extremities are mainly affected,
he passed the current through the cervical cord, and
when the lower extremities are the principal offenders,
the lumbar cord. It is recommended to continue the
treatment’ for several months, but few patients will
persevere with so prolonged a course. Dr. Steavenson
and Dr. Garrod both mention the use of the electric bath.
‘hey consider that it exercises a favourable influence
-over the course of the disease. A bath tub is used of
some non-conducting material, such as wood or porcelain,
and this is filled with water at about the normal tem-
perature of the body. A copper plate connected with the
negative pole is placed at the foot of the bath, and a
similar plate at the head is in connection with the posi-
tive pole. A galvanometer, measuring at least 250
milliamperes, is used. The strength employed is about
200 milliampéres, and it is computed that only 40: pass
through the body, while the remainder pass through
the water. The full current of 200 milliampéres is
used for about ten minutes. During the first six days
the bath is given daily, and afterwards every second
day.

2. Thermal Treatment.—Treatment by means of hot
mineral waters, and other accessories, is of the greatest
TREATMENT. 149

value. To the consultant the choice of a suitable thermal
water becomes of the first importance, but unfortunately
no fixed rules can be laid down. In some cases the
alkaline, or indifferent, and in others the sulphurous
waters appear to answer best. Of the alkaline, or indif-
ferent, Bath and Buxton in this country are the most
frequented. Owing to its situation Bath is much warmer
than Buxton in winter, and in the majority of cases is
more. suitable. In summer Buxton is preferred by
many. Of the sulphurous Strathpeffer has latterly
come to enjoy considerable repute as a summer resort,
whilst Harrogate still maintains its ancient character for
efficiency. Amongst the many other spas in this country
are Woodhall (Iodine), in Lincolnshire, and Llangammareh
(Bromine), in Wales, both of excellent service in certain
cases; but for the average case the indifferent or alkaline
waters are preferable. And of these, Bath maintains
its premier position. Abroad we have the thermal waters
of Wildbad, Carlsbad, Wiesbaden, Téplitz, Homburg, Kissin-

gen, St. Moritz, Bourboule, Mont D’Or, Aix-les-Bains,
Hammam R’Hira, and Hammam Meskoutin, and Arkansas,

Virginia, and Banff, in America. When anemia and de-
bility are prominent symptoms, the chalybeate waters of
Langen Sehwalbach, Rippolsau, Spa, Franzenbad, ete., arc
of use. At Aachen special attention is paid to rheumatoid
arthritis by means of douches and massage in conjunc-
tion with the general baths. Rademacker” has found
great benefit from this plan of treatment, even in
advanced cases.

The Bath thermal waters have been used for ages in
this as well as in other joint complaints, and have come
to possess a name and repute, for alleviating the symp-
toms of such disorders, second to none—in fact so much
so that due discretion is not always observed either by
the bathers or their medical advisers. Beyond all doubt
150 RHEUMATOID ARTHRITIS.

they are most useful in the early stages, and again when
the disease is subdued they come to be almost equally |
invaluable. But no greater mistake can be made than
to imagine that they will cure all and every condition.
I hold that alone, during certain stages, they, like all other
mineral waters, are not of the smallest use, but given a
proper and successful medication we derive much help
‘and good from them not only in alleviating symptoms,
but in counteracting the effects of stiffness, deformity,
and muscular weakness. I know of no waters, in this
disease, of more avail than those of Bath. It has been
said more than once that patients have derived no bene-
fit from our waters, but so it may be said of any waters.
Combined with suitable internal treatment, which must
often be of a prolonged nature, no case should leave Bath
unrelieved if not cured. But we must make it clear that
once a joint is disorganised no power on earth can renew
the diseased tissues. We may,alleviate and relieve pain,
give greater movement, and, in short, make life bearable,
but we cannot make a joint quite perfect—there must
always remain some symptoms to show how severe the
attack has been. In severe and advanced cases improve-
ment can only be obtained after months of treatment, a
period often most trying both to.the patient and the
physician in charge. These facts should in all cases be
laid before the patients and their friends to prevent
disappointment and discouragement in protracted cases,
which apparently make little progress, but-which in the
long run will usually yield to the means adopted for
their amelioration. This I consider to be our duty not
only to our patients but to ourselves as medical men.

At first, immersion in the Bath waters acts as a gentle
counter-irritant—the gentle excitation of the cuticle
being passed by reflex action throughout the body—
an increased oxidation and production of heat being the
TREATMENT. 150

result. The circulation improves, and the tissues receive
fresh supplies of blood to reinforce their vital powers.
Again, wet and dry douching stimulates. and exhilarates.
The latter has to be used with care, as where the joints
are sensitive it may do much harm. If practised as at
Aix-les-Bains much benefit may be derived from it, how-
ever. In Bath this system has been carried to high per-
fection, where the attendants are not only highly qualified,
but do their work with a thoroughness and care not often
met with. The massage or shampooing combined with
the douching has often a marvellous effect in the chronic

‘stages. By its means the muscles are strengthened
and further atrophy prevented, and it also seems to have
a soothing effect on the joint pains and nerves. Itis also
of use in the insomnia which so often accompanies rheu-
matoid arthritis. When practised dry it appears to have
a more exciting effect, and its results are not altogether
so good. Massage again, where walking is difficult or
impossible, keeps the muscles healthy and the skin ina
condition of activity. It may be employed along with
electricity, but certainly its best results are obtained
when it is carried out in a bath by a skilful operator. When
the attack is acute, only the lightest and slightest
massage is permissible. As the joints stiffen it
may become more forcible, and deeper, and should
be combined with passive movements, under which
treatment deformities and ankylosis often improve
and do well.

In Bath we have one of the finest bathing establish-
ments in existence, filled with all the necessaries and ac-
cessories so essential to the comfort of theinvalid. Bathing
may be carried out with or without the douche; douching
with or without wet or dry massage; local vapour baths ;
specially prepared mud, medicated and electric baths; and
baths and douches for special organs. The waters them-
152 RHEUMATOID ARTHRITIS.

selves are drunk not only on account of their constituents,
but from the fact that they help to wash out impurities
of the blood by flushing the kidneys; thus assisting the
elimination of toxic products. The baths also act ina
two-fold fashion, assisting the elimination of the toxic
materials through the skin and lungs, as well as assisting
in the improvement of the more purely mechanical
defects.

Care must be taken not to push thermal treatment to
such an extent as to debilitate the patient, and, therefore,
it is probable that the course should cover a long period,
with baths at considerable intervals, rather than a large
number crowded into a short time.

Should it not be possible for a patient fe go to a spa
for treatment, as, alas! too many cannot, by careful
bathing in an alkaline warm bath, much may be done at
home. Massage and rubbing can usually be obtained
anywhere, and gymnastics can be improvised. What
answers well is a gentle course of gymnastics, pulleys,
dumbells or elastic bands with handles, all of which if
not carried too far are of much use.

