Chapter I: Preface

“A knowledge of the real nature of gout ... is, in my opinion, at the very foundation of all sound pathology,” wrote Todd many years since; and the passing years have but invested his reflection with deeper significance and something of prophetic insight. For who can doubt that he who would elucidate the pathological groundwork of gout must be at once a clinical physician, a bio-chemist, a bacteriologist, a morbid anatomist? and well may we ask, Who is sufficient for all this?

How vivid the light thrown upon the problems of clinical medicine by the bio-chemists! The story of the fate of protein and purin substances in the animal body, at one time a medley of guesses and gaps, is gradually evolving into one of relative certitude and completeness. Revolutionary, in truth, the change, and many a cherished shibboleth has been ruthlessly cast aside! With admiration not unmingled with awe we see them laying well and truly the foundations upon which in the ultimate scientific medicine must inevitably rest.

Of these the very corner-stones are _chemical physiology_ and _chemical pathology_, the rapid evolution of which is profoundly altering our conceptions of health and disease. Those vital processes of the organism that but yesterday we saw “as through a glass, darkly,” are now in great part illumined, and the distortions wrought in them by disease made more manifest.

How pregnant, too, with warning their findings! Processes that to our untutored minds seem simple are revealed as infinitely complex. Through what a maze must we thread our way if we would disentangle the intricacies of metabolism! Intricate enough, forsooth, in health, but how much more so in disease! For, as Sir Archibald Garrod eloquently phrases it, “it is becoming evident that special paths of metabolism exist, not only for proteins, fats, and carbohydrates as such, but that even the individual primary fractions of the protein molecule follow their several katabolic paths, and are dealt with in successive stages by series of enzymes until the final products of katabolism are formed. Any of these paths may be locked while others remain open.”

It is with chastening reflections such as these that we may best approach our study of gout, that riddle of the ages upon which so many physicians from time immemorial have expended their dialectic skill. But, vast though the increase in our knowledge of the chemical structure of uric acid and its allies, uncertainty still dogs our steps, and, doubtful of the pathway to solution of the pathological mystery of gout, we must perforce approach the problem in a more strictly catholic attitude.

_Uric acid_ has apparently failed us as the _causa causans_. Neither this substance nor its precursors can be held responsible for the fever, local inflammation and constitutional disturbances in gout, being, as they are, practically _non-toxic_. Albeit, though I hold this view, I do not for one moment suggest that _uric acid_ has nothing whatever to do with gout. The fact that _tophi_, its pathognomonic stigmata, are compounded of _biurate of soda_, would _per se_ stamp such an attitude as untenable. On the other hand, _uric acid_ must be viewed at its proper perspective as a _concomitant_ or _sequel_ of _gouty inflammation_, the essential cause of which must be sought elsewhere.

“The old order changeth, giving place to new,” and happily with the advent of _bacteriology_ our views, or rather our hazards, as to the nature of joint diseases underwent profound modification. But, strange to say, though quick to apprehend the significance of infection, its causal relation to other joint disorders, we still seem unaccountably loth to discard our timeworn conception of “gouty” arthritis as of purely _metabolic_ origin. This to my mind is the more remarkable in that the onset, clinical phenomena, and course of acute gout, and no less the life history of the disorder as a whole, are emphatically indicative of the intrusion of an _infective element_ in its genesis.

The extreme frequency with which _infective foci_ are met with in the victims of gout, the frequency, too, with which exacerbations of the disorder are presaged by _acute glandular affections_ of undeniably _infective_ source, is by no means adequately realised. For our forefathers gout began, and, forsooth, often ended, in the “stomach,” or it was the “liver” that was impeached. But the portal to the alimentary canal was for them only a cavity, the contained structures of which, albeit, to their mind often betrayed evidences of a “gouty diathesis.” They distinguished “gouty” teeth, “gouty” tonsillitis, “gouty” pharyngitis, even “gouty” parotitis; but all these they classed as tokens or sequelæ of gout, not possible causes or _excitants_ thereof.

Now as to the true significance of these acute glandular affections held by clinicians of repute to be of “gouty” origin. What of “gouty” tonsillitis, pharyngitis, parotitis? Still more, what of our deductions regarding the relationship of these same when met with in association with _non-gouty_ forms of arthritis? Do we not hold them each and all as evidences of _infection_? and, we may well ask, why not in gout?

