COLUMBIA LIBRARIES OFFSITE HEALTH SCIENCES STANDARD HX641 25599 RC71 .Sm5 Introduction to the RECAP '!'!w,vl'/Xv.VA"/! /v^ / / rti ^ ILibrarp PRE SENTED IN >IE>IOR\' OF ^MLLL\MHEXRYDRAPER 1830-1901-PaxdS-1855 AND HIS SON WILLIAM KlNNiCUTT DRAPER 1863-1926-P.AND S.-1888 ifa i M t yAfe4?.-Ai^-^-:^^-A/rA^ A^-Afa^fa^^^ Digitized by the Internet Archive in 2010 with funding from Open Knowledge Commons http://www.archive.org/details/introductiontoouOOsmit ilacmillan'5 iHanuals of jaetitctnc anti Surgcrg DIFFERENTIAL DIAGNOSIS WITH CLINICAL AIEMORANDA The^)^^- INTRODUCTION TO THE OUTLINES OF THE PRINCIPLES OF DIFFERENTIAL DIAGNOSIS WITH CLINICAL MEMORANDA BY Fred. J. SMITH, M.A., M.D. Oxon, F.R.C.P. Lond. PHYSICIAN (with care OF OUT-PATIENTS) AND SENIOR PATHOLOGIST TO THE LONDON HOSPITAL THE MACMILLAN COMPANY LONDON: MACMILLAN & CO., Ltd. 1899 A^/ rights reserved Copyright, 1899, By the MACMILLAN COMPANY. Norfajooti 3prc8» J. S. Cushhig & Co. — Berwick & Smith Norwood Mass. U.S.A. PREFACE The number of works on medicine, and its various quasi-special branches, that claim the time and attention of over -burdened students and practitioners is so great that only one excuse should be offered for adding to it, viz. either to say something new or to put forward a more rational and simpler arrangement of what is old. Very little that is new will be found in the following pages, but I claim that I have attempted to arrange the old, old phenomena of disease in such a manner as to show more clearly their funda- mental meanings and relationships. I have utiHsed the data of physiology, and the facts of pathological anatomy, as the source from which to draw inferences and deductions, which in their turn constitute a critical analysis of clinical symptoms ; I have endeavoured by this analysis to lead up to the underlying principles which govern disease as well as health. Once these principles, which are few in number, are recognised, bedside symptoms become merely illustra- tions of them, varied, it may be, by local and individual peculiari- ties, yet ever stamped with such a likeness that the simplest induction will speedily explain the organ of their origin. Isolated, or apparently isolated, facts thus lose their isolation, and become members of a related community ; they no longer require separate efforts of memory for their retention, but fall naturally into their places as deductions from a universal law. vi DIFFERENTIAL DIAGNOSIS I thus hope that what I have written will serve not as a text- book of medicine, or, indeed, as a storehouse of facts, but as a series of pegs whereon to hang a chain of knowledge which will be ever increasing link by link as experience grows more ripe, and a larger and larger number of varieties of symptoms are recognised as varieties, and not elevated to the rank of species by ignorance of the connecting links. Inasmuch as there is little here that is new, I have mentioned very few authorities for the clinical points I have utilised ; they are the common possession of the medical profession at large. A few original ideas of my own are scattered throughout the work ; time and clinical testing alone can show their value, but they are at least founded on some considerable experience, and the method of their exposition is that which I have found useful in teaching by the bed- side. My great wish has been to be as accurate as possible, so as not to mislead by false statements, and so sin by commission ; the omissions are only too glaring, but limitation of space forbade further inclusions. FRED. J. SMITH. 138 Harley Street, W. CONTENTS CHAPTER I PAGE Introduction — Definition of diagnosis : Steps in diagnosis — Antitoxin treatment — Causes of disease : Comments on the various classes of causes — Processes of disease : Inflammation ; Degeneration ; New growths ........ I CHAPTER II Physical signs v. symptoms — Pathology, meanings of — Contagion v. in- fection . . . . . . , .21 CHAPTER HI Micro-organisms and disease — Reasons for believing a disease to be due to microbes — Differential diagnosis of exanthems : General explanation of the phenomena ; Special diagnostic points — Varicella v. Variola — Variola v, syphilis — Diphtheria v. ulcerated throat — Measles, rotheln, and scarlet fever — Typhus v. typhoid — Cholera v. diarrhoea — Erythema — Influenza — Venereal diseases . . ,25 CHAPTER IV Diseases of thoracic organs — Section I. Lungs and pleura — Pyrexia — Cough, useless and useful — Sputum, quantity, quality — Respiration viii DIFFERENTIAL DIAGNOSIS PAGE — Dyspnoea — Pressure effects — Pain in chest, secondary or idio- pathic — Physical signs — Comparison of two sides : Inspection ; Palpation ; Percussion ; Auscultation — Laryngeal affections — Pneumothorax: Cavities — Phthisis, pneumonic, fibroid, haemor- rhagic, miliary, diagnosis of — Pneumonia, incipient, central ; Is it a specific disease ? — Acute bronchitis and bronchopneumonia — Chronic bronchitis, its pulmonary complications — Pleurisy, causes of — Pleuritic effusion — Intrathoracic growths — Growth v. aneurysm . 47 CHAPTER \N— Continued Section II. Heart and pericardium — Local symptoms and physical signs — General symptoms and physical signs — Heart organs : Hyper- trophy and dilatation ; Compensation and failure ; Diagnosis of hypertrophy and dilatation, of compensation and failure — Endocardial V. exocardial sounds — Indications and meaning of bruits — Morbus cordis without bruits — Ulcerative endocarditis : Its pathology and diagnosis: Prognosis in heart disease . . . .112 CHAPTER V Diseases of nose, throat, and alimentary system — Haemorrhage : From nose, causes ; Issuing by mouth, local causes — Hsematemesis v. haemoptysis : Causes of haemoptysis ; Causes of haematemesis — Issuing by anus — Causes of melaena — Causes of haemorrhage per anum — Vomiting : Causes — Colic : Diagnosis of causes of ; Treat- ment of — Colic without collapse : Differential diagnosis of causes of — Colic V. peritonitis — Differential diagnosis of forms of calculus — Diarrhoea and constipation, causes and diagnosis of — Diarrhoea in phthisis — Ascites, primary groups of — Ascites v. encysted fluid — Dyspepsia v. gastric ulcer . . . . . .148 CHAPTER VI Diseases of the urinary organs — Normal urine, variations in health ; Variations in disease, frequency, quantity, colour, specific gravity, pathological constituents, tests for and meaning of — Albuminuria — Surgical kidney — Pyuria, causes and diagnosis of — Haematuria, indications of locality and cause — Casts — Urates — Oxalates — Phos- CONTENTS ix PAGE phates — Uric acid, consideration of — Sugar, consideration of — Uraemia, diagnosis of — Suppression v. retention : Causes of suppres- sion and retention — Bright's disease, varieties of — Urine in consecu- tive nephritis — Stone, tubercle, and carcinoma of kidney — Diabetes, phosphatic, insipidus . . . . . .185 CHAPTER VII Affections of joints — Symptoms of joint trouble — History of illness, etc. — Charcot's joints — Flat foot — Gonorrhceal rheumatism — Gonorrhoeal rheumatism v. simple — Traumatism — Hysteria — Synovitis — Tubercle — Rheumatism — Gout — Rheumatic gout — Rheumatoid arthritis — Differential diagnosis of last four affections — Arthritic diathesis . 229 CHAPTER VIII Section I. Anatomy and physiology of the nervous system — The neuron — The peripheral nerves — The cord — Medulla — Brain — Functions of the same — Motor, sensory, and reflex tracts — Trophic influences — Inco-ordination — Section II. Table of diseases of the nervous system — Section IH. Differential diagnosis of nervous diseases — Essential V. secondary ; Organic v. functional — Peripheral neuritis — Spinal cord, systems of, indiscriminate lesions of — Cord v. peripheral nerves — Medulla and pons, tracts and cells in — Mid-brain hemiplegia — Cranial nerves — Brain — Jacksonian epilepsy — Traumatism — Organic lesion — Tumours of brain . . . . . .247 CHAPTER IX Urgency cases — Haemorrhage — Other vascular lesions — Traumatism — Sudden death — Lesions of nervous system — Poisoning — Differential • diagnosis ........ 326 CHAPTER I INTRODUCTORY REMARKS ON DIAGNOSIS IN GENERAL Dr. Pye Smith once defined pathology very pithily as "a chat about the etiology of disease." Though I think the definition some- what too narrow, we may accept it provisionally and then define diagnosis as "the complete analysis of etiology," for we cannot consider a diagnosis as absolutely final and finished until we have probed etiology to the bottom. The process of diagnosis, thus scientifically considered, will then consist of three stages : — (i) The collecting of as complete a list as possible of the immediate pheno- mena of disease w^hich are universally and by common consent termed symptoms and physical signs, e.g. cough, pain, diarrhoea, paralysis, palpitation, etc. (2) Inferring or deducing from these collective phenomena a primary or gross diagnosis as to the organ or organs affected and the general nature of the disease, e.g. bron- chitis, dyspepsia, neuritis, morbus cordis, etc., thus arriving at what we may call the generic title of the affection. (3) A final step, viz. the identification of the specific cause at work, thus adding a specific name to the generic one, e.g. tubercular bronchitis, gouty dyspepsia, septic pneumonia, rheumatic arthritis. The first of these three steps is naturally the simplest proceed- ing, for it consists only in taking a complete history of the case. Each hospital school has its own particular method of case-taking, and each teacher naturally thinks his own school the best, and I therefore give a preference to the following card, which is in use at the London Hospital. It has, I believe, at least the merit of not omitting anything of importance if used systematically. C . B DIFFERENTIAL DIAGNOSIS chap. Instructions for case-taking in Medical Wards : — I, The Clinical Clerk to enter the heads of the case, and date of the Patient's entry to Hospital, and fill in the registered number as soon as possible. Insert dates at which the notes are taken. II. State what the patient complains of — using his or her own words verbatij7i as far as possible, and when using the names of the days of the week, be sure to insert also the day of the month. III. Family History — Number and condition of health of those living. Ages and diseases of those dead. Note any family tendency to disease. This section is especially useful for the following diseases — rheumatism, gout, phthisis, haemophilia, nervous diseases, asthma, heart disease ; though it must not be omitted in any case. Personal History — Habits (stating quantity and kind of alcohol taken), occupations, residences, previous diseases and illnesses, noting especially the dates of illnesses or changes. If in Hospital before, get the registered number, and insert it in the present notes. Especially, never omit to inquire for any disease which may stand in etio- logical relationship with the present illness, e.g. rheumatism with tonsillitis or morbus cordis, gout and lead poisoning with cirrhotic kidney, syphilis with many conditions ; these three diseases should never be omitted^ their absence, as well as presence, being equally carefully noted. Present Illness — Date and manner of commencement : order of symptoms and dates of occurrence. A useful question here is — When were you last quite well ? and trace the ill- ness step by step from this. Probable Cause — Insert here your own opinion and also that of your patient, and any higher available opinion. IV. Present Condition — General condition. This should never be omitted ; the most important items are perhaps — expression of face, colour of face (anaemia, cyanosis, etc.), oedema, nutrition, distension of veins, sleep, easy respiration, etc. ; note position of patient in bed, whether sitting up or lying down, whether restless or comfortable and quiet, etc. V. Digestion — Tongue, teeth, throat, appetite, vomiting, hasmate- mesis, bowels. Syinptoms — Fulness or pain after food, flatulence, colic or other disturbance. Abdominal pain or tenderness. I DIAGNOSIS IN GENERAL 3 Liver — Size and character as determined on percussion and palpation. Whether tender or not. Jaundice. Spleen — Percussion, palpation. Abdomen — Its physical condition as indicated by palpation, percussion and mensuration. Distension, retraction. Ascites. Tumour, Abdominal pain. VI. Vascular System — Pulse frequency and characters, condition of arteries, veins, capillaries. Heart palpate, percuss, auscultate. Syvipto77is — Palpitation, pr£ecordial dulness, pain, etc. VII. Respiratory System — Dyspnoea, frequency, characters of respir- atoiy movements, Cough, expectoration, hsemoptysis. Physical examination^ inspection, palpation, percussion, auscul- tation, condition of larynx. VIII, Nervous System — Geiieral condition. Intelligence, mental state, sleep, speech. Vertigo, delirium, coma. Complaints of head pain, vomiting, numbness, neuralgia. Paralysis, convulsions, spasms, tremor. Motor power — Limbs, trunk, action of sphincters. Ability to walk and do ordinary work. Power over large joints, small joints, finer movements of fingers, e.g. writing. Cranial nerz'es — Movements of eyes, tongue, face, palate. State of pupils. Special senses — Ophthalmoscopic appearances. This should never be omitted, but is more especially important in (i) anaemia, (2) Bright's disease, (3) cerebral and spinal diseases, (4) syphilis, (5) any disease in which amblyopia is complained of. Sensibility — Tactile sensibility of skin, anaesthesia, hyper- assthesia, dyssesthesia (perverted sensations, e.g. numbness, burning pain, etc.). Sensibility to heat and cold. Reflexes — Superficial and deep. Patellar, plantar, wrist, ab- dominal, cremasteric, etc. In Spinal Cases., gait in walking, power in each limb, condition of sphincters. In any nervous case the special points to be attended to without exception in any case are (i) hereditary, (2) manner and time of onset, (3) condition of reflexes, (4) static and locomotor equilibration. 4 DIFFERENTIAL DIAGNOSIS chap. IX. Locomotor System — State of bones, muscles, joints, scars, nodes. Skin^ moist or dry. Bed sores. X. Lymphatic Glands — Neck, groins, axilla. Size, mobility, sup- puration. XI. Urine — Frequency of micturition. Quantity, colour, reaction, specific gravity. Albumen. Sugar. Deposit. Microscopical and chemical characters of deposit. XII. Generative System — Menstruation, frequency, duration, quan- tity in excess or otherwise, whether painful, other discharges. Conditions of uterus and pelvic organs (when examination is possible). XIII. Treatment — Prescriptions and diet to be entered, and all alter- ations noted with dates. XIV. Progress of Case to be noted as occasions may require. Pulse should be recorded whenever the temperature is taken. Urine must be noted at least once a week. When important symptoms or complications occur, besides a description in the text, an indication should be given in the margin. As a good general hint for note making, remember m all cases^ without exception^ a note should be made on the first day after admission ; in all acute cases a note should be made every day while the symptoms persist; after this, notes may be made less frequently, but any fresh symp- tom or complication must be immediately noted. XV. Result — A description of the patient at the time of discharge, or the mode of death, should be given at the termination of the case. This is, in some respects, the most important part of a Clerk's duty, and must on no account ever be ojnitted in any case. The description need only be of that system or systems which have been affected by the disease. The Clinical Clerk to sign his name in full on completion of the case. At the second step diagnosis frequently stops short ; possibly, though let us hope rarely, from carelessness or indifference on the part of the observer, as when a cough or diarrhoea is treated by a dose of opium (reluctance on the part of the patient to submit himself to thorough examination has sometimes too to be over- come) ; more frequently and excusably because further information is useless in the present state of our therapeutical knowledge, or because some very obtrusive symptom must be immediately subdued I DIAGNOSIS IN GENERAL 5 if the patient's life is to be saved even temporarily, as may happen in hyperpyrexia from any cause, or in the agony of calculous colic ; most frequently and really unavoidably because the further informa- tion required is absolutely unattainable until death has afforded the opportunity for more thorough investigation, as in a case of severe haemoptysis, for example, or rapidly fatal septic pneumonia or per- forative peritonitis. Like the first step, this second one is in many cases a very simple matter, but to the student and young prac- titioners it is apt to appear easier than it really is. Nothing but wide experience by the bedside and, above all, in the post-mortem room, will convince us of the difficulties which surround even the simplest accurate diagnosis, and there can be no greater mistake than that of at once accepting the most obvious as the most correct. Apart from the above exceptions and difficulties, it should ahvnys be our endeavour to take the third and final step in diagnosis. Of its importance generally in clinical medicine examples are almost superfluous, the point is so universally admitted. I need only mention the flood of light thrown on an obscure case of albuminuria by the recollection of a forgotten attack of — it may be mild — scarlet fever, what a relief to our anxieties it is to find a bad sore throat as a precedent fact in a case of squint, and, per contra, how the dis- covery of the bacillus tuberculosis in the sputum redoubles our anxieties about what was previously looked upon as a simple catarrh. But beyond all this the discoveries of the last quarter of a century in bacteriology have made this third step of much greater importance still, for they have held out to us hopes of cure in many cases hitherto incurable. Whether these hopes are destined in the future to be realised or disappointed it would be rash to prophesy, though certainly the results hitherto obtained are encouraging. As the basis on which these hopes are founded is very germane to the completion of a diagnosis, we may here enunciate its principal points. Stated in order the argumentative propositions run thus : — (i) Many groups of symptoms or diseases are caused by microbes invading the body. (2) In many of these, if not in all, the actual symptoms are caused by a toxin or toxins manufactured by the microbes, either directly from their own metabolism or indirectly from the tissues of the victim. (3) The spontaneous cure of such symptoms is, at least in some cases (possibly or probably in all), effected by an anti- toxin or neutraHser of the previous toxin; this in turn 6 DIFFERENTIAL DIAGNOSIS chap. may apparently be produced either by the microbes or the tissues. (4) Such antitoxin can be obtained, with more or less success (by methods which need not here be entered upon), in quantities and condition available for therapeutic uses. (5) It should follow, and has in many cases already been proved to follow, that the injection of such antitoxin, if effected early enough in the disease, is efficacious in curing the patient. These propositions would appear to be scientifically demon- strated, but there is one point which is still in doubt, and that the most important one from our present point of view; it is this — does each separate and identifiable microbe produce a special and specific toxin, i.e. a poison of definite composition — as definite, say, as morphine or other alkaloid — peculiar to itself and requiring for its neutralisation an equally definite and specific antitoxin? or, on the other hand, do many diiferent microbes produce a common toxin, so that the antitoxin produced by one microbe or method of preparation can be used for the toxin of another kind of microbe? All the evidence — at least the weight of evidence — we at present possess points in the direction of the former of these two supposi- tions being the true one. Witness the almost conclusive clinical experience in the treatment of diphtheria, of rabies, and of tetanus, as well as the brilliant successes and the disappointing failures in cases of septic disease, in which the particular microbe at work is less definite or less famihar, and where success has been com- pulsorily attributed to the right antitoxin, failure being due either to the wrong antitoxin or to a too late application. I think, there- fore, we shall be obliged ultimately to admit its truth, and we can see at once on this admission how enormous is the importance of the third step in diagnosis, to be able to say, " This case of illness is due to this particular microbe, and I must use its antitoxin as quickly as possible." Besides this therapeutical use of a completed diagnosis, the principle of toxins and antitoxins has lately been applied to that completion itself, vide Typhoid Fever. May we not hope in the future to see the two procedures more frequently working hand in hand, complementary to one another? Causes of Disease in General In the special sections of this work we shall always be consider- ing diagnosis as an induction from symptoms. We may here in the. I DIAGNOSIS IN GENERAL 7 introductory or general chapter briefly review the matter from the other standpoint, and see what are the causes of disease and the general processes by which these causes produce the symptoms which we have later to analyse. The fundamental causes of disease belong to but few really separate categories, which may be presented in comprehensive forms as follows : — Causes of Disease A. From without (environment in the larger sense) : — O •5 <^ O ^ to c '6 o U r Chemical (on the surface of the body). Traumatism \ Grossly physical eftects, and those of excess of heat I and cold. . , . I External — fleas, lice, Alacroscopical or coarselv I , •^ . ' - bug's, etc. microscopic . • K . 1 ^ 1^ Internal — worms, etc. (i) Essentially patho- genic, or (2) rend- ered so by peculiar Parasitic Poisons flj 2 c c £ ^ c 2 o 3 ° ^ . a rt rt .£ •- c ^ Finely microscopic (mi- crobes) (opportunities ofvital- ity or food supply. arsenic, alkaloids, pto- ^ Recognised as such maines, etc. Ordinary articles of food rendered injurious by circumstances of too free indulgence, imperfect mastication, decomposition, etc., and also by unusual changes in digestion with absorption of poisonous ptomaines, etc. /Perforation of a hollow tube from any cause what- ever. Direct extension of processes of disease from one organ to another. Carried in the blood or lymph stream, convected from place to place. Forced malpositions, as twisting of tubes and dis- locations of more solid organs. B From within (idiopathic, so to speak) {a) The more or less direct effect of altered function in one organ upon another organ, e.g. the inter- 8 DIFFERENTIAL DIAGNOSIS chap. related functions of liver, stomach, kidney, pancreas, etc. b) The effects of wear and tear, age in its physiological sense. {c) Congenital or inherent debility of tissue either absolute or relative to the work demanded of it. {d) New growths of intrinsic formation. That the apparently innumerable causes of disease should be reducible to such a small number of independent types is at first somewhat startling, but I think a little consideration and comment will show that the above errs on the side of excess rather than defect, and that some of the groups overlap. Traumatism. — In its widest sense — of injury — this would in- clude nearly all the other causes of ill health which arise from the environment of the individual. Food imperfectly masticated or otherwise by its physical qualities unsuitable for digestion is, for example, very likely to cause a wound of the stomach with its attendant evil consequences. In its grosser sense the cause belongs almost entirely to surgery. We may recognise its probable single action when health speedily returns after the removal of an exciting causa causans. Mr. Hutchinson would refer most skin diseases to this category or the next. Parasites. — Of the grosser forms of external parasites the action is mildly irritative or traumatic, increased largely by scratching or rubbing. If through the wounds thus produced microbes find an entry to the blood or lymphatic vessels — the skin teams with ever watchful enemies of this character — the result may be as bad as, in fact is identical with, the other microparasitic troubles, the skin, instead of some mucous or other surface, being the point of entry which is thus more easily traceable. Of the larger internal parasites — collectively denominated worms — the results are more varied. Thus round and tape worms may reside within us without causing any trouble whatever, but they may cause much irritation with reflex symptoms, they may block passages, e.g. the common or cystic bile duct, or cause tumours (hydatids), or by migration of the young {Trichina spiralis^ cause serious symptoms in any organ ; the Anchylostoma duodenale may produce profound anaemia by abstraction of blood. To the second^finely microscopic — group of parasites the ever- multiplying discoveries of medical science are rapidly relegating every disease to which human flesh is heir. Possibly enthusiasm I DIAGNOSIS IN GENERAL 9 rather than hard facts is having something to say in this matter. When present in numbers, or with virulence sufficient to create a pathological disturbance in the body, they have one almost invari- able and common result, viz. pyrexia (in primary syphilis, in gonor- rhoea, and possibly a few others — chronic rheumatoid arthritis, for example — this is least marked, and even in tubercle it is doubtful how much of the fever is due to the specific bacillus), a result to be expected when we consider the enormously preponderating influ- ence which metabolism has in the production of our supply of body heat, and then remember that in microbic disease either a toxin or a contagium vivum is, or may be, carried all over the body, stimu- lating every part of it to a metabolic antagonism.-^ This pyrexia itself, however, almost immediately offers points of difference aiding diagnosis, in suddenness of onset and rise, in duration, in irregular variability or regular periodicity; cf. typhoid and typhus, scarlet fever and measles, malaria and general septicaemia, etc. In many cases, too, the seat of inoculation or of first morbid appearances is available, the uterus in the puerperium, the tonsil in diphtheria, the genito-urinary apparatus in venereal diseases. Still later we have the selective seat in which the poison has left its traces, such as the peripheral nerves in diphtheria, the kidneys in scarlet fever, the spleen in malaria, etc. Further points will be found in the special sections. Poisons. — Poisons, as ordinarily understood, may be divided into three classes : (i) Those which act upon the alimentary canal, and are practically not absorbed, e.g. all corrosives and many irritants; (2) those which only act after absorption, e.g. most alka- loids; (3) those which act in both ways typically, phosphorus, arsenic, and oxalic acid. The first and last classes will show ali- mentary symptoms in excess, vomiting and diarrhoea within a short time of being taken, and have one point in common, in marked contrast to the common symptom in microbic invasion : this is a subnormal temperature, largely induced by shock and mental anxiety. The second class in its entirety, and the third in the later phases of a case, show appropriate features according to the selective affinity of the poison for special organs, digitahs for the heart, conium and strychnine for the motor nerves, phosphorus for liver and muscles, opium and belladonna for the cerebral cortex, etc., and thus the case may be provisionally or even finally diagnosed in conjunction with the history. 1 This metabolic activity or antagonism not only explains the phenomenon of pyrexia, but also lies very close to the root of ^vhat ivide Processes of Disease) we know as inflammation. lo DIFFERENTIAL DIAGNOSIS chap. When articles of diet become injurious, they too, like the more virulent poisons, produce symptoms in one of two ways: (i) by acting as immediate irritants to the alimentary canal, with vomiting and purging, as in ptomaine poisoning, or in actual surfeit of food otherwise wholesome; (2) by pouring into the blood or lymph stream a greater supply of nutriment than can be adequately disposed of in the great chemical laboratories of the body ; hence arise, more immediately, unpleasant sensations in the shape of sleepiness, biliousness, headache, etc., and remotely, a storing up of an undue amount of fat — obesity — flabbiness of body and mind, general lassitude, etc., and perhaps more remotely still, gout and goutiness, with all their pains and penalties, and possibly also a lessened resistance to attacks of microbic troubles. Immediate Surroundings. — From the little world of its own special environment every internal organ, which has no immediate and direct communication with the larger external world, gets all its serious troubles. The blood and lymph that bathe its tissues bring with them the chemical or vital poisons that interfere with its physiology, or cause grosser mischief still, e.g. nephritis, acute yellow atrophy, meningitis, endocarditis, etc. ; the perforation of a tube allows its contents to become a serious source of irritation to neighbouring structures — gangrenous inflammation from extra- vasation of urine, for instance, when ureter, bladder, or urethra is ruptured, or peritonitis when the contents of the alimentary canal are allowed to escape freely into the peritoneal cavity. Inflamma- tion has but slight respect for the fascial or fibrous boundaries laid down for its guidance by anatomists, but spreads with but Httle hesitation from meninges to brain or cord, from endo- or peri- cardium to myocardium, from stomach to liver, etc. Displacements of the heart by pleural effusions or more solid growths will cause serious interference with the circulation ; a displaced kidney brings about a great deal more than simple mental worry ; twisting of the gut, or even of a pedicelled tumour, may, and often does, bring about a fatal illness. All these are illustrations of the working of the internal environment, and yet there are but few of them which with equal propriety might not be put under the heading primarily of poisons or traumatism. Arising from within — Idiopathic Diseases. — It is only by courtesy — because we cannot always discover the original culprit — that disease in one organ, almost certainly arising from the wrong- doing of another, can be called idiopathic, or that this group can retain its position amongst the primary causes of disease. We often I DIAGNOSIS IN GENERAL ii speak of a primary congestion of the liver, or of an idiopathic anemia, but in both cases it is extremely probable that the ali- mentary canal is the first offender by passing an excess of suitable, or some unsuitable, material to the liver or blood, which in turn exhibit the symptoms of complaint ; and even now we have to throw the blame rather on the individual, who has by over-feeding or neglect of defecation originally induced a plethora of nutrient material or absorption of poisonous products of food decomposition unavailable for nutritive purposes. In pneumonia and bronchitis danger but rarely arises from obvious asphyxia ; it is almost constantly due to the difficulties the heart experiences in keeping up the circula- tion. This in turn may be due to the imperfect oxygenation of the blood by the lungs. Still the lung trouble is originally derived from without. When the functions of the kidney are imperfectly per- formed every organ in the body feels it, owing to imperfect removal of waste ; yet the kidney itself has suffered for the fault of stomach, or from the introduction of microbic toxins. In fact, the more we inquire into this group of causes, the less the reason for retaining it, and the more does it divide itself up amongst the other groups. Wear and Tear. — In wear and tear we get the first trace of disease really independent of external conditions ; they are the essential conditions under which all living things exist. It is a common idea with the laity that in seven years every cell of the body is changed in its constituent molecules. As far as I know, there can be no exact foundation for this belief, but it probably, for all that, contains a pregnant approximation to the truth, and should loss — however gradual — be not equalled by repair and re- placement, function must suffer, with the inevitable reaction known as dis-ease. The deficit in childhood is evidently nil, and as age advances, with waning elasticity in power of repair, it may be extremely minute, so that many years may elapse before the resultant loss of function is sufficient to attract attention. I think it probable that many cases of so-called cirrhotic kidney — and a better illustration of a chronic insidious disease could not be given — are thus induced. The kidney mischief — want of repair in epithelial cells — acts and reacts in turn upon the vascular system, where indeed, in the shape of arterio-capillary fibrosis and atheroma, the effects of age are more visible and pronounced, and also more serious than in any other organ or tissue. This vascular degenera- tion operates in two ways: (i) directly, the vessels themselves becoming brittle and absolute rupture taking place, or by losing 12 DIFFERENTIAL DIAGNOSIS chap. natural elasticity ^ they gradually yield to the blood pressure within them, and aneurysms, large or small, single or multiple, form, with all their attendant dangers; (2) indirectly; the minuter vessels by their pathological changes either (thrombosis) starve outright the tissues to which they are distributed, or (by thickening and altera- tion of wall) interfere with that due interchange of nutrient and waste material which is the life of the tissues, and thus lead to such impaired vitality that the tissues cannot adequately resist untoward influences — toxins, etc, — nor properly repair damage inflicted upon them. It is by such considerations as these that we are led easily to understand how in old people or those prema- turely worn out (alcoholic excesses, physical toil, chronic lack of nourishing food) the prognosis of disease is made much worse, and also to appreciate why symptoms in such patients may be unexpectedly obscure or insidiously vague ; pyrexia, that constant accompaniment of metabolic resistance and cell warfare, may be but slight, or even absent in cases which would otherwise be termed acute ; the foundations of life may be sapped and death intervene while we are still waiting for the explosion of general and local manifestations that should tell us where the enemy is attacking; a smouldering pneumonia, an apyrexial empyema, a chronic and insidious uraemia will illustrate the point. Congenital or Inherent Debility of Tissue. — Considered strictly, this whole group can only be a particular illustration of the influence of the immediate environment, of the physiological — or pathological rather — influence of one organ upon another, for during intra- uterine life the foetus is as much a part of the mother as her kidneys or heart, and is as much dependent for its health and integrity upon the due interrelation of her organs as are those organs them- selves dependent upon one another. For more practical or clinical purposes, however, the matter assumes a different aspect, and we may divide these into three fairly distinct categories. First, those cases in which an active process of disease is going on in the child at the time of birth, a disease which has actually attacked it — been transmitted to it conveys a slightly different impression — while it was part of the mother. Syphilis and the acute specific fevers offer us typical examples of this, and recent reports would seem to render it possible, if not probable, that tubercle may in a similar way attack a child in utero. Simple anatomical deformities might ^ It must be remembered that elasticity essentially consists in a " power to return to an original form after a distorting force of any kind — pull, pressure, or twist — has ceased to act." I DIAGNOSIS IN GENERAL 13 be placed in the same class. Secondly, those cases in which inherent defect of tissue is assumed — rather than proved — to exist to explain certain so-called idiopathic affections. A child, for instance, is born healthy to all appearance, and remains so for years, and yet without any ascertainable cause disease makes its appear- ance in certain structures or organs ; mental deficiencies, primary sclerosis of parts of the nervous system, primary myopathies, haemo- philia, would be examples of this class, amongst many others, in which we invoke heredity as a deus ex machina. Thirdly, the prin- ciple may with a little extension be used to explain those delightful words, " idiosyncrasy," " dyscrasia," " diathesis," etc., which are such beautifully simple ways of explaining (! !) our ignorance of etiology. Thus, a number of people take a similar dose of a drug; some exhibit marked effects, others none. Why ? Oh, idiosyncrasy ! Again, a dozen individuals are exposed to the same unusual dis- turbance of gross environment ; one gets acute rheumatism, another nephritis, another pneumonia, another pleurisy, another chorea, and some show no trace of the storm. Why? Oh, different diatheses is the glib reply. However, explain or mystify the matter as we may, the facts remain, and we utilise them clinically when we insist upon the importance of careful inquiry into the family history of a patient, and into the previous illnesses that may have occurred of a similar nature to that for which our advice is sought. The layman puts the same idea into different words when he exclaims, " The old doctor is the man for me; he understands my constitution." New Growths. — Of the exact etiological factors underlying the starting of a primary new growth, our real knowledge up to now amounts to — nil. Pathologists were lately — and perhaps even now are — keen in the pursuit of a hypothetical cancer microbe — a psorosperm, it was called. If such exists, its entrance, its life, and its death are still mysteries to us. The only clinical causes we can yet appreciate are blows as the starting-point of many sarcomata, and chronic irritation for many epitheliomata, but we still await anything like an explanation of the vast bulk of growths of a malignant — or innocent, for that matter — nature. Cohnheim's theory of foetal remnants is perhaps as fascinating as any ; but even this goes but a little way. Processes of Disease However few the really independent causes of disease are thus seen to be, the individual morbid processes which they excite are 14 DIFFERENTIAL DIAGNOSIS chap. still fewer, for they overlap one another even more than the causes, both in their intermediate phases and in their final results. Of intermediate phases only two are possible. Every organ and tissue in the body possesses two primary attributes — structure and function, — and the processes of disease can only exhibit themselves as inter- ferences with one or the other, or more probably with both, of these attributes ; the diagnosis and discrimination of these interferences constitute the whole of our morbid anatomy and physiology. With microscope and naked eye we attempt, after death, or in fragments removed from the living, to find and to study the alterations in structure, and with the clinical eye we endeavour to penetrate the mysteries of altered function. Our instruments of sight, natural and artificial, aided even by most elaborate staining processes, are very imperfect for studying the finer — molecular? — structural changes, and hence, though much has been revealed, very much more remains to be discovered. But the omissions are the less important from a clinician's point of view, because, firstly, we cannot be sure that what is seen was there during life ; and, secondly, because of the limited capabihty of nature and the still more restricted power of drugs to restore structural damage, even when it can be detected or surmised. We cannot, moreover, determine what is reparable and what is not, except by that means which is our only therapeutical hope, viz. by endeavouring to promote to the utmost harmonious function, the loss of which is indeed but too frequently our only means of guessing that structure has suffered. The power, on the other hand, of the clinical eye is only limited by the amount and character of the intelligence which can, by reading and experience, be brought to bear upon unravelling the intricate web and woof of symptoms, upon determining which of them are primary and essential, and which are secondary or of less moment ; which we can directly influence, and which must be left to the control of other organs. The gross or comprehensive processes by which these inter- ferences with structure and function are brought about are : — 1. Inflammation. 2. Degeneration. 3. New growths. Inflammation. — Into the microscopic details of diminished drainage from, and excessive entrance of blood and serum into, an inflamed area or organ I do not propose here to enter, nor into the diapedesis of white and red corpuscles, nor to the differ- I DIAGNOSIS IN GENERAL 15 ence between these cells and pus, nor into the vexed question of the origin of fibroblasts. Collectively, all these constitute the struc- tural changes which we can see, and the student is too apt to lose himself in these details of a microscopic slide and not to think of the fundio Icesa of vessels and tissue cells which, from the medical, as opposed to the surgical, point of view, is the chief, if not the only, object that requires attention. It is true that we frequently call upon a surgical colleague, and rightly too, to empty by artificial means a serous cavity which has become filled with the products of inflammation, but it is immaterial to a chnician whether the nucleated cells that appear at a focus of inflammation are pro- fessional policemen or special constables sworn in for the occasion ; it is immaterial whether repair be executed by builders called in for the purpose from a distance, or by the inhabitants living in the neighbourhood ; they all have to be nourished by the food in the blood, they all are worried by similar irritants, and our only concern is to remove the irritant as speedily as possible and do our best to keep the blood in good condition. The functio Icesa of capillary blood-vessels leads to excessive, insufficient, or improper food supply to, and imperfect drainage from, the special or specific cells of a part ; this leads to altered vitality in these cells, and this in turn is exhibited by disturbance in their function — excess, perversion, or diminution, — and eventually, if the trouble be severe enough or long enough continued, the cells die outright. It is thus that we must think of inflammation in its earlier active phase — kidney cells treated in this manner allow wrong materials, albumen, etc., to escape in the urine ; they fail to pass on the right substances, or even cease to secrete at all ; hepatic cells cease their glycogenic and bile formation functions, or perform them wrongly ; the cells of the alimentary mucous membrane ex- crete vitiated digestive fluids, and when digestion has thus been improperly performed, absorption becomes a harmful process, the gut muscle too is hurried into excessive action, and diarrhoea ensues, or, if it be involved seriously in the trouble, its function ceases, and paralytic obstruction — the most serious of all forms of recoverable obstruction — occurs ; in the lungs excessive secretion or effusion fills the air cells, and thus brings about cessation of the aerating function ; imperfect nutrition of nerves sends them astray in functioning, and their property of irritability becomes excessive, insufficient, or perverted, and so the illustrations might proceed through the body. The fimctio Icesa of the tissue cells may thus be secondary to 1 6 DIFFERENTIAL DIAGNOSIS chap. that of the capillaries, but more frequently in medical practice we see it as a primary phenomenon due to a toxic condition of the nourishing plasma which surrounds them ; under these circum- stances the cells cease to a large extent their own specific activities and take up ones that are foreign to them, manufactory of an anti- toxin and other unusual metabolic processes. When thus struggling against unnatural conditions they are very liable to be attacked by fatal structural changes unless relief be speedily afforded them. It is thus I understand the evil effects of the working of blood- poisoning, whether this be generalised over the whole body, as in zymotics, or whether it arise from some quite localised process, as in a poisoned wound with absorption therefrom. When these destructive phases of inflammation have ceased and nature exhibits her limited power of parenchymatous-cell reproduc- tion, we must remember that the new or young cells have to learn their business and get accustomed to variations in their environ- ment ; they are likely at first to be of feeble vitality and resisting power, and chronic exfoliation may thus be kept up till irreparable damage is done to the organ of which they form the essential constituent. And lastly, when repair is complete we have to realise the strangling effects of the new-formed fibrous tissue, which, in us, is the best that nature can do to fill up a gap. This fibrous tissue cannot pick out urea nor biliary constituents from the blood, it cannot absorb peptones or fats or oxygen, it cannot transmit messages, nor can it contract and relax in response to messages received ; it has only one function, that of contraction into a con- dition of stable equilibrium, and this it exercises with most per- nicious effects on vessels and parenchymatous cells, strangling the one and starving the other. I have written at some little length on the local processes of inflammation in the hope of making it clear that a scar in the kidney is identical with one in the lung or liver, that a catarrh of the bronchi is identical in its processes with one of the gut ; that, in fact, the principles once grasped, details can be evolved with readiness for special cases, and pathology thus changed from a heterogeneous collection of wearying facts to a splendid illustration of fundamental laws working on lines variable within small and special limits. Degeneration. — In text-books of pathology it is usual to de- scribe this process as either a primary or a secondary phenomenon, and then to give particulars of many varieties : amyloid, brown. I DIAGNOSIS IN GENERAL 17 glassy, cloudy, fatty, mucoid, colloid, fibroid, etc. Important as this knowledge is from many points of view, it may for our present purposes be largely ignored, for both forms and all varieties mean cHnically very much the same thing, viz. diminution in vitality and functional capacity, and ultimately death, of the parenchymatous cells, whose fate is being discussed. The primary form, strictly speaking, has for its underlying essence either natural wear and tear, or congenital and inherent poor quality of material, both of which have been already alluded to as primary causes of disease ; but it is usual in clinical medicine to think of and accept as primary many varieties of degeneration, fatty, etc., which are in reality induced by an insidious form of chronic poisoning or starvation through the blood supply, which in its turn is influenced primarily by the alimentary canal and the substances put into it and absorbed thence. These are thought of as primary because it is difficult, and perhaps impossible, in some cases to appreciate the alimentary errors which are at the bottom of the matter. In other cases of so-called primary degeneration typically in the nervous system the death of the (neuron) cell, and the con- sequent atrophy and degeneration of its processes, may be brought about by the agency of very insidious microbic toxins, syphilitic for example. This probably is the explanation of many cases of tabes dorsalis, and other primary affections of the nervous system not directly traceable to inherent weakness. To see with the actual or with the clinical eye the process of secondary degeneration is usually comparatively easy and simple ; for whereas in the primary form the trouble arose from insidious qualitative changes in the supply of nutriment and the removal of waste, here it is due either to a gross interference with the quanti- tative nutritive supply, or to an equally gross mechanical interference with the protoplasm of the cells — squeezing or distortion. A few illustrations will make the position clearer. The absolute block- ing of a large (or microscopical) artery by thrombos is, embolus, or ligature, leading to coarse (or fine) gangrene or necrosis of tissue, is the most obvious illustration of the former process. It is well seen and very common in the brain, spleen, kidney, or lung. It occurs, though less commonly, in the intestine, liver, and other organs (in surgery it is common enough in limbs, or part of them). The secondary degeneration of the processes, long and short, of the neuron cells of the nervous system is a less obvious but equally certain illustration ; it differs in that the nutritive supply or stimulus reaches the process (and indeed probably also gland cells, muscles, c 1 8 DIFFERENTIAL DIAGNOSIS chap. etc.) through other channels than obvious vessels, but the degener- ative result follows as surely as does general wasting of the body at large when the stomach is seriously incapacitated. The actual rupture of a vessel may act in both ways ; it is certain that the blood supply to the part concerned is stopped, and at the same time the blood, escaping from the vessel often at high pressure, mechanically tears asunder the cells of the tissue and exposes them to every form of distortion and violence. Inflammation, again, in its reparative stages, is a potent cause of secondary degeneration through the cell strangulation its scar contraction brings about (in its acute destructive phases the destruction is wrought by the action of poisons and excessive reaction to them), and this not only in gross cases of localised trouble, but also in the more chronic and diffused forms, as, for example, in cirrhosis of the liver of alcohohc origin, in pneumonokoniosis and other forms of cirrhosis of lung. The influence of cardiac disease {q.v.\ with its back-pressure stagna- tion and increased transudation from the capillaries, acts in a very similar manner to the diffuse forms of inflammation — loss of function, then death, with a very imperfect or altogether absent power of reproduction of cells of highly speciaHsed function, this in turn followed by a fine fibrosis to fill the spaces left by the absorption of dead cells — these are the processes induced in organs and tissues by cardiac failure. New Growths. — But one diagnostic difficulty here presents itself, and that is of establishing by physical signs the presence of a malignant growth. This is frequently great, and sometimes even insuperable without surgical aid (will the Rontgen rays ultimately assist us here ?) ; but whether this difficulty be overcome or not, the pathological processes which a maHgnant growth starts in the body are comparatively simple to understand. Thus a malignant growth acts : — Mechanically \ coarsely or > or biologically ) insidiously. Of the coarse mechanical form of trouble the blockage of a hollow tube, either by projection into its lumen or by pressure from without, is at once the simplest and most common illustration. Thus the intestine, ureter, or bile-duct may be blocked, and gastric dis- tension, with vomiting and emaciation, or intestinal obstruction, with retention and absorption of faecal products, occur, or retention of urine or bile, with a more or less rapidly following toxaemia by I DIAGNOSIS IN GENERAL 19 products that should be discharged from the body. Arteries, capil- laries, veins, and lymphatics suffer in precisely the same way, with resulting anosmia, or even gangrene, oedema, or effusion, simple or chylous, according to the function of the blocked vessel. Solid organs, too, may suffer from the same gross pressure, with disturb- ance of function and distortion of structure. The brain gives us a common illustration of this class, but, owing to the fact that it, with its vessels of all kinds, are enclosed in an unyielding box, the results are complicated, for they may be due to direct pressure on specialised cells, as well as to indirect effects of altered circulation. More insidious, but equally real, mechanical (pressure, strangu- lation, disturbed circulation) effects are produced by the creeping processes of the growth, and explain the symptoms and cause of death in many cases, thus in the lung and liver, structure and function frequently suffer far out of proportion to the naked-eye bulk of the tumour. In the intestine the muscle is paralysed by these processes, and so contributes by this paralysis a large share to the obstruction. In the brain, too, it is thus that we must explain the fatal effects of a small tumour growing into a very im- portant area of the organ. This insinuation of the growth into a tissue, with violent separation of the elements, frequently sets up a diffuse inflammatory reaction in the cells of an organ, and this must also be reckoned amongst the insidious mechanical effects. The biological or vital morbid processes started by and in tumours would seem to depend somewhat upon what we may call the physiology of new growths, which may be thus summarised : — 1. They possess a great power of increase in bulk, or vitality of reproduction. 2. They would seem to possess some form of internal secretion or metabolic activity whereby chemical products are poured into the blood stream — products which are foreign to the normal tissues, and apparently of considerable power for evil in some cases. 3. They appear to possess but little or even no power of resist- ance against irritative, especially microbic, influences. (i) has already been considered as starting all the mechanical effects, both gross and fine, of tumours. It also explains (microbio- logical researches may alter in some ways this view) the phenomena of recurrence after appai^ejit extirpation, and metastases due to the transference from place to place of cells endowed with this special power of reproduction. (2) would appear in some measure to explain the anaemia and cachexia which frequently, but by no means invariably, accompany 20 DIFFERENTIAL DIAGNOSIS chap, i the existence of a malignant growth. Starvation and the mechanical effects mentioned above doubtless play the chief role, but many cases occur in which these are not sufficient to explain the great cachexia occasionally met with even when the growth does not affect an important organ. Thus does a growth insidiously under- mine health. {3) It is to the feebleness of the powers of resistance (the pro- tective reaction to irritation possessed by normal tissues) must be largely attributed the ease with which malignant growths become the seat of destructive phases of inflammation, with but little cor- responding power of allowing or promoting the reparative phases. When microbes invade, as tl^ey so frequently do, malignant neoplasms, they are but seldom killed by the growth, or even diminished in vitality, and thus it very frequently, indeed, happens that secondary septic processes carry off a patient who begins by suffering from carcinoma ; thus in epithelioma of the lips or tongue death is very often due to inspiration-pneumonia ; and, indeed, in carcinoma of the lung it is as often as not a pneumonia that finishes the scene. In carcinoma of the gut, peritonitis is to be feared long before perforation can occur, as though the growth encouraged the penetration of microbes or their toxins. Such exhibitions may with justice be termed the grosser forms of biological active processes induced by growths, an empyema or a purulent peritonitis being the immediate diagnosis. We have thus completed an outline sketch of the primary causes and processes of disease. From these, physiological deduction will lead us to expect certain morbid phenomena as the result of certain untoward influences in our environment. We must now proceed to discuss diagnosis by inductive methods, accepting the morbid phenomena (the physical signs and symptoms discovered in or com- plained of by our patients) as the threads of Penelope to lead us out of the maze, or to discover the fountain-head, and thus apply therapeutical measures with some idea of what results we hope or intend to produce. CHAPTER II notes on a few of the terms used in medicine and medical diagnosis Physical Signs v. Symptoms Symptoms are those uneasy or abnormal sensations or feelings of which the patient complains either spontaneously or as the result of verbal inquiry, e.g. pain, cough, shortness of breath on exertion, etc. It is customary also to include many other phenomena in the term, such as the results obtained by chemical, bacteriological, or microscopical research, and even some unusual conditions of the nervous system assuredly only found by physical examination, e.g. absent knee jerks, etc., but I think it well to have a sharp line of distinction where possible. Physical signs is a term used to describe those phenomena of disease (especially of the chest and abdomen) which only become apparent to the observer's senses by means of what is termed a physical examination, including, in its completest extent, inspection, palpation, percussion, and auscultation in their simple and modified {e.g. succussion) forms. If these definitions are not in every particular absolutely satis- factory, they at least form a sound and workable conception for clinical purposes. That some such definition as the above is useful, my own experience would tend to show, for I have been asked the distinction between the two sets of phenomena in a court of law, and it is no unfrequent occurrence for a student to glibly enumerate a string of the easier and less important physical signs when asked for the more perplexing and intricate, and withal more germane, symptoms, a reply which may not unfairly be allowed to annoy an examiner and create in his mind a bad impression of a candidate's 22 DIFFERENTIAL DIAGNOSIS chap. clinical knowledge. Nevertheless, it must be borne in mind that neither in science nor in ordinary usage is there a fundamental dis- tinction based on clear conceptions of existing facts. For example, pain may certainly be claimed as a symptom, and cardiac bruits as physical signs, but what shall we say of the pain-drawn face, or the cardiac bruit that is audible and troublesome by its noise to the patient ? It follows clearly that where no pressure from counsel or examiner is brought to bear, the two terms will be used almost indis- criminately. Pathology No term in medical science is used in such a loose sense, and with so many confusing ideas attached to it, as this, and one cannot wonder at the student's difficulties in trying to answer a question such as, " Give, describe, or state what you know of the pathology of such and such a disease." " A chat about the etiology " seems at first sight to be a very happy definition, but frequently the term is used much more or much less comprehensively. It cannot be too strongly insisted upon that there are at least three separate and, in some respects, different and distinct ideas contained in the word as commonly employed : — 1. The changes in organs, tissues, and fluids of the body to be found by the naked eye and microscope after death = morbid anatomy. 2. The explanation of symptoms (and often, indeed, of physical signs also) by reference to the known morbid anatomy ; this = morbid physiology or the etiology (from within) of symptoms = symptomatology. 3. The explanation of the morbid anatomy or morbid physi- ology by reference to the action or influence of the en- vironment on the organism = etiology (from without) of disease. That all these three meanings may simultaneously be read into the word is obvious from its derivation (ttci^os and Aoyos), the theory of, or a discourse on, suffering; but its everyday, and especially its examinational, meanings are ill defined. For instance, the path- ology of inflammation chiefly concerns itself with the naked eye, and especially the microscopical anatomy of the inflamed area and the changes going on in its neighbourhood, together with specula- tions as to the precise origin of the cells seen. The pathology of gout, diabetes, and blood dyscrasias in general, principally requires II TERMS USED IN MEDICAL DIAGNOSIS 23 a discussion of the primary seat of perverted metabolism, with a hypothetical explanation of the morbid physiological phenomena which arise in consequence of this perversion, morbid anatomical facts receding in the background as results rather than causes ; while, again, the pathology of pneumonia or other specific fever would be very incomplete without considerable reference to the micro-organisms which cause them, and the modes by which these parasites enter the body and attack the tissues. If no suggestions are given as to the precise form of answer required, a clear exposition of the pathology of any disease is best given by a brief, concise, but complete as possible, summary of the main (anatomical, symptomatic, and etiological) facts observed in its history, followed by a statement or discussion of those theories which have been propounded as best explaining or Hnking together these facts. As an example we may sketch an answer to the question, " What is the pathology of cirrhotic kidney ? " The most important facts observed in connection with cirrhotic kidney are : — A. Anatomical. — The almost universal discovery on autopsy that hypertrophy of the heart and degeneration of arteries have coexisted with the cirrhotic kidneys. B. Symptomatic. — The extreme frequency w^ith which patients thus afflicted suffer, and even die, from uraemia, cerebral haemorrhage, or intercurrent inflammation of some organ. The condition of the urine. C. Etiological. — That such patients are almost invariably at or past middle age, or have been gouty, or suffered from plumbism, or suffered from repeated attacks of acute or subacute nephritis. The theories suggested to account for the anatomy are: (i) Johnson's stopcock theory. (2) Gull and Sutton's arterio-capillary fibrosis. " Renal inadequacy " (a term associated with the late Sir Andrew Clark), especially if of long duration, will largely account for the symptoms, while the condition of the kidneys, as revealed by the microscope, give a sufficient explanation of this renal inadequacy. Or, to take a shorter example, the pathology of Addison's disease : — The only constant anatomical fact is destruction of the supra- 24 DIFFERENTIAL DIAGNOSIS chap, ii renal organs, and that almost constantly of a caseous, probably tubercular, nature. Pigmentation of the skin is not nearly so constant. Symptomatic facts are few and summed up in progressive debility and frequent gastric crises and a very poQr pulse. Etiological facts none constant, but tubercle bacilli often found in the glands. A theory has then to be stated and argued out as to the func- tions of the suprarenals, interference with which can produce these symptoms ; it must be compatible, too, with the fact that destruction of the organs, other than tuberculo-caseous, frequently enough does not produce the same symptoms. Contagion v. Infection These terms are often used to indicate different methods by which a disease is communicated from person to person. Unfor- tunately (as is so often the case with terms originally possessing one specific meaning), habit and common usage, but especially increased recognition of facts, have so broken down the limits between the meanings, that the words now only remain as puzzles for students. Contagion should mean transference by actual contact of person with person, while infection should be a more comprehensive term, indicating that the disease to which the adjective " infectious " is applied can be communicated from one individual to another, and should include contact as one method of such communication. The essential fact of clinical importance is the communicability of the disease; observation and laboratory work must teach us the ^^how" leaving the clinician to use such expressions as " communicated by contact," or " by microbes floating in the air and gaining entrance to a second individual either by means of milk, water, food, or by the breath, etc." Such expressions, if cumbersome, at any rate convey a definite meaning ; and until science supplies us with more accurate knowledge, " communicable " is quite sufficiently under- stood to include all such terms as contagious, infectious, etc. CHAPTER III MICRO-ORGANISMS AND ZYMOTIC DISEASES From communicable diseases to microbes is nowadays Hardly a step in thought, for the researches of the last quarter of a century have taught us that the two are essentially effect and cause. In this work, dealing mainly with clinical problems and practical medicine, I do not propose to give more than the very briefest outline of those fundamental principles of bacteriology which have now" be- come essential for all medical practitioners. Beyond those principles and their correct understanding I do not hold that it is necessary, or even desirable, that students or medical men in practice should go ; the extraordinary intricate details and scrupulous exactitude required for the scientific laboratory working of bacteriology are too engrossing for, and demand too much time from, those who do not intend to devote their life to purely scientific work of this descrip- tion. The healers of the sick must patiently wait for the results of laboratory work, recognising and using those which are immediately available for practice. These already represent a greater amount of accurate and minute knowledge of the causes and processes of disease than all the previous centuries have yielded. Meanwhile the following numbered paragraphs contain the principles of the subject in a form easily assimilable, and only to be acquired from monographs by a very tedious process of analysis. . I. Micro-organisms do exist in countless myriads everpvhere in nature where the conditions of moisture, temperature, and access of air are suitable. 2. Their genera and species are probably more numerous than those of all animals or plants visible to the naked eye. 3. They are too small to show generic or specific distinctions 2 6 DIFFERENTIAL DIAGNOSIS chap. in their organs, consequently the classification of them for scientific purposes rests on : — {a) Gross outward shape — cocci, bacteria, bacilli, spirillum, etc. {b) Their methods of aggregation and segregation. {c) Motility or the reverse. {d) Their chemical and vital reactions to and on their artificial environment, e.g. aerobic or an^robic, whether they liquefy gelatine with or without the production of gas, or whether they do not liquefy it, what nutrient medium do they best flourish in or on ; colour and appearance of the growth, etc., etc. {e) Their reactions to various staining and decolourising re- agents. (/) And most importantly, their influence upon their host after inoculation into a vein or tissues or serous cavity, etc., e.g. whether they produce any symptoms of ill-hfealth or not, the character of the symptoms, and the anatomical results on autopsy of the animal, etc. In this way they have been divided into two broad groups, the pathogenic and the non-pathogenic, a distinction which frequently breaks down when microbes gain access to a part of the body in which they are not usually found, e.g. the bacterium coh commune is a natural inhabitant of the alimentary canal, but it seems to cause very serious mischief when it gets into the tissues generally. 4. Those now known to produce, and generally accepted as producing, disease (the pathogenic group), constitute probably only a minute fraction of the whole number of species. 5. To prove that one particular microbe and no other is the cause of a given disease or symptom-complex, the following condi- tions must be rigorously fulfifled : — (a) It must be constantly found in the blood, tissues, or dis- charges of the individuals suffering from the disease in question, {b) From this source a culture must be prepared in a sterile medium, and the particular microbe isolated and grown in pure culture for some generations. {c) From such absolutely pure culture it must be introduced into a fresh healthy individual of the same species as the original sufferer. Ill MICRO-ORGANISMS AND ZYMOTIC DISEASES 27 {d) This inoculation must reproduce the disease in the second individual. (e) The special microbe must again be found in the second animal in the same situations as before. In the strict fulfilment of these laws are contained all the difficulties of scientific bacteriology. They can only be appreciated by those of experience, and to publish the crude and inaccurate results of the dabblers in the science is merely to waste paper, and to retard the progress of medicine. 6. AppHed to man and practical medicine there is only one microbe which has gone completely through the trial and come out triumphant, that is the organism w^hich produces cutaneous erysipelas. The reason why no others have been intentionally put to the test is self-obvious ; but laboratory accidents (only too frequently), experi- ments on animals, and justifiable deduction have so far proved the position as to leave no reasonable doubt that a microbe is at the bottom of the following w^ell-known diseases : — Group I Tuberculosis (of every form and organ). Pneumonia (? one only). Anthrax. Typhoid. Asiatic cholera. Diphtheria. Malaria. Leprosy. Gonorrhoea (.'' one only). Rabies. Tetanus. Plasrue. Of which it may be said that the type of the disease is fairly con- stant, and that one special microbe has been identified and universally accepted as the essential cause of the malady. Group II Cerebro-spinal meningitis. Dysentery. Influenza. Measles. Scarlet fever. Small-pox. Typhus. Varicella. Whooping cough. Syphilis. Of which we may say that the con- ditions and circumstances under which they occur, together with the regularity of their symptoms, leave no reasonable doubt about each being caused by a definite species or genus of microbe, though such has not yet been satisfactorily isolated so as to be universally accepted. 28 DIFFERENTIAL DIAGNOSIS chap. Group III Pycemia. ) The diseases hitherto enumerated under lists I and Septicaemia, j II have a group of symptoms and dinical courses which are so far constant and distinctive (rash, periodicity, anatomical products, etc.) as to deserve a specific and constant name, and to lead to the belief that one, and one only, species of microbe is the causa causans. In these two diseases, on the other hand, the symptoms (fairly constant, but with no absolutely pathognomonic feature), the course, and careful bacteriological investigation, all tend to raise a conviction that more than one, if not indeed several, species of microbes may be concerned. To satisfactorily and simply account for the manufacture of the words it is necessary to state briefly the clinical classification of pathogenic micro-organisms. For this purpose, then, we may divide them into three classes : — (a) Those which, under any circumstances of the patient, are able after entry to the body to grow into, attack, and destroy healthy tissues, and hence can be, and are, easily carried by the blood- stream to distant parts of the body. ip) Those which, under no known circumstances of the patient, are able thus to attack healthy tissues, but cause symptoms by living and growing on dead or dying tissues, and from there dis- charging into the blood-stream doses of a chemical poison extremely active, indeed, but incapable of multiplication. ic) Those which seem to be of an intermediate character, and depend for their activity and virulence to a large extent upon the conditions of vitality of the tissues upon which they alight, and also on their own temporary condition of vigour. Pyaemia, then, is a disease produced by a member of class (a), and in strictness must include anthrax, and nearly all the other specific diseases. Septicaemia is a. disease produced by a member of class (^). Artificial cultivations and experimental inoculations would seem to show that between all three groups no line of strict demarca- tion can be drawn ; but this does not entirely destroy the clinical value of the distinction in cases of disease. For when in a natural state the distinction can be moderately well made, and it is prob- able that clinical (as opposed to laboratory experimental) diseases arise from the invasion of microbes of a natural (to them) healthy activity. 7. Pathogenic microbes would seem to be able to attack tissues Ill MICRO-ORGANISMS AND ZYMOTIC DISEASES 29 in one or both of two primary ways with a subdivision of the second method. (a) By a sort of hand-to-hand fight, microbe v. cell = phago- cytosis. (^) By a weapon in the shape of a secretion = chemiotaxis, about which weapon two theories exist : — (i) The secretion is itself a poisonous chemical substance = a toxin. (2) The secretion is of the nature of a ferment, comparable to trypsin, say, and = a toxinogen. On the other hand the cell defends itself either — (i) By bodily eating the microbe. (2) By secreting a substance neutralising the toxin, or fer- ment, or the products of the ferment ; in either case it is called an antitoxin. This is the most natural place in which to insert the clinical reasons for suspecting that a disease is due to microbial influences. (a) The occurrence of an epidemic of the disease in question, in which the logic of events seems to prove, or, at least, strongly suggest, that on the one hand all the cases arise from a common (aerial, aquatic, or telluric) source, from which all gross metallic, e.g. lead, copper, arsenic, mercury, or organic, e.g. decomposing food, poisons can be and are excluded ; or on the other hand that consecutive cases arise from previous ones, the latter a mode of spreading often better noticed in the smaller sporadic outbreaks, where observation is closer and the methods of " catching " the complaint more easily distinguished. (d) The existence of localities where endemic diseases flourish, where a purely local cause must be at work, but where, again, all metallic and ordinary organic chemical poisons can be excluded. (c) In both these cases the a priori argument will be enormously strengthened by a posteriori reasoning when the common, local, or personal factor has been removed, and the disease has ceased to attack fresh individuals, and the removed factor has been shown to contain no organic or metallic poison. {d) The character of the disease itself an active acute onset, follovred by definite fastigium, with crisis or defervescence, and a complete restoration of the patient to health. le) The finding of a definite microbe in the blood, tissues, 3© DIFFERENTIAL DIAGNOSIS chap. fluids, or excretions of the patient. Modern discoveries have made this an almost necessary part of routine clinical study, but the microbe must be put through the above strict scientific proof before its causative role will be accepted. Into the extraordinarily fascinating subject of attenuation of microbes, causes of immunity, and protective and curative inocu- lations I do not propose, further than the observations recorded on p. 31, etc., to enter. The work that has been done in this direction would fill many libraries were it all published, but it is entirely founded on the above principles. We will now proceed to consider the differential diagnosis of the ordinary zymotic diseases of England. For the student to attempt to learn by rote the apparently chaotic variations in the incubation periods, symptoms, compHca- tions, and sequelae of these diseases seems to me a useless, difficult, and never-ending task, but to give a working hypothesis as to the essential causes of these discrepancies and variations is a compara- tively simple matter, bringing rule and order out of confusion. I say hypothesis advisedly, because though we have every reason to believe that incidents occur in the body in precisely the same potential sequence as in the test tube, we have no absolute proof that they do so. In the test tube there is no variation from hour to hour in the bulk and quality of the cultivation menstruum, except such as are brought about by the mixture of bacterial pro- ducts ; there are no policemen leucocytes exercising their unceasing vigilance in getting rid of foreign substances ; it is doubtful how far these cells and the renewal of the menstruum can fundamentally change the phenomena, apart from their undoubted power to hinder, delay, or prevent them altogether. So far, then, as science has allowed us to follow the workings of microbes, we are scarcely using the language of metaphor or analogy when we speak of the invasion of the body by specific germs in precisely the same terms as we use when describing the invasion of a geographical country by a hostile nation ; the differences between the engaging forces are almost nothing but those of size and the nature of the weapons used. The first event, then, is an attempted landing of the invading forces. To say that the expedition may be wrecked by storms on sea or land is nothing more than to say that multitudes of malignant and pathogenic microbes enter the apertures of the body or alight on the skin, but are immediately swept away by the forces of respira- tion (sneezing, coughing, etc.), by food and drink, by smoking, by Ill MICRO-ORGANISMS AND ZYMOTIC DISEASES 31 accidental rubbing of clothes, by washing, etc. ; that, in fact, they never get a foothold in the tissues or blood. Date of infection. Incubation period. Reason why in an epidemic all ex- posed do not sicken ; meaning of immunity ; ab- ortive cases also. Malaise of incuba- tion period. Onset sudden gradual. or Ingravescence of dis- ease and fasti- gium. Defervescence, or crisis, or death. Convalescence and death from ex- haustion in it. A successful landing is the moment of infection, and from now onwards we have the varying incidents of a campaign. The invaders have to strengthen their position, increase their numbers (for our story it is im- material that they do this with inconceivable rapidity by reproduction), and provide food ; the time thus occupied represents the incubation period. Even now, or at a somewhat later stage, when the march through the country has begun (abortive cases), a complete miscarriage of the whole expedition may occur through (a) a want of suitable food in the district, or {b) the energy of the local inhabitants and first line of home defences, who may annihilate the in- vaders as soon as they emerge from their local camp. It is possible in either or both of these ways to explain immunity, natural or acquired, permanent or temporary only. The slight excitement caused by the rumours of an invasion represent the malaise and slight symptoms of the incubation period. The relative strengths of the contending parties explain the nature of the onset. In one set the invaders are so powerful, or have become so numerous, that their attack and onward march cause the utmost consternation through- out the land ; in the other they are so insigni- ficant in strength or numbers that only a slight disturbance is caused at first, though later their power may be enormously increased by reinforcements, etc. As the invaders march through the country the war rages with increasing violence, until either, in repeated conflicts, or in one great pitched battle, the invaders are destroyed, or per contra, the defenders are completely defeated. When the invaders have been thoroughly routed comes the time for rebuilding cities, towns, and villages, and for recuperation of the in- habitants, and it may happen that the whole 32 DIFFERENTIAL DIAGNOSIS CHAP. Persistent debility, or even stronger than ever. Complications and sequelae. (i) Specific to the disease, e.g. otor- rhcea. (2) A second specific disease succeed- ing the first. (3) Non - specific complications, e.g. abscesses from pyogenes, coli commune, etc. nation is so exhausted that this is impossible, and life ceases in the country. Rebuilding and renovation may remain for ever incomplete, or may be such as to make the country stronger than before. In such a war of invasion there may be found three well-marked classes of events : — (i) The attacks on the principal cities by the original invaders. (2) A separate descent upon the country of a different invading force, which, eating different food, or fighting with different weapons, may go through all the vicissitudes of the first force. (3) Turbulence and riot on the part of a mal- content native or alien population which had previously, under pressure from local authority, lived more or less quiet, and even useful, lives. Dropping now the possible suspicion of using metaphorical language, we know for a certainty we have the following variables in every equation of infectious disease : — 1. The inherent constitution of the individual's tissues, cells and body fluids, including the presence or absence of certain materials for the growth of microbes, the power of manufacturing antitoxin, or of eating up these microbes. 