Within the last few years, the hot-air bath has been
used and found to be of much benefit, but only in the
more chronic cases, and where the disease is not
extensive. ,

Let us now for a moment glance at certain other
methods and systems of treatment for special conditions.
If pain, as we so often find it in the knees, be severe, and
apparently from the rubbing of the ulcerated cartilages
one upon another, the only method to deal with this is by
extension by weights. Where fluid is exuded we seldom
come across this difficulty, but now and again we see it,
and are often puzzled as to the best means of subduing
it. The weights should not be heavy, but should be
applied continuously. Again, should there be an excess
TREATMENT. 183

of fluid present it may be desirable to tap the joint, and
withdraw the fluid. I have often seen the mere fact of
puncture relieve tension and give ease. One should not
therefore be discouraged if no fluid is found. I find
patients once relieved by this means ask for it to be done
again and again. Should the jaws become either totally
or partially ankylosed we are on the horns of a dilemma.
If only partially ‘ankylosed, probably a series of small
blisters will relieve the difficulty (I never apply one
larger than a shilling piece). Should it be unrelieved, we
have to consider the advisability of exeision. This has
been done in several cases with fair success. It has
_also been practised on other joints, such as the knee or
elbow, where there was little power and great crippling.
In three cases I have seen the result, which was fairly
successful in two. In both, there was before operation
great deformity, and the limb was useless, not so much
from pain as from inability to use it. In both, bony
ankylosis ultimately resulted and there was no return of
the disease in those joints. Of course the other joints
remained in statu quo ante. In the other case, the pain
and disease returned within a few months, probably from
an insufficiently extensive operation. In a few cases I
have recommended the operation as desirable, but in all
it was declined. My personal knowledge therefore on
this subject is slight. In Germany surgical treatment
has recently become common, and successful results have
been reported by, amongst others, Madelung,” Miller,”
Felix Franke, and Schiiller.*! In some of the cases
reported by Schiiller, after the excision of one joint,
improvement followed in other affected joints.
Climate.—Whatever may be said, there can be no
doubt that those who can afford it should not winter in
this country. Egypt is par excellence the place for such
to winter in. Biskra and some of the other Algerian
154 RHEUMATOID ARTHRITIS.

health resorts are nearly as good. What one has to bear
in mind is that it is a dry warm atmosphere which is
required, not a dry or a damp cold one. The northern
Mediterranean sea-board, except during mild winters,
and except in a few spots, is not advisable. It is better
to live at home where all the comforts and necessities
are so much better and more easily obtained. . For those —
who have the time and money, a winter in the dry
Karoo of South. Africa is of advantage. I am not in
favour of a long sea voyage, nor yet of residing near the
sea. The moisture is invariably undesirable. A voyage
_ often, by mere rest and absence of anxiety, may do
wonders, but as routine treatment it is not advisable.

Such then is our armamentarium. Its constituents
are numerous and various, but although many are inter-
changeable, yet each has its own peculiar mission for
which it is best adapted. Every case must be carefully
considered, from every point of view, thoroughly in-
dividualised, and the treatment best adapted to obtain
the end in view firmly laid down and persisted with. A
disease which has been gradually coming on for months,
and of such a destructive character, cannot be expected
to yield to a week or two of treatment, however skilfully
devised or carefully carried out. Time is required, for
it is not by any dexterous legerdemain, but by skilful
application of remedies and by the steady accumulation
of trifling advantages that we are finally enabled to
subdue and overcome the enemy.

To summarise.—In the acute stages the patient should
be kept in bed, on a light nutritive diet. The joints may
_be kept at rest, on a light splint, and painted with guaia-
col and olive oil or iodine, or with methyl salicylate, or
else fomented with carbolic acid solutions. Internally
guaiacol carbonate or salophen should be given. If
sleep is not readily obtained this must be attended to,
TREATMENT. 155

as must also be the gastro-intestinal and genito-urinary
tracts. If the patient can stand it, light massage, and
baths for short periods, as may be ordered. As it be-
comes more chronic the patient is allowed up, and the
thermal treatment pushed—electricity and gymnastics
often now being useful. The diet must be carefully ©
supervised, the use of cod-liver oil and maltine being
indicated. Internally, the treatment as in the acuter
stages.

THE BATH THERMAL WATERS.

The springs which supply the waters of Bath are three in
number, giving a daily yield of 507,600 gallons, at a temperature
of 117-120° Fahr. If compared with other thermal waters of
Europe and America, we see that those of Bath stand high in the
scale.

EUROPE:
GERMANY,

Aix-le-Chapelle (Kaiserquelle) ..........0.00.cccesseeeeeeeeeseeees 131:0°
Baden Baden (Hauptquelle)
Hims (Kesselbrunnen) ........0.......06.cccccscceeeeeteseeeetstenee
Karlsbad (Miilbrunnen) ............0.. sc cceeeeeeceeeeceeeeeteteeeees
Karlsbad (Sprudel) ......... oe soeigcoen
Karlsbad (Schlorsbrunnen) .. as
Nuenahr (Mariensprudel) ............c:scccecseeeeeescceeneeeseeees
Schlangenmbad i. ...0i assesesewnacess evesesatasussacengrncrsan oveansaenen
Worm Dru eis 2c. sie sends vs pin sc cb06s veswereagmeamnenadd ds eateienateus
Wiesbad6tt css .0scevssicasereeeecenonies

Wildbad.  sevwcecncecenzatapcaseturoneasieeds va plalee smatmhadartaceoeasnsess

  
 

DAR veces cass senahaiwinnasnines ps ble sbine SicevinhereacuahameMecanaOede uaaminnclges
Monte Doré aod
Ba r6 Bess ajc ccewuisisnves dose vaca ee ranmieanni reatabonaneued re eentatebsee

 

Veatba Qiao. iis scivess wesses vvsasanssaiatedacsecdentaiennes ue neniweneenem
156 RHEUMATOID ARTHRITIS.

AustRo-HunGary,
Bad On: jee tnesccacaesesetty suse: etaes wate ddnenledeuamezcemanveuanaeeusa oe
Téplitz fiatptansliay = Beco doy con aur nenegietnreo wemtaaunbamanten a mnmiee y
GaSbele wisn ses casesuauassncetssavaetaginn a os os ta nt anachoasinantaba nema 87:0°
SWITZERLAND,
DCU sass eetenawnicaelnn eSeaa eigoeeae ee ead es odtedeeners dered AeA ates 123-°0°
ENGLAND
Bathiceseacics ds sraaasencaa cinta pn anaaeateciadigt tamaiceuapanacnstea ile 120-0°
BURG sa scenaapeijeostic vargas via coiaig iaasvu spap'ed samiete ig uiee ae eunies@nta Hes 82-0°
AMERICA :
Hot Springs, Garland, Arkamnsas............000....0000068 93-0°-150-0°
~ Chalk Creek Hot Springs, Colorado’ se. csscevinesseneeeomanesss 130°0°
_Des Chutes _,, és QLEGON 2... ese asec ees ss eaeeie 143°-145-0°
Madison Co. ,, 55 Ni CarOlnaic sscess sinushwecteetancenis 102-0°

If compared with the waters of Buxton, those of Bath are seen
to be much stronger :-—

 

In an Imperial Gallon. Bath. | Buxton.
Carbonate of Lime ................. cece cceeeeceeee eee 9001 | 9-185
95 "MASHESIS, op sicssscaanageanowes sialon ave 0°399 | 4:°746 5
EVOL, decane saxtnqaawreniaeneceeanraas 1:217 | 0:087
SOG: cs ccvewnxaa se sea eiuedeaegeaeenstiensts 15017 sae? ee
Sulphate of AmMonium ........... eee eeeeee eee e eens this 0-014
é, ILI Gs Se. acietuacusmtuadens ane wee acaat 69°984 | 0-673
5 Potash: —cvowvensicsnsaane marae es 6°702 | 0°678
35 Magnesia .........ccceeceeeeeeeeeeeeees 35°042 tes 5
Sod aij -—. s.vessarsaseasunteuenemay eghenies 23°140 | 0-202
Chloride Of SOU, vie cdcdsacesadencaeeessavisa cei 17°894 | 4:517
Potassium................ -Buauirte ooehae eee 1°823 aoe
Silicate OL SOC ai iiss ccasseaevatetan aesiveedoucenieanneanawstes 0:399 oe
Nitrite Of Lime, cass cst csesssieeesstenmenes v9 455 easascnan 1°562 | 0°266

 

 

 

In an Imperial Pint of the Bath Waters there is :—Oxygen 0°74;
Nitrogen 4°60; Carbonic Acid 4°17 cubic inches.

The total amount of solids in each pint of the Bath waters i is
168 grains. The amount of the gases, free and in combination,
TREATMENT. 157

is of the utmost importance, as they act as powerful stimulants
by the excitation of the cuticle which they produce.