The marvel then is that even to-day many still hold that the tonsillitis, pharyngitis, even the gingivitis, like the subsequent articular lesions, are one and all attributable to the underlying _gout_. We certainly should not do so in the case of any arthritis other than “gouty,” and to my mind the time is ripe for a change of attitude.

The “gouty” throats, like the “gouty” teeth, should be regarded not as symptomatic of gout, but _etiologically_ related thereto. We should cease to talk of “gouty” throats, teeth, etc., should renounce the prefix, for there is nothing _specific_ of _gout_ either in the tonsillar, pharyngeal, or dental lesions. We should instead view these various local disorders in their true perspective as _foci_ of _infection, causally_ related to the subsequent and _secondary_ “gouty” arthritis.

Similarly, when we come to analyse the component elements of an acute paroxysm of gout, how strongly indicative of the intrusion of an _infective_ element the following features: the onset, temperature curve, character of local articular changes of the disorder, the presence of _leucocytosis_, with secondary anæmia and enlargement of the lymphatic glands! Again, how suggestive the occasional complication of acute gout by _lymphangitis_ and _phlebitis_! Of like significance, too, the paroxysmal nature and periodicity of the disorder, and the compatibility of the morbid anatomical changes and the cytological content of the aspirated joint fluid with their genesis by _infection_.

As to correlation of the metabolic phenomena of gout with the postulated infective element, I would suggest that, although abnormalities of metabolism form an integral part of gout, they are of themselves inadequate to achieve its efflorescence. As we shall see when we come to consider those elemental manifestations of gout, _i.e._, uratic deposits, or _tophi_, neither the purely physical nor the purely chemical theory of their origin will suffice, nor, for that matter, can any solution of their formation be gleaned from even a blend of the twain. In short, such hypotheses are too _mechanical_.

The intrusion of some other factor, “something vital, something biological,” seems essential for the elucidation of _uratosis_, _i.e._, uratic deposition. For this, _not uricæmia_, is the specific characteristic phenomenon of gout. If we cannot explain uratosis on physical or chemical grounds, then how much less, in view of the _non-toxicity_ of _uric acid_, can we on this basis account for the _inflammatory_ phenomena of the disorder!

Now _inflammatory reaction_ is, I hold, an invariable _antecedent_ in all gouty processes, whether of _articular_ or _ab-articular_ site. Granted that inflammatory reaction is a necessary prelude, the specificity of gout is attested by the fact that the same is followed by local deposition of urates. But while this sequential uratic deposition invests all forms of “gouty” inflammation with a specific character unshared by any other disease, it follows that the cause of the said inflammation must, if possible, be ascertained.

Now, as I believe, “gouty” subjects are _ab initio_ victimised by innate tissue peculiarities, doubtless reflected in corresponding obliquities of tissue function and metamorphosis, and through their medium the general resistance of the body to invasion by _infections_ is lowered; in other words, under the influence of these morbific agencies the latent morbid potentialities of the gouty become overt and manifest. For in the gouty, as Walker Hall observes, “a slight injury or indiscretion of diet, an overloaded intestine, or increased toxicity of the intestinal flora, may be followed by a disturbance of the general nuclein metabolism and a local reaction in certain tissues.”

Enough has been said to disclose the dominant trend of this work, and although there are many aspects of the subject in regard to which I hold somewhat iconoclastic views, yet exigencies of space forbid me even to allude to them in this foreword. I hasten therefore to discharge the pleasing duty of acknowledging my great indebtedness to the acumen and discrimination which has been brought to bear on this subject by a long succession of eminent physicians, in proof of which I need only adduce the names of those giants of the past the illustrious Sydenham, Sir Thomas Watson, Sir Charles Scudamore, Jonathan Hutchinson, not to mention Trousseau, Charcot, Lecorche, and Rendu. But I should fail in my duty did I not in a special sense express my deep indebtedness to the classic and epoch-making work of Sir Alfred Garrod. For the rest, too, I have derived much enlightenment from Sir Dyce Duckworth’s treatise and the various works on the subject by Luff, Lindsay, and others.

From the bio-chemical aspect I owe much to the researches of Walker Hall, and to those of our American _confrères_ Folin, Denis, Benedict, Pratt, McLeod, Walker Jones, Gideon Wells, etc.