2. The quasi-accidental temporary powers of the same at the time of infection. 3 and 4. Similar powers on the part of the invading microbes. 5. The actual number of the latter gaining admission (antago- nism between different microbes landing at the same time). Scientific laboratory work has proved beyond all doubt that each of these is of the utmost degree of importance, but it has not given us even an inkhng as to the laws which govern the variations on the part of the body forces, and is only on the threshold of in- vestigations into those regulating the microbes ; the strongest men often enough fall victims to epidemics while the weakhngs escape, some in contact with the patients are smothered with microbes and escape, while for others or even the same persons at another time, a single contact is sufficient to produce a most virulent attack. Although these unknown variables and their unknown laws make Ill MICRO-ORGANISMS AND ZYMOTIC DISEASES Z3 any tables of comparatively little scientific value, the following may be found of some practical utility in clinical work as well as for examination purposes. Table of Incubation Periods Anthrax . > ' 2 or 3 days. Cholera . up to 15 ,, Diphtheria Have been known to 2 to 4 ,, Influenza. develop within 24 hours 3 or 4 „ Pneumonia of infection, though the annexed periods in Relapsing fever 4 to 10 ,, Scarlet fever days are very much 2 to 5 „ Septiccemia commoner. Tetanus . up to 21 ,, Yellow fever J . up to 18 ,, The following, arranged roughly in ord^r of duration, are : — Gonorrhoea 2 to 3 days. Pertussis . . 6 to 1 2 days. Typhus . 2 to 12 ,, Measles. . . 8 to 12 ,, Glanders 3 to 18 ,, Malta fever . . about 10,, Typhoid 4 to 20 ,, Rotheln . . . 10 to 21 ,, Variola . . II or 1 2 days (curiously constant). Varicella . . 10 to 14 ,, Erysipelas . 10 to 14 „ Mumps . . 12 to 21 „ Syphilis . . 18 to 28 „ Rabies . 40 days and upwards Tubercle . . Unknown, probably . 1 ,' t 1-j 1 5ome weeks. Our previous considerations have led us a priori to expect what we actually find, viz. that the variations are much too great and too irregular to serve any diagnostic purpose ; but they explain why three weeks has been adopted as the period of segregation of individuals who have been exposed to infection, where such segregation is possible, as in schools and pubUc institutions. When the incubation period is at an end, and the actual onset of the disease begins, diagnosis rapidly narrows itself down. Many of those enumerated above show characteristic features, apart from pyrexia, almost at once, thus : — Anthrax Cholera Ring of vesicles with central black slough. Characteristic diarrhoea, except in fulminat- ing cases. D 34 DIFFERENTIAL DIAGNOSIS CHAP. Diphtheria Pneumonia . Wound-Septicaemia Gonorrhoea Syphilis and venereal poisons Glanders Erysipelas Tetanus Mumps Membrane on infected spot. Cough and disturbance of respiratory rhythm, vide p. 35. Wound inflamed and discharging. Urethral trouble. A chancre of some description. Particularly acrid nasal discharge. Sharply defined red blush surrounding a wound. Stiffness of jaws, or abdominal muscles. The swelling of both parotids. The bulk of the remainder is constituted by the common so- called zymotic diseases or exanthems of our country. In them the presence of an epidemic gives the primary and the strongest clue to the diagnosis. I might go so far as to say that in many aberrant and abortive cases this forms the only guide, for without it many cases of sore throat, or of rashes in a scarlet fever epidemic, of nasal catarrh in an outbreak of measles or influenza, would go unrecognised. Next to epidemicity, the manner of onset in fairly typical cases gives the best clue to differential diagnosis. Thus they are all accompanied with pyrexia, which in — Influenza Relapsing fever Scarlet fever Typhus Variola Measles Pertussis Rotheln Typhoid Almost invariably comes on very rapidly, reaching its probable maximum within twenty-four hours. Comes on much less rapidly, taking two or three days or even longer (especially in typhoid) to reach its height. After the onset a period elapses, nearly constant for each zymotic, before the further diagnostic point of the characteristic rash is available. We may utilise this period to draw attention to those symptoms which, if not actually the result of a temperature above the normal (a point made doubtful by many considerations), are at any rate the twin results with pyrexia of the toxaemias of disease. They are very important, as, when they are present, they suggest the continual use of the clinical thermometer; they also give the student a rational and firm basis for a written description of the symptoms of any Ill MICRO-ORGANISMS AND ZYMOTIC DISEASES 35 zymotic, of which indeed, ^^^th the rash, they form the bulk, stress being only laid on special points. Following the plan laid down on p. 2, we have : — The Symptoms of Pyrexia Tongue. Appetite. Thirst. Bowels. Respiratory and vascular symptoms. Urinary system. SkiiL Alitnentar)' System Usually a tendency to get dry and dirty, in typhoid and in scarlet fever often typical. Much diminished, probably digestion is nearly in abeyance. Almost constantly increased. Constipation the rule, in measles and typhoid diarrhoea not uncommon. The respiration and pulse are quickened, and in simple case in their ordinary ratio of i to 2-5-. It is a sufficiently accurate and good clinical rule to expect an increase of about 10 beats per minute in the pulse rate for each degree F. that the temperature is over the normal. The principal exceptions are scarlet fever, in which the pulse rate is often acceler- ated out of all proportion, and influenza, in which there is very little acceleration. If the ratio of 2^ to i is markedly altered, pulmonary or cardiac (endo- myo- or peri-cardial) compli- cations must be strongly suspected and care- fully looked for. The urine is usually diminished in quantity, increased in colour and specific gravity ; urates are very frequently deposited in excess on cooling. There seems to be no doubt that the toxins of all diseases are irritating to the kidney (by which channel they are largely excreted), hence the presence of a trace of albumen is very common ; it has little signifi- cance either as a signal of future kidney dis- ease, or as a diagnostic point, except in scarlet fever, where obstinate nephritis is an only too frequent sequela, and in diphtheria, when albuminuria helps to decide the nature of an otherwise doubtful sore throat. Is often hot and dry, or may be moist and covered with sudamina. 36 DIFFERENTIAL DIAGNOSIS chap. Nervous system. Headache, especially at back of eyes, a feeling of languor and debility with aching sensations in the limbs and back more or less severe, and the consequent restlessness, are all that can be ascribed to ordinary pyrexia ; should the temperature be over 105° delirium or coma may supervene, but these, with subsultus tendinum, floccitatio, etc., belong much more to poisoned than to heated blood, and may be seen with a subnormal temperature. It is worth while to note that small-pox, even in comparatively mild cases, is associated with a back - ache of quite disproportionate severity. The characteristic rash of each disease now begins to appear, almost constantly as in the table below. With its appearance, though probably long before, the diagnosis will be complete. Such are the usual features of the rashes of our zymotics, and they will, if anything like typical, be found sufficient to finally clinch a diagnosis which even for the most experienced may have remained doubtful previous to the appearance of the rash. Desquamation. — Inasmuch as desquamation is usually considered very strong if not conclusive evidence in favour of a past infectious disease, it may not be out of place to state definitely once for all that it may be seen of almost any degree and character in patients who have been in bed for any disease. It is extremely copious in the course of some skin affections (dermatites), also after excessive doses of thyroid gland, and after prolonged (some days) bathing, as in typhoid ; but I have also seen it after pneumonia, in the course of kidney disease, as well as in patients affected with chronic spinal cord mischief. We have now concluded the symptomatological diagnosis of our infectious diseases ; it simply remains to tabulate a few of the most salient features of contrast of the individual affections which are likely to be confounded, or which are of special interest to students. [Table Ill MICRO-ORGANISMS AND ZYMOTIC DISEASES 37 Table referred to on page 36 Disease. Date of Rash after Onset. Locality. Characters. Varicella Within 24 hours Anywhere, fre- Clear vesicles, not quently several umbilicated, but crops of them. they often leave scars. Scarlet Within 48 hours Chest first, rapidly Bright, boiled-lobster fever spreads to trunk, colour, disappears face, and limbs. on pressure (except in malignant cases), followed by large flaky desquama- tion, which con- tinues longest on hands and feet. Rotheln.i About 3rd day Trunk Mottled like measles, or red like scarlet fever, followed by small branny des- quamation. Variola 3rd day Forehead first, but At first felt rather soon nearly uni- than seen as a soft. versal ; only one velvety feeling of crop, V. varicella skin with nodules under it ; soon um- bilicated vesicles, becoming pustules in 4 or 5 days, and almost invariably leaving scars. Measles 4th day Forehead first, Mottled, patchy, does and limbs, soon not absolutely dis- spreads to trunk appear on pressure. Desquamation is small and branny. Typhus 5th day Wrists very early, Mottled and ha^mor- soon universal. rhagic spots, not dis- One crop only. appearing on pres- sure, conspicuous. Typhoid 7 th or 8th day Abdomen and back, Small red, slightly successive crops elevated spots, dis- appearing on pres- sure, and usually want looking for. ^ There is some dispute as to the existence of this disease ; its clinical features, as allowed by the believers in it, are exactly intermediate between scarlet fever and measles. SS DIFFERENTIAL DIAGNOSIS chap. VARICELLA v. VARIOLA Fever and constitu- Scarcely marked, and Usually very severe, tional symptoms. even if pyrexia and especially the severe, still not back-ache, much constitutional disturbance. Date of rash. First day. Anything in first two days will be prelimi- nary atypical and probably hsemor- rhagic ; typical rash on third day. Rash itself. Often successive crops, Always one crop only. non - umbilicated, Umbilicated and hemispherical; often confluent, practically never confluent ; contents Contents always puru- rarely more than lent ; forehead al- milky ; appear any- most always the where. first. It is but very rarely that any serious difficulty arises in the differential diagnosis of these two diseases, only an extraordinarily severe case of varicella could be mistaken for a mild attack of modified variola and m'ce versa. It is well to emphasise the fact (usually unnoticed or denied) that varicella does frequently leave pitted scars which may easily be mistaken individually for those left by smallpox, their greater number after the latter will be the best guide. VARIOLA V. SYPHILIS A far more difficult problem may occasionally arise to decide between the rash of variola and a varioliform syphilide. In both, the fever and constitutional symptoms may be very severe, and the actual spots may be identical in appearance, umbilicated and puru- lent. The most reliable point will be the situation of the rash, which in syphilis is nearly sure to be confined to the forehead, where it may be very copious ; it is almost certain to be much more widely spread in variola. If doubt remains, a history of a chancre must be sought, and may clear up the diagnosis. Ill MICRO-ORGANISMS AND ZYMOTIC DISEASES 39 DIPHTHERIA v. "HOSPITAL," OR "ULCERATED' SORE THROAT The following points are usually made in separating these troubles : — Diphtheria. Ulcerated Sore Throat. Always derived from a previous May arise de novo (at least with- case. out known exposure to previous throat case), from smell of drains, septic wounds, etc. Temperature not high as a rule, Temperature higher, on an average 102° maximum. 101° to 105°. False membrane includes necrosed False membrane only an exudate, epithelium, if removed leaves a if removed does not leave a bleeding raw surface. bleeding surface. Albuminuria. No albumen in urine. Knee jerks often lost, and neuritis No loss of knee jerk or neuritic as sequela. sequela. Klebs-Loeffler bacillus found. Other microbes but not the Klebs- Loeffler. Notwithstanding the discovery of the Klebs-Loeffler bacillus, which must be by all admitted as the only cause of one specific form of disease called by the name of diphtheria, I am strongly convinced, as the result of personal experience, that there are several kinds of microbes which can give rise to forms of ulcerated sore throat, which by every clinical test are indistinguishable from the diphtheria produced by the Klebs-Loeffler bacillus ; there may be sloughing and bleeding on removal of the slough, there may be albuminuria, and possibly disturbance of function of peripheral nerves — in fact, everything. This statement may be accepted without its being held that I am preaching a dangerous doctrine, for I hold that the same care should be given to every case of ulcerated throat, and that the same isolation, especially as regards kissing and breathing the breath of the patient, should be practised, whatever the microbe may be, for all such cases are undoubtedly infectious. Nor do I dis- approve of the use of antitoxin. I hold very strongly that if the throat be due to the Klebs-Loeffler bacillus, the injections will cure, when the case without them would be hopeless ; and if the 40 DIFFERENTIAL DIAGNOSIS CHAP. throat be due to other microbes, the injections will certainly do no harm. It may be that the acceptance of my view tends to vitiate the statistics of diphtheria, and hence those of antitoxin cures. This I cannot help, for I believe I am stating truth, and that even the most experienced will admit it. The confusion — if confusion there be — is due to the fact that we do not yet know all the powers for evil of all microbes, nor the laws which govern their growth on human tissues, and the powers of resistance of these same tissues. We have already noted that rotheln as a distinct disease is not recognised by some observers. Accepting its existence, how- ever, the following table, constructed from Dr. Roberts' Medicine^ shows the principal characters of the three diseases — rotheln, measles, and scarlet fever — their likenesses and contrasts : — MEASLES ROTHELN SCARLET FEVER Eight to twelve days, never a few hours only. Incubation Ten to twenty days, never a few hours only. Two to five days, often within twenty- four hours. Fairly sudden, with rapid increment. Onset Sudden, but gets no Very sudden, acme in worse. twelve hours or so. Symptoms of Onset Catarrh of nose and Sore throat, but not Throat symptoms very eyes. so bad as scarlet prominent, fever. About 102°. Temperature 102° or lower. 102° or higher. Appears about fourth day, distinctly to be felt,mottled patches, Rash Appears second day, papules brighter than in measles but Appears in twenty-four hours, not raised nor to be felt, large Ill MICRO-ORGANISMS AND ZYMOTIC DISEASES 41 does not completely disappear on pres- sure, symptoms soon lessen when rash appears, rash lasts three or four days. Proportional to fever. patchy, may coal- esce and be bright like scarlet fever. Symptoms nearly gone when rash ap- pears, rash lasts al- ways four or five days, and may be eight or ten, longer than either of the other two. Pulse Proportional to fever. areas, uniformly bright red ; disap- pears entirely on pressure; symptoms worse if anything when rash is at its height ; rash lasts four or five days. Frequent, out of pro- portion to fever. Varieties (only to be noted in Epidemics) Sine eruptione, sine No marked varieties, Sine eruptione, angi- catarrho, malignant (haemorrhagic). but may occasion- ally be rather severe. nosa (throat speci- ally bad), maligna (haemorrhagic). Sequels and Complications Eyes, nose, and ears. None usually ; very Nephritis and dropsy, but especially cat- rarely nephritis. rheumatism, ear dis- ease, endocarditis, cellulitis of neck, cancrum oris, ab- scesses. arrh of air passages, also catarrh of in- testinal tract. Can- crum oris. Without the rash and without the presence of an epidemic to guide one, there are no features that will enable a diagnosis to be made between some cases of bad sore throat and the throat which may accompany either scarlet fever or (occasionally) measles. Quite recently there have been described small whitish spots on the mucous membrane of the mouth and palate, which are said to be a pathognomonic indication of incipient measles. TYPHOID V. TYPHUS Typhus. I. Only seen in crowded poor communities ; almost absolute contact required for infection. Typhoid. I, Epidemics common in sparsely populated districts, conveyed by milk or water to a distance. 42 DIFFERENTIAL DIAGNOSIS CHAP. Typhus. 2. Incubation, two to twelve dayi. 3. Onset very sudden. 4. Symptoms markedly nervous and cerebral. 5. Rash prominent to eye, as much on limbs as body, usually hsemorrhagic, appears earlier than in typhoid, five or six days. 6. Constipation the rule. 7. Crisis almost invariable ending. 8. Complications septic in charac- ter anywhere in the whole body. 9. No characteristic lesions after death. 6. 7. Typhoid. Very indefinite, may be a fort- night or more. Onset usually insidious, but may be rather sudden. Symptoms markedly gastro-in- testinal, though headache often severe. Rash usually requires to be looked for ; almost confined to trunk ; rarely more than ery- thematous spots, entirely dis- appearing on pressure, rarely present in first week. Diarrhoea the rule, at any rate in second week. Lysis almost invariable ending. Chief complications abdominal, — perforation, peritonitis, or haemorrhage, but periosteal ab- scesses not very uncommon. Characteristic lesions of intes- tines. Considering the absolute contrasts that these two diseases offer, it would seem impossible that they should have been so long confounded ; but we must remember that in those days typhus was very much more common than now, and therefore there were probably many cases aberrant from the type. If we remember, too, that what is now known as the " typhoid state " (dry, brown tongue, delirium, subsultus tendinum, and collapse) is the charac- teristic condition of any severe blood-poisoning of any nature, we may cease to wonder at the confusion. The separation of the two is now of almost purely academic examinational (and historical) interest, for typhus is so rare that scarcely i per cent of medical men ever see a case. The above table is quite sufficient should the differential diagnosis be required. Weidal's test (the influence of the serum of a suspected person upon cultivations of typhoid bacilli) has recently been discovered. Its reliabihty would up to date seem to be of the very highest degree, in fact almost absolute if done by a skilled bacteriologist. Ill MICRO-ORGANISMS AND ZYMOTIC DISEASES 43 CHOLERA ASIATICA v, CHOLERA NOSTRAS (Severe Diarrhcea or Ptomaine Poisoning) In England, luckily, we are not often called upon to deal with an epidemic of true Asiatic cholera ; but, frequently enough, it is imported into our seaports, and occurs sporadically from this origin, so that the diagnosis is of some importance. The essential etiological pathology of all such intestinal fluxes is the same. An irritant reaches the intestinal canal and causes a severe diarrhoea, to which, in the main, and not to the specific nature of the irritant, the symptoms are due. The diagnosis must then eventually rest upon the scientific discovery or proved absence of the comma bacillus of cholera, but the following clinical points are worth bearing in mind : — 1. If the outbreak or case be due to some ordinary irritant (chemical or living) in the food there will usually be an obvious history of such being the case, e.g, a. public dinner, or all the mem- bers of a family being simultaneously attacked after a meal. 2. Children are almost the exclusive sufferers from our summer diarrhoea. If adults are also attacked, then paragraph (i) is nearly sure to be true. 3. In food-poisoning cases all the patients will be attacked so nearly simultaneously or under such circumstances as to exclude the possibility of infection from patient to patient. 4. Cholera nostras occurs with us almost exclusively in very hot summer weather, or in the autumn, when there is much spoiled fruit about. 5. Rice water stools are said to be very typical of true cholera. They are seldom passed by patients \\dth ptomaine poisoning. 6. In a fatal case, with none of the above guiding indications, bacteriology must be called upon for the diagnosis. ERYTHEMA SIMPLEX v. OTHER RASHES To separate simple erythema from the er}nhematous rashes of more serious disease is a problem rather frequently arising in children. A new blanket, or underclothing of wool, a little dys- pepsia, \nll frequently produce a rash closely resembling that of scarlet fever or erysipelas. In all cases of the slightest doubt an appeal must be at once made to the clinical thermometer, and again in twelve hours or so. Two or three observations on the tempera- 44 DIFFERENTIAL DIAGNOSIS chap. ture will clear up most cases. There is seldom pyrexia, at any rate of more than a few hours' duration, with the simpler troubles, and still less frequently an apyrexial condition when infectious disease is the cause of the rash. Besides the temperature the following points will be of assistance :- — Erythema. Erysipelas, etc. Margin of rash gradually fades into Outline of blush very distinct. healthy colour. Locality erratic, Locality usually recognisable as no discoverable wound. that of a specific fever, or round a wound. No constitutional disturbance. Usually considerable disturbance headache, vomiting, or chilliness. of bodily health. Probable history of some contact Probable suspicion of infection. with irritating clothing material or known slight trouble. Little tendency to spread after once Usually spreads distinctly under it is out and discovered. observation, while symptoms re- main or get worse. INFLUENZA Of late years we have had a repeatedly recurring recrudescence of this pest, and many opportunities for estabHshing its differential diagnosis. In the several epidemics it has almost seemed as though we had as many separate diseases to deal with — now an outbreak of contagious meningitis, now a pulmonary epidemic, and now one of gastro-intestinal catarrh or worse. In some a severe catarrh of the nose and eyes with a mottled rash has aroused suspi- cion of measles, while in others a severe tonsilHtis and a bright red rash have made a diagnosis of scarlet fever seem almost justified. The view which seems to me to best explain these vagaries is to assume that the microbe of influenza (it has not yet been isolated to the satisfaction and acceptance of everybody, though its existence is universally believed in) has but little specificity of its own. If it has a particular affinity it is for the nervous system, which it attacks with undue violence, causing disproportionate headache and pains, and followed by a debiUty out of all proportion to its pyrexia. Should the victim of its attack possess, however, a distinct locus mi?tons resistentiae it will attack that locus, and cause what is apparently a simple non-specific inflammatory attack, a pneumonia, a nephritis, a tonsilHtis, a diarrhoea, etc. Ill MICRO-ORGANISMS AND ZYMOTIC DISEASES 45 As regards its actual diagnosis, my own experience would lead me to say that in cases uncomplicated by any actual inflammatory disease of an organ its main characteristics are : — 1. The absolute suddenness (even to the minute) of the onset of malaise and chilliness. 2. The presence of pyrexia, above 99.5 say, separates it from an ordinary cold in the head, especially in conjunction with — 3. The great intensity of the aching in the limbs and eyes. 4. During the first twenty-four to forty-eight hours the diag- nosis, at least in children, must remain in doubt if any other epidemic is about. 5. At the end of this period, when we are expecting a rash or some other specific symptom, the temperature falls, and the patient is convalescent, unless some definite complication has occurred. 6. If such a local affection arise, the fact that it is due to in- fluenza can only be determined by the prodromal symptoms which are absent in the simple cases. In those cases where a rash and coryza or tonsillitis occur a certain and unquestionable diagnosis is at first impossible, unless there be a definite epidemic of influenza in the air, but we may remember : — {a) The rash is more evanescent in influenza than in scarlet fever or measles. {b) The whole febrile period without complications is also much shorter. if) Scarlet fever and measles but seldom occur more than once in a lifetime, and therefore a previous history of either is pro tanto a point in favour of influenza. {d) Just the reverse holds of influenza, and a previous attack makes the present one more probably of that nature. {e) In adults first attacks of scarlet fever and measles are com- parative rarities, while influenza mayhave its first incidence at any age. VENEREAL INFECTIOUS DISEASES These include gonorrhoea, syphilis, and septic inoculations. The diagnosis of gonorrhoea, with its special power of producing a suppurative discharge from mucous membranes, need not delay us. It is the truthfulness of the history more than the nature of the urethritis that requires consideration. To differentiate a simply septic venereal sore from a true syphilitic chancre is much more difficult, and the fact that the 46 DIFFERENTIAL DIAGNOSIS CHAP. Ill syphilitic and septic microbes are, with extraordinary frequency, inoculated together and grow side by side renders it often impos- sible to tell whether a given sore will ultimately prove syphilitic or not. Remembering, then, that many sores are both, the following points must be taken only as guides, not as infallible supports : — Septic. Incubation only a day or two. Suppuration ana ulceration fairly free. Frequently multiple, and can be inoculated on to a separate part of the body intentionally or acci- dentally. Induration, if present, fades off gradually, and is only inflam- matory oedema. Bubos often form, enlarge, soften, and abscess forms. No rash, sore throat, or other con- stitutional disturbance at a later period. Syphilitic. Some three weeks. A sore (the date of inoculation for which can be sworn to) cannot be purely syphi- litic if it appears within a week, but it may be both. Pure syphilis does not suppurate, and probably not ulcerate ; but if a sore does ulcerate and become phagaedenic, it is curious that it almost always contains also the syphilitic virus. Most usually single, and cannot be inoculated on to a distant part of the body. Induration is sharply defined like a wad let into the skin. Is some- thing special to syphilis, not simple inflammatory. Bubos are hard and isolated, and if due purely to syphilis have no tendency to suppuration. Rash and sore throat coming on some weeks later are the only real pathognomonic features of true syphilis. One cannot too strongly insist on the fact that a very large majority of venereal sores have the syphiHtic virus in them, though its presence is for a long time obscured by the more active and rapidly-developing septic microbe, the work of which is soon pro- minent enough. The positive features of syphilis may later become most distinct, but a negative is proverbially difficult to prove, and nothing but six months from the date of inoculation will prove it satisfactorily. The question whether this is too heavy a price to pay for certainty belongs to the region of treatment, and cannot be discussed here. CHAPTER IV DISEASES OF THORACIC ORGANS Section I. — The Lungs and Accessories The principal symptoms arising from disease within the thorax are : — (i) Pyrexia. (2) Alterations in respiratory movements and rhythm. (3) Alterations in cardiac sounds, position, and rhythm {vide Section II). (4) Pain, and — (5) Various other pressure effects. The physical signs consist of alterations in the normal or average condition noticed on — (i) Inspection. (2) Palpation. (3) Percussion. (4) Auscultation. I propose first to analyse some of these phenomena from the point of view of diagnosis, and then to offer a few remarks on the individual diseases producing them. PYREXIA This, qua thoracic disease, is only likely to be present as the result of inflammation of some thoracic organ, or produced by nervous reflex from irritation of the vagus, with or without inter- ference with respiration or circulation. Of the latter form there is but little in an elementary book to 48 ^ DIFFERENTIAL DIAGNOSIS chap. say. It would certainly seem that hyperpyrexia might sometimes arise from this source, for it is seen occasionally in cases of peri- carditis and pleurisy, and when rheumatic hyperpyrexia is accom- panied by visible organic disease, this is almost constantly a pericarditis, so that arguments are not wanting to establish the position of a reflex hyperpyrexia through vagus irritation, though other factors, e.g. the rheumatic poison, may have a good deal to do with the temperature variations. In cases of organic disease of the intrathoracic organs, on the other hand, the thermometer affords many useful points in differ- ential diagnosis. In cases, for instance, where the physical signs tell us that bronchitis is present, it is a common rule of practice to consider that a temperature of ioi° or over indicates the extension of the inflammatory process to some of the alveoli, so that broncho- pneumonia is present, even though there be no tubular breathing, etc., suggestive of consolidation of lung, within the range of the ear. Again, we may suspect that an undoubtedly catarrhal area has been invaded by tubercle, or we may think of tubercle when a persistent cough exists without physical signs of a catarrh ; here a nocturnal elevation of temperature with a normal reading in the day is a very strong piece of evidence in favour of the more serious condition, though it must be admitted that tubercle is sometimes apyrexial, and simple catarrh may be febrile even after its acute stage has passed. Lastly, in pleurisy with effusion, a nocturnal elevation of temperature, especially if associated with sweating, strongly suggests that the effusion is purulent, or, if proved clear, that it is due to concealed tubercle. The non-subsidence of a pyrexia after apparent removal of the cause, e.g. tapping, must be carefully watched to ascertain the meaning of the hitch in the proceedings ; and similarly when a pyrexia, whose cause is known and whose course is usually constant, as in the common zymotics, does not follow the average rule, pulmonary complications must be suspected and carefully looked for. It is important to remember that when breathing power is very seriously interfered with, as in some cases of pneumonia or broncho- pneumonia, or in an ordinary case of bronchitis becoming capillary, the temperature may sink and become normal, or more probably subnormal, while the disease is making rapid strides to a fatal issue, so that a subnormal temperature in such cases is even more to be feared than pyrexia of moderate, or even severe degree, say up to 103.5 or 104. The same may be said in severe cardiac failure from any cause, though increased temperature is here less likely as IV DISEASES OF THORACIC ORGANS 49 an initial phenomenon except in recent endocarditis, of which, indeed, pyrexia and a bruit are the chief indications. In all cases of old or chronic lung and heart mischief, the thermometer is an important aid in determining whether the physical signs are produced by old changes in the tissues or by active processes still going on. If the former, there will most prob- ably be no fever ; if the latter, pyrexia may be present ; at least if pyrexia is present, then the changes are probably active. Alterations in Respiratory Rhythm (a) Cough Cough, as we know, is a peculiar modification of respiration which can be produced voluntarily, and can also often be suppressed by an effort of the will when the act would be attended by pain ; but it is essentially a reflex act arising from irritation of nerve terminals or trunks, in direct or indirect communication with the respiratory centre, principally of the vagus or of the fifth nerve. It is designed primarily with the object of removing this irritant from the terminals of the pneumogastric in the air passages of the lung; but inasmuch as the respiratory centre is incapable of dis- tinguishing between an irritant of terminals and one of nerve trunks, and between a removable and an irremovable irritant, the act is in many cases necessarily ineffectual. We are thus led naturally to a division of coughs into (a) coughs useful, (b) coughs useless, the former requiring to be helped, the latter to be suppressed as far as possible ; and hence our first point in diagnosis is to try to separate the two classes. First, as regards the sound and features of the cough itself : — Cough Useful Cough Useless Moist, accompanied by a rattling Dry, barking, or ringing cough, or wheezing sound with each characteristically paroxysmal in blast ; if at first dry and in- many cases, e.g. whooping cough effectual, ultimately results in in later stages ; always ineffec- the expulsion of some mucus tual in removing the essential or other material from the air cause of irritation. It may re- passages more or less proper- suit in the bringing up of a tionate to the efforts made. small plug of mucus, but totally out of proportion to the efforts made. E so DIFFERENTIAL DIAGNOSIS CHAP. JV.B. — In both classes may be included a few unusual or rare cases of gross foreign bodies in the tubes, or of the membranous casts of plastic bronchitis, in each of which the cough may be dry, barky, and severe, or moist and wheezy, but may still result in the expulsion of the irritant. Now as regards the clinical causation of the two groups. These we may tabulate as follows : — Cause. Disease of external ear. Elongated uvula. Acute pharyngo-ton- sillitis. Laryngitis, bron- chitis, broncho- pneumonia, ordi- nary pneumonia, pleurisy. Tuberculosis of larynx or of lung. Cough Useless Principal Diagnostic Points. The evidence will be chiefly negative, absence of other possible cause for a slight dry cough. Under such circumstances it has only to be remembered that a foreign body in the ear, or a little eczema, may cause such a cough for the diagnosis to be suggested, and the sugges- tion will lead to a careful examination of the part. Suspected by the cough and tickling in the throat being much worse (possibly only then notice- able) on lying down. Absence of thoracic signs of disease and presence of the long uvula complete the diagnosis. Cough (as opposed to mere laboured hawking of phlegm) slight, but attended with much pain, therefore often suppressed. Condition obvious on examination of mouth and pharynx. In all these acute inflammatory conditions of the air passages the cough is, at least in the earlier stages, — say twenty-four to thirty-six hours — of the useless type, and may safely be mitigated with sedatives ; the temperature, the history, and the painful cough are sufficient for a tem- porary diagnosis. For a complete one, vide under the appropriate subsections (pp. ()j et seq.). Both these forms of tubercle, in the stages of deposit, before ulceration or suppuration has occurred, are associated with a troublesome dry cough. In the former additional suspicion is aroused by hoarseness or loss of voice, and the laryngoscope will clear up the diagnosis. For a complete diagnosis of phthisis, vide pp. 84 ^/ seq. IV DISEASES OF THORACIC ORGANS 51 Cause. Malignant or syphi- litic deposit in larynx before ul- ceration. Tumour pressing on pneumogastric or its branches, or on trachea or bronchi ; aneur- ysm, enlarged glands, malignant growth. Morbus cordis in early stages. Principal Diagnostic Points. Cough and symptoms similar to tubercle, diagnosis made with laryngoscope. N.B. — In the later ulcerative stages of all these deposits in the lar)-nx, though the cough may be in some degree useful, it is always persistent and dis- tressing to a degree that renders some mitiga- tion of it necessary. Any of these tumours, in any form, may cause a dn,', hacking, or brassy cough, which in itself should arouse suspicion of some such condition. Absence of other obvious cause, and especially if combined with paralysis of one or both cords, will be the chief diagnostic feature, but vide p. 105 for further indications. The back pressure of a leaking mitral will, on any extra exertion, cause a cough which — at first, at any rate — is distressing and useless. The diagnosis depends primarily on the presence of a bruit. Should this be absent and yet no - other cause for a cough on exertion be found, the consideration of the heart sounds on p. 125 will be useful. Cough Useful As remarked above, cough may be looked upon as useful, and encouraged accordingly, when it removes irritating material from the air passages in something like proportion to its activity and force (the force may need reinforcement in the aged or debiUtated). Hence we find it in — The later stages of all acute inflammatory affections of the air passages and lungs when secretion has become excessive or suppura- tion estabhshed, or often enough when the disease has become chronic. The later stages of phthisis when ulceration and breaking down of lung tissue has occurred. In bronchiectasis, how-ever arising. In some cases of pleuritic effusion or of morbus cordis when it would appear that the air tubes are used as the means of carrying off excess of fluid. In the bursting of abscesses, empyemata, etc., into the tubes. The differential diagnosis of these conditions will be the object 52 DIFFERENTIAL DIAGNOSIS chap. of several sections in the succeeding pages. So far as the mere act of coughing is concerned, they offer no differentiating points. It is, however, worth while to draw attention to the suggestions given by the time of day at which a cough is worse. If it is worse at nighty after the patient has got warm in bed, the suggestion is that it is due to some cause other than a mere mechanical stimulus or natural secretion, i.e. in an adult suggestive of phthisis or pneumonia, in a child of pertussis or bronchopneumonia. On the other hand, if the cough is worse duriiig the active working hours or on change of atmosphere^ this is suggestive of simple catarrh, as in mild bronchitis. It is possible that the explanation of this clinical fact may lie in a suggestion that the activity of the more virulent microbes is inde- pendent of the circumstances of the patient, whether active or quiet, asleep or awake, while the milder ones may be more dependent on respiratory activity, as we know natural secretions are. The Sputum as an Aid to Diagnosis Sputum is the natural sequel to a useful cough. As a guide to the naming of a disease it is not often by its naked-eye characters (its microscopical -bacteriological examination is most important) of great capital value, but as a guide to the improvement, or the reverse, of the condition of our patient's air tubes, during treatment, it is of very great significance. It is well to draw the student's and young practitioner's attention to the fact that the repeated physical examination of the chest which is allowable, and even necessary, in hospital work for teaching purposes, is not in private practice always advisable ; and many patients will so strongly object to it that some other means must be adopted for estimating progress, and none are so useful as a few questions on the violence and frequency of the cough, and the amount of trouble experienced in getting up the phlegm, followed by an ocular and mental inspec- tion of the sputum, which should always be kept for the purpose. Phlegm, as the natural secretion or excretion of the mucous membrane of the air tubes, should be small in quantity, and consist merely of almost colourless mucus, with occasional cells and detritus of inhaled particles. It is what it should be, in country dwellers and non-smokers; but in towns, in smokers and others with dusty occupa- tion, it becomes more or less coloured in agreement with these factors ; hence black phlegm, unless we see it is due to dark blood, need not be a cause for alarm under such circumstances. IV DISEASES OF THORACIC ORGANS 53 In disease the quantity is, as a rule, enormously increased, and much besides mucus is present. Quantity. — Speaking of quantity only, quite apart from quality, it is important to note one point particularly, i.e. whether the excess is brought up in large mouthfuls or gulps at a time, with quiescence in the somewhat long intervals, or whether it arises from an increased frequency in the act of coughing, with but a moderate expectoration each time. The former indicates or suggests to us that there is a cavity or potential cavity of some kind communicating "with a bronchus, and emptying itself by cough at intervals ; such may be bronchiectasis, or abscess either of lung itself or neighbouring organ, or empyema. The latter tends to negative such a suspicion if roused by other methods of examination, and suggests instead a bronchitis, bronchopneumonia, or ordinary pneumonia, with excessive secretion, but without organic dilation of tubes ; the absorption of a pleuritic effusion, or the presence of morbus cordis, will occasionally very much increase the quantity of sputum. Quality. — As regards the quality of the sputum, the following are the principal pathological constituents to be found by clinical examination : — Mucus (excess only is pathological), Pus, and nummulation, Blood, Bile, Lung tissue. Hydatid booklets and other parasitic detritus, Microbes (particularly of tubercle and actinomycosis), Foetor, on each of which I propose to make brief comments. Mucus. — As this is the natural secretion of the air tubes, it follows that its excess or defect is the pathological phenomenon. In the early hours of a catarrh it is defective (hence cough useless and sedatives required). Later it becomes excessive but very sticky. This excessive stickiness is almost pathognomonic of pneumonia (cough still useless, or at least violent and out of proportion to result, and to be helped by liquefaction of phlegm). This indicates an acute bronchitis or pneumonia. Later still it becomes mixed with pus, and looser, indicating that the catarrh has caused suppurative processes which, unless very excessive, are known not to be of unfavourable omen. Fus, — ^As mentioned above, this is found in the later stages of 54 DIFFERENTIAL DIAGNOSIS chap. all catarrhal affections of the bronchi, and hence, as a rule, is of little diagnostic significance; it causes mucus to assume a yellowish or green colouration. There are two conditions of suppurative sputum which it is important to bear in mind : {a) when the pus comes up very freely and almost pure, i.e. without much mucus, rousing suspicion of, or corroborating other indications of, the bursting of an abscess or empyema into an air tube, or the presence of bronchiectasis ; {b) the condition known as nummula- tion of the sputum, in which small masses of pus float quite separately and isolated in the spittoon ; it suggests the presence of small loculi where the pus can collect before being expectorated ; it is seen in its most typical form in, and is very suggestive of, the later stages of tubercular destruction ; it is found, but less frequently and typically, in pneumonia and bronchitis, especially if some of the smaller tubes have dilated. Blood. — " Blood-spitting " is a very common complaint, and requires considerable care to ascertain its exact source, vide pp. 150 et seq. Suppose, however, we are satisfied that it arises from some pulmonary affection, we have still to consider its significance. It may appear in small isolated streaks in the mucus, or clotted and free, or it may be more intimately mixed with the sputum, imparting a uniform tinge to the excretion. If of laryngeal Probably only in streaks or tiny clots, with origin. pain in larynx and alteration of tone of voice. Unless other source obvious, a laryngeal examination must be made, and this will clear up the question. If tracheal or acute Again probably only in streaks and tiny clots ; bronchitis. other signs of tracheitis and bronchitis. In chronic bron- Often profuse, condition is fairly obvious in chitis. diagnosis, but the occurrence of haemoptysis in the disease is frequently forgotten. In phthisis. Whether in an early or late stage the haemor- rhage may be smart, diagnosis must rest on other factors. Apices are especially likely to give added physical signs on deep inspira- tion. Bacillus, if found, is conclusive. In pneumonia. It is especially in pneumonia that the blood stains the sputum uniformly. Colour anything from mere rusty to dark prune - juice ; the darker the worse the prognosis. In morbus cordis. Presence of bruits, or, more significantly, other signs of cardiac failure, vide p. 124. IV DISEASES OF THORACIC ORGANS 55 In malignant The sputum of patients with recognisable disease. malignant disease often contains small masses of blood - stained material likened to red- currant jelly ; the point may be of importance in separating such from other consolidating lung trouble (vide p. 105). Such are some of the main lines of thought towards a diagnosis in cases of pulmonary haemorrhage, but it is easy to see that the bleeding itself or its character is of relatively small importance ; other factors of much greater weight are involved. Bile. — This is but a very rare constituent of sputum, but if present is practically pathognomonic of communication between an air tube and a pathological excavation of the liver. Limg Tissue. — If fragments of elastic tissue are found in the expectoration (boiling with caustic potash and examining the detritus under the microscope is the simplest plan), the important caution is to be sure that what we see has actually come from the lung. It is not enough to find elastic fibres, which may have come from tiny fragments of food accidentally present ; they must have the shape of a more or less open figure 8 indicating their origin from the bronchioles or alveoli. If such are present, they prove pulmonary ulceration to a demonstration, and render tuberculosis almost certain ; doubt can only arise in some few cases of chronic disease of the lung, either fibroid pneumonia, or bronchitis with associated bronchiectasis. An acute gangrene will reveal itself by other more important features. Hydatid Hooklets, or other parasitic detritus or eggs, are of course immediately pathognomonic of their source. Microbes. — The bacilH of tubercle and other bacilli are of course equally pathognomonic ; the only cautions are, first, to be sure that the staining processes have been properly carried out ; and secondly, to remember the difficulty of proving a negative, and so excluding tuberculosis too summarily from the absence of bacilli in a few fields of the microscope. Foetor. — This proves that the microbes of putrefaction have not only reached the dead material of the sputum, but have had time to effect their pecuHar changes in it ; hence foetor almost certainly indicates that the sputum has lain for some time in a potential cavity, i.e. a place where such changes could go on undisturbed, or that a piece of lung has itself died outright, or some foreign body is present in an air tube capable of putrefying ; consequently careful search must be made for : — 56 DIFFERENTIAL DIAGNOSIS chap. (i) Bronchiectasis. Usuallyassociatedwithchronicbronchitis. Phthisi- cal cavities are curiously almost exempt from this putrefactive process, though their contents have a peculiar mawkish smell very charac- teristic. (2) Abscess of lung. The main diagnostic features of intrinsic abscess Intrinsic or are {a) fcetid expectoration, which {b) consists bursting into of nearly pure pus, with putrefying detritus, lung from with- and {c) the discovery over a localised area of in. the lung of pathological physical signs {vide pp. 64 etseq.). Abscess arising elsewhere and burst- ing into the lung will have revealed itself be- fore rupture probably. The foetor (if present) and coughing up of quantities of pus merely indicate that communication has been estab- lished with the air tubes. (3) Gangrene. The foetor of pulmonary gangrene is utterly in- describable ; once smelt it cannot be forgotten, and when occurring with symptoms of serious blood-poisoning leaves no room for doubt or error. It is well to insert here a caution against mistaking foul breath for foetor of sputum ; the latter is only one cause of the former, and that a rare one, the nose, mouth, and stomach being far and away the most frequent sources of foul breath. To sum up the diagnostic value of an examination of the sputum, we may say that nearly every disease of the respiratory apparatus has, or may have, a form of expectoration which is fairly characteristic which, at any rate, lends strong corroboration to other physical signs and symptoms, and at times takes a leading position as an indicator of the essential condition of the organ — improvement or the reverse — under treatment. Besides cough and its attendant expectoration, there are one or two general alterations in respiratory movements which deserve a brief mention and analysis for diagnosis. Generally accelerated Respiration. — This, apart from intentional or voluntary quickening of the movement, essentially means that the supply of oxygen to the tissues is insufficient for their immediate (it may be) temporary needs. This may be analysed into : — A. Conditions in which an extra supply is required. {a) Exertion, A purely healthy and physiological condition, exaggerated in convalescence when the tissues IV DISEASES OF THORACIC ORGANS 57 are rebuilding their stable capital of nutritional material. {b) Pyrexia arising Oxidation is quickened throughout the body. I from any dis- have already (p. 35) noticed the importance ease. of the temperature-respiration-ratio in draw- ing attention to pulmonary complications when other complaints of lung trouble by the patient are absent. This rule is particularly valuable in the specific fevers, when cough may be de- liberately suppressed because of the pain it causes, or when the patient is too weak to cough. B. Conditions in which increased frequency of respiratory movement is required to keep up the ordinary normal supply. (. Produced by the circulatory apparatus. Vide subsequent section. As regards their characters and meanings, we may classify them as follows : — A. ( I ) Natural Breath Sounds Point where heard. Normal sounds. Significance. Over larynx and Inspiration and expira- In laryngeal obstruc- trachea. tion, distinctly a tion stridor and noisy, non- musical hoarseness may be rush of air, and detected, both equally so = tracheal breathing. 70 DIFFERENTIAL DIAGNOSIS CHAP. Point where heard. Over larger bronchi, e.g. interscapular space or R. sterno clavicular articula- tion. Normal sounds. Inspiration louder than expiration, but the latter very dis- tinct and audible = bronchial or tubular breathing. Over ordinary lung tissue. Inspiration distinct, ending in or con- stituting vesicular murmur ; expiration scarcely or not at all heard. Significance. Has no abnormality in itself, only becomes abnormal by — {a) Being heard in the wrong place = too free conduction through solid lung or dilated tube. {p) Not being heard in the right place from compression of a tube, etc. Its absence is certainly abnormal, e.g. over lung solidified by any cause. In babies, in unusually thin adults, and in one lung which is doing the work of two, the vesicular mur- mur is undoubtedly exaggerated, and constitutes the harsh breathing of some authors.^ (2) Additional or Adventitious Sounds are in their nature essentially pathological, so we have only to discuss their variations and mean- ing. They may be subdivided as follows : — I. Interrupted : ^ I. Fine sounds (crepitations) are such as would be pro- duced by the separation of two sticky surfaces, that ^ Some authorities on auscultation will not admit the use of the term " harsh breathing," but I must say I know of no other term that can better describe the sounds heard in the three conditions mentioned above. ^ By thus strictly defining the terms "crepitations" and "rales" according to the time in the respiratory cycle in which they are heard, it seems to me that they gain in accuracy for use, and indeed also in meaning and significance. The adjectives " coarse " and " fine " may still be used for either, occurring in its proper time ; and from the coarseness or the reverse, and from the time definition, we may form a tolerably accurate opinion of either (i) the probable size of the tube in which the sound arises ; (2) whether the air has an actual thoroughfare through the tube, or only goes into and back again out of it ; (3) the state of the secretion, the more liquid, the coarser the IV DISEASES OF THORACIC ORGANS 71 is, in fact, the actual cause of them, and their place of origin is the alveoH and very finest air tubes of the lung. They are heard during inspiration only. 2. Coarser sounds and moister (rales) are produced by the passage of air through a more or less viscid secretion, and represent the bursting of air bubbles in the fluid ; they are produced in all tubes larger than those causing crepitations only by the passage of air through the secretion. They are heard therefore during doth expiration and inspiration. XL Continuous sounds : These are the equivalent of the term rhonchus as used by the late Dr. Fagge, the main point of the defini- tion consisting in the sound remaining at a certain level or pitch, possessing, in fact, a certain musical tone and quality throughout inspiration or expiration, or both. Of the sounds themselves there are many varieties : whistling, cooing, snoring, etc., according to the depth of tone or originality of term-invention of the listener. They are produced by secretion adhering in local masses to the wall of a larger tube, thus forming a sudden and adventitious narrowing of the lumen round which the air passes with a musical note. (3) Voice Sounds, Palpation.) (For Tactile Vocal Fremitus vide under Over trachea larynx. and Over larger bronchi. Abnormally. Hoarseness the only detectable variation, owing to irregular growths or secretion covering the cords. No idiopathic abnor- mality, only abnor- mal like the breath sounds by hetero- topy. sound, and the more likely, in the finer tubes, to allow air to actually bubble through it both ways. The two may both occur in the same breath consecutively to one another, a circumstance which would strongly suggest that an alveolar or capillary affection were supervening on a catarrh of the larger tubes, a most useful danger signal, therefore. Normally. Loud and fairly dis- tinct. Not so loud, and more indistinct. 72 DIFFERENTIAL DIAGNOSIS CHAP. Over lung tissue. Normally. Abnormally. Mere confused mur- Increase of spoken mur or not at all. words (broncho- phony) denotes a pathological, in- creased facility for transmission from the larynx (solidifi- cation of structure, dilated or ruptured tube, cavity, etc.). Increase in whispered words (pectoriloquy) denotes still greater facilities for sound transmission from the larynx. Altered sound of voice, only one noticeable form (aegophony), a pecu- liar bleating tone strongly character- istic, if not patho- gnomonic, of pleural effusion. In addition to the above classes of regular voice and breath sounds, we must notice one or two important modifications of them. Cavernous Breathing is primarily an exaggeration in loudness of tubular breathing, but it has in addition a musical character of its own — comparable to the notes produced by blowing over the mouth of an empty bottle, and due to the same essential cause, viz. interfering currents of air echoing in a hollow. When heard in typical form this cavernous breathing is characteristic of a cavity, pulmonary or pleural, communicating freely with a tolerably large bronchial tube. Tinkling Sou7ids produced by the falling of drops into the body of a liquid contained in a resonating chamber ; hence they are only heard when the liquid has been violently driven over the surface of either a pulmonary or pleural cavity by coughing or succussion. Cogwheel Respiration is a peculiar form of interrupted inspiration, as though the air entered in a series of little jerks. It is almost con- fined in its appearance to the upper lobes of the lungs, and was formerly thought to have much, now only a very little, significance IV DISEASES OF THORACIC ORGANS 73 as indicating early stages of phthisis, causing unequal difficulty of air entrance into certain lobules. My own experience would lead me to say that it is frequently met with in perfectly healthy lungs, and that its chief significance is a very minor one, viz. that the patient is nervous, and totally unaccustomed to breathe by in- tentional or voluntary movements. B. Pleural Friction Sounds are well known, to-and-fro rubbing sounds. There are only two sources of difficulty in their diagnosis : the one is to separate them from fine crepitations, and the other from pericardial friction ; the latter is identical in character. From the former they are separable by being coarser, and sounding more immediately in contact with the stethoscope, but principally and essentially by being heard both with expiration and inspiration ; a doubtful sound heard wdth both movements must be either a rub or rales, and the latter will be evidently bubbling. The need for separating them from pericardial friction sounds arises only in the neighbourhood of the pericardium, and there the simple manoeuvre of listening while the patient holds his breath will usually be suffi- cient, pleural sounds then of course ceasing, except in the occasional cases when pleuro-pericardial adhesions exist, and then the import- ant diagnostic point is to recognise by the continuance of the sound during the cardiac cycle that the pericardium is affected. Pleural Creeks are rare, and only heard in exceptional cases of very old-standing chronic dry pleurisy. C. Sounds heard by Tapping the Chest and by Succussion. — These include : — Bell Soimd^ the ringing echo across a chest produced by laying one coin on the w^all and striking this with another coin. The necessary condition for its production is a fairly large empty space, and hence it is useful in detecting a pneumothorax, and its presence may be corroborative of other evidence of a pulmonary cavity. Splashing Sounds produced by shaking the patient ; can be but seldom required, but indicate, when heard, air and fluid in the pleura. This classification gives in a fairly comprehensive and com- prehensible manner the chief ordinary pathological sounds heard in the thorax. For these abnormalities of natural phenomena my chief aim has been to indicate the principles and reasons which, when well grasped, wdll give a rational foundation for explaining any others that may be found in a given case. In practice the difficulty is not so much to hear and understand the physical meaning of 74 DIFFERENTIAL DIAGNOSIS chap. intrathoracic sounds, as to know what name others have given to the sounds we hear, and thus to avoid serious misunderstandings and confusions of nomenclature. Tubular and bronchial breathing, harsh breathing, rales and rhonchi and crepitations are illustrations of disputed points in affixing labels to aural perceptions. I here assume tubular as identical with bronchial breathing, and shall endeavour in the succeeding paragraphs to follow my own defini- tions of the remaining sounds. Having thus cleared a good deal of the ground of symptoms and physical signs, we will now proceed to discuss some of the diseases on which the phenomena depend. LARYNGEAL AFFECTIONS The symptoms that are likely to call attention to the larynx as the seat of disease are : — (i) Pain felt locally. (2) Cough, at first almost certainly useless, and only later, if ever, useful, i.e. with equivalent expectoration. (3) Especially a combination of (i) and (2). (4) Alterations in voice, hoarseness, huskiness, aphonia, etc. N.B. — In one great and dangerous group of laryngeal affec- tions, viz. paralysis of abductors from disease at a distance, there are very often no symptoms whatever (if a possible slight shortness of breath be excepted), and the condition is only discovered by laryngoscopic examination, either as a routine matter or because other features of the patient's complaints have suggested that a paralysis might be found. , The causes to which those symptoms may be due are inflam- mation, acute and chronic, new growths, and paralysis of laryngeal muscles. To endeavour to associate symptoms with causes and to make an exact diagnosis without a laryngoscopic examination is simply to attempt the impossible, and in what follows the final necessity of such examination must always be assumed, though a strong degree of probability may certainly be arrived at by a fair consideration of the history and circumstances of the case. Hoarsetiess of voice, if it occurs in a child, is almost certainly due to either acute laryngitis (simple or membranous) or to papillo- mata of the cords. Ulcers of syphilitic, tubercular, or malignant nature are practically unknown in childhood, and so is paralysis IV DISEASES OF THORACIC ORGANS 75 of the cords, except post - diphtheric, and then the history is tolerably obvious on slight inquiry. The acute pyrexial illness with catarrh and obvious faucial congestion will easily decide that acute laryngitis is present, but only the laryngoscope will prove that there is or is not also a papillomatous condition, or show a case of pure and primary false membrane of the larynx. In adults the same hoarseness of voice may have the ulcers above mentioned as addi- tional causes, but not every conjunction of apical phthisis with hoarseness, of gumma of the liver, with the same voice disturbance, has distinct ulceration of the cords as the necessary and sole cause of this latter symptom. Phthisical and syphilitic patients are not exempted from a simple laryngeal catarrh. The following table gives the main points of distinction between the various forms of — Ulcers of the Larynx Tubercular. Slow in progress, and not much destruc- tion till a long in- terval has passed. Shallow, superficial ulcers, without much swelling or infiltra- tion. Curiously painful on swallowing ; com- moner from say twenty to forty-five years. Almost certainly evi- dence of pulmonary infection of tubercle, of chronic type. Cords freely movable. Syphilitic. Rapid in extension when once broken down. Deep, ragged, sloughy ulcers, with much tumefaction. Little painful ; com- moner from say thirty-five to fifty. Pulmonary association of a chronic type ; very rare ; may be septic aspiration- pneumonia. Cords not so free. Malignant. Intermediate in rapid- ity. Ulcer itself not very deep, but much ex- cess of tissue for- mation, and not much simple swell- ing. Little painful ; com- moner over fifty. If lungs affected at all it is with acute septic bronchopneu- monia. (Schluck- ungs-pneumonie, ) Cords often quite fixed and immovable. 76 DIFFERENTIAL DIAGNOSIS CHAP. Laryngeal Paralyses The functions of the larynx with its vocal cords are three. These, with their natural nerves and muscles, may be thus tabu- lated : — Function. Action of Cords. Muscles. Nerve. Speech Approximated Made tense with Arytenoids, lateral crico-arytenoids Crico-thyroid Recurrent laryngeal. Superior varying tension laryngeal. in voice expres- sion Cough (or extra- ordinary res- piration) First opened by then firmly closed by then suddenly Posterior ^ crico-aryte- noid All the other muscles Recurrent laryngeal. opened by Force of air and re- laxation of adductor muscles. Possibly by action of posterior Ordinary breath- Very little move- crico-arytenoid Slight abduction in in- Recurrent ing ment, but what there is tends to spiration ? Slight adduction in expira- laryngeal. allow free tion? (No movement entrance, with gradual exit of air according to Semon) We should naturally expect, then, that paralysis of muscles should interfere with some or all of these functions. In the main the in- ference is correct, but the exceptions are very important. The affection may be uni- or bi-lateral : it may be of adductors or abduc- tors, or both. The results, with their reasons, are as follows : — Speech. Unilateral Abductor Paralysis Very little or not at all affected, because (i) the cords can still approximate ; (2) they can still be made tense by the crico-thyroid. 1 Even for a student fairly well up in anatomy it may be a little difficult to remember the action of the laryngeal muscles, The O in posterior may help him to remember that this is the only muscle which always and consistently Opens the larynx. IV DISEASES OF THORACIC ORGANS 77 Cough, or extra- ordinary respira- tion. Respiration. In the later phases of the act unaffected ; same reasons as for speech. In its first violent in- spiration possibly a little difficulty or stridor, because extraordinary inspiration requires the larynx to be as widely open as possible. Ordinary, unaffected, because the slight respira- tory movement can easily be affected by the other cord. Speech. Cough. Respiration. Speech. Cough. Respiration. Speech. Bilateral Abductor Paralysis Still frequently unaffected. Reasons under Uni- lateral Paralysis. In later stages of the act unaffected, because — reasons above. In violent inspiratory phase probably considerable difficulty or stridor, because the lax cords may be drawn together by the draught of air, and completely close or seriously narrow the aperture of entrance. Ordinary, probably unaffected, but may be occa- sional severe dyspncea. Reasons under In- spiration of Cough. Unilateral Adductor Paralysis Probably unaffected, because the tensor is still sufficient to put the cord in a vibratory condi- tion. Hence a further deduction may be made, that if the voice is altered, and only unilateral adductor paralysis seen, the probabilities are in favour of a source for the paralysis high up, before the superior laryngeal nerve is given off. In later explosive phase probably weakened, because the air begins to escape past the lax cord as soon as pressure increases in the ex- piratory effort. Extraordinary inspiration unaffected. Unaffected to any appreciable degree, because air can get freely in, and the exit aperture is so little increased. Bilateral Adductor Paralysis Even now may be unaffected materially except for shortness of breath through loss of expira- tory control, because — vide argument above in unilateral trouble, which still holds good. 78 Cough. Respiration. DIFFERENTIAL DIAGNOSIS CHAP. Later explosive stage almost nugatory, because air now escapes very freely directly any excess of pressure behind is produced by expiration. Extraordinary inspiration unaffected ; aperture of entrance very free. Probably a little quickening of respiration, because of the loss of control over expiration, so that air escapes too freely. Speech. Cough. Respiration. Total Laryngeal Paralysis May even now be nearly perfect as regards tone, but shortness of breath will be noted in con- tinuous speaking, because — if the tensors have escaped they are still sufficient, or nearly so, for tone in single words, but adductor paralysis will cause shortness of breath {vide above). If voice is quite lost, and tensors also para- lysed, we are justified in diagnosing a central lesion in the medulla affecting both roots. Non-explosive and nugatory, because of adductor paralysis. Inspiratory phase, possibly dyspnoea and stridor, because of adductor paralysis. Ordinary, as in all the others may still be unaf- fected for the reasons above. N.B. — An opposite and complementary line of reasoning may be applied to spasms of the larynx, which are much rarer and only in laryngismus stridulus seen to perfection. Into the actual causes of these paralyses I do not propose to go very deeply here ; a few will be noted below under Tumours of the Thorax, and the subject will be apparent again in the nervous section. The following outline classification is, however, useful; it is mainly after Sir F. Semon {B. M. J.^ January i, 1898), but rearranged : — Functional. Toxsemic. So-called hysterical. ' Lead, arsenic, and possibly other X metals. Diphtheria, typhoid, rheuma- tism, etc. IV DISEASES OF THORACIC ORGANS 79 Organic. Primary disturbance in the central cells of-| medulla or cord. Primar}' disturbance in j the nerve trunk. 1 Traumatism. Bulbar paralysis. Tabes dorsalis. Disseminated scle- rosis. Haemorrhage. Softening. Tumours of medulla. Such cases of the toxic group as have ended in per- manent destruc- tion. Pressure of aneur- ysms, malignant tumours, inflam- matory thickening (pleural, pericar- dial, meningeal). Syphilitic processes similarly situated to inflammation. ' Surgical. Suicidal. Accidental. Homicidal. The point of greatest practical importance is to determine whether a given paralysis is organic in origin, with practically no chance, or functional, with a fair chance, of recovery. For the toxsemic group of functional cases the great point is to be aware of their existence, and should paralysis be discovered a history of previous or coexistent illness must be carefully inquired for, and its possible treatment by metallic drugs investigated. The affection itself has no distinguishing features, though it may be expected to be of a bilateral type owing to its origin in circulating toxins. For the so-called hysterical paralyses the following points are probably sufficient : — 1. The patient will come mth a predominant complaint of loss of voice. 2. Close physical examination will reveal no gross organic lesion, but will probably show — 8o DIFFERENTIAL DIAGNOSIS chap. 3. Other features of nervous instability. 4. The sex will probably be female. 5. The age will usually be under thirty. 6. The type of paralysis will be adductor and tensor, the combination of the two indicating a cerebral origin, which this undoubtedly owns. As no danger (of asphyxia at least) can arise from adductor paralysis, vide table for reasons, the mental association of this form with the usually good prognosis in hysteria may help the student to remember the clinical fact that by far the majority of cases of adductor paralysis are functional, while a much greater proportion — in fact, all cases of abductor paralysis — are of grave and probably very serious import. PNEUMOTHORAX Is a condition in which air in the sac separates the two layers of the pleura ; this may occur either over the greater part or whole of the lung, or over much smaller areas limited by previous ad- hesions. It is a condition easily liable to be overlooked or mis- understood, and yet of frequent occurrence, so that it is well we should understand the principles of its natural history and mechanism, which are not, I think, sufficiently clearly set forth in most text-books. In origin, then, the gas must be : — I. Admitted from without. Traumatism. Surgical procedures. External fistula opening into sac (rare). 2. Developed in situ. From decomposition of a pleural effusion (also rare). 3. Admitted from within. (Esophagus (cancer, etc.) (a) Bursting of a gas -holding Stomach (ulcer, cancer, etc.) viscus or cavity other than Subdiaphragmatic abscess. I ^ pulmonary. {b) Laceration of visceral pleura Phthisis (most commonly), and lung. Abscess or gangrene. Emphysema. Violent respiratory efforts in healthy lungs (very rare). Penetration of broken bone through pleura. IV DISEASES OF THORACIC ORGANS 8i Admitting that the condition exists, the diagnosis of the source, according to the above table, presents but few difficulties. In the first group, "Admitted from without," both the cause and the condition are obvious, and require no discussion. In the second group, "Developed i7i situ^" the pleural effusion will probably have already attracted attention ; the smell of a little fluid withdrawn by aspiration will leave no doubt about decomposition : such cases are, however, extremely rare, and our further analysis will be partly applicable to them. In group 3 [a) the previous symptoms will prob- ably have made the source clear if the pneumothorax be discovered, as, indeed, they will also probably have done in group 3 (b), but it is especially to this last group that our argumentative analysis applies for the estimation of the occurrence of the accident. We must first claim one or two postulates which are, I think, justifiable :— Postulate I. That the pleura must be healthy (or at least not adherent). Over the area of separation this must be true, except under conditions of gaseous pressure too high to take into clinical consideration. Postulate 2. If the pleura be healthy or non-adherent, the admission of air to its cavity must allow of some collapse of the underlying portion of the lung. Postulate 3. This collapse must diminish (it may be in slight degree) the utility of the affected lung. Postulate 4. Laceration of healthy pleura must be attended by some pain if consciousness is still present. Postulate 5. (Not quite so obvious, but justified, I believe, by post-mortem experience.) The opening into the pleura must be {a) a round hole ; or {p) a valvular rent ; or (c) a slit more or less irregular. Postulate 6. That the admission to the healthy pleura of air or any foreign material will cause cough of greater or less severity. Granted these postulates, we may divide the immediate symptoms of the occurrence of pneumothorax into the inevitable or constant, and the quasi-accidental or variable. The Inevitable or Constant are : — I. Cough. — This is, in fact, the actual cause of the accident, by the increased air pressure it produces in the lung ; so while usually preceding pneumothorax it will certainly . continue after it, except in cases of sudden death. G 82 DIFFERENTIAL DIAGNOSIS chap. 2. Pain in the side. — Must be present by postulate 4. It is usually sufficient to attract attention, but may be so slight or so mixed up with other discomfort as only to be found by leading questions. 