. Compared with other waters we find the total amount of solids
In each gallon to be :-—

ISBIN GEN, eset geil eu ue vamoue cal cmansuiendtaapad ‘

ine ee
Bad OM bts sie sitisanionns aes Guan ve cated dewteeensactisiacoas sa dane ies 840-000
RATS DAG snag iclsneedi teh Sato setcsisioknth Acawsamnuteinaedeaenidanistea Cbiainc 496:071
Babs 3s a conten nteesoceeuieuenes cud cues ie ek sn eaapaaeheneel wale ane 168-400
Mont DOT E :aisdahce ori toiat sn Mowe ard 2a tenets cis talasesied Geese tisk oseakiase 114°360
LOPLGZS asics saaes vets soshte Mictawes sash yuo. seen demmataadensaiiaie Mune 48°740
Warm bean nen scicciegecets vast tal rece casalttinnnctdedeat si-useees 40°380
Wald bad ieesisinsce taeussscicancasdsatda suas abeeuuie’ deresats ousiicn simntae os vesg 35870
GEISHA Deis etcetera sete dare atc gi ok redone ies tata aan 26°680
RGM OEP bad seis caense.ca suhaah iSagaes ves wentniphbadentheneree undead ie 22°370
SPS UA Mie coistins etch ce ass wet Se erapree circ ted ao ah pee a taht cade ame 20°579
Blom DSPs 25303 eis 25 devas ou densities Neuse oda aavesuies eek clades 20°170

REFERENCES.

Hudeod.— Creasote et Tuberculose,”’ Genéve, 1893.
Powell, Douglas.—‘ Diseases of the Lungs.” p. 549.
Hoelscher.—“ Berlin. Klin. Woch.,” 1892, No. 3.

Bates.—‘‘ New York Med. Journal,” April 2, 1893.
Bouchard and Gimbert.— Gaz. Hebdomadaire,” No. 31,

1877, p. 488. .

Jaccoud.—'‘ Gaz. Hebdomadaire,” No. 31, 1877, p. 156.
Rosenthal.— Berlin. Klin. Woch.,” No. 32, 1888.
'D’Or.-—“ Rev. de Médicin,” February, 1890.

Rosenbach.—Uited “‘ Medical News,” April 28, 1888.
Flint.—“‘ New York Med. Journal,” July, 1890.
Bogdanovitch. Cited ‘ Brit. Med. Journal,” vol. i., 1888.

Sahli.—‘Correspb. f, Schweitzer Aertze,” 1887, No. 30.

Picot.— Semaine Médicale,” March 14, 1891.

Fagge, H.—‘‘ Principles and Practice of Medicine.”

Garrod.— Rheumatism and Rheumatoid Arthritis.”
Howard.—‘ Pepper’s System of Medicine.”

Compagnon.— De l'utilite du Sal. de Soude dans le Treat-

ment du Rhumatisme,” 1880.

Stolzeburg.——‘‘ Berlin. Klin. Woch.,” No. 5, 1894.

fuinossier and Lanois.— Union Médicale,” April, 1894.

Anders, J. M.—“ Therap. Gazette,” March 15, 1895.

21. Champonniére.—“ Bull. de Académie de Médicine,” July 30,
1895.

92. Erb.— Handbuch der Electropathie,” s. 648.

23, Rademacker.—“ Aachen als Kurart,” s. 111.

Re ee :
NPARBORSSHIS giRpH

wee
Soe
158

24,
25.
26.
27.
28.

29.
30.

81.

s

RHEUMA TOID ARTHRITIS.

Solis-Cohen.— Practitioner,” Sept. 1896.
Hyde.—* Rheumatoid Arthritis,” 1897.
Sireday.—“ Journ. de Méd.,” Aug. 25, 1897.
Roger.— Lancet,” vol. ii., 1897.

‘Madelung. —Quoted “Batimler Congress f. Innere Medicin, ?

Berlin, 1897.
Miiller.—“ Langenbach’s Arch. f. Klin. Chir, .,” B. 47, 1894.
Franke Felix.—‘‘ Abdruckan’s Chir. Beitr. Festschrift f.
Benno Schmidt,” Leipzig, 1896, s. 66. ,
Schiiller.—“‘ Congress f. Innere Med.,” Berlin, 1897.

 
 

159

CHAPTER VII.
SENILE ARTHRITIS.

Morbus Coxe Senilis—Senile Arthritis—Monarticular Rheuma-
toid Arthritis—In whom seen—Symptoms—Morbid Anatomy
—Changes in the Bones—Trophic Phenomena—Treatment.

Morbus coxe senilis, senile arthritis, or, as many call
it, monarticular rheumatoid arthritis, is most typically
seen in the hip or shoulder joints of elderly people. It
has been maintained, by some, that it is a similar con-
dition to rheumatoid arthritis; but to this I cannot
agree. For one thing it does not involve the peripheral
joints, being confined almost entirely to the hips and
shoulders. It is unaccompanied by any nerve or trophic
phenomena, and the muscular wasting present is merely
that induced by disuse, and mal-position of the bones.
Taking it all round, it is quite distinct both clinically
and pathologically. It is usually monarticular, but not
invariably so, and, as I have said, principally affects the
hips or shoulders. There is no symmetry, and it is
most common in men—women more rarely being affected.
It, as a rule, follows some injury of a very trifling
nature, as with diseased arteries and tissues whose
vitality is impaired it is possible, nay probable, that an
injury will so affect the joint structures, both through
their vascular and trophic supply, that a joint lesion
may follow on what would otherwise be the most harm-

~ Jess incident.

Adams first gave to this disease the name of “ Malum
coxe Senile,” but later on substituted ‘Chronic Rheu-
matic Arthritis.” Much has been written on the subject,
160 RHEUMATOID ARTHRITIS.

and, amongst others, we find Robert Smith,' Colles? and
Wilmot? have done so with special reference to the
disease as it occurs in the hip joints. Canton‘ refers to —
a similar condition in the shoulders, and Geist® describes.
the disease as a form of senile gout. Waldman® main-
tains that it is a separate disease from rheumatoid
arthritis.

Symptoms.—As a rule, the disease begins as a gnaw-
ing pain, which speedily results in the loss of the use of
the limb. If in the hip, the pain is often referred to
the knee likewise, but, as a rule, the principal pain is
felt over the trochanter or else in front in the groin.
The pain is rarely, at first, so severe that the limb can-
not be used, but, in the later stages, it.may become
marked. It is- found the patient cannot cross the
affected leg over the unaffected one without using his:
hands. There is inability to rotate the limb, and there
is atrophy of the gluteal muscles, as well as of the
muscles of the thigh. The tendon reflexes are increased.
_As the disease progresses we have considerable shorten-
ing, owing to absorption of the head of the bone. There
may be eversion with some adduction. The movement
of the joint is limited and attended with considerable
pain, and distinct grating. Again, we may, occasionally,
find cysts sometimes intimately in connection with the
joint; but in others, at some distance from and free
from it. They vary in size and are filled with thick,
glutinous, straw-coloured fluid. As the progressive
shortening of the limb proceeds, we have thickening. of
the trochanter, from the deposition of lime salts about
its base, and it seems unduly prominent from the mus-
cular wasting. The pelvis is often raised on the diseased
side, as the patient, by introducing another joint, by
walking on the toes, hopes to prevent shocks and jars to
the diseased parts. The toes may be turned in or out,
SENILE ARTHRITIS. 161

but more usually the latter. The symptoms in the
shoulder are somewhat similar. The arms cannot be
raised from the side and any attempt to do so causes
acute pain. When at rest the pain is not so acute as in
the case of the hip. There is, however, a similar wasting
‘of the muscles.

Post Mortem.—We find the joint distorted, the liga-
ments thickened, and the synovial membrane the seat
of chronic inflammatory changes. The articulating sur-
faces are worn down—the cartilages being altogether
destroyed or else still remain in patches, showing the
bone here and there bare underneath. What remains of
the cartilage can be easily stripped off, showing a rarefied
condition of the bone.. Instead of being hard and indur-
ated, as one would find in the chronic stages of rheuma-
toid arthritis, we find it soft
and yellowish in appearance,
and it breaks down readily—
apparently due to general wast-
ing of the bone with fatty de-
generation of the medullary
substance. In the case of the
hip, the neck may become so
absorbed, that the head comes
to rest on the trochanter. .
There may be an apparent
widening of the acetabulum
from the same reason. Occa-
sionally there is true new bony cates °itortes Coxe Beailis. "Ay
formation around the neck, but ee cele ends sbueebed, cath
this is rare. It may also occur slignbpepontan of tine sel
round the articulating surfaces. The disease consists
m a pure degeneration or wasting of the bone, followed
by that of the cartilage. The changes in the bone are
the primary and principal ones, those in the cartilages

11

 
162 RHEUMATOID ARTHRITIS.

and synovial membrane being secondary. The bone is
characterized by an increase in the number of its
spaces; the trabecule are fewer in number; thinner
and farther apart, and the spaces are filled with a
yellowish marrow, consisting of round cells, granular
corpuscles, and others having undergone fatty degenera-
tion. It differs widely from the bone marrow in normal .
bone, and also from that found. in true rheumatoid
arthritis.