Reverting to my own colleagues at the Royal Mineral Water Hospital, Bath, I would tender my deep thanks to the Honorary Physicians, Drs. Waterhouse, Thomson, Lindsay, and King Martyn, for the uniformly generous manner in which they afforded me opportunities for studying cases under their care.

To Dr. Munro, our senior pathologist, I am especially beholden for invaluable, nay indispensable, help in the matter of blood examinations, the cytological study of joint fluids, and the microscopic verifications of tophi. To Dr. MacKay also my cordial thanks are due for the skiagraphs contained in this work.

For the section dealing with the ocular disorders met with in the gouty my most sincere thanks are due to Mr. W. M. Beaumont, of Bath, whose singularly wide experience in this sphere renders him unusually equipped to deal with this highly controversial aspect of gout. To Drs. Cave and Gordon, of Bath, also I am indebted for many valuable suggestions kindly afforded me while writing this volume. To my brother Dr. Bassett Jones I am under deep obligation for unwearying assistance in our joint endeavour to ascertain the exact relationship of gout to lumbago, sciatica, and other types of fibrositis.

For the preparation of the index of this work I would proffer my grateful thanks to Mr. Charles Hewitt and to Miss Donnan and Miss Crosse for having undertaken the arduous task of typing the manuscript thereof.

Lastly, I would express my thanks to my publisher, Mr. Heinemann, for much consideration and many courtesies.

LL. J. LL.

31, UPPER BROOK STREET, W. 1.

TABLE OF CONTENTS

CHAPTER I

HISTORICAL AND INTRODUCTORY

The Antiquity of Gout. Prevalence of Gout in the Anglo-Saxon
Period. Views of the Humoralist. The Aphorisms of Hippocrates.
Introduction of the Word Gout. Early Views as to the Nature of
Tophi. The “Honour of the Gout.” That Gout confers Immunity
from other Disorders. Growing Infrequency and Attenuation of
Gout _pp._ 1-13

CHAPTER II

THE PEDIGREE OF GOUT

Tardy Dissociation of Chronic Gout. Identification of Muscular
Rheumatism. Differentiation of Chronic Gout from Arthritis
Deformans. Cleavage of Arthritis Deformans into Two Types.
Elimination of the Infective Arthritides _pp._ 14-20

CHAPTER III

EARLIER THEORIES OF PATHOGENESIS

Garrod’s Theory. Antagonistic Views. Histogenous Theories.
Antecedent Structural Changes. Hepatic Inadequacy.
Hyperpyræmia. Nervous Theories. Growing Scepticism as to
Garrod’s Pathogeny of Gout _pp._ 21-34

CHAPTER IV

DEFINITION, CLASSIFICATION, ETIOLOGY, AND MORBID ANATOMY

Definition. Classification. Suggested Classification
of Articular Gout. Etiology and Morbid Anatomy. Bodily
Conformation and Individual Temperament. Locality, Race,
Climate. Food, Drink, Occupation. Lead Poisoning. Mental and
Physical Over-exertion. Summary. Morbid Anatomy _pp._ 35-58

CHAPTER V

PATHOLOGY OF GOUT-PROTEIN METABOLISM

Revelations of the Bio-chemist. The Formation of Urea. Fate
of the Amino-acids. Seat of Formation of Urea. Amino-acids
in Relation to Gout. The Glycocoll Theory of Gout. Urea
Excretion in Gout. Creatine and Creatinine. Inborn Errors
of Metabolism _pp._ 59-70

CHAPTER VI

NUCLEIN METABOLISM

The Isolation of Nucleic Acid. Researches on Spermatozoa. The
Discovery of Purins. Uric Acid a Derivative of Nucleic Acid.
The Chemistry of Uric Acid and the Purin Bodies. Chemical
Constitution. Properties of Uric Acid. Uric Acid in the Blood.
Gudzent and Schade’s Theories. Organic Combinations. Complexity
of the Problem _pp._ 71-82

CHAPTER VII

SOURCES OF URIC ACID

Exogenous Purins. Exogenous Uric Acid Excretion. Fate of the
Unexcreted Purins. Endogenous Purins. Source of Endogenous
Purins. Proteins and their Derivatives. Amino-acids and
Dicarboxylic Amino-acids. Endogenous Uric Acid Excretion.
Factors influencing Endogenous Uric Acid Excretion.
Physiological Conditions. Pathological States. Ingestion of
Certain Drugs. Synthetic Formation of Uric Acid _pp._ 83-97