3. Shortness of breath {vide under Quasi-Accidental). The Quasi- Accidental or Variable Sympto7ns are really only one, viz. shortness of breath or dyspnoea (the quickened pulse, the collapse, the sweating, etc., are merely variable concomitants of the amount of asphyxia). This short- ness of breath may be so slight as to be quite unnoticed, or may be so severe as to lead to death, appalling in its suddenness, with every conceivable degree between the two. For the primary explanation of the degree we must draw a distinction between the symptoms setting in immediately with the accident, and those which develop in the course of a little time. For that which comes on at once, one quite sufficient explanation is obvious, viz. the share in aeration of the blood previously taken by that portion of the lung now collapsed and useless. That which arises in continuance of the primary trouble may own this same explanation, but probably in associa- tion with another, viz. the possible valve-like action of the torn pleura allowing an inspiratory pumping-in of air to the sac, but preventing expiratory escape, so that more and more healthy lung is allowed or forced to collapse ; this may go on to a degree incompatible with life, or by the establishment of pressure and tension equilibrium it may remain stationary, life being still possible. In all cases and under all circumstances the ultimate degree of shortness of breath has then the above foundation, viz. tlie previous uiility of the collapsed area. The physical signs of pneumothorax, per se and apart from the disease causing it, may be naturally divided into (a) those found over the area of separation ; (b) those observed elsewhere. {a) The former will be : — On iilspection. — Nil, unless a large area of lung be collapsed, when that side of the chest may be a little sunken, and probably deficient in m.ovement. IV DISEASES OF THORACIC ORGANS 83 On palpation. — Nil, unless the opening into the sac be a free one, when increase of tactile vocal fremitus may be appreciated, owing to the freer conduction of aerial vibrations with a resonating chamber. On percussion. — Hyper-resonance, owing to the air coming into immediate contact with the chest wall, and so allowing unusual vibratory opportunities. On auscultation. — The signs will vary from tubular breathing with amphoric resonance — if the opening be patent — to complete silence when the lung is collapsed, and the opening a mere slit, so that the air pressure in the pleura prevents the lung from expanding. {b) The latter refer to (i) the increased work thrown on the still functionating area of lung, leading to increased loudness of the breath sounds previously heard, of whatever nature; (2) the dis- placement of the heart's apex beat, which may be much or little, right or left, according to the amount and side of the collapsed area of lung; (3) frequency of pulse and severity of asphyxial symptoms, dependent as before on the previous utility of the portion of lung now hors de combat^ and possibly in some degree on the cardiac dislocation. The sequelce and subsegimit history of a case of pneumothorax depend upon the admission to a living serous membrane of foreign material. If this is merely aseptic air, and the opening is such as can readily be healed, recovery is likely to be complete with the restoration of the status quo a?zte. If it be tubercular or septic, it is almost inevitable that pleurisy of a corresponding type shall arise, with its appropriate symptoms. With this analysis, the diagnosis of pneumothorax can hardly require further discussion, bearing in mind that it always occurs suddenly as an acute episode in health or chronic disease. It is, however, somewhat frequently assumed that the condition may be mistaken for 'a pathological cavity in the lung. When, as is frequently the case, the two coexist, diagnosis is difficult, I admit, and probably immaterial ; but under other circumstances the two offer more contrasts than likenesses, as may be seen by comparing the above with the following : — 84 DIFFERENTIAL DIAGNOSIS chap. INDICATIONS OF A PULMONARY VOMICA On inspection. Sinking in of chest from the old fibroid disease which remains from the original trouble that caused the excavation. On palpation. Increased T.V.F. from the consoHdation sur- rounding the cavity, and from the resonance of the chamber. On percussion. Dulness and increased resistance, again arising from induration and consolidation around the cavity. On auscultation. Tubular breathing with amphoric resonance, frequently adventitious sounds of the nature of rales, and clicky or resonating crepitations ; the former arising in and from the cavity, the latter from the fluid in it and from the consoli- dating catarrhal mischief going on around it, so that their absence is a good sign as indicat- ing inactivity of disease or its obsolescence. These are the signs usually ascribed to a vomica in the lung, and the reasoning is sound as far as it goes, because chronic phthisical processes (tubercular or non - tubercular, vide below, Fibroid Phthisis) are far and away the commonest causes of these excavations. But even with this causation there are two or three conditions that must be fulfilled before the signs will be present in typical form: (i) it must be fairly superficial to prevent its appro- priate signs and sounds being overwhelmed by those of overlying healthy or diseased lung ; (2) it must be of fair size, at least as large as, say, a nut, to cause amphoric echo ; and (3) it must communicate by a patent opening with a bronchus to allow access of air. The two acute processes, viz. abscess and gangrene, which may produce rapid excavation of the lung, are by their very acuteness sufficiently distinguished, qua excavation, from tubercular mischief. N.B,—\\, is advisable, or even imperative, in doubtful cases of excavation, to listen to the chest actually while the patient is coughing^ as well as to note alterations in signs after a cough, because the tube or tubes leading to the cavity may be blocked with material only to be removed by coughing. PHTHISIS "An assemblage and progression of symptoms associated with and dependent upon the ulcerative, or suppurative, destruction of a IV DISEASES OF THORACIC ORGANS 85 more or less circumscribed non-malignant deposit in the lungs," was the late Sir Andrew Clark's definition of the disease, and I do not think a better one could be devised, although it excludes miliary tuberculosis, for it is wide enough to embrace all the non- tubercular chronic destructions of the lung which are associated anatomically with suppuration and ulceration. Both before and since the enunciation of this definition an enormous amount of literature has appeared containing exhaustively detailed descrip- tions of the anatomical results of phthisis in the lung, and classifications of the disease of such endless variety, that the student of the subject must get confused in trying to get an intelligent idea of the whole of it ; for under such a weight of exposition he is in great danger of losing sight of that unity of principle with diversity of result which underlies and explains the varying aspects of phthisis and chronic diseases of the lungs. It is to this unity of principle that I wish to draw special attention, with a few brief notes on the results and conclusions. The frequency of tubercular — as compared with all other forms of — chronic irritation and destruction of the lung, and the special anatomical results of this special form, have led to a tendency to view inflammation in the lung as always something special, with special laws of its own. Such a view is erroneous and misleading, and the first great principle in our present subject is that the lungs offer no exception to the rules that govern the processes of so- called inflammation, as it occurs amongst vascular tissues anywhere in the body. These processes we must briefly indicate in a series of paragraphs : — 1. The collective phenomena known by the name of inflamma- tion are the invariable result of a locally acting (not necessarily locally produced) irritant of any kind whatever^ provided this be not sufficiently severe to kill the tissues outright ; and then, be it remembered, the processes go on in the surrounding living tissue, the dead mass sharing in, or being the efficient cause of, the irritation. 2. The first phenomenon is interference with the freedom of circulation through the part, a coincident out-soaking of fluid, and the appearance in the area of numbers of small round cells. The majority of these cells are of feeble vitality, if not actually dead, representing as they do to a large extent the dead and wounded in the fight between invaders and defenders. The tissues, too, in and near which the fight is going on, suffer in vitality from the disturb- ance in their normal circulatory refreshment ; this is the functio S6 DIFFERENTIAL DIAGNOSIS chap. /^sa of inflammation, whether in mesoblastic or epiblastic ele- ments. 3. Paragraph 2 represents the destructive phase of inflamma- tion. It may reach any degree of intensity^ from the microscopic-in- quantity-but-identical-in-quaUty of the heahng of an aseptic wound up to the quarts of pus and sloughing of septic cellulitis ; and it continues in the immediate neighbourhood of the irritant so long as this — or its products — remains in such a condition and position as to come in contact with irritable tissues. 4. Following this, as the defenders locally or generally get the upper hand, comes the reparative phase in which granulation tissue is formed, consisting of new nucleated cells (the precise origin of these and of pus, though perhaps important, has no bearing on our present purpose), endowed with vitality because of, and in propor- tion to, their proximity to supplies of nutriment in the shape of newly-formed blood capillaries and intercellular lymph spaces. 5. Following granulation tissue comes the formation of fibrous or scar tissue, which possesses primarily some peculiar properties : (a) it is practically non- irritable, hence should the irritant still remain active in situ^ it serves to shut it ofl" from its field of opera- tion on irritable tissues, and eventually causes its death by isola- tion ; ib) though poor in vitality itself, it is not irritating to healthy tissues, and has no tendency like dead material to cause a spread of inflammation ; {c) it is extensile and contractile, almost mechanic- ally so, so to speak, very different in these qualities from naturally existing fibrous tissue, exhibiting either quality to an extreme degree, unbalanced by intermingled muscular fibres ; id) though in general it is produced in an amount which is simply reparative, it is occa- sionally liable to excessive growth, as is seen in false keloid and in some thickened pleura. 6. The dead material that arises as the result of the destructive phases of inflammation, if left i7i situ and isolated by scar formation, and if it does not become the seat of a fresh development of irritating energy (septic microbes, etc.), has a tendency to dry up and be converted into cheesy material, and ultimately into a cal- careous mass by the deposition of lime salts. 7. The two phases of inflammation — the destructive and the constructive — must go on so long as the irritant remains in contact with irritable tissues. The fight must always be to the death or impotency of the tissues, or of the irritant. Hence in the case of a living and propagating irritant (microbes) it may be prolonged indefinitely ; the microbes striving, and, alas ! too often with over- IV DISEASES OF THORACIC ORGANS 87 whelming success, to cause destruction, the tissues as continuously, but with indifferent success, to efface their enemies by scar formation. 8. From a given primary focus inflammation may spread by (a) direct continuity as the irritant extends its area of influence wider and wider (this method of extension, if of any distinct degree, is almost conclusive proof of microbic invasion, for a simple mechani- cal irritant cannot spread ; a non-reproductive chemical one would rapidly become neutralised by combination ; and it is only by direct multiplication of the microbe, or by the continued production of toxins, toxicogenic zymins, etc., that we can understand the widening area of irritation) ; (d) mechanical transference of the irritant to other points, either by the blood stream or per lymphatic channels, or, especially in the lungs, by air currents or mere mechanical dropping under the influence of gravity into parts which are for the time being lower than the original focus. These are the essential principles of inflammation wherever occurring, undeviating in their action, only modified, not obscured or fundamentally altered, by the nature of the invading irritant and the elementary anatomical details of the organ attacked. Of the modifications introduced by the nature of the irritant, we must note that in tubercle (the same is true to a certain extent of the other infective granulomata) there is a special tendency to the early and rapid formation of a small mass or nodule of granulations with a vitality and cohesion somewhat in excess of that met with in the results of the inoculation of more virulent microbes. These nodules would apparently seem to belong to the reparative side of inflammation, for they do occasionally — it is true very rarely — become quite fibrous even in a miliary tubercle, but owing to their low degree of vitality and lack of capillary nutrition they cannot individually grow to any size without caseating or softening down. Owang to the great pertinacity and multiplication of the irritant they are, however, persistently produced in the immediate vicinity of the original focus, and by their union and coalescence may constitute masses of caseous material as large as the thumb or larger. If the irritant be of a more virulent type, the destructive phases of inflam^- mation are more prominent, with suppuration and tissue death (microscopic = necrosis, macroscopic — gangrene), and, possibly, the development of foul smelling gases as the predominating processes. If different irritants of different virulencies be at work at the same or successive times, the results are likely to vary according to the above sketch, first one and then another becoming the predominat- 88 DIFFERENTIAL DIAGNOSIS chap. ing feature of the case, e.g. catarrh followed by tubercle, pneumonia by gangrene. Of the modifications introduced by the anatomical peculiarities of the lung, we have only to note the air passages with their enormous area of mucous membrane, lined with epithelium, to which air must necessarily be freely admitted ; air, too, which cannot always be filtered through nasal vibrissce, and which consequently often, or even usually, contains multitudes of microbic, mechanical, and chemical irritants of every kind. Hence we have (i) an extraordinarily ex- tended frontier offering opportunities of invasion ; (2) the most favourable opportunities for the accumulation, in tubes through which air currents are feeble, of mucus and dead epithelial, and other cells (catarrhal products), on which microbes may implant themselves without opposition, and grow and multiply till they reach irritable tissues ; (3) the physical signs of such tubercular nodules or of catarrhal and pneumonic products will naturally be essentially identical in local details over small areas, for they all produce con- solidation or collapse of lung tissue, or sticky fluid contents for the air tubes ; it is this which causes so many difficulties in diagnosis. We may now apply these principles and their modifications to explain the correlated pathology of, and the adjectives applied to, the varieties of phthisis. Pneumonic Phthisis This term may be used to refer either to the amount of con- solidation of the lung, or to the clinical history of the case, resem- bling at some period of its course a pneumonia (croupous or catarrhal). In the former case we have the tubercular nodules rapidly forming and coalescing (scrofulous or acute pneumonic phthisis of authors) until large areas are involved, giving the physical signs of a pneumonia, but without the definite limited symptoms of that trouble ; the softening of the masses will add still further likeness to the resolution stages of ordinary pneumonia. For the latter signification of the term, i.e. a clinical history re- sembling that of a pneumonia, it is a common enough event for the tubercular nodule to cause an inflammation of a non-tubercular nature to surround the original focus with consolidation (tuberculo- pneumonic phthisis of authors), and this may occur at any period of the progressive destruction. In both these cases the tubercular bacilli are the original irritating invaders. But another common sequence is the primary invasion of the pneumococcus (croupous) or of less definite microbes (catarrhal), causing a wide-spread con- IV DISEASES OF THORACIC ORGANS 89 solidation or pneumonia, and in the weakened tissues and dead material thus produced the specific tubercle bacilli find a favour- able nidus for growth, and proceed more or less rapidly to con- tinue the mischief after the acute symptoms of the original invasion have subsided. This sequence of events explains the term catarrhal phthisis, though the term might equally well be applied to the ordinary cases of not very acute tuberculosis of the lung in vrhich large areas are not simultaneously solidified. Fibroid Phthisis This term includes all varieties of chronic lung destruction, of whatever nature, in which the reparative or scarring phases of inflammatory reaction have reached a considerable degree and extent. Inasmuch as the bacillary or simple irritant invasion is entirely a matter of accident, we have the following easily understood varieties : — Tubercular. Another name or v>'ay of expressing a ver}^ chronic case of tubercular phthisis, in which the fight being a pro- longed one, the scarring is very evident. (The term must obviously be also applicable to cases of cured phthisis.) Tuberculo-fibroid. Nearly the equivalent of the first variety, only that subsequent to the tubercular scarring other irritants continue the inflammatory reaction and healing. Fibre-tubercular. In which the primary scarring is due to in- definite bacillary or even mechanical (pneumonokoniosis, stonemasons' or coalminers', etc., lung) irritants, and on the weakened tissues the tubercle bacillus makes a descent, and continues the destruction - with - healing processes. Fibroid. A condition of fibrosis of the lung, starting as above (most commonly, perhaps, from an unresolved pneumonia or bronchopneumonia), but in the production of which the tubercle bacillus never at any time plays any part. N.B. — Post-mortem experience would almost lead me to believe that in any of these cases the scar may take on a keloid-like exten- sion, independent of obvious irritation. HEMORRHAGIC PHTHISIS When haemorrhage of noticeable extent occurs as the result of "ulcerative destruction of the lungs," the blood may either coagu- 90 DIFFERENTIAL DIAGNOSIS chap. late in situ round the focus, or it may also be mechanically carried into distant air tubes and alveoli. The ulceration may or may not be due to the action of tubercle bacilli ; in the former case, extrava- sated blood is likely to be more or less impregnated with the bacilli, and in proportion as it is impregnated it acts locally or at a distance, like a laboratory plate culture, causing a rapid multiplication of the points of infection. (This is the old phthisis ab hcemoptoe. The older pathologists did not recognise, as we now do, that the bacilli were there before the haemorrhage, and that it is only their exten- sion which is due to the bleeding.) In the latter case, when tubercle bacilli are not present, the haemorrhage, qiia haemorrhage, is harmless enough, or, at least, has to be considered from a totally different standpoint of causation. Miliary Tubercle Is a condition in which thousands of tiny nodules are scattered through the lungs (and other organs, liver, spleen, etc., including tubercular meningitis), and only requires notice here to insist upon the fact that it is never a primary form of attack fro?n without of the tubercle bacillus. It invariably arises from some caseous or softening tubercular ^ focus within the body, the bacilli being carried thence by lymph or blood stream. This focus can always be found by a sufficiently close search on the post-mortem table. Diagnosis of Pulmonary Tuberculosis From the above consideration of the pathology of, and anato- mical changes in, chronic and even acute pulm.onary disease, it will be seen that an accurate and exact diagnosis of their causa causans is not to be obtained by physical signs alone. All such affections are, or may be, indifferently associated with crepitations, rales, and rhonchi, and with consolidation of small or large areas of lung, with or without signs of pleuritic involvement. We may be inclined in one direction by the localisation of these morbid phenomena to an apex or to a base, and led in another by their universal distribution over the whole of one or both lungs. The ^ In all that relates to phthisis the terms ' ' tubercle " and ' ' tubercular " are used in strictly concomitant association with assumed specific bacilli. The terms "nodule" and " nodular " are used in their strict meaning of a little lump, or referring to a little lump. It is the confusion in these terms that has led to much confusion in translating tl^.e meaning of the older authors, who made tubercle the equivalent of a little lump, with- out reference to the presence or absence of bacilli, of which, indeed, they naturally knew nothing. IV DISEASES OF THORACIC ORGANS 91 family history may show a special proclivity to tubercular disease. ^ We must weigh the circumstances of occupation as affording 0})por- tunities for pneumonokoniosis ; we must note with anxiety a failing appetite, with wasting and sweating, and carefully watch the pro- gress of our patient when acute symptoms (cough, fever, haemo- ptysis, etc.) have subsided. But when all these points have been duly weighed in the balance, remembering that tubercle may pre- cede, accompany, or succeed any other irritant, we shall still have before us the one crucial question, "Is the bacillus tuberculosis present in the expectoration or not ? " Universal consensus of opinion warrants the statement that if the bacillus be found, it is at any rate a prominent sharer, if not the sole factor, in the production of the patient's illness, so that if we would guard against disappoint- ment in prognosis and errors in diagnosis, the search for the microbe must be undertaken in every case permitting of doubt. The most likely cases for error and doubt are the following : — (a) Bronchitis and Bronchopneu77ionia in Babies a?id Young Children. — Here sputum for examination is practically unobtainable, and we must rely mainly on the following considerations : — If the disease is simple in origin the patient should get well in from two to three weeks, and the improvement in the child should correspond fairly w^ell to the clearing up of the morbid lung sounds. If the child does not rapidly pick up after this time, a very careful search must be made for empyema, which very commonly develops and retards convalescence. Should no evidence of pleuritic trouble be found, and the child still not improve, then tubercle must come strongly under suspicion, and every system and part of the body must be carefully examined for corroborating or contradicting evidence. Pulmonary tubercle under the age of say ten or eleven years is practically only of one kind, viz. miliary, or at least very widespread, and hence a wide area of persistent morbid phenomena will be suggestive. Those other unknown irritants which maintain a chronic catarrhal condition have a contrary tendency, viz. one to preserve their morbid activity only in one locaUty, and that usually at the base. These basic chronic catarrhs, especially if occurring after a specific fever, such as measles, by no means infrequently persist, and form the origin of a genuine purely non- tubercular fibroid phthisis. 1 Modern opinion, in more strict accordance with the bacillary or infective theories of tubercular processes, is inclined to attribute more weight to the view of direct infec- tion by personal contact with a sick relative or friend, or by inhalation of germ- infected air of the sick-room, and less to the mere possession of tubercular ancestors. 92 DIFFERENTIAL DIAGNOSIS chap. (b) Repeated attacks of " Cold and Cough^'' ivith slight symptoms of Mild Bronchitis. — This group of symptoms constitutes the very commonest history of the commencement of an ordinary case of phthisis, and must, therefore, ab initio., arouse our strongest suspi- cions. Sputum may be available, and may decide the diagnosis out of hand, but it must be remembered that even tubercle takes a little time to soften and ulcerate, so that expectoration may be unobtainable, or, again, its examination may yield merely negative results. We must then proceed to carefully examine the lungs for a small localised area over which the auscultatory phenomena are not only pathological, but different from the universally heard rhonchus of bronchitis, and suggestive of consolidation. Such are commonly, but by no means invariably, found at the apices of the chest. They are found frequently enough at the apex of a lobe, or, in my experience, often in the neighbourhood of the pericardium. I do not think that a visible want of expansion or altered percus- sion note is of much use in deciding doubtful cases. By the time they are definite enough for observation the general symptoms have rendered their aid superfluous. I am accustomed to rely more upon the sharpness of the crepitations — "clicky" is the term I usually apply to them — and a slight increase in voice and expiratory breath sounds. If these go with a pulse frequency, and a loss of weight and appetite out of proportion to the apparent illness, I feel at any rate judgment must be suspended, and the case declared one of doubtful and suspicious nature, and the more suspicious, the stronger the lead given by the patient's history, whether family or personal. These are the cases that made our predecessors in medicine divide their patients up into constitutional types of liabi- lity to consumption : the blonde, with thin flaxen hair, the brunette, with flushed cheeks, the sprightly or ethereal, the clumsy or scrofu- lous ; their descriptions are still true in the main, for they were founded on an experience which is still ours. (c) HcE7noptysis. — It may be said at once that genuine pulm.onary haemoptysis, and especially if free or repeated, when found w^ith the physical signs and symptoms considered under ib\ adds so enor- mously to the probabilities of tubercle as to render diagnosis nearly certain ; but the symptom is so common and so alarming to our patients, that it may be discussed at a little greater length. We have already (p. 54) enumerated and briefly mentioned the possible causes of hsemorrhage, and on p. 152 given the diagnosis between haemoptysis and hsematemesis. It remains here to consider the question commonly enough asked, "What do you expect to hear IV DISEASES OF THORACIC ORGANS 93 in the chest of a patient who comes to you complaining of ' spitting of blood ? ' " We may, I think, reply accurately enough by saying, " If blood-spitting is his 07ily complaint, it is probable that we shall hear nothing." The reasons for this reply are: (i) that in a very large proportion of such cases the blood comes from elsewhere than the lungs — gums, pharj^nx, nose, larynx, etc. ; (2) that in again a large proportion of the cases in which the blood does really come from the lungs, it is symptomatic of advanced heart or lung disease, which will have given rise to marked symptoms previous to, and different from, the haemorrhage ; and (3) it is a common experience that we hear nothing — not even the crepitations of blood in the bronchioles — in those cases which time shows only too clearly were really cases of tubercular haemorrhage. In connection with the diagnosis of the causes of pulmonary haemorrhage, I cannot conclude better than by quoting a few sentences written by Sir Thomas Watson many years ago, and which still hold good. He says (^Lectures o?i the Principles a7id Practice of Physics^ 5th edition, 187 1): " Cceteris paribus, the disposition to pulmonary hsemorrhage is in- creased by whatever tends to diminish the capacity of the thorax, and to compress the lungs, or the heart and great vessels. It is partly on this principle that we may account for the frequency of haemoptysis in persons with crooked spines: in tailors who sit continually in a stooping posture ; in young women who lace their stays too tightly ; and even in those who labour under dropsy or other cause of distension of the belly." He then quotes in full detail a case of vicarious menstrual hemoptysis, and proceeds : "It is, however, a melancholy truth that capillary haemorrhage from the mucous membrane of the air passages is dependent in a very large proportion of cases upon incurable disease — tubercular phthisis or organic disease of the heart. When haemoptysis is thus actually symptomatic of tubercular disease of the lungs, it is liable to con- siderable variety in regard to the period of its first occurrence. There are many persons in whom the first attack of haemoptysis precedes, even for years, the primary symptoms of unequivocal phthisis. There are others in whom the first attack of haemoptysis is immediately followed by all the signs which announce the pre- sence of tubercles in the lungs." He then mentions heart disease and pulmonary apoplexy, and after quoting Andral to say that : " Of those individuals whom he had known to spit blood at some period or other of their lives, there was only one in five whom he did not know to have tubercular phthisis." He deplores his in- ability to alter the opinion he had long held and expressed: "That 94 DIFFERENTIAL DIAGNOSIS chap. if from any given number of persons who have been known to spit blood — excluding the streaks of bronchitis, the rust -coloured ex- pectoration of pneumonia, and injury to the chest — we subtract those in whom that symptom was connected with irregularity in the uterine functions, and those in whom it was symptomatic of cardiac disease, there will be very few indeed left in whose lungs the exist- ence of tubercle or other fatal disease may not be confidently predicated." Except that we do not now regard pulmonary tuberculosis with quite such a hopeless feeling as regards prognosis, these statements of Sir Thomas Watson are, I think, as true now as when he wrote them. (d) Pneumonia that does not clear up rapidly after the Temperature has fallen. — Here the very fact that the lungs do not clear up in, say, three or four weeks, constitutes in itself proof that somethiftg other than the pneumococcus is at work. This something may be tubercle bacilli or others not yet sufficiently identified (there is just a possibility that the lung tissue — the soil — of the individual may be peculiarly weak, and allow well known microbes to continue the irritation). Expectoration is always present, and can be obtained for bacteriological examination, so that diagnosis requires no further remark beyond calling attention to the fact that an unresolved pneumonia is not necessarily at any time tubercular^ but may at any time become so, and is, therefore, a standing menace to its possessor. (e) Chronic Bronchitis. — Vide below, p. 98. Here I can only say sputum is again available, and must be examined. Of pyrexia in these various cases I have said but little, as its indications are of dubious significance. On the one hand, it is certain that a slight rise of temperature (loi or less) in the evening (especially with early morning sweating) is strongly suggestive of tubercle in those cases, as in group (p), where the physical signs are doubtful; but, on the other hand, it is equally certain that typical hectic temperature (102, 103, or 104 at night; 97 to 99 in the morning) is due more to septic processes, either with or without tubercle, than to tubercle itself, so that in the other groups we get very little assistance from thermometric observations. There is only one other point in phthisis that I propose to mention, that is diarrhoea. It is important to remember that it may be due to any of the following : — {a) Simple dietetic errors, from which phthisis is no protection. Inquiry into food will possibly suggest this cause. (b) Simple irritability of alimentary tract, which is very common IV DISEASES OF THORACIC ORGANS 95 in these patients, and may be increased by swallowing septic or irritating matter which ought to be expectorated. The diagnosis of this form can only be made by exclusion, and by noting that it moderates or ceases under appropriate treatment, and warning against swallowing sputum. (c) Tubercular ulceration of gut. The diagnosis will mainly rest on the intractability of the diarrhoea, and possibly some tenderness of abdomen, together with an exclusive consideration of the other three conditions. [d) Amyloid or lardaceous disease. This generally admits of easy diagnosis from the enlargement of the liver and spleen, and considerable quantities of albumen (without pus) in the urine. It is very rare for the intestine to be the sole or even the principal seat of the deposit. Should this, however, happen to be the case, it may be difficult or impossible to differentiate the condition from tubercular ulceration. In both cases the patient will probably be anaemic and cachectic ; in both the flux will be persistent and in- tractable. We may remember that amyloid degeneration never occurs in early phthisis before suppuration has been long estab- lished ; intestinal ulceration may, on the other hand, be a much earlier feature. Diarrhoea from amyloid disease, again, is usually stated to be entirely free from abdominal pain, while ulceration is frequently associated with colicky disturbances. PNEUMONIA Of the diagnosis of a well-developed attack but little needs to be said. The flushed or bluish face, with sweat standing in large drops on the forehead, the working of the alae nasi, the rapid breathing, the painful efforts at subduing a distressing cough, makes up such a typical picture that we can often diagnose the disease at sight j and when woodeny dulness on percussion and tubular breath- ing on auscultation are added, the diagnosis is complete. But there are one or two points still that are worth a little discussion, even in an elementary work. Diagfiosis in Early Stages. — Primary or idiopathic pneumonia is particularly characterised by the very sudden rise in the temperature (probably 103 or 104 within twelve hours), and a corresponding sudden onset of symptoms; while the physical signs, being much slower in development, are still in abeyance. These symptoms are usually a rigor, or convulsions (convulsions in children often take the position of rigors in the adult as an indication of severe invasion 96 DIFFERENTIAL DIAGNOSIS chap. by microbes), speedily followed by headache with intolerance of light, frequently enough delirium, and vomiting of a nervous type, i.e. independent of food. Now these are precisely the symptoms suggestive of an acute toxaemia, or of intracranial inflammation ; and hence many cases of incipient pneumonia may hastily be assumed to be something more dangerous than ultimately proves to be the case. Careful attention to the following points may assist us in form- ing an opinion, but for twenty-four or even forty-eight hours it is often absolutely impossible to make a final diagnosis. Inquire of the patient or friends as to any possible local source of infection, such as a wound, a boil, or an abscess, or even a blow on the head, and especially as to any discharge from an ear ; the throat and ears must then be examined for signs of septic mischief, and time would not be wasted by asking if the patient has had the opportunity of acquiring an infectious disease from a sick friend. If negative replies are received to these inquiries, note the pulse- respiration -temperature ratio, vide p. 35, which even from the commencement is very likely to be markedly deranged in a case of pneumonia. Should the indications be still undecided, judgment must be withheld temporarily, until a cough with expectoration or physical signs come to our aid. Central Pneumonia. — It occasionally happens that a pneumonia develops in, and remains confined to, the central part of one base, and thus the physical signs, even in the later stages, are concealed or ill developed. In such cases the sputum becomes a most valu- able sign, and quite possibly gives an absolutely decisive indication ; it is probably extremely sticky, but little aerated and non-purulent. If with these features it is uniformly stained with blood pigment, we are justified in saying that some pneumonia is present — the staining may be of any degree from rust to prune-juice colour, and the deeper it is, the worse the outlook. Is Pneumonia a Specific Disease ? — The facts suggesting such a theory are : — (i) The sudden onset of symptoms before, and independently of, the lung consolidation. (2) The sudden cessation of the symptoms while the consolida- tion still remains. (3) The definiteness of the phases through which a typical case of the disease passes. (4) The undisputed occurrence of small epidemics, and the appearance of attacks in which the evidence of infection from a IV DISEASES OF THORACIC ORGANS 97 previous case is overwhelmingly strong (noticed in anxious wives or mothers too closely attending their sick charges). (5) A microbe of very definite character has been pretty con- stantly found in sputum and lungs of typical cases ; it has been isolated and cultivated, and to a limited extent has been put through the tests on p. 26. Nos. (i) and (2) undoubtedly prove to a demonstration that the symptoms of pneumonia are not due to the lung consolidation as such, while (5) offers a plausible explanation of them; and we may, I think, sum the matter up by asserting that " One particular microbe is capable of producing a form of disease to which the term ' idiopathic pneumonia ' is applicable, but that facts do not prove that this is the only microbe capable of producing a set of clinical phenomena indistinguishable from such pneumonias." Accurate post-mortem evidence, coupled with scrupulously exact bacteriological work, would, I suppose, clear up every case and prove its precise causation, but there can be no disputing the fact that consolidations of large areas of the lung, coupled with symptoms indistinguishable per se {i.e. apart from the clinical history of the case previous to their onset) from those of an ordinary pneumonia, do occur in the course of bronchial catarrh, of puerperal, and other septic troubles, and of influenza amongst many other diseases. Admitting this, it is difficult to believe that the lung mischief is necessarily due to diplococcus pneumoniae, and that we must deny to other pathogenic organisms — specific or common, known and unknown — this power over the lung. Again, on the other side of the question, the diplococcus pneumoniae has been found frequently in morbid effusions in joints and elsewhere, under circumstances strongly suspicious of a causative relation, so that it cannot be said to confine its attention to the lungs. The only possible deduction from these facts is to give to clinical pneumonia a modified specificity, perhaps equal to that given to clinical diphtheria (^-v.), while denying to it one so com- plete and unequivocal as that given to measles, syphilis, or scarlet fever. ACUTE BRONCHITIS AND BRONCHOPNEUMONIA The late Dr. Sutton used to teach that healthy children did not suffer from bronchitis. If this be so, then the zymotics, poor feeding, and neglect are responsible for much subsequent disease amongst our young population, for bronchitis is a very common II 98 DIFFERENTIAL DIAGNOSIS chap. disease in infants, and as bronchopneumonia is a direct extension of the morbid processes to the bronchioles and alveoh, it is a common difficulty to decide whether a given case shall be called bronchitis or bronchopneumonia. My own opinion is that prac- tically all cases of bronchitis amongst young children, if severe, have some degree of alveolar extension, so that from the point of view of treatment the diagnosis is of little moment, being more of academic or examinational interest. If dulness on percussion and tubular breathing are present over localised areas they settle the matter at once, but as these are easily obscured by non-affected lung tissue and the rhonchi of the bronchitis, and as children are awkward at, or incapable of, deep voluntary respiration, I usually rely upon the following two features: (i) The Temperature: if ioi° or over, it points to alveolar extension ; if below i o i ° and yet above normal, it points to uncomplicated bronchitis ; if markedly subnormal, it again points to very dangerous and universal bronchiolar involvement. (2) Rales and crepitations : if these are so abundant as to markedly predominate over the rhonchi of bronchitis, I again assume that bronchopneumonia is present. Dr. Osier, in his deservedly popu- lar work on medicine, will not allow any difference between capillary bronchitis and bronchopneumonia. As regards the nature of the morbid process he is obviously right, for one cannot draw an imaginary mathematical line between bronchioles and alveoli ; but as regards extent in area I think he is wrong, and I would define bronchopneumonia as a local (few or many patches), capillary bronchitis as a universal, extension of the catarrhal process to fine tubes and alveoli. This definition best explains the undoubted difference in prognosis ; capillary bronchitis I regard as uniformly and inevitably fatal, while recoveries from local consolidation are numerous and, indeed, the rule. CHRONIC BRONCHITIS AND ITS ASSOCIATIONS It is a very common observation that one attack of bronchitis (irrespective of the nature of the irritant causing it) predisposes the sufferer to another. A little consideration of the pathology of inflammation easily explains this. It is almost inevitable that, in a mucous membrane that has once been inflamed and shed a good deal of epithelium, slight scar changes, diminishing its vital resist- ance, should be left behind. Proceeding further, if we allow that these changes (scar tissue) will diminish the natural vital IV DISEASES OF THORACIC ORGANS 99 elasticity of the tubes, it is easy to see that with repeated attacks two consequences are likely to follow: (i) the stiffening process will extend farther and farther down the tubes, or become more and more marked in local segments of them ; from this it will follow (2) that increased air pressure, w^hether expiratory or in- spiratory matters not, must be felt more and more by the smaller air tubes and alveoli, which were never meant to stand such a strain, and consequently yield to it, giving us bronchiectasis, local or general, and emphysema. If the lung trouble is of such a nature as to be associated v>'ith much scar tissue, then this may by con- traction constrict air tubes, leading to dilation above the obstruction, or if it has a distant point of support its contraction may lead to a pulling open of tubes. We must not forget, too, that in elderly people, at all events, there is yet a third factor, and an important one, in the production of these degenerative or fibrotic processes ; this is arterial degeneration or wearing out of arterioles, with conse- quent imperfect nutritional changes in fine tissues. It is a clinical fact that an enormous numerical preponderance of cases of "bron- chitis and emphysema " in persons over forty, say, have atheroma of arteries well marked, and I believe the association is causative, and not an accidental accompaniment of age. We are thus led by simple deductive reasoning to appreciate the pathology and occurrence of — The Pulmonary Complications of Chronic Bronchitis (i) Brotichiedasis^ of which the principal diagnostic features are : large quantities of expectoration, often brought up in mouthfuls at a time, and frequently foetid ; this foetor is a most important diagnostic point between bronchiectasis and a phthisical cavity, for the latter never or hardly ever possesses foetid contents ; otherwise the physical signs of the two conditions are almost identical. (2) M??iphysema, of which hyper-resonance or too great an exten- sion of resonance is the main sign, coupled with prolonged expiration and shortness of breath out of proportion to the cardiac condition or the signs of bronchitis. (3) Collapse, arising from constriction of a tube or from plug- ging of it by catarrhal products. Over a collapsed area there is likely to be a little alteration in the percussion note — dulness or woodeny sound — but absence of breath sounds loo DIFFERENTIAL DIAGNOSIS chap. will be naturally the chief feature, and, possibly, slight fine crepitus on very forced inspiration. (4) Hce?noptysis, from rupture of a vessel, either owing to de- generation or to mechanical stretching, or possibly to venous distension in a violent paroxysm of coughing. (5) Pleurisy or pleuritic effusion^ arising from extension of in- flammation or from passive disturbance of circulatory ex- changes ; diagnosed by a rub or dull percussion note with segophony, etc. {^ide below). (6) Bronchopneii77ionia and capillary bronchitis^ arising from ex- tension of the catarrhal process to bronchioles and alveoli, either in an ordinary and direct manner, or by the insuffla- tion of the decomposing contents of a bronchiectasis. These are perhaps the most important complications of all, for they are very frequently the direct cause of a fatal ending to the case. Moreover, tubercular bacilli may suc- ceed, by their assistance, in implanting themselves on the weakened tissues or catarrhal contents of the tubes. The on- set of capillary bronchitis {vide definition above) is marked either by a prominent rise (inflammatory reaction), or, more probably, by an equally prominent fall, in the temperature to subnormal (asphyxial or exhaustive decline). This alteration will be associated with a very marked exaggeration of the breathlessness and cyanosis, the pulse will speedily become extremely frequent, small, and thready, and the patient will rapidly pass into a condition of extreme danger from asphyxia; in true universal capillary bronchitis he never rallies, but cold, clammy perspiration soon appears, and death foflows in less than forty-eight hours. The diagnosis of bronchopneumonia, when associated with a smart febrile attack, does not present any difficulty; but when we are attending an elderly patient, the subject of chronic bron- chitis, we must be on our guard to examine the lungs pretty frequently, as this alveolar extension often creeps on in a most insidious manner (pleuritic effusion may behave similarly, vide below), a little extra cough and shortness of breath, a little flushing of the face, perhaps, or sense of weakness or exhaustion, being the only outward indications of the mischief, which is most serious in its result. If we do, however, discover by care such a smouldering danger, we must not forget to test the sputum for bacilli, as this is the IV DISEASES OF THORACIC ORGANS loi common history of tuberculosis supervening on chronic bronchitic trouble. PLEURISY AND PLEURITIC EFFUSION To discover the mere presence of these troubles is usually easy; to estimate aright their clinical significance is far more important and difficult. Acute Pleurisy Sympto??is aytd Physical Signs. — Of the diagnosis of the presence of acute pleurisy I shall only say that pyrexia, associated with cough and pain in the side made worse by forced respiratory move- ments, is very characteristic, and if friction sounds are heard dis- tinguishable from pericardial ones {vide p. 126), the diagnosis is complete. I have already (on pp. 61 ^/ seq.) drawn attention to other more obscure cases of pain in the side. Causes of Acute Pleurisy. — These may be divided into the general and the local. As regards general causation, experience shows that the following are very hable to an attack : — (i) Those who are suffering, or are hable to suffer, from rheu- matism, acute or subacute. (2) Those who are affected with, or recently convalescent from, an attack of an acute specific fever, including influenza. (3) The \dctims of chronic nephritis of any form, with its associated imperfect elimination of waste products, and its anaemia. (4) It is undeniable that a fourth group must be inserted of individuals who are apparently in perfect health, but get an attack of pleurisy as the result of what is ordinarily termed a chill. Recent observations on the subsequent history of such individuals tend to reduce the number of genuine idiopathic cases very materially, as a large proportion of them have proved to be con- cealed tuberculosis. The local causes are : — (i) Traumatism, blows, fractured ribs, crushes, etc. (2) Extension of inflammatory processes — {a) From the lung, tubercle, pneumonia, bronchopneumonia, infarction, absccss, gangrene, etc. {f) From the pericardium (rarely). I02 DIFFERENTIAL DIAGNOSIS chap. (c) From abdominal viscera, liver, spleen, etc., through the diaphragm. (3) Rupture of morbid collections into the pleura, independ- ently of the inflammatory process reaching it — phthisical cavities, abscesses, hydatids, etc. Pleuritic Effusion Symptoms. — Inasmuch as effusion may be, and frequently is, an associate or sequel of the acute affection, however arising, the symptoms of acute pleurisy will suggest an examination for fluid ; but, on the other hand, effusion frequently takes place very in- sidiously, without obvious precedent disease or symptoms of suf- ficient severity to induce the subject to take medical advice, and only a troublesome shortness of breath or vague chest discomfort leads him to submit to examination. Physical Signs. — On the affected side we find : — On inspection. — Some loss of mobility compared with the sound side, possibly a visible displaced heart's apex beat. On palpation. — Tactile vocal fremitus, absent or much dimin- ished, possibly heart's apex beat felt in wrong place. On percussion. — Absolute dulness with increased resistance to the pleximeter finger. On auscultation. — Weak or absent breath sounds, probably of a distant tubular character owing to compression of alveoli and finer tubes ; a peculiar nasal twang is given to the voice sounds, known as segophony. Heart sounds heard most clearly in a displaced position. Over the still uncompressed lung the sounds, qua effusion, will b3 healthy, but the breath sounds will be exaggerated from over- work. Causes of Pleuritic Effusion and Hyd7'o-Thorax: — (i) All the causes of acute pleurisy already enumerated, in any of which eff"usion may be a predominant feature, or may remain after the acute symptoms have subsided. (2) Heart disease, with its obstructed circulation. (3) Malignant disease and other growths {e.g. hydatid) within the thorax. (4) Tuberculosis of lung or pleura, either evident or concealed {vide Causes of Acute Pleurisy). IV DISEASES OF THORACIC ORGANS 103 A general review of the above paragraphs leads to an inevitable conclusion that pleurisy and pleuritic effusion must in almost all cases be reduced to the rank of a symptom, possibly it may some- times rise to the dignity of an independent disease, and as a symptom it may occasionally possess the importance of causing a fatal event ; but, on the whole, its features and pathology must be analysed from the point of view of what hes behind, and not as the " be all and the end all " of a diagnosis. The Nature of the Fluid. — Physical signs alone enable us to say that fluid is present, but they give no direct information as to its nature — unless, indeed, we have a pointing empyema, which is, or should be, very rarely seen nowadays. Indirectly, by their persist- ence, they tell us that the fluid is not being absorbed, but this may be, and generally is, due to circumstances other than its nature. Should there be no indications of these circumstances, such, I mean, as obvious morbus cordis or pneumonia, etc., we are then justified in saying that this non-disappearance is probably due to the fluid not being simple serum, or to there being some hidden and persistent cause for it in the thorax, e.g. tubercle or carcinoma; cases of simple idiopathic pleuritic effusion resisting absorption for any length of time are rare. The symptoms, again, strictly speak- ing, are not of much use : excessive sweating, anaemia, weakness, and hectic temperature are certainly suggestive of pus, but they do not exclude tubercle with simple serous effusion, nor, indeed, car- cinoma, which I have found on the post-mortem table after such precedent history. There is but one method of ascertaining with certainty the nature of the fluid, and that is to withdraw a little by a syringe and examine it with the naked eye and (or) microscopi- cally. The following considerations will show that even now our diagnosis is far from complete: the fluid may be (i) clear watery, (2) bloody or blood-stained, (3) milky or purulent, (4) stinking. {a) If it be clear, it is either hydatid-cyst fluid — which will not coagulate on boiling and will show booklets — or it is serum ; in this latter case no strong deduction can be made from the information, for every single cause may have at times clear effusion, except ruptured abscesses and gangrene, both of which have probably given other and clearer proofs of their presence. It is in clear effusions that inoculation experiments on animals are so useful in clearing up a doubtful tubercular diagnosis. {b) If it be turbid or definitely purulent, the suggestion is that the attack is strong or the defence weak, which is not very 104 DIFFERENTIAL DIAGNOSIS chap. conclusive information ; empyema is common in children and in old people without further obvious cause, and also in renal cases and drunkards, but I have met with it as the product of carcinoma. (c) Blood or blood-stained serum is naturally to be expected in severe traumatism or ruptured aneurysm, in purpuric or scorbutic patients, but when occurring without such immediately obvious antecedent, it certainly leads us strongly in the direction of tubercle or carcinoma, for it is very rare in simple or rheumatic cases. {d) If it be stinking, we have conclusive proof that the microbes of decomposition have gained access to the fluid, but how, or why, they got there, we must learn from other evidence than their pres- ence. Some cases of stinking empyemata unquestionably do perfectly well after simple drainage, proving that the access of the microbes was not gained by gross lesions. It will thus be seen that the nature of the fluid per se gives but little definite or decisive indication ^ as to the real meaning of pleuritic trouble; serum clear or blood-stained, pus, or stinking fluid may each apparently occur or succeed one another in the same case ; the point is of great importance for prognosis and treat- ment, but we must look elsewhere for clearer indications of causa- tion. The presence of acute rheumatism, or the history of its previous occurrence, an account of severe exposure to weather, a present or recent attack of an acute specific fever, of pneumonia, of bronchitis or bronchopneumonia, advanced tubercular changes in a lung, are all fairly obvious on slight inquiry or observation. So, too, heart disease or chronic nephritis will yield unmistakable evidence of their presence, if we only bear them in mind as possible causes and look for them. Any of these would be admitted as a satisfactory and final explanation of the origin of the trouble, beyond the natural history and clinical significance of which we need not go either for diagnosis or prognosis ; but if the case offers no such leading indications, we have now to decide between (i) an unusual case of apparently idiopathic pleural effusion ; (2) malignant growth ; (3) tubercle of lung or pleura concealed by the fluid. If the fluid has persisted, without signs of absorption, for longer than, say, two or three weeks without a causative diagnosis becoming reasonably certain, we should, I think, empty the chest as completely as possible by mechanical means, even in the absence of urgent symptoms or other reasons, solely for the purpose of establishing, as far as ^ Microscopic or bacteriological examination may possibly in some cases g^ve absolutely conclusive proof of tubercular or malignant disease. IV DISEASES OF THORACIC ORGANS 105 possible, a fundamental diagnosis from the nature of the fluid, and from the changes in the chest produced by its withdrawal. The nature of the fluid we have already seen to be very dubious in its indications, though so7tiethmg may be guessed from it. The changes in the physical signs may be thus analysed : — In simple idiopathic pleurisy aspiration will certainly cause a restoration of some degree of resonance to the previously dull area, and the lung will soon expand with a return of distinct breath sounds, probably intermingled with fine and coarse crepitations, owing to the renewal of the circulation through previously compressed lung tissue. If the case is a tubercular one, it is again probable that there will be some restoration of more natural physical signs on percussion and auscultation, but it will not be so complete as in the former case, and there is likely to be some evidence of patchy consolidation, and quite possibly friction sounds will be heard. It is, too, more probable that the fluid will return, though in either case this may happen. In growth of more gross character it is unlikely that the removal of the fluid will alter to any marked degree {vide below) the physical signs found previously ; there is no re-expansion of lung with renewed air entry, rapid return of the fluid is practically certain to take place, and suspicion becomes greater the more rapidly this return appears without pyrexial phenomena to account for it. If the fluid withdrawn be turbid or purulent^ this is in itself strong, but not absolute proof against malignant growth. The most important point to bear in mind with pus is that the fibrinous coagula, etc., are apt to prevent expansion of the lung, so that greater care must be exercised in pronouncing judgment from the absence of this expansion. It is also very rare — I should say un- known — that tubercle, otherwise indetedable^ should cause a purulent effusion as the first sign of its presence. INTRATHORACIC TUMOURS Those which I propose to discuss here are: (i) malignant growths ; (2) aneurysms. Both have their chief features in common, viz. irritation and pressure, and to discuss in detail every variety of each, and its separate diagnosis, would require a monograph to itself. I only propose to give the principles on which such differentiation must proceed; this necessitates as a foundation a brief sketch of the nature and anatomical relationships of the two affections. . io6 DIFFERENTIAL DIAGNOSIS chap. Malignant Growths Are in nature — (i) Primary. {a) Carcmoma. (b) A group to which we may loosely apply the term " lymphosarcoma." ^ (2) Secondary. Every growth or form of it which can cause meta- static deposits, or invade the thorax by simple local extension. Their anatomical relationships may be thus tabulated : — Starting Point. Progress. k;^ Almost invariably at the root of c3 the lung, either in the root .S itself or glands of posterior Ph or upper mediastinum. >^ c3 (a) Anywhere in the lung tissue. fi {b) Creeping into the medias- H tina. Into the mediastina, sur- rounding and compressing the structures there, and forming a large solid mass. Into the substance of the lung, solidifying it. Into and over the surface of the pleura pericardium, etc. I have grouped these together, allowing a growth to proceed in any direction, a course which is theoretically true, and may now and again be taken by any of them, but clinical experience in the post-mortem room shows that : — 1. Primary carcinomata almost always spread either into the lung tissue or on to the pleura, or both ; they practically never invade mediastinal tissues alone. 2. Primary lymphosarcomata practically never invade either lung or pleura, but grow steadily in the mediastina, compressing the lung ; the pericardium is surrounded, and may be actually invaded on its inner surface, causing effusion and cardiac difficulties. 3. Secondary metastatic deposits from a distance practically always form nodules in the lung substance, solidifying and invading it without compression. 4. Secondary extensions from mamma or oesophagus, e.g.^ are the especial tumours which may spread in any direction. ^ This term must include true sarcomata, and also the ill-understood enlarge- ments of lymphatic glands, lymphadenoma, Hodgkin's disease, etc. IV DISEASES OF THORACIC ORGANS 107 Aneurysms May be classified according to the part of the arch from which they spring, but I think more usefully according to the clinical indi- cations, thus : — Anatomically. Of the ascending arch. Of the descending arch. Of the descending thoracic aorta. Of the transverse arch. Clinically. The aneurysms of physical signs especi- ally : __ {a) Externally bulging tumour with expansile pulsation. {b) Dulness on percussion. {c) Audible bruits. The aneurysms of symptoms, principally or entirely pressure effects on neigh- bouring soft tissues {vide p. 108). The progress of any aneurysm — upwards, downwards, forwards, or backwards — is governed by the precise point in the circumference of the vessel at which it first starts, spreading from that point in all directions except towards the parent vessel. This sketch shows that the two conditions cannot be separated by anatomical considerations alone. We will now discuss in parallel columns the more likely explanation of certain conditions. Aneurysm. Sex. Many times commoner in males. Occupation. The more laborious oc- cupation probably ex- plains the greater fre- quency in men. Age. Usually thirty-five to fifty. Alcohol. Excess undoubtedly a pre- disposing factor. Syphilis. Is undoubtedly also a pre- disposing factor. Growth. No predilection for either sex. Would seem to have no influence in inducing a growth primarily. Primary commoner under thirty-five, but second- ary at any age corre- sponding to the primary growth. Without influence. Has no influence on or- dinary growths ; and gummata, large enough to cause doubt, are ex- cessively rare. io8 DIFFERENTIAL DIAGNOSIS CHAP. Complaint of pain. Inspection of patient. Auscultation. Aneurysm. Acute pain is certainly suggestive in cases of doubt, but no conclusive evidence from this point. Bulging expansile tumour pathognomonic ; but, of course, usually no evi- dence from inspection in cases of doubt. CEde- ma of an arm occasion- ally seen, but of one side of chest alone very rarely if ever. A systolic or double bruit, if not traceable to val- vular disease, is very suggestive ; even if valvular it only loses significance if patient be young and has suf- fered from a recognised cause of endocarditis. The degenerative pro- cesses of age tending as much to aneurysm as to valve destruction. Growth. If present it is more commonly a dull op- pressive pain, but neur- algia may occur. A mass of enlarged glands or growth above clavicle also pathognomonic ; a malignant tumour else- where is very suggestive in doubtful cases. OEdema of one side the chest wall very sus- picious, and if without oedema of arm almost conclusive. Bruits have no connection with tumour as such ; may occasionally occur if heart is displaced, or aorta or pulmonary artery distorted, but this is very rare. Pressure and Invasion Effects On lungs. Usually causes compres- sion only, with irritat- ing cough, but may start an acute inflamma- tory attack with free haemoptysis. May cause compression only by growing on the pleura {q.v.\ but more frequently assumes the characters of an insidi- ous consolidation — often multiple in secondary infection — and only at the last when breaking down causes aspiration-bron- chopneumonia. IV DISEASES OF THORACIC ORGANS log On trachea and bronchi. On pleura. On veins. Aneurysm. Tracheal tugging ^ very characteristic if present ; may cause a bronchitis, and possibly dyspnoea, but vide Nerves. Acute pleurisy a much commoner result than quiet effusion ; this is because an aneurysm is much more acutely ir- ritating than a soHd neoplasm. Aneurysm, until too large to be mistaken, rarely presses on any vein ex- cept the left innominate, and hence the oedema mentioned under In- spection not usually aA-ailable in doubtful cases. Growth. Probably causes only a slowly progressive shortness of breath from compression, which also leads to collapse of cor- responding area of lung. A clear or blood-stained effusion, very common when the growth reaches to and spreads over the pleura ; it is probably more due to venous blockage than a real inflammatory reaction. Tumour of size or extent to be still doubtful fre- quently catches the in- tercostal veins, causing oedema of chest wall ; also the vena azygos, causing enlargement of abdomino - thoracic veins; the left innomin- ate, too, or even a vena cava, may be caught early. Is now and again blocked by a growiih, and occa- sionally chylous ascites has appeared from this cause. Tumours of thorax proper more rarely than aneur- ysm cause dysphagia ; should they do so its amount is likely to be unvar}'ing. Carcinoma of the oesophagus itself is the only likely one, . . and then the gradual but persistent history of ^ A peculiar shock s}Tichronous with the pulsation of the aneurysm, felt by two fingers laid on the trachea when extended to its utmost by throwing back the head as far as possible. Thoracic duct. On oesophagus. Practically never inter- fered with by a doubtful aneurj'sm. Aneur^'sms cause dys- phagia, but when it arises from this cause it is likely to var}' in degree on occasions. no DIFFERENTIAL DIAGNOSIS CHAP. Aneurysm. On nerves. On bones. Effect of rest or treatment. Duration of symptoms. The intermittent beating of an aneurysm appears to be more .irritating than a growth ; the re- current laryngeal is the nerve par excelle7ice of aneurysmal trouble, being frequently paral- ysed by small aneurysms of the arch. Destruction of bone by aneurysm is very pain- ful. The symptoms of aneur- ysm show spontaneous variations in intensity which it is difficult to account for ; they are almost invariably im- proved, for a little while at all events, by rest in bed and other treat- ment. From clinical histories it would appear certain that aneurysms may last for a long time before causing a fatal event, hence a history of symptoms for many months or a year or two is very suggestive of aneurysm as against growth, though perhaps more against either of them. Growth, dysphagia as the only symptom is the strongest circumstantial evidence. A growth appears to cause but little active irrita- tion to nerves, but no general rule can be laid down. Pain is certainly less common in growth than in aneurysm. Intrathoracic growths rarely reach and erode bones, but one growing from the bones of the thorax would cause pain not so acute as that of aneurysm. The symptoms of growth rarely show even the faintest trace of im- provement under rest and treatment, while judgment is suspended. All cases of definite tum- our end fatally within a year, hence if condition has early and rapidly become severe, it is so far in favour of growth V. aneurysm. IV DISEASES OF THORACIC ORGANS iii These points, I think, include the bulk of the evidence we shall have to weigh in a given case. Few only of them are decisive or pathognomonic, but if all are carefully considered I think we shall usually arrive at a correct conclusion. CHAPTER \N— Continued DISEASES OF THORACIC ORGANS Section II. — Diseases of the Heart and Pericardium Errors of judgment — if not of actual diagnosis — occur more frequently in connection with heart disease than with the troubles of any other organ. The reason is somewhat as follows : — Before the days of the invention and perfection of the stethoscope heart disease was either not diagnosed at all, or it was guessed at by pain and morbid sensations in the thoracic cardiac area, or it was recognised by evidences of circulatory disturbance and the character of the pulse. These indications, without the assistance afforded by the stethoscope, were apt to be misleading. Now the pendulum has swung too far the other way, and, armed with an instrument of precision, we are all too apt to think we can immediately diagnose heart disease by bruits thus brought within the sphere of our objective consciousness. This is just as great a mistake as the former condition of uncertainty. That we can thus detect a leaking valve or a stenosed orifice must in general be admitted — though even here great caution is necessary in interpreting our aural perceptions — but this is often enough a very different matter from morbus cordis. Sir Andrew Clark was, I believe, the first to draw public attention to this. He compiled a very long list of patients in whom he had by systematic examination detected a cardiac murmur, but whose symptoms and complaints, as he showed, had no derivation whatever from a diseased heart. His experience we all of us can now confirm from out-patient practice, but it seems somehow to have escaped the recognition it deserves at the hands of students and practitioners. It may then well be asked what are the features (symptoms CHAP. IV ISEASES OF THORACIC ORGANS 113 and physical signs in combination) by which we are to recognise genuine heart disease. The conditions leading to a suspicion of heart disease are divisible into two main groups: (i) local in the thorax or cardiac area; (2) general, expressed in or by distant organs or tissues ; and each may again be divided somewhat indefinitely into symptoms and physical signs (p. 21). We will proceed to comment briefly on each division. Local Thoracic Symptoms which may Indicate the Presence OF Morbus Cordis 1. Pain. — Pain is a very variable feature indeed. It may be slight, or it may be extraordinarily severe (typical angina), and almost any degree of it may be associated with a cardiac condition of absolutely no moment at all, or of one of the very greatest danger to life. The only general statement that can be made about it is, that when due to the more serious troubles, it is very liable to spread from its original position and extend to the right, or to the upper chest and down the left arm. On the other hand, when owning a gastric (its most common source) or other than cardiac origin, it more commonly remains fixed to the cardiac area. It must not be forgotten that the pain of aneurysm, of pericarditis, and of left pleurisy, all instances of serious organic disease, more commonly also remain as a stationar}^ pain. In any and all cases we must, however, make a careful physical examina- tion, for by the results of this our judgment of the pain is, after all, mainly influenced. Pain alone must not be accepted as evidence of morbus cordis, though, when we are satisfied that the pain is genuinely severe, we must be doubly cautious in exonerating the heart, even if at the time of examination there remains very little or no evidence of abnormality. 2. Shortness of Breath may be very briefly dismissed, inasmuch as it may be due either to pulmonary or cardiac conditions, and it is only a physical examination of the patient that can determine which. From either source it is probably associated with cough, and made worse by physical exertion. That produced by cardiac disease is perhaps more definitely relieved by raising the patient to a sitting posture. 3. Cough. — Cough perhaps more properly belongs to the general group of back pressure symptoms, but as its alternative causation is local, it may be mentioned here. If due to cardiac disease, it will be either dry, ineffectual, and useless cough, and is then I 114 DIFFERENTIAL DIAGNOSIS chap. suggestive of nervous irritation, perhaps aneurysm, or it will be accompanied by some expectoration, but this will be simple frothy mucus, unless, indeed, there be hemorrhage, when the mucus will be blood-stained or replaced by pure blood {vide Haemoptysis, p. 54). If pus or other organic elements be present, it is a certain demonstration that the cough is x\q>X. purely cardiac in origin. 4. Palpitatio?i. — This simply means that the beat of the heart has become perceptible to the owner of the organ. It is extremely common in all sorts of diseases and conditions of ill-health, and especially as the result of mere introspection and morbid self- consciousness. Accordingly, when standing alone, without objective signs of morbus cordis, it is almost an indication against that con- dition as its real source ; but when associated with definite abnor- malities of mechanism or rhythm, and especially if then constant, it acquires considerable significance in the case. We thus see that the local symptoms, without exception, require a careful physical examination to determine their value and significance. Local Thoracic Physical Signs which may indicate the Presence of Morbus Cordis These include everything which can be seen on inspection, felt by palpation, appreciated by percussion, or heard on auscultation. I do not propose to discuss these in any detail, but shall merely indicate seriatim what aids they give us in diagnosis. Inspection is very frequently quite negative in its results. It may show a heaving impulse of great hypertrophy, or the pulsating tumour of an aneurysm ; the apex beat, too, may be visible to the eye, and its position is of great importance {vide p. 102 for its use in pulmonary diseases). A rippling wave of apex beat is suggestive of irregular action, or possibly of pericardial effusion, and recession near it in systole might possibly indicate adherent pericardium. Palpation will further determine the apex beat and be convincing of a strong, heaving beat. It may rouse suspicion of irregular heart action. Stress is laid by some on a thrill which may possibly thus be felt. It certainly is corroboration of probable mitral stenosis when a doubtful presystolic bruit is heard, but is frequently felt with faihng heart from any lesion, and also may be appreciated often in thin subjects whose hearts are above suspicion, so that I hold it very cheaply unless other and more certain indications of trouble are present. IV DISEASES OF THORACIC ORGANS 115 Percussion gives, with very variable results, the area of uncovered heart, and possibly some idea of the gross size of the organ. But it is so subject to personal variations in the observer, so liable to vary in health in different individuals, so subject to fallacies from the position of the lungs in health and disease, that it is wise to reduce it to a very low level of diagnostic utility. The preposterous claims made on its behalf by the recent upholders of the Schott (and other) systems of treatment have reduced its value still lower, and left it as an object of ridicule to thoughtful men, at any rate as indicating the size of the heart. It is, however, of some little use in helping us to differentiate between a pericardial effusion and a hypertrophied heart. Auscultatio7i. — By auscultation we become aware of several factors in the heart beat which are of very unequal significance individually, but collectively constitute our most important know- ledge of the condition of the heart. They may be enumerated as (i) the ordinary sounds of the heart; (2) the frequency of the beat; (3) the regularity of cardiac action and its rhythm; (4) ab- normal sounds or bruits added to or replacing the natural sounds. (i and 2) The Ordiftary Soimds and Fi'equeticy. — In health it is well known that the first sound should be materially longer than the second, the now classical lubb-dup well representing the difference. As the frequency of the rate increases this difference must, of course, absolutely diminish, and in rates of over (say) 150 is practi- cally inappreciable ; but when moderate or low frequency is present, even in the absence of other abnormality, a comparative shortening of the first sound is a serious indication of some change in the action. It may indicate mere nervous hypersensitiveness, and then the rate is likely to be high, and other evidence of nervous instability may be present in the patient. More usually, and especially with moderate frequency of beat, it is suggestive of muscular debility or hurry, probably the result of degeneration, or, at least, of imperfect nutrition, and makes us anxious about the supervention, already present or to come, of a pathological yielding of the muscle and incapacity to continue to stand the strain of present pressure. (3) Regularity. — So long as the action of the heart is regular, and its rhythm even, so long may we make a very substantial deduction from the prognostic gravity of almost any evidence of defective mechanism or circulatory disturbance. If irregularity be detected especial care must be taken to ascertain if it be a regular periodic irregularity, i.e. an occasional dropped beat say every four, ii6 DIFFERENTIAL DIAGNOSIS chap. five, or six beats, or if it be a totally irregular irregularity, defying exact description, and rhythm totally absent. The former is often a harmless condition, and may even be beneficial to a heart working under some unusual strain, so that in the absence of other definite indications of cardiac failure it requires only to be noted for future reference, but is not to be treated by direct efforts at cardiac medication. The latter, a tumultuous irregularity with many beats of very variable strength, is a very grave sign, and indicates the urgent need of prompt interference on behalf of an overburdened heart. (4) Abnonnal Sounds. — The presence of an endocardial bruit (vide p. 127, to differentiate endo- from exocardial bruits) heard in the situation and conducted in the direction usually laid down in text-books, is strong evidence of leakage through, or narrowing of, a valvular orifice, but the deductions as to cardiac disease to be made from this evidence are of very unequal importance in different cases. In rheumatic fever or other disease, such as the specific fevers, known to be a possible cause of endocarditis, the first occurrence of a bruit is of very great importance, for we then know that a valve is inflamed and softened, and we get a strong indication for giving such valve as much rest as possible. Again, in a case of smoulder- ing but persistent pyrexia, the source of which is not obvious, if we hear a cardiac bruit which was not present before, or even if we were previously aware of its presence, but it seems to vary in char- acter at times, it will throw strong suspicion on that valve as the seat of a septic or simple inflammation, keeping up the temperature and threatening very serious danger. Thirdly, when some of the features of circulatory disturbance through an organ or district are present, a bruit is certainly suggestive of central cardiac failure as a probable contributory factor, though regularity and evenness of the cardiac beat are much more important features than the bruit itself. In the more chronic cases of valvular trouble, where a bruit or bruits have been known to exist for some time, neither the bruit nor the precise form of trouble indicated by it is of great importance, for we can neither treat the one nor place any great rehance on the accuracy of the other. Speaking then in general terms, bruits are only of value to remind us (i) when they first appear, they are evidence of a softened valve which may yield on pressure; (2) when old, that the heart is working with imperfect machinery, which has not the same elasticity for emergencies that the original sound mechanism possessed. IV DISEASES OF THORACIC ORGANS 117 General Symptoms in other Organs which may indicate Morbus Cordis There are at least two factors in the production of those symp- toms which are exhibited by other organs or areas, but which are usually accepted clinically as indicative of cardiac disease. They are : (i) the work of the heart and aorta; (2) the work of the smaller arteries, arterioles, and capillaries interacting with the lymphatic circulation through the part in question. The heart is a driving and suction pump, introduced into the closed system of tubes, by means of which the blood is kept circul- ating, and as such its nervous, valvular, and muscular mechanisms are perfectly adapted for fulfilling its part in the total result, viz. that of keeping up a sufficient head of pressure in the aorta and pulmonary artery, and relieving by suction the largest venous trunks of their low pressure contents. The aorta in turn, distended and stretched by this charge of blood at high pressure, should, by its elastic recoil, be able to transmit the charge and pressure in gradu- ally diminishing degrees to the arteries smaller than itself. The greater or less frequency of the heart beat, and its greater or less force, are regulated by the central nervous system only according to the very general needs and conditions of the body at large as a whole. It is to the second of the above factors, viz. arteriolar, capillary, and lymphatic action that we have to mainly look for the regulation of the blood supply for the local needs of individual organs for particular purposes, and also for an explanation of the finer problems of local nutrition and function. That this is in many cases the most important factor is strongly suggested, if not proved, by cases where death has taken place with the patient in a water-logged condition, and yet post-mortem examination has shown the heart itself healthy enough, in both muscle and valve, to keep up its part of the circulation for a long time if local conditions had allowed or assisted their share of work to be done. It must be admitted that improvement in the heart's action is frequently fol- lowed by the happiest possible results in distant parts, so that it is impossible in clinical medicine to separate and identify the exact shares of each factor ; none the less the effect of digitalis or supra- renal extract on the one hand, and of iodide of potassium, nitro- glycerine, or erythrol tetranitrate on the other, compel us to bear m mind the peripheral as well as the central circulatory factors. Whichever of the two is at fault, or if both be so, the ultimate local ii8 DIFFERENTIAL DIAGNOSIS chap. result from a clinical point of view is much the same. It is to be remembered, too, that the precise nature of any valvular defect in- fluences only the time when circulatory disturbances appear, and then the order or sequence in which they occur ; it has no general influence on the result, provided that cardiac muscular failure actually supervenes. The result itself is, in the first place, a dimin- ished arterial supply of fresh blood, together with an imperfect or inadequate removal of the impure venous blood, and renewal of nutrient lymphatic plasma. This circulatory disturbance leads in its turn to interference with the work of organs with an active function, and to oedema or effusion in areas of less functional activity. In the second place, this sluggish capillary venous and lymphatic circulation, with excessive pressure on the venous side, leads to an alteration in the quantity and quality of the natural exchanges between blood capillaries and lymphatic channels, and, in fact, alters in toto the vital conditions existing in the part in question. Thus we find not unfrequently that a venule actually ruptures with gross effusion of blood, or individual red cells escape and die in an extra vascular situation, or finally the blood may coagulate in the venules from unnatural composition, leading to a condition known as in- farction. Ultimately, but gradually, fibrin coagulates from the altered lymph, and causes a thickening of the capillaries and fibrosis of the tissues, and the pigment from the dead red corpuscles stains the tissues. Again, we have embolism occurring, not as the result of general circulatory conditions, but owning a particular cause in either loosened vegetations from endocarditis, or clotting of blood in the irregularities of a cardiac chamber, with subsequent loosening of the clot into the circulation. The symptoms occurring in these various ways throughout the body may be tabulated briefly as follows : — o - r u 1 Post-mortem appearances Organs. Symptoms of back ^^^^^ ^^ . ^f ,^rt » P'^^^^^'^^- organs. Lungs. Shortness of breath, Drier than usual and cough dry or with tougher, more re- simple frothy mu- sistant to attempted cous expectoration, laceration by finger; moist sounds at one probably discoloured or both bases. In- from old blood pig- farction or embolus ment (brown indur- leads to bloody ation) ; round or sputum, and prob- wedge-shaped area IV DISEASES OF THORACIC ORGANS 119 Organs. Pleura. Liver. Spleen. Stomach tines. Kidneys. and intes- Brain. Limbs. Symptoms of back pressure. ably pleuritic pain and rub with physi- cal signs of con- solidation : this used to be termed pul- monary apoplexy. Pleural effusion com- mon, with appropri- ate physical signs. Tender or even pain- ful, and somewhat enlarged to the ex- amining hand. Possibly enlarged, may be vague pain in region. Dyspepsia, flatulence, and constipation fre- quent ; severe vom- iting often seen. D iminution in secretion even to almost com- plete suppression ; slight albuminuria very common. Headaches, confusion of mind, sleepless- ness, noises in head, flashes of light, etc. ; apoplexy of some form common enough. Pitting oedema, especi- ally in the legs. Emboli of arteries. Post-mortem appearances known as " heart" organs. of consolidation = infarction or em- bolus. Excess of fluid in the cavity. Congestion of intra- lobular veins, well- known nutmeg liver. Very firm, may be small or large, and possibly wedge- shaped areas of em- bolism. Veins very prominent, and mucous mem- brane dark and congested ; possibly slight ulceration. Kidneys very firm on section; cortex equally congested with the medulla. (?) serous apoplexy ; brain often seems more juicy than normal. Embolus a well-known cause of softening. It is particularly important to remember that any organ whose vitality and circulation are thus interfered with is in a condition in which very slight irritation will cause an acute outburst of inflam- I20 DIFFERENTIAL DIAGNOSIS chap. mation. Bronchitis and acute nephritis are thus two very common compUcations, and it is often a matter of some importance, but great difficulty, to determine whether the bronchi and kidneys are simply venously congested or actively inflamed. I am accustomed to rely upon a muco-purulent v. mucus sputum, and the presence or absence of dry musical rhonchi in the one case, of epithelial casts with facial oedema in the other case, as the most reliable points of distinction. Such, then, are the means we have for determining the presence of real heart disease, and, like similar evidence on any other point, each factor has to be weighed first individually^ and then in addi- tion to, or subtraction from, all other factors, and a balance struck with every possible care. The matter will be referred to again in dealing with nervous v. valvular and muscular heart troubles {vide pp. 137 ^^ seq.