The disease appears, to me, to be a pure degeneration,
due to some trophic or vascular malnutrition. With
regard to treatment, nothing can be done beyond pallia- _
tion. Relief of pain is our principal object, and is
accomplished, more or less inefficiently, by the use of
local applications, such as belladonna, small blisters, the
continuous current, massage, bathing, ete. By good
‘feeding, rest and stimulants, the progress of the disease
for a time may be arrested, leaving only a. permanent
disorganization, which nothing can repair.

 

REFERENCES.

Smith, Robert—‘ Dublin Journ. of Med. Sciences,” 1835, vi.

Colles.—Quoted Garrod, “Rheumatism and Rheumatoid
Arthritis.”

Wilmot.—Quoted Garrod, loc. cit.

Canton.—‘‘ London Med. Gazette,” 1848, N.S., vi.

Geist.—‘‘ Klin. der Greisenkrankheiten Erlanger,” 1860.

Waldman.—“ Volkmann’s Samml. Klin. Vortr.” No. 238, 1684.

Soe ge. bo
APPENDIX.

For reference the report* furnished by Dr. Blaxall, of the British
Institute of Preventative Medicine, on the micro-organisms found in
Rheumatoid Arthritis by Dr. Wohlmann and myself, is herewith
appended.

‘“‘THIS investigation was undertaken at the request of Dr.
Bannatyne, of Bath, who stated that he, with Dr. Wohlmann,
had arrived at the conclusion from the clinical aspect of cases
suffering from rheumatoid arthritis, that the disease was due
to a micro-organism, and further that by microscopic examina-
tion of the synovial fluid from affected joints, they had found
an organism, constant and distinct, and this micro-organism
they considered to be specific.

“Synovial fluid from affected joints was sent me from Bath
the fluid was aspirated with antiseptic and aseptic precau-
tions, with such success that out of eighteen cases which have
been submitted to me, only twice. have I found it con-
taminated.

“My first attempts to obtain organisms in the synovia and
to obtain cultivations from it, resulted in failure. I adopted
the ordinary methods of bacteriological procedure, staining
films of the synovial fluid for a few minutes with aniline dyes,
and inoculating serum tubes and all ordinary culture media,
as well as making plate cultivations of nutrient agar-agar and
‘gelatine after Koch’s method. But I was unable to observe
any organisms in the microscopic specimens, or to recognize
any appearance of growth upon any of the culture media.

“J then varied the staining methods, leaving the specimens
in the dyes for a prolonged time in the cold, applying heat,
and using concentrated solutions. By these means organisms

 

* This report appeared in the ‘‘ Lancet,’’ April 25th, 1896.
'

164 _ RHEUMA TOID ARTHRITIS.

could be perceived in the specimens corresponding exactly to
those described by Drs. Bannatyne and Wohlmann, and
morphologically identical with those seen in their microscopic
specimens. But their recognition was unsatisfactory, owing
to several causes. In the first place, it was evident that the
organisms took up the stains with great difficulty, and only by
their prolonged action, or by the application of heat; but
‘these means resulted in a very dense colouration of the
synovial film. Secondly, they were decolourized with great
ease, for attempts to decolourize the substratum left the
organisms unstained. ,

 Aoain, the microbe being very minute, it was exceedingly
difficult in heavily stained specimens to discriminate it from
débris or from precipitate of the dye used. It was necessary
then to find a method by which the organism should be well
stained, should retain the stain, and yet allow the synovial
film to be sufficiently decolourized, and one that should obviate
all precipitate of the dye. I cannot claim to have attained
this result, but after many trials I have adopted vie following
procedure as being most satisfactory.

“A thin film of synovial fluid, drawn out between two
cover- glasses, i is dried over the flame and fixed in the usual
way, by passing through the flame five or six times, as other-
wise the organisms are apt to be washed out. The cover-
glass is then immersed in dilute acetic acid for about two
minutes, well washed with water and dried again, this second
drying being to prevent the cover-glass sinking in the staining
fluid. The stain which I have found most useful is aniline
methylene blue. The cover-glass is placed, specimen side
down, on a watch-glassful of the stain, and the whole placed
in a moist chamber in the dark, for three to five days. It is
then washed in gently running water for some hours, rinsed
in distilled water, dried and mounted in the usual way. More
expeditious, though not giving such clear and well defined
specimens, are aniline gentian violet and carbolic fuchsin.
This latter stain I have found it advantageous to dilute one-
third with distilled water. Twelve to thirty-six hours are
APPENDIX. 165

sufficient for these in a moist chamber. The cover-glasses are
washed in running water in the same way, then well rinsed
with thirty per cent. alcohol, washed in distilled water, dried
and mounted. The acetic acid clears the synovial film and
allows the dye to penetrate more readily. The prolonged
staining deeply colours the organisms, so that the washing
process leaves them well stained, though the film is decolour-

- ized ; and the moist chamber, by preventing the evaporation
of the dye obviates the precipitate.

“Microscopic examination of the specimens reveals an
organism possessing peculiar characteristics. At first-sight it
appears to be a diplococcus, the two cocci being distinctly
stained, but separated by a clear unstained interval—about
equal in length to the diameter of either stained end. This
interval I have never succeeded in staining. But careful
observation will show, especially where the substratum is
faintly coloured, that the intervening portion is nearly as
broad as the diameter of either stained extremity, and that it
has parallel contours. I therefore consider the organism to be
a bacillus, which exhibits very marked polar staining. The
average length is 2u and the average breadth ‘6s, but this
latter measurement varies greatly with the intensity of the
staining. But the organism, as seen under the microscope,
appears much smaller than the measurements would indicate,
‘owing to the limited portions stained.

“The number of organisms met with in a cover-glass
specimen of synovial fluid from a joint affected with rheu-
matoid arthritis varies greatly. Sometimes the field is
crowded with them ; at other times they are scattered and
hard to find.. These differences appear to follow very closely
the acuteness or chronicity of the disease.

“The organisms are generally evenly distributed through
the film, showing, however, a tendency to congregate around
the leucocytes. Their arrangement is always discrete; I
have never seen chains or masses formed.

“Though the staining methods mentioned above have given
me the most satisfactory specimens, yet the organisms can be
166° RHEUMATOID ARTHRITIS.

seen when stained for a much shorter time, especially with

gentian violet, methyl-violet, or carbolic fuchsin. But it is

found that these stains if allowed to evaporate, deposit upon

the cover-glass a precipitate of dye, which so closely resembles

the organism, that it is by no means easy to recognize them

when but few are present in a preparation so observed—be-

‘cause after such a brief staining, attempts to remove the pre-

cipitate by washing and the use of re-agents, bring about more

or less completely the decolourization of the organism ; whereas.
after a longer contact with the stain, the microbes are coloured

more firmly, and are less easily decolourized. But there is

one exception to this statement, in a method which I have
devised and found useful.

“Impressed with the small size of the organism and the
minute portion stained, it occurred to me that the protoplasm
might take up dyes more readily if it came into contact with
them while moist. With this in view I mixed a drop of
synovial fluid with a few drops of the stain (aniline methylene
blue being best) on a cover-glass, and rubbed out with a
platinum needle. The cover-glass, with the stain and synovial '
fluid together, was then dried slowly over a burner, and when
quite dry, fixed by passing several times through the flame,
then freely washed with water, dried and mounted. ‘In this
way I obtained very fair results, the greater part of the stain
being washed off, leaving the organism well coloured. For
rapid diagnosis, this method is very useful.