CHAPTER VIII

FORMATION AND DESTRUCTION OF URIC ACID

Distribution of the Enzymes. Stages in Disruption of Nucleic
Acid. Destruction of Uric Acid _pp._ 98-106

CHAPTER IX

URIC ACID IN RELATION TO GOUT

Uric Acid Excretion in Gout. Uric Acid Variations in Acute
Gout. Uric Acid Variations in Chronic Gout. Retarded Exogenous
Uric Acid Output. Lowered Endogenous Uric Acid Output. Other
Anomalies in Excretion in Gout. Purin Metabolism in other
Disorders. Purin Metabolism in Chronic Alcoholism and
Plumbism _pp._ 107-116

CHAPTER X

THE RENAL THEORY OF GOUT

Anomalies in Uric Acid Excretion in Gout. Uricæmia in
Nephritis. The Relationship, if any, between the Amounts of
Uric Acid and of Urea, and Total Non-protein Nitrogen in Human
Blood. Uricæmia not necessarily due to Renal Defect. Uricæmia
not Peculiar to Nephritis. Uricæmia does not necessarily
Portend Gout. To what may be ascribed the Deficient
Eliminating Capacity of the Kidney for Uric Acid. Uratic
Deposits in Nephritis. Differentiation of Uratic Deposits in
Gout and Nephritis. Clinical Associations of Gout and Granular
Kidney _pp._ 117-132

CHAPTER XI

URICÆMIA IN GOUT

Folin and Denis’s Method. Uric Acid a Normal Constituent of
Blood. Effect of Exogenous Purins. Uric Acid Content of Blood
in Gout. Hyperuricæmia in Non-gouty Arthritis. Variations
in Uric Acid Content of Blood independently of Diet. What
Relationship, if any, Exists between the Uric Acid Content of
the Blood and Attacks of Gout. Discussion of the Foregoing
Data. The Significance of Uricæmia. Sources of Fallacy in Uric
Acid Estimation. Disabilities of Modern Tests. Need for further
Investigations _pp._ 133-148

CHAPTER XII

URATOSIS IN RELATION TO GOUT

Constitution of Tophi. Mode of Formation. Localisation of
Uratic Deposits. The Causation of Tophi. Solubilities of Uric
Acid. Tophi in Relation to Uricæmia. Tissue Affinities for Uric
Acid. Retention Capacity of Tissues for Uric Acid. Clinical
Evolution of Tophi. The Cause of the Inflammatory Phenomena.
Non-toxicity of Uric Acid. Are the Precursors of Uric Acid
Toxic? _pp._ 149-170

CHAPTER XIII

THE RISE OF THE INFECTIVE THEORY

Boerhaave’s Forecast of the Infective Theory. Ringrose Gore on
Infective Origin. Leucocytosis in Acute Gouty Polyarthritis.
Chalmers Watson’s Researches on Gout in a Fowl. Trautner’s
Suggestion of a Specific Infection _pp._ 171-176

CHAPTER XIV

GOUT AS AN INFECTION

Local Foci of Infection: Dental, Nasal, Pharyngeal, etc.
Gastro-intestinal Disorders. Variation in Free HCL. Intestinal
Disorders. Infection or Sub—infection _pp._ 177-187

CHAPTER XV

GOUT AS AN INFECTION (_continued_)

Analysis of the Acute Paroxysm. The Evolution and Life History
of Gout. Analogies between Gout and the Specific Infective
Arthritides. Correlation of the Metabolic Phenomena of Gout
with the Postulated Infective Element _pp._ 188-199

CHAPTER XVI

CLINICAL ACCOUNT

Acute Localised Gout. Prodromal Symptoms. Dyspepsia.
Premonitory Symptoms of Tophus Formation. Premonitory Articular
Pains. The Acute Paroxysm. Detailed Consideration of Phenomena.
Mode of Onset. Localisation. Nature of Pain. General Phenomena.
Pyrexia. Changes in the Blood. Uric Acid Excretion. Local
Phenomena. Tophus Formation _pp._ 200-213

CHAPTER XVII

CLINICAL ACCOUNT (_continued_)