\ We may now consider the pathology of, and the meaning of, the terms — HYPERTROPHY AND DILATATION, COMPENSATION AND FAILURE Hypertrophy It is a provision of nature, distinctly tending to the preservation of individuals, that healthy muscle should increase in volume and strength (growth or hypertrophy) in proportion to the work it is called upon to do, provided that this at first lies within the original capabilities of the muscle. The heart is no exception to this rule, and when its circulatory work from any cause (nervous, valvular, or connected with increase in general blood pressure from kidney disease) is persistently maintained above its original average, the cardiac muscle hypertrophies or grows to meet the demand, pro- vided that the nutritional powers in general of the individual are fairly good. Temporary increase in work is inherently provided for by a reserve excess of potential energy over that habitually put forth. It is easy to understand in general terms that if the mechanism of the heart was originally adapted to work with the greatest pos- sible efficiency (and we have every reason for such belief), any alteration in that mechanism must involve increased expenditure of energy to produce the same result, i.e. increased work. We have just seen in the previous paragraphs that the symptoms of disease of the heart as expressed by organs other than itself are largely (the IV DISEASES OF THORACIC ORGANS 121 vasomotor factor must not be forgotten) indicative of failure of the heart to do this increased work. All the means which unaided nature can take to bring about a fresh balance of work and power are collectively spoken of as compensation, and hence compen- sation clinically means regained (if lost) or maintained capabi- lity of the heart to do its work under unusual or altered conditions. For a per7nanency this is, to all intents and purposes, hypertrophy. Tenipora?y natural compensation was mentioned above as a mere use of potential inherent energy, and artificially we can produce temporary compensation by diminishing the work, as by rest in bed or vasodilator drugs. Following this argumient, it is obvious that hypertrophy has only one cause — increased work. It is actually the result of, and can only be equal to, this increase, and then it must logically be deduced that the symptoms of hypertrophy are — the absence of symptoms of heart disease. Disappearance of these symptoms when present means the development of compensation, and if per- manent this means hypertrophy. It must be admitted that there are circumstances under which hypertrophy may be indirectly the possible cause of some trouble. If, for instance (as in athletes, soldiers, etc.), great physical exer- tion has called forth considerable hypertrophy, then, when the work is permanently given up, the heart probably will not diminish in bulk in proportion to its diminished duties, and its beat may become inconveniently apparent to its owner. It is possible that its powerful action may rupture an artery that is healthy. Certainly it is a source of danger to vessels that are not healthy, and arterial disease and degeneration are unfortunately only too frequent results of the same conditions as those which require hypertrophy of the heart. In this sense hypertrophy of heart may be described as a predisposing factor in cerebral haemorrhage, but in all other senses hypertrophy is a purely defensive expression of nature — a physiological and not a pathological phenomenon. Dilatation We may say at once that this term is used in two distinct, and in some respects almost opposed, senses. The first is a mere mechanical increase in the capacity of a chamber. The second sense takes note of only one of the possible consequences of this increased capacity, and is the equivalent of cardiac failure. As regards the first meaning, theoretical considerations would 122 DIFFERENTIAL DIAGNOSIS chap. show that it is an inevitable and universal result of valvular in- capacity, though I am strongly inclined to doubt if it is possible to prove the position by post-mortem evidence (the conditions of rigor mortis, and the effects of pressure upon dead muscle, do not suffi- ciently closely correspond to the reaction of living muscle to its environ- ment) ; anyhow, the occurrence of dilatation in this sense has no possible importance from a clinical point of view, provided that the energy of contraction and the strength of the chamber i?z question are in- creased in proportion} the object of the muscular walls being merely to empty the cavity with sufficient force. The second sense in which dilatation is used is exactly repre- sented by the absence of this requisite energy of contraction and absolute strength, and it is precisely this that 4S the cause of the symptoms of morbus cordis. This is heart failure, or absence of compensation. It is under these circumstances that a previously hypertrophied heart becomes a nuisance to its possessor by its tumultuous efforts to cope with the work to which it is no longer equal. It is when this failure or stretching becomes excessive that relative incompetency of healthy valves supervenes, for they are no longer capable of closing an orifice which has become too large. DIAGNOSIS OF HYPERTROPHY AND DILATATION As the presence of one or other or both of these conditions is, one might say, the very essence of 99 per cent of cardiac patho- logy, the recognition of them becomes at once the cardinal point in diagnosis. Of dilatation in its first or simple sense there is no positive objec- tive sign at all, and its presence is a matter of no moment if the requisite muscle strength is present to compensate it. Its pre- sence is assumed in all cases in which a large heart is due to val- vular alterations ; in other cases {e.g. that due to renal disease — so-called concentric hypertrophy) it is probably absent. In all cases, and in any sense of the word, the condition of dilatation, as well as that of hypertrophy, demands for its presence a heart larger than usual {i.e. for an average environment of age, work, etc.), and therefore we require as the first element in diag- nosis the signs by which we may recognise an enlargement of the heart. ^ It must be remembered that this proportion is a large one, viz; the cube of the figure representing increase in diameter. IV DISEASES OF THORACIC ORGANS 123 The ordinary physical signs by which this is done, and the principal fallacies, are the following : — Insf'ectio?!. — The apex beat may be seen displaced outwards, or downwards and outwards. A lifting of the whole cardiac area of the chest may be seen at each beat, or possibly a persistent bulging. Palpatio )i. — The displacement of the apex beat may be felt, as well as the heaving. If a thrill is felt it is also a suspicious sign, and must be noted. Percussion. — There will be in- creased area of cardiac dulness, both absolute and relative. Fallacies. These physical signs found by in- spection, palpation, and percus- sion may be : — 1. Obscured — as by abundant fat or muscle over the chest, by emphysematous lung, by peri- cardial effusion. 2. Rendered unduly prominent by wasting of fat or muscle, by re- traction of lung, by deformity (pigeon breast. Pottos curvature, etc.) of the chest. 3. Their interpretation may be a mistaken one, in that tumours or effusions, etc., may displace the heart, its apex beat, and cause transmitted pulsation and bulging. Auscultation is interfered with by much the same circumstances as the other methods. But, in addition, we have to differen- tiate heart sounds from those of pericardial, pulmonary, and pleural origin {vide p. 127). Auscultation will confirm other in- dications, or decide by itself the position of the apex beat. If bruits of organic origin {vide p. 129) are present, and known to have been so for some time, the presence of a heart larger than usual is at once certain. If no bruits are present the character of the two sounds must be noted. They are chiefly of use to separate pure hypertrophy from dilatation or failure. If by these means we have ascertained that a large heart is present, the only other problem requiring solution is this : Is it capable of continuing to do its work or not ? In by far the greater number of cases the answer is obvious at a glance. The symptoms of failure are too obtrusive, or, on the other hand, the absence of such symptoms is quite complete ; but, excluding the extremes, we meet with many cases in which the most careful attention to every feature may still leave us in doubt. 124 DIFFERENTIAL DIAGNOSIS chap. Such, for example, as a young woman, possibly pregnant too, com- plaining of some puffiness of the ankles at night, and we find her anaemic and the possessor of a mitral bruit (the relative shares of anaemia and heart and pregnancy require much consideration) ; or, again, an elderly patient with renal trouble complaining of short- ness of breath — Is it cardiac or renal, is the heart begt?i?itng to fail ? By attention to the following considerations we shall not com- plete our diagnosis, but we shall at least get a strong body of evi- dence condemning or acquitting the heart of being particeps criinmis : — Inspection \ Will none of them help us much. They will reveal fre- Palpation \ quency and irregularity, but these are much better deter- Percussion j mined by auscultation. Auscultatio7i will give us accurate information on — 1. Frequency of Pulse. — It is not the absolute frequency that is of so much importance. A weak and failing heart may be either slow or frequent, fatty hearts are often slow, and sound hearts often beat over 90 per minute. What is of importance is the rapidity with which the heart settles down after a temporary in- creased frequency. The patient should be made to exert himself smartly for a few moments, and then the number of beats in the next four or five quarters of a minute should be registered and com- pared. If the muscle is good the numbers will rapidly diminish with each succeeding fifteen seconds, till the rate is regained which was previously present. If the increased frequency continues it is a suspicious circumstance against the muscle. 2. Irregularity of Beat in a large heart is very suspicious, and if due to muscle failure will, I believe, be invariably associated with grave features which cannot be misunderstood. It is only in hearts of average size that its indication is doubtful, and then, I think, it makes one suspect the nerves rather than the muscle in any case where there is room for genuine doubt as to the presence of heart failure {vide pp. 117^/ seq^. 3. The Character of the Sounds. — If the natural heart sounds be replaced entirely by bruits we lose the assistance they usually afford us, and we must rely all the more upon the regularity of the beat and other indications. If they be not thus entirely lost, but are audible with greater or less distinctness, it must be borne in mind that, with an increase in bulk of healthy muscle, there is an increase in the contrast between the first and second sounds. The first sound is lengthened, and the second sound made sharper. As the IV DISEASES OF THORACIC ORGANS 125 muscle becomes unhealthy or fails in power this contrast becomes less, and we may lay down the rule — " The more the first sound approximates in character to the second, the more do we fear that hypertrophy is being overtaken by dilatation or weakness." If the first sound is very weak, almost inaudible, this is, excluding fallacies of emphysematous lung, etc., a sure sign of failing muscle. General Sy77ipto7ns. — We can only repeat again that back pressure effects, if definitely present, are essentially signs of failure. Their absence or amelioration is provided for by hypertrophy, and hence they conclusively prove by their presence that the muscle is feehng the strain. We may now, with these views of hypertrophy and dilatation, briefly examine the elements of the problem, " How is the heart itself affected by various valvular affections ? " ^ , t h / Competent. \ Incompetent. [ Relative, from too wide an orifice. < Absolute, from intrinsic disease ( (thickened, puckered, etc.). Orifices must be i. Correctly adapted for their valves. 2. Narrowed (by adhesions). 3. Too large (by dilatation of chamber). A moment's consideration of any single valve trouble will at once show that any pathological change in the structure or orifice leading to the leakage or stenosis must throw extra work on to that chamber which (reckoning from the direction of the blood stream) immediately precedes the lesion, and hence we might infer that hypertrophy should be the immediate result. But as the extra work is thrown on to the chamber at very different periods in its cycle of work and rest, the results are not quite the same in the two cases. In pure stenosis the extra strain comes during systole when the muscle is expecting to work, and here we can easily understand that almost pure hypertrophy results. In simple incompetency of a valve, however produced, the strain comes on the precedent chamber at a moment when the muscle is relaxing or resting, and hence, being caught unawares, so to speak, it is likely to yield somewhat, and an increase in the volume of the cavity is likely to ensue, or dilatation in its first sense, and, unless compensating energy or strength appears, dilatation in the second sense will soon appear. This precedent chamber (in incompetency at any rate) contains a larger quantity of blood than usual, which will, in systole, be forced into the succedent chamber at a time when it is relaxing 126 DIFFERENTIAL DIAGNOSIS chap. or resting, and hence in this chamber, too, there must occur some degree of dilatation to be again compensated by hypertrophy. When two or more valves are affected, and possibly in different ways, the problem becomes more difficult to follow, but the above principles will help us, provided we have the data as to time and amount of the several affections. Such data are, however, practi- cally never offered to us, and we have to be content with accepting the general clinical result that in all cases of chronic valvular disease of the heart the organ becomes larger in its dimensions as ascer- tained by physical examination. This enlargement is nature's effort at compensation, and when the hypertrophy reaches its limits, or the muscle from any cause becomes badly nourished, cardiac failure and serious symptoms will supervene, whatever be the actual capa- city of the chambers. CARDIAC BRUITS, AND SOUNDS THAT MAY BE MISTAKEN FOR THEM If, on auscultation of a chest, an abnormal sound be heard in the cardiac or aortic region, the first point to determine is, whether its origin lies in the cardiac or pulmonary organs. This, as a rule, is not difficult to decide. Pleuropericardial friction sounds re- sembling a pericardial rub, and compression of a small portion of lung tissue by the heart's movements, with a noise resembling a short systolic bruit, are the chief difficulties. In the first place, they will either of them only be heard locally where they arise, somewhere along the margin of the heart. This and their rough character will alone be sufficient to separate them from endocardial bruits, which are heard over the bulk of the heart, and always conducted at least a little way from the point of maxi- mum intensity. Then if by making the patient hold his breath for a few seconds the sound entirely ceases, we know at any rate that the inside of the pericardium is free from acute inflammation, and this is the most important clinical point, for an acute pleurisy here is only of additional importance from the liability to spread to the inner surface of the pericardium. If the sound does not entirely disappear on holding the breath, the heart movements must take some share in its production. Probably the pericardium is adherent to the heart on the one hand, and the pleura on the other. The position in which such sound is heard, on the boundary or just out- side the limits of the heart, and a history of previous pericarditis or IV DISEASES OF THORACIC ORGANS 127 pleurisy, will help us in deciding pleura v. pericardium, though frequently it is quite impossible to decide the point. Nor is the decision of very great importance practically, for either solution suggests adhesions which may in the long run interfere with the cardiac muscle, and are consequently to be feared in the future. It is well now to make the patient hold his breath — first at the end of deep inspiration, and secondly at the end of deep expiration. Should the abnormal sound be heard at one of these periods, and entirely disappear at the other, or, at least, be materially altered in character and loudness, it is probable that it depends on the forcible emptying of a small tongue of lung tissue by the mechanical pressure of the heart in systole. This is, however, a rare sound to hear. If we have thus decided that the sound has its origin in the cardiac organs, the next point is to determine whether it is peri- cardial or endocardial. At the apex of the heart very little diffi- culty will be experienced, for the to-and-fro rubbing of pericarditis present throughout the whole cycle of the heart's action is very unlike any apical endocardial bruits, and the galloping rhythm of a rapid heart only requires a little careful listening to distinguish it. At the base, where pericardial bruits are perhaps more common, the difficulty of distinguishing them from double aortic murmurs is a little greater. The following table correlates and contrasts the most important distinguishing features in all cases : — Exo- or Pericardial Sounds. Endocardial Sounds. Character. Time of occurrence. Conduction. Almost always a fric- tion or rubbing sound ; practically never musical. At any period of cycle, not specially with systole or diastole. Are not conducted along the blood stream or to apex, though they may be heard over a wide area. More usually blowing in character ; often musical. Always in connection with, if not actually at, systole or dia- stole. Conducted upwards, or to the apex and axilla, except pre- systolic bruits, which have such special characteristics as to barely allow of mis- takes. 128 DIFFERENTIAL DIAGNOSIS CHAP. Exo- or Pericardial Sounds. Endocardial Sounds. Position of maximum intensity. Effects of pressure. Variation from day to day. Pulse and associated symptoms. May be heard any- where, but where heard do not gradu- ally lose in intensity on gradual shifting of stethoscope. In yielding chests firm pressure is likely to cause marked altera- tion in sound. Probably vary in area from day to day, and may disappear rather rapidly, but do not dodge about, appearing and dis- appearing alter- nately. Pulse rate sure to be accelerated in acute pericarditis (in chro- nic cases no rub because of adhe- sions, or if present is pleuropericardial, vide supra). Apex, for mitral bruits, base or mid ster- num,foraortic bruits, are points of maxi- mum intensity, and the bruits gradually diminish from their point of greatest distinctness. Pressure makes no real difference in the sound, though the closer fit of the stethoscope may en- able it to be heard more distinctly. More likely to be con- stant, except in recent or ulcerative endo- carditis ; they have at times a curious habit of appearing and disappearing in a most capricious manner. Pulse rate entirely dependent on the recentness of the in- flammatory attack or on physical condition of patient, so that in chronic cases it may be for years quite natural. Considerable precision may thus enter into our decision as to whether the source of an abnormal sound is endo- or exocardial, but when we come to consider the various problems connected with unusual sounds of endocardial origin, we are on very treacher- ous ground indeed. We can now and again decide some of them with a tolerable degree of accuracy, but on other occasions and for other problems even the keenest judgment of the most mature ex- perience will only with diffidence and hesitation express an opinion. IV DISEASES OF THORACIC ORGANS 129 Epitomised and tabulated the position is this : — I. What is the exact origin of the bruit? Blood states, poverty of blood, either of quantity or quality. It may be due to Organic disease oC] valves obvious to the naked eye on post - mortem ex- amination. ^litral. Aortic. Pulmonary. Tricuspid. Leakage of valves^ I without naked eye ^May be due to ^ changes. J \ Aneurysm. Insufficiency or sten- osis, recent inflam- mation or effects of old trouble. [General dilatation of walls of cavities, or improper or feeble action of individual musculi papillares. 2. What is the vital significance to the patient of the bruit thus detected? Here I shall attempt only a complete solution of some of the simpler problems, with an indication of the principles that must guide us in attempting to decide the more complex ones. ^.— WHAT IS THE EXACT ORIGIN OF THE BRUIT? (a) Hccmic v. Organic Bruits It is usually comparatively easy to determine whether a bruit is due to poverty of the blood — ordinarily termed hsemic bruits — though the precise cause of such bruits is a matter of very great dispute and uncertainty ; Dr. Byrom Bramwell offering us a choice of (i) pulmonary, (2) mitral, (3) left appendicular. Whatever its cause, the following particulars will suffice to separate it from bruits owning a definite organic lesion as causative factor : — Position. If of Haemic Origin. Rarely heard at the apex, and if so, not conducted into axilla ; usually heard at the base, and better a little to the left of the ster- num. K If of Organic Origin. Heard at apex, and often conducted into axilla ; basic organic bruits are almost always better heard a little to the right of the sternum ; pulmonary organic bruits being rare, ex- cept as congenital con- dition. I30 DIFFERENTIAL DIAGNOSIS CHAP. Time. Character. Conduction. Loudness al- tered. Associated con- ditions. If of Hsemic Origin. Always systolic, never diastolic or presys- tolic. Not very distinctive, but they are never regu- larly musical. Rarely conducted any distance beyond their point of maximum in- tensity; somewhat sud- denly cease to be heard as stethoscope is moved. Become very much louder on patient lying down on the back. Patient obviously anaemic, and as this improves, the bruit is likely to disappear. If of Organic Origin. May be, of course, sys- tolic or diastolic, or both, or presystolic. May be musical. Usually conducted some way from maximum point, and gradually die away in intensity as stethoscope is shifted. Not markedly altered by patient lying on the back ; any alteration usually in direction of diminution. Not necessarily anaemic ; aortic disease is most likely to cause anaemia. This anaemia is not likely to yield to treat- ment, and if it does, the bruit still persists. (b) Valve of Origin of Bruits of Organic Origin The rules commonly laid down for discriminating the various sources of bruits due to organic valvular trouble may be briefly indicated as follows : — Mitral systolic, indi- cating regurgita- tion through an in- competent mitral valve. Mitral presystolic, indicating abnor- mal narrowing of mitral orifice. Systolic in time, i.e. aocompanying or replacing the first sound ; best heard at the apex, con- ducted into the axilla even to the angle of the left scapula ; pulmonary second sound usually accentuated ; apex beat displaced down and out in old standing cases, indicating some degree of enlargement of the left side the heart ; pulse small. Presystolic in time, leading up to a sharply ceasing first sound ; best heard a little above the apex, not conducted very far from its point of maximum intensity ; pulmonary second IV DISEASES OF THORACIC ORGANS 131 Aortic systolic, indi- cating obstruction at aortic orifice. Aortic diastolic, in- dicating incompe- tent aortic valves. Tricuspid systolic, indicating regurgi- tation through in- competent valves. sound very accentuated ; apex beat if dis- placed at all, chiefly to the left — outwards — indicating enlargement of the right side. (If the word ' abrupt ' be pronounced with a very rolling r the word becomes almost onomato- poeic of the phenomena to be appreciated in connection with this bruit.) Systolic in time, best heard over mid sternum about the third cartilage, or in the second right space ; conducted upwards towards the vessels of the neck ; apex beat displaced in old cases farther down and out than with any other bruit, indicating the greatest hyper- trophy of the left ventricle ; pulse small. Heard with or replacing the second sound, best over mid sternum opposite the third cartilages or in second space on the right ; conducted down to the apex or to the ensiform cartilage, and so conspicuously as to be sometimes best heard at those spots ; apex beat displaced down and out, again indicating a great degree of enlargement of the left ventricle ; pulse peculiarly collapsing — the water-hammer or Corrigan's pulse. Systolic in time, best heard over the right ven- tricle, and conducted a little outwards to the right ; ver\' rare except in the later stages of heart failure, and is accompanied with a venous systolic pulse in the neck ; indications of hypertrophied right ventricle pushing apex beat outwards. Best heard to the left of the sternum, veiy rough; conducted upwards to the left. Too rare to notice here. Pulmonary systolic, or stenosis of pul- monary orifice. Pulmonary diastolic ; tricuspid presys- toHc. In many cases, if used with discrimination, these rules vriSS. give tolerably accurate results, and are sufficiently useful to be remem- bered ; but even in the most competent and careful hands they are apt to mislead, for statistics have shown ^ that "out of every hundred hearts we listen to, in thirty-six the bruits will give us exact information, in ten they will lead us absolutely astray, and ^ Thesis for M. D. Oxon. based on some 700 autopsies. 132 DIFFERENTIAL DIAGNOSIS chap. in fifty-six they will give us information in excess or defect of the truth." The matter is of less importance, as we must iterate and reiterate the fact that every heart, with (or without) bruits, has to be judged on the merits of its muscle power and energy, and not by the bruits, the patient's condition must be taken as we find it, and not as one deducible from a theory of what it ought to be by the murmurs present. Of all factors by which our clinical judg- ment is influenced, that of the bruits present is the one of smallest weight. The above rules will equally apply to bruits arising under cir- cumstances which lead us to think that they are more likely due to relative incompetency or muscle imperfections, such, for instance, as a case in which cardiac failure is already noted, and a bruit becomes audible, unexpectedly developing under observation without pyrexia. The pathology of such cases will be touched on a little further in a subsequent section {vide pp. 135 et seq.). (c) The Bruits of Aneurysm v. Valvular Disease We have already (pp. 105 efseq.) dealt with the separation of aneu- rysms from intrathoracic solid tumours ; we have here to separate them from lesions of the heart itself. Aneurysms of the transverse or descending aorta can scarcely give rise to suspicion of valvular mischief. The tumour and bruits and other local indications are too far removed from the situations where enlargement of the heart or valvular bruits would be observed. It is those of the ascending arch that require some care in discrimination, though even here the presence or absence of implication of the valves is of more importance than the presence or absence of an aneurysm as such. The bruit of aneurysm is most The bruit of valvular disease is frequently systolic, only occa- most frequently double, occa- sionally double, practically sionally systolic or diastolic never diastolic only, often also only (very rarely found to have absent altogether ; rarely con- been completely absent when ducted very far, and never down post-mortem shows gross valvu- the sternum. lar disease) ; usually conducted a good distance, and often heard down the sternum or at apex of heart. Then the question of associated cardiac enlargement must be considered. My experience in the post-mortem room, in agree- IV DISEASES OF THORACIC ORGANS 133 ment with recent observations, tends to show that aneurysms as such, i.e. when so situated as not to interfere with tlie aortic valves, have but little influence in causing hypertrophy of the heart. Aortic valve disease, on the other hand, is the especial trouble pre-emi- nently calculated to produce hypertrophy and dilatation of the left ventricle ; hence, if with the bruit there is well-marked enlargement of the heart, the probabilities are strongly in favour of valvular disease ; if there is but httle or no evidence of such enlargement, the probabilities are in favour of an aneurysm as the cause of the murmur. Again, if there be a dulness extending suspiciously to the right of the sternum, the position of the heart's apex beat will give us help. Should this be displaced outwards much more than downwards, it is probable we have to deal with an enlarged right ventricle (lung trouble or mitral stenosis) ; if much downwards as well as outvrards, aortic valve trouble is again probable. If not very materially displaced, aneurysm again is strongly suggested (or soHd tumour). It has to be admitted that the general conditions, viz. severe physical exertion over long periods, alcoholic excess, syphilis, advanced age with senile degeneration, renal disease, etc., which are predisposing factors in aneurysm, are equally the predisposing factors in primary aortic valve disease (the valves are, in fact, merely a part of the aorta, and degeneration with aneurysmal yield- ing may occur at any point), so that it is by no means an unfrequent thing, in fact I think it is a rule of the majority of cases, that when aneurysm occurs it shall be associated with vah^ular lesions, and hence it is frequently impossible to exclude the aneurysm, although we have positive evidence that the heart is affected. The diagnosis is of less importance in that the condition is a grave one, and what is likely to help the heart is likely to help the patient to bear with, or to cure the aneurysm if it exists. ^.— WHAT IS THE VITAL SIGNIFICANCE TO THE PATIENT OF THE BRUITS? This includes two problems, the first of which, viz. the bruit as an indication of the condition of the muscle of the heart, has really more to do with prognosis than diagnosis ; it has already been touched upon in dealing with the symptoms that suggest morbus cordis, and will be further considered {vide pp. 135 etseq.); the second is the bruit as a direct indicator of leakage or stenosis, and the 134 DIFFERENTIAL DIAGNOSIS chap. influence of these on the patient's condition ; this we will now con- sider. Bruits of hsemic origin may certainly be ignored in cardiac pathology. They are accidental phenomena in diseases of other origin, and disappear with the disappearance of the blood dys- crasia, and their significance is nil beyond the significance of this dyscrasia. Bruits of aneurysmal origin, too, have the significance of the aneurysm itself. They add nothing to our knowledge of the course the arterial disease will take ; they give no guidance in treatment, and their disappearance, if they do disappear, does not necessarily mean the cure or amelioration of the condition. This work does not deal with treatment, but I cannot refrain from putting on record an emphatic protest against any extremes of active treatment in aortic aneurysms, such as starvation and severe bleedings. The lesion is one that will kill quite fast enough without our assistance, and our efforts had better be directed to making life bearable by counsels of moderation in all things than to rendering miserable the remaining years of a threatened life. Bruits of undoubtedly organic valvular origin have the following significations : — (i) To determine the presence of recent inflammation {vide p. ii6). (2) To determine excessive dilatation of a chamber {vide p. 122). (3) By their disappearance to determine muscular weakness {vide p. 140). (4) To determine single or combined alterations of old stand- ing in the valves, with their significance. This last (4) is the problem to the decision of which I devoted some time ago a very considerable amount of statistical inquiry. Omitting the actual figures, the tables I prepared showed that, sup- posing the patient died from the effects of heart disease — {a) Mitral incompetency gives, amongst single lesions, the worst prospect of prolonged life. {b^ Aortic incompetency also amongst single lesions gives the best prospect. {c) The question between aortic stenosis and mitral stenosis depends on other factors to such an extent that the IV DISEASES OF THORACIC ORGANS 135 isolated lesion is of very small importance, and probably the prospects are about equal, (d) If aortic stenosis be combined with mitral incompetency, the patient gains about three and a half years of life from what he would enjoy with aortic stenosis only. {e) Mitral stenosis combined with aortic stenosis is a very fatal combination ; but if the pulmonary or tricuspid be also stenosed, the patient gains about seven years of life. Such a marked difference points strongly to the lung as the weak spot in heart disease. These results, at any rate the first one (which seemed to be the most firmly established by figures), are so startling and so contrary to what is apparently one's general experience of the innocuousness of a mitral systolic bruit, that I was then (1890), and still am, driven to the conclusion that they illustrate more forcibly than any other argument the futility of attempting to lay any weight on the nature of the bruits in estimating the value or power of a heart whose valvular machinery is damaged. I leave them, without further com- ment, to be refuted or corroborated by future investigators. HEART DISEASE IRRESPECTIVE OF MURMURS In discussing hitherto the pathology of cardiac disease and hypertrophy and dilatation, we have had in mind chiefly chronic organic disease of the valves as the essential cause of the disturb- ance. It is certain that the nervous and muscular mechanisms, connections, and structures are capable, in an otherwise fairly healthy individual, of obviating to an almost complete extent, and for a very long time, such defections in valve arrangements ; but if the patient is to die, as many do (though very many do not) from chronic valvular trouble, a time eventually arrives for him when such compensation fails from malnutrition or overstrain of muscle (? of nerve too). The case then, from its causation, goes into a special group, but from its clinical features remains an illustration of the class of cases which we must now consider, viz. those in which the nervous or muscular mechanisms have broken down, or possibly (as in valvular trouble ?) both have given out. The precise pathology of the various examples of this class is often most obscure, and probably the essential elements in it vary from time to time, now nerve, now muscle being at fault. So far as can be understood, 36 DIFFERENTIAL DIAGNOSIS CHAP. Muscular defects of degeneration (whether fatty or fibrous or other is not ■< very material ; the muscle is no longer nat- ural). Nervous influ- ences or de- fects. Of slower onset through months and years. I think the following table represents fairly completely the causes which may be at work in producing the clinical features of the case: — Malnutrition from the circulat- ory disturbances in the heart itself, of valvular disease ; common. Malnutrition from more general conditions, e.£: age, vascular degeneration, kidney disease, J gout, obesity, etc. ; common. Definite new growths, syphilis, tubercle, malignant disease, hydatids, etc. ; all are rare. Fibrosis or scar formation from any cause, especially peri- or endocarditis, syphilis, etc. ; also common, at any rate as revealed by the microscope. ' Acute febrile disease, especially perhaps pneumonia, typhoid, and septicemia (from pyrexia, or toxins, or both). Poisons, <{ such as tobacco, alcohol, etc., which may affect the muscle as well as the nerves. (This group may come on more in- sidiously.) ' From diseases of any organ, Purely reflex. \ e.g. intestines, stomach, ovary, etc. (? thyroid). Pressure on peripheral part of nerves, enlarged glands, e.g. central pressure of tumours, meningitis, etc. Loss of control of nerves from actual neuritis or smaller de- ■l gree of nerve illness. Poisons — tobacco, alcohol, prob- ably thyroid secretion, etc. Diphtheria, influenza, and other specific diseases prob- ably should also be placed here. Of more rapid onset, possibly days or weeks. Direct effects on vagi or acceler- ators. IV DISEASES OF THORACIC ORGANS 137 The clinical features of the cases are as varied as the possible causations. Sometimes they assume the shape of the most dangerous and serious illnesses we can meet with ; sometimes, on the other hand, they indicate but a trivial malady ; yet the former may prove of no moment, while sudden death may terminate the latter. They may present all the general indications of back pressure, or they may confine themselves almost entirely to local pain and distress. Diag- nosis becomes increasingly difficult with the absence of indubitable signs of organic disease, and mistakes must constantly occur even to the most experienced. Still, a careful inquiry into the history of the case, and an equally careful weighing and balancing of all avail- able factors must be undertaken, and will help us materially in, at any rate, basing our opinion on a sound foundation of probability, beyond which clinical medicine can rarely go ; certainty is rarely attainable where the exceeding delicacy of ill-understood physio- logical balances is in question. It may be laid down as a general rule (not perhaps without some very grave exceptions — vagus neuritis, for example, after diphtheria) that affections of the nerve apparatus are less serious in their outlook than those of the muscle. Remembering how easily the heart beat is affected, at least in frequency, by every passing mental shock, by pain, by gastric disorder, by, in short, reflex in- fluences from every quarter, the general truth of this rule in practice must, I think, be accepted. Hence our first efforts at diagnosis should be directed to an endeavour to determine on which side weakness lies. The following paragraphs in parallel columns will show the points of distinction more clearly, and bring them into sharper contrast. DERANGEMENTS OF THE DERANGEMENTS IN THE NERVOUS CONTROL MUSCLE APPARATUS Points in the Previous History If previous attacks of symptoms Previous attacks of symptom have have occurred, they have prob- probably not cleared up entirely, ably cleared up entirely, leaving but have left permanent short- no trace of permanent and per- ness of breath or other evidence sistent signs of ill-health. They of ill-health. They were prob- were not associated with decided ably associated with definite evidence of back pressure effects. signs of back pressure. In I -.8 DIFFERENTIAL DIAGNOSIS CHAP. The first attack was probably associated with some mental shock or dyspeptic trouble, or if with a definite illness, it was more likely influenza or diph- theria (both known to cause nerve changes) than rheumatism or scarlet fever, etc. (known to produce endo- or myocarditis). Attack more likely to be quite sudden in onset, without obvious exciting cause. young people the first attack traceable to rheumatism or other disease known to produce organic changes in endo- or myocardium. In elderly patients there will probably be found an admission of progressive feebleness and shortness of breath previous to an actual attack of symptoms calling for medical aid. Points in the Symptoms Complained of More likely to be stress laid on the local symptoms, pain more or less sudden and spasmodic in the cardiac area (rapidly sub- siding after eructations or vomit- ing), palpitation, fluttering sen- sations, choking, etc., also pro- minent, but soon subsiding. Likely enough to return on a repetition of the recognised cause, e.g. heavy meal, tobacco, alcohol, etc. Faintness is again a very common phenomenon in such cases, but fatal syncope extremely rare. Local symptoms less prominent, and usually masked by the general distress. If they are prominent there is no doubt about their genuine severity (angina, vide p. 1 1 3), and they do not subside suddenly after mere eructation or vomiting. Exciting cause much more frequently physical exertion of some kind, or very violent excitement. Faintness of an ordinary char- acter is not common, but fatal syncope is fairly frequent. Points ascertained by Examination of the Patient General Considerations and Conditiofts Age. — In the young the two great causes of cardiac mtisde weakness are valvular trouble (congenital or acquired) and acute pyrexial disease. If these two can be excluded, cardiac complaints in younger subjects are almost certainly nervous in origin. In older patients, when their complaints may point to a cardiac source, we are much more anxious about the condition of the muscle. This anxiety will be increased very much by evidence of renal disease or arterial degeneration. The latter, in fact, is a better gauge of age than the calendar's tale of years. The coronary IV DISEASES OF THORACIC ORGANS 139 arteries so frequently share in this degeneration that a degenerate radial or temporal is an absolute bar to our regarding lightly any history of ca?-diac attacks ; they compel a serious view being taken of such a case. Fatal angina or an aneurysm, otherwise undiscoverable but with a gloomy outlook, must inevitably occur to our minds under such circumstances. In later life, too, one is inclined to look more favourably on the same symptoms in a woman than in a man. Sex. — Of sex, apart from age, but little can be said. Women, as a rule, are certainly more hable than men to view with appre- hension slight symptoms or disquieting sensations in the cardiac region ; hence, if there is no obvious origin for heart disease, one would be more inclined in a woman towards a neurotic explanation of a case. If, on the other hand, ob\dous hysterical manifestations of other kinds are present — Grave's disease, influenza, tobacco, alcohol, sexual indulgence, masturbation, puberty with its strain on the system, a neurotic heredity — if any one of these gives us a clue, sex at once becomes of very little account in comparison with such indication. Back Pressure Effects. — These we have already (p. 118) considered in some detail. For our present purposes we may divide them into — (i) disturbances of function; (2) disturbances of structure — oedema, fibrosis, etc. — and we may state that — In ner\-ous affections of the heart In muscular troubles both classes the latter class is seldom are common, and, indeed, the (? never — vagus neuritis, for characteristic feature. Provided example) seen. Evidence of there is no local cause for a the former class is fairly com- member of the second class, its mon : shortness of breath with- occurrence is practically patho- out rales or bloody expectora- gnomonic of heart muscle failure, tion, disturbances of general cerebration, or of special senses, or irritability of stomach, etc. Local Examination of the Cardiac Region Inspection., palpation., zxid percussion are only of essential utility in determining the presence or absence of hypertrophy and dilatation, and as one indication of frequency and irregularity. Hypertrophy and Dilatation., either or both In purely ner\-ous affections of the In m.uscular troubles alteration in heart the organ is but rarely the size of the heart is constant 140 DIFFERENTIAL DIAGNOSIS CHAP. much larger than normal. The chief exception is long-standing Grave's disease. except in acute febrile disorders (on the presence of which the diagnosis mainly rests). This, in fact, when marked, constitutes the type case. Frequency and Irregularity Tachycardia and bradycardia are the commonest features in nervous affections of the heart. In fact, either of them, possibly with some irregularity, but with- out other objective signs of heart disease^ constitutes the type case, and under such circumstances, in combination, a pulse of over 160 or under 50 may safely be regarded as due to nervous in- fluences. Tobacco in excess, Grave's disease, influenza are the common causes of such tachycardia and palpita- tion, and careful inquiry must be made for them. In the more slowly developing defects of muscle, frequency rarely rises much beyond 130 without at the same time being associated with marked tumul- tuous irregularity and signs of back pressure ; nor, on the other hand, is it often reduced below 60 without similar indica- tions. In the more rapidly developing muscle failure of poisons and pyrexia frequency may be very high without such other symptoms, but then the feebleness of the sounds is our best guide. Irregularity alone as the sole indi- cation of muscular trouble never occurs, at any rate for long. Should it be the first warning others will very soon appear. Vide frequency also (on p. 124) under Hypertrophy and Dilata- tion. Bruits. — In nervous troubles bruits of any kind are exceedingly rare, and still rarer is it to find one that follows the rules laid down for those of valvular origin, though I think it probable that some of the obscurer murmurs may be due to irregularity of nerve influence on individual muscle bundles. The presence of bruits in muscle troubles has already been dis- cussed (p. 1 1 6). Here we need only mention that the disappear- ance of a valvular bruit with in- crease in severity of symptoms is pathognomonic of muscle failure, as, indeed, is its first appearance under such cir- cumstances of increase in symp- toms. IV DISEASES OF THORACIC ORGANS 141 The Ordinary Cardiac Sounds Nervous affections of the heart Muscle troubles, on the other hand, have a peculiar tendency to render the sounds sharper and more distinct as noises, though the contrast between the first and second may be lost in ex- treme frequencies. If any sound disappears in nerve troubles it is the second. have a tendency to shorten the first sound, and, at the same time, to render it less audible. So much so, that in some cases of poisoning, prolonged pyrexia (as in typhoid, etc.) or fatty heart, the first sound may be- come almost inaudible. This is true whether bruits are present or not. Their presence only renders its appreciation more difficult. Such, in detail, are the individual points requiring attention in the diagnosis of the nature and meaning of cardiac complaints. In practice the difficulty lies not so much in estimating these sepa- rately as in weighing them collectively and striking a balance between those which point in opposite directions. It is here that clinical experience and acumen have their most brilliant oppor- tunities for making a reputation for their possessor, and no hard and fast rules can replace them. The only advice I have to give of general application is, " Don't be in too great a hurry to express a decided opinion. Time and circumstances will often throw a clear light on a case which is at first apparently obscure and perplexing." ULCERATIVE ENDOCARDITIS To understand the diagnostic problems of ulcerative endocarditis it is necessary to enter into the outlines of the pathology of endo- carditis in general. The four following postulates constitute the essential foundations : — 1. That acute endocarditis arises, precisely like inflammation elsewhere, as the result of an irritant applied to the membrane. 2. That the severity of the anatomical lesions, produced by the inflammation, is strictly proportionate to the relative strength of — on the one side, the toxicity or nature of the irritant ; on the other side, the resisting powder of the membrane. 3. That in clinical practice the irritant is always either chemical 142 DIFFERENTIAL DIAGNOSIS chap. substances produced by (i) unnatural metabolism of the tissues,^ (2) microbic activity, or it is the microbes themselves and their activities locally exerted on the membrane. 4. That a previously damaged valve forms a locus minoris resistenticB to the influence of any poison circulating in the blood. In connection with postulate (2) and our knowledge of the anatomical changes that ordinarily accompany any inflammatory process, we may tabulate endocardial changes thus : — Phenomena of constant Phenomena whose occurrence depends on occurrence at the circumstances defined by postulate (2). onset in every case of acute endocarditis. '{a) Simple swelling without loss of epithelium, no vegetations, and ultimately complete resolution. Active congestion, with \{b) Swelling plus loss of epithelium (micro- effusion of serum and j scopic ulceration) ; appearance of vegeta- cells and swelling of \ tions ; ultimately some thickening or the valve. J scarring left behind. ic) Swelling, loss of epithelium, vegetations plus loss of other tissues and naked eye ulceration. {a) Must be allowed to occur in those cases of rheumatic fever and other illnesses in which a definite valvular bruit occurs, but finally entirely disappears. Q}) Is the most common clinical occurrence in such illnesses (rheumatic fever) as leave a permanent organic valvular bruit. These must in strictness be also termed ulcerative endocarditis, but as the loss of tissue is of microscopic proportions, the term is usually reserved for the third class. {c) It is to this condition that the term ulcerative endocarditis is usually applied. I have put it in serial continuity to the other forms to emphasise what I believe to be its real position, viz. an endocarditis, the severity and course of which depend upon circum- stances which may be called accidental, in support or explanation of which statement we will now consider the clinical occurrence of severe endocarditis. First of all, cases of the following type are unfortunately by no means rare. A patient, probably under twenty, is attacked wirh ^ This is inserted in view of the doubt whether rheumatism is a microbic disease IV DISEASES OF THORACIC ORGANS 143 rheumatic fever. A valvular bruit develops and persists, but the patient becomes more or less convalescent from distinct rheumatic symptoms. Then, without any pyrexia, or very slight and tem- porary fever, one or other, or perhaps one after the other, some of the following incidents occur: attacks of pain in and swelling of the spleen, renal pain with haematuria, cough with bloody sputum and a pleuritic rub, cedema with loss of circulation in a limb or part of one, hemiplegia, etc., each and all evidences of an embolus being swept from the heart into the organ specified. The patient may yet live on in an invalid condition for some months, and even for years, and eventually succumb from cardiac failure or from an embolus proving fatal. On autopsy we find the areas of embolism, corresponding to the symptoms, each and all in what may be termed a quiescent condition, i.e. one the ultimate end of which will be simple fibrosis or scarring after absorption of very slightly irritating dead tissue. We find on the valves of the heart a greater or less amount of vegetations, on the removal of which losses of substance — ulcers — may be plainly visible in the valve tissue, but, and this is the point, from neither the valves nor the eiiibolised areas can any growth of pathoge7iic 7nicrobes be obtained. Such a case must be termed severe — and ulcerative — endocarditis, though its origin is purely rheumatic. Now let us sketch the other form. An attack of rheumatic fever, followed by the appearance of a bruit as before, but the patient gets quite well of all symptoms and remains so, a murmur being the only evidence of his attack. One day an entrance to his system is effected by potent-for-evil microbes, and now follows a train of symptoms which in gross may be termed septicaemic — hectic, sweating, rigors, diarrhoea, ups and downs — and quite probably evidences of emboli, as in the previous case. The patient dies, not of an apyrexial exhaustion or cardiac failure, but evidently of some acute febrile process. On autopsy we find, not quiescent, absorbing embolised areas, hut the seat of each embolus is occupied by a soft, semi-purulent collection of debris, the heart valves or endocardium may be in precisely the same condition to naked eye as in the previous case — though it is probable that the loss of tissue will be more evident — vegetations may or may not be equally abundant, but from the ulcer and from each embolised area can be obtained a culture of pathogenic microbes. Microbes of many kinds have thus been found — gonococci, pneumococci, pyogenes albus, p. aureus, etc. The difference between the two cases is clinically real enough 144 DIFFERENTIAL DIAGNOSIS chap. and serious enough, though the anatomical changes to naked eye may be practically identical, at least in the heart. But the differ- ence is, I maintain, a quasi-accidental one, and due to a contamina- tion of the blood by virulent microbes, which {vide above) may be of almost any kind, and hence ulcerative endocarditis is not a specific disease to the same degree as are scarlet fever, syphilis, or small- pox, for example. It is more like pneumonia, which can be produced also by many microbes. Diagnosis of Ulcerative Endocarditis Septic or malignant or ulcerative (they are all used synony- mously in clinical medicine) endocarditis is either endocarditis plus blood-poisoning, or it is blood-poisoning plus endocarditis, according as the valves have been previously or are now only for the first time damaged. Its three diagnostic features are: (i) symptoms of blood-poisoning; (2) embolic phenomena; (3) valvular bruits — and we have to see how it is to be separated from the diseases which may at times present these features. Simple endocarditis, by which we must here understand one from which recovery, except as regards scarring of the valves, is easily possible and indeed the rule, has been sketched above, and the principal point of difference between it and the malignant form is the absence of those extreme variations in temperature, of diarrhoea, and of rigors, which indicate that blood-poisoning has been superadded to the valvular trouble, though the emboli and the murmurs may be common to both. To diagnose septic endocarditis from an ordinary case of septicaemia, no matter what was the point of entrance of the poison, is a work of supererogation ; they are identical. The only point is, that the presence of a bruit renders it probable that the enemy has effected a lodgment in a position — the cardiac valves — whence his spread over the country is supremely easy. If the bruit materially and distinctly alters from day to day, we have strong proof that active anatomical changes are going on in the valve — destruction of tissue or disposition of fibrinous vegetations on a raw surface — and these make the diagnosis nearly certain. But there are still three specific and special causes of toxaemia which are likely to cause confusion. These are typhoid fever, acute tuberculosis, and ague. Typhoid fever, in its pyrexia and in its diarrhoea, may resemble, and is, a septic disease; per contra^ a person with old valvular IV DISEASES OF THORACIC ORGANS 145 trouble is not thereby protected from enteric, and in such a person the likeness to septic endocarditis may be very close. The following differences will, however, usually help us : [a) the fever in typhoid is usually more regularly persistent, not so intermittent or remittent in its type ; (p) the abdominal tenderness, the headache, and the rash are none of them common in ulcerative endocarditis ; and lastly, {c) the serum (Weidal's test) test for typhoid will, with almost mathematical precision, tell us whether typhoid is or is not present ; moreover, (d) if a bruit is present in a patient with typhoid alone, it will not alter from day to day in any marked degree. With refer- ence to this last point, I must add that, in my view of the pathology of septic endocarditis, it would certainly be possible for typhoid to relight ulcerative changes in the valves. The diagnosis from acute tuberculosis must mainly rest on the positive evidence of this disease being present — a preponderance of pulmonary signs and symptoms, proof of other tubercular lesions, etc. If a cardiac bruit be present, it must be watched for the same indications as when typhoid is suspected. Too often, it must be admitted, the diagnosis is only cleared up by post-mortem examination. Malignant endocarditis has been mistaken for ague only by reason of a temporary regularity in the rigors and pyrexial extremes. The effects of quinine and a few days' delay have never left the matter long in doubt, unless death has too rapidly intervened. Many cases have now been reported in which, while cardiac bruits have been absent during life, autopsy has revealed the presence of (septic ?) valvular lesions. Of such cases it can only be said that, without the assistance of a combination of septic symptoms and embolic phenomena, diagnosis is simply impossible. We can only guess at it by an attempted process of exclusion. Prognosis in Heart Disease This involves two separate lines of thought. First, the imme- diate prognosis {a) in a case of acute endocarditis, {b) in a case of cardiac failure without evidence of acute inflammatory changes; secondly, the general prognosis of a case of chronic cardiac trouble as regards occupation, etc. In a given case of acute endocarditis the prognosis depends entirely upon the severity of the inflammatory process, and the extent to which it weakens the muscle by its spread. The deter- L 146 DIFFERENTIAL DIAGNOSIS chap. mination of this is entirely beyond our powers of direct observa- tion ; we can only indirectly estimate it to some degree by the symptoms of cardiac failure, and prognosis can only be made from day to day by noting each day's progress. When the temperature (rarely much raised) becomes quite normal we have a right to assume that the active stages of inflammation are at least not pro- gressing, and then intensification or amelioration of back pressure symptoms gives us a daily despair or hope, always with a tendency to look on the bright side, because, as a matter of clinical experi- ence, it is but rarely that acute — provided that it is not septic — endocarditis kills directly. Recovery is the rule, at least to the extent of a capability of leading a life which may be useful, and even enjoyable. When, as in repeated attacks of acute rheumatism, we have reason to believe that fresh outbursts of inflammation keep on recurring, the outlook must necessarily become more gloomy with each attack, though even here we may, to a large extent, accept the above suggestions. In considering those cases in which we do not suspect recent endocarditis, whether the primary trouble has originally been valvu- litis or is now essentially a primary muscular degeneration, the most important question is. What is it that has caused this heart to fail 710W ; is it that the work has been too great or the power too small ? — for evidently the ratio between them is one which cannot be maintained. Careful inquiry must be made into the duration and progress of each symptom, however trivial, and into the habits and surroundings of the patient ; and the less obvious appears the excess of work — we must never forget that worry or anxiety, mental work, in fact, may be equally or more detrimental than bodily exertion — the more anxious are we lest it be power that is failing below a standard compatible with prolonged life. When we have duly weighed the items of this consideration, we can only await next the verdict of treatment. Statistics of bruits, with ages at death, are but of httle use. As age or degeneration, i.e. loss of vital elasticity, advances we must naturally expect a slower response to remedial measures, if, indeed, response be not entirely absent ; but even now it is astonishing to see how cases may improve by a judicious combination and alternation of drugs and of rest and in- creasing exertion. The latter, though an obvious common-sense method of treatment, has recently been brought into fashionable prominence under the name of Schott or Nauheim treatment. The prognosis of other cardiac affections, though requiring frequently the nicest of judgment, can generally be regarded with IV DISEASES OF THORACIC ORGANS 147 lenient eyes. In nervous affections, as a group, the outlook is certainly good, and the patient must be encouraged to live an ordinary life, with a few hints as to the avoidance of excesses of mental or bodily strain ; and if a cause, such as tobacco or alcohol, can be discovered, moderation or total prohibition must be en- forced. Even when associated with other phenomena of Grave's disease, a rapid heart is comparatively harmless, though a prolonged period of ill-health must be accepted as inevitable. When our advice is asked by a patient who has recognised valvular disease, with no present symptoms of failure, we must look, and encourage the patient to look, on the cheerful side as much as possible. Nothing can be more injudicious in such cases than to pull a long face and condemn such a patient to a life of idleness, ticketed with a label, " Heart Disease." Habits of depressing intro- spection are sure to arise, and it is these that kill more surely and rapidly than any valvular lesion. Pregnancy is a serious considera- tion, but I have known a girl of seventeen with severe mitral trouble of rheumatic origin marry at twenty, bear eight healthy children, and survive till the age of seventy-seven. In questions w^here a possible pregnancy has to be considered, I think a past history of back pressure symptoms of more importance than the present character of a bruit. CHAPTER V DIFFERENTIAL DIAGNOSIS OF SOME SYMPTOMS AND AFFECTIONS OF NOSE, THROAT, AND ALIMENTARY TRACT AND ANNEXA HEMORRHAGE HAEMORRHAGE may appear at the nose, mouth, or anus as the three natural openings of the system ; but it may originate from many situations, and we shall try to indicate the reasons which lead us to assign to it its actual seat of origin. Epistaxis, OR Bleeding from the Nose The nose differs very materially from the mouth and anus from our present point of view, because there is practically no difficulty in ascertaining that the blood does come from somewhere in the naso-pharyngeal cavity itself. When blood makes its exit from either of the other two openings the question of precise origin is very much more intricate, as we shall presently see. Only as the very rarest of clinico-pathological curiosities could one imagine a gastric or pulmonary haemorrhage giving rise to more than a pass- ing suspicion that the naso-pharynx was its seat, and very Httle inquiry into the mode of onset, and physical examination of the cavities, will be required to rapidly settle that suspicion should it have momentarily arisen. Consequently, in a case of epistaxis of some duration and amount, the only primary questions of diagnosis that can arise are (i) its precise seat, and (2) its cause. The determination of question (i), though often difficult, or even impossible, is, if it be necessary at all, entirely a matter of local inspection with mirror and speculum, and will not be further CHAP. V SOME SYMPTOMS AND AFFECTIONS 149 considered. The answer to question (2) is a matter of the very widest clinical importance, and we will proceed to classify the — I. Local Causes : in Nose, etc. — (a) Traumatism, fractured base of skull, blows, etc. (d) Adenoids. (c) Malignant growth or in- nocent polypi. (d) Ulcers, lupus, syphilis, etc., and necrosis. (e) Diphtheria and similar acute local trouble, or even simple catarrh. 2. General Constitu- tional Causes — (a) Haemophilia. (3) L e u c o c y- thsemia. (c) Vascular de- generation. (d) Onset of acute fevers. (e) Scurvy. (/) Purpura. (g-) Puberty. Causes of Epistaxis Diagnostic Points. History usually obvious ; difficulties only arise when patient is drunk, or otherwise no?z C07n- pos mentis or unconscious. Subject a young child ; suspected by nasal voice, sunken bridge of nose, habit of mouth breath- ing ; proved by inspection ^vith finger and mirror. Subject adult probably ; may be complaint of local pain, and of nose being stuffed ; inspec- tion clears up the case. Detected by speculum; very probably associ- ated with ozsena. History of illness preceding the epistaxis, and probably other local signs, sweUing, etc. Invariably (in first attack) a young subject, most likely a boy ; history of previous attacks of hsemorrhage markedly disproportionate to the lesion, e.g. tooth extraction, etc. ; family his- tory sure to give evidence of heredity. Probably a young subject ; examination of spleen and blood will clear up the case. Subject old (physiologically, if not in years) ; radials thickened, heart hypertrophied ; pos- sibly also renal symptoms. Subject young ; obviously out of health ; ther- mometer proves pyrexia. Swollen and spongy gums. Always (if epistaxis) purpuric spots elsewhere. Age the most important guide, coupled with the knowledge that epistaxis does occur frequently at this epoch without other obvious causation. I50 DIFFERENTIAL DIAGNOSIS CHAP. 2. General Constitu- Diagnostic Points, tional causes — *= {h) Vicarious men- Obviously a female, and with a history of sup- struation (?). pressed natural menstruation, but the occur- rence of well-established cases is very doubtful ; the bleeding would be periodical. These causes, as well as those which follow, emphasise the absolute necessity of a careful systematic examination of a patient with epistaxis if the diagnosis is not at once obvious. ;. Local Conditions other than Nasal — {a) Distinct kidney disease. {b) Cirrhosis of liver. {c) Morbus cordis. (^ Pregnancy. {e) Coughing, sneezing, etc., to excess. Diagnostic Points. This is only a slightly special branch of 2 {c) in which the kidney trouble is, and has been, a prominent feature in the case. It is not absolutely essential that contracted kidney should be present. A consecutive nephritis {q.v.) will sometimes cause it. History or other strong indication of alcoholic excesses ; liver probably enlarged. Bruits present, or at least other evidence of car- diac disease. An occasional cause of epistaxis. History and abdominal examination sufficient. History distinctive ; onset after such excessive respiratory movements. Differential Diagnosis of Blood issuing by the Mouth Blood which issues by the mouth may have obviously many sources : — 1. Naso-pharynx. 2. Mouth and pharynx. 3. Stomach or oesophagus. 4. Lungs. 5. Aneurysms bursting into either viscus. The history of the way in which the blood comes up for evacua- tion may in some cases be sufficient and diagnostic, but even in intelligent adults the question of vomiting v. coughing is often very difficult to settle, so that the differential diagnosis must proceed on definite exclusion lines by objective guides as far as possible. SOME SYMPrOMS AND AFFECTIONS 151 Our first care, then, must be, in a doubtful case, to carefully wipe away the blood from nose and mouth and fauces ; a careful local examination, with thorough exploration with eye or finger, will then soon show us whether the blood is coming from above, and reference to the causes of epistaxis will probably clear the matter up after a systematic examination of the patient. N.B. — Do not be led away from a careful examination of nose and throat by a definite history of haematemesis i^q.v?) or haemo- ptysis {q.v.\ especially if other symptoms pointing to stomach or lungs are absent. Suppose, now, that local examination reveals the mouth or fauces as the seat of the bleeding vessel — the following conditions must be borne in mind as further elements in the exact diagnosis : — Causes of Hemorrhage from Mouth and Fauces 1. Traumatism from external vio- lence. 2. Traumatism from teeth or food. 3. Gums. 4. Ulcers. 5. Acute tonsillitis and pharyngitis. 6. Chronic pharyn- Sfeal conditions. Diagnostic Points. History obvious. Wound found on gums, tongue, cheek, or fauces ; its history must be most carefully inquired into, whether consciously done by the teeth or dur- ing a meal, or attack of coughing, or whether the patient is unconscious of its origin. A bitten tongue with no history^ and with blood on the pillow in the niorni7ig^ in a youngish subject is prima facie strong presumptive evi- de7tce of 7ioctur7tal epilepsy. Spongy, from scurvy or purpura or anaemia, all of which will show definite features elsewhere. Gingivitis in dentition, or from want of cleanli- ness in mouth, easily recognised by age, or by tartar encrustation. All fairly easily recognised — malignant, syphilitic, lupus, tubercle, or simple or gangrenous (can- crum oris). Easily recognised by dark purplish red coloura- tion, or by actual ulceration. Blood only in spots ; dilated and varicose veins seen on posterior pharyngeal wall. As sources of haemorrhage of a serious degree none of these 152 DIFFERENTIAL DIAGNOSIS CHAP. require much consideration beyond mention of the fact that any deep or progressive ulceration may open a large vessel ; but as sources of alarm to a patient they have a very great and real im- portance, and a discovery of one of them may go a long way in establishing a reputation for care or carelessness. Leaving the mouth and parts open to inspection, we have now to consider those seats of a haemorrhage appearing through the mouth, which are out of sight. These are — 1. The air passages, 2. The alimentary tract, and our first point in diagnosis is to determine which of these two main tracts is at fault, in other words, to distinguish — Sensation accompany- ing the voidance of the blood. Precedent condition of patient. Associated condition of patient. Voided blood itself. Associated mena. pheno- H^MOPTYSIS Cough or tickling in throat, or possibly no warning at all. Cough or known lung mischief. If pallor present, it came on subse- quently to the hae- morrhage, i.e. the bleeding excites cough before it is sufficient to cause pallor. Usually frothy, and often bright (mix- ture c air), always alkaline. Melaena not marked as a rule ; some phy- sical signs, rales, etc., possibly found in lungs. N.B. — Their absence does not exclude haemoptysis. V. H^MATEMESIS Nausea first, followed by act of vomiting Dyspepsia or marked gastric disturbance. Pallor often precedes the ejection of blood, i.e. blood pouring into stomach causes it before the blood is voided. Never frothy, usually dark, and frequently acid from admixture of gastric juice. Almost certainly fol- lowed by melasna ; possiblylocal pain or tenderness over ab- domen or stomach. Caution — muscles may be tender from coughing or strain- ing. Having satisfied ourselves that it is (i) the lung which is the source of the blood, diagnosis must next proceed to the — SOME SYMPTOMS AND AFFECTIONS 153 Laryngitis, trache- ites, bronchitis acute, and granu- lar pharyngitis. Pneumonia. Phthisis. Gangrene, abscess bronchiectasis. Degenerative bron- chitis and em- physema. Foreign body. Aneurysm. MaHgnant growths. Blood aspirated into lung in hsemate- mesis. Causes of Hemoptysis Diagnostic Points. If within reach of the laiyngoscopic mirror, cause soon cleared up (tubercular, syphilitic, or malig- nant ulceration, q.v.