“Treated by Gram’s method, the organism is almost com-
pletely decolourized.

“TI have been able also to detect the organism in the
synovial fluid in the hanging drop specimen, but this is far
from easy, unless they were present in larger numbers.

“T have now stained and examined the synovial fluid from
various joints from eighteen cases affected with rheumatoid '
arthritis, and in every case have cbserved the organism which
I have described above; but in fluids from distended joints,
due to other causes, as chronic synovitis, gonorrhceal and
tubercular affections, I have entirely failed to find them.
APPENDIX. 167

CULTIVATION.

“At first all attempts at cultivation, both aérobic and an-
aérobic, yielded apparently no result. But I imagined that
this might be due in part to the small size of the organism,
so that if it formed colonies they might be scarcely per-
ceptible, and judging from the scattered distribution in
synovia that the tendency to a free growth might be small,
and in part to a slow development. Keeping these points in
view I resolved to try it upon a large scale, and in such a
manner, that any change in the medium might be easily
detected. Into litre and half-litre flasks were put 250 ces. of
peptone beef-broth, filtered repeatedly until it presented a
perfectly clear and bright appearance. Great care was taken
over this to avoid the slightest obscuration. The flasks were
sterilized and placed in an incubator kept at blood heat for
several days to prove their sterility, and also to be sure that
the fluid remained perfectly clear. If these conditions were
fulfilled, the flasks were carefully opened, and a drop or two
of synovial fluid from an affected joint allowed to enter.
The flasks were then incubated at blood heat. Similar flasks,
but uninoculated, were also incubated at the same time to
serve as controls.

_“T was fortunate enough to attain success with the first
experiment. The first point noticed was that for three days
the beef-broth remained perfectly clear, pointing strongly to
the conclusion that the synovial fluid contained no ordinary
organism. But, from the fourth day and onwards, there
could be seen floating in the clear fluid very minute particles,
and these increasing gave rise to an appearance resembling
‘gold dust.’ This effect was enhanced by lightly shaking the
flask. Sometimes the growth seems to stop at this ‘gold
dust’ stage, but at other times it may become slightly floc-
culent, recalling to mind the appearance of a commencing
growth of tubercle bacilli in glycerine beef-broth. The beef-
broth never becomes turbid, but always retains its bright
appearance.

“The control flasks showed no such development. Micro=
168 RHEUMATOID ARTHRITIS.

‘scopic examination of such a culture, stained as before, dis-

plays the organisms in considerable numbers, but it can be
readily understood from the delicate nature of the cultures
and the imperfections of staining methods, that a too great
reliance on stained specimens was not advisable,.and that
additional evidence would be helpful.

“Verification was obtained by making hanging drop speci- °
mens, and this is the easiest method of demonstrating the
presence of the organism.

“In the hanging drop the microbe appears precisely as in
the stained specimens, with two bright refractile ends, and an
intermediate part much less obvious. They may occur in
zodgloea masses, or as discrete individuals hugging the edge
of the drop. They are non-motile, but have a marked oscil-
latory movement. I have been fortunate enough to see them
undergo division in the hanging drop specimen.

“The intervening portion lengthens out, the ends appearing
to pull against one another energetically, and. the whole
organism oscillating the while uneasily. The middle part

‘lengthens out more and more, so that the organism appears to

be about twice its ordinary length ; then. suddenly the link
snaps, and freed ends fly off in contrary directions, and are
rost amidst their fellows.

“This phenomenon helps, I think, to explain some variations
in length frequently noticed in stained specimens from culture.
In these some bacilli will be seen very short, the stained ends
quite close together, with a minute unstained connecting link,

_ very suggestive of a diplococcus.

“These I take to be quite young organisms. Some, how-
ever, are much longer, attaining a length of 3+, or possibly 4y,

‘the stained edges widely separated, and a clear unstained

sheath faintly visible with the highest powers. These I

‘Imagine to be the older forms, soon about to divide. In these

older forms too, the staining is sometimes somewhat different.
Instead of the staining portion being more or less spherical
at the ends of the organism, the coloured part is in the form
of a conical cap, the base towards the centre of the bacillus,
APPENDIX. 169

and spreading faintly down the edges of the sheath. These
forms show best the claim of the organism to be considered a
bacillus. It will be obvious, however, that it is very difficult
to bring out these ‘subtle differences in a photograph—and
indeed the limited staining of the organism and its minute-
ness, render the production of good photographs by no means
easy.

“The organism also grows upon nutrient agar-agar. If
beef-broth cultures are inoculated on tubes of sloping nutrient
agar-agar, and incubated at blood heat, growth takes place in

‘about three days, and in a very characteristic manner. ‘This
‘growth is exceedingly delicate. It appears no more than as a
fine transparent film, which under a lens can be seen to
consist of minute colonies no larger than a pin point, and
perfectly transparent. To the naked eye it bears a very close
resemblance to condensation water, though control tubes and
the obvious tests show that this is not the case.

“Tt grows also in Léffler’s serum, but here the growth is even
more difficult to recognize, owing perhaps to the opalescence
of the medium. It occurs as minute points, less difficult to
observe at the lower part of the tube, where the condensation
water has washed off the cholesterin. Stained cover-glass
specimens, and hanging drop specimens made from such
cultures, reveal an organism identical morphologically with
that described as present in the beef-broth cultures and
synovial fluid.

“T have also grown the organism in milk, where it appears
to flourish, but without causing curdling, or precipitation of
the casein. On nutrient gelatine, however, at 22° ¢., I have
never succeeded in getting a growth, and in liquid gelatine
incubated at 37° c. there is no visible growth.

«Examination of the blood in cases affected with rheu-
matoid arthritis has also afforded me positive results of the
presence of the organism.

“] have examined the blood taken near to an affected joint,
and also that from a distance, and in both have been able to
detect the organism in microscopic specimens. Out of five
17 RHEUMATOID ARTHRITIS.

specimens of blood submitted to me, I have been successful in

three, and these were the most severe cases. But further:

. proof of the presence of the organism in the blood is the fact
that twice I have been able to obtain cultures from it. The
method was the same as previously described. The blood
was inoculated into flasks of clear sterilized beef-broth and

inoculated at blood heat temperature. Subcultures were also.
made from these flasks on to agar-agar and blood-serum.:. The
organism found was identical in every respect with tliat
which grew from the synovial fluid, and with that which was-_
observed in the stained specimens.

“Some animal experiments have been made, for which 1 am
indebted to the Council of the Royal-College of Surgeons, and
to Dr. J. Sims Woodhead ‘Two cems. were injected subeu-
taneously into mice, guinea -pigs, and rabbits, but without a
fatal result. There is some reason to think, however, that
the cultures set up a disease in rabbits; which affected the
joints ; but further experiments are necessary to arrive at pane
truth with regard to this matter. : ea op

“As far as I am aware only one organism has been pre.’
viously associated with rheumatoid arthritis, which it’ is
necessary to discuss. This was described by Schiiller.* He
writes of a bacillus 2-6 long and “75-995 broad, which -
exhibits polar staining. It is easily coloured by ordinary
stains, especially carbolic fuchsin, but very easily decolourized.
It is noteworthy that Schiiller thinks it incumbent on him to
point out the distinction between his organism and tubercle
bacilli, :

“Tt grows readily upon gelatine at 25°c. In two, three, or
six days, small white grains or knobs appear. The gelatine is
liquified, and eventually the organism grows to such an éxtent
that the whole mass becomes opaque white. On agar-agar it
grows as greyish white flecks or films.

“It is obvious that the organism. described by Schiiller

 

_* Max Schiiller: “ Berliner Klinisch. Wochensehrift,” Septembér
4th, 1893. Crna Ee ep.
APPENDIX. 171

differs markedly from the one under discussion. In fact the
only points of resemblance are the polar staining and the easy
discolourization. It therefore appears to me to be indisputable
that this organism of Schiiller’s is not that which was dis-
covered by Drs. Bannatyne and Wohlmann.