Acute Gouty Polyarthritis. Mode of Invasion. Distribution of
Lesions. Local Characters. Constitutional Symptoms. Changes in
the Blood. Leucocytosis. Collateral Phenomena of Gout. Lumbago,
Sciatica, etc. Incidence of Gouty Stigmata in Various Types of
Fibrositis _pp._ 214-224

CHAPTER XVIII

CLINICAL ACCOUNT (_continued_)

Chronic Articular Gout. The Joint Deformities of Chronic Gout.
Tophi: Their Evolution and Distribution. Other Sites of Tophi.
Affinities between Gout and other Diseases. Gout in Relation to
Glycosuria. Gout in Relation to Phlebitis. Cutaneous Disorders.
Gout and Nephritis. Prognosis in Gout _pp._ 225-246

CHAPTER XIX

ETIOLOGICAL AND CLINICAL DIAGNOSIS.

Articular Gout. Etiological Diagnosis. Clinical Diagnosis.
Introductory Remarks. The Diagnostic Status of Tophi. Tophi
in Relation to Arthritis. Frequency of Tophi in True Gouty
Arthritis Underestimated. Difficulty of Detecting Tophi _pp._ 247-257

CHAPTER XX

CLINICAL DIAGNOSIS (_continued_)

Acute Articular Gout. Localised Variety. Differential
Diagnosis. Infections. Acute Gonococcal Arthritis. Traumatic
Lesions. Acute Osteoarthritis. Static Foot Deformities. Hallux
Valgus with Inflamed Bunion. Hallux Rigidus. Metatarsalgia.
Gout in the Instep. Gonococcal Arthritis. Tuberculosis and
Syphilitic Disease of the Tarsal Joints or the Related Joints.
Pes Planus. Gout in the Heel. Referred Pain. Local Sources
of Fallacy. Post-calcaneal Bursitis. Synovitis of the Tendo
Achillis. Gout in the Sole. Plantar Neuralgia. Erythromelalgia.
Anomalous Sites for Initial Outbreaks _pp._ 258-267

CHAPTER XXI

CLINICAL DIAGNOSIS (_continued_)

Acute Gouty Polyarthritis. Differential Diagnosis. Acute
Articular Rheumatism. Acute Gonococcal Arthritis. Etiology.
Onset. General Symptoms. Distribution of Lesions. Local
Characters. Associated Phenomena. Secondary Syphilitic
Arthritis. Acute Rheumatoid or Atrophic Arthritis. Age and
Sex. Onset. General Symptoms. Distribution of Lesions. Local
Characters. Associated Phenomena. Infective Arthritis of
Undifferentiated Type _pp._ 268-274

CHAPTER XXII

CLINICAL DIAGNOSIS (_continued_)

Chronic Articular Gout. Chronic Monarticular Gout. Monarticular
Gout in Large Articulation a Rarity. Chronic Gout of
Oligo-articular Distribution. Its Confusion with Chronic
Villous Synovitis. Villous Synovitis Static and Non-gouty in
Origin. Clinical Symptoms of Villous Synovitis. Bilateral
Hydrarthrosis. Peri-synovial and Peri-bursal Gummata. Chronic
Gout of Polyarticular Distribution. Differential Diagnosis.
Osteoarthritis. Local Characters of Joint Swellings. Rheumatoid
Arthritis. Local Characters of Joint Swellings. Nerve
Arthropathies. Hæmophilic Arthritis _pp._ 275-285

CHAPTER XXIII

CLINICAL DIAGNOSIS (_continued_)

Skiagraphy. Significance of Local Areas of Rarefaction. The
Radiographic Types of Gouty Arthritis. Differential Diagnosis.
Infective Arthritis. Hypertrophic or Osteoarthritis. Rheumatoid
or Atrophic Arthritis _pp._ 286-292

CHAPTER XXIV

IRREGULAR GOUT

Historical Account. Murchison’s Views. Retrocedent Gout. Gout
in the Stomach. Cardiac and Cerebral Forms. Other Irregular
Manifestations. Conclusions. Infantile Gout _pp._ 293-307

CHAPTER XXV

OCULAR DISEASE IN THE GOUTY

Evidence of Gout in the Eye. Deposition of Urates. Gouty
Diathesis. Significance and Location of Tophi. Relative
Incidence of Iritis. Metastasis. Arthritic Iritis. Gouty Iritis
not a Clinical Entity. Ocular Symptoms in Hyperuricæmia.
False Gout. Retinal Hæmorrhage. Neuro-retinitis. Glaucoma.
Conclusions _pp._ 308-326