^ all of them common causes of slight hjemoptysis) ; blood either in little pellets or thin streaks ; sputum very sticky and frothy; pain locally on swallowing or coughing. Sputum usually uniformly stained either slightly or up to prune -juice colour, very sticky and usually nearly or quite airless ; associated dul- ness, tubular breathing, and temperature, etc., commonly distinctive enough. Far and away the commonest cause of profuse haemoptysis ; bacilli if found distinctive, but diagnosis in early stages often impossible. All rare causes of haemorrhage ; associated foetid smell of sputum, and local physical signs char- acteristic. Condition described by Sir Andrew Clark: haemor- rhage fairly free, physical signs of bronchitis and emphysema, without any distinctive bacilli or evidence of excavation or dilated tubes. History usually sufficient of choking with aspira- tion of the foreign body. As a cause of haemoptysis rare, but when aneur^^sm is present haemoptysis is tolerably frequent ; if other signs of aneurysm present, haemoptysis adds to their weight, and especially if there are signs of pressure on a large air tube. N.B. — Slight haemoptysis may precede for a long period the actual rupture of the sac. Said to be like red-currant jelly, but in my ex- perience the haemorrhage here is only dis- tinguishable by the physical signs of the growth, and has nothing distinctive in itself. Vide tests between hsematemesis and haemoptysis ; if definite haematemesis proved to be present there will only be slight pellets of blood or blood-stained mucus coughed up for a few hours or a day or so after the vomiting. These causes really fall into two clinical groups, viz. those in which the source and cause of the haemorrhage are obvious or 154 DIFFERENTIAL DIAGNOSIS CHAP. easily detected, and those in which probabiUties have to be nicely balanced. To the former group belong visible laryngeal and pharyn- geal troubles, obvious gangrene, abscess, aneurysm, pneumonia, and carcinoma secondary to an obvious primary growth. To the latter belong those cases of definite haemoptysis in which no physical signs at all are to be found, and those in which the physical signs are those of bronchitis plus a few rales and fine crepitations, indicating the present situation of the semi-coagulated blood ; in this group our main anxiety is the determination whether phthisis is at the bottom of the matter or not, and the question will be found dis- cussed under that heading {vide pp. 54 and 92). We will now assume that (2) the blood has come from some part of the alimentary system. We have to consider the — Causes of H^ematemesis Swallowed blood (rarely of notice- able extent). Vicarious menstrua- tion (very rare). Bloodstates in — Purpura, Scurvy, Yellow fever, Acute yellow atrophy of liver, etc., Traumatism. Gastritis or simple vomiting. Diagnostic Points. « Already considered ; local examination usually sufficient to clear up the case, except in a few cases of malingering, with deliberate drinking of blood. Of very doubtful occurrence ; can only be thought of in a girl, probably young and hysterical ; no other local symptoms, periodicity of bleeding. All rare as causes of hsematemesis. The condition of the patient induced by the named disease usually quite suffi- cient for diagnosis. Aneurysm. History sufficiently obvious, either of an external blow or of swallowing a corrosive or violent irritant, or some mechanical lacerator of mucous membrane. Haemorrhage slight as a rule, and usually only in streaks ; the history of severe vomiting pre- ceding the blood usually sufficient, except in those cases where the violence has actually ruptured a large vessel ; vide below, Aneurysm and Ulcer, etc. Quite possibly unrecognised till post-mortem is made ; only diagnosable during life when SOME SYMPTOMS AND AFFECTIONS 155 Cancer. Ulcer. Diseases of other organs leading to venous conges- tion — (a) Morbus cordis. (i>) Chronic pulmon- ary disease. (c) Cirrhosis of liver. (d) Portal conges- tion. Diagnostic Poii previous examination has revealed a tumour of abdomen with expansile pulsation, Hccmor- rhage very profuse, and probably rapidly fatal. Haemorrhage usually of coffee ground type, great loss of flesh, and probably a tumour ; patient usually beyond early middle age. Haemorrhage usually free, with clots ; in simple ulcer, patient usually a young person and more commonly a female. I have known a tubercular ulcer in a phthisical patient cause fatal hcemorrhage, but such cases are very rare. Presence of bruits and other evidence of cardiac back pressure. Evident physical signs of lung disease, associated with failure of circulation. History of alcohol, or dyspepsia and vomiting suggestive of alcohol ; liver enlarged probably. Produced by ascites, carcinoma of peritoneum, enlargement or diseases of spleen, etc., with tolerably obvious features. Such is a practically complete hst of the causes of the presence of blood in the stomach leading to hsematemesis. In numbers they look formidable enough on paper, but in practice they are comparatively simple in diagnosis. Thus, hemorrhage from the stomach is nez^er the first and totally unexpected symptom of serious bloodstates, nor of those forms of back venous pressure commonly attributed to portal congestion. There are and have been some prodromal or leading indications in all cases, the haematemesis forming a culminating calamity, so to speak, not perhaps expected, but not altogether unforeseen. There is only one group of cases that really presents much difficulty, viz. those in the middle period of hfe, especially in men, where we have to try and decide between cirrhosis of the hver, carcinomatous or simple ulceration, and an unexplained cause which provisionally may be termed simple varicosity of veins. More than one such case has occurred to me in which age and sex, history of alcohol, slight dyspeptic pheno- mena, and the entire absence of positive objective signs (enlarged liver, tumour, dilated stomach, etc.), have together formed a 156 DIFFERENTIAL DIAGNOSIS chap. symptom-complex, in which the diagnostic points have been so nicely balanced that a positive diagnosis has been impossible in the absence of a post-mortem. Luckily for the patient the diagnosis, from a therapeutical point of view, is here of comparatively little moment, for absolute rest in bed, combined with physiological rest for the stomach, constitute the main, if not the only means of com- bating all form of serious gastric haemorrhage. For some further indications, vide under the headings of Ulcer, Cirrhosis of Liver, etc. Anal Appearance of Blood We must now consider blood passing from the bowel by the anus. It may be laid down as a working rule that blood in a comparatively unaltered state, i.e. recognisable as such by the laity, passed per anum comes from the colon or rectum, or the lowest two feet or so of the ileum. Blood coming from the stomach or upper part of the small intestine will be so altered by the digestive processes as to appear as melaena or black tarry stools. The only exception (it occurred to me once in tubercular ulcer of the stomach, verified post-mortem) is a case in which the bleeding is so profuse as to practically fill the intestine, and so appear at the anus simply darkened in colour. Such cases are almost invariably fatal. The following are the Causes of Mel^ena Blood passing from These cases constitute an enormous majority the stomach. (probably 90 per cent) of cases of melaena ; hsematemesis is very likely to have occurred ; for differential diagnosis, vide table above. Duodenal ulcer, or Rare as causes of melasna ; suggested chiefly by simple, tubercular, the presence of the symptom (melcena) com- or malignant dis- bined with the absence of the commoner ease of small in- causes ; possibly some tumour felt or some testines. abdominal symptoms suggesting ulceration, but not of a gastric type. Anchylostomiasis. Very rare indeed in England as a cause of melaena and anaemia ; only to be detected by finding eggs in the faeces. Causes of Haemorrhage (recognisable as such by the Laity) PASSING per Anum A. Lower ileum— Diagnostic Points. Ulcers : Typhoid. Haemorrhage appearing in course of a definite attack or of a vague pyrexial illness, when the hemorrhage clears up the diagnosis. SOME SYMPTOMS AND AFFECTIONS 157 Tubercular. Dysenteric. Simple and car- cinomatous. Traumatism. Drugs, especially violent purges. Blood conditions. Intussusception. B, Csecum, colon, and sigmoid flexure. Diagnostic Points. Usually distinct indications of tubercle, but diagnosis often impossible, ante mortem, from typhoid ; vide Typhoid v. Tuberculosis. History of recent or old dysentery fairly obvious. To me unknown causes of severe haemorrhage, but might conceivably give rise to the symptom, but would not be diagnosable, except by ab- sence of above three troubles, and in carci- noma possibly a tumour. History of a blow or swallowing a foreign body. If such a case arose it would be quite a patho- logical curiosity. History of administration. The same as in the stomach, but all rarer ; occa- sionally has occurred as a sequel to the very debilitating scourge of influenza ; such was the cause of death of a lately deceased distin- guished member of our profession. Signs of intestinal obstruction, presence of strain- ing, etc. All similar causes to those of ileum, but dysen- teric and carcinomatous ulceration are' here very common causes of haemorrhage instead of being rare, while the reverse is the case with typhoid and tubercular troubles, intussuscep- tion commencing in colon very rare indeed. C. Rectum — Traumatism. Piles. Pol>^i. Prolapse. Intussusception coming do^^^l. Ulcers — dysenteric, malignant, etc. Strictures. Fissures, fistulae, etc. Vaginal sources, to be looked for in females. All within reach of the examining finger or speculum, so that their diagnosis requires no discussion ; examination of the rectum also discloses the fact that the blood does come from the lowest six inches of the bowel. Like haemorrhage appearing by the mouth, the causes of melsena and rectal haemorrhage are much more formidable on 158 DIFFERENTIAL DIAGNOSIS chap. paper than in practice, and it is but very rarely that some clinical features will not be found leading unmistakably to a definite diagnosis. VOMITING Vomiting is a very complex process, of which the actual emptying of the stomach forms only a culminating objective feature. According to physiology, the whole series of phenomena ending in emesis is best explained by the hypothesis that there is situated in the medulla oblongata a group of neuron cells (termed a vomiting centre), the dendrites of which are connected with the nervous system in such a way that, on the one hand, they may receive afferent impulses from any part of the body, which im- pulses are capable of stimulating them to special activity, and, on the other, they may transmit messages to the salivary glands, to the respiratory mechanism, and to the voluntary muscles which, when thus stimulated, produce the emptying of the gastric contents. By accepting this explanatory hypothesis, we are in a position to gain a more or less rational understanding of the innumerable pathological or clinical incidents that may be associated with vomiting. The afferent impulses (as from a crush or severe pain, however excited) from any part may be so strong as to cause it, or, on the other hand, the condition of the blood circulating through the centre, or the physical condition of the brain, may be such as to independently start the centre into action. Lastly, and far most frequently, the contents or condition of the stomach itself may start the afferent impulses. A purely scientific or physiological analysis of vomiting should therefore start with a division into central or direct, and peripheral or reflex, each with its subdivisions; but from a clinical and diagnostic point of view a more useful classification is into the following : — SOME SYMPTOMS AND AFFECTIONS 159 Causes of Vomiting Diagnostic Indications /'Cerebral — Tumour. Meningitis. Cerebritis, etc. General shock. ^ Gastric crises of tabes dorsalis, or G.P.I. Hysterical. Cardiac disease. Pulmonary diseases attended by cough — phthisis, etc. Acute Infective dis- eases — the zymo- tics, pneumonia, etc. Ursemia and other kidney troubles. Simple pain. Not usually associated with much nausea, independent of food ; almost invariably as- sociated with marked corroborative evi- dence — optic neuritis, fits, paralysis, etc. — may be quite intermittent for even long periods, and then its apparent causeless- ness is its great feature. Apparently quite causeless in its onset, and equally mysterious in its cessation after a day or two's duration : also independent of food, associated with more local pain than cerebral form. Probably in a young person, and one who is not losing flesh, notwithstanding the asser- tion that for months everything has been vomited. Distinct evidence of bruits and back pressure on other organs than the stomach. On inquiry patient will say, " I cough till I am sick." Physical examination rarely fails to show good cause for the cough, but it is astonishing how patients will complain of the vomiting and forget the cough till a leading question on it is put : " Are you sick because you cough, or are you sick independently of coughing ? " Although vomiting, especially in children, is common at the onset of febrile acute illnesses, it must be very rarely that the cause is not soon obvious, for the ther- mometer will rapidly remove doubt. Vomiting again causeless, and independent of food ; uiinary examination soon clears up the case, even if it be unattended with commoner symptoms of uraemia. Statement made by patient quite sufficient. i6o DIFFERENTIAL DIAGNOSIS chap. Pregnancy, tumour, Physical examination of the abdomen very obstruction, etc. soon clears the matter up ; abdominal pain or discomfort usually marked. Addison's disease. Vomiting usually associated with pain, but the accompanying physical weakness, and especially the almost imperceptible pulse, will point to the disease even if typical 5 -< bronzing be not present. Gastric trouble — Vomiting due to actual disease of the Ulcers. stomach is, broadly speaking, characterised Irritation. by being in some definite relationship to Inflammation. food and to pain or discomfort produced Pyloric obstruc- by food. tion, etc. etc. For other points separating the various ^ Poisoning. gastric troubles, vide Gastric Ulcer, etc. If we are called upon to investigate a case of vomiting, very little observation is required to eliminate certain of the above groups — the pyrexia and aspect of acute general diseases, the collapsed features or the history of obstruction, the evident dropsy of morbus cordis, the pain or shock of an accident, etc., will at once put even the most careless observer on the right track. The diagnostic difficulties begin when the vomiting is the sole obvious feature that attracts the anxious attention of the patient or of the friends in the case of children. In quite young babies, i.e. in the first year of life, it is almost safe to conclude at once that food and consequently gastric irrita- tion, is at the bottom of the mischief, though we must not forget to look for signs of congenital syphilis. After the first year up to, say, puberty the insidious onset of tubercular meningitis with causeless vomiting must never be absent from our minds, however obvious may seem at first sight the apparent cause for the symptom. It is also during this period of childhood that all acute illnesses are apt to have vomiting for a prominent feature in their early stages, from which fact we may safely deduce as a golden rule — No case of vomiting in a child can be safely despised till a few days have passed without the development of any more guiding symptoms. It may, how- ever, be said that in acute gastric conditions food will be at once rejected, while in all other forms of sickness the food will usually stay down for some little time, and that without pain or discomfort. In adults we may draw attention specially to " morning vomiting " ; this, when repeated, is almost confined to the following conditions : pregnancy, alcohol and alcoholic dyspepsia; occasionally the vomiting V SOME SYMPTOMS AND AFFECTIONS i6i of uraemia and of cerebral tumour assumes this type, as almost invariably does the vomiting which is brought on by the cough of chronic bronchitis. Once reminded of this peculiarity diagnosis is not difficult. COLIC Strictly speaking, the terms " colic " and " colicky pain " should be reserved for intermittent or at least remittent painful sensations in the abdomen, or referred to the abdominal viscera ; but I wish here, for convenience' sake, to use the expression in a more comprehen- sive sense to include all forms of severe pain referred by the patient (either by voice, or gesture in those unable to speak) to the ab- dominal or pelvic region. Pain thus referred may arise from disease of any structures of the trunk below the thorax, for none of the viscera were intended for organs of special localising sense, so that pain arising in one part is frequently misreferred to another spot. For this very reason the differential diagnosis of the various causes for the symptom assumes here a greater importance than in any other region, especially as the treatment for one cause of the pain w^ould be absolutely and rapidly fatal if another cause were at work, e.g. perforation of stomach z'. a gall-stone. The causes, then, are many and various. They may be divided most simply into groups : — CAUSES OF ABDOMINAL PAIN Group I. — Affectio7is of the Peritoneum arid Alimentary Canal itself (a) Irritating contents of the gut causing either congestion of mucous membrane or painful peristalsis, or more likely both together. Food unsuitable in quantity or quality. Foreign bodies of any description. Drugs, active purgatives, or poisons. (d) Ulceration and other disease of the walls ; simple ulcer or tubercle, or carcinoma, etc. {jV.B. — It is astounding how frequently such diseases exist without causing any pain directly by their mere presence.) {c) Embolus of a mesenteric artery I have known to cause intense agonising colic with other symptoms like obstruc- tion. M 1 62 DIFFERENTIAL DIAGNOSIS chap. {d) Obstruction and strangulation of the gut, whether acute or chronic, and however arising (intussusception bands, hernia, twists, etc.). ((?) Peritonitis, acute or chronic, local or general, however aris- ing, independently or through — (/) Perforation of any hollow viscus, or rupture of a solid one. {g) Some blood alterations or blood-carried poisons must be inserted here ; of these lead and gout are the only two of practical importance. (^h) Nervous disturbance of gut from independent disease or functional condition of cord or brain ; e.g. the gastric crisis of tabes, or of G.P.I. ; or disease of the supra- renals ; or abdominal nerve complexus as met with in Addison's disease, etc. Group II. — Affections of Organs in Direct Connection with the Gut (a) Liver : — Inflammation or abscess, primary or arising in connection with a previous painless affection. Carcinoma and other rapidly increasing growths. Gall-stones when trying to leave the gall-bladder. Rupture (only traumatic). (3) Pancreas : — Acute inflammation. Stone in the duct (very rare, and practically outside the range of certain diagnosis). (c) Spleen : — Abscess. Enlargement, especially if also mobile enough for difficulties to occur in the circulation to and from it. Embolus (pain rarely very severe). Group III. — Affections independent of the Ali77ientary Tract and its Connections (a) Of the urinary tract : — Stone or other painful kidney trouble. Kinking or disease of ureter. Bladder : distension or rupture. {S) Abscess from any source ; its presence or its rupture may cause acute pain. V SOME SYMPTOMS AND AFFECTIONS 163 (c) Aneurysm : its presence or rupture. (d) Affections of the bones of the vertebral column, especially caries. Group IV. — In women the pelvic reproductive organ must be borne in mind as the possible primary source of growths, abscesses, peritonitis, bladder disturbance, etc. In dealing practically with such a heterogeneous collection of causes for acute abdominal pain, it is obvious that we must have some guiding principle on which to work ; though a general, and often even a precise and exact, diagnosis is by no means so difficult to arrive at as might at first sight appear. The simplest method appears to me to take events in the chronological order in which they occur, with possible or probable narrowing of the field with each. On a message being received to see a patient in this condi- tion, the first information naturally given is, roughly, the age of the patient, baby, child, or adult. We may say at once that in subjects under puberty direct alimentary disturbances are almost alone to be thought of — intestinal obstruction or strangulation, simple colic, possibly appendicular trouble or peritonitis, or may be even a renal stone — but such cases as tabetic crisis, Addison's disease, aneurysm, gall-stone, etc., may be at once excluded. After puberty no such general rule can be laid down, though it is true that certain troubles, e.g. gall-stone and malignant obstruction, are much more frequent in stout elderly patients than are others, e.g. intussuscep- tion or perforating acute ulcer. The next step, as things occur in practice, is to inquire of the friends as to the previous illnesses of, or similar attacks experienced by, the patient, and also as to symptoms additional to the pain : — Is this the first attack ? A. If not, has the patient previously — Been jaundiced ? Passed gravel ? Had urinary trouble or difficulty ? Complained of anything suggestive of G.P.I, or tabes? Suffered from marked irregularity of bowels ? Lost much flesh, or rapidly emaciated ? B. If it is, How did it come on ? Was it — (a) More or less gradually in the course of a fairly definite 1 64 DIFFERENTIAL DIAGNOSIS chap. illness, or at least has the patient been complaining long? e.g. Typhoid. Gall-stones. Addison's disease. Gastric ulcer. Dyspepsia. Phthisis. Gout. or, {B) Suddenly, in the midst of perfect health ? e.g. Latent gastric ulcer with perforation. Hernia or other strangulation of gut. Appendicular trouble. Indigestible meat, poisons, etc. The answers to these questions, and independent statements by friends, will very probably have thrown great light upon the case, excluding certain causes almost to a certainty, and bringing others forward into equal prominence as probabilities. Any symptoms additional to the pain will also very likely throw great light in certain diagnostic directions. Those more particularly to be asked for if information is not volunteered are — Vomiting. Constipation or other state of bowels, such as straining at stool, or diarrhoea. Strangury, or frequency of micturition, or other obvious urinary trouble. History of blow, or other accident. After gaining as much information as possible from what may be called external sources, the next step is to visit the patient and make as careful an examination, verbal and physical, as circum- stances will permit. We will now for a moment leave diagnosis itself, to consider the object we have to gain by it, viz. correct treatment of the condition. Treatment of acute abdominal pain must proceed on one of four lines : — A. Absolutely expectant, except for the outward application of hot fomentations, or an ice bag; B. A hypodermic injection of morphia, or inhalation of general anaesthetising agents, such as chloroform or ether ; C. An emetic or purge ; D. Prompt surgical interference : manipulative or by the knife ; V SOME SYMPTOMS AND AFFECTIONS 165 and it is primarily the object of diagnosis to determine upon which of these Unes we may most safely proceed. The last is out of all proportion the most important from every point of view, so we will first investigate the symptoms which indi- cate that a condition is present which demands this Hne of treat- ment. The conditions themselves are : — 1. Perforation or rupture of any hollow or solid viscus (gut, bladder, uterus, liver, etc.), or of any pathological tumour in the widest sense of the word (aneurysm, cyst, abscess, etc.). 2. External strangulation (strangulated herniae of all sorts palpable externally), or internal strangulation of a viscus or tumour by twist of its pedicel, or by band, etc. (internal herniae, etc.). 3. Acute general peritonitis of unknown origin (as well as most cases of known definite causation). 4. Acute pancreatitis and embolus of a mesenteric artery, which cause symptoms precisely resembling those of strangulation of the gut, and can only be distinguished on operation. 5. Distended bladder. 6. Displacements of pregnant or pathological uterus, causing urgent symptoms. Luckily most of these conditions are, even in their earliest stages, usually associated with such diagnostic features as to be at once recognisable as a group of cases. Thus the — Pain. — Is very sudden in onset, rapidly becoming agonising in character, may be continuous or intermittent, and in many external hernial cases so correctly localised as to direct attention at once to the seat of trouble. Aspect of the Patient. — Is frequently distinctive, with ashen pallid face, and eyes deeply sunk, and pinched features ; collapse very profound, with cold and clammy sweat. Pulse. — Is small, thready, and frequent. Tongue. — Is very dirty, and with great tendency to dryness. Vomiting. — Is often incessant, most distressing, very rarely indeed quite absent; if any delay has occurred may be stercoraceous. i66 DIFFERENTIAL DIAGNOSIS chap. Constipatio7i. — Absolute since the onset of pain ; thus dis- tinguishing such cases from virulent poisons, in which diarrhoea is present with vomiting. Abdomen. — Is very tender to touch as well as painful, and may be already distended or rapidly becoming so ; evident laboured waves of peristalsis may be present and give useful information. Urine. — May be much diminished, or totally suppressed without strangury. Should all these indications be present, or even two or three of them in well marked form (especially small, thready pulse, dry tongue, and incessant vomiting), there can be no room for hesitation if life is to be saved — piompt surgical measures must be adopted, manipulative or by cutting, according to circumstances. It how- ever only too frequently happens that the symptoms are not so well marked at the onset, and diagnosis must perforce be postponed for an hour or two. The only safe and golden rule is then : " In any case presenting the above features in doubtful form, but where suspicion is in the slightest degree aroused, no morphia must be administered"; for thereby many of the most important developments are masked or prevented ; but the patient must be placed under intelligent observation with hot or cold abdominal applications, and his case must be reinvestigated in an hour or two, by which time the diagnosis will have become more certain. Measures may then be taken accordingly. A distended bladder, though possibly a cause of acute abdominal pain, ought not to be difficult of diagnosis ; if the distension is sufficient to cause pain, the viscus will always be easy to feel as a centrally placed abdominal tumour. A bladder ruptured through disease, though probably causing symptoms belonging to (i) (where, indeed, it has been placed), will have invariably been pre- ceded by a long history of urinary trouble and difficulty, and will have thus been diagnosed. The pregnant uterus will likewise not offer, under these circum- stances, any diagnostic difficulty. Cases of rupture come under (i), and the blanched, bloodless aspect of the collapsed patient will be suggestive in a woman known or suspected to be pregnant. Into the more definite diagnosis of these cases I do not propose here to enter : the keenest diagnostician must frequently content himself with saying, " Laparotomy is urgently indicated," leaving the operation to disclose the exact condition. Thus, acute pancrea- V SOME SYMPTOMS AND AFFECTIONS 167 titis presents all the features of acute intestinal strangulation^ and acute perforative peritonitis is often identical in its symptoms with volvulus or internal hernia. Abdominal Cases without Marked Collapse Collapse developing very early in the case (almost from the instant of onset), with its attendant facies, pulse, etc., we have hitherto taken as the guiding principle in diagnosis. We have now to consider those cases of abdominal pain in which it is not so marked, may be even absent, at any rate in the earlier stages. Such cases, especially if on examination no pathognomonic sign is present, still call for the keenest eye, clearest understanding, and most incessant watchfulness, that at the earliest moment the cloven hoof betraying serious developments may be detected — something more than pain written in the face, some smallness and frequency of pulse out of proportion to the expected; a persistency of vomiting, or alteration in the character of the vomited matters — any or all of these features may be found on a second visit. In no case of painful abdominal affection can it be said that collapse must be absent, but it is, at any rate in severe shape, an exceptional feature in otherwise fairly healthy people (at the ex- tremes of life or in broken down subjects great caution in judgment is necessary), when one of the following is present, causing complaint of abdominal pain : — Simple colic, from improper contents of gut, or due to lead, gout, or Addison's disease, or nervous troubles ; Liver diseases, apart from a possible suppurative peritonitis arising from it ; Chronic obstruction of bowels \ Typhlitis ; Aneur3^sm ; Caries of spine ; Retroperitoneal growth ; and we shall now proceed to discuss their differential diagnosis on the assumption that the patient is capable of giving intelligent answers to questions, and that a thorough examination of the abdomen is allowable and allowed. On approaching the patient definite jaundice, if present, will at once attract notice {N.B. — by artificial light this is very easily over- 1 68 DIFFERENTIAL DIAGNOSIS chap. looked, in fact, impossible to detect, and the question of its presence must always be asked), and direct attention to the liver as in some way the cause of the trouble. The discovery of jaundice would also lead to questions as to its previous occurrence, if such had not already been put. The pigmentation of Addison's disease would at this stage possibly attract attention, and if present go far towards the elucidation of the diagnostic problem. General inquiries to estabhsh points left doubtful by the friends may then be put to the patient ; their scope has been already indicated. The abdomen must then be exposed, and the patient asked to point out the seat of greatest pain, and the direction (if any) in which it seems to travel ; this point is often useful, but as already noted, too much stress must not be laid upon it, owing to the vagaries of referred pain. The orderly methodical examination of the abdomen by inspec- tion, palpation, and percussion, and even by the stethoscope, may be proceeded with, and if there is still a doubt, a vaginal or rectal examination, or both if necessary, must be made. This examination will almost for a certainty have revealed any of the following points which are present : — 1. Whether the pain is greatly increased by pressure, or some- what relieved as a steady pressure becomes firmer and deeper ; the former suggestive of peritonitis or serious organic disease, the latter of simple colic. 2. Hardness or increased resistance of the muscles, either locally or generally, suggestive of some inflammatory trouble beneath them. 3. Tumour or swelling of liver, spleen, kidney, or bladder, or independently existing in abdomen, suggestive of its being the real seat and possible cause of the pain, or indirectly affording an opportunity for obstruction or strangulation of the gut. 4. Per vaginam, fixity, or swelHng of uterus, or other palpable abnormal condition of female reproductive organs again directly or indirectly causing the mischief. 5. Per rectu77t^ ballooning, or the peculiar smell of carcinoma (not easy to describe, but like some other smells once experienced never forgotten) or definite stricture, or tumour within reach of finger, all suggestive of carcinoma or other serious rectal disease, or intussusception reaching the rectum. 6. In cases still obscure we shall have tried to elicit pain on flexing thigh against resistance, suggestive of renal or appendicular or psoas mischief, or tenderness on tapping or jarring spine, sug- gestive of caries or other serious bone mischief. V SOME SYMPTOMS AND AFFECTIONS 169 Founded upon these and similar features, we may epitomise the principal points of differential diagnosis in such cases as follows : — Differential Diagnosis of Causes of Abdominal Pain not USUALLY associated WITH MaRKED CoLLAPSE, OR URGENTLY demanding active interference Colic^ Si7nple or Functional^ of Intesti?te Probable history of an over-full, indigestible, or unsuitable meal ; pain probably relieved or not made worse by pressure ; vomiting severe, but not prolonged, and diarrhcea probably present, or soon sets in. Lead and gout must be thought of in adults as a possible cause, and a blue line on gums or tophi looked for, and inquiries made of occupation, etc. Tabes dorsalis and G.P.I. must also be remembered in this con- nection, and the knee jerks and pupils investigated. After all is said and done, the most important problem is here to separate these cases from commencing local or general peri- tonitis, and from forms of intestinal obstruction which begin in- sidiously (overlooking a gall-stone or renal calculus is less serious, but vide below), and the -vdtal importance of the subject must be my excuse for repeating and bringing into closer contrast the likenesses and differences of the two conditions. Besides the mere pain itself, then, they may be alike in — 1. The vague localisation of the pain. 2. The suddenness of its onset. 3. The universal tenderness of the abdomen on light pal- pation. 4. The intensity of the pain. But they more frequently and essentially differ in — Functional colic. Obstruction and Peritonitis. Locality. Very vague, usually epi- Not unfrequently cor- gastric or umbilical. rectly localised. Suddenness. Gradually rising to a Most commonly abso- maximum, and waning lutely sudden, and and waxing. then persistent at a high pitch. Superficial tender- Often great, in fact. May be great, but is ness. greater than when never greater than 170 DIFFERENTIAL DIAGNOSIS CHAP. Collapse, includ- ing sunken eyes, small pulse, dry tongue, clammy sweat, etc. Vomiting. Constipation. Diarrhoea. Abdominal swell- ing or tympan- ites. Muscular rigidity. Functional Colic. fairly firm pressure is applied, which may completely check the pain. Rarely present, except at extremes of age and in broken - down sub- jects. Rare, except in acute poisoning by drugs or food, and then never stercoraceous, and only excited by food. Not common, except in lead poisoning. Far more frequent than constipation, except in lead colic. Practically do not occur, at any rate early in the case. Easily overcome, if pre- sent, by gentle, steady, persistent pressure. Obstruction and Peritonitis. that caused by firm pressure. Usually comes on at once, and in any case develops very rapidly; only in the rarest of instances is it quite absent. Very common indeed, usually very persist- ent, and may be ster- coraceous, independ- ent of food. Usually complete (even to wind) after the onset of pain ; bowels may have been open just previously or pain may come on during defsecation. Only exists in the shape of tenesmus, with pass- ing of mucus and blood. N.B. — In sus- picious caseSj when diarrhoea is complained ofy examine the alleged motions. General distension fre- quent, and forms a very suspicious feature indeed. May arise very early in the case. May be quite local, but is usually present, and cannot be overcome, any effort to do so causing great increase in the pain. In the remaining conditions causing severe abdominal pain, SOME SYMPTOMS AND AFFECTIONS 171 immediate diagnosis on the first or even second visit is of less vital consequence, though important enough, as it must essentially be, if medicine is to maintain any grounds of claim to rank as a science. Affections of the Liver Simple non-purulent inflammation or congestion. Suppuration. Carcinoma. Gall-stones. Two cases have recently come under my care in which I believe this condition was present ; the pain was localised to the right hypochon- driac and epigastric region, and both were associated with a distinctly appreciable liver edge, which was very tender on pressure or manipulation ; in both alcohol was much in evidence, and both subsided in a few days without further symptom. Probable history of dysentery or tropical resi- dence ; pain localised correctly in liver ; fre- quently a swelling to be made out ; a hectic type of temperature, and especially if associated with night sweatings is very suspicious. Easily diagnosed if tumour is felt ; if no tumour, then rapidity of loss of flesh is most important feature, when the locality of pain, and age of patient, rouse a suspicion. Possibly previous history of jaundice ; patient usually stoutish and middle-aged or older ; distended gall-bladder, if present, almost con- clusive. It is usually assumed that gall-stones, renal calculus, and simple colic are very likely to be mistaken for one another. The following table shows their contrasts and Hkenesses : — Gall-stones, renal calculus, simple colic may be alike in — 1. Sudden onset of pain. 2. Sudden cessation of pain. , 3. Indefinite locality of it. 4. Severity of it. 172 DIFFERENTIAL DIAGNOSIS CHAP. They more commonly differ in- Gall-stones. Renal Calculus. Simple Colic. 5- Locality Usually referred Usually in back. Usually referred and — more correctly than the others to the right hypo c h on- drium. loin, and groin. to umbilicus or epigastrium. 6. Direction Pain fixed, or Travels down Fixed in umbili- of pain. seems to pass groin to testi- cus, or travels upwards. cle, which is frequently re- tracted. across abdo- men. 7. Character. Not intermittent. More intermit- tent than gall- stone. Usually is actu- ally intermit- tent. 8. Calculus found. In faeces if at all. In urine if at all. None. Associated Jaundice ; urine Strangury or fre- Urination not in- symptoms, dark coloured quent micturi- terfered with. if any. perhaps; other- tion ; possibly except possi- wise the func- bloody urine ; bly quantity tion not inter- function pretty diminished if fered with ; certainly inter- much vomit- vomiting may fered with; ing, which is occur from the vomiting less more probable pain or asso- likely than with than in the ciated gastric biliary colic. other two. disturbance. Previous his- Of jaundice and Of gravel in urine, Of "bilious at- tory. similar attacks. or other patho- logical condi- tion of urine. tacks," if any- thing, or of dropped wrist. Age. Middle or later. Any age. Middle and young most likely. Chronic Obstruction of Bowels. — Previous history of notable irregularity of bowels ; rectal examination may give very important information ; possibly a tumour in known line of colon (malignant or intussusception). Typhlitis. — Pain usually correctly referred to right iliac fossa; dulness on percussion and great tenderness, especially at SOME SYMPTOMS AND AFFECTIONS 173 M'Burney's point If definite swelling and redness diagnosis nearly conclusive. Aneurysm. — Tumour has expansile pulsation ; pain more in back and worse at night ; bruit possibly heard over tumour. Vessels elsewhere degenerate : history of syphilis and hard work and alcohol probably. Caries. — Pain also referred to back, probably worse on jarring heels or tapping spine ; this or aneurysm may cause definite cord symptoms. Retroperitoneal Growth. — Only guessed at by excluding other causes for pain or cord symptoms. Possibly a tumour of irregular outline may be felt, lying deeply, and without expansile pulsation. DIARRHCEA AND CONSTIPATION The causes of these conditions or symptoms may thus be tabu- lated : — I. Contents of the gut. Too liquid. Too solid. Too irritating. Foreign bodies. 2. Walls of the gut. {a) Ulcers : if not too deep to par- alyse. {b) Growths. {c) Inflammation. Clinical Illustrations. Doubtful if this condition per se ever causes diarrhoea, possibly excessive drinking might do it ; unduly active peristalsis may thus cause it by preventing absorption. Probably unusual sweating, habitual neglect of the bowels ; fever thus possibly causes constipation by too great absorption of water. Improper fermentation, unripe fruit or other indigestible material. Either by their presence cause irritation pos- sibly, or by their size cause obstruction, e.g. purgative drugs, or gall-stones, etc. Tubercular, typhoid, dysenteric, and simple. May cause irritation, and so diarrhoea, or paralysis, and so cause constipation ; sometimes by bulk or cicatrisation may also cause obstruction. of peritonitis leads to paralysis, the most 174 DIFFERENTIAL DIAGNOSIS CHAP. (d) Altered structure. (e) Altered circula- tion. (/) Blood conditions or toxaemias, which may either cause excessive peristalsis or ex- cretion into gut, or both, or, />er contra^ may act in the reverse manner. (^g) Reflex nerve in- fluence, again acting either on peristalsis or secretion, or both. (h) Pressure from without acting mechanically or reflexly, (/) Some unexplained causes. Clinical Illustrations. obstinate form of obstruction ; milder forms of this may by irritation cause diarrhoea, as in some cases of appendicular or cascal trouble. Lardaceous disease, leading to obstinate diar- rhoea. Heart disease, cirrhosis of liver, either con- stipation or diarrhoea. Bright's disease (urgemia) ; gouty habit ; probably some of the diarrhoeas of zymotic cases, critical or otherwise, are thus caused. Lead is the best known example of the opposite condition, viz. constipation. Cord diseases ; mental states, as fear, anxiety, insanity, etc., dentition in babies, com- monly causing diarrhoea, but not unfre- quently the reverse ; and here possibly may be placed the too solid motions of habitual neglect. If an abdominal tumour presses on the gut it is likely to cause constipation, but some- times it may cause diarrhoea reflexly, or by direct irritation. e.g. To what shall we attribute the almost universal constipation of the early days of sea -air, or other changes of climate and temperature ? The majority of the above cases offer no difficulty in diagnosis, for the constipation or diarrhoea is merely a concomitant symptom of some obvious disease or departure from the ordinary habits — dietetic, physical, or general — of the individual ; but a few guiding rules of procedure are required for the elucidation of those cases in which the diarrhoea or constipation is the only obvious symptom from which the patient is suffering, or, at least, of which he complains. In any such case the first and most important thing to ascertain is the precise meaning attached by the patient to the words he uses — ask how often the bowels act, whether much tenesmus or not, and V SOME SYMPTOMS AND AFFECTIONS 175 the quantity and character of what passes, and inspect the motions for this purpose if necessary. A case recently has occurred to me in which the patient complained of an obstinate diarrhoea. Some- what puzzled by my ineffectual efforts at drug treatment, I was led to ask him to save everything passed for twenty-four hours ; I then found all the motions solid and natural, and further inquiry led to the conclusion that it was simply a case of a gross feeder whose bowels required naturally a more frequent relief. This inquiry and inspection will probably result in the discovery of any of the follow- ing conditions of the stools : — Natural in Consiste?icy and Quantity. — As in the above case. If motions very narrow and ribbon-Uke, probably a stricture, organic or spasmodic (of sphincters), is present. Much Fecule?it Material., but too Watery^ Light ^ or Dark. — If light or natural colour, suggestive of simple irritation of upper bowel by unsuitable food j if dark and tarry, strongly sug- gestive of hemorrhage (^.^'.), high up. Masses of Undigested Food or Curds {in Children), so-called Lien- tery. — Suggestive primarily of unsuitable or too free feeding, e.g. too much milk in typhoid ; and if this question is satis- factorily determined in the negative, then suggestive of undue nervous influences, perhaps best treated by bromides or ner\-ine tonics. Pea-soupy Stools. — Might rouse a suspicion of insidious typhoid, and should lead to the use of the thermometer. Scybalous Knobs or very hard Fceces ; probably with much Mucus. — Suggest a false diarrhxjea, due to undue constipation ; hardening of the fasces ; a most important class of cases, because they are so common. Pus^ or Pus a7id Blood; Mucus, or Blood and Mucus. — Rupture of an abscess into bowel. Much mucus is a pathognomonic sign of colonic trouble, and if present with hardened lumps almost certainly indicates constipation, either simple or due to organic obstruction, as the real trouble ; if with blood it is suggestive of dysentery, malignant or other stricture, piles, fistula in ano, etc. Me??ibra?20us Masses floating in Water. — Membranous colitis ; in the absence of an acute illness rather suggestive of malignant disease, or occasionally chronic obstruction or simple con- stipation. The anus at least, and better also the rectum, should then be 176 DIFFERENTIAL DIAGNOSIS chap. inspected and examined to see if any pathological condition is there present which can cause diarrhoea, or at least explain the patient's complaint, thus : — Piles or Simple Polypi. — May explain blood and mucus, excessive straining pain, etc. Fistula. — By its discharge may have given a false impression of diarrhoea, as well as altering the material of a stool. Balloofiing. — If well marked is strongly suggestive of a stricture just out of reach, or that can with an effort be just touched. Stricture. — MaHgnant, syphilitic, etc., will explain either diarrhoea or constipation, or a marked alternation of the two con- ditions. Rectu7n full of Hardened Fceces. — A very common thing to find in complaints of either diarrhoea or constipation. It must be emptied, and then a fresh examination made, as the condition may be a simple one, or it may be merely a symp- tom of some serious trouble to be discovered by the ex- amination of the empty viscus. Uterine a?td Ovarian Troubles. — In women a rectal examination is often required as well as vaginal ; it is possible for almost any organic disease or pathological position of the genitory organs to cause a disturbance of defaecation. A systematic examination of the abdomen, which may precede or follow the rectal one, may very likely reveal an efficient explana- tion of the trouble. Almost every pathological condition of the abdominal viscera may cause alteration in alvine evacuation, e.g. liver diseases {q.v.\ splenic enlargements, any abdominal tumour, dilated stomach {q.v.), tubercular peritonitis, or any other form of peritonitis, or ascites, etc. ; as, however, most if not all of them will have given rise to complaints other than of diarrhoea or con- stipation, they mil not here be further considered. Should the history and examination thus far have left matters still in doubt, the patient must next be thoroughly overhauled for evidence of some general disease, or a local one not situated within the abdominal region, which may be associated as cause with the symptoms under consideration. These are chiefly phthisis, lard- aceous disease, plumbism, Bright's disease, typhoid, leucoc3'thaemia, and other blood dyscrasias or definite disease of the spinal cord or brain. These, like the troubles mentioned in the preceding paragraph, hardly require in this connection any further mention. The chronic V SOME SYMPTOMS AND AFFECTIONS 177 cachexia, or suppuration, with the enlarged spleen and urinary con- dition of lardaceous disease ; the blue line, colic, and occupation of plumbism ; the temperature of typhoid ; the blood of leucocy- thaemia and ansemia ; the low specific gravity aiid diminished urine of approaching uraemia (the diarrhoea is really a uraemic phenomenon) ; these are all sufficiently distinctive ; and so are the physical signs in the chest of a phthisical patient ; but it must not be forgotten that in consumption there are several possible sources for the diarrhoea which require a little consideration, owing to their importance ; thus : — Causes of Diarrhcea in Phthisis {a) Accidental, as it were, due to food, or change in climate, etc., from which phthisis confers no immunity. This may be sharp while it lasts, but is quite temporary, rapidly ceasing or yielding to treatment. Some change in residence or diet will probably give the clue to its origin. ib) In association with the dyspepsia, w^hich is such a trouble- some accompaniment of phthisis, particularly in its earlier stages. In fact, when lung mischief is doubtful but sus- pected, this dyspepsia is a very suspicious piece of diag- nostic evidence. {c) Due to tubercular ulceration of intestine. Usually occurs in later stages, when the lung trouble is very distinct. Associated with slight colicky pains, and very intractable to treatment, though often ceasing spontaneously. The presence of the ulceration cannot be diagnosed with certainty, but pain, and especially tenderness in the abdo- men, are suggestive when in combination with an obstinate diarrhoea. {d) Lardaceous changes supervening ; painless in itself, absolutely rebellious to treatment ; associated with distinctive signs of lardaceous trouble already mentioned in spleen and liver, and possibly kidney. {e) That of exhaustion in the very last stage of the disease ; the active cause, in fact, of the fatal ending in many cases not apparently due to either {c) or {d). Ascites The methods to be adopted to determine the presence of excess of fluid in the peritoneal cavity are so distinctly laid down in all the N 178 DIFFERENTIAL DIAGNOSIS chap. text-books that I do not propose to discuss them except in tabular form, to separate ascites from cystic formations in the abdomen i^ide p. i8i). The causes of ascites recognised at the bedside belong to only two categories, or perhaps three, if we include chylous ascites. A. Irritation of the membrane itself — /Tubercle \ Either of the mem- ^ ) Carcinoma (secondary) ( braneor of an organ ^ \ Sarcoma (primary or second- f covered by it, e.g. \ ary) / ovary, etc. Inflammatory affections of the peritoneum apart from growths rarely cause marked effusion, unless in conjunction with severe kidney mischief. B. Undue pressure of blood in the portal system, which may arise from — 1. Local Causes in Abdomen^ practically confined to the Liver and its Fissures^ e.g. cirrhosis of liver, alco- holic or otherwise ; perihepatitis ; glands or growths (including a gall-stone very rarely) in the transverse fissure, whether primary or secondary. 2. Produced by a Pathological Condition of other Organs — 'Either secondarily through the right heart, or by extension of growths and inflammation from the pleura through the diaphragm. When due to kidney trouble, it arises probably from altera- tion in composition of blood, not from pressure. C. Undue pressure upon the receptaculum chyli or the thoracic duct, leading to transudation of a milky fluid into the peri- toneum-chyle. To determine to which of these primary groups a given case of ascites must be referred is usually a comparatively easy task ; to further differentiate the precise individual cause at work is more difficult, and often impossible, without exploration. In practice one usually first proceeds to exclude Group B 2. The history of the onset of the swelling of abdomen will here give Heart Lungs Kidneys V SOME SYMPTOMS AND AFFECTIONS 179 us very important information — whether, that is, the ascites was the first complaint, or whether the patient had long suffered from other troubles, such as cough, or shortness of breath, puffiness of face or limbs, etc. A careful examination of the thorax and of the urine will then speedily give us either a negative or positive result. If the thoracic organs and the urine are found to present no morbid features, we may be at once sure that some local-abdo- minal cause is at work. Should any of them, on the other hand, be found in a markedly pathological condition, we know at once that a powerful accessory factor is present in the case, whether local causes are at work or not. The indications from the above examination of the thoracic organs will rarely if ever be of doubtful significance, for ascites does not arise from such causes alone until and unless they are of pronounced severity. To ascertain the exact local cause at work it is certainly advisable, and, if much fluid is present, often necessary, to empty the abdomen. In my opinion, this should always in the first instance be done by a small surgical incision, and not by a trocar, however small : {a) it is more scientific ; {b) safer for the patient ; {c) gives more informa- tion as to the exact condition of affairs ; {d) it has been known to cure cases otherwise deemed incurable ; {e) it allows at one operation removal of a removable cause should such be found. The character of the fluid (in whatever way it be obtained) will at once detect chylous ascites. A microscopic examination must be made for this purpose, not only to differentiate fat droplets from pus corpuscles, but also for the further intention of deciding the possible presence of cells of heterotopic character. (Physiological injections into animals will, if necessary, detect tubercle.) Should chyle be present, we know at once that we have to deal with a growth, either malignant or glandular, or possibly (very rarely indeed) with a blood parasite — Bilharzia or Filaria. Should the fluid prove to be clear or purulent, we have to deal with one of the causes in Group A or B (i). Purulent peritonitis is almost invariably associated with {a) severe kidney disease, which will have been already detected; {b) perforation of a viscus, the occurrence of which will have been only too obvious ; or, {c) in women, extension from vagina, uterus, or Fallopian tubes, a mode of production always to be suspected in the sex if no other cause is ascertainable. If the fluid has been obtained by incision, this will by itself have probably completed the diagnosis, but if circumstances should have prevented exploration, the following are the principal i8o DIFFERENTIAL DIAGNOSIS chap. diagnostic factors, attention to which, in addition to what has been said already, will usually clear up the case : — Tubercular Peritonitis. — History of vague attacks of colic and irregularity of bowels. Abdominal walls probably feel thick to pleximeter finger or examining hand ; increased resistance. Irregular masses, with equally irregular dulness, may be appreciated. Patient usually young, though (even old) age does not exclude tubercle. Carcinoma. — Physical signs almost identical with tubercle in the small nodular form, and even on the post-mortem table the two may very closely resemble one another. More com- monly the primary growth is obvious as a tumour — ovarian, gastric, renal, etc. Sarco7na. — If secondary, indistinguishable from carcinoma for clinical purposes. If primary (of omentum) a tumour will be felt giving a sensation to examining hand identical with ballottement of pregnancy. Under thirty-five this cause may be almost at once excluded. Acute Ltflajnmation. — Recognised by the great pain and tender- ness on palpation ; board-like muscles {vide purulent effusion above). Cirrhosis of Liver, — Admitted history of alcohol, or if not of alcohol then of morning vomiting ; possibly piles or hsema- temesis. Liver usually enlarged, but surface regular, or at least without large bosses of carcinoma. N.B. — Youthful age does not exclude this cause, unfor- tunately. May be a history of syphilis, which points either to cirrhosis, gumma in portal fissure, enlarged glands, or peri- hepatitis. Perihepatitis. — To me, as an independent affection this is unknown, but I have seen it in connection with chronic peritonitis of tubercular or malignant origin, and also with syphilis and with heart disease. It is to be thought of when in a case of morbus cordis ascites is the prominent back pres- sure symptom, but I do not believe that it ever arises or causes trouble as a primary and separate disease. Glands and Growths in Portal Fissure. — If they cannot be felt, will only be diagnosed by a process of exclusion of other troubles ; but when the cause of ascites^ can usually be felt after withdrawal of the fluid. SOME SYMPTOMS AND AFFECTIONS i8i Inspection of ab- dojuen. Palpation. Percussion, Thrill. Other means. Free Ascitic Fluid. v. Symmetry usually main- tained ; flanks usually bulge markedly. No tumour to be felt, or if so it is a hard, solid mass. Dulness, particularly in the flanks with patient on back, possibly only here appreciable, and definitely shifts by imperceptible move- ment as the patient shifts his position. Cystic Tumours, or Encysted Fluid of Ordinary Origin. Usually some definite asymmetry to be per- ceived ; flanks do not bulge particularly. Tumour or tumours to be distinctly appreciated ; possible mobile, and feel cystic and fluctuat- ing. Dulness usually only appreciable over the tumour, not specially in flanks ; if it shifts with position of patient there is a perceptible movement of some- thing inside the ab- domen, detectable by palpation also. Usually not obtainable at all ; if it is so, it wdll only be in a limited area through the body of the cyst, not through the whole abdomen. Bimanual in a female shows movements of uterus with ovarian cyst ; other cystic for- mations may be felt definitely as such, of limited extent or mobi- lity, or both. In ovar- ian cyst menstrual irregularities may also help us. The only case which is likely to cause much trouble is that of a large, thin-walled ovarian cyst, which has practically filled the whole abdomen. Here even a careful attention to the above points may still leave us in doubt. The history of menstrual irregularities, and of a previous asymmetry, together with an absence of all presumable Frequently to be tected through whole abdomen. de- the In females bimanual examination gives no very distinctive infor- mation. 1 82 DIFFERENTIAL DIAGNOSIS chap. causes of ascites, will probable put us right ; such cases are nowa- days very rare, and, of course, they can only occur in the female sex. Very great obesity of the abdominal wall is a great obstacle to phy- sical examination, and such a case demands extra care, with which difficulties may vanish, but frequently only an examination under a general anaesthetic will clear up a doubtful abdominal case. Simple Dyspepsia v. Gastric Ulcer Even in an elementary work dealing with diagnosis it seems impossible to omit all reference to this subject, for the cases are so common in which we desire to have guidance, and yet the definite separation of the two conditions — perhaps it would be more correct to say the exclusion of ulcer — is so extraordinarily difficult, that I feel it is much easier to criticise the criteria mentioned in text-books than to offer any distinction of my own. If we take a number of cases of gastric ulcer, either proved such by autopsy or diagnosed as such during life, we find the following points more or less marked : — 1. The subjects will roughly divide themselves into two groups : {a) those whose ages range from seventeen to thirty ; (b) those from forty onwards. Group («) will be almost entirely composed of the female sex, and the majority will have suffered from ansemia, and they will not have wasted. Group {b) will be composed of either sex indifferently : anaemia — except for hsematemesis — will not have been marked, but loss of flesh will commonly have appeared. 2. Severe pain will have been a prominent feature in the history of the illness, and this pain will have frequently displayed the following peculiarities : — {a) Caused only by taking of food. \b) Appeared some little time after the ingestion of food, not at once, (c) Locahsed to a limited area, usually in the epigastric angle. {d) Increased by pressure on the spot, and often only then apparent. {e) ReHeved almost immediately by vomiting when this has occurred. 3. Vomiting is also likely to have been frequent, with chief characteristics : — (a) It occurred rather late after food. V SOME SYMPTOMS AND AFFECTIONS 183 {b) It relieved the pain almost at once. {c) It has been actual blood or blood-tinged at least once. 4. In the cases fatal from ulcer there will almost invariably have been, in addition to the above : — (a) Perforation with acute peritonitis ; or (b) Very severe haematemesis ; or at least {c) Such constant severe pain and vomiting as to have led to death by exhaustion — this last mode of death is commoner in the group of older patients. Hence with regard to diagnosis it is very easy to say that an ulcer is present when the above symptoms occur in typical severity. It is the converse of this proposition, viz. to exclude an ulcer when gastric symptoms are slight, that offers such enormous difficulties ; in fact, there can be no hesitation in saying that it is impossible by cli7iical methods alone to prove this negative. Will the Rontgen rays here again help us ? It is being constantly proved in cases that are operated upon for perforation, less commonly in ulcers found on autopsy, that pain may be — {a) So slight as to be practically unnoticed. {b) Relieved by taking food. {c) Generally diffused and not localised. id) Unrelieved, or only very gradually so by vomiting. That vomiting may be — {a) Absent altogether. {b) Not bloody nor blood-stained. In fact, that in certain cases every one of the guiding indications may have been absent, or what is perhaps worse, may have been absolutely contra - indicative. These exceptional cases are far more common in the group of young subjects ; in the older group the features are more constant, though not even there entirely without exceptions. Dr. S. Fenwick has adopted, if not invented, a simple method of attempting to solve the diagnosis by getting the patient to swallow about a drachm of common salt in a tumbler of water when the stomach is empty ; should an ulcer be present, the salt coming in contact with a raw surface will excite a lively attack of pain ; if ulcer be not present, pain is not likely to be caused by the simple procedure. The same plan may be adopted to determine whether an ulcer, which has been diagnosed as present, has healed. 1 84 DIFFERENTIAL DIAGNOSIS chap, v Apart from this clinical manceuvre we can, I think, only lay down the following rules : — 1. Never to think too lightly of an attack of dyspepsia in a young woman, especially if she be anaemic as well. 2. Whenever it is possible, even at some inconvenience to the patient, to insist on a soft diet and a few days' rest in bed in all cases of dyspepsia which have not arisen from a fairly definite cause. 3. A persistent-local (epigastric usually) pain in an older patient must similarly put us on our guard, to insist upon treatment appro- priate to ulceration. By attention to these rules we may cause some trouble to ourselves and our patients, but we shall at least have the satis- faction of having avoided anything likely to make matters worse. CHAPTER VI DISEASES OF THE URINARY ORGANS One of the most striking facts about kidney troubles is the fre- quency with which they occur without local symptoms. In acute nephritis it is true that aching pain in the loin is frequently present, and new growths of the kidney, including stone under that head, are usually associated at some period of their growth with more or less severe local pain : but chronic Bright's disease, lardaceous degenera- tion of the kidney, and, in fact, the majority of those cases in which the most serious degeneration and disintegration of the kidney structure are present, only betray themselves by general symptoms due to imperfect depuration of the blood, and by alterations in the urine of such a character, or so insidious in onset, that they may not have attracted the attention of the patient. For a discussion of the general symptoms refer to the heading Uraemia. The alterations in the urine are sometimes sufficiently obtrusive to be called symptoms, sometimes so insidious that they must be relegated to the class of physical signs, but in either instance they are so exceedingly important that they must be rather fully discussed for diagnostic purposes. Before we can appreciate or estimate pathological changes in the urine we ought to have a satisfactory general idea of the quantity and quality of the healthy excretion, and also of its physiological or healthy variations — a subject, which long experience of students has taught me, is dreadfully neglected, and forgotten as soon as the examination in physiology is passed. Normal Urine Should possess the following characteristics : — Quantity. From forty to fifty ounces in the adult. Appearance. Clear and bright. 1 86 DIFFERENTIAL DIAGNOSIS chap. Colour. Amber to sherry, light or dark. Reaction. Acid. Sp. gravity. 1015 to 1025. It should, in an adult, be passed about four or five times in the twenty- four hours, and should on analysis show about 2 per cent of urea. The colour is due to various urinary pigments, ultimately, no doubt, derived from bile pigments and from haemoglobin. The reaction is due to the presence in fairly large quantities of the acid phosphate of sodium NaHgPO^ {and probably of the analogous potassiuin salt also in smaller quantities^ It is truly wonderful how this simple, well-established fact is forgotten by students, who will persist in ascribing the acidity to uric and hippuric acids, regardless of the feeble acidity of these bodies, and their insignificance in quantity. Variations in Health In health the following are the chief factors influencing the urine, and a brief epitome of how and why. I. Exercise. — Physical work must undoubtedly — by mere wear and tear of fixed tissues as well as by quickening circulation, and therefore oxidation of more floating capital — have a tendency to throw more waste products into the blood. These waste materials are the ultimate oxidation products of organic food stuff's, HgO, CO2, and urea or uric acid (as urates) ; the HgO and COg pass off in large measure through the lungs by increased respiratory move- ment, and through the skin with the sweat, which is also markedly increased by exercise ; hence there follows as a natural deduction, just what is seen in actual practice, viz. that with exercise the urine shall as a rule be lessened in quantity, but increased in specific gravity, by a higher proportion of nitrogenous waste material and inorganic salts. At first this nitrogenous waste takes the form of uric acid, so that a copious deposit of urates and biurates is the familiar result of a hard day's work in one who is unaccustomed to physical labour. As uric acid is a less oxidised product than urea, i.e. contains a smaller proportion of oxygen, it is probable that this deposit is due in some way to an inefficient supply of oxygen to burn up the increased waste suddenly produced. When the body has had time to accommodate itself to the circumstances, the more usual metabolism of nitrogenous waste into urea again comes to the fore. VI DISEASES OF THE URINARY ORGANS 187 2. Food. — The ingestion of food influences the urine in two ways : — A. Directly : by the simple excretion of excess of water taken in — the student is apt to forget that the so-called solids of the food (^7) contain a large proportion of free water, {b) produce much water by their oxidation, so that it is not only the drink alone of the food, but the solids also that produce this excess. B. Indirectly : during gastric digestion a quantity of HCl is required, the manufacture of which sets free a corresponding quantity of sodium in the blood, with the result that the phosphate of sodium in the urine is more likely to become NagHPO^ or even NagPO^ rather than NaH2P0^. By both these processes, then, the quantity, the specific gravity, and the acidity of the urine are likely to be influenced — the first in- creased, and the last two diminished ; the acidity to such a degree that it is quite within physiological limits to find the urine neutral or even alkaline after a full meal. 3. Weather, — This simply has reference to the temperature to which the skin is exposed when no compensating influences — such as exercise — are at work on the circulation through it. Cold causes the skin to contract, and diminishes consequently its circulation and excretion of sweat, \\4th the result that the amount of urine passed is increased \ external heat will have the contrary effect. 4. Mental Conditions., such as fear, certain hysterical states on the borderland of health, and especially doubt as to opportunities for voluntary micturition, undoubtedly have an influence on the secretion of urine \ but their exact mechanism is obscure, and we can only record the fact. Thus we see that — V^^ yj J ]y[ay all be profoundly altered by exercise, food, P- 5 _•) "j weather, and mental conditions. Reaction, \ ' We will now proceed to discuss from a diagnostic point of view the variations in urine due to disease. i88 DIFFERENTIAL DIAGNOSIS CHAP. Variations in Disease Increased Frequency of Micturition May to due to — Acute inflamma- tion or irritation of kidney. Stone, or other growths of kid- ney, with colic. Cystitis and bladder calculus. 4. Prostatic troubles. 5. Polyuria. Chief diagnostic points. Very small quantities at a time, total quantity much diminished, probably blood in it ; stran- gury not infrequent. Also like acute inflammation, but with severe pain (renal colic, ^.2/.) probably running down into groin. Total quantity probably about normal, possibly alkaline and ammoniacal, certainly much mucus deposit ; probably pain in bladder or perineum, which may only be at end of act, and often referred to the glans penis. If acute the act is itself very painful ; if chronic the increased frequency of micturition is chiefly at night, with possibly some difficulty in starting the act during the day, and the catheter (possibly passed with difficulty) shows residual urine ; total quantity normal or greater than usual. Vide next section ; total quantity much in- creased. Acute congestion or inflammation, if primary. If on the top of old mischief. Large white kid- ney. Blocking of ure- ter. Retention, heart disease, and gen- eral circulatory disturbances. Total Quantity Is Di?ninisked in Frequent micturition ; strangury ; smoky or definitely bloody urine ; albumen and casts ; possible history of turpentine or copaiba, etc., administration. The same features, but with history of previous increased quantity. Vide section on L.W.K. Urine nearly solid with albumen ; patient very anaemic. If of both, total suppression {q-v.) ; if one only, such urine as escapes possibly normal; probably severe pain in groin and loin. Vide Suppression v. Retention, p. 216. Moderate quantity of albumen ; history of gradual di7ninutio7i in quantity of urine, and presence of other signs of heart disease or circulatory disturbances. VI DISEASES OF THE URINARY ORGx\NS 189 Is Increased in /Cirrhotic kidney. Consecutive neph- ritis. Lardaceous kidney. o ^ u < ^ o U 1) c o f^ / Hydronephrosis. Diabetes insipidus. Diabetes mellitus. Hysteria, after rigors of malaria, occa- sionally after crisis of acute disease. Low specific gravity, little albumen, patient probably over forty-five years of age ; few if any casts. Probably considerable number of casts ; fair quantity (up to one quarter) albumen, and history of acute kidney trouble. Probably also enlarged spleen and liver, and known cause of lardaceous degenera- tion present ; albumen considerable, casts may or may not be numerous, and possibly show lardaceous microscopic re- action. Increased quantity only at irregular intervals, and urine quite likely without much change from normal ; abdominal tumour in renal region often detectable. Quantity enormous, up to 300 or 400 ozs. ; specific gravity very low ; absence of albu- men or other pathological constituent. Specific gravity usually above 1025, but^ N.B. — sugar may he present in U'ri7ie of specific gravity below 1020; presence of sugar; urine of peculiar appearance and general symptoms of diabetes. Urine offers no special peculiarities ; the polyuria is quite temporar}', and the attendant circumstances are quite sufficient for diagnosis. Colour Of pathological variations in colour due to changes in the urinary pigments very little is known, and still less use can be made for clinical purposes of the knowledge we do possess (perhaps with the exceptions of melanin and indican) ; but the follow- ing substances when present will produce evident colour variations from the ordinary, and these variations form the first preliminary or simple test for the respective substances, and should therefore be remembered : — 190 DIFFERENTIAL DIAGNOSIS CHAP. Bile pigments. Blood. Chyle. Carbolic acid. Rhubarb. Santonin. HcB7tiatoxylin. Iodides and bromides. Methylene blue {occa- sionally given for rheumatoid - arth- ritis'). Urine a yellowish green tinge in thin layers, almost black in thicker ones ; if shaken the froth possesses a beautiful yellow colour. This yellowness of the froth is pathognomonic of bile in urine (? rhubarb or santonin). Urine either of a smoky tinge and not clear, or possesses the red colour of blood more or less marked. Urine distinctly milky throughout, and often co- agulates into a soft jelly. Urine of a green colour, looking almost black in thick layers. Brownish yellow colour, becoming red on adding alkali, disappearing with an acid. Bright yellow ; disappears with free acid. Reddish, also disappears with free acid, thus differing from red colour due to blood ; vide Hsematuria. Dark colour appears on adding nitric acid, due to setting free of iodine or bromine. Urine of a bright blue colour. I have recently seen a case of eosin in the urine mistaken for blood — it arose from eating sweets coloured with eosin. Specific Gravity Apart from the knowledge of the total quantity passed in twenty- four hours, variations in specific gravity have very little positive patho- logical significance. A high specific gravity (over 1027) should, however, at once rouse a suspicion of glycosuria i^q.v.\ while a low one (under 1015) should immediately start inquiry into the total quantity passed, etc., leading in the direction of suspected cirrhotic kidney, unless other obvious explanation be at hand. Constituents of Urine not usually found in Health, ANJ) essentially PATHOLOGICAL By their presence. Blood, pus, casts, sugar, albumen, chyle, phos- phate of lime if in quantity, bile. Or by excess. Urates, mucus. Or by altered condi- Triple phosphates, ammonia, tions of urine. For convenience of discussion, and because of its practical utility in urine analysis, we may divide these constituents into those VI DISEASES OF THE URINARY ORGANS 191 which form, or are chiefly found in association with, a deposit of some sort, and those which still leave the urine quite clear notwith- standing their presence, thus : — Forming, or chiefly found in, a Deposit. Leaving the Urine clear. Phosphates of lime. Sugar. ,, triple. Albumen. Urates and uric acid. Blood. [If in quantity Oxalates. Chyle. 4 usually makes Mucus. Bile. [ urine opaque. Pus. Casts. Blood staining a precipitate. It is obvious that there are two questions requiring answers in connection with these abnormal constituents — (i) By what tests shall we recognise them ? (2) What clinical diagnostic use can we make of the information thus acquired ? To the first of these questions I propose to give merely an outline of a reply; for details of manipulation special manuals must be consulted, as I am chiefly concerned with clinical and not scientific questions. Tests for the Nature of an Abnormal Constituent OF THE Urine There are three methods to be adopted in testing urine, all of which should be employed in turn as corroborating one another : (i) ordinary physical examination by the eye and nose; (2) chemi- cal experiments; (3) microscopical investigation; if very great accuracy is demanded, the spectroscope may be used to detect blood and bile. Smell Of ammonia. Indicates decomposition, and so far gives a clue to the improbability of a deposit being urates, but suggests pus or triple phosphates. Of violets. That the patient has been taking turpentine. These are the only two indications that smell is likely to give one, but asparagus and possibly other articles of diet do alter the 192 DIFFERENTIAL DIAGNOSIS CHAP. natural smell of healthy urine, though the fact is not of much clinical value. Appearance to Naked Eye of Urinary Deposit or Urine Phosphate of lime?- Triple phosphates? Urates. Uric acid. Oxalates. Mucus. Pus. Blood. Sugar. Casts and Albumen. Bile. White, more or less granular deposit ; some- times in large amount ( = phosphatic diabetes), and may be hummocky from intermixture of mucus. Only recognised accurately by microscope in a deposit ; urine ammoniacal. Usually coloured pink or red ; if white they may be distinguished from phosphates by the fact that they usually adhere to the side of the vessel at the top of the urine. Only seen as isolated little cayenne-pepper grains at the bottom of the glass, or entangled in mucus. Usually seen (if at all by naked eye) as small shining crystals entangled in the mucus. Practically a constant feature even in health ; it forms a translucent, semi-transparent, floccu- lent cloud towards the lower part of the glass, and often floating free in the middle of the urine. White or greenish white, often hummocky deposit at the bottom of the glass, not granular, but easily mistaken for phosphates or white urates ; mucus cloud usually excessive above it ; urine commonly, though by no means invariably, ammoniacal. Smoky or definite red colour of blood, light or dark. Peculiar greenish yellow tinge in typical diabetic urine, but perhaps more often nothing very distinctive. Only observable under the microscope ; not any characteristic appearance. Vide colour and chemical changes, p. 190 ^ Students are very apt to forget that phosphates of sodium and potassium are soluble in water, and therefore do not occur in precipitates. ■^ These crystals are called triple phosphates, because all three atoms of hydrogen are replaced by metals (2 by Mg, i by Am) ; they can only occur when decomposi- tion has taken place in the urine, either within or without the body ; for without decomposition ammonia does not appear in the urine. PLATE URINARY DEPOSITS 1. Uric Acid. 2. Amorphous and Soda Urates. 3. Triple or Ammonio-Magnesic Phosphate. 4. Oxalates. 5. and 6. Casts of Uriniferous Tubes x 215 Diam. To face page 192. ,# Fig. 1. Uric Acid. i^^'-ff'' '^••A '■'^■'^■^■- ■■■■. ^o^ Fig. 2. Amorphous & Soda Urates. '^- ^ ^^^ ^ Fig. 3. Triple or Ammonio- Magnesic Phosphate. Fig. 4. Oxalates. .^& Oxalate. /.;! ^ o o, ^'m. a ^ c . oc ^#?. ^^^^mrnmmm i^€ <:^ ^ — — \ o IViple phospliate. Figs. 5 and 6. Casts of Uriniferous Tubes x 215 Diam. URINARY DEPOSITS. To face page igz. VI DISEASES OF THE URINARY ORGANS 193 Heat and Chemical Tests First ascertain by litmus paper the reaction of the urine. Inas- much as all the deposits may occur in acid or alkaline urine, with the exception of triple phosphates {vide footnote, pp. 192 and 209) and excessive urates, an alkaline reaction gives no very definite information beyond a strong probability that a deposit is not urates, but it is important in the heat test for albumen.^ Then take a little of the urine in a clean ^ test-tube (if there be a deposit to be tested take care to get plenty of it in the test-tube), and apply heat very cautiously and gradually, watching the urine carefully all the time. Bring it to active ebullition, and finally add a drop of nitric or, better still, acetic acid. The meaning of this is as follows : — 1. From cold up to, say, a little below blood heat urates will gradually dissolve: .'. Watch the deposit to see if it gets lighter — the diminution represents urates ; if no diminution up to this point, no urates ; and, N.B. — all urates are now dissolved, and so cannot be mistaken for albumen. 2. From about blood heat up to boiling albumen will, if present, be coagulated and appear as a precipitate ; the more albuminous a liquid the lower the temperature at which the albumen will begin to coagulate : . •. Watch the deposit (or clear urine) to see if it gets thicker (or clouds). Any precipitate now appearing is either albumen or phos- phates,^ and neither will disappear on boiling, so we add one drop of acid (acetic is best, as it is weaker and so avoids fallacies of nitric dissolving traces of albumen), which — 3. Dissolves any phosphates, but (if not too much be added) leaves the coagulated albumen untouched : ^ This is owing to the fact that when decomposition takes place any albumen present is converted by the ammonia into alkali-albumen, which is not coagxilated by heat alone. 2 Dirty test-tubes, especially with acid, will often prevent precipitation of albumen. 3 It is doubtful to what cause this deposition of phosphates is due ; possibly escape of CO2 which held them in solution, or possibly some subtler chemical change in them produced by boiling (Ralfe), O 194 DIFFERENTIAL DIAGNOSIS chap. .*. The part of final precipitate clearing up with acid = phos- phates ; remainder = albumen or other proteid body; if brownish red, probably due to blood or stained by blood. 