“To sum up :—

“(1,) In the synovial fluid in eighteen cases of rheumatoid
arthritis an organism has been demonstrated, which is constant
in its characteristics.

“(2,) The organism is a minute bacillus, exhibiting
marked polar staining. It is difficult to stain and easily
decolourized.

“(3,) The organism can be grown in culture media, and
presents striking characteristics. In beef-broth it gives the
appearance of gold dust; and on agar-agar and serum its
growth is almost invisible.

“It does not grow on nutrient gelatine at ordinary tem-
perature.

“(4,) It is present in the blood of severe cases.

“(5,) It has not been found in the synovial fluid from
distended joints due to other causes.

“Jt should be added, that it has been impossible to examine
sections of the synovial membrane, owing to the want of
pathological specimens.”
 

 

173

LIST

OF AUTHORITIES.

PAGES |

Apams 4, 6, 7, 8, 48, 44, 48, 55,
56, 68, 68, 159
Anders. - - 139
Arloing - 36
BakeR - 104
Ball 116
Ballet 120
Barjon : 78
‘Barlow - - 90
_ Barthelémy - ‘ 78
Bates - - - 138
Baiumler -s e 9, 22, 27, 78
Beardsley = - ze o5 = 144
Beau - - 114, 116
Beauvais, Landré - 4,5,6
Béclére - 78
' Begbie - 16
Besnier - 8, 63, 116
Bezancon 36
_ Billroth 56, 64
Blaxall 28, 80, 81, 82, 83
Bécker - ~ 107
Bonnet - - 118
Bouchard = - 36, 83
‘Bowlby -  -- - - 68
Brabazon == - - 3, 4,9
Bristowe - - 121
Broca 4, 6, 7, 68
Brodie - 55, 56, e
Brown-Séquard
Buzzard 20, 29, i
-CAMPAGNON - 144
Canton 6, 160
Casselberry - 107
Cavafy . - 75
Cazin 18, 32, 35
Champonniére - -  - 139

Charcot 1, 4, 7, 8, 15, 23, 33, 48,
44, 47, 73, 77, 89, 106, 110,
"119, 114, 115, 120, 125, 144
Charrin - - 36, 83

 

PAGES

Chauffard - 4,9, 14, 74, 83
Chiaje - - 5
Chomel - - 6
Chvéstek 28, 51, 56
Cohnheim - .40
Colles - = 7, 55, 160
Colombel - 125
Cornil 7, 60, 65, 66, 67, 69, 73
Croeq ~- - 114
» Cruveilhier 4, 6, 7, 55
Da Costa - - 146
pace Lloyd 92
ebove - - 70
De Sauvage - 5
Desplats - 146
Deville 4,6,7
Dori, Lacaze - 8, 92
Drackmann - - - 127

Duckworth, Sir Dyce 8, 16, 43,
44, 77, 88, 110, 117, 120

Duplay . 18, 32, 35
EDINGER 82, 35
Erb - 148
Evans = 40
Live 5
Ewing 50
FaccE 64, 125, 145
Ferrier 33, 35
Fodor 50
Folli - 17, 84, 71
Forsbrooke 9, 15, 37
Franke - - - - 148
Fuller 4, 7, 8, 43, 55, 63, 92, 93

Garrod, Dr. A. EB. 9, 19, 22, 39,
48, 44, 47, 55, 56, 63, 77, 88,

89, 92, 101, 106, 110, 116, 144,
145, 148

Garrod, Sir A. 3, 4, 8, 43, 77, 89,
92, 116, 144

 
174

Geisen, Van -
Geist

Gley

Golgi -
Goodhart
Gowers -
Griffiths
Gwilt

HaBERSHON
Hadden

Hall

Haller -
Haygarth
Heberden
Henoch -
-Herringham
Hoelscher
Homolle -
Hoppe-Seyler
Howard
Hudeod’
Hunter -
Hiisse
Hutchinson
Hyde

JACCOUD
Jenkinson

Kry
‘Klein
Klippel -

- Kohts

Kéliiker -
Kussmaul .-

LakER
Lane, A.
Lane, H.
Lanois
Lebert -
Lecorché
Leis
Leyden
Linossier
Lobstein
Lorain
Lorenze -
Lunn

‘McARDLE- -
Mackenzie
Madelung

RHEUMATOID ARTARITIS.

PAGES

4, 5,

110
2.1387
8, 68, 101

63

© 101, 117, 144
- 137

36, 38, 40, 41
69

8, 15, 88
so ae

91, 109, 117
144

6

49

- 17, 72
47

- 60
69

37

8

9

- 147
5, 59
77

6

47

- 147
6

89

- 145
64

88
-- 87
- 158

 

PAGES

Mannaberg 40
Maragliano 40
Marie - QL
Massolongo 17, 72
Mathieu - 8
May 5
Meyer 6
Miller - 84
Mitchell _- 124
Money - 92, 127
Monocoro 92
Moore 5
Moullin - - 64
Miiller 148
Musgrave 5
‘Mussy - - - 144
NEPVEN - 75
Newsholme - 39
ORD 8, 16, 18, 46, 106
Orth — - - 48
Osler+ - 37
Oudin - 78
PaGet 23, 33, 124
Pasteur 90
Payne 117
Petrie 5
Pfeiffer -. 17
Picot- - 139
Pitrés 18, 72
Pitt 75, 117
Playfair 116
Powell - - 137
Pye-Smith - 15,43
RaDEMACKER 149
Ramond 4, 9, 14, 74, 83
Ranvier 7, 60, 65, 66, 67, 69
Redfern - - 7
Remak - 16
Rindfleisch 55, 60, 64, 66
Ringer - 144
Riva .- - 28
. Roger - - 49, 147
Rokitansky 61
Romberg 115
SABOURIN 24, 32
Sandifort - : - 7
Schiiller 9, 11, 83, 88, 148
Scudamore - 6
See 144
Semmola - - 86
LIST OF AUTHORITIES. 175

PAGES PAGES
Senator 8, 16, 44, 55, 63 | Turner 61
Sireday - 147
Smith - = 6, 7,160 | VarnL1aRD 18, 72
Smith, Shingleton- - 28 | Vallat 24, 32, a
Solis-Cohen - — - 145 | Vergely -
Spender 4, 8, 23, 34, 101, 120, | Vidal 4, 1, 195
; 125, 145 | Vierordt - 86
Steavenson 148 | Virchow - 4,5, 8
Stewart 10, 22, 26, 28, 47, 48, | Volkmann 56, 67, 68, 69, 96
51, 89 | Vulpian 23, 33
Still 74, 91, 92, 116
Stolzeburg - 146 | Wacner - 91
Striimpell 24,32 | Waldman 28, 89, 160
Sydenham 5 | Walzer - 141
Syers -- - 43 | Weber 6, 66
Wilmct - - 160
TESSIER - 118 | Wohlmann 9, 14, 28, 29, 78, 83
Todd . 4,7, 55,115 | Wynne 67
Trastour 7, 48, 114° Wreckowitcl 48
Een ere 4, 44, 55, 57, 63, 73,
146 | ZEIGLER - 68

 
177

INDEX.