CHAPTER XXVI

TREATMENT OF GOUT

Radical Treatment of Local Foci of Infection or Toxic
Absorption. Diet in Acute and Chronic Gout. The Fallacy of
Fixed Dietaries. Thorough Physical Examination a necessary
Prelude to Dieting. Need for Collaboration of Clinician and
Bio-chemist _pp._ 327-341

CHAPTER XXVII

TREATMENT OF GOUT (_continued_)

Regulation of Diet in the Gouty. The Individual Foodstuffs,
Proteins, Carbohydrates, Fats, Vegetables, Fruits, Condiments.
Special Dietaries. Amylaceous Dyspepsia. Hyperchlorhydria _pp._ 342-371

CHAPTER XXVIII

MEDICINAL AND OTHER MODES OF THERAPY—ACUTE GOUT

Initial Purgation. Colchicum in Acute Gout. Method of
Administration. Preparations and Dosage. Colchicine, Salicylate
of Colchicine. Atophan. Alternative Remedies in Acute Gout.
Salicylates. Alkalies. Quinine. Thyminic Acid. Anodynes in
Acute Gout. Local Measures. Analgesics. Liniments, etc.
Ionisation. Massage. Surgical Methods _pp._ 372-388

CHAPTER XXIX

MEDICINAL AND OTHER MODES OF THERAPY
(_continued_)—INTER-PAROXYSMAL PERIOD

Prophylactic Measures. Treatment of Atonic Dyspepsia.
Hyperacidity due to Organic Acids. Treatment of
Hypochlorhydria. Alkalies, Atophan, and Colchicum as
Prophylactics _pp._ 389-396

CHAPTER XXX

MEDICINAL AND OTHER MODES OF THERAPY (_continued_)—CHRONIC
ARTICULAR GOUT AND ASSOCIATED MORBID CONDITIONS

Alkalies. Contrasts between Salts of Sodium and Potash.
Differential Indications for their Usage. Alternatives.
Salicylates. Benzoates. Hexamine. Iodides. Iodine. Albumen
Compounds. Collosol Preparations of Iodine. Guaiacum. Local
Measures in Chronic Articular Gout. Treatment of Tophi.
Ionisation. Surgical Measures. Treatment of Associated
Morbid Conditions. Fibrositis. Lumbago. Sciatica. Acute
Brachial Fibrositis. Local Massage. Oxaluria. Glycosuria.
Hyperchlorhydria. Gouty Phlebitis. Gouty Eczema. Gouty
Nephritis _pp._ 397-417

CHAPTER XXXI

CLIMATO-THERAPY, HYDRO-THERAPY, ETC.

Climate. Choice of Residence. Clothing. Exercise. Massage.
General Hydro-therapy. Importance of thorough Physical
Examination. Individual Reactive Peculiarities. Prophylactic
Measures. Contra-indications and Untoward Complications.
Methods of Application of General Hydro-therapy. Immersion
Baths. Aix and Vichy Massage. Vapour Baths. Indications for
Sub-thermal Baths. Local Hydro-therapy. Varieties of Douche.
Treatment by Hyperæmia _pp._ 418-430

CHAPTER XXXII

MINERAL SPRINGS AND CHOICE OF SPA

Difficulties of Definition and Classification. Radio-activity.
General Principles of Spa Treatment. Physiological Action
of Radium Emanation. Activation of Body Ferments. Influence
of Uric Acid Metabolism. Increased Excretion of Uric Acid.
Subjective Phenomena of Gout in Relation to Blood Content and
Excretion of Uric Acid. Therapeutic Action and Application.
Alimentary Disorders. Glycosuria. Raised Blood Pressure. Choice
of Spa. The Spare and the Obese. Waters Suitable for Various
Types of Dyspepsia. Bickel’s Experiments. Mineral Waters in
Associated Morbid Conditions. Glycosuria. Oxaluria. Phlebitis.
Respiratory Disorders. Fibrositis. Gouty Eczema. Uric Acid
Gravel. Arterio-sclerosis. Chronic Nephritis. Concluding
Remarks on Spa Treatment _pp._ 431-465

INDEX _pp._ 457-469