4. If the deposit is unaltered or only slightly thickened by boiling, it is either phosphates or pus. Now take a fresh specimen in a clean test-tube, and add a drop or two of acetic acid or weak nitric acid, this — Makes mucin stringy; Dissolves phosphates ; Does not affect urates ; Does not materially affect pus. To a similar specimen add a few drops of caustic potash ; this — Causes pus to become jellified or ropy ; Dissolves urates ; Does not affect urates markedly. To test for sugar, boil some Fehling's solution, and while boiling hot add a few drops of urine ; if sugar be present, red or yellow oxide of copper is rapidly precipitated. There are many other tests for sugar, and great controversy still exists as to which is the best ; but the above, known as Fehling's test, is sufficient and accurate enough for ordinary clinical purposes. If bile be suspected by the colour, Pettenkofer's test with fuming nitric acid, giving a play of colours if bile pigments be present, may be applied as confirmatory evidence. But the simplest of all tests for bile is the yellow colour imparted to the froth that appears when urine is shaken. Microscopical appearances of Urinary Deposits and Elements Oxalates. Phosphates — Amorphous or crystalline. Triple phosphates. Pus. Blood cells. Urates. Uric acid. Casts. VI DISEASES OF THE URINARY ORGANS 195 CLINICAL SIGNIFICATION OF ABOVE We may now proceed to discuss more fully the second question mentioned above, viz. What is the clinical significance of the various morbid constituents, and how far are they of diagnostic value ? Albuminuria The causes that may produce albumen in the urine are many, but we can distinguish in clinical work three groups of albuminuria : — Group I. — In which the albumen is only a sub- Blood {vide Haema- sidiar}'- factor, and its presence completely turia). accounted for by the other constituent, viz. — Pus {vide Pyuria). Spermatorrhoea (?). Group II. — Present With abundant casts, indicating acute kidney with other factors disease, or consecutive nephritis in earlier explaining its an- stages, atomical source, viz. — Group III. — In Cirrhotic kidney. which it is often Consecutive nephritis in later stages, the only obvious Lardaceous kidney. morbid constitu- Surgical kidney (hydro-nephrosis). ent, though a few Stone in pelvis, probably with pus or crystals, casts or crystal- Cardiac disease or general back pressure, line substances Abdominal disease or pregnancy, with local back may be present in pressure. some cases. With or after some specific fevers — diphtheria, scarlet fever, etc. So-called cyclical or functional albuminuria. Leucorrhea in women. Anaemia (occasionally). Debility in or after many general diseases. To determine to which of these groups a given case belongs it is obvious, then, that we must examine the urine carefully (and repeatedly in some cases) by chemical and microscopicaP tests. ^ If no obvious deposit is present let the urine stand for twelve hours in a conical vessel covered from dust. The late Dr. Ralfe used also to dust a little powdered starch on its surface, to carry down mechanically any floating casts. If a centrifugal- ising machine is available this is the best method of obtaining a deposit. 196 DIFFERENTIAL DIAGNOSIS chap. These will be practically certain to differentiate Groups I. and II., and by exclusion lead us to believe that some member of Group III. is causing the mischief. Then note the quantity of albumen present ; if only a trace, it is most likely due to — Cirrhotic kidney. Back venous pressure (local or general). Surgical kidney (first or second stage, q.v,\ Specific fevers (not reaching stage of actual nephritis). Leucorrhea. Anaemia. Cyclical or functional {^q.v.\ If more than a trace, probably — Lardaceous kidney, or Consecutive nephritis without many casts, or Chyluria. Most of these conditions will become tolerably obvious when the patient as well as his urine is carefully overhauled, but one or two of them require a little further consideration. Cyclical or Functional Albuminuria These are terms invented to describe cases which were, I believe, first noticed by examiners for life assurance (but the con- dition has subsequently been investigated by many observers), who found albumen in the urine without obvious cause, and with an entire absence of other guiding pathological constituent or even symptom. Its exact pathology, and above all its precise clinical significance from a prognostic point of view, are still but imperfectly understood, but before we can allow ourselves to rest content with such a diagnosis, the following propositions and conditions must have been rigorously investigated : — 1. That the patient must have been most carefully examined in every system, without finding evidence of disease (more especially, perhaps, the condition of the vascular system). 2. That the urine and the urinary system must have been also repeatedly and carefully examined without the discovery of any morbid constituent or local condition, especially casts, blood, pus, stricture, stone, phimosis, leucorrhea, fever, phthisis, leucocythaimia, etc. VI DISEASES OF THE URINARY ORGANS 197 3. That the albumen shall never have been more than a trace. 4. It is a condition hitherto found almost exclusively in adolescents (boys or girls), or youngish adults, though it is uncertain how far it may persist into later life. 5. The circumstances found to influence the presence and quantity of the albumen have usually been position of body, exer- cise, exposure, and certain articles of diet, e.g. eggs j and hence the urine must be examined on several occasions — Before and after rising in the morning ; „ „ cold bathing; „ ,, food of suspected kinds ; „ ,, exertion (slight and severe). If these various testings give various results while other condi- tions remain the same, a preliminary diagnosis of functional may be given, but one to be willingly abandoned on the discovery of some indisputably organic change. Surgical Kidney as Cause of Albuminuria Surgical kidney is a convenient, but somewhat invidious, expres- sion used to denote a kidney which has been damaged by obstruction to the free outflow of urine from its pelvis. It would appear that an intermittent obstruction is equally, if not more, efficacious than a permanent one in producing the condition. In its typical form it is essentially a surgical trouble with surgi- cal treatment, and its description and discussion must be looked for in surgical manuals ; but as its earlier manifestations and irregular forms may easily come before a physician, its main features are here glanced at. There are three forms or stages of it readily distinguishable when met with alone, but they are far more usually — on the post- mortem table at any rate — mixed with one another : — 1. Simple atrophy of pyramids from pressure. 2. No. I, plus chronic inflammation of kidney from irritation. 3. No. I and No. 2, plus septic infection of the urinary tract. As regards the causation, there are three well-known causes, viz. stricture of urethra, stone in the bladder, and enlarged prostate, and when either of these is in operation it is probable that both kidneys will suffer. The disease is here mentioned in a medical work chiefly on account of a group of cases which arise from very 198 DIFFERENTIAL DIAGNOSIS CHAP. ill-understood causes that are supposed to give rise to intermittent kinking of the ureter, with a consequent intermittent increase of pressure in the pelvis. Definite diagnosis of such cases is in all probability impossible in their earlier stages, but the following symptoms would render the condition highly probable : — 1. Albuminuria probably not more than a trace, and very pos- sibly intermittent. 2. Marked irregularity in the quantity of urine passed in succes- sive days. 3. The presence in the abdomen of a tumour, possibly ill-defined, diminishing and increasing according as the amount of urine passed is large or small. The remaining conditions of albuminuria in Group III. may be more briefly dismissed in tabular form : — 2. Condition. Cirrhotic kidney^ or consecutive nephritis i?i the later stages. Lardaceous kid- ney. 3. Heart disease. 4. Abdominal dis- ease. 5. Nephrolithiasis. 6. Diphtheria^ scar- let fever., or other zymotic; ancemia^ leucor- rhea^ convales- cence from even acute nephritis. Guiding Indications. Specific gravity low ; quantity increased ; heart hypertrophied ; vessels probably degenerate ; distinct history of nephritis in consecutive cases. Albumen considerable ; quantity of urine greater than usual ; some obvious cause for lardaceous change, not forgetting syphilis and phthisis ; liver or spleen, or both, almost sure to be enlarged ; painless diarrhoea may (rarely) be present. Bruits probably present, or at least alterations from health in the cardiac sounds ; nearly sure to be oedema of legs ; quantity of urine di7ni?t- ishi7tg lately., pari passu with the onset of other back pressure symptoms. Ascites or tumour or pregnant uterus ; swelling of abdomen probably obvious. Vide Stone in Kidney. The history of such disease is usually obvious enough ; albumen likely to diminish as convale- scence proceeds, but casts must be anxiously looked for. In connection with all the groups, but especially perhaps with VI DISEASES OF THE URINARY ORGANS 199 this last group, of causes of albuminuria, a very anxious question will often arise — Is this patient weak and anaemic because he is albu- minuric, or is he albuminuric because he is weak? The question is important because of treatment. If we feed him up to cure anaemia we may further damage his kidneys : if we starve him to relieve the kidneys we may perpetuate the anaemia, and also the debility of renal tissue. To answer this question fully would require an essay, but the following points are worthy of attention : — It is obvious at once that all albuminuria depends upon and is caused by — (i) Acute or gross disease in or near (2) Simple nutritive (or original) debility of some part of the kidney structures, which, when healthy, prevents or does not cause a transudation of albumen into the excretion. Acute or gross disease includes — (a) All those cases (stone, tubercle, carcinoma, perirenal abscess, etc.), the treatment of which is or should be almost entirely surgical, and of which a brief note will be found under the appropriate heading. (d) Inflammation of the kidneys or bladder, of which, when acute, the treatment and management are obvious enough. Difficulties and doubts arise when the acute trouble has subsided and the case become one in which the albumen remains (with the anaemia in the secondary cases, possibly without it in the primary ones) as practically the only sign of disease. These must be placed for our present object along with the group in which no such acute local trouble has been present. The following important proposi- tions may then be made on them, each proposition having weighty therapeutical deductions : — 1. Albuminuria of so-called functional or cyclical origin may exist for years without the subject of it showing any marked deterio- ration of health, and the same is true of many albuminurias which are the sequel of known acute Bright's or other gross renal mischief. 2. If the urine on boiling becomes practically solid, this only means about 2 per cent of albumen — say the equivalent of an egg or a couple of ounces of beefsteak in twenty-four hours ; while what is ordinarily spoken of as a trace of albumen means from J to ^ per cent or less — the equivalent of about one ordinary mouth- 200 DIFFERENTIAL DIAGNOSIS chap. ful of food — so that as a mere drain of nutrient material from the body albuminuria may be certainly neglected. 3. Experience has shown, after many trials, that no drug and no plan of low diet expressly used, ad hoc, has hitherto been found capable of preventing or eliminating the last traces of albumen from the urine. 4. It is the life-work of the kidneys to excrete some of the waste products from the body, and these oxidation products come from two sources : — {a) . The result of the ordinary never-ceasing activity (life, growth, and decay) of all the body tissues and cells. (b) A possible, or even probable, luxus consumption of materials taken in by the mouth as food, but never really assimilated into the structures of the body. Now, any rational system of management of albuminuria must take all these facts into account. Wear and tear of tissues cannot be checked entirely, but it may be kept within moderate limits by avoiding excessive physical exertion. Luxus consumption can also probably not be entirely avoided, but may be reduced considerably by avoiding excess of nitrogenous food. Beyond these extremes I do not think we should be too strict either in diet or exercise with albuminurias, for constant worry of obeying rules is worse than occasional lapses from them. Pyuria or Pus in the Urine The sources of pus found in the urine may thus be tabulated, with their most prominent guiding features : — Source. Chief Points. Urethra, in either Quantity small ; escapes at any time, indepen- sex. dently of micturition, and stains and stiffens the linen ; micturition probably painful ; squeezing urethra towards meatus shows a bead of pus. Vagina in female. Similar indications, and speculum clinches the diagnosis ; also vaginal epithelium revealed by microscope. Bladder^ Most probably associated with frequent distress- ing micturition and other symptoms of cystitis \ urine possibly ammoniacal on voidance ; much bladder epithelium under microscope ; if no symptoms (or very slight) of cystitis, pus prob- VI DISEASES OF THE URINARY ORGANS 20I Source. Ureter. Kidney and pelvis thereof. Chief Points. ably in small quantity, but the cystoscope must be appealed to as final arbitrator. Practically indistinguishable from kidney. Quantity usually considerable ; stone and tubercle most common causes ; urine most commonly acid, and but little disturbance in frequency of micturition, except in stone ; pain of a colicky nature not unfrequent ; renal epithelium frequently found under the microscope. If we have ascertained the place of origin of the pus, the next point is the cause of the suppuration itself : — 2. In vulva vagina. I. In urethra. Hunterian chancres have been known to occur in the urethra ; the finger would readily detect them ; instrumental irritation. Strain has lately been asserted on good authority to cause a urethritis independently of sexual connection. Gonorrhoea, recent or old (with stricture), is, after all, far and away the commonest cause. If the matter is legally disputed the gonococcus would be the only possible distinctive feature, though this is more likely to lead to hard swearing than to scientific conviction. and Such causes as foreign bodies (pessaries, etc.) are obvious on inspection with a speculum, as are also chancres, epithelioma, etc. It is indisputably proved that in young sub- jects dirt, masturbation, etc., may start a sup- purative inflammation without a suspicion of criminal violence. A diagnosis without a his- tory is impossible, but the fact of such vulvitis occurring must be remembered by a medical jurist. That suppuration may occur in the bladder, or at least that pus may enter the urinary tract at the bladder without general cystitis, is true ; but its occurrence is so rare that practically the causes of cystitis and of suppuration through or from the bladder are the same. They are : — 3. In Bladder, 202 DIFFERENTIAL DIAGNOSIS CHAP. {a) Foreign bodies. (b) Distension from {c) Extension of inflamma - tion. {d) Debility. (. »+H +-> u CO t/3 \n W £ "y. in rt ^ u y3 p ^ c Posterior roots. J Lateral pyramidal tracts. ) Direct „ „ j Ascending antero-lateral tract of Cowers. Anterior roots. Direct cerebellar tract. Many unnamed fibres, both in white and gray matter. a u .B (V ■i-> 3 u (U a C ,£5 ■*-> « rC (n +-• C a> u ;h a 3 (U ^ C rili O The ganglion on the posterior root of peripheral nerves. Rolandic or motor area of cerebral cortex. The reticular formation of medulla and pons, and also in the ordinar}^ gray matter of cord, as intracordal neurons. xA.nterior cornua. Clark's column, and probably also cerebral and cerebellar cortex. In gray matter = intracordal neurons. 250 DIFFERENTIAL DIAGNOSIS CHAP. D. The Medulla Oblojigata. — Structurally, this is the continua- tion upwards of the cord, but the arrangement of its neuron cells and stems is more complicated and intricate. Only the more important (as far as our present knowledge is concerned) and apparently simple ones are here tabulated : — Cells of the Medulla Groups just below the floor of the fourth ventricle in serial continuation of those of the anterior cornua. fFuniculus gracilis. Groups in-! „ cuneatus. [ ,, rolandi. Groups scattered through the reticular formation. s ° ^ S ^ I O X W3 Vh o (D 3 o y O a o bo Motor cortex of brain. Posterior root ganglion, and also (above the cells of the funiculi) cells of cortex of cerebrum, and cerebellum. Clark's column, and also cere- bellar cortex. Cells in tricle. floor of fourth ven- E. T/ie Pons. — The main bulk of the superficially visible fibres run in a transverse direction ; the deeper parts are really the con- tinuation upwards of the medulla. The cells and fibres most essen- tially pontine are the following : — VIII DISEASES OF THE NERVOUS SYSTEM 251 Cells of Pons Groups round the central canal. Groups in the roof. > 0^ (/) SJ <« £ -S W ^ U <+5 U Fourth nerve. Third ,, (chief oculo-motor). Going to cerebrum and cere- bellum. Fibres of Pons Transverse. Oblique. Vertical or pyramidal. Transverse and oblique, passing in all direc- tions. g bo "^ o u OJ o o u Cerebellum. Cerebrum and cerebellum. Motor cortex of brain. Probably scattered through the whole cortex of cere- brum and cerebellum and formatio reticularis, and also basal ganglia. F. Cerebrum and Cerebellum. — In these organs the connections and arrangements of neurons attain their highest degree of com- plexity and obscurity. Some few we think we know, but of the vast majority our knowledge is practically nil. In the section on cerebral localisation more details of the anatomy and functions of the brain will have to be given. For our present purposes the fol- lowing table will be sufficient : — Cells of Cerebrum and Cerebellum Ascending frontal parietal and rest of motor cortex so called. Frontal lobes. y '^ Oh o U oj tfl Corona radiata, anterior two- thirds of posterior limb of internal capsule and pyra- midal tracts. Fibres running antero - pos- teriorly to opposite cerebellar lobes, and to the rest of cortex cerebri also. 252 DIFFERENTIAL DIAGNOSIS chap. Fibres of Cerebrum and Cerebellum Of frontal, occipital, and tempore - sphe- Convolutions of same noidal convolutions. w side and of opposite o «^ side (through corpus 2 vn callosum). .^ '?^ Convolutions of cere- u r* bellum. to of motor convolutions. -g bo Oray matter of cortex. of internal capsule. g c ... ^ r^ TO /^ Frontal cortex. of anterior limb. I -5 t;J I t,^ , ... I rt *" I Motor cortex. of posterior „ anterior two-thirds. V ^ \ r\ ■ •. ^ j^ .^ " . 1 • 1 "^ J Occipital andtemporo- of „ „ posterior one-third. I i, -j i i. " " -^ J \ sphenoidal cortex. Note. — Between the anterior and posterior roots of the spinal cord on the one hand, and the cerebral hemispheres on the other, there is a total decussation of impulses, if not of actual fibres. But such functions and anatomical connections as the cerebellum exerts on, and possesses with, the cord are apparently not crossed. After this brief dogmatic sketch of the structural connections of the nervous system, we must proceed to a similar tabulation of the — FUNCTIONS OF NERVE MATTER We will commence as before with The Neuron. 1. The Cell. — While there is still some dispute as to whether the cell possesses any function of a transforming or reinforcing character, there is unanimity in accepting a purely nutritive function as the chief, if not the only, function properly belonging to the cell. At any rate, it is a clinical fact that neuraxons, collaterals, and den- drites, and consequently the synapses of the dendrites, all undergo complete degeneration and death when separated from the neuron cell, or when the neuron cell itself is killed ; and nutritive disturb- ance of the cell is rapidly followed by similar changes in the other parts of a neuron, and structures (non-nervous, e.g. muscles) to which the nerves are distributed. 2. Neuraxons and Collaterals. — The only ascertained function of these parts of a neuron is to transmit unchanged along their length impulses derived, or started {a) from sources external to the body, including in this term food in the alimentary canal, and air and its impurities in the air passages, as well as stimuli applied to the skin, VIII DISEASES OF THE NERVOUS SYSTEM 253 etc., (fi) from the synapses with dendrites of other neurons. They are thus purely and absolutely analogous to telegraph wires, carrying to and from every structure of the body messages which result in the performance of every possible physiological process, whether motion, perception, nutrition, secretion, etc. 3. Deiidrites^ a?id Sy?iapses of Dendrites. — It is by these we now assume that impulses are transmitted from neuron to neuron, and transformed in character. It would seem as though the synapses afforded an opportunity for a sort of inductive action of neuron on neuron ; the actual resultant of any impulse from any source depending upon the inherent qualities of the neuron brought into induced action and its connections {a) with other neurons to which the impulse may be again transmitted, or (b) with terminal organs, muscle, gland cell, or other tissue capable of exhibiting a final resultant. Peripheral Nerves. — As these are simply neuron complexes, their functions in gross are those of their units; in detail they carry the impulses which eventuate in — A. — Movements in Voluntary Muscles which — In Health. Are possible to an amount known by experience to each indi- vidual ; are under the control of the will, and capable of co- ordination for any purpose. In Disease. Are weakened, or absent, or inco- ordinated. J Time or order. \Amount. Involuntary J Tonic, spasms. \ Clonic. In volition B. — Sensory Perceptions — A known experience of the indi- vidual, differing materially in different individuals. Excessive ^ Weakened Lost Delayed Perverted in [Temperature, -relation-! Pain, to [Touch, etc. C. — Reflex Processes^ any of which may incidentally affect consciousness and become a percept. They are divisible into three groups : — Group I. — Experimental, or acting through cutaneous external stimuli :— 254 Superficial — DIFFERENTIAL DIAGNOSIS CHAP. In Health. In Disease. Plantar, cremas- Present, but somewhat Obviously increased. teric, etc. variable in amount. ,, Absent. decreased. Deep — Knee jerk. Elbow jerk, etc. Present, but also some- Increased, diminished, what variable. absent. Group II. — Natural from the viscera with contents or condi- tion for stimulus, and involuntary movement or secretion, etc., as the resultant. Of these there must be very many, but in only a few cases and conditions are of much use to us clinically : — Those of bladder. ,, rectum. In Health. Co-ordinated for pur- poses of voluntary micturition and de- faecation. In Disease. Inco-ordinated, and often removed from voluntary control. Group III. — Vasomotor regulating the supply of blood to a part — In Health. In Disease. The essential point is the local control over This local control Is fre- local blood supply. quently lost or per- verted. D. Trophic Influences. — Clinical evidence, as well as experi- mental, tends to suggest that, besides the above noted trophic influence of the neuron cell on its own processes, there are influ- ences constantly ascending and descending peripheral nerves which are essential for the proper nutrition, growth and decay of the structures which, in their ordinary functions, are under the control of the nerves distributed to them — muscles, for instance, or sensory end organs, glands, etc. — and there is a certain amount of evidence to show that these influences are something active, liable to excess or perversion, as well as absence, for it is found that irritation or inflammation of nerve structures is more efl'ectual in producing destruction or degenerative effects than is mere section of a nerve trunk. Illustrations of trophic changes will be noted presently {vide p. 266). E. — Special Sense Nerve Phenomena and Mental Processes. — These VIII DISEASES OF THE NERVOUS SYSTEM 255 will be noted when the brain is under consideration. We may here merely mention — Sight ^ . ,, ^ ^. Hearing- ^ . And in disease may be increased, ° 1 prnitv in . ...... Taste r 111 perverted, or diminished. Smell ' '^'^^*- Spinal Cord. — To enumerate in detail the functions of the cord would in large measure be to repeat what we have said on peripheral nerves. Its cells are constantly engaged in the task of superintending the nutrition of peripheral nerves and other struc- tures, as well as of intracordal fibres or neurons, as has already been noted. The principal function of the cord, as a whole, is to act as a sort of subordinate office to the brain's head office, and by its complexes of neurons to arrange and co-ordinate impulses passing through it. Thus it is the final manager of efferent impulses to voluntary muscles arranging their order ; it is the primary manager of afferent impressions, enabling our minds to become precisely and accurately conscious of our environment ; and lastly, it possesses innumerable mechanisms for the perform- ance of reflex functions of all descriptions : and these may (a) be performed entirely by the cord without notification to the sensorium, or (^) cause such notification so that we perceive the reflex, but (c) they are always liable to control from the head office of the brain under all circumstances. Brain, or Encephalon. — As the seat of what is termed the mind, the encephalon remains the supreme governor and controller of every process going on in the body. It is the head office to which all information from every part must be sent, whether we are conscious of such information or not, and it retains to itself the power to intervene in and control everything, but allows generally to the cord a very large measure of home rule in those processes which are mainly concerned in the mere sustentation of the animal framework. Having thus considered anatomical structure and physiological function as separate entities, we have now to associate the two into mechanisms for purposes. This, even in the peripheral nerves, is not always a matter of mathematical precision; in the cord the difficulties become much greater, while in the brain they are as yet insurmountable except in a few special cases, and in a most general manner. We shall arrive at the most available certainty \\ith greatest clearness by taking functions and tracing their path- 256 DIFFERENTIAL DIAGNOSIS chap. ways ; the following tables are apparently reliable as far as our present knowledge goes, but being based upon clinical experience and experiment, are liable to some alteration as our knowledge grows in exactitude. Motor Tracts or Pathways of Voluntary Muscular Movements The nerve impulses are centrifugal ; so, taking the same course, we have — 1. Highest volitional, or will centres of doubtful locality, prob- ably (according to Hughlings Jackson) the cortex of the frontal lobes. 2. Rolandic region of cortex. 3. Corona radiata. 4. Anterior two-thirds of posterior limb of internal capsule. 5. Pyramidal tracts — {a) In crura cerebri. {d) In pons. {c) In medulla (including the decussation). {d) In cord (crossed and direct). 6. Cells of anterior cornua. 7. Peripheral motor nerves. 8. End plates. 9. Muscles. In any given voluntary movement the parts played by these various structures are as follows : — In (i). — The wish starts by psychological processes or influ- ences from without, and takes a less amorphic shape as nerve im- pulses, which pass along the processes of the neurons concerned ; by dendritic synapses these impulses are transmitted or passed on to the neurons of the rolandic region. In (2). — These physical impulses are marshalled and co-ordinated in a manner that may be compared to the first sorting of letters at the General Post Office into those for each sub-district or "route," and just as by arrangement letters can be sent by an alternative route, when one is blocked, with slight resultant confusion in their delivery, so by the dendritic synapses of innumerable cortical neurons can these impulses be transmitted by other than the usual path, with resultant delay or disturbance in movement. Herein lies VIII DISEASES OF THE NERVOUS SYSTEM 257 the commencement of the explanation of the common statement that " Movements and not muscles are represented in the cerebral cortex (and cord)." Each neuron of the rolandic cortex has to share in many movements, but never completely causes one ; hence slight cortical damage is likely to impair many movements, but not absolutely to paralyse any. From (2) impulses pass through (3), (4), and (5) in a compara- tively simple manner along the neuraxons, and break on the complicated synapses of their terminals with the dendritic com- mencements of (6). In (6), \Yith its connections, goes on the final sorting of impulses for delivery along the neuraxons of the appropriate members of (7); thus is completed the explanation of the statement inserted above relative to movements rather than muscles being represented in brain and cord. Along (7) messages are carried again in a very simple manner to reach (8) and (9), and produce in them appropriate reaction. For clinical diagnosis it is important to note the absolute inde- pendence of the nutrition and life of the neurons of (i), or level A, of (2) to (5), or level B, and of (6) to (9), or level C. A lesion of destructive character in level A leaves the mechanisms of levels B and C, qua a piece of machinery, quite untouched and ready to start and carry out co - ordinate movements, provided only that impulses can reach them somehow; and, similarly, B and C are nutri- tionally quite independent ; hence we find at the bedside that a paralysis due to lesion in level C is characterised by the flaccidity with rapid wasting of the affected muscles, and probably other trophic disturbances of the skin and its annexes. A paralysis due to a lesion in levels B or A is characterised by retention of the tone and of volume of the affected muscles, and absence of trophic disturb- ance of other structures. Sensory Tracts or Pathways of Afferent Impressions from without These impulses are centripetal, and hence we begin with — 1. Peripheral sensitised end organs in skin, muscle, or special • sense mechanisms (these are the best understood clini- cally and microscopically, but analogous nerve structures must exist in every tissue and gland of the body). 2. Sensory nerves of descriptive anatomy. s 2 58 DIFFERENTIAL DIAGNOSIS chap. 3. Cells in the ganglia on the posterior roots. 4. Posterior root of spinal nerve. 5. Posterior columns of cord, external and internal, and probably also Gowers' antero-lateral tract, and the direct cerebellar tracts. 6. Cells in funiculi gracilis, cuneatus, and rolandi, and also Clarke's column. 7. Cells and fibres in formatio reticularis and fillet of medulla and pons, tegmentum of crus cerebri, inferior peduncle of cerebellum, and the cortex of both cerebrum and cerebellum. With regard to the part played by these various structures in the perception of an external stimulus, we are very much more in the dark than is the case with the corresponding motor tracts ; but the following statements would appear to be justified : — In (i) the external impulse, whether of touch, temperature, pain, etc., is received and converted into what we can only call a common nerve impulse, which is then carried by way of (2), (4), and (5), as along telegraph wires, until it breaks on the dendritic synapses of the terminals of these, and thus can impress itself in some way on the terminals of the neurons in (6) and (7). It is commonly assumed and universally accepted as a legitimate deduction from experiment and clinical evidence that Nos. i, 2, 3, 4, and 5 form a lowest level or neuron complex, corresponding to the lowest level on the motor side, and that this lowest level is dependent for its nutrition on No. 3 ; the injury or destruction of which results in corresponding degeneration or destruction of the whole level. But after we leave this level precise knowledge ceases, and speculation reigns as to the number of serial neuron levels and as to the exact paths by which impulses reach the sensorium, and even as to the locality of the sensorium. And, again, as regards co-ordination of, or judgments upon external impressions, we only know that disease of the lowest level (as in tabes dorsalis) leads to great perversion of them ; e.g. a touch is referred to a totally wrong spot, but . we do not know whether this lowest level is the only co-ordinator of afferent impres- sions, or even if it is the chief one. Reflex Paths So far as is known, there are no special paths reserved entirely for reflexes; the impulses travel by the ordinary sensory and motor VIII DISEASES OF THE NERVOUS SYSTEM 259 nerves. We may, however, discuss a few points in this connection. For a reflex phenomenon we require a chain of structures which we may thus tabulate : — A sentient receptive surface or end organ on which the stimulus may act. An afferent nerve. A central connection of afferent and efferent mechan- isms. An efferent nerve. A terminal organ to exhibit the reflex, whatever its nature. Skin or external surface in the experimental class. Mucous membrane or epithelial cells in visceral class. Tissue elements (?) in vasomotor class. The ordinary afferent nerves of the organ or area in question. This, so far as we can judge, is not an organic or structural connection, but merely the functional synapses of the dendritic terminals of the re- spective sensory and motor neurons in the central system, allowing a transmission of impulse. The motor nerves of voluntary or involuntary muscles, corresponding to the class of reflex in question ; and nerves carrying efferent im- pulses for other organs. Voluntary muscles in Class I. Involuntary muscles, fibres, and epithelial cells of glands of viscera in Class II. Involuntary muscle fibre in arterial coats in Class III. For the reflex to take place it is essential that this chain should be complete in each link, and that there should be no strong in- hibitory influence at work capable of stopping the reflex. Class A. — The true or superficial reflexes m.ay occur from any area of skin or from the conjunctiva. Those most commonly looked for are : — Plantar, involving health of i, 2, and 3 sacral nerves and connections. Cremasteric „ „ i, 2, and 3 lumbar „ „ Abdominal „ ,, 8 to 12 dorsal and i lumbar „ „ Thoracic „ „ i to 8 dorsal „ „ Conjunctival „ „ 5 and 7 cranial „ „ but in special cases many others are looked for as indications of health or disease of specific nerves and segment of the cord. Of the so-called deep or tendon reflexes at knee, elbow, wrist, etc., we know that the path for them must, in some of its details, be different from that of the superficial ones, for the two 26o DIFFERENTIAL DIAGNOSIS CHAP. can vary independently of one another in degree ; the knee jerk, for example, is often absent, while the superficial reflexes of the leg are still obtainable. The knee jerk has been more fully studied than any of them, and about it we may make the following state- ments, with deductions : — It requires for its production — (i) A certain degree of myotatic irritability (Gowers) in the quadriceps extensor muscle. (2) The integrity of the third and fourth lumbar nerves, and their synapses in the cord. It is capable of being modified by influences from the en- cephalon, which influences are found to travel by the pyramidal tracts of fibres, and are believed to be of two kinds : {a) restraining from the cerebrum ; {d) reinforcing from the cerebellum (Jackson). As deductions from these premises — {a) Diminished cerebral control. {b) Increased cerebellar influence. {c) Increased irritability in some link of the spinal and peripheral chain. {a) Increased cerebral control. {I?) Diminished cerebellar influence. {c) Diminished irritability (or break) in some link of the spinal and peripheral chain. When the knee jerk is found to be materially altered in character from an average expected normal, we should try and estimate which of these influences is at work. The common clinical examples are : — Indicated by Apoplectic seizure of ordinary type. Increased knee jerk means Diminished or ab- sent knee jerk means Knee jerks increased from cause (a). of Paralysing lesion rolandic cortex, or internal capsule. Lateral sclerosis pri- mary. Old transverse myelitis above lumbar en- largement, causing, e.g., lateral sclerosis of lower part of cord. Chronic history of in- creasing weakness and jerkiness in walking. History of acute para- plegia. VIII DISEASES OF THE NERVOUS SYSTEM 261 From cause {b). From cause (r). Knee jerk diminished or absent from cause {a). From {b). From {c). Occasionally apparent- ly in cerebellar tu- mour, causing more irritation than de- struction. Peripheral neuritis in early stages. Occasionally apparent- ly in tumour of cere- brum. Meningitis, vertical and even basic. In shock their absence is probably partly thus explained; gen- eral paralysis of in- sane in later stages. Occasionally apparent- ly in abscess and tumours that have destroyed some parts of cerebellum. Peripheral neuritiSjlater stages, acute or chronic anterior po- liomyelitis. Tabes dorsalis. Pseudo - hypertrophic paralysis. Myelitis of lumbar region. Indicated by Headache, vomiting, and optic neuritis. Pins and needles, and weakness. Headache, vomiting, optic neuritis, etc., Jacksonian epilepsy. Pyrexia with cerebral symptoms. Mental features. As above. Rapid or chronic wast- ing of muscles with R.D. Lightning pains; Arg}'ll Robertson pupils, etc. IMethod of getting up from the floor. Acute paraplegia. In some of the above cases the meaning of the alteration is fairly clear and definite, but it must be confessed that in tumours and in inflammation within the cranium neither the result nor its cause is always very obvious. In epilepsy, again, the frequent absence, and in general paralysis of the insane the frequent exaggeration, are not at once readily explicable ; in hysteria the knee jerks are very variable, and I have, I believe, found them absent in an otherwise perfectly healthy individual. Class B. — Visceral. For the bladder and rectum (it would seem probable also that the rest of the alimentary tract and other 262 DIFFERENTIAL DIAGNOSIS CHAP. viscera are under similar control by means of the appropriate sym- pathetic and ordinary nerves) it is assumed, with great probability, I^olanpic vtotor area Voluntary abdovi. muscles Diagram to represent nerve impulses concerned in normal micturition. that in the lumbar enlargement of the cord the synapses of the sensory and motor neurons of the lower sacral nerves (probably) are so arranged that afferent impulses, started by the condition or VIII DISEASES OF THE NERVOUS SYSTEM 263 contents of the viscus, on reaching the cord can, and do in health, diverge in three directions : one impulse or message goes by cither the posterior or anterolateral ascending columns of the cord to the sensorium, and there produces by appropriate synapses a wish to micturate or defcecate ; following this message to its termination, and supposing the nervous system is quite intact, the desire can result in restraint of the act or in the act itself, according as circum- stances of a social nature are unfavourable or the reverse ; the former being one illustration of inhibition {vide p. 267). In either case the messages (though of different import) pass down the pyramidal tracts (?) to the appropriate cells of the anterior cornua, and thence by peripheral neurons (i) to the voluntary abdominal muscles, (2) to the sphincter, and (3) to the detrusor musculature of the bladder, in- fluencing them in a manner appropriate to the control or permission of the act. The second and third divisions of the afferent message are, as it were, short circuited, passing simply into the cord by the posterior roots and immediately becoming transmitted by synapses to the efferent neurons controlling the sphincter and detrusor muscles of the bladder, and causing action or inaction of those muscles respectively. It is by this short circuit that micturition and defaecation are provided for in the absence of consciousness. A diagram shows this somewhat complicated description very simply. Theoretically, then, it is possible for the acts to be interfered with by lesions in any part of this course, but clinically such interferences may be reduced to one of four categories, which, with the possible explanation in each case, may be thus stated : — I. Retention of urine, distension of the bladder, with overflow and consequent constant dribbling. This is perhaps the commonest form, and is found under many widely different clinical circum- stances. Its possibility is due essentially to the fact that the sphincter fibres of the bladder are more powerful than the detrusor fibres. It occurs in — {a) Parturition, es- Probably then due to a spasm of the sphincter, pecially primi- produced locally by irritative prolonged pres- parae. sure of foetus. {p) Operative pro- Probably due to intense reflex stimulus of unusual cedures about character through tinusiial channels, leading to perineum, etc. spasm of sphincter. [c) Tabes dorsalis Probably due to an inability of afferent messages occasionally. to reach the efferent neurons with sufficient energy. 264 DIFFERENTIAL DIAGNOSIS CHAP. {d) Senile and other mental condi- tions, especially so-called hy- sterical. [e) Enlarged pro- state and stric- ture, etc. Probably the original fault lay with highest will centres in checking the voluntary act from deliberate motive ; this was followed by blunting of sensorium, while the sphincter still retained its ascendency in physical power. Difficulties probably purely mechanical and not nervous at all, except that habit blunts the sensory terminals in the bladder. 2. Complete incontinence, bladder never full, urine constantly dribbling as fast as it reaches the bladder. Indicates essentially a paralysis of the sphincter fibres. This form is rarely found except in — Acute transverse Due to destruction of the motor efferent neurons, myelitis of lum- and consequent absolute sphincter paralysis, so bar enlarge - that gravity causes the escape of urine, ment. It is a curious, but very important fact, that such absolute in- continence is never found in purely functional peripheral troubles, and only as the rarest of curiosities even in organic definite peripheral neuritis. 3. A co-ordinated more or less normally complete emptying of the bladder without the intervention of the will or of consciousness. The occurrence of this form essentially indicates that the lumbar (sphincter and detrusor) centres are intact with all their reflex mechanisms, and proves to a demonstration that the higher centres are not essential for the act, but that the lumbar cord is quite competent when necessary to control the entire proceeding. It occurs pretty frequently, e.g. in : — {a) Nocturnal incon- tinence in chil- dren (enuresis). (Ji) Transverse mye- litis above the lumbar enlarge- ment. {c) Tumours and other forms of pressure, caus- ing paraplegia. May indicate unusually powerful stimuli (stone, hyperacidity, etc.), or undue irritability of the local nervous mechanism. Here it is a localising indication of the position of the lesion, and is of considerable value as indicating that the mischief has not reached the lumbar cord. Again a localising symptom of some importance. 4. Slighter degrees of interference with co-ordinate micturition. VIII DISEASES OF THE NERVOUS SYSTEM 265 These form rather a heterogeneous group of cases in their outward manifestations. It includes : — Probably due to irregularity in arrangement and arrival of reflex messages on the afferent side. Probably the messages on the afferent side are abnormal in their meaning ; possibly also there may be local irritation of sphincter, so that distension with overflow may result. Indicates merely a little weakness of sphincter. Probably only indicate the great intensity of natural stimuli, the nervous mechanism being intact. id) Tabes dorsalis with what is termed stam- mering blad- der ; may be present in other forms of sclero- sis of cord. {p) Temporary re- tention in spas- modic stricture, stone, etc. {c) Discharge of ur- ine on cough- ing, especially in women. id) Strangury and frequent mictu- rition of cystitis or of enlarged prostate at night. Although we have thus dealt at length with the bladder only, it is extremely probable that defaecation is under precisely similar control, and worked by precisely similar mechanism j but the clinical manifestations of its pathological performance are not so marked, nor so easily followed in detail. This is no doubt due in part to the greater capacity and distensibility of the colon, which acts towards the sphincter ani, like the body of the bladder to its sphincter ; but chiefly to the fact that the bladder is being constantly filled with a fluid secretion, while the rectum is being intermittently filled with a (more or less) solid material; a few doses of saline aperient will render the likenesses in action more apparent. Class C. — Vasomotor reflexes. Of the nerves and paths by which these pass we are profoundly ignorant, except that they seem to run in the so-called sympathetic chain, and to pass to and from the cord with the anterior roots. We recognise the loss of vaso- motor control in paralysed limbs and under many other conditions, but we are not able to make much clinical use of our observations as regards localising indications. 266 ' DIFFERENTIAL DIAGNOSIS chap. From the fact that all reflexes may in health or disease be attended with sensory perception of their occurrence, it follows as a legitimate, and indeed inevitable deduction, that the path of the afferent impulse must have at least two dendritic connections in the spinal cord or central system : one with the appropriate motor neuron, and the other with those neurons which ultimately conduct an impression to the sensorium. An anatomical basis has been discovered for this deduction in the division of all afferent nerves into two branches — one going towards motor neurons, and one continuing in the direction of the sensorium. Seat and Paths of Trophic Influences But little can be said on this head beyond what has already been noted in the general description of a neuron and the functions of its component parts. It would appear that for the perfect nutri- tion of all structures they must have a perfect connection with a (at least one, and probably several) neuron cell, the physiological health of which they equally enjoy ; failing with it, and recuperating too with it. Obviously the most simple and uncomplicated evidence of this probable connection is most likely to be found and established in the case of the peripheral neurons of the limbs, the dendritic synapses and relationships of which are fairly well understood ; and the following clinical examples go far to establishing the general proof of the theory : — 1. The rapid atrophy of the corresponding motor nerves and muscles (or parts of muscles) after complete destruction of all (or some) of the cells of the anterior cornua. 2. The defective growth of all parts of a limb that has been in childhood severely paralysed by anterior poliomyelitis. 3. The changes in the skin and annexa when the sensory nerves or cells on the posterior roots are damaged. 4. The mysteriously rapid onset of bed sores from very slight causes (pressure, warmth, etc.) in many cases of acute myelitis. 5. The equally malignant cystitis and renal trouble that so frequently accelerates or causes death in similar cases of myelitis, notwithstanding most rigorous asepticism in artificial emptying of the bladder. 6. Certain very suggestive dystrophies after experimental divi- sion of nerves, e.g. the fifth cranial, etc. VIII DISEASES OF THE NERVOUS SYSTEM 267 Special Sense Tracts The olfactory, optic, auditory, and glosso-pharyngeal nerves require only to be mentioned here. Their connections will be better studied when dealing with the principles of brain localisation {vide Cranial Nerves, p. 303). These facts of anatomy and associated function form the main foundation upon which are laid the principles of differential diagnosis of nervous diseases ; but before proceeding to construct tables from them, there are a few general points and terms to which attention must first be directed. Inhibition and Interference By these terms are understood the power which one neuron or group of neurons possesses of so influencing another neuron or group as to check or interfere with in any direction the function which the second mechanism intrinsically possesses. This power may be exercised either voluntarily through the will, of which our daily actions are almost one continuous example, or it may be, and probably is, the inherent function of large numbers of neuron com- plexes which may thus act without any effect on consciousness, the most constantly occurring clinical example of which is the hy- pothecated influence of the cerebral and cerebellar cortex on spinal reflexes \ the former being supposed to check them, the latter to increase them. Inhibition and interference constitute almost insuperable diffi- culties in the w^ay of drawing satisfactory and conclusive deductions from the experimental destruction of limited areas of nerve tissue in cord or brain. Direct and Indirect Symptoms By direct symptoms are understood those negative or positive morbid phenomena, directly appreciable by the observer, which arise as the direct result of destruction or irritation of a certain group of fibres with known definite function, e.g. blindness from laceration of optic nerve, noises from irritation of the auditory nerve, paralysis from the destruction of the pyramidal tracts, etc. Indirect symptoms, as the term is used clinically, are really of two kinds : {a) those which must be assumed to exist as the plainest corollary from the hypothesis of inhibition and interference, and 268 DIFFERENTIAL DIAGNOSIS chap. may be of a positive or negative character, e.g. increased knee jerk from destruction of brain areas ; or diminished knee jerk from irritation of similar areas ; {f) those which might perhaps be more properly spoken of as temporary symptoms, in that they are the result of mere increase of pressure which is often capable of removal ; examples of which are very common in tumours of the brain or pons, and haemorrhage anywhere into the central nervous system or its containing cavity. These pressure symptoms must be allowed to subside in acute (haemorrhagic probably, or inflammatory) lesions before an exact diagnosis is possible ; and in more chronic cases of tumour their possible presence and significance must be very carefully considered. Inco-ordination For every movement, whether voluntary or reflex, at least two (and often many more) muscles or groups of muscle fibres are called into action ; and in order that the movement may be co-ordinated these several muscles must all act in harmonious relationship to each other (i) in time, (2) in amount, i.e. if one of the muscles con- cerned acts out of its turn, or with a force disproportionate to that exerted by the other muscles concerned, the movement will become disorderly, inco-ordinate, and even perhaps inadequate to its avowed object. Now, by arguments which cannot be introduced here, it is proved that afferent impulses from the muscles to the cerebrum and cerebellum (not necessarily, and in fact not usually, causing a con- scious perception) are as important for co-ordination as are the motor or efferent impulses to the muscles ; and in fact clinical experience almost allows the deduction that if inco-ordination of voluntary movement be present there is a lesion of afferent tracts either of the ordinary class or of the special senses ; disseminated sclerosis being almost the only exception, and even here it is assumed rather than proved that the inco-ordination arises from delay in the transmission of motor, and not afferent impulses. It is more commonly complained of in walking (giddiness or stumbling) than in other actions, because this requires very complicated and delicate adjustments of very many muscles, but clinical examination very frequently reveals much that is not complained of by the patient. The following are the principal clinical causes of inco- ordination, and the leading indications pointing to the probable diagnosis. VIII DISEASES OF THE NERVOUS SYSTEM 269 Cause. Peripheral neuritis. Affections of pos- terior columns (? of antero-lateral ascending tracts too). Cerebellar or cere- bral disease. False optical impres- sions. Alcohol or other general action on the sensorium. Leading Features. "Pins and needles," and other sensation abnormali- ties and weakness complained of; skin dystrophy or anaesthetic patches ; knee jerks increased or absent ; inco-ordination made worse by closing the eyes. Histor}'- of lightning pains ; knee jerks absent ; inco-ordination worse on closing the eyes. Very possibly severe headaches or optic neuritis if a tumour ; if other trouble of chronic nature history clears up the cause ; closure of eyes not likely to make matters worse, because inco- ordination is central. A squint, found by appropriate tests ; inco-ordina- tion iinproved by closure of the affected eye, or of one if both are affected, because this at once stops the wrong perceptions. History generally obvious ; there are also mental alterations, marked in directions other than that of co-ordination of movement \ effect of closure of eyes variable. Reaction of Degeneration By this term is understood those peculiar changes in the elec- trical reactions of a 77iuscle which are produced in it by the death of the peripheral neurons distributed to it. They are of two kinds — quantitative and qualitative. The essential points to be remembered about R.D. are : — I. It is a phenomenon of muscle only (nerves simply lose irri- tability rapidly after severance from their nutritive cells). It always indicates that the peripheral neuron going to the muscle fibre is dead or dying. It is a phenomenon exhibited by each muscle fibril, and consequently is only exhibited in a simple and typical manner when at least a large majority of the individual • neurons going to a gross anatomical muscle are affected ; thus is explained its common absence in typical form in some cases of progressive muscular atrophy, and other slowly progressive neuron destructions. 2 70 DIFFERENTIAL DIAGNOSIS chap. 4. The quantitative element may be thus represented : — 1st Period. 2nd Period. 3rd Period. 4th Period. c - C normal or + C + + C-o F - F - F - F-o where C and F represent irritability to the constant and Faradic currents respectively, and period roughly represents a week or ten days or less. The qualitative element is that — fKCC. fACC. The natural A.C.C. , K.C.C. A O r becomes order of K.O.C. K.O.C. A.O.C. during the first two or three periods, but when C and F both become diminished — as between the 3rd and 4th periods — the above change may occur without our being able to make the definite statement that R.D. is present. Section II. — Diseases of Nervous System Proceeding now to consider pathological diagnosis, it will conduce to clearer views of analysis if we insert a — Tabular View of the Causes of Diseases of the Nervous System 1 . Traumatism. Recent. History obvious. Past. May lead to secondary changes of sclerosing or neo- plastic nature. 2. Vascular Disturbances^ with Probable Post-Mortem Eviaence. A. Inflammation.! (I) Primary of nerve -| Cerebritis. Structures, with I ,^ ,. . r ■, • J J > Myehtis of cord, rapid deg-enera- i ,. . . ^. J S • \ Neuritis, pohomyehtis, etc. tion and softening, y '^ ^ ' * The term " inflammation" is used here as the most convenient, because long- established, to express the fact of an acute and very rapid destructive degeneration of neuron cells or processes, or both, which may, however, and often does, occux" with- out very obvious changes in the blood-vessels of the area. VIII DISEASES OF THE NERVOUS SYSTEM 271 (2) Primary of intersti- tial or meningeal origin, extending to nerve struc- tures. B. Haemorrhage. C. Plugging of a Vessel. (i) Embolic. (2) Thrombotic. 3. Tumours. Malignant, carcinoma and sarcoma. Simple connective tissue type. Tubercular. Syphilitic. Abscesses, i.e. cysts of inflam- matory origin. Cysts of non - inflammatory origin. 4. Scleroses. Primary. i Meningitis. I Perineuritis. Vascular degeneration. Aneurysms. Septic arteritis. From cardiac valves, aorta, etc. From endarteritis obliterans, syphilis, tubercle, etc. All primarily irritants, and later \ destructive by pressure or by invasion of nerve fibres. Either of a distinct system, e.g. pyramidal tracts, or of quasi- accidental patches. Secondary. Following destruction or separa- tion of processes from the neuron cells by any means whatever, e.g. lateral sclerosis after cerebral destruction. 5. Nutritional Disturbances. — A group of cases more easily com- prehended by the imagination than defined in words. It is usually intended to include hysterical and other cases in which recovery is (usually) complete and (not unfrequently) very rapid. They probably all have as their essential foundation a primary lowering of the vitality of a neuron, with loosening of its synapses with other neurons, thus interfering with the transmission of impulses. It is obvious that if this process goes beyond a mere chemical or molecular disturbance the case may soon have to be put in some organic degenerative group. Any of these pathological changes 77iay occur anywhere through- out the nervous system, but each one has its seat of election, and hence, when the locality of a lesion in any case is settled, we are often cariied very far in the direction of a diagnosis of its nature, 272 DIFFERENTIAL DIAGNOSIS CHAP. and vice versa. The history of the onset is such an important factor in the diagnosis of the nature of a nerve lesion as to necessitate the insertion of the following table, copied from Sir W. Gowers : — Disease. Onset. Sudden, Acute J few minutes, traumatism. \ Acute, (^ few hours or days. Sub-acute, one to six weeks. Sub-chronic, , six weeks to six months, growths. I ^, ^ I Chronic, over six months. Pressure and Disease. Vascular lesion. ► Inflammation. Degeneration or scleroses. An occasional exception may occur, the most important of which is the suddenness with which tumours may now and again cause symptoms either by haemorrhage taking place into them when otherwise quiescent, or by some slight mechanical alteration in the relation of parts when tumour is present. Section III. — Differential Diagnosis of Nervous Diseases With this introductory outline of the structure, functions, and general phenomena of the nervous system, and of its disturbances, we may proceed to the more specialised differential diagnosis of nervous diseases. The first point in the precise diagnosis of an apparently nervous group of symptoms must be the determination as to whether the symptoms are primarily and essentially caused by an actual lesion (organic or nutritional — Gowers) of the nervous system, or whether they are secondarily, i.e. purely reflexly, connected therewith, due to pyrexia, for example, or local disease of other organs. To exhaust from this point of view in tabular form the differen- tiation of all the varied phenomena of disease would be confusing and unpractical, if not even impossible, considering that it is only through our nerve structures that we are made conscious of, and adapted to, all the variations of our environment, both local and general, and that the co-ordinate or harmonious working of each and every organ throughout the body is possible. VIII DISEASES OF THE NERVOUS SYSTEM 273 The following table, then, is but the veriest fragment of an outline of the subject, inserted more for logical completeness of the ideal object of this book than for serious practical utility, though I have endeavoured to make it serviceable as well. Chronic and Sub-Chronic Symptom Groups If Caused by Essential Affection of Nervous System. Absence of obvious primary peripheral local disease ; es- pecially examine blood and urine and pelvic organs. Motor complaints largely in the ascendent ; weakness and loss of power in limbs or unsteadi- ness ; movement or its loss rarely associated with pain. Sensory complaints often also prominent ; usually numbness or parsesthesise, if painful most likely of a neuralgic, i.e. inter- mittent and shooting character, or without obvious objective causation. Complaints of vague alterations from the usual harmonious ease of the acts of micturition and defaecation. 5. Insidious onset, very variable progression, and unlimited chro- nicity. 6. Reflexes probably altered. If Secondarily or Reflexly Nervous. :. Such disease is present; cau- tio?i — secondary trophic lesions not to be mistaken for pri- mary. ;. Such complaints absent, except with obvious disease of muscles or alteration in outline of joints or limbs : gout, rheumatism, epiphysitis, etc. (. Such complaints practically only of a painful nature, and frequently with obvious causa- tion, e.g. chronic pleurisy, cold, abscesses, etc. 4. Complaints about these acts usually of a straightforward difficulty in act, or definite alteration in frequency, e.g. stricture, enlarged prostate, etc. 5. Onset fairly marked, progress more uniform and chronicity limited, e.g. rheumatoid arth- ritis, chronic Bright's disease, etc. 6. Reflexes probably unaltered. Comments on the Table, and Additional Remarks I. The examination of blood and urine are expressly mentioned to avoid the mistaking for primary nervous affections the numerous vague and obscure secondary phenomena that occur in anaemia and other primary blood dyscrasiae, and are the prominent symptoms of chronic and even acute uraemia. A careful examination of the T 274 DIFFERENTIAL DIAGNOSIS CHAP. pelvic organs will often reveal a very substantial cause (neoplasm, parametritis, etc.) for a puzzling sciatica. 2, In children, and even sometimes in adults, it is difficult to distinguish between the refusal to move a limb or part because such movement causes pain (pseudo-paralysis) and the incapability of such movement ; the effect of passive movement painful in the former, not in the latter, is the simplest test, and usually sufficient. Other cases in which movement causes exaggeration of already present pain will be referred to in various places where the fact is of use in separating individual complaints. Inco-ordination of movements, and tremors on effort, are very suggestive of primary nerve lesions, the various forms of Grave's disease being the chief fallacy. General convulsions and local spasmodic twitchings of muscles constitute evidence of such importance as to require separate con- sideration. Vomiting, if reflex from nerve lesions, is usually paroxysmal, very persistent during a paroxysm, and not accompanied by much nausea as a rule ; it may be excited by food, but occurs equally independent of it {vide p. 158). Mental changes, except when accompanied by pyrexia, are almost always indicative of an essential nerve lesion, most commonly of the nutritional type when the symptom is primary ; when it is secondary to some organic destruction its cause is usually fairly obvious. Wasting, if general, rarely points to organic disease of the nervous system ; but if local, it becomes very suggestive of such a causation {vide p. 252). Acute and Sub-Acute Symptom Groups :1 V^^ S rt o "3 o >H g kI P-i a rt o rt o If Caused by Essential Affection of Nervous System. 1. Pathological activity, or pos- sibly inactivity of nerves (headache, pain, spasm, de- lirium, etc.), out of propor- tion to the degree of fever, and not necessarily abating with defervescence. 2. Rapid onset of actual loss of function of nerves — paralysis, anaesthesia, etc. a. \ If Secondarily or Reflexly Nervous. This activity or its re- verse is more or less proportional to the fever ; usually abates with it. No paralysis, or if so, it is pseudo-paralysis. VIII DISEASES OF THE NERVOUS SYSTEM 275 On this tabular differential diagnosis of acute symptom complexes it is only necessary to remark that there are but few general points that can be utilised for the purpose. In the cases in which the greatest difficulties and the most serious mistakes are likely to occur the differential points are rather special than general, and consequently the diagnosis ^^'ill be found in special tables; vide — Meningitis v. Pneumonia, pp. 95 and 96. Tubercular Meningitis v. Gastritis, pp. 159 and 160. Infantile Paralysis v. The Exanthemata, p. 292. Acute Mania v. Delirium Tremens. Organic v. Functional Lesions We may now continue with general differential diagnosis, on the assumption that the case before us is really and essentially nervous. The next point to determine is whether it be organic or functional. Even in an elementary work it is impossible to avoid glancing at a definition of these terms. The difficulties in the way of an accurate investigation of the microscopical details of the (whole of the) nervous system have hitherto been so great as to practically prevent a final decision of the question, "Is the picture of structure normal or abnormal, physiological or pathological ? " and then of the question, " Did the ill-regulation of function during life depend upon the peculiarities of structure which have been noted ? " As modern methods of microscopical technique (hardening, preserving, staining, etc.) become more and more perfect, we are coming more and more to the conclusion that a final answer can be given to the first of these questions, and probably, in consequence, to the second, so that the field of genuine functional diseases is rapidly becoming more and more restricted. Theoretically, we can conceive that a piece of living m.achinery that was originally (in congenital troubles the same argument applies to the development of structure) capable of carrying out its due function properly and in harmony with the functions of other nervous complexes may work improperly or inharmoniously ( = disease) by assuming (i) that its structure has got damaged, or (2) that its supply of nutriment is faulty (excessive, inadequate, or deleterious), or (3) that it individually is suffering from wrong con- trol (imperfect, excessive, or perverted) by other "centres." The last two would correspond to functional, the first to structural, 276 DIFFERENTIAL DIAGNOSIS chap. disease; but it is very easy to see that what was at first purely functional, qua a given "centre," may readily result in organic destruction if the untoward influences persist. As common examples of diseases which are at present frequently thought of as functional, and illustrating the above theory, I would mention — Epilepsy. — Due primarily to a fine (some day, I believe, to be definitely described) organic change in structure of a centre or centres, kept up or made worse by improper nutriment. Witness the bad influence of some diets (meat) on epileptics. Hysteria and Neurasthenia. — Due primarily to imperfect nutrition of higher centres, and then a consequent loss of control of these over lower centres which exhibit the symptoms. (Some cases are very close to deliberate malingering.) Neuralgias. — Often due to organic (inflammatory) changes, but strictly to improper nutrition. Delirium and other Pheiiomena of Fevers and of Apyrexial Toxcemia. — Due at once and essentially to deleterious substances supplied to the nerve, often ending in definite structural trouble. (Witness diphtheria, influenza, etc.) Manias and Permanent Menial Obliquities. — In causation closely allied to the temporary troubles of fevers, etc. ; but more frequently the cause ends in fine microscopical changes, which are already being investigated with success. Occupation Neuroses. — Essentially due to overwork, which in turn leads to, or is associated with, imperfect nutrition by excess of waste products. (These cases are very often ones of definite neuritis.) Minor Symptoms of Diseases of Brain. — Are in themselves nothing but functional, and are illustrations of perverted control. Typical examples are alteration of reflexes, disturbances of visceral functions, etc. Considering the very small capability of repair possessed by the nervous system when once a cell has been damaged, it would seem almost suflScient to define organic as that which is incapable, functional as that which is capable, of repair. Excepting inflamma- tory troubles, this is very nearly my meaning in what follows. Most commonly the point will be obvious from the general aspect and history of the patient, but in cases of doubt the follow- ing table will assist us : — VIII DISEASES OF THE NERVOUS SYSTEM 277 Organic. Onset. If sudden, usually the symptoms are fairly definite and local- ising. If chronic, it is still usually fairly constant in character, and con- sistent in progress. Motor Symptoms. Pa?'alysis. — Far and away the most common result ; if flaccid it is rapidly followed by R.D. ; in all cases its distribution is in accordance with known anatomical structure, and ob- jective signs may frequently be found when due to lower level lesions ; constant in posi- tion when once apparent, at least does not dodge from limb to limb ; may be incom- plete. Spasm. — Rarely due to organic lesion except in Jacksonian epilepsy and the convulsions of meningitis; may occur during sleep; when organic usually a definite known causa- tion in history. Sensory Symptoms. Not common as the sole com- plaint ; if it is the only com- plaint it is usually definite and localising. Reflexes. Experimental. — Most usually definitely and permanently altered, and in a constant direction for the individual case. Functional. If sudden, it is less definitely local- ising, and symptoms more vague, frequently prominently mental. If chronic, it is very inconstant in features, and inconsistent in pro- gress. Also tolerably common, but even if flaccid, R.D. never develops ; in most cases it is apparently due to lower level lesion, and yet no objective signs to be found ; its distribution varies from time to time ; usually complete in the member complained of. Verycommon; usually ceases during sleep ; no ascertainable cause in the history. Often enough the sole complaint, indefinite and non - localising ; definite hemianaesthesia will be unassociated with any features pointing to organic brain trouble, e.g. hemiplegia or unconscious- ness at onset. Variable in diflferent cases which are otherwise similar, and also in the same case from day to day. 278 DIFFERENTIAL DIAGNOSIS CHAP. Organic. Visceral. — Micturition and defas- cation often seriously affected, as also many other visceral functions. Vascular. — Often loss of vaso- motor control, limbs cold, and circulation too easily influ- enced by local conditions ; may cause serious anxiety. Mental Changes. When present usually persistent, and are associated with other definite indications of organic trouble. Total Aspect and Course. Constant. Consistent. Definite. Functional. Rarely or never serious visceral mischief, but there may be troublesome retention of urine. Such loss of control only shows itself in turgescent directions (factitious urticaria, e.g.)^ or very temporary coldness and white- ness : never looks serious. Characteristically variable, and present before illness, or at least not directly caused by it ; unas- sociated with other definitive in- dications. Inconstant. Inconsistent. Indefinite. The mimicry of organic disease by functional changes is, how- ever, sometimes so complete and so intricate that further details can only be given in special cases. Assuming that we have determined the case to be one of organic disease, one of the first questions that requires an answer will be — "Is it of the brain or encephalic structures, or is it of the cord (in- cluding medulla) or periphery ? " The clearest method of reply is to divide all cases into two categories: (i) acute, a week or less; (2) chronic, a month or over. A. — Acute Nervous Lesions Before deciding as to an apparently acute case it is exceedingly important to make inquiries into the previous history of the patient, because the following acute incidents in chronic diseases may mis- lead us : — Fits in epilepsy. „ general paralysis of the insane. „ chronic poisoning (alcohol, lead, etc.). cerebral tumours. VIII DISEASES OF THE NERVOUS SYSTEM 279 Crises in tabes dorsalis. Acute features in chronic spinal caries. „ „ ear disease, etc. ,, ,, meningitis. Excluding such cases, the following points are most important : — Onset. Consciousness. Motor Symptoms. Cranial Ne? ves. Paralysis or paresis or excessive move- ment. Sensory Symptoms. Reflexes. Intracranial. Very sudden onset is extremely common. Very often interfered with in some degree. Often implicated some degree. m Almost invariably on one side ; if on both, nearly sure to be much interference with consciousness or with cranial nerves, as in ven- tri cular h asmorrhage or pontine lesions. Comparatively rare alone ; if present, they are of the hemi- type. Of eye frequently lost. Knee jerk frequently altered on one side Cord and some Peri- pheral Lesions. Such suddenness is rare. Practically never inter- fered with. Rarely or never impli- cated, unless it be as regards the dila- tion of pupil, and in post - diphtheritic paralysis. Almost invariably on both sides, owing to nearness of the two sides in the cord, and to the sym- metry of peripheral nerves in liability to poisoning ; area of disturbance very small if one-sided. Very common indeed, and of the para- type; because motor and sensory tracts are so close together in cord, and both have a nearly equal tendency to suffer in poisoning (? except diphtheria). Of eye lost sometimes in lesions high up in cord. Frequently altered, but more probably on 28o DIFFERENTIAL DIAGNOSIS CHAP. Intracranial. only, unless great excess of intracra- nial pressure. Bladder and rectum rarely affected, un- less consciousness is much interfered with. Cord and some Peri- pheral Lesions. both sides, and that without evidence of intracranial pres- sure. Bladder and rectum often interfered with in acute cord lesions, and that without interference with mental clearness. If the case be a less acute one (over a month), and seems to be stationary or progressing, the following table may be constructed : — B. — Chronic Nerve Lesions Intracranial. v. History. More frequently a history of an acute attack or attacks, and if such be the case, symptoms very possibly stationary or improving ; tumours the great excep- tion. Motor Symptoms. Jacksonian epilepsy {q.v.) common enough. One side most likely alone affected. Cranial motor nerves often affected. Sensory Symptoms. Again one-sided and cranial ; "pins and needles," and other parsesthesias, if pre- sent, are of one arm or leg, or one side. Extracranial. Less frequently such history with stationary symptoms ; the symp- toms are likely to be progressing, except in cases of definite myelitis. Such uncontrollable movements only take the shape of twitching in legs or arms. Both sides most often affected. Cranial nerves rarely affected except in disseminated sclerosis and in tabes dorsalis, in both of which the lesion may extend to encephalic centres. Both sides, and not cranial ; " pins and needles," if symmetrical, almost pathognomonic of a peripheral lesion ; sensory disturbances in cord troubles nearly sure to be acutely painful or completely anaesthetic. VIII DISEASES OF THE NERVOUS SYSTEM 281 Intracranial. v. Extracranial. Reflexes. Often one-sided change ; if Equally affected, and that without both sides, nearly certain mental symptoms, to have cranial nerves affected, or mental symp- toms. Mental Changes Common. Never present in a purely cordal lesion, or in one of peripheral nerves. It is impossible to pursue the plan of general tables for differ- ential diagnosis farther, owing to the mass of details necessary for complete diagnosis, which w^ould be quite irrelevant in many in- dividual diseases. We must now proceed to consider the separate affections, with tables to differentiate those which are more nearly similar. Peripheral Neuritis The existence of lesions of the peripheral nerves, independent of trouble in the cord and brain, has only been determined within quite a recent period ; consequently, the first and commonest diffi- culty in their diagnosis arises from a want of famiHarity, not with cases of the disease itself, for they are only too frequent, but with the idea of its existence ; and non-acquaintance has, as its natural corollary, non-recognition. It may be laid down as a law that — " In the gross total of nervous diseases peripheral neuritis, in some one of its many forms, is exceedingly common, and its possible presence must always be borne in mind." Now, how — in what connections — does it occur, and what are its prominent features ? As far as diagnosis is concerned, it occurs in two fairly distinct forms : — {a) More or less localised to individual-named nerves and their branches ; a search along which will often reveal the cause of the trouble, e.g. a septic wound or tumour causing pressure, though it must not be forgotten that general constitutional poisons, such as rheumatism, gout, or lead, may, and often do, produce such local asymmetrical affections. {b) More universal affection of a large number of nerves (multiple neuritis of authors), almost invariably due to a poison carried by the blood, e.g. alcohol, etc., and almost invariably sym- metrical. 282 DIFFERENTIAL DIAGNOSIS chap. It is rather a peculiarity of peripheral nerve troubles that they are often either of sensory or of motor nerves only, a point apt to be overlooked ; but mixed cases, both sensory and motor, are per- haps more commonly met with. The prominent symptoms are the following : — 1. Motor Side. — Weakness and wasting of muscles, -^ith.Jlacdd paralysis, and possibly R.D. ; certainly R.D. if the case is severe, because the peripheral neuron is the main channel by which nutri- tion of terminal organs is maintained. 2. Sensopy Side. — The inflammation acts as an irritant of the peripheral sensory neuron, possibly proceeding even to complete destruction of function ; hence we get — (a) " Pins and needles " and numbness. If these are well marked and persistent, and on both sides, they are almost, if not quite, pathognomonic of a peripheral lesion. (p) Pain and hyperaesthesia in the known area of distribution of certain sensory nerves. {c) Anaesthetic patches. These require to be looked for, as the patient has very probably not appreciated their pre- sence. Possibly these anaesthetic regions or areas may be the alleged seat of painful sensations — paradoxical or painful anaesthesia. 3. Reflex Side. — Experimental reflexes, especially the knee jerk, either grossly exaggerated (in early stages), or more probably absent ; visceral reflexes are almost universally unaffected, so that serious disturbance of micturition or defaecation is practically con- clusive proof that the cord or brain is affected. 4. Trophic Side. — Muscles waste rapidly {vide Motor Side) ; the skin and its appendages show very characteristic appearances ; nails become brittle and crack very readily ; hair falls out or is tempor- arily excessive in growth ] skin becomes very smooth, shiny, and thin. 5. Cranial nerves may be affected, but if so, entirely without general symptoms, and also without any pathological mental pheno- mena. If, then, in a given patient some or many of the above are present, we must suspect a peripheral lesion, and inquiry or volun- teered statements may then very likely reveal the presence of some antecedent condition known either to predispose or to excite such changes. These, with the leading feature of the resultant neuritis, are given in the following table in rough order of frequency. VIII DISEASES OF THE NERVOUS SYSTEM 283 Clinical Causes of Peripheral Neuritis Injury, including local in- flammation and pressure ; septic wounds ; necrosis of bone, syphilitic, tubercular, cancerous, aneur^j-smal, etc., tumours ; probably as a sub-group come occupation neuroses (often neuritis). Diphtheria. Causation obtrusive ; only the pain or paralysis, or both, make one say neuritis is present ; the case is named from the causation, and not necessarily called neuritis. 