 

PAGE PAGE
AACHEN . 149 | Atmospheric: conditions, a
Aconite ; i» 246 cause 26 1. AT
Acta racemosa .. 144 | Atony of muscles .. 114
ae rheumatism, diagnosis Atrophy of the skin, etc. . 125
°. sis os oe -» 96
. Acute rheumatoid arthritis 90 | Bacinnus, cause of the
——— age at which it disease . ais -» 26
occurs a8 i -» 90 | — mode of growth ay .. 81
—_— — appearance of joints —shapeof .. sts -. 80
im wes ae at -. 93 | — staining of vs .. 81
_— — — cardiac troubles in 94 | — pyocaneus.. ee .. 49
——-—feverin .. .. 94 | — tuberculosis ee «» 49
——-—inchildren.. _ .. 90] Bacteria, effect on joint
Se muscular atrophy in 94 tissues 30
+- — — painin we -. 94 | — effect on endocardium and
— — — pigmentation in .. 94 pericardium + 81
Adhesions es “te .. 62: | — where they propagate .. 380
Aitiology ¥ i .. 41 | Bacterial products .. .. 81
_ Age, as a cause a 44 | — — how absorbed .. -. 81
' Aix-la-Chappelle | 155 | — — selective action of .. 32
.  Aix-les-Bains .. é -. 149 | — — their action on nervous |
_ Alcohol... 5 - 20 | system” .. a -. 384
Alcoholic muscular ‘atrophy 118 | Baden Baden .. .. 154
Alkalies '.. 144 | Banff .. 149
Alkalinity of the filbod .. 50 | Baréges 154
Alimentary tract, RyEreHne Bath .. -. 148
due to . 126 | — waters 2 -» 154
Ammonia "4, 145 | — — constituents of . 155
Anemia Lie 86,122 | — — effect of -. 150
Anatomy, morbid 55 | — — how used -» 150
Ankylosis é > 108 — — suitable cases for . 149
— bony a ae -. 68 | Battaglia .. 154
— fibrous 58, 108 | Belladonna .. 145
Anterior cornua, multipolar Benzo-naphthol - 136
nerve cells of as Benzosol 138
Arkansas, hot springs .. 149 | — nature ‘of ‘and mode of
Arsenic .. a : . 148 administration or -» 142
Arthrite séche eh .. 7 | Betol .. a oe .. 143
Arthritic diathesis .. .. 15 | BNaphthol . 143
Arthritis, chronic rheumatic 4 | Blisters , «. 145
— deformans .. at ne Blood, action of toluylene-
Arthropathies, nerye «x 96 diamin on .. es as
ABPUERMtON: of joints .. 153 | — changes in.. ies -. 73

12
8 INDEX.

PAGE

ood, destruction of .- 88
injoints .. -. 64
me, appearances of .. 68
- erosion of . a 68
hypertrophy of .. .. 68
-marrow.. wa (0
ones, enlargements of 103
- nodules of . : -. 103
mny-loose-bodies ah -. 61
ourboule waters 149
ronchitis aes .- 126
albar warnings sia .. 28
urse .. ave ae 103
axton 148
\JUPUT . 145

vcium phosphate i in urine 127

umpagnon 144
unphor 7 145
urbolic acid, external appli-

cations of .. 146

urdiac condition, “due to
micro-organisms .. 115
irdiac lesions, statistics of 116

urlsbad . 149
irtilage, appearances of .. 59
-changesin..  .. -. 64
. fibrilation of 5 66
- marginal overgrowths of 67
osseous changes in ». 67
- prolification of .. .. 66
irtilaginous changes .. 64
- loose bodies sia »» 61
vtarrh of mucous mem-
branes es ts .» 45
puses . Ss oe we. AL
vuse, age as a 44

- atmospheric conditions asa 47 -

- catarrh of mucous mem-

branes as a . ae -. 45
- emotional causes as «. AT
- genito- a complaints
asa .. 46
- heredity as a ha ate Sa,
- injury as a. ae -. 48
-S@CX asa .. 48
antral nerve system, de-
generation of . -» 70
hanges in the joints os 57
haulmoogra oil 145
aildren, rheumatoid arth-
ritis in se ae ss “90
hili paste... x .. 145
hloralose: 146
aloroform 145

 

PAGE

Cholesterin .. 63
Chromatogenic functions of

. the skin a a .» 125-

Chlorosis 26 i

Chronic rheumatic arthritis 3

Chronic rheumatism of the

joints 3
Chronic rheumatoid arth- é
ritis .. 89, 94

— — — its characteristics 94
Circulatory aes nee

due to - 120
Climacteric .. sia .. 44
Climate +» 153-
Clothing * - -- 186
Cloves, oil of .. ne -- 146
Cod-liver oil .. apa -. 134
Colchicum vi .. 142
Cold, as a cause ae ee AE
Conjunctivitis... - Fi »» 127
Corpuscles, granular and

amoeboid in diagnosis .. 63
— nucleated, in blood - 74
Counter irritants .. 145
Creasote .. 138
— action of , .. 141
Crepitation in joints .. . 104
Cysts 104

— in connection with senile

arthritic joints ni -. 160
Damp .. Ms 2 -. AT
Dax oa -» 154
Deafness he -. 127
Deflection of hands als -. 109
Deformities. 4 -. 108
— in gout, chronic rheu-

matism, ree bi aes

ete. .. : » 114
— types of .. 110
Diagnosis 8 2. 95
Digitorum nodi i « @
Diphtheritic muscular

atrophy ‘ se -. 119
Dislocations .. 114
Douche baths .. 150
Dyspepsia oe ae .. 126
Dystrophic theory .. .. 16
EBURNATION .. a .. 68
Ectasine . mo -. 36
Effusion, analysis of. -» 68
— into joints . we -- 63
— micro-organisms in .. 63

Electrical bath - ..

“

. 147
INDEX. 179

‘ PAGE
Electrical treatment ». 147
Emotional causes... . AT
Ems... Se a ,. 148
Endocarditis .. ae z« 115
Endocardium, changes in .. 73
Eucalyptus .. tg -. 145
Excision of joints .. -. 151
Exostosis ss as -. 68
Exposure, a cause .. -- AT
Extension by weights +» 151
FaravIsm ae Aes ». 147
Fats... be hd -. 184
Fever a . 120
Fibrous nodules oe see
Fluid in joints® a -. 68
Franzenbad . 149
Fraxinus excelsior .. .. 144
GALVANISM.. ae . 147
Gastein -. 148
Germicidal power of blood .. 50
Glands, changesin .. .. 74
— symptoms due to .. . 116
Glossy skin . 124
Gonorrhea, a cause .. .. 49
Gout, a cause .. se .. 49
— diagnosis of as -. OF
— rheumatic . 3
Goutte asthenique primitif 3
Guaiacol 3 -. 140
— applied externally .. 146
Guaiacols, the ie .» 138
Guaiacol carbonate .. - 140

— — nature of and mode of

administration aif .. 139
Guaiacum a i «» 145
Gymnastics - 136
HMoGENESIS 8 .. 37
Hemoglobin .. ae .. 74
Hemolysis .. 37

Hemolytic process in anemia 37
— value of the red corpus-

eles .. : 86, 38
Hemoptysis .. i .. 122
Heemorrhages.. 34 -- 122
Hammam Mes Koutin .. 149
Hammam R’Hira .. .. 149
Hand, deformities of.. .. 109
Harrogate | Read .. 148
Heart, changesin .. - 7
Heberden's nodes... woe 18
Heredity e .. 41

Hips, deformities of . .. 111

 

PAGE

Hips, senile arthritis of 160
Holland, prevalence of the
disease i In: (23 os -. 48
Hyoseyamus .. ey -» 145
IcutHyoL i hy «» 145
Influenza, va ae -. 62
Injury, a cause 48
Integumentary system, ab-
normalities of 4 -. 125
Todides . re se ». 144
lodine .. -. 144

— external application of .. 145
Ireland, prevalence of the

disease in .. ae -. 48
Iritis  .. vs aa .. 127
Iron... és an .. 148
JOINTS, appearances of -- 102
— changes in ss .. 87
— distension of Ce .. 57
— effusion into we -. 63
— hemorrhage into .. .. 64
— suppurationin .. ». 64
— swelling of.. sa -. 102
—— temperature of .. .. 103
— treatment of id «» 182
— — — by excision ». 152
Kipney, changes in .. -. 7
Kissingen .. 149
Knees, deformities of .. 112
LanGEn SwWaLBACH .. -. 149
Lecethin bs - -- 68
Ligaments, changes it in, .. 62
Liver, hemolytic process of 38
Llangammarch is .. 148
Local sweatings as -. 85
Loose bodies in ve .. 60
Luchon.. es ‘ .. 154
MALARIA 6 ay -. 89
Maltine es ae .. 135
Malum coxe senile .. .. 159
Marienbad_ ... ee .. 157
Massage .. 151
Melon-seed-like bodies ga iL,
Mercury 145