3. Rheumatism and gout. 4. Alcohol (with this, but in- finitely rarer, must be put poisoning by CSg, aniline, and a few other trade products). 5. Lead. 2. Diphtheria. Symptoms almost entirely motor, and especially of the eye and palate, but knee jerks almost invariably absent. Almost entirely sensory, and pain in the course of a nerve, with a history of gout or rheumatism, the chief guides. Both sensory and motor ; here " pins and needles " is a very constant feature, with progressive weakness in legs and arms ; history of alcohol (possibly denied) or of trade occu- pation. As a peripheral nerve trouble, usually confined to wrist drop, and colic (? nervous) ; blue line on gums is the guiding feature. 6. Arsenic. Sensory and motor, usually preceded or accompanied by coryzal symp- toms. 7. Diabetes. Glycosuria ; mainly neuralgic symp- toms in a given nerve ; also absence of knee jerks. 8. Cases occurring in the course of the exanthemata, which present no special diagnostic points ; also in anaemia and other cachectic conditions, e.g. senility. 9. Malaria, leprosy, beri-beri, and other tropical forms too rare in England to require further notice here. The presence of one or more of these causes will then often go far towards clinchmg the diagnosis. Cases will, however, often enough occur in which the cause is not obvious — overlooked, denied, or forgotten — and we may have to depend on the symptoms alone for a diagnosis. 284 DIFFERENTIAL DIAGNOSIS CHAP. For what affections can the symptoms of peripheral neuritis be mistaken ? Simple neuralgia and affections of the cord and brain are the ones chiefly requiring distinction. Neuritis v. Neuralgia I have adopted the word " neuralgia " here to indicate a pain not due to gross organic changes in a nerve, for the diagnostic problem I wish to try to solve is the following : Is this pain complained of by the patient a purely reflex phenomenon, or at least only due to nutritional (so-called functional) changes, or is it due to gross organic changes, of which actual neuritis is our present example? The following table gives the main points of difference : — Table Reflex or Functional, i.e. Neuralgia. More likely to be paroxysmal in character. Spontaneous in onset, independent of use of nerve, and, in fact, often better during bodily activ- ity. Intermittency complete, and history may show long intervals of in- termittency. Situation often variable from day to day, but almost invariably unilateral in any given attack. If points douleureux present, which they rarely are, pressure on them causes pain at the periphery. Little or no local tenderness along nerve trunk, and especially a light pressure will cause as much pain as a heavier one. Wasting or other trophic dis- turbances never present at first, and only rarely after a long time. Organic, i.e. Neuritis. Less likely to be of this character. Pain usually excited by movement, often subsides when a posture of rest adopted, and always worse after use. If intermittent, rarely completely so, and not for long. Situation never variable from day to day ; more commonly bilateral, but may be either. Points douleureux usually present, and pressure on them causes very distinct local pain, as well as perhaps peripheral. Generally local tenderness along nerve trunk, and pain much more proportional to amount of pressure. Wasting and trophic disturbances nearly certain to appear rapidly, and may even proceed to R.D. in muscles. Some of these points can be investigated with a definite result in any stage of the malady, but for others time must be allowed, and often in the early days of symptoms a definite diagnosis is VIII DISEASES OF THE NERVOUS SYSTEM 285 impossible ; but if the cause be organic the nerve is almost sure in a very short time to show very definite signs of loss of function and degeneration, whereas a reflex or functional pain may continue for years without such signs. To avoid needless repetition, the further distinction between peri- pheral neuritis and cord troubles can be better discussed after we have considered an outline of the functions and affections of the cord. DISEASES OF THE SPINAL CORD Of the real exciting causes of primary affections of the spinal cord we know very little, indeed practically nothing. This is in great contrast to our knowledge of causes of peripheral troubles, but traumatism (external and internal), tumours, acute inflamma- tion, and a slowly destructive process — ultimately ending in de- generation of neurons and a condition known as sclerosis — are the chief clinical causes of those pathological symptoms which we discover by examination. It must be accepted as a fact that the last-mentioned cause (and often also acute inflammation) has, to an extraordinary degree, a habit or power of attacking parts of the spinal cord possessing analogous function, and symmetrically situated on either side of the middle line. So constantly is this the case that these affections are now spoken of as system diseases in opposition to the indiscriminate lesions produced by tumours, haemorrhages, etc. System Lesions of Spinal Cord The systems thus picked out are : — 1. The cells of the anterior cornua ; 2. The fibres of the pyramidal tracts (crossed and direct) ; 3. The fibres of the posterior columns ; and the names given to the diseases thus produced may usefully be tabulated as follows : — Anterior Cornua — p . j Chronic = Progressive muscular atrophy. ^ I Acute = Infantile (or adult) spinal paralysis. Secondary to acute = Myelitis or tumour pressure, etc. Lateral Columns OR Pyramidal Tracts — Primary = Primary lateral sclerosis or spastic para- plegia. 286 DIFFERENTIAL DIAGNOSIS CHAP. Secondary 1 = Secondary spastic paraplegia, caused by any destruction of the nutritive cells in the rolandic cortex, or by division or destruction of the main neuron stems from them, such as is left by an acute transverse myelitis. Posterior Columns — Primary = Tabes dorsalis or locomotor ataxy. Secondary = Acute myelitis or tumour pressure, etc. Besides these pure or simple lesions we have two named com- binations — • Combination of anterior cornua and = Amyotrophic lateral sclerosis. pyramidal tracts. Combination of pyramidal tracts = Ataxic paraplegia. and posterior columns. The diseases in the right-hand column form then the labels of the system lesions of the cord. With the exception of acute anterior poliomyelitis they are all, when primary, i.e. without obvious cause, chronic in onset (a year or more). After or during an indiscrimi- nate lesion (tumour, haemorrhage or softening, traumatism, acute myelitis, all of which except tumour are acute or sub-acute in onset) the symptoms of the system lesion constitute the evidence of loca- tion vertically and horizontally. We will now proceed then to tabu- late the known functions of the systems to get a firm foundation for differential diagnosis : — Motor Table Functions of Systems of Cord Pyramidal Tracts. Anterior Cornua. Telegraph wires conveying motor mes- sages from cells of rolandic cor- tex to dendrites of cells of an- terior cornua. Receive by their dendrites motor mes- sages from pyramidal tracts. Posterior Columns. Nil. 1 This is not usually named as a separate disease, but a symptom-complex or residual condition produced by or left after the lesions mentioned — tumour, haemor- rhage, inflammation, etc. VIII DISEASES OF THE NERVOUS SYSTEM 287 Sensory. Pyramidal Tracts. Nil. Anterior Cornua. Nil. Reflex. Trophic. Transmit im- pulses from the brain having a restraining in- fluence on spinal reflexes. Nil. Form a link in the reflex chain for any given level. Forms the main source of tro- phic influences for the peri- pheral neuron and for the muscles. Posterior Columns. Sensory telegraph wires convey- ing messages from skin, muscles, etc., up to medulla and brain. Also form a link in the chain at a given level. Possibly transmit trophic influ- ences to skin. The Consequent Symptoms of Irritation or Destruction of the Systems a7'e Pyramidal Tracts. Anterior Cornua. Posterior Columns. Motor. * At the seat of lesion. * Below the seat of lesion. Movements or paralysis cor- responding to the fibres going out at the level. Movements or paralysis pro- portional in extent to the number of fibres d e- stroyed, hence may be merely general weak- ness ; paralysis not flaccid. Paralysis flaccid, and with R.D. in muscles. No influence on lower cells and muscles. Inco - ordination without loss of power ; due to interruption of afferent im- pulses from muscle by the sensory nerves to the encepha- lon or head co- ordinat ing centre; no para- lysis or convul- s i V e m o v e- ments. * The reason for the difference in symptoms at the seat of lesion, and above and below it, should be most carefully noted. It is that the posterior columns and the pyramidal tracts are merely bundles of telegraph wires, the vast majority of which 288 DIFFERENTIAL DIAGNOSIS CHAP. Pyramidal Tracts. Sensory. ■^ A t the Nil. seat. * Below the Nil. Anterior Cornua. Nil Nil. Reflexes A of Experimental Production. * At the seat. * Below the seat. Absent from break in chain. Posterior Columns. Root pains pos- sibly, girdle sensation. Anaesthesia of opposite side proportional to the number of fibres d e- stro.yed ; pains possible from irritation of un- destroyed fibres. Absent from break in chain. Absent knee jerk in destructive lesions from break in chain. Increased from absence of re- straint in de- structive lesions ; in irri- tative lesions knee jerk is variable. are in any given section of the cord merely passing through the seat of section, con- ducting impulses which actually exhibit themselves lower down or higher up as motion or perception ; it is only a very few that at any point leave the cord as the direct con- tinuation of a peripheral neuron with incoming or outgoing message. The reverse is the case with the cells of the anterior cornua, which are all of them in any section individually in relationship with peripheral neurons proceeding from that plane of section (or at least from very closely situated planes) ; they have no serial functional relationships (of clinical utility at present at any rate) with more distant cells above and below. A similar, I might almost say the same, explanation may be given of the term "root symptoms," an expression frequently used in nervous clinical patho- logy. It means symptoms, motor or sensory, which can be traced to irritation (usually), or destruction of the peripheral neurons constituting a motor or sensory root of a spinal nerve, either just outside the cord or just within it (after they have left the cells of the anterior cornua in motor cases, before they have been separated in the posterior columns in sensory cases), but leaving the cord at that plane; they will obviously be segmental in distribution, i.e. a girdle pain or a local pain in the back corresponding to the sensory nerve, or, on the other hand, a twitching or paralysis and atrophy of certain muscles corresponding to named motor nerves. VIII DISEASES OF THE NERVOUS SYSTEM 289 B of Viscera, Pyramidal Tracts. Anterior Cornua. Posterior Columns. No voluntary as- sistance to the act possible, but the centres may work har- moniously. Trophic to Skin and Muscles. * At the No effect, because seat. peripheral neu- ron unaffected. ■^ Below. Nq effect. Loss of expulsive or containing power if in lumbar region, and so drib- bling or reten- tion of urine ; in regions other than the lum- barresult on vis- cera unknown. Rapid wasting, with R.D. of muscle fibres or whole muscles, cor- responding to destroyed cells. No effect. No consciousness of acts, and great mischief may ensue if centres do not work harmoni- ously. Bed sores not in- frequent, either from anaes- thesia or absence of usual trophic influences. Same as at the seat. In addition to these three systems we have clinical evidence that the antero-lateral ascending tract of Gowers conveys impres- sions of pain and touch to the sensorium, and that the gray matter has, amongst other functions, the power of conveying impressions of changes of temperature to the brain, and probably also of control- ling the nutrition of the skin and sub-cutaneous structures. Sir W. Gowers has brought forward much evidence in favour of the first pro- position ; the known thermal ansesthesia of syringomyelia is sugges tive of the correctness of the second ; and the third is one possible explanation of the rapid development of bed sores in acute myelitis. These tables show very distinctly that if a system disease be present in a typical form confusion is impossible, for their symptoms present positive contrasts rather than comparisons. The combined chronic lesions are rather more confusing, and it is moreover true that atypical and indiscriminate lesions are frequent, and hence the differential diagnosis requires some little discussion. The first caution and golden rule is, " Don't be in a hurry to make a final and definite diagnosis, to find, as it were, a ready-made label * See footnote, pp. 287-288. U 2 90 DIFFERENTIAL DIAGNOSIS chap. for a case." Consider well the abse?tce as well as the presence of posi- tive symptoms, and then let the diagnosis run, " From what I have observed, I have reason to believe that such and such parts of the cord are affected, and, owing to the absence of certain features, other parts are exempt." If the case be typical the appropriate label will then be found, and if atypical no opinion will have been expressed which may afterwards have to be withdrawn. Indiscriminate Lesions Inasmuch as an indiscriminate lesion of the cord can only be diagnosed, so far as its symptoms are concerned, by its effects upon those systems or parts of the cord with the functions of which we are more or less acquainted, i.e. by the same phenomena — motor, sensory, reflex, and trophic — already several times noted, there follow as immediate and necessary deductions (i) that the history of onset of the illness, and the grouping of the signs, will be of much more importance than their individual presence ; (2) that the vertical or horizontal localisation will also assume an equal impor- tance to ascertain if local therapeutical measures offer a prospq^t of radical cure, e.g. tumours. The lesions themselves are practically only three, viz. trauma- tism, vascular lesions (blocking, rupture, or inflammatory), and tumours, though syringomyelia and disseminated sclerosis ought also to be enumerated if they had not such special characteristics of their own. They all of them cause either irritation followed by destruction, or immediate destruction of the cord, and may be classified from that point of view as follows : — A. Irritative period Meningitis, simple chronic. long, weeks or Tertiary gummata and other tumours of months, or even meninges. years. Aneurysmal erosion of bone and compression. Spinal caries when products cheesy and possess but feeble potency of irritation, or when gradual bone displacement causes pressure. Tumour of the bones. Traumatism that has only excited slight inflam- matory changes. B, Irritative period Spinal caries with suppuration or sudden displace- short : hours or ment of bone. days. Syphilis within two years of infection. VIII DISEASES OF THE NERVOUS SYSTEM 291 Tumours of any origin (occasionally). Meningitis, acute general. Meningeal haemorrhage. C. Irritative period Acute myelitis (this often occurs in cases where almost non-ex- longer irritative period might be looked for, istent. e.g. acute meningeal inflammatory affections). Haemorrhage into cord, or softening from blocking of a vessel. Traumatism when severe. Hence it is obvious that it is hardly possible to mistake any of the members of Groups B and C for a system lesion (except perhaps acute infantile paralysis), the history of the onset of the symptoms stands in such absolute contrast. The cases of Group A, too, are almost invariably characterised by one distressing symptom, which is as invariably absent from system lesions, viz. severe local pain or tenderness in the back, a root symptom (^.z'., p. 288, foot- note). Besides these two fundamental differences I only propose to give the following brief notes on the diagnosis of indiscriminate lesions. Traumatism. HAEMORRHAGE INTO OR SOFTEN- ING OF CORD. HAEMORRHAGE INTO MENINGES. Tumour of menin- ges. A definite history of some violence always to be obtained ; in slight cases interference with mic- turition is the most suspicious circumstance, suggesting serious cord trouble ; a chronic meningitis or myehtis may arise from this cause analogous to concussion of brain. Exceedingly rare, onset instantaneous, consequent and subsequent symptoms those of an acute myelitis, unless the clot or area of softening be very small, when they will be those of a system lesion, only of acute origin, and probably asymmetrical. Also excessively rare except from traumatism, or ruptured aneurysm, in each of which diagnosis is obvious ; if a small meningeal haemorrhage were met with it would be indistinguishable from localised meningitis or tumour except by very sudden onset. Focal or root symptoms very prominent ; com- plete symptoms more rapid in onset than sclerosis, less so than inflammation ; jumpings of a limb with pain in it for some months prin- cipal characteristics from pressure on posterior or lateral tracts. Tumour OF SUB- STANCE OF THE CORD. 292 DIFFERENTIAL DIAGNOSIS chap. Very rare ; symptoms similar to meningeal tumour, but much more rapidly progress towards a paralytic as opposed to an irritative aspect. System Lesions v. Peripheral Neuritis We may now return to peripheral neuritis and those affections of the cord for which it may be mistaken. There are two systems of the cord, disease of which can obviously cause mistakes, viz. the anterior cotnua (motor) and the posterior columns (sensory), and that because anterior poliomyelitis and tabes dorsalis are, in fact, lesions of the same peripheral neuron as motor and sensory peri- pheral neuritis respectively. Pathologically the difference lies in the exact point in the neuron where the trouble begins. This is in the cells of the anterior cornua, and of the posterior roots ^ in the system lesions, with consequent rapid secondary degeneration of neuraxons. While in peripheral neuritis the affection, if not limited to the neuraxon, at least begins in it, and only secondarily involves the neuron cell in severe cases. Clinically we are fortunately able to find a good many differences, so that in the majority of cases but little difficulty arises in diagnosis ; though it must be confessed that often also only time and very great patience will but partially unravel the mystery. A. — The Onset The onset of the system lesions is, as a rule, in marked contrast to that of the peripheral troubles. Anterior poliomyelitis occurs as : — 1. Acute, (a) Idiopathic infantile paralysis. ij)) „ adult „ {c) Part of an acute myelitis. 2. Chronic, or progressive muscular atrophy. Sclerosis of the posterior columns is, as an idiopathic affection, always chronic. Now, acute infantile paralysis commences with a sharp outburst of fever, and cannot be diagnosed from a zymotic fever until its special symptom, viz. paralysis, has supervened. Inasmuch as there is a concomitant congestion of the spinal cord, this onset may be associated with a pain in the back, leading to a suspicion of variola or of meningitis ; the rash will soon differentiate the former, and the latter will soon be excluded by the subsidence of the pain and the ^ This is the view now entertained of tabes dorsalis. VIII DISEASES OF THE NERVOUS SYSTEM 293 very rapid appearance of the paralysis; if meningitis were the trouble the pain would persist and the paralysis (if any) would be long delayed until the inflammation had had time to attack and destroy neuraxons. In adults, while the course of events is precisely the same, the general symptoms are much less pronounced, though the onset is equally rapid ; still, the age is in itself very important, for anterior poliomyelitis is as rare in adults as a mysterious, i.e. without obvious cause, neuritis is in children, and vice versa. On the other hand, peripheral neuritis rarely, if ever, has such an acute pyrexial onset with pain in the back ; it may have a smouldering fever lasting several days, or even a week or two (the febrile period in poliomyelitis is at most three or four days, generally only twenty-four or forty-eight hours), but then it has not the pain in the back ; if it has the pain in the back (lumbago and sciatica) it will not have the pyrexia unless this be associated with definite joint (rheumatism or gout) trouble. In those cases in which the acute poliomyelitis is only part of an acute transverse lesion, the early bladder and rectal disturbance and the complete paraplegic anaesthesia will be sufficient to prevent mistakes. In the more chronic forms of trouble also the onset presents more striking differences than likenesses. Thus, in a peripheral motor lesion there is probably more wasting and paralysis in six weeks to two months than a case of progressive muscular atrophy will show in six months or a year; and, again, the locality will be different, for in the neuritis the whole limb, or whole muscles, will have suffered (except in isolated nerve cases, w^hich will probably have an obvious local cause), whereas in progressive muscular atrophy the changes will be confined to hand or foot (common type), or to shoulder muscles (upper arm type), spreading thence very slowly. The latter disease, progressive muscular atrophy, may be finally dismissed by stating that it has no other nervous features except a progressive weakness going hand in hand pari passu with the wasting, and R.D. is not to be obtained typically; while in peripheral neuritis the paralysis is out of all proportion in the early days to the wasting, and R.D. is typically present. The reason for these differences is obvious if we remember that in the system disease the cornual cells suffer one after another in very slow progression, and consequently individual neuraxons with their nutritional functions die and cause atrophy of individual muscle fibres or bundles ; while in the peripheral troubles many neuraxons are simultaneously involved. 294 DIFFERENTIAL DIAGNOSIS chap. B. — The Course of Established Symptoms The system lesions in their course, though sometimes appar- ently standing still, rarely or never lose their typical physical signs by which they have been diagnosed, but they frequently show im- provements or exacerbations quite unaccounted for by anything that can be called treatment or neglect. Peripheral lesions, on the other hand, proceed almost steadily in one of three directions : (i) straight downhill to the grave in less than a year or eighteen months; (2) downhill for so long as the cause acts and a little longer, and then with the cessation of the cause (usually alcohol) steady improvement sets in up to complete recovery, unless and until the cause again operates, when history repeats itself; (3) persist for an indefinite time without any apparent alteration. The perennial root of the tree is attacked in the system lesion ; in the other a branch is cut off which may or may not grow again, but, on the other hand, it may be so necessary to nutrition that the whole tree dies. We will now conclude the subject of cord and peripheral troubles with a few tables of special interest. Peripheral Neuritis and Tabes Dorsalis These often have the following in common : — 1. Inco-ordination of movement ; 2. Pains in limbs ; 3. Absent knee jerks ; but more frequently they differ in the following : — Peripheral Neuritis. Tabes Dorsalis. Inco - ordination seldom a very Inco-ordination especially marked ; marked feature ; paralysis very paralysis and weakness for common. simple movements never present. Pain is in the nerve, never a girdle Pain shoots along a limb ; if a pain. girdle pain present it is very strong evidence (root symp- tom). Paraesthesias common. Paraesthesiae rarely present Knee jerks sometimes exaggerated. Knee jerks never exaggerated. Viscera never affected. Visceral crises and disturbance of function common. VIII DISEASES OF THE NEPvVOUS SYSTEM 295 Peripheral Neuritis. Eye affections may be present; if so they are prominently complained of, and may stand as the sole symptoms ; optic neuritis or atrophy extremely rare. Tabes Dorsalis. Pupillary or oculo-motor troubles nearly constant, but in addition to other symptoms ; atrophy of optic nerve frequently found. m- Infaniile Paralysis will resemble Diphtheritic Peripheral Neuritis (a) History of acute illness ; (b) Rapid onset of paralysis ; (c) Some wasting of muscles ; but the two will probably differ in — Diphtheria. Acute illness almost certainly with prominent local (throat, vagina, wound, etc.) symptoms. Paralysis almost always of eye or palate first, and rarely of limbs at all. Wasting not great, and R.D. typi- cally present only in severe cases. Very symmetrical paralysis. May get worse for some days after onset ; recovery is always practi- cally complete if the patient does not die. Infantile Paralysis. Acute illness with only general symptoms or some pain in spine. Almost always of limbs only, very rarely cranial at all. Wasting considerable, and R.D. nearly constant, in some muscles at any rate. Ultimate paralysis characteristi- cally local and asymmetrical. After twenty-four or forty-eight hours any alteration is always in the direction of improve- ment ; recovery is never abso- lutely complete. Ataxic Paraplegia v. Peripheral Neuritis The combined motor and sensory phenomena may arouse suspicion of some peripheral affection, but the course of the cord disease is in itself almost sufficient to separate it from the latter ; the cord trouble is always slow in onset, and months elapse before it advances fair, while the neuritis is almost invariably acute or sub- acute. The very marked inco-ordination, too, of the cord trouble, especially taken with the exaggerated knee jerk, adds further confirm- atory differentiation. 296 DIFFERENTIAL DIAGNOSIS chap. Amyotrophic Lateral Sclerosis v. Peripheral Neuritis Dr. Gowers says, " The wasting from disease of single nerves or at a plexus is sufficiently distinguished by its limitation, coupled with its rapid onset and associated sensory symptoms " ; and from some forms of multiple neuritis, he says, " It is necessary to wait for slower wasting in other parts than those first affected before a diagnosis can be made ; a careful search will generally reveal other symptoms of neuritis, and a known cause is usually obtrusive." Lateral Sclerosis v. Peripheral Neuritis Any affection of the pyramidal tracts can only be mistaken for a case of pure motor peripheral trouble. If sensory phenomena are present to an extent sufficient to attract attention the disease is not primary lateral sclerosis. The cases of motor neuritis which could rouse an idea of lateral sclerosis must be either of arms or legs. Now, if it be of the arms, the note at the bottom of p. 287 shows us that if the lateral columns are affected as high as the origin of the brachial plexus, the knee jerk is exaggerated and ankle clonus probably marked ; but, per contra, the peripheral brachial nerves have no such influence on the rest of the cord, and there will be no disturbance of reflexes lower down. The same test will also apply if the trouble be in the legs, for, except in the earliest stage of neuritis (and that arising in a manner and under circumstances which preclude all idea of lateral sclerosis), the knee jerk is absent and ankle clonus not to be obtained. Peripheral Neuritis v. Disseminated Sclerosis Insular sclerosis most usually offers a fairly typical symptom complex which cannot be mistaken for anything except functional (or hysterical) nervous disease ; but inasmuch as its very name implies a random distribution, it is possible that cases may arise in which the peripheral nerves are suspected. Of the many symptoms that may occur in disseminated sclerosis there are three which, notwithstanding its indiscriminate distribution, are almost constant, viz. — 1. Intention tremors ; 2. Nystagmus ; 3. Increased knee jerk ; and it is as rare to find a case of peripheral neuritis exhibiting these VIII DISEASES OF THE NERVOUS SYSTEM 297 three in combination without other obvious indications as it is to find a case of disseminated sclerosis in which they are not all three present. Disseminated Sclerosis v. Hysteria or Functional Troubles To distinguish the early stages of sclerosis from what is usually accepted as functional disease is probably to try and make a distinc- tion between identicals, for the death of neurons by sclerosis is in all probability preceded by a stage of functional debility in which recovery is certainly possible, but as the recognition and demon- stration of this recoverable condition is all-important from a thera- peutical and prognostic point of view, I have drawn up the following table of points most worthy of attention in rough order of im- portance. Functional. Tremors very common, but not so violent as to prevent comple- tion of intention. Nystagmus very rare and ill- marked ; double vision rare except very temporary. Knee jerks probably glib, but variable from time to time. 4. Speech probably voluble, or 4. obstinate silence; seldom scanning, varies from time to time. 5. If bladder trouble at all it is retention, and pain not com- plained of. 6. Optic neuritis or atrophy un- known. 7. Recovery rather sudden and 7 complete, and possibly no return ; if return it is sudden and in the same guise. 8. Sensory hemi - anaesthesia not 8 uncommon with recovery. Established Disseminated Sclerosis. 1 . Tremors so violent as frequently to quite frustrate intention. 2. Nystagmus common and very distinct ; double vision not uncommon. 3. Knee jerks grossly exaggerated and invariable \ should a patch have caught the reflex chain they will be absent, but still invariable. Speech scanning usually, and not variable. 5. Bladder trouble frequent ; in- continence, stammering blad- der, and even painful retention. 6. Optic atrophy if present is conclusive, for it is sclerosis. 7. Apparent recovery curiously frequent, but return of symp- toms soon occurs ; may be in another guise. Hemi - anaesthesia rare, and what anaesthesia occurs is little likely ever to be removed. 298 DIFFERENTIAL DIAGNOSIS chap. Functional. Established Disseminated Sclerosis. 9. Perversion of will power a fre- 9. Perversion of will power not quent cause, or concomitant, often observed to any extent ; and very variable at times. if it is present it remains. 10. Spasticity and inco-ordination 10. If spasticity or inco-ordina- variable from time to time. tion occurs it is likely to be permanent. 11. If any wasting occurs it is li. If wasting occurs it is likely likely to be general, and very to be local and fairly slow in onset, and arises from rapid, though when lateral mere disuse. columns are affected this will not hold. AFFECTIONS OF MEDULLA, PONS, AND CEREBELLAR PEDUNCLES In dealing with the peripheral nerves and spinal cord I have dealt at some little length with the points of differential diagnosis because the cases are more commonly met with, and because the problems of diagnosis are comparatively simple in themselves if due attention is paid to the elements that lead to conclusions. In dealing with intracranial troubles we are introduced at once to so much that is absolutely unknown, and still more that is only guessed at or in dispute, as regards anatomy and physiology, that complete diagnosis is frequently impossible, and I shall only attempt to sketch a clear outline of the principles of regional and pathological diagnosis, and introduce independently a few important subjects which are but ill remembered and worse understood by students. An accurate knowledge of the precise regional relations of the various tracts of fibres and groups of cells whose functions are more or less known is absolutely essential for a clear understanding of the diagnostic problems offered by disease in this region. The best way to learn this is by careful study of sections compared with the figures to be found in every text-book of anatomy. They may be tabulated for study thus : — Fibres of Pons, Medulla, and Cerebellar Peduncles A. — Old Tracts already noticed in the Cord I. Pyramidal, cross- Constitute the crossing of the pyramids, and then ed and direct ; the pyramidal tracts through the medulla, pons. VIII DISEASES OF THE NERVOUS SYSTEM 299 functions purely motor. Antero -lateral ascending tract ; function to con- vey centripetal impulses. Direct cerebellar tract ; function centripetal (? en- tirely). Posterior col- umns : function centripetal. Bulk of unnamed white fibres of cord, function nearly or quite unknown unless commissural. and cerebral "crura." In tracing these down from the motor cortex it must be noted that some of them turn out to join the nuclei of origin of the motor cranial nerves, in which case the relationship between cortex and nucleus is always crossed^ precisely the same as that of cortex and anterior comua of cord. Some are traceable as fibres in the formatio reticularis, reaching thus the superior cere- bellar peduncles and so the cerebellar cortex ; others are lost in the formatio reticularis, and their further course unknown. Form a large part of the restiform bodies or inferior peduncles of cerebellum. This is the only known ending of these fibres. End in synapses with the cells of the funiculi gracilis, cuneatus, and rolandi. Constitute probably the bulk of the fibres of the formatio reticularis. Their destination is un- known and also their function, though they are assumed to unite successive segments of the mid-brain. B. — New Tracts of Fibres^ or in some cases New Names for Old Tracts Originate in. I. {a) Cells of nuclei gracilis, cuneatus, and rolandi. {U) Unnamed white fibres of cord. ic) Olivary body and other cells in the region of the upper medulla. 2. Direct cellebellar tract of cord, internal and external arcuate fibres. Tract. Reaching to. {a) Function afferent, reach- ing the inferior peduncles .S2 of cerebellum as inter- ^ nal arcuate fibres, pass- o ing to cerebellar cortex, t) {b) Reach cortex of cerebrum o and cerebellum, or end t5 in cells of formatio reti- S cularis {vide 5 above). <2 id) Many go as arcuate fibres Q to cerebellum, many also of unknown destination u, ^ ■ and function. .2 ^ ^ Cerebellar cortex and nuclei. 300 DIFFERENTIAL DIAGNOSIS CHAP. Originate in. 3. Cells of nuclei gracilis, cuneatus, and rolandi, also independent cells in for- matio reticularis, and many of cells of the olivary body. 4. Begins by axons from cells of nuclei gracilis, cuneatus, and rolandi, added to by axons from cells of for- matio reticularis, of oli- vary body, etc. 5. Cells of reticular formation at one end, cells near the nucleus of third nerve at the other, and from inter- mediate cells. 6. From cortex of one cere- bellar hemisphere. Tract. (U u CO Reaching to. Functions probably afferent, reaching cerebellar cortex by inferior peduncles. Is the principal afferent (? entirely) passage to brain from the cells in medulla, reaching to corpora quad- rigemina and optic thala- mus. Probably motor in function, serving for connections between motor cranial nerves, especially in their associated (quasi - reflex) movements, e.g. lips and tongue, the two eyes, etc. To the other hemisphere, probably engaged in co- ordination. Of funiculi — Form Gracilis, f(^) Cuneatus, i(^) Rolandi, ((^) In formatio — Form Reticularis. ((^) \ (A Cells of cranial Form nerves from three to twelve. Cells of the region some of the neuraxons of — Fillet. Internal arcuate fibres. Others of unknown destination. neuraxons going to — Reinforce fillet. Connect different segments. External arcuate fibres. Reinforce posterior longitudinal bundle. the neuraxons of their respective nerves. Now, in applying these facts of anatomy and physiology to the problems of diagnosis, it cannot be too strongly insisted upon that in intracranial lesions, just as in peripheral (and cord) ones, there is VIII DISEASES OF THE NERVOUS SYSTEM 301 nothing essentially mysterious or beyond the power of the youngest student to grasp. The mystery, so far as there is any, lies simply and solely in our ignorance of the exact path of nerve impulses, and of the amount and nature of control and interference exercised by one neuron group over another. Lesions, of whatever nature, affect the structure and function of individual neurons in precisely the same way here as elsewhere, and this affection (whether of defect or excess) it is that constitutes our means of localising diagnosis. The elementary facts to grasp are : — 1. That every anatomical nerve in the body has the power of communicating with, or of receiving messages from, the cortex of cerebrum and cerebellum for purposes of harmonious functioning in the healthy body. 2. That for some reason (several explanations of the fact have been offered) that portion of the cerebral cortex which is thus in connection with a peripheral nerve is in the opposite named (right or left) hemisphere to that side in which occurs the peripheral dis- tribution of the nerve in question. 3. That, per contra^ the relationship of the cerebellar cortex to a nerve is an uncrossed one. 4. That this crossing of impulses and of fibres lies — A. For motor nerves and impulses — {a) In the lower part of the medulla, so far as spinal nerves are in question. ip) For the cranial nerves, just a little nearer to the cortex than the nuclei of origin. B. For sensory nerves and impulses — {a) Distributed throughout the cord and medulla for the spinal ones, each nerve crossing at once. (3) For the cranial nerves, just a little nearer the cortex than the nuclei of origin. 5. It is at once an obvious and necessary deduction from these elements of crossed influence that a lesion of a strand of fibres above, i.e. nearer the cortex cerebri than the nucleus of origin of the peripheral nerve in question, must exhibit its effects on the opposite side of the body to that on which the lesion lies. If it be at, or on the peripheral side of, the nucleus, its effects must be exhibited on the same side as that of the lesion ; and further, from what has 302 DIFFERENTIAL DIAGNOSIS chap. been said on p. 252 about the function of the neuron cell, must almost inevitably be associated with some trophic alteration (excess or defect) in the muscles affected. 6. A self-obvious statement, but one too frequently forgotten, that the closer the nerve fibres (or cells) lie together the more likely are they to be involved together by a small lesion. In this fact, however elementary it may seem, lies the clue to at least one-half of the localising problem. Thus, taking the motor side and a destructive lesion as an illustrative example, a cortical or sub- cortical small lesion may easily be understood to be capable of producing a monoplegia, but the nearer we get to the (anterior two- thirds of the posterior limb of the) internal capsule, the more fibres will be caught by the lesion, and the wider will be the peripheral area of disturbance, until when we arrive at the crura cerebri, pons, and medulla the motor fibres are collected so closely together that it is almost impossible but that a paralysis shall be at least a hemi- plegia, and possibly even a complete paralysis of all four limbs. Further, speaking of our present region — the mid-brain — it is almost impossible but that some at least of the motor cranial nerves shall have participated in the disturbance; for this reason they give us tolerably exact information of the locality of the trouble. This will at once explain the following clinical experience, viz. that given a hemiplegia^ then if it is due to a lesion — In CPUS Cerebri. — The third nerve on the opposite side is nearly sure to be paralysed. Any other cranial paralysis will be on the same side as the paralysis of the body. In Upper Pons. — We may look for some weakness in the opposite fifth nerve (motor part), and possibly some anaesthesia, though there is a considerable distance between the motor pyramidal fibres and the sensory root of the fifth. In Lower Pons. — Very probably a paralysis of the opposite seventh, because its peripheral course lies so close to the motor fibres which are destroyed. (The explanation of the contraction of the pupils, a constant feature, is not quite so obvious.) In Medulla. — We may look out for a paralysis of the opposite sixth, very possibly of the opposite seventh, because the seventh nerve winds round the sixth nucleus. (A paralysis of both sixth nerves is not such a precise indication, owing VIII DISEASES OF THE NERVOUS SYSTEM 303 to their exposure to pressure between the pons and the bone.) In the lower part of the medulla one twelfth nerve or a spinal accessory is very likely to be affected, leading to deviation of protruded tongue, or to paralysis of a vocal cord. CRANIAL NERVES The last paragraph has shown the importance of these nerves as indicators of locality of a lesion. I propose now to add a few notes on the individual nerves and their lesions. Firsts or Olfactory. — This, strictly speaking, is not a nerve but an integral part of the cerebral cortex. Chnically, if the sense of smell is impaired, we must first suspect and investigate the external cavities. Tf these are declared free from suspicion the trouble may be situated in the anterior fossa of the skull, causing pressure on the olfactory bulbs. The cortical connections of the bulbs are supposed to exist in the tip of the temporo-sphenoidal lobe, so that in cases of suspected abscess or tumour, interference wdth the faculty of smell is a suggestion that the lesion is not far from that situation. Second^ or Optic. — Like the olfactory, is a distinct outgrowth of the brain, with a primary connection with the corpora quadrige- mina. Its cortical representation is found {a) in the occipital lobes for coarse optical impressions, i.e. for an appreciation of the fact that something is affecting the optic nerves; {b) in the supra- marginal and angular gyri round the end of the sylvian fissure for optical perceptions and judgments, i.e. for an appreciation of the precise object that is stimulating the optic nerves, and its exact nature and associations. Hence, as regards localising deductions from the nerve, we have — {a) Optic neuritis {vide p. 324). lb) If hemianopia be due to a lesion of the optic tracts the pupil will not react when light is thrown on the blind half of the retina, because the lesion is in front of the centre for reflex of light ; if it lies between the corpora quadrigemina and the optic lobes the pupil will react, but the patient will not perceive that anything is stimu- lating the retina ; if the lesion is between the occipital and the supramarginal lobes he will perceive the object, 304 DIFFERENTIAL DIAGNOSIS chap. but will not judge its nature correctly. (This is the condition known as word blindness when testing a case of aphasia.) Thirds JFourth, and Sixth. — These nerves, taken collectively, form the motor apparatus (with muscles) of the eye-balls, built and arranged to subserve the purpose of single vision with two eyes, for which very accurate associated action of the muscles is required. This is provided for undoubtedly by the close approximation of the nuclei of the nerves, and by the posterior longitudinal bundle serving as a rapid means of communication; hence it certainly follows that nuclear lesions of these nerves or of the posterior longitudinal bundle will cause squinting, or at least double vision (squint is merely a deviation of the visual axes from their normal position visible to the observer). Such lesions are known, though not very common ; their exact discussion would be too intricate to follow out here. It must not be forgotten that these three nerves lie very close to one another and to the orbital branch of the fifth at the entrance to the orbit, so that a tumour or sclerosing lesion in that situation may produce a total paralysis of all four nerves. Simpler problems are presented by considering the individual nerves and their branches, i.e. peripheral lesions. Ihird Nerve. — If affected by a crural lesion it is probable that there will be a complete paralysis of the whole of the third on the opposite side to that on which the paralysis of the body is said to be. If affected in the more peripheral parts of its course, it is more probable that the paralysis will be incomplete, i.e. of one or more branches only. The reason for this is better discussed along with pathological diagnosis. Fourth. — To this nerve the same remarks apply as to the third, remembering that it only supplies one muscle, viz. the superior oblique, which assists in downward m.Qis&v[).^xi\.'^ of the globe. Hence double vision on looking downwards only. Fifth. — When affected at or above its nucleus never, according to Bastian, exhibits trophic, vasomotor, or secretory disturbances of function ; when affected in its peripheral course does exhibit such disturbances in the appropriate area of distribution. Sixth. — As above remarked, the exposed position of these nerves between the pons behind and the bone in front deprives a double paralysis of much locahsing value, but if one only is affected we have strong ground, in an otherwise doubtful case, for believing that the vin DISEASES OF THE NERVOUS SYSTEM 305 lesion is in the medulla or in front of the pons ; in front, that is, as regards the cranial fossae. If one sixth and the same named (right or left) seventh are involved together, we can fix the lesion pretty accurately as at that spot in the medulla where the seventh nerve winds round the sixth nucleus. Seventh. — In small lesions at or above, i.e. nearer the cortex, its nucleus, it is a clinical fact that the occipito-frontalis muscle almost invariably escapes, probably because the muscle is most commonly used reflexly, and stimuli reach it by the posterior longitudinal bundle. If the nerve is affected between the brain and the bottom of the internal auditory meatus it is very likely that deafness of the same ear may be found, because the seventh nerve lies in actual contact with the eighth. In lesions beyond this point, up to the exit from the stylomastoid foramen, it is likely that the paralysis will be absolutely complete. Beyond this point individual branches may be caught by a lesion, but we shall have probably gross mani- festations of a swelhng (parotitis, etc.) or inflammation to help us outside the skull. It is also to be noted that in peripheral lesions there will be no associated hemiplegia. Eighth. — In central lesions it is not likely that the auditory nerve will suffer alone, its nuclei are too wide spread. In peripheral lesions it will be likely to suffer alone, or, as above noted, in con- junction with the seventh only of the same side. Ninths Tenth, and Eleventh. — Individual lesions of any of these nerves alone at their nuclei are excessively rare. A central lesion of any of them will, therefore, locate itself in the medulla by being associated with an affection of all three. A peripheral lesion will define itself by features external to the skull. Twelfth. — The tongue is so intimately connected with the power of articulate speech as to lead to a conclusion that the cortical representation of the twelfth nerve is to be found in Broca's con- volution on the left side, and in a corresponding area on the right hemisphere j and we find that a lesion on the left side (? on the right side in left-handed people) in Broca's convolution, or between it and the twelfth nuclei, disarranges the function of the tongue so far as that subserves speech (pure motor aphasia). Again, in deglutition, and in practically all uses of the tongue, the two halves are so accustomed to work together that it would seem a great convenience (or, probably, almost a necessity) that they should be capable of being stimulated from either side of the X 3o6 DIFFERENTIAL DIAGNOSIS chap. brain. Furthermore, as a matter of anatomical fact, the nuclei of the right and left twelfth nerves lie so close together in the floor of the lower half of the fourth ventricle as to be almost intermixed. Hence, as a matter of clinical experience, we find that (barring speech defects) in lesions above the nuclei, if a one-sided paralysis of the tongue occurs, it is likely to be incomplete and also to be comparatively temporary, and certainly unassociated with any trophic lesions. In lesions at the nuclei the paralysis is almost sure to be bilateral, and {vide p. 252) associated with atrophy. From lesions peripheral to the nucleus we may again get a one- sided paralysis, but this time with trophic lesions. DISEASES OF THE BRAIN What we know about the brain is, that it is composed of neurons and supporting (mechanical and nutritional) tissue. The former so arranged and connected as to subserve in the best possible manner the great purpose of bringing us into more or less har- monious communication with the world at large — co-ordination of functions in the very widest meaning of the word. Here resides the consciousness of change in the environment, both internal, of organs, and external, of the body, and here is initiated the necessary process to adapt everything to that change. What we hypothecate is, that through these neurons, and their synapses with one another, messages can with very great ease pass from one hemisphere to the other (commissural fibres), or from every part to every part of the hemisphere of the same side (internuncial fibres), and also with both direct and crossed influence from cerebral to cerebellar cortex and me- chanisms. To completely analyse the tracks by which this is done — even those which are tolerably well known — would require a large volume, and would in the present work serve no useful purpose. So far as bedside diagnosis is concerned, the principal difficulties in the way of accuracy are : (i) want of precise knowledge of actual structural continuity of tract with tract; (2) a still greater lack of precision in knowledge of functional continuity; (3) the fact that direct patho- logical lesions, and still less their effects as regards pressure, so very seldom confine themselves to those individual tracts, or tracks, about which we think we know something. VIII DISEASES OF THE NERVOUS SYSTEM 307 The following tables give some of the principal points of localisa- tion, either approximately proved or strongly suggested : — Cortex of the Brain — Ascending parietal, as- cending frontal, and corresponding median cortex. Frontal. Occipital. Supramarginal and an- gular. Superior temporo- sphenoidal. Tip of the temporo- sphenoidal lobe. The rest of the cortex. Cortex of Cere- bellum. Possess the function of initiating the motor side of i?wve?nents in various parts of the body on the opposite side. In this area of cortex are represented in order from above downwards the foot, leg, arm, face, so that a pure cortical destructive lesion produces weakening of these move- ments. For irritative lesions, vide Jack- sonian Epilepsy, p. 309. Suggestively the seat of connected thought and reasoning ; lesions here have, in some cases at least, impaired this power, e.g. general paralysis of the insane. In- dubitably this region comes into structural continuity with the anterior limb of the internal capsule, and so functionally is supposed to be connected with the cere- bellar and occipital cortex. Probably in the main the seat of subjective consciousness of sensory stimuli ; it is almost certainly proved also to be the seat of the primary registration of optic impressions. Proved almost conclusively to be the seat of the final registration of optic impressio^is, i.e. visual concepts as opposed to mere percepts, and to be for this purpose in close connection with speech (on its motor side) and appropriate common motor areas. These facts are such, at least, for the left hemisphere {vide Optic Ner\'e). Stands in precisely the same relation to auditory stimuli that the supramarginal does to visual ones {vide Auditory). Represents the olfactor}'- sense in a similar though perhaps less efficient manner. Very few or no facts essentially proving a local or definite function. All we can say about this is, that when, by damage to its peduncles, messages 3o8 DIFFERENTIAL DIAGNOSIS chap. are unable to reach the cortex, defects of equilibration become a marked feature in the disease, but we cannot say more precisely how or why these are caused. White Matter underlying Cortex — Inasmuch as this is engaged in carrying messages to and from the cortex, it is difficult, or even in many cases impossible, to differentiate lesions of it from those of the overlying gray matter. All that can be said, in general terms, is, that the nearer to the cortex the more likely is subjective consciousness — apart from a mere unconsciousness in the ordinary sense of the word — to be implicated in the pathological disturbance, and on the motor side the less likely are we to get mere twitching (or loss of power) in groups of muscles as opposed to actual purposive (but unconscious) movements or weakening of such movements. We know a little about some tracks, or tracts, in the white matter. Thus : — That in the frontal lobes is collected mainly into the anterior limb of the internal capsule. We do not know much about lesions of this, except that we should expect inco-ordination of movement to some extent, and incoherence of thought, i.e. we only know it so far as we know the function of the frontal cortex. That corresponding to the motor cortex is gathered together as the corona radiata, and then more concentrated still in the anterior two-thirds of the posterior limb of the internal capsule. As it conveys the motor impulses lesions of it will cause hemiplegia or hemiconvulsions. That corresponding to the occipital cortex conveys impressions to the sensorium from everywhere, per the posterior third of the posterior limb of the internal capsule, and lesions should produce hemianaesthesia and lesions of sight corresponding to what has already been said on that subject : also interference with the afferent impulses necessary for co-ordination. That of corpus eallosum can only be said to connect the two hemispheres ; of its special function, and of evidence of its lesions, we can say nothing here. Basal Ganglia with their Fibres and Cells — Of the corpus striatum, optic thalamus, and cells of the teg- mentum of the crura cerebri, it is impossible to say anything definite without going into minute detail. We recognise in them anatomically complete neuron groups (cells and processes) in very VIII DISEASES OF THE NERVOUS SYSTEM ^ 309 intimate connection with one another and with cortical groups — evidently very complex and delicate mechanisms for the rapid distribution and adjustment of nerve stimuli ; but, notwithstanding the attention they have received of late, we are still almost as much in the dark now as ever we were as to the precise part played by theiTi in conscious, or in reflex life. We can still only say that the corpus striatum probably has something to say to the correct adap- tation of means to ends on the motor side, while the optic thalamus and tegmentum play a similar role in connection with the correct appreciation of afferent stimuli on their way to the cortex. Of the corpora quadrigemina and gray matter in connection with them we can say that they play a conspicuous part in the correct manipulation of the eyes, including in that term not only gross movements but also accon;modation and reflex to light. We may now conclude this elementary outline of localisation of the brain functions by a note on one or two points of special diag- nostic interest as illustrations. ON THE MOTOR SIDE A. — Jacksonian Epilepsy — This term has been given — in honour of the first accurate investi- gator of the phenomena — to attacks of convulsive movements which commence locally in an extremity, or in the face, and are due to an irritant lesion of some kind in that portion of the rolandic (or motor) area corresponding to the given peripheral commencement of the movements. Any given attack may be quite local, and limited in distribution almost to the spot originally attacked, or it may be spread more and more widely so as to involve the other limbs of the same side, and even those of the other half of the body, and may even end in unconsciousness, hence it may closely resemble idiopathic epilepsy. The important points to remember about it are, that for the same patient — • (a) It invariably begins in the same place (thumb, great toe, and mouth are the commonest). {h) It invariably spreads in the same direction, though not necessarily to the same extent ; the extent apparently depends upon the nature and amount of the te??iporary exciting cause of extra activity, but the direction is prob- ably governed by lines of least resistance, which soon become established in any patient, and remain constant for that patient. 310 DIFFERENTIAL DIAGNOSIS chap. {c) It is always followed by an (at least temporary) paralysis of the convulsed muscles which — {d) Is always most marked in the muscles first affected. Thus its presence Is a very strong piece of localising evidence for an irritant in a particular part of the rolandic region. In the above particulars it may closely resemble idiopathic epilepsy, especi- ally if the aura of the latter is local, but the following points will usually serve to distinguish them : — Jacksonian. Idiopathic. 1. Inmost cases either a marked If cause be present it will be in the and obvious cause, e.g. shape of a family history or some- traumatism, or evidence thing general, not local. Ab- suggestive of a neoplasm as sence of evidence of gross intra- cause. cranial disease other than that afforded by the fit. 2. The commencement always Onset not often local in the situa- local, and movement pre- tions chosen by Jacksonian ; when cedes sensation. it is thus local sensation precedes movement. 3. No tonic stage, at least not Tonic stage nearly constantly pre- marked. sent. 4. Comparatively rarely goes so Loss of consciousness is a constant far as general loss of con- feature, though it may be only sciousness. momentary. 5. After a fit, paralysis, or at Paralysis after a fit not present, a least weakness, is a marked feeling of tiredness in general the feature in the locality of the only evidence of motor distress, commencement. 6. No sleepiness after a fit. Sleepiness very frequent after a fit. B. — Other Motor Disturbances of Voluntary Move- ments — Besides Jacksonian epilepsy, the following involuntary movements are usually assumed to be due to damage of the brain, because (i) they are usually associated with mental deterioration; (2) they cease during sleep as a rule ; (3) they are more complex in gross aspect than we are accustomed to see in pure spinal movements. Paralysis agitans. Coarse rhythmical movements, usually of the head and hands, more marked during inaction ; often, too, these are of the hemi- type, another argument for a brain origin. VIII DISEASES OF THE NERVOUS SYSTEM 311 1 Chorea. • Coarse, involuntary imitations of purposive move- ments, continuous during" waking hours ; also often of hemi- type. General paralysis of Principally of lips and tongue during speech, also insane. seen in the limbs ; the morbid anatomy of this disease is known to be a fine cortical sclerosis. Chronic alcoholism Coarse tremor of hands upon attempted fine or mercurialism. movements. Athetosis. Peculiar rolling movement of affected digits ; frequently post-hemiplegic, and then indicates that the lesion is probably near the cortex. C. — Symmetrically used Muscles — In those symmetrical muscles of the two sides of the trunk and face which are almost never used independently in health, e.g. inter- costals, eye muscles, etc., complete paralysis is never seen from a one-sided central lesion ; the explanation of this, known as Broad- bent's hypothesis, is that such muscles are stimulated into action with nearly equal facility from either hemisphere, either through the corpus callosum or through mechanisms in the mid-brain (? cere- bellum). ON THE SENSORY SIDE Information and facts are much less definite and numerous in considering afferent than efferent impulses. When once the sensory impulse has reached the medulla on its centripetal journey we know little or nothing about it and its neuron complexes, or series of complexes, till it reaches the posterior third of the posterior limb of the internal capsule. It is clinical observation that has taught us that afferent impulses are absolutely necessary for the co-ordinate and harmonious working of the whole body ; but, so far as inco- ordination in the narrower sense of mere movement is concerned, we have only one fact of importance to guide us, viz. that if inco- ordination be due to spinal or peripheral lesions, as in tabes, in all probability the knee jerk will be absent, if it be due to intracranial lesions the knee jerk will be either natural or exaggerated. HEMIANiESTHESIA Due to an organic cause is an excessively rare phenomenon when standing alone ; when with hemiplegia it almost conclusively proves a lesion of the internal capsule, because it is only here that 312 DIFFERENTIAL DIAGNOSIS chap. the sensory fibres are sufficiently close together and to the motor ones to be thus affected by a lesion small enough to not cause such an interference as will either rapidly prove fatal or have such an effect upon consciousness as to prevent trustworthy observations. N.B. — This last statement should be carefully borne in mind, for it is the clue to the reason why many bizarre effects in cerebral troubles have not been noted ; if the lesion is great enough to damage tracts widely separated, it is either multiple or so large as to cause rapid death. Hemianaesthesia as the sole evidence of disease is almost in- variably due to functional and recoverable causes probably affecting the internal capsule. ON THE MENTAL SIDE If there be no pyrexia or other evidence of local disease outside the nervous system, then, qua localisation from mental phenomena, all we can say is that the disease is above the pons and crura, and in all probability is in the cortex of the cerebrum. They arise in all probability from a loosening of, or at least alteration in, the synapsial connections of the cortical neurons. Clinical experience would tend to suggest that the frontal lobes have more to do with the mind than any other part, but nothing beyond this can be said. % ^ ^ % M- % We have now to deal with the differentiating points, and especially to note them as regards the intracranial portion of the system. I propose to discuss the matter, so far as necessary, under the following headings : — 1. Traumatism. 2. Functional troubles. 3. Ordinary organic lesions. I. Traumatism Speaking generally, the incidence of an accident of gross nature and its immediate results are easy enough to appreciate, but there are a few cases of nerve troubles not perhaps usually included in the term, but which, I think, should be so included, for they are essentially traumatic in constitution. Chorea after fright, neuritis or so-called occupation neurosis, i.e, after prolonged special use of nerves, and the results of shock, are illustrations of my meaning. VIII DISEASES OF THE NERVOUS SYSTEM 313 Probably in all there may be an underlying functional or structural weakness of the nervous system, but this does not really affect my point. If we thus widen our conception of traumatism, we have the following separate groups of possible results : — {a) Gross laceration or bruising of tissue, with acute inflamma- tion, followed or not by suppuration and abscess forma- tion, of all of which the traumatism, with entry of pyogenic germs, is at once an obvious, complete, and satisfactory diagnostic explanation. (J?) Tumour of malignant or simple character, where again nothing more need be said, for the tumour is either a blood clot, or it remains in the shape of a cyst, or is of a heteroplastic nature — there are too many cases on record of the last incident to leave any room for discus- sion as to the sequence of events. (For further notes, vide p. 323.) {c) Sickness or degeneration of neuron processes, which may end in recovery, or in ultimate death and sclerosis of the whole neuron, according to the severity of the changes started in it and the general recuperative power of the animal functions of the whole body. This is, I think, the explanation of such cases as those mentioned above — shock, chorea, occupation neurosis — and possibly others. I believe that the potential (to use an electric analogy) of the stimuli sent through the neuron processes has been so high, or the current so long continued, as to have heated, melted, or disturbed the molecular constitution of the wires or connections, with resultant temporary or permanent loss of conducting power. This analogy must not be driven too close in detail, but in broad outline seems to me to offer the best explanation of such cases. However this may be, the relationship of external cause with the clinical symptoms is admitted by all. Of the diagnosis of chorea and shock little needs to be said; their features are unmistakeable. The only problem connected with them is whether the connections or wires of the nerve mechanisms can be repaired, and this point can only be proved by time. Suffice it to say, that repair is the rule, though this may be not quite complete. Of the identification of an occu- pation neurosis or neuritis one can only emphasise the great fact, from which, indeed, they derive their name, viz. that the pain or spasm, or inco-ordination, complained of by the patient is only pro- 314 DIFFERENTIAL DIAGNOSIS chap. duced by the special movements peculiar to the particular occupa- tion (writing, violin playing, etc.). None of them appear when the same nerves and muscles are used for other combinations. This is at least true in the early stages of the malady, but recent observa- tions tend to show that a definite neuritis does frequently exist. If and when this is so, it is easily explained on the above hypothesis. The fact that these neuroses are exhibited only in the performance of one special combination of movements is a strong argument in favour of a primary lesion in the cortex, where combined movements and not muscles are chiefly represented {vide supra^ p. 257). It may also be mentioned that the following, amongst others, suggest a cortical seat for the troubles causing chorea and shock : — {a) That they are practically always associated with some altera- tion in the mental or psychological conditions of the patient. ip) That they very frequently exhibit themselves on one side of the body only. {c) That the trouble is exhibited by complex combined move- ments which are originated in the cortex. 2. Functional Troubles On p. 275 will be found a definition of the term "functional," and the tables and remarks throughout this section may be used to locate the weakened neurons, for it is only by perverted function as exhibited peripherally that we can locate the weakness. Here I wish to draw attention to a division of these cases into {a) those due to traumatism as defined above, and (J?) those due to a general constitutional cause resulting in a loss or perversion of will power. In the latter group of cases, constituting the hysteria of the layman, or the " cussedness of the individual," I believe that the primary and essential lesion resides in the cortex of the brain (? and cere- bellum), and consists in imperfections of the synapses of the inter- nuncial neurons with one another, perhaps associated with altered stability of the molecular constitution of the neurons themselves. 3. Ordinary Organic Lesions There is one exceedingly important general observation to be made which links all these into one. It is this : We must never for- get the great frequency with which acute vascular lesions are found as a complication — very frequently forming the closing episode — in VIII DISEASES OF THE NERVOUS SYSTEM 315 the more chronic troubles, particularly in tumours and in sclerosing lesions ; so that, while recognising the acute condition, we must never omit to inquire very carefully for evidence of a possible pre- existing chronic trouble {vide also pp. 272 and 278). By putting the definite question, " When was the patient last quite well and in his normal condition ? " and further, by inquiring for any slighter mani- festations of ill-health that may have preceded the actual attack for which our assistance is required, we shall not only get evidence of a second lesion if one exists, but we shall also gain informa- tion that may be of the greatest service in deciding between the various possible causes of the attack. We may now proceed to an analysis of the lesions themselves individually. Those which I propose to discuss briefly are : — Inflammation, haemorrhage, thrombosis, and embolism (acute vascular lesions). Idiopathic afl'ections of neurons. Tumours. The following analysis, with the appropriate change in locality, wdll frequently apply as well to the cord and nerves as to the brain. Broadly speaking, they divide themselves clinically into two groups: (i) irritative, (2) destructive lesions; but the distinction, though useful, cannot be maintained in its entirety. For in the life history of an irritative pathological lesion (physiological stimuli apparently have no such limits) there is to be noted, first, a period of excessive functioning in the affected neurons (pain, parEesthesias, twitchings or contractions of muscles), followed by a period in which this excess becomes less and less, until it becomes a nega- tive quantity, finally function is completely abolished (ansesthesia and paralysis), in which stage the symptoms are those of a para- lysing lesion — another reason for carefully ascertaining the whole history of the case. Then, again, the distinction of irritation v. destruction w411 depend in some cases on the situation of the lesion, meninges, or perineurium v. bulk of brain, cord or nerve strands. Inflammation, hsemorrhage, and frequently also tumour, will at all times offer good examples of this variability with locality. Acute Vascular Lesions Acute Iiiflamf nation. (For diagnosis of Peripheral Neuritis, vide pp. 281 et seq. and pp. 2 9 2 (?/ seq. ) As it attacks the central nervous system it occurs in two well- 3i6 DIFFERENTIAL DIAGNOSIS chap. marked forms, i.e. meningitis and encephalitis or myelitis, which require separate notice. Of the Membranes, Meningitis. — Here, as anywhere else, acute inflammation excites general symptoms, viz. pyrexia, with malaise and discomfort. The special points leading us to locate it in the nervous system are the concentration of the pain in the back, or in the head, with rapid onset of grave symptoms of impHcation of nerve matter, or of pressure on it (affections of cranial nerves — squint, facial paralysis, etc. — vomiting, optic neuritis, unconscious- ness, jumping of muscles, feebleness of gait, or paraplegia, etc.). In its irritative stage it may require separation from meningeal haemor- rhage or tumour. From the former, its slower onset and the pyrexia will be sufficient ; from the latter, the pyrexia again and its more rapid (a day or two at most v. a week or two at least) onset should usually leave no doubt. In its paralytic stages it becomes essentially a cortical myeHtis or cerebritis, and only the history shows that such began as a meningitis. Of the Cord. — The rapid onset of a complete paraplegia could only arouse suspicion of blocking or rupture of a vessel apart from a myelitis. Thrombosis or plugging of spinal vessels is so rare as to be a mere curiosity, but both this and haemorrhage will be in their earlier stages sufficiently separated from myelitis by their absolutely sudden onset, and by the absence of pyrexia. In their later stages all three lesions would be identical. Of the Brain. — A primary cortical acute cerebritis is extra- ordinarily rare. If it occurred it would precisely resemble an acute meningitis, except that there would be a more rapid onset of para- lytic phenomena, especially in the limbs (vertical meningitis), or in cranial nerves (basal meningitis). Acute primary medullary cerebritis, i.e. in the mass of the brain, is practically only known in the shape of an abscess, and then the principal point is to separate it from a tumour. Their likenesses and differences may be summed up thus. Both will be equally likely to have — 1. Vomiting. 2. Optic neuritis. 3. Headache (intense). 4. Localising paralytic phenomena, or irritative. VIII DISEASES OF THE NERVOUS SYSTEM 317 On the other hand, they will probably differ as follows : — Abscess. 1. A history of some peripheral suppuration — ear, nose, and other discharges — which has possibly ceased just previous to symptoms of cerebral trouble. 2. Symptoms may quite possibly come on with great rapidity, and rapidly get more serious. 3. Temperature a little raised, or more probably subnormal. 4. Irritative phenomena rare, para- lytic phenomena at once or rapidly coming on. Tumour of other Nature. Probably no such history, but there may be a tumour elsewhere sug- gestive of a primary growth, to which the cerebral one may be secondary. Symptoms rarely increase with great rapidity unless it be with instantaneous exacerbation, indi- cating haemorrhage into tumour. Temperature either quite normal, or with greater and more irregu- lar ranges than in abscess. Irritative phenomena commoner, and lasting longer than in ab- scess. Hcemorrhage, Thrombosis^ and Embolism — The one essential feature common to all these, and the one by which they are as a group separated from all other lesions, is the instantaneous rapidity with which their symptoms commence, and speedily reach an acme. The two latter never as a simple diagnos- able lesion occur in the meninges, but the former frequently does so, and it is of some importance to distinguish this situation of it if we can : — Meningeal Haemorrhage. 1. Commoner when idiopathic in young subjects. 2. Very rare, except as the result of traumatism, forceps at birth, e.g.^ or blows on the head or back. 3. Commencement of symptoms sudden, but generally some minutes or even hours before they reach their acme, ix, more ingravescent. Haemorrhage into Bulk of Brain or Cord. Commoner in older subjects when without exciting cause. Very common, without any history of traumatism : is equally rare as the result of violence, unless this be very severe. Instantaneous commencement, and acme reached almost with the same rapidity ; gradual ingra- vescence is much rarer, though well recognised as occasionally occurring. 3i8 DIFFERENTIAL DIAGNOSIS chap. In this point of contrast it is obvious that exceptions must occur in connection with the size of the vessel which has ruptured, e.g. the middle meningeal or the basilar, on the one hand, the symptoms of which will be indistinguishable almost from intra- cerebral haemorrhage ; or, on the other hand, a very small branch of an intracerebral artery, the symptoms of which may be very slowly ingravescent. Concussion, or brain bruising, is another exception, but its onset is always traumatic and sudden. , , . , TT I- Haemorrhage into Bulk of Brain or Meningeal Hsemorrnage, r d 4. The symptoms usually go The symptoms cannot be said to through an irritative stage, have any irritative stage ; they which is easily observable are destructive from the earliest and may be prolonged (pain time of observation, or convulsive movements). 5. The subsequent course may Recovery never complete, and the show complete recovery, focal lesion will always be found though possibly an irritative to be a destructive one. focus may be left behind. In discussing the separation of the three troubles as they occur in the bulk of the brain or cord, it must be admitted once for all that a positively certain diagnosis (ante-mortem) is impossible, but a more or less intelligent and probably correct guess may be hazarded by attention to the following points : — 1. That in the spinal cord the communication of the vessels is so free and easy that embolism and thrombosis are of the very rarest occurrence of sufficient extent to cause a definite paraplegia. 2. Age. — Though the cause leading to embolus direct from the heart (acute endocarditis) is commoner in young subjects, and also syphilis and tubercle as active causes of local thrombosis, yet none of them cease absolutely as age advances. Moreover, atheroma, another principal cause of thrombosis or embolism (from debris), is distinctly an affection of advancing years. Hence age, per se, gives us no very strong and leading guidance ; nevertheless it must be stated that, ceteris paribus (which they seldom are), the older the patient the more do our thoughts go in the direction of haemorrhage., 3. Marked premonitory symptoms of slight attacks are likely to make us think of thrombosis, especially if syphihs is present, or tubercle a probability. The reason for this is that preliminary small haemorrhages are rare, and so also, I believe, are small VIII DISEASES OF THE NERVOUS SYSTEM 319 emboli, while as an artery gets gradually obliterated we should expect premonitory evidences of disturbed nutrition in areas which are ultimately going to die. 4. State of Consciousness. — If we bear in mind that haemorrhage forces asunder (by a pressure increasing as the cube of the radius of its bulk) the fibres of the brain, and adds materially to the bulk of the intracranial contents by blood which should be escaping by the veins, thus increasing the intracranial pressure ; if, too, we bear in mind that loss of consciousness (under the circumstances we are now considering) is probably due to increase of pressure on the cerebral cortex, or to violent impressions upon it, and then consider that the plugging of a vessel from any cause has no such tendency, w^e shall see the probable explanation of Trousseau's statement (which is, I believe, still in accord with clinical experi- ence), that " Whenever hemiplegia, complete and absolute " (there- fore due to a rather serious lesion), " occurs suddenly " (therefore due to vascular lesion) " without the loss of consciousness " (there- fore without much pressure), "it is more likely to be due to softening (plugging) than to haemorrhage." 5. State of Heart. — If in a young subject, otherwise in usual health, we hear cardiac bruits, they will be, ipso facto^ suggestive of embolus, provided the heart is acting fairly quietly and regularly, and the more suggestive the more recently the bruits are known to have developed. If, on the other hand, we find a powerful heart acting violently with or without bruits, we suspect that this power has ruptured a weakened vessel, especially if the attack (hemiplegia) came on during exertion or excitement (one of the great dangers of alcohol when taken by a person with damaged vessels). Finally, if the heart beat is very feeble, as after a severe illness of any sort, and during convalescence, the feebleness of the circulation is sug- gestive of thrombosis, either locally at a distance from the heart, i.e. in the brain, or of clotting in the irregular chambers of the heart and propulsion of an embolus thence. 