Micro- organisms, ‘discovery of 79
— — found in the joints .. 79

Monarticular rheumatoid
arthritis we de .. 159

Mont D'or at i .. 149

Morbid anatomy se -. 55
180

. PAGE
Morbid anatomy of the bones 68
— — — — cartilage -. 64
— — — — ligaments -. 62
— — — — synovial mem-

branes . aie -. 59

Morbus coxe senilis am 70, 151
— — — bone marrowin .. 70
Morphia : ae .. 156
Motor cells of "anterior cor-

nua of cord . 23, 33

Multipolar ganglion cells .. 33

— — — degeneration of .. 33

Muscles, changes in .. an 0
Muscular atrophy 23, 32, 117
— — an aid to diagnosis .. 97
— — cause of of .. 118
— — its extent ie -. 33
— — its nature S% .. 33
— — neuritisacauseof .. 118
— — reflexes in i .. 118
— — result of neuritis .. 119
— — selected musclesin .. 118

— — selective character of 118
—~ — vaso-motor reflex spasm

' @ cause es ae .. 33
Myositis . ae 88
Myotatic srvitebility | .. 124
‘Naxep eye eee of

the joints. .. war DN
Naphthols, the Pe .. 148
Nephritis aa a4 -. 127
Nerve arthropathies .. -. 96
Nerve changes ~ 2a ane
— central system, changes

in - 70

— inflammatory condition of 72
— peripheral, changes in .. 72

— phenomena, early -- lol
~— system, epee due to 123
Neumahr ‘ vs .. 155
Neuritis sie on .. 123
—a cause of muscular
atrophy 118
— asa cause ‘of the ‘disease 18
— descending. . ae -- 712
Nodes, Heberden’s sis -» 75
Nodosity of the joints . 38
Nodules, fibrous a ge 74
Nomenclature. . se ox @
Norse Viking’s bones sae
OLIGOCHROMAMIA .. .. 87
Opium .. a4 o- 146

Osteitis, rarefying 5s -. 69

 

INDEX.

PAGE
Osteo-arthritis 4, 84, 87
— — its meaning . 8
Osteophytes .. 61, 69
Osteophytic nodules . .. 103
Osteosclerosis .. a -- 68
Osteosclerotic cases .. « 8
Pain, a symptom ' 101, 104, 108
—itscharacters .. -. 108
Paraffin ae ae «. 145
Paraldehyde .. a -. 146
Paralysis agitans .. -. 109
Pathology a -. 14
Periarticular connestive tissue 62
Pericarditis .. id -» 115
Pericardium, changes of .. 73
Phenols, the is «> 142
Phosphates in urine .. .. 127
Phthisis . ia -. 127
Pigmentation, abnormalities
Of es Ps aay oe WEDD,
Plombiéres.. si .. 155
Polypi of synovial mem-
brane 59
Post gonorrhoeal rheumatoid
arthritis .. 88
— gouty rheumatoid arth-
vitis .. é ys 88
— rheumatic rheumatoid
arthritis .. afi .. 87
Potassium iodide .. -. 144
Premonitory symptoms _.. 100
Primary symptoms .. .. 102
Prognosis Ee . 127
Progressive muscular ‘atrophy 34
Psoriasis a - 127
Puberty 3 44
Pulmonary " hypertrophic
osteo- aes nk «. 96
Pulse rate ‘ +. 120
Purpura +. 122
Pyrogallic . acid, action on
blood... oe ds -. 39
QUININE, the use of ... 142, 144
Reaction of degeneration .. 118
Reflex action, @ cause 19
Reflexes in muscular atrophy 118
— — neuritis - 123
Rheumatic arthritis, "Heber-
den’s nodes in oh -. 75
Rheumatic gout ne i 8
Rheumatism, a cause 23, 49
INDEX.

PAGE
Rheumatoid arthritis, acute 90
— — acute © rheumatism,
diagnosis from as - 96
—— — aconstitutional disease 7°
— — anemia in hee se 121 4
— — best term to employ.. 1

— — changes found in an-
cient bones .
—— connection with acute

rheumatism ie «. 49
—— — deformities in. «. 108
— — different from rheuma-

tism, gout, ete. .. 1 67
— — dislocations in .. 114
—— due to reflex nerve

impulses .. ais 19
—-—due to simple wear

and tear as ie, se
— — fever in ae .. 119
— — functional depression

& cause : we 19
— — gout, diagnosis from... 97
— — hemorrhages in » 199
— — Heberden’s nodesin.. 75
—-—inchildren .. -» 90
— — integumentary system

in ow. a is «. 125
— — its causes ae s> 41
— — its diagnosis .. ». 95
— — its frequency . se dL
—— itsmeaning .. 2
— — its morbid anatomy . 55
— — its pathology .. -. 14
— — its varieties .. 86
— — micro-organisms in ‘14, 79

, ~—natureof¢hanges .. 4
— — nerve symptomsin .. 123
— —neuritisin .. 18, 123
— — only a form of chronic

rheumatism
— — rheumatism, gout and

gonorrhoea, as causes ». 49
— — symptoms of .. -- 100
— — tabetic resemblance .. 21
— — tachycardia in -» 120
—— toxic products, a

cause -- 20

— — trophic phenomena i in 124
— — uterine derangements

in .. i a ais
— — vaso-motor disturbances

in .. Pe we -. 124
— — various terms applied
toit .. .

— — views held in France ‘1, 15

 

Rhumatisme prsremlnaee
primitif fixé..

—_—— généralisé .

— chronique BE imitif.

— fibreux ae

— noueux

Rippolsau

Rémerbad ...

Sv. Moritz ..

Salicylates, the use of

Salol .. .

Salophen

Sand, hot Ag

Schlauzenbad ..

Scleroderm

Sclerosis of bone

Sclerotitis

Sea voyage 7 :

Secondary symptoms :

Selective action of bacteria
and their products

— character of muscular
atrophy aif

Senile arthritis

— — pathology of ..

— — symptoms of ..

— — treatment of

Senility, a cause

Sex .

Skin, appearance over
joints .

— changes

Spondilitis

Stimulants, the use of

Strathpeffer ae

Sulphonal

Sulphur

Suppuration in joints |

Sweating ‘

Symmetry of symptoms

Symptoms...

— due to alimentary tract .

— — — the ae eys-
tem . =

— — — micro- ‘organisms i

— — — the nerve system ..

— premonitory

— primary ..

— referable to heart. .

— — to glands

— — to joints

— secondary .

Synovial membrane, thicken-
ing of ae °

181

PAGE

1. 162

-. 102
» 124

108

.. 132
.. 148
-. 146
-. 145
-.» 105
«. 125
. 107

. 100
. 126

119
102
123

- 100

102

i £8
"146
402

117

. 102
182

Syringo-myelia es

TABES DORSALIS
Tachycardia ..
Temporo-maxillary joint
Tenderness of joints .
Thermal treatment ..
Thumb, deformities of
-Toluylenediamin ie
Toplitz'. a

Toxic products, a cause
Treatment

Trophic changes

— phenomena
Turpentine

UratE of soda apport
Uric acid 7
Urine, changes in

INDEX.

PAGE

21

.. 96
36, 120
106

ss » 104
.. 148
. 110

.. 89
. 149

.. 20
. 130

se A?
.. 124
. 145

ae 19%
7, 127
. 127

Usure des cartilages articu-

laire .. .
Uterine derangements,
cause

‘a
ee

 

PAGE

Vacuotation of nerve cells 71
-Vapour baths .. . 145
Vaso-motor disturbances .. 124

— — — action of toxines on 35,

40

Vegetables 5 : . 138
Vegetations of the synovial

membranes . 59
Velvety appearances “of the

cartilage .. 65
Villi of the synovial mem-

brane .. 59

Virginia, hot springs of . 148

WARMBRUNN ..
White corpuscles, increase of 40
Wiesbaden oe . 149
Wildbad ‘ , .. 149
Women, frequency of the
disease in . 43
— uterine derangements i in 44
Woodhall Spa.. . 142
Wrist, deformities of... . 110

 

 

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