6. Te7?iperature. — Haemorrhage always causes a fall in the tem- perature, which may continue till death or be replaced by irregular pyrexia. Plugging of a vessel rarely causes much fall, and, if it does so, the temperature soon rises to normal, and continues there with very slight or no variation, so that the greater the excursions of the thermometer the more do we think of haemorrhage. If these various indications are properly balanced, a correct con- clusion will more often than not be arrived at, though many mis- taken diagnoses will undoubtedly occur. 320 DIFFERENTIAL DIAGNOSIS chap. It must not be overlooked on the post-mortem table that a fatal plugging may yield no very obvious signs, because the softening which we look for as proof of plugging is a phenomenon which only commences some little time after the circulation through the part has ceased. It may not be out of place, too, to mention that, whether the softening be white, red, or yellow, it is merely an acci- dental result of (i) the age of the process; (2) the amount of blood or other pigment, or their derivatives, left in the area by circumstances of absorption ; it has no special significance suggestive of a difference in the pathology of the lesion. Idiopathic Affections of Neurons Though in no sense of the word idiopathic, there is no other connection in which the effects of hgemorrhage or plugging can be more appropriately placed ; consequently, we must tabulate the above heading as follows : — 1. Secondary to their death by gross violence, whether from haemorrhage or plugging. 2. Idiopathic — {a) Acute, usually termed acute inflammation. lb) Chronic, usually termed primary sclerosis. I. Of the secondary form but little need be said; it undoubt- edly occurs as a sclerosis of a tract, or track, after haemorrhage from or plugging of a vessel has destroyed the nutritive mechanism, but it adds litde or nothing to the clinical picture already portrayed. The paralysis, or anaesthesia, or both, and the exaggerated reflexes appear rapidly as the result of the death of the neuron ; the subse- quent sclerosis merely fixes these in rigid features, and adds certain confirmation to a previous diagnosis of organic mischief. 2 {a). The acute primary affection has its chief, if not its only, seat in the neuron cells of the motor areas (nuclei of nerves), at any rate this locaUsation property is so constant that cUnically it affords one of the strongest points of evidence in favour of the particular pathological lesion, i.e. of primary acute inflammation or degeneration. We find it most commonly in the spinal cord as acute anterior poliomyelitis, the diagnostic points of which have already been considered on p. 292, but it must not be forgotten that the nuclei of origin of the motor cranial nerves are absolutely analogous in function, if not even serially homologous in structure, to those of the anterior cornua, and are therefore found to be VIII DISEASES OF THE NERVOUS SYSTEM 321 liable to the same affections ; hence an acute bulbar paralysis or an acute affection of an isolated cranial nerve nucleus may and does occur. Its history will be one of acute {i.e. complete within twenty- four hours) onset, accompanied probably by a slight pyrexia ; the latter may be so slight or fugitive as to escape observation, and hence the disease may resemble at its onset a small haemorrhage or softening. The differences in such an acute case will principally consist in the following : — {a) Although it is possible, yet as a matter of clinical experience, the onset rarely is so instantaneous as in hemorrhage. (B) There will be at any rate in a few hours after onset an almost complete absence of any sensory phenomena. ic) In the bulb if the cause of the trouble were a haemorrhage or softening, it is almost inevitable but that some limb paralysis or anaesthesia should be found, for the vessels supplying these motor nuclei do not confine their nutri- tive supply to these alone; and we have already noted the peculiar precision with which this lesion does pick out the motor cells only. In the identity of its results upon the peripheral nerve and the muscles supplied by it (degeneration and atrophy), it has to be separated from purely peripheral lesions ; difficulties arise here more in theory than in practice ; nuclear lesions are seldom quite com- plete {e.g. of third, seventh, sixth, twelfth, etc.), while peripheral ones are specially prone to be so, particularly if the nerve {e.g. the seventh) passes through a bony canal. Again, if the peripheral lesion be only partial, its causes (meningitis, gummata, tumours, etc.) are associated with general symptoms or local phenomena (swelling, pain, etc.) of such obtrusiveness as to leave little room for doubt if the case be seen in an early stage. In later stages diagnosis will be impossible without the history to guide us. 2 {b). In the chronic form of primary sclerosis of tracts, of which the following are the chief types : — Tabes dorsalis ^ Lateral sclerosis > of the cord ; Progressive muscular atrophy J Disseminated sclerosis of cord and brain ; Chronic bulbar paralysis of bulb ; ? Paralysis agitans 1 r ^ ■ :i o -1 ^ r of bram cortex: - ? benile tremors J Y 32 2 DIFFERENTIAL DIAGNOSIS chap. the principal feature which separates them at once from every other lesion — except a very slowly growing tumour — is the extreme chronicity of the process, so that symptoms are slowly developing for many months at least, and often even for years. The extreme precision with which this affection, i.e. primary sclerosis, picks out certain tracks and strands (except disseminated), is also as marked a feature as in the acute form, so that, when combined with chroni- city, it leaves little room for doubt, at any rate in advanced cases. The individual diseases have already received {supra) sufficient attention ; it remains here only to remark on the likeness of the process to functional disorders. If we consider the minute patho- logical processes underlying the gross sclerosis (the final stage), it is easy to see that in the early stages of the trouble we are now con- sidering, it is probable that a time will occur in which only function will have suffered, and consequently this will be a stage in which the greatest difficulties may occur in separation ; in fact, there may be, and even probably must be, identity of symptoms with a differ- ence only in future progress. Attention may be drawn to p. 297, where the differences between disseminated sclerosis and functional troubles are discussed. Besides what is there recorded there is only the general consideration of the element of time ; this, in the beginning of a simple functional trouble, which is not going to proceed to sclerosis, is likely to show confusion in many systems, as opposed to stress on one system in a case that is going to end in sclerosis ; and then, again, later will show a stationary or im- proving condition in the former versus a downhill course if the fundamental meaning of the symptoms is the starting of a pro- gressive process of decay and degeneration. Tumours of Brain (and of Cord) By their comparative chronicity or comparative acuteness, according to the point of view from which we regard them, these troubles separate themselves almost conclusively from vascular and acute inflammatory lesions on the one hand, and, on the other, from chronic idiopathic scleroses. From the latter, too, they are also separated by the fact that they are very indiscriminate in the pressure they exert : they spare nothing that comes within their sphere of influence (hence the predominance in the cord of root symptoms). As they affect the cord they will receive no further notice, but from their importance in the recent advances of cerebral pathology and treatment they must be discussed a little more fully as they affect intracranial structures. VIII DISEASES OF THE NERVOUS SYSTEM 323 It Is common knowledge that the tripod on which their diagnosis mainly rests has for its three legs : — Headache. Vomiting. Optic neuritis. To these are frequently enough added some specific features indicating its locality, and occasionally its precise nature. For the former, vide Jacksonian Epilepsy and the Cranial Nerves; of the latter it is only necessary to mention a definite history of syphilis, tubercle in the choroid or elsewhere, and a primary focus in some organ of sarcoma or carcinoma. Now, any one of these three legs may be permanently knocked away and yet the diagnosis stand, while even two may be removed for some time without a complete overthrow of the diagnostic super- structure ; but if all three be gone it is only in the rarest of instances, and more by inspiration than logic, that we should venture to assert that a cerebral tumour was present because of some incidental localising suggestions. Headache. — Pain in the head, even severe, is such a common complaint that not much stress can be laid on this symptom until the other common sources of it have been excluded. We may say that unless at least one of the other two guiding indications were present it would hardly arouse suspicion of a cerebral neoplasm (not but that the neoplasm may be there, without our suspecting it), except it possessed in rather a marked degree some or all of the following features : (i) very persistent and resistant to remedies, and possibly paroxysmal; (2) so severe as to keep the patient awake at night ; this should be made a very strong point, as patients vary very much in their estimation of the intensity of a headache ; (3) located in one, and that perhaps an unusual part of the head ; (4) often associated with acute additional pain or tenderness on percussing the head in that region (this is commoner in superficial tumours, and when definitely present is a valuable localising sign). Vo??iiting. — If of cerebral origin {vide pp. 158 and 159) is usually stated to be unassociated wdth much, or any, nausea ; totally inde- pendent of food (often attempted with an empty stomach), and of a peculiarly forcible (pumping) character ; certainly none of these features is absolutely constant, even in the certain presence of a tumour, but we may safely say that w^hen a patient makes special comiplaint of vomiting as the chief symptom, and no definite gastric or alimentary trouble can be found to account for it, it is imperative 24 DIFFERENTIAL DIAGNOSIS CHAP. upon us to examine the fundi oculorum and inquire more particularly about the headache. The diseases likely to cause such vomiting of remote or obscure origin are tabes dorsalis and Addison's disease, neither of which should offer any difficulties in exclusion, at least from the possible occurrence of a tumour. Optic Neuritis. — Inasmuch as a definite optic neuritis occurring as a totally independent disease, apart from any discoverable causation, is the very rarest of phenomena, if not absolutely unknown, it necessarily follows that if we can establish its certain presence, and if we can exclude other causes, we have almost proved to a demonstration the presence of gross intracranial mischief of but few categories. As regards its recognition it can?iot be too strongly insisted upon, no? too often repeated^ that severe optic neuritis and other pathological changes in the fundus may be present without the slightest volujitary co7nplaint on the part of the patieitt of subjective disturbances of vision^ nay more^ he may deny such even when the direct question is put to him, so that the ophthalmoscope is absolutely necessary for diagnosis. The following is a tolerably complete list of causes of the changes found in the fundus, with the main characters of separa- tion : — Gout, cirrhotic kid- neys, albuminuria. Specific fevers, ty- phoid, e.g. Leucocythsemia and purpura. Embolism of central artery. Anasmia. Haemorrhages, or white atrophic spots, the chief feature in the fundus ; the examination of the urine, and other evidences of vascular degenera- tion, leave no room for mistakes. The pyrexia, the rash, and general symptoms too well marked ; the neuritis itself may be indis- tinguishable. Again hemorrhages are the prominent feature in the fundus ; examination of blood and en- larged spleen in the one case, and haemor- rhages in the skin in the other, are sufficient to prevent mistakes. Changes are in the yellow spot, not In the disc, except as atrophy ; arteries and veins small instead of large. Loss of sight probably com- plete in the eye affected. Optic neuritis rare, except in cases of very marked pallor ; examination of blood gives certain information. I have known even Dr. Jackson deceived in such a case, however, and diagnose tumour from the headache and optic neuritis when they were dependent upon simple anaemia. VIII DISEASES OF THE NERVOUS SYSTEM 325 Lead poisoning. Errors of refraction. Tubercle. In tumour of ordin- ary character, or syphilitic or tu- bercular, and in abscess or men- ingitis of any causation. It is very rare that optic neuritis is the only sign of plumbism in a doubtful case ; wrist drop or colic, or blue line, nearly sure to be present ; occupation or opportunities for absorption important. This is rather a pitfall in estimating the presence of a neuritis than a definite cause of that con- dition. They must be carefully excluded as the possible causes of visible fundal pecuharities before other ones are sought ; and the results of their correction noted. Visible as small nodules in the choroid ; their presence is absolutely conclusive as to the nature of a tumour or a meningitis if previously doubtful, but they are only rarely present even when tubercle is the cause we are seeking for certain symptoms. The optic neuritis when present has usually no distinctive characters peculiar to each (? tubercle above), but is very frequently present with any of them as very strong evidence of a gross diagnosis. Such are the principal means we have for a pathological diag- nosis in general terms. We have already considered the separation of meningitis and also of abscess. The question of the space of time during which a lesion is developing its features has already been repeatedly alluded to, and so also have those features which assist us in forming an opinion as to the precise locality of a disturbing factor. The question cannot be pursued farther with- out going into very special discussion unsuitable for the present work. CHAPTER IX URGENCY CASES Under this heading I propose to discuss the diagnosis of a very mixed group of cases with which the daily press has from time to time made and kept us famihar under the attractive (?) title of " Drunk or Dying," in allusion to the fact that so many of them, while ending fatally, have a very close resemblance to the varied phases of alcoholism in its numerous stages. It is for lack of some definite principles in diagnosis (and treat- ment) that so many mistakes have occurred, mistakes from which no extrication is possible, and through which more than one medical reputation has foundered, and public institutions have had much undeserved censure cast upon them. We may define the group to which I refer as " Cases in which we are called upon — usually in a great hurry — to examine and treat a patient in whom sudden and apparently severe illness has super- vened, and whom we have not been previously attending, or with whose previous history we are at the time unacquainted." This last condition is put in to temporarily exclude cases of illness which are known to be complicated with sudden storms, though the following analysis will show that such are not usually present. We will commence with a bare enumeration of the lesions which are liable to take place suddenly, or, perhaps more appropriately to our subject, are liable to cause sudden symptoms in persons who are apparently in perfect health, or at least are able to go about the public thoroughfares unattended. They divide themselves fairly naturally into groups as follows : — I. Haemorrhage. II. Vascular lesions other than haemorrhage. CHAP. IX URGENCY CASES 327 III. Traumatism. IV. Sudden death. V. Lesions and conditions of the nervous system. VI. Poisoning. This is a fairly complete list of " urgency cases." It may seem a very formidable one to carry in mind, but in practice it is not so, for many cases are self obvious from the first, and early treatment can proceed on but very few lines. Group I. HEMORRHAGE {a) Through breach of skin. e.g. Traumatism, varicose veins, etc. {b) Appearing externally e.g. Hsematemesis, hjemoptysis, epis- through rupture of vessel taxis, or haemorrhage from internally. rectum. {c) Concealed haemorrhage. e.g. Rupture of aneurysm, or of tubal gestation, or of a vascular organ, especially spleen ; heemorrhage into stomach without vomiting, or into in- testine without appearing in a stool. (Cerebral haemorrhage is not included in this group, as it is brain laceration and compression that cause its symptoms.) From the point of view of a provisional or preliminary diagnosis guiding U3 to first or immediate treatment, this group stands almost by itself, and may at once be dismissed rather summarily. Sub- divisions {a) and {h) are at once obvious by the blood round the patient (if the body has been removed or the blood cleaned up there will obviously be some history of such having been done). Group {c) offers a little more difficulty, but here it is fair to assume that if the haemorrhage is sufficiently severe to necessitate the attendance of a medical man, it will be sufficient to cause very marked blanching of the face, and faintness, with the small pulse, weak or husky voice, and sighing respiration characteristic of a severe loss of blood. A ruptured aneurysm, spleen, or ectopic gestation is, besides the faintness and blanching, also very likely to cause severe local pain, directing attention to the region in question. 328 DIFFERENTIAL DIAGNOSIS chap. Group II. — Vascular Lesions other than Haemorrhage e.g. Simple fainting, angina pectoris. (Blocking of blood-vessels is excluded here, as the symptoms entirely depend on the locality of the block.) A diagnosis of either of these conditions is usually, like that of haemorrhage, fairly easy. Either of them may have ended in rapid death (a subject of special grouping, vide below), in which case let me strongly urge that no diagnosis should be given without a complete autopsy. Fainting, if not due to actual haemorrhage {vide above), is commonly very transient ; if prolonged, it can only be diagnosed as a simple lesion by exclusion of the indications of Groups V. and VI. {vide pp. 331, ZZ'^\ Angina, if of any severity (and it is only then that it becomes an " urgency case "), will be recognised by the position of the pain in the chest, and the fixed attitude of the patient from the fear of death on movement. Group III. — Traumatism The only conditions that can arise from traumatism are — (i) The actual injury to limbs or viscera. (2) Shock to the nervous system, which may be sufficiently severe to cause death. (3) Unconsciousness, from — {a) Sh^ck, pure and simple, {b) The nature or locality of the injury, e.g. of brain. (4) Death. If the victim is conscious, and thus a history obtainable, no difficulties in forming a preliminary diagnosis can arise, and we are not here concerned with anything deeper or more accurate, the discussion of which indeed involves a whole treatise on trau- matic surgery. If, on the other hand, the victim is unconscious though not dead (again vide Sudden Death), and no history obtain- able from friends or bystanders, the patient must be carefully examined for any signs of injury (fractured base of skull, or severe crush, bullet wounds, etc.), and then, should nothing be found to account for the unconsciousness, the case must temporarily be placed as " unconsciousness " amongst the group of nervous lesions, and its diagnosis sought by means of the indications given under IX URGENCY CASES 329 that heading. The position of the body, as at the bottom of a ladder or stairs, etc., may suggest a fall, but even if the fall be proved, it may still be due to epilepsy, apoplexy, etc. The shock of traumatism, especially if the latter be not very severe, may take the shape of a mental condition closely resembling alco- holism {q.v.). Group IV. — Sudden Death The interest of this group is purely medico-legal. There can be no clinical diagnostic problem involved, unless it be to give a warn- ing to friends as to the possible sudden death of any patient, so that worldly affairs may be put in order in time. It is, however, impossible to ignore the condition in an article on " Emergency Cases," and so I have inserted the following table, which is but slightly altered from Professor Dixon Mann's article in the Lancet for June 26, 1897 ; the great assistance of which I wish to acknow- ledge. Dr. Mann states that in a case of sudden death one of three conditions will be found on autopsy : — 1. A recognisable disease or condition known to be commonly associated with a sudden end. 2. A recognisable disease, but which is not usually terminated suddenly. 3. No recognisable pathological condition anywhere in the body. Tabulated and arranged, with a few additions and alterations, this first list gives the following : — {a) Morbus cordis (in about Valvular disease. half the cases. — Mann). Possibly congenital abnormality. Atheroma of coronary arteries (with or without history of angina pectoris). Fatty heart. Sclerosis of muscle. Rupture of wall of a cavity. {b) Haemorrhage. Ruptured aneurysm. Ruptured spleen. Into pancreas. Into brain (apoplexy). Into stomach or intestine. Ectopic gestation. Varicose veins, internal or external. Traumatism of a large vessel. 33° DIFFERENTIAL DIAGNOSIS chap. {c) Asphyxia, with a condition Air, serum, blood, or pus in pleural or disease known to pro- cavity. duce it rapidly. CEdema of, or membrane in, glottis or polypoid growth. Pressure of tumour (solid or liquid) on larynx or trachea. Embolus of air in a vein, or clot in a pulmonary artery. Blood, or other vomited or swallowed foreign body in air passages. {d) Miscellaneous group, in Perforation or strangulation of gut, and which precise mode of peritonitis, death not obvious. Exophthalmic goitre, though the morbid con- Addison's disease, dition is easily recognis- Nephritis of any kind, able, and is known on Pneumonia, especially in old people, occasions to cause very Abscess or tumour of brain, rapid death. Meningitis. Obvious damage to a viscus from trau- matism. In his second list Professor Mann includes some of the con- ditions I have put in the first one, and also the following : — Diphtheria, without membrane being the apparent cause ; prob- ably neuritis. Phthisis, with exhaustion probably. Ulcerative endocarditis ; may be signs of septic infarction. Pericarditis, with effusion of serum or pus. Adherent pericardium, probably with recognisable changes in the muscle of the heart. Gall-stone colic ] May find the stone in the duct or ureter, Nephritic colic J but it may have sHpped back or out. Gout, especially in corpulent individuals, recognised probably by the cirrhotic kidney corroborating the joints or tophi. Hydatid tumour, which has ruptured. The third list of Professor Mann's I have enlarged by including in it several conditions which he has placed in the first and second; my reason for so doing is that it is only in very exceptional circum- stances that the results of the autopsy are sufficient for a diagnosis ; there is required in addition a reliable history of the patient in some form, or a witnessing of the last scene. It includes : — IX URGENCY CASES 331 Asthma — possible signs of asphyxia. Pertussis — possible signs of asphyxia. Overlaying of infants. Epilepsy — possible signs of asphyxia ; "i /i -ki ,,--, 1 • • , •! T f anQ possiDiy Convulsions m children ; L i v.' f Spasm of glottis — possible signs of asphyxia ; T i _. (Laryngismus stridulus) ; ) Acute rheumatism — cardiac syncope. Zymotic diseases — occasionally by intensity of the poisoning — without a rash. Hyperpyrexia — sunstroke, acute rheumatism, etc. Influenza. Excitement or fright as in quarrelling, or near approach of any danger — thought of an operation, etc. Chronic alcoholism — probably some neuritis of pneumogastric. On these lists I do not propose to say anything further ; their importance is obvious and enormous ; but when we have admitted the fact of sudden death, and have made a thoroughly careful post- mortem, clinical medicine ceases its functions, and legal procedures come to the front with all the available evidence as to what was happening, or had just happened, when death took place. We now come to the two groups which include the real crux of the position, and are the essential clinical elements in drunk or dying. They must be considered in. some considerable detail. Group V. — Lesions and Conditions of the Nervous System Cerebral plugging or rupture of a vessel, constituting apoplexy of the laity. Epilepsy — including post-epileptic states, and also malingering of fits. Hysteria. Plumbism — lead encephalopathy. Lunacy — especially G.P.I. Cerebral tumour — with epileptiform convulsions. Sunstroke. Meningitis, and acute encephalitis. (Simple fainting will be here considered; as its main symptom is apparently cerebral.) 332 DIFFERENTIAL DIAGNOSIS chap. Group VI. — Poisoning, including two Sub-Groups A. Autogenetic. Uraemia. Diabetic coma. B. From without, which may include any and every poison, however administered, but from our present point of view has especial reference to — Alcohol. Opium and other narcotics, such as chloral. Belladonna as a deliriant. Strychnia as a convulsant. Both for diagnosis and treatment it will be well to maintain a chronological order of events, as this will render the discussion much more practical, even if it introduces a little theoretical incon- sistency. Commencing then with the history. While getting ready to go or going with the messenger we must inquire into the particulars of the seizure as closely as possible : asking, for instance, Has the patient taken anything ? — if so. Of what known nature ? — Whence obtained ? — Is he in a fit ? etc. From the answers to these questions, if they be intelligent or even intelligible, valuable hints may be obtained, I am bound to admit that in the majority of cases there will be either no history at all, owing to the absence of witnesses, or the history will be unintelligible, owing to the anxiety, fright, or imbe- cility of the messenger ; or, again, it may be purposely misleading in some few criminal cases. Such as it is, however, listen to it, and use your own judgment as to its value. On arrival, the first thing is to clear the room or a space round the individual, to give him air, to prevent bystanders doing mis- chief, and to enable you to exert your own efforts without unneces- sary interruption. Secondly, while doing this, you will have a few moments in which to note the general aspect of the patient. Is he motionless and apparently dead, or is he in a fit, convulsed and obviously living ? Is his face natural in colour, or is it blue with livid lips, and is froth issuing from them ? — if so. Is the froth blood- stained ? Is he sweating profusely, or is his face dry ? Thirdly, while noticing these facts loosen everything from the neck, cutting the clothes if necessary for rapid action to prevent imminent asphyxia. And lastly, if convulsed, restrain him in some way, so as to prevent him from injuring himself by the violence of his movements. IX URGENCY CASES 333 We are now in a position to take diagnosis into consideration, and this obviously proceeds in two directions, according to whether the patient has convulsions and is living, or whether he is quiet and possibly dead. If he is in a " fit," this may be due to — Cerebral (hcemorrhage, tumour, etc.); Epilepsy ; Hysteria ; Malingering ; Poisoning — strychnine especially, but possibly opium or other poison ; Uraemia ; Dentition, etc., in babies ; Tetanus ; and the following are the points most worth attention to decide which of these is present. 1. Age and Sex. — Of age little need be said, for at all ages many things are possible. It is obvious that dentition can only occur in babies, and in these young subjects convulsions are very common from every form of reflex irritation ; the precise cause can only be cleared up by the same careful examination as in adults j the condition, though very common, hardly gives rise to difficulties in our present connection,/.^, with "urgency." Sex, too, has only this influence, that in females, and especially from seventeen to forty years of age, we lean more strongly to a diagnosis of functional trouble of no great immediate danger. 2. The Eyes. — A most, perhaps the most, important seat of clues. Are they open or shut ? — if shut. Is there much resistance to your opening them by lifting the lids? — Is the patient looking round furtively ? This furtive glancing and resistance to opening the eyes is very suggestive indeed of hysteria or malingering. Then the state of the pupils, note are they equal or unequal, dilated or contracted, do they react to hght or not, is the conjunctival reflex present. In epilepsy the pupils are dilated and insensible to light, or occasionally oscillating without obvious cause : in hysteria they react readily to light, and in malingering (unless artificially tampered with) they will obviously do the same. In poisoning they will usually not act to light, if it be by strychnine, the only likely convulsant, they will be dilated, as will also happen if asphyxial convulsions are due to some poison; should it happen to be a case of opium poisoning with 334 DIFFERENTIAL DIAGNOSIS chap. convulsions they will be contracted. In uraemia the pupils are as a rule fixed and dilated, they react very slowly, if at all, to light, but it may happen that they are of natural size. If the pupils are unequal we shall think of pontine or other cerebral haemorrhage, or of general paralysis of the insane. The conjunctival reflex will be absent in 'epilepsy, uraemia, and other more dangerous conditions ; certainly present in hysteria and malingering. We may sum up the matter by saying that if ( i ) fixed (small or large), or (2) irregular and unequal, pupils are present, or if (3) the conjunctival reflex is absent, then the condition is serious, and may be a dangerous one. If, on the other hand, the pupils react readily to light, it is probably a less serious matter, and if the conjunctival reflex is present this adds greatly to the probability of a recoverable condition. 3. Froth coming from Mouth, — This is usually present in epilepsy, and very possibly blood-stained from biting of the tongue. If it be blood-stained, epilepsy is certainly most probable in the absence of motive for malingering. Malingerers will use soap for froth-making purposes, so that the mouth must be examined for this article. Froth may be present in poisoning, but has then no special significance except as suggesting hydrocyanic acid, but then fits are not present. 4. Note the Nature of the Convulsions. — They are most exag- gerated perhaps in hysteria, and most universal. The malingerer is apt to over- or under-do the movements. In poisoning by strych- nine an attack is soon over and followed by complete relaxation of muscles ; in tetanus this relaxation is incomplete ; moreover strych- nine convulsions are more marked in head and trunk (opisthotonos or emprosthotonos), while tetanus is more likely to be concentrated in the jaws and neck. In epilepsy, too, opisthotonos is usually absent, and malingerers cannot keep it up for long, even if they can assume the position at all. In cerebral haemorrhage or blocking with convulsive movements, these will take the shape of conjugate deviation of head and eyes, a most important sign, hardly ever met with except with such gross lesion. 5. The General Appearance of the Face. — In malingerers certainly, and usually in hysteria, the face is hot and flushed, and the body as well bathed in hot perspiration (note the state of the weather or atmospheric pressure) if the movements are at all violent. In epi- lepsy the face is possibly blue and congested, or more probably pale ; it may be moist, but it will be with a cold sweat, and the same coldness will be present in poisoning. In uraemia the face IX URGENCY CASES 335 may be flushed, but it is more usually natural or pale without sweat. 6. The Getter al Coftscioitsness and Capability of being Roused to Speech. — In malingering and hysteria he can certainly be roused ; in epilepsy and uraemia he cannot be ; in poisoning he is either totally unconscious (hardly in this group), or is perfectly conscious and rational between the fits. 7. The Pulse. — Over this the patient can have no control. In malingering and hysteria the pulse will be full, bounding, and rapid from exertion. In uraemia and poisoning it is likely to be very small and rapid ; in epilepsy it is usually somewhat accelerated ; in gross cerebral lesions it is likely to be very slow, from cerebral com- pression. Such are the most important means of immediate or rough diagnosis, none of them individually trustworthy ; each has to be considered in relation to the others. I do not propose to consider the more accurate diagnosis any further, as the main object of this chapter is to draw a line between those cases for which a bucket of water or a police cell is advisable, and those for which skilled medical attention in a place of rest and quietude (bed at home, or in a hospital) is the only safe line to pursue. We will now pass on to the second group of cases, viz. those in which convulsions with (genuine or feigned) unconsciousness are not present. Here the cases may be divided into three classes, though I shall speak of them only in two : — /. — Those who are actively conscious (this consciousness may be very perverted in its judgment), and perhaps noisy and abusive, especially when undergoing physical examination. // — Those who are unconscious, but can be roused by speaking, pinching, pricking, etc. ///. — Those who are absolutely comatose, and cannot be roused at all. Firstly, then, those who are actively conscious and may be noisy. Practically there are four things to be thought of here : — ■ ( 1 ) Alcoholism — drunkenness ; (2) Head injuries and cerebral disease; (3) Lunacy; (4) Poisoning other than alcohol — rarely ; and it must never be forgotten that the first may be combined with any of the others ; a complication the possibility of which forms the principal crux of the problem. 336 DIFFERENTIAL DIAGNOSIS chap. Here again, the first thing is the history from others or from the patient, and it is very probable that in this class of cases it will throw strong light on the diagnosis, especially when taken with the manner in which it is told. Lunacy, under these particular circumstances, is almost sure to betray itself either by the absolute nonsense the patient talks, or by the direct contradiction of, or lack of confirmation from, the story of those with him. The manner of relating his tale differs materially in the lunatic and the "drunk," The lunatic may relate his tale perfectly quietly and with pseudo- rationality, the drunken man is nearly sure (in this stage) to be very excitable and inco- herent : the speech of the former will be complete in its individual words (except in general paralysis of the insane, when the long words may be slurred), that of the latter will have the easily recognised character of drunken speech. If actual lunacy can be excluded, but we have a strong suspicion that alcohol has been at work with or without an accident of some kind, the tale of others may be of most material value. In cases of head trouble, whether from traumatism (shock is here an important element) or from disease, a little alcohol goes a long way, so that if there be the slightest suspicion of serious trouble, abuse and noisi- ness must be largely discounted, and the patient taken under pro- fessional care. A case in point occurred within my experience some years ago. The patient was at first quiet, but began to be noisy, abusive, and very pugnacious when examined. He was thought to be drunk, and was on the point of being sent away when another house physician saw him, thought he looked very ill and peculiar, and advised his admission to the wards : he died before reaching them, and the autopsy showed that it was a case of cerebro-spinal meningitis. See, therefore, how noisy and abusive conversation fits in with other facts in the history. If what you hear is not sufficient, see what you can ascertain with your eyes. The colour and appearance of the face may help. In alcoholism it will be flushed ; in head mischief, whether haemor- rhage or inflammation, the face is possibly flushed, but it is much more likely to be pale, or blue and congested — bloated ; in a lunatic the face will seem natural, or possibly flushed with exertion ; in deliriant poisoning the face will be dry and flushed, or cold and clammy. The condition of the pupils is as important here as in the case of convulsions ; in alcoholism they are sure to be dilated, and probably fairly active ; indeed, if the patient is not comatose from alcohol they are sure to be active. In head conditions, IX URGENCY CASES 337 though the pupils may be active, they are more likely to be fixed, dilated, contracted, or unequal, or at least sluggish in movement. In lunatics (except general paralysis, when they are unequal or sluggish) they are active enough. In poisoning in this stage they would be widely dilated and inactive, with brightly glistening eyes. If still in doubt the temperature should be taken. This in serious cases is pretty sure to be markedly raised or lowered. If a normal temperature is found in a man who is actively conscious, or can be roused very easily, and if at the same time his pupils are active, the probabilities are that there is nothing very serious the matter. If, on the other hand, the temperature is raised, inflam- matory conditions must be suspected, either in the brain or possibly elsewhere (unsuspected pneumonia, e.g.), and if markedly lowered we know that there is a depression likely enough to be or become dangerous, and the case had better be watched. These points, if carefully considered, will be, as a rule, sufficient to prevent serious mistakes, but keep all your faculties on the stretch for any little suggestive point ; finally, if in doubt, act as if the case were a serious one. We will now pass on to the other group of cases — those in which the patient is quiet and actually unconscious, though he may be capable of being roused momentarily. There is here only one golden rule of treatment : Never allow AN UNCONSCIOUS PATIENT TO BE LEFT ALONE. If hc is SCCU at a hospital take him in. Far better to take in fifty drunken men in one night, and let them lie on mattresses under supervision in a warm room, than let one die unattended. The one action can at the worst only subject you to mild chaff and cause temporary incon- venience, the other may ruin you or your hospital for ever. If seen elsewhere than at a hospital have him removed at once to a hospital or to his home (or some one else's), and do not leave him till some reliable person is in charge. This is a golden rule, from w^hich no possible concurrence of circumstances should ever allow you to depart. Accurate diagnosis is therefore, from the point of view of imme- diate treatment, but of little use, but for further treatment, and for our reputations' sake, we must endeavour to make one. Any one of the conditions hitherto enumerated in this chapter may be present, or a combination of tw^o or more. A drunken man, for instance, is not absolutely free from the chance of being injured by blows or falls, and he is even more likely than a sober one, i:efen's paribus^ to have an intracranial haemorrhage, for if a man's z 338 DIFFERENTIAL DIAGNOSIS chap. vessels are diseased and he gets drunk, the arteries, which can do so, dilate, the diseased ones cannot, and rupture may occur. A hysterical woman may have a genuine epileptic fit with post-epileptic coma, and she may have got drunk previous to either, and finally have been damaged. Your preliminary actions are here the same as in the other groups. Clear a space round the patient, free his neck, listen to any history that is forthcomiing, and if definitely pointing to poison act promptly on it. Do not forget that coma from alcohol is as much poisoning by that substance, and often as dangerous, as is poisoning by opium or any other drug. S?nell the Bi'eath. — In the absence of a definite reliable history (either of an alcoholic bout or of only one glass given by anxious friends) the smell of alcohol is of equal importance with the smell of other poisonous substances. If a definite history is forthcoming an alcoholic smell must be judged by it. Camphor, turpentine, carbolic acid, hydrocyanic acid, chloro- form, aether, opium are the principal commoner poisons that will have imparted a distinctive odour to the breath. In diabetic coma the breath will be sweet like apples. Lately, on entering a patient's bedroom, I thought I had gone by mistake into an apple storeroom. Occasionally patients in uraemic coma are said to smell of ammionia. Note the Face as Before. — If it is pale and dry the case is quite likely to be only simple fainting, if there are no other distinctive symptoms ; if it is pale and sweaty, with cyanosed lips, cerebral haemorrhage or poisoning are most probable ; if flushed brightly it may be alcohol or belladonna poisoning, or possibly fever; if the face be purple and bloated, this points almost conclusively to serious cerebral mischief, probably compression. Next Proceed to Examine the Pupils. — In the other sections we have already considered the broad outlines of the conclusions to be drawn from the condition of the pupils. We may here finally tabulate the possible conditions, with a few remarks on their special influence on final diagnosis. The pupils may be — - As regards As regards As regards Reaction to Light. Absolute Size. Relative Size. Active. Dilated. Equal. Sluggish. Normal. Unequal. Totally inactive. Contracted. And finally either one or both may be irregular in outline. IX URGENCY CASES 339 Conditions in which the Pupils are still Active. — This is only likely to be the case when the condition of the brain causing the unconsciousness is either of a temporary character or in a very early stage. Inasmuch as we can but rarely see the patient in the latter condition, it is almost a fair clinical deduction to say that still very active pupils indicate no immediate danger. Thus they will be found in malingerers, in simple fainting (then indica- tive of returning consciousness), in hysterical and cataleptic con- ditions, and in the later stages of post-epileptic coma that is not going to prove fatal. The malingerer may be aware that he can, by stimulating the palm, dilate the pupil on that side, but this is such a temporary phenomenon as to cause little or no difficulty. In poisoning the pupils are frequently unaffected in the early stages, but this can hardly occur when absorption has so far advanced as to cause coma. The absolute size of active pupils will depend upon the amount of light in the examination room • Conditions in which the Pupils are Sluggish This occurs in — General paralysis of in- They will probably also be unequal, and sane. behave otherwise in a bizarre manner, possibly dilating with light. Uraemia. ^vlay be small, natural in size, or dilated. Disseminated sclerosis. In any condition, like ursemia. Early stages of apoplexy. Will probably cease to act before the ex- amination is completed. Conditions in which the Pupil ceases to React to Light at all The first and most important deduction from this state of the pupils (if we can exclude a glass eye and previous total blindness) is that the condition of brain underlying it is very serious, and even likely to prove fatal ; it marks the dividing line between coma and stupor. The commonest examples are : — Pupils very small. Opium poisoning (very rarely dilated). Pontine hsemoiThage (also often unequal). Possibly in general paralysis of the insane, or in tabes dorsalis. Pupils large and Belladonna (and its allies) poisoning, and also in equal. the later stages of most poisons, especially if 340 DIFFERENTIAL DIAGNOSIS chap. asphyxia is or has been a prominent feature. In connection with the large pupils of alcoholic poisoning it is worth while to note that even in a condition of coma due to this cause the pupils will still react to powerful peripheral stimuli, such as pinching the patient or pulling his hair forcibly. I know of no other grave condition of which this can be said. Pupils unequal. Frequent in one-sided pontine lesions. Also in one-sided considerable increase in intracranial pressure, as from haemorrhage. In general paralysis, too, it may continue during a final coma if previously present. After the examination of the eyes look for localised paralyses anywhere. Is the face reasonably symmetrical ? Are the eyes in a natural axis or markedly deviating ? Do the arms or the legs drop equally powerlessly when raised ? A localised paralysis of this sort is almost pathognomonic cJf coarse cerebral lesion, but of course in deep coma the point is often difficult to appreciate. The next point is the respiration. If this is stertorous the probabilities are in favour of a cerebral lesion ; but one must not forget that it may become stertorous in every form of dangerous coma. Then the pulse. If it be small, compressible, and slow, it is very likely to be opium poisoning (occasionally opium produces a very rapid pulse) or pontine lesion. If it be small and thready and rapid, no conclusion can be drawn, as this pulse is met with in so many conditions of coma where death threatens. A slow, labouring pulse, especially with a thickened artery, is suggestive of cerebral haemorrhage, or post-epileptic coma. Now draw off some of the urine. If sugar be present, diabetic coma is rendered probable though it occurs when anything presses on the fourth ventricle ; e.g. I have found it in cerebellar haemorrhage. If it is urasmic coma, there is likely to be albumen, or possibly blood, or both, and the urine will be of low specific gravity ; this latter is especially important, as the urine of cirrhotic kidney often enough contains no albumen, or such a faint trace as to be easily overlooked. A cirrhotic kidney, too, renders haemorrhage very likely. After noting the foregoing points, try how far the patient is capable of being roused ; the danger increases pari passu with the depth of IX URGENCY CASES 341 the coma. In uraemia, even when likely to prove fatal, some signs of consciousness can usually be obtained by pretty forcible stimula- tion ; this forms a valuable — not conclusive — distinction between uraemia and the coma of cerebral hcemorrhage. Lastly, take the temperature. This may give some information; it will be very high in sunstroke or other forms of heat apoplexy, and gives instantly the best guide to treatment. It almost certainly will be raised in the comatose condition of general paralytics, or of inflammatory conditions, and hence will be of great use in separating these from haemorrhage, uraemia, etc., in which the temperature (at the time we are considering) is invariably subnormal. In conclusion, I must again repeat that no one of these indica- tions is sufficient by itself; all must be considered and a balance struck. The history may be absolutely conclusive, and now and again an individual feature (e.g. conjugate deviation) may be so marked and obtrusive as to outweigh everything ; but whatever conclusion we finally arrive at, we must never leave a comatose patient WITHOUT EFFICIENT SUPERVISION ; HE MUST ALWAYS BE WATCHED carefully TILL A SUFFICIENT TIME HAS ELAPSED TO ALLOW OF AN ALCOHOLIC COMPLICATION HAVING PASSED OFF. INDEX Abdomen, pain in, vide Colic physical examination of, i68 Abortive zymotics, meaning of, 31 Abscess, of lung, foetid sputum in, 56 V. tumour, of brain, 316 Acid, uric, 209 Addison's disease, pathology of, 23 Adenoids as cause of epistaxis, 149 Adhesions as cause of abdominal pain, 63 Age and chronic bronchitis, 99 and disease, 12 and tubercle, 238 in hemiplegia, 318 old, shortness of breath in, 58 Ague V. ulcerative endocarditis, 145 Air in pleura, causes of, 80 Air-tubes, pressure effects on, 59 Albuminuria, 195 cyclical or functional, 196 eye changes in, 324 treatment of, 199 Alcoholism, coma in, 338 • inco-ordination in, 269 in urgency cases, 336 peripheral neuritis in, 283 pupils in, 336, 340 shock in, 329 tremors of, 311 Anaemia, cardiac bruits in, 129 eye changes in, 324 nervous phenomena in, 273 respiration quickened in, 57 Anaesthesia, paradoxical, 282 Anchylostomiasis, 156 Aneurysm as cause of colic, 173 as cause of pressure, 61 bruits of, V. valvular disease, 132 pain in, 61 pressure of, on cord, 290 thoracic, 107 Aneurysm, treatment of, 134 V. growth in thorax, 107 Angina pectoris as urgency case, 328 Antitoxin, arguments for existence of, 5 in diphtheria, 39 special or general, 6 Anviria, causes of, 217 Anus, blood appearing at, 156 diseased conditions of, 176 Aphasia, motor, 305 Apoplexy and sudden death, 331 Appendix and pain, 173 Arsenic, peripheral neuritis from, 283 Arteries, pressure on, in thorax, 59 Arterioles, degeneration of, in emphy- sema, 99 Arthritic diathesis, the, 244 Arthritis, rheumatoid, z/. true rheumatism, 242 Ascites, 177 causes of, 178 purulent, 179 tapping V. incision for, 179 V. encysted fluid, 181 Asphyxia and sudden death, 330 Ataxic paraplegia v. peripheral neuritis, 295 Ataxy, locomotor, vide Tabes Dorsalis Athetosis, 311 Atrophy, progressive muscular, v. peri- pheral neuritis, 293 Auscultation of chest, 69 Bacteriology, principles of, 25 Ballooning of rectum, 176 Barometer, living, meaning of, 243 Bell sound on percussion, 73 Bile in sputum, 55 in urine, tests for, 190 Bladder, causes of pus from, 202 haemorrhage from, 204 344 DIFFERENTIAL DIAGNOSIS Bladder like rectum, 265 reflexes of, 263 Blood dyscrasise as cause of nerve symptoms, 273 Blood from kidneys v. from bladder, 203 in urine, 203 Blood-spitting, causes of, 54 Bone, features of pain from, 60 pressure on, in thorax, 60 Brain, abscess of, v. tumour, 316 acute vascular lesions of, 315 difficulties in studying, 306 diseases of, 306 haemorrhage into, v. meninges, 317 effect of heart failure on, 119 functions of, 255 localisation in, 307 peduncles, affections of, 298 softening of, P.M. table, 320 softening of, v. haemorrhage, 318 softening of, varieties of, 320 tumours of, 322 tumours of, headache in, 323 V. cord, lesions of, 279 white matter, functions of, 308 Breath, foul, v. foetid sputum, 56 shortness of, in heart disease, 113 shortness of, in old people, 58 shortness of, v. dyspncea, 58 smell of, in urgency cases, 338 sounds, 69 Breathing, cavernous, 72 diaphragmatic, 58 Bright' s disease, 217 Bronchiectasis, 99 foetid sputum in, 56 sputum in, 53 Bronchitis, acute, and bronchopneu- monia, 97 Bronchitis, acute, and uraemia, 216 acute, cough in, 50 acute, temperature in, 48, 98 acute, V. tubercle, 91 capillary pyrexia in, 48, 100 chronic, and its associations, 98 chronic, and phthisis, 94 ■ chronic, complications of, 99 chronic, blood-spitting in, 54 Bronchopneumonia and tubercle, 100 and chronic bronchitis, 100 pyrexia in, 98 P5Texia in, v. bronchitis, 48 V. tubercle, 91 Bruits, exocardial v. endocardial, haemic v. organic, 129 importance of, 116 127 Bruits of aneurysm, 132 valve of origin of, 130 vital significance of, 133 Bulbar paralysis, 321 V. haemorrhage, 321 Bulging of chest, 66 Bursae, enlargement of, 233 Calcium phosphate in urine, 208 Capsule, internal, functions of, 308 Carcinoma of kidney v. stone or tubercle, 224 Caries affecting spinal cord, 290 as cause of chest pain, 61 as cause of colic, 173 Case taking, instructions for, 2 Casts in urine, 205 Cavernous breathing, 72 Cavity in lung, signs of, 84 Cells of body, disturbed functions of, 15 of body, disturbed functions in blood-poisoning, 16 Cells of nervous system, affections of, 320 Cerebellum, functions of, 307 inco-ordination from, 269 Charcot's joint, 231, 232, 235, 240 Chemiotaxis, definition of, 29 Chest, comparison of two sides of, 64, 65 Chest, inspection of, 65 oedema of, 66, 108 pain in, 61 palpation of, 66 tumour of, 66 veins enlarged on, 66 wall, bulging of, 66 Cheyne-Stokes breathing, 58 Children, cholera nostras in, 43 Cholera, asiatica v. nostras, 43 Chondroarthritis, 239 Chorea a cortical trouble, 311, 314 and traumatism, 312 Choroid, tubercle in, 325 Clicky crepitations, 92 Cogwheel respiration, 72 Cold and cough, origin of phthisis in, 92 Colic, 161 and sudden death, 330 causes of, 161 differential diagnosis of, 163 renal, v. biliary or intestinal, 171 simple V. obstructive, 169 with collapse, points in, 165 with collapse, operation in, 165 without collapse, 167 Coma in alcoholism, 338 INDEX 345 Coma in uraemia v. cerebral haemorrhage, 341 Coma, temperature in, 341 V. stupor, pupils in, 339 Communicable v. infectious, 24 Comparison of two sides of chest, 64, 65 Compensation in heart disease, 120 Concussion, 318 Congenital disease, 12 Consciousness in hemiplegia, 319 Constipation and diarrhoea, 173 consideration of, 175 Contagion v. infection, 24 Convulsions, nature of, in urgency cases, 334 Convulsions v. rigors, 95 Co-ordination of motion, 268 of sensation, 258 Cord, spinal, continuation of, into medulla, 299 Cord, spinal, diseases of, 285 function of, general, 255 function of systems of, 286 gnmmata of, 290 lesions of, indiscriminate, 290 lesions of, irritative v. destructive, 290 Cord, spinal, lesions of, system, 285 meningitis of, 290 pressure of aneurysm on, 290 syphilis of, 290 V. brain, 279 Corona radiata, 308 Corpora quadrigemina, 309 Corpus callosum, 308 striatum, 308 Cough, at night, 52 classification of, 49 in ear trouble, 50 in heart disease, 113 in lar}Tigeal trouble, 50, yj in thoracic tumours, 51 useless, causes of, 50 Coughing during auscultation, 84 Cranial nerves, 303, 305 Crepitations, clicky, 92 definition of, 70 Cyst, abdominal, v. ascites, 181 Damage, old, and elasticity of function, 60 Death, sudden, causes of, 329 Defaecation and micturition, 265 Degeneration as process of disease, 16 causes of, 17 reaction of, 269 Degeneration, secondary, 17 Delirium, 276 Desquamation, point in, 36 Diabetes, insipidus, 227 pathology of, 213 peripheral neuritis in, 283 phosphatic, 227 Diagnosis, definition of, i second stage in, 4 three stages in, i, 5 Diaphragmatic breathing, 58 Diarrhoea and constipation, 173 and constipation, causes of, 173 and uraemia, 216 considerations in case of, 174 in phthisis, 94, 177 severe, v. cholera, 43 Diathesis, 13 arthritic, 244 Diet and disease, 10 Dilatation of heart, 120, 121 Diphtheria and antitoxin, 39 as cause of epistaxis, 149 paralysis in, v. infantile paralysis. Diphtheria, peripheral neuritis in, 283 V. hospital sore throat, 39 Disease, abortive, meaning of, 31 and diet, 10 and new growths, 13 causes of, 6 congenital, 12 processes of, 13 reasons for thinking it microbic, 29 Disseminated sclerosis v. peripheral neuritis, 296 Drunk or dying, 326 Dullness on percussion, degrees of, 67 Duodenum, ulcer of, 156 Dying or drunk, 326 Dyspepsia v. heart pain, 32 V. gastric ulcer, 182 Dyspnoea v. shortness of breath, 58 Ear, cough from, 50 Eburnation of bone, 240 Effusion, pleuritic, 102 pleuritic, and pleurisy, 10 1 Elasticity, definition of, 12 Embolism, eye changes in, 324 of mesenteric artery, 161 Emphysema, 99 Empyema, sweating in, 48 Endocardial v. exocardial bruits, 127 Endocarditis, pathology of, 141 t}T3es of, 142 346 DIFFERENTIAL DIAGNOSIS Endocarditis, ulcerative, 141 ulcerative, diagnosis of, 144 ulcerative, v. ague, 145 ulcerative, v. tubercle, 145 ulcerative, v. typhoid, 144 Enuresis, 264 Environment and disease, 10 Epilepsy, 276 as urgency case, 333 Jacksonian, 309 Jacksonian, v. idiopathic, 310 nocturnal haemorrhage in, 151 — — pupils in, 333 Epistaxis, causes of, 149 Erythema simplex v. other rashes, 43 Etiology as part of pathology, 22 Exanthemata v. infantile paralysis, 292 Exercise, influence of, on urine, 186 Exocardial v. endocardial bruits, 127 Eyes, the, inco-ordination from, 269 the, in "fits," 333 the, in anaemia, purpura, gout, cirrhotic kidney, albuminuria, fevers, leucocythaemia, 324 Eyes, the, changes in fundi, in plumbism, refraction errors, tubercle, tumours, 325 Face, the, in coma, 338 the, in urgency cases, 334 Faeces, points in examination of, 175 rectum full of, 176 Fainting as urgency case, 328 Fat as alterer of physical signs, 66 Fever, eye changes in, 324 symptoms of, 35 Fibroid phthisis, origin of, 91 Fits, causes of, in urgency cases, 333 Flat foot, 235 Fcetor of sputum, 55 Food, influence of, on urine, 187 Foot, flat, 235 Fremitus, tactile, 66 Frequency of micturition, causes of in- crease in, 188 Friction sounds, pleural, 73 Frontal lobes, function of, 307 Froth at mouth in urgency cases, 334 Function of cells in disease, 14, 15 Functional nerve troubles v. sclerosis, 322 nerve troubles v. organic, 275 Ganglia, basal, of brain, 308 Gangrene of lung, fcetor in, 56 Gas in pleura, 81 Gastritis v. meningitis, 160 Giddiness and uraemia, 216 Girdle pain, 288 Glycosuria, 212 Gonorrhoeal rheumatism, 235 Gout, 233 changes in fundi oculorum in, 324 in joints, 238 pathology of, 210 peripheral neuritis in, 283 G. P. I. , tremors in, 311 Granulomata, inflammation in, 87 Grating in joints, 231 Growths as cause of disease, 13, 18 intrathoracic, and pressure, 61 intrathoracic, v. aneurysm, 106, 107 Gummata and cranial nerves, 321 Gums, haemorrhage from, 151 Haematemesis, causes of, 154 V. haemoptysis, 152 Haematuria, 203 Haemic v. organic bruits, 129 Haemophilia as cause of epistaxis, 149 Haemoptysis, causes of, 54, 153 in chronic bronchitis, 100 its indications, 92 V. haematemesis, 152 Haemorrhage and sudden death, 329 and tumours of brain, 314 brain v. meninges, 317 from mouth, causes of, 150 from nose, 148 into tumours, 272 in urgency cases, 327 V. acute bulbar paralysis, 321 Headache and uraemia, 216 in cerebral tumours, 323 Heart and pericardium, diseases of, 112 bruits, exocardial v. endocardial, 127 Heart bruits, importance of, 116 bruits, organic v. haemic, 129 bruits V. sounds of like nature, 126 dilatation of, 121 disease, age in, 138 disease and epistaxis, 150 disease and sudden death, 329 disease, cough in, 51 disease, general symptoms of, 117 disease, local signs of, 113, 114 disease, nervous v. muscular, 137 disease, pain in, 61 disease, sex in, 139 disease, without bruits, 135 enlargement of, diagnosis of, 122 INDEX 347 Heart, failure of, it8 failure of, as cause of disease, i8 failure of, character of sounds in, 124 Heart, failure of, definition of, 120 hypertrophy of, 120 hypertrophy of, diagnosis of, 122 hypertrophy of, symptoms of, 121 its functions, 117 ■ natural sounds of, 115 organs, 118 pressure on, 59 regularity of, 115 ■ state of, in hemiplegia, 319 • valvular lesions, effects of, 125 • valvular lesions, influence of indi- vidual, 134 Heat in joints, 233 Hemiansesthesia, 308, 311 Hemianopsia, seat of lesion in, 303 Hemiplegia, diagnosis of seat of lesion in, 302 Hemiplegia, heart in, 319 softening v. haemorrhage, 318 temperature in, 319 Trousseau on, 319 Heredity and disease, 12 in tubercle, 91 Hoarseness of voice, 74 Hospital throat v. diphtheria, 39 Hydatid hooklets in sputum, 55 H}'perpyrexia, a source of, 48 Hysteria, 276 and laryngeal troubles, 79, 80 micturition in, 264 V, disseminated sclerosis, 297 Hysterical joint, 236 Idiopathic disease, 10 Immunity, meaning of, 31 Inadequacy, renal, 216 Inco-ordination, 268 causes of, 269 in peripheral neuritis, 294 knee jerk in, 311 Incubation, meaning of, 31 period, table of, 33 Indigestion and uraemia, 216 Indiscriminate lesions of cord, 290 Infection, date of, 31 V. contagion, 24 Inflammation as process of disease, 14 in the lung, 85 in nervous system, 270 ■ nature of irritant in, 87 phases of, 86 Inflammation, reparative side of, 16 Influenza, diagnosis of, 44 V. scarlet fever, 45 Inhibition and interference, 267 Inspection of chest, 65 Interference and inhibition, 267 Intestine, ulcers of, as cause of haemor- rhage, 156 Intrathoracic tumours, 105 Irregularity of heart, 124 Irritant, nature of, as influencing in- flammation, 87 Irritation of nerves, stages in, 315 Irritative lesions v. destructive, 315 Jaundice and artificial light, 167 Joint, Charcot's, 240 gout in, 238 grating in, 231 heat in, 233 hysterical, 236 pain in, 230 osteoarthritis v. rheumatic gout, 239 Joint, redness in, 233 rheumatism in, 238 stiffness in, 230 swelling of, 231 traumatism of, 236 tubercle of, 232, 237 uric acid in, 240 Joints, affections of, 229 affections of, family history in, 234 affections of, personal history in, 234 Joints, affections of, differential diagnosis of, 241, 243 Joints, affections of, eburnation in, 240 affections of, weather influence on, 243 Keloid, explanation of, 86 Kidney, cirrhotic, eye changes in, 324 cirrhotic, patholog}^ of, 23 conditions causing secondary changes in, 222 Kidney disease and epistaxis, 150 disease, forms of, 218 Kidney, stone in, v. tubercle or carci- noma, 224 Kidney, surgical, 197 tubercle of, 226 Kidneys, casts from, 206 effect of heart failure on, 119 haemorrhage from, 205 latent disease of, 223 348 DIFFERENTIAL DIAGNOSIS Kidneys, malignant disease of, 227 ■ pus from, 202 Knee jerk, 279 as test of locality of inco-ordina- tion, 311 Knee jerk in hysteria, 261 modifications of, 260 occasionally absent in health, 261 Lactation, prolonged, and salicylates, 241 Laryngeal paralysis, 76 trouble, blood-spitting in, 54 recurrent, pressure on, 60 Laryngitis, cough in, 50 Larynx in hysteria, 79 necessity of laryngoscope, 74 symptoms of disease of, 74 tumours of, 51 ulcers of, 75 Lead poisoning, eye changes in, 325 peripheral neuritis in, 283 Lesions, indiscriminate, of cord, 290 irritative v. destructive, 290 Leucocythaemia, eye changes in, 324 epistaxis in, 149 Levels in the nervous system, 257 Limbs, effects of heart failure on, 119 Liver, cirrhosis of, 180 cirrhosis as cause of epistaxis, 150 diagnosis of pain from, 171 effects of heart failure on, 119 painful affections of, 162 Lumbago v. poliomyelitis, 293 Lunacy in urgency cases, 336 Lung, abscess, foetor of, 56 cavity in, signs of, 84 changes in, in pleural effusion, 105 collapse of, 99 consumption of, 200 disease and haemoptysis, 153 effects of heart failure on, 118 gangrene of, foetor of, 56 inflammation in, 85, 88 malignant disease of, 55 tissue, in sputum, 55 Lymphatics, pressure on, in chest, 59 Manias, meaning of, 276 Measles, spots in mouth in, 41 V. rotheln, 40 Medulla, affections of, 298 anatomy of, 301 physiology of, 301 Melaena, causes of, 156 Meninges, tumour of, 291 Meningitis and cranial nerves, 321 Meningitis, of cord, 290 V. gastritis, 160 V. myelitis, 316 V. pneumonia, 96 poliomyelitis, 293 Menstruation, vicarious, and epistaxis, 150 Menstruation, vicarious, and hasmate- mesis, 154 Mental changes, functional 77. organic, 278 in brain dfsease, 312 Mercurialism, tremors of, 311 Mesentery, embolus of artery in, i6i Microbes and disease, 27 classification of, 26 in sputum, 55 proofs of specificity of, 26 reasons for suspecting, 29 rules governing, 25 Micturition, increased frequency of, 188 pathological variations of, 263 reflex, 264 V. defsecation, 265 Mind, influence of, on urination, 187 seat of, 307 Monarthritis, 234 Morbus cordis, haemoptysis in, 54 pain in, 61 prognosis in, 145 Motions, examination of, 175 Mouth, froth at, 334 haemorrhage from, 151 Movements, central representation of, 257 Movements, course of nerve impulses in, 256 Movements, inco-ordination of, 268 Mucus in sputum, 53 in urine, 192 Murmurs, and sounds mistaken for them, 126 Muscles not represented centrally, 257 reaction of, degeneration in, 269 symmetrically used, 311 Myelitis, acute, 291 micturition in, 264 Neoplasms, how they kill, 18 and septicaemia, 20 physiology of, 19 and disease, 18 Nephritis, dangers of, 219 forms of, 218 Nephrolithiasis, 225 pathology of, 209 Nerve cells, primary affections of, 320 INDEX 349 Nerve diseases, central v. peripheral, 279 diseases, differential diagnosis of. 272 — diseases, toms, 267 direct v. indirect symp- Nerve diseases, organic v. functional, 275 diseases, primary v. reflex, 273 impulses, motor, course of, 256 Nerves, cranial, 303, 304, 305 cranial, like motor spinal, 320 cranial, lesions of, 303 cranial, peripheral v. central lesions, 321 Nerves, irritation of, stages in, 315 peripheral, functions of, 253 thoracic, pressure on, 60 Nervous system, anatomy of, 247 and \irgency cases, 331 causes of disease in, 270 diseases of, 247 functions of, 252 levels in, 257 onset of diseases in, 272 physiology of, 247 Neuralgia, 276 V. neuritis, 284 Netir asthenia, 276 Neuritis, diphtheritic, v. infantile par- alysis, 295 Neuritis, inco-ordination in, 269 in occupation neuroses, 314 optic, 324 optic, and vision, 324 peripheral, 281 peripheral, forms of, 282 peripheral, v. amyotrophic lateral sclerosis, 296 Neuritis, peripheral, v. ataxic para- plegia, 295 Neuritis, peripheral, v. disseminated sclerosis, 296 Neuritis, peripheral, v. lateral sclerosis, 296 Neuritis, peripheral, v. neuralgia, 284 Neuritis, peripheral, v. progressive mus- cular atrophy, 293 Neuritis, peripheral, v. system lesions of cord, 292 Neuritis, peripheral, v. tabes dorsalis, 294 Neuron, the, 247 the, functions of, 252 Neuroses, occupation, 312 Night, cough worse in, 52 sweating in abscess of liver, 171 Nomenclature of chest sounds, 74 Nose, bleeding from, causes of, 149 Nummulation of sputum, 54 Nystagmus, 297 Obstruction of bowels, 172 Occipital lobes, function of, 307 Occupation neuroses, 276, 312 Oculo-motor nerves, 304 CEdema of chest, 66, 108 CEsophagus, pressure on, 59 Olfactory nerves, lesions of, 303 Operation in uraemia, 216 Optic nerves, lesions of, 303 neuritis, 324 Organic v. functional nerve lesions, 275 Osier, Dr. , on bronchopneumonia, 98 Osteoarthritis, 239 lipping of bone in, 232 Oxalates in urine, 208 Pain, from old adhesions, 63 gastric v. cardiac, 62 girdle, 288 in abdomen, vide Colic in bone, features of, 60 in chest, 61 in gastric ulcer, 182 in heart disease, 113 in joints, 230 Palpation of chest, 66 Palpitation in heart disease, 114 Pancreas, painful affections of, 162 Paradoxical anaesthesia, 282 Paralysis, acute bulbar, 321 after Jacksonian epilepsy, 310 agitans, 310 infantile, discussion of, 292 infantile, v. diphtheria, 295 infantile, v. exanthemata, 294 in urgency cases, 340 laryngeal, 76 organic v. functional, 277 peripheral, v. central causes of, 321 Paraplegia, ataxic, v. peripheral neuritis, 295 Paraplegia in meningitis, 316 Parasites and p}Texia, 9 as causes of disease, 8 Parturition, disturbances of micturition in, 263 Pathogenic microbes, classification of, 28 Pathology, definition of, i, 22 Peduncles of brain, affections of, 298 Percussion of chest, 67 Pericardio-pleural friction, 73 3S^ DIFFERENTIAL DIAGNOSIS Pericarditis, and uraemia, 216 pain in, 61 Pericardium, diseases of, 112 Perihepatitis, 180 Peritoneum, cancer of, 180 tubercle of, 180 Peritonitis and uraemia, 216 Phagocytosis, definition of, 29 Phosphates, triple, meaning of, 209 Phosphatic diabetes, 227 Phosphorus, forms of, in urine, 208 Phthisis, 84 ad hcB7noptoe, 90 after pneumonia, 94 and chronic bronchitis, 94 blood-spitting in, 54 catarrhal, 89 ■ cough in, 51 definition of, 85 diarrhoea in, 94, 177 fibroid, 89 fibroid and keloid, 89 from cold and cough, 92 hsemorrhagic, 89 pneumonic, 88 scrofulous, 88 tuberculo-pneumonic, 88 Physical signs, definition of, 21 give physical conditions only, 65 of thoracic disease, 64 Piles, 176 " Pins and needles," 282 Pleura, air or gas in, 81 air or gas in, origin of, 80 effect of heart failure on, 119 effusion into, causes of, 102 effusion into, nature of, 103 effusion into, symptoms of, 102 Pleurisy, acute, causes of, loi acute, pain in, 61 • ■ acute, symptoms of, loi and pleural effusion, loi and tubercle, loi and uraemia, 216 in chronic bronchitis, 100 V. empyema, pyrexia in, 48 Pleuro-pericardial friction, 73 Plumbism, eye changes in, 325 Pneumonia and phthisis, 94 and uraemia, 216 — central, 96 cough in, 50 — ■■ — diagnosis of, 95 haemoptysis in, 54 is it a specific disease? 96 — — — V. intracranial inflammation, 96 Pneumothorax, 80 physical signs of, 82 postulates for, 8i sequelae of, 83 shortness of breath in, 82 symptoms of, 81 Poisoning, pupils in, 333 Poisons as cause of disease, 9 PoliomyeUtis, diagnosis of, 292 Polyarthritis, 234 Polypi, rectal, 176 Pons, affections of, 298 Portal fissure, obstruction in, 180 Posterior longitudinal bundle, 300, 304 Pregnancy and epistaxis, 150 and heart disease, 147 Pressure, intrathoracic, 59, 60 Processes of disease, general, 13 Prognosis in heart disease, 145 Progressive muscular atrophy, 293 Prostate, enlarged, micturition in, 264 Pseudo-paralysis, 274 Ptomaine poisoning v. cholera, 43 Puberty and epistaxis, 149 Pulse, frequency of, in morbus cordis, 124 respiration ratio in pyrexia, 35 the, in urgency cases, 335, 340 Pupils, the, in alcoholism, 340 the, in epilepsy, 333 the, in fits, 333 the, phases of, 339, 340 the, in urgency cases, 338 the, stupor v. coma, 339 Purpura and epistaxis, 149 eye changes in, 324 Pus from bladder, 202 in nephrolithiasis, 224 in sputum, 53 in urine, 200 Pyrexia and parasites, 9 in old thoracic disease, 49 in phthisis, 94 in pleurisy v. empyema, 48 in thoracic diseases, 47 pulse-respiration, ratio in, 35 quickens respiration, 57 symptoms of, 35 Pyuria, 200 causes of, 201 Rales, definition of, 71 Rashes of zymotics, table of, 37 Reaction of degeneration, 269 Rectum, ballooning of, 176 diseases of, 176 haemorrhage from, 157 INDEX 351 Rectum v. bladder, 265 Redness of joints, 233 Reflexes, paths of, 259 • superficial v. deep, 259 varieties of, 253 vasomotor, 265 Refraction, eye changes in, 325 Renal inadequacy, 216 Repair, limits of, in nerve tissues, 276 Resiliency of chest wall, 68 Respiration, accelerated, 56 accelerated, in anaemia, 57 accelerated, in chronic disease, 57 accelerated, in heart disease, 57 cogwheel, 72 in coma, 340 in lar}'ngeal paralysis, jj ratio to pulse in pyrexia, 35 rhythm, alterations in, 49 Retention of urine, causes of, 217 V. suppression, 216 Rheumatic gout, 238 Rheumatism, cases where salicylates are no use, 241 Rheumatism, gonorrhoeal, 235 joints in, 238 peripheral neuritis in, 283 simple V. gonorrhoeal, 236 V. rheumatoid arthritis, 242 Rheumatoid arthritis, 239 V. rheumatism, 242 Rhonchus, definition of, 71 Rigors V. convulsions, 95 Root s}TTiptoms, 288 Rotheln v. measles and scarlet fever, 40 Salicylates, occasionally no use in rheu- matism, 241 Salt as detector of gastric ulcer, 183 Scar tissue, functions of, 16 Scarlet fever v. influenza, 45 V. measles, 40 V. rotheln, 40 Scarring in varicella, 38 Schott treatment of morbus cordis, 146 Sciatica from pressure, 274 V. neuritis, 284 V. poliomyelitis, 293 Sclerosis, amyotrophic, v. peripheral neuritis, 296 Sclerosis, disseminated, v. functional trouble, 297 Sclerosis, disseminated, v. peripheral neuritis, 296 Sclerosis, early stages of, v. functional trouble, 322 Sclerosis, lateral, v. peripheral neuritis, 296 Sclerosis, primary, of nerve cells, 320 secondary, 320 Segregation, necessity for, 33 Sensation, cortical seat of, 307 pathways of, 257 Septicaemia, 28 from neoplasms, 20 Serum-therapy, arguments for, 5 Shock and alcoholism, 329 nature of, 313 Shortness of breath v. dyspnoea, 58 Sight, cortical seat of, 307 Signs, physical, of thoracic disease, 64 physical, v. symptoms, 21 Sixth cranial nerve, localisation from, 302, 304 Smell, cortical representation of, 307 Sodium phosphate in urine, 208 Spasm, organic v. functional, 277 Speech in laryngeal paralysis, 77 anatomy of, 249 Spinal cord, functions of, 255 diseases of, 285 Spleen, heart, 119 painful affections of, 162 Sputum, the, as aid to diagnosis, 52 blood in, 54 foetid, V. foul breath, 56 foetor of, 55 in pneumonia, 96 nummulation of, 54 qualitative changes in, 53 quantity of, 53 Squint, inco-ordination in, 269 Stiffness of joints, 230 Stomach, effects of heart failure on, 119 Stone in kidney, 202, 225 V. carcinoma, 224 V. tubercle, 224 Strangury, micturition in, 265 definition of, 204 Structure in disease, 14 Succussion, 73 Sugar in urine, 212 Suppression v. retention of mine, 216 causes of, 217 Supramarginal lobes, functions of, 307 Surgical kidney, 197 Sweat, the, in urgency cases, 334 Sweating at night, 171 in empyema, 48 Swelling in joints, 231 S}Tnptomatology, definition of, 22 Symptoms, definition ol, 21 352 DIFFERENTIAL DIAGNOSIS Symptoms, direct v. indirect, in nerve, 267 Symptoms, root, 288 V. physical signs, 21 Synovitis, 237 Syphilis of cord, 290 V. septic venereal trouble, 46 V. variola, 38 Systems in spinal cord, 287 lesions of, v. peripheral neuritis, 292 Tabes dorsalis, micturition in, 263, 265 V. peripheral neuritis, 294 Tactile vocal fremitus, 66 Tegmentum crura cerebri, 308 Temperature in bronchitis, 98 in bronchopneumonia, 98 in capillary bronchitis, 48 in coma, 341 in hemiplegia, 319 in urgency cases, 337 Thalamus, optic, 308 Thorax, pressure effects in, 59 symptoms of disease in, 47 tumours of, 105 Throat, hospital, v. diphtheria, 39 Tinkling sounds, 72 Tissue debility as cause of disease, 12 Tongue, the, functions of, 305 Toxaemia, functions of body cells in, 16 nervous phenomena in, 276 Tracheal affections, blood-spitting in, 54 tugging, 109 Tracts in cord, functions of, 288, 289 motor, 256 sensory, 257 Traumatism and degeneration, 313 and tumours, 313 as cause of disease, 8 as urgency case, 328 of joints, 236 of nervous system, 290, 312 Tremors, functional v. organic, 297 Triple phosphates, meaning of, 209 Trophic influences of nerves, 254, 266 Trousseau on hemiplegia, 319 Tubercle and age, 238 and bronchopneumonia, 100 and pleurisy, loi and tubercular v. nodule and no- dular, 90 Tubercle, cough in, 50 heredity in, 91 in choroid, 325 in joints, 237 Tubercle in kidney, 202, 226 in kidney v. stone or carcinoma, 224 Tubercle, miliary, 90 pulmonary, diagnosis of, 90 V. bronchitis, 91 V, bronchopneumonia, 91 V. ulcerative endocarditis, 145 Tugging, tracheal, 109 Tumour bulging from chest, 66 of thorax, 105 of brain and cord, 322 and cranial nerves, 321 eye changes in, 325 haemorrhage into, 315 headache in, 323 vomiting in, 323 Typhoid, eye changes in, 324 state, the, 42 V. typhus, 41 V. ulcerative endocarditis, 144 Ulcer, duodenal, as cause of melaena, 156 Ulcer, gastric, and hsematemesis, 155 gastric, salt as detector of, 183'' gastric, v. dyspepsia, 182 of larynx, 75 of nose as cause of epistaxis, 149 Ulcerative endocarditis, 141 Unconsciousness in urgency cases, 337 Uraemia, 214 as cause of vomiting, 159 as urgency case, 333 diagnosis of, 215 pupils in, 334 V. haemorrhage as cause of coma, 341 Urates in urine, 192, 207 Urea and uric acid, 210 Ureter, blocking of, by tubercle, 226 blocking of, by stone, 225 Urgency cases, 326 diagnosis of, 332 Uric acid, 209 in joints, 240 Urinary organs, diseases of, 185 Urine, the, acidity of, 186 • blood in, 203 bile in, 190 casts in, 205 characters of healthy, 185 coloior of, 189 deposit in, 192, 194 incontinence of, 264 in disease, 188 INDEX 353 Urine, in urgency cases, 340 in Bright's disease, 221 oxalates in, 208 pathology of, 190 phosphates in, 208 pus in, 200 quantity of, 188, 189 specific gravity of, 190 sugar in, 212 suppression of, 216 urates in, 207 variations in health, i85 Uvula, elongated, causing cough, 50 Varicella, scarring in, 38 V. variola, 38 Variola v. poliomyelitis, 292 V. syphilis, 38 V. varicella, 38 Vasomotor reflexes, 254, 265 Veins, enlarged, on chest, 66 pressure on, in thorax, 59 Venereal infection, differential diagnosis oi, 45 Venereal infection, septic v. syphilitic, 46 Vessels, lesions of, in urgency cases, 328 Vision, and optic neuritis, 324 as cause of inco-ordination, 269 double, 304 Voice, hoarseness of, 74 sounds, 71 Vomica, signs of, 84 Vomiting, 158 causes of, 159 in cerebral tumours, 323 in colic, 165 nervous, 159 Watson, Sir T. , on haemoptysis, 93 Wear and tear as causes of disease, ix Weather, the, and joint trouble, 243 the, influence of, on urine, 187 Zymotics as cause of vomiting, 1 59 diagnosis of, 30 rashes in, 37 THE END DEFECTIVE EYESIGHT: The Principles of Its Relief by Glasses. BY D. B. ST. JOHN ROOSA, M.D., LL.D., Professor Emeritus of Diseases of the Eye and Ear; Post-Graduate Medical School and Hospital; Surgeon to the Manhattan Eye and Ear Hospital, etc., etc. ; author of "A Clinical Manual of Diseases of the Eye " ; "Ophthalmic and Otic Memoranda "; "A Practical Treatise on the Diseases of the Ear"; "The Old Hospital and Other Papers"; "A Vest-Pocket Medical Lexicon." Cloth. i6mo. $i.oo, net. Dr. St. John Roosa has revised and very carefully enlarged the first edi- tion of this work, which was published under the title, "The Determination of the Necessity for Wearing Glasses," so as to make it a complete manual for the student and practitioner. The treatise takes up all conditions re- quiring the use of glasses, and indicates in the most careful manner the indications and rules for describing them. It contains six chapters, and is illustrated, so that a perfect understanding of the text is made easy. It is well known that the author is aconservative in regard to the value of glasses, believing that there is a limitation to their use, and that they ought not to be prescribed unless of positive value. The revolution which has been pro- duced in modern ophthalmic practice by the invention of a practical and exact instrument for measuring the radius of the cornea, is fully dwelt upon. No pains have been spared to make the manual a complete guide to the practitioner who wishes to understand and practise the rules for the pre- scription of lenses for the improvement of impaired sight. The book may also be interesting to educated men in all departments of life, who desire to be informed as to advances that have been made in this interesting subject, one which concerns such a large proportion of the human race. THE MACMILLAN COMPANY, 66 FIFTH AVENUE, NEW YORK. I A Brief but Comprehensive Text- A Handy Book of Reference for Book for the Student. the Skilled Physician. KLEMPERER'S CLINICAL DIAGNOSIS. BY DR. Q. KLEflPERER, Professor at the University of Berlin. Second American from the seventh and last German edition ; au- thorized translation by Nathan E. Brill, A.M., M.D., Adjunct Attending Physician, Mt. Sinai Hospital, and Samuel M. Brickner, A.m., M.D., Assistant Gynaecologist, Mt. Sinai Hospital Dispensary. With 6i Illustrations. Cloth. i2mo. Price, $i.oo, net. "Those of us who have heretofore made the acquaintance of Klemperer's Clinical Diagnosis abroad, will have reason to hail its appearance in Enghsh with satisfaction, and for the others we cordially recommend that they do not fail to become famiUar with it. . . . We feel sure that the work will have success here, and there is no reason why its status with German clinicians should not be repeated with us, for well and happily translated as it is the text can scarcely meet with less appreciation than it has so long enjoyed." — N. V. Medical JournaL THE MACMILLAN COMPANY, 66 FIFTH AVENUE, NEW YORK. COLUMBIA UNIVERSITY This book is due on the date indicated below, or at the expiration of a definite period after the date of borrowing, as provided by the rules of the Library or by special ar- rangement with the Librarian in charge. DATE BORROWED DATE DUE DATE BORROWED DATE DUE c2e:e38)M50 RC71 ^^^ Smith Introduction to the outlines of the T^e of fUfferential diagno- ^.^j; M r« -I 7-. I iS c ''■',' •> '• ' • r» »•» 1 » . '. > '.•Ivl'tv'/Xv'.''.' *y.'-»i»'t.>» •'»'.■, y>yy.>' wyA< 1 »''.'->\'»S \ I mm: -:^m;:SM;:/- 'M'''iVXsVi'''M' '.'>'' '\y^'y',\'\w''y ,' ;.,',;;:v;;:vi'y\>;s>; v;v^;v>;^•;v^;S';•;';':^^■;^^v^;^*^^^'^ ''^'.'.ii'i!! ,.,...,■,.,.•..,.» ',>> ♦l•.'•■,»,'^''»^^'■*^.■•'.?^"w^