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disease of the sympathetic, which belief was borne out bythe numerous physiological experiments by which glycosuriawas produced by acting on the vaso-motor sympatheticsystem. It could not be expected that lesion of the vaso-motor nerves should always produce glycosuria, for the area,of vascular dilatation might be too extensive or the lesionmight be irritative and not paralytic. In support of thisview, as was pointed out, some of the other symptoms mightbe explained by supposing the disease to have affected thevaso-motor system-e.g., polyuria, thirst, red tongue, coma.In one or two cases contraction of the pupil and hyperidrosisunilateralis have been observed. Diabetes might be due toone of three causes :-First, affection of the vaso-motornerves in some part of their course between the vaso-motorcentre and the liver, as in the four cases here recorded.Secondly, affection of the vaso-motor centre itself, as seen inthe cases in which glycosuria was due to cerebral lesion.Thirdly, affection of the vaso-motor centre reflexly, as in thecases of neuralgia, sciatica, &c., with glycosuria as recordedby Frerichs.-Mr. C. B. LOCKWOOD said that the anatomicalrelationships of the semilunar ganglia were different on thetwo sides of the body. Had both ganglia been. examined ?In injury of the frontal region of the brain glycosuria some-times occurred.-Dr. HADDEN had examined portions of thebrain, medulla, and semilunar ganglia as well as the sympa.thetic nerves going to the liver in some cases of diabetes.He found all these parts normal, and could not satisfy him-self that the appearances were abnormal in Dr. White’sspecimens.-Dr. PYE SMITH thought no one could doubtthat the specimens were abnormal.-Dr. HALE WHITE saidthat in one case both ganglia were examined and presentedthe same lesions. Frerichs gave two cases of disease of thetrigeminus in which there was glycosuria.The following card specimens were shown :-Mr. G. R.

Turner: Congenital Tumour of the Perineum. Dr. HaleWhite: Congenital Malformation of Lung and a specimen ofPatent Dactus Arteriosus. Mr. D’Arcy Power (for Dr.Mackinder) : A Pouched or Duplicate Bladder. Mr. Riving-ton : A specimen of Osteitis of the Upper Part of the Tibiawith Disease of Knee-joint.

CLINICAL SOCIETY OF LONDON.

Discussion on Charcot’s Disease.THE adjourned debate on this subject was resumed, but

not concluded, at the meeting held on Dec. 12th, Sir AndrewClark, President, in the chair. Oll the motion of the Pre-

sident, it was determined that an extra meeting should beheld in order to finish the discussion, and the date fixed wasDec. 19th, which, however, as announced elaewhere, wassubsequently changed to the 23rd.

Dr. DUCKWORTH read a précis of two letters which he hadreceived from Professor Charcot. Two specimens sent byCharcot were specially referred to. One was from a cast ofpied tabetique, and the other was the pelvis and the upperextremities of the femora of a case of locomotor ataxia.Charcot had not met with the joint disease apart from tabesdorsalis. He admitted that rheumatic arthritis may super-vene in the course of tabes dorsalis, but that was anothermatter. Reference was made to the porosity and fragilityof the bones. Dr. Duckworth repeated his conviction thatin Charcot’s disease we had a definite clinical conditiondetermined by disease of the spinal cord or some part of thecentral nervous system.

Dr. MOXON proposed a vote of thanks to Professor Charcot;this was seconded by Mr. MORRANT BAKER, and carriedby acclamation.Dr. MoxoN, in proposing the vote of thanks, professed

much admiration for Charcot. Assuredly no connoisseurhad ever brought so proud an imagination to his science,and no scientific imagination ever bad a better power ofobservation subordinated to it. Without pretending toa Carlylese worship of a fact, yet he had great respectfor facts. In reviewing the discussion he experienced anindefinite state of mind, which was uncomfortable to him.Referring to Sir James Paget’s speech, he consideredthat he might beg, with Sir Andrew Clark, that Sir Jameswould make more clear what it was that he meant.When he remembered the range of thought and accuracyof utterance which were at Sir James’s disposal, heconfessed to a certain degree of disappointment, and he

was particularly sorry to find that herpes zoster had beendragged in. Herpes zoster was a narrow clinical puzzle,just as such substances as selenium, iridium, and rubidiumwere narrow chemical puzzles. He did not think that theturning on of herpes zoster could throw any possible light onCharcot’s disease. He referred to a typical case of herpeszoster in which a medical man had told the patient that thedisease at its beginning was a mixture of gout, neuralgia,and rheumatism. As far as he knew, Charcot’s diseasewas extremely like rheumatic arthritis, and he fell in withthe views of Mr. Hulke, and could see nothing peculiar inthis so-called peculiar disease. He thought that the morevaguely he spoke the better it would suit the occasion.Charcot’s disease seemed to him to be hopelessly indefinite,and whereas herpes zoster was definite, typical, and full ofnerve from beginning to end, this so-called peculiar jointdisease had no nervous phenomena at all. Sir James hadfailed to fit the case altogether. Looking at the line ofindefiniteness which surrounded Charcot’s disease and rheu-matic arthritis, might it not be through our ignorancethat they do coincide? So far he had dwelt on negative points,but he despised negativism, and would now advance a posi-tive contribution. Locomotor ataxy has branches, andhe did not think that Charcot’s disease was a grafted branch.Eight years ago Westphal pointed out that in generalparalysis of the insane the conditions of locomotor ataxywere present. This statement of Westphal’s drove him toSt. Luke’s-as an observer,-and he also took with him agalvanic battery and several Guy’s men. He found that athird of the general paralytics had the physical conditionsof locomotor ataxy. Dr. Savage had found that the sameholds good for Bethlem, and he had also Dr. Savage’s per.mission to state that no case of Charcot’s disease had occurredamongst the general paralytics. Might there not be somerelation between this absence of disease of joint in caseswhich were paralysed and ataxic? He suggested that simplerheumatism might be changed into an exaggerated unrepre-sentative, irritative, severe, strange, and peculiar diseasewhen occurring in cases of ataxia, and in illustration of hisremarks he showed a specimen of the shoulder-joint of anex-cabman who was thrown from his cab a year before hisdeath. Here he thought that the constant jolting of thearms had led to the wearing away of the head of the humerus,and compared this jolting to a "locomotor ataxic actioa"on the shoulder-joint. He considered that this specimenwas halfway to a Charcot’s joint; there was no productionof new bone about it. If half a Charcot’s joint can bemade bv wobbling alone was it not possible that a whole onecould arise as the result of wobbling when the nerves werein a diseased state. If careless and continued use couldproduce such changes, it was surely better to search fortraceable causes. When he was demonstrator of anatomyhe taught that the nerves going to a muscle also suppliedthe skin over that muscle on the side towards which motionwas effected, and further that the joints were also supplied,generally on the side towards wnich motion takes place.There must be some meaning in that. It was a requisite ofjoint life that the moving agency should be duly checked.And if we took away this sensibility, this agency for check-ing movement, must we not measure that before we aretold that there is a special disease ? Common rheumatismafter long experience of insensitive joint and spasmodicmuscle might be turned into Coarcot’s disease. If the cab-man had had an insensitive state of joint as well as thespasmodic action of muscles, he could not help thinking thatthe half Charcot’s joint would have been a whole one. Heconfessed that the narration of the following case cost himpain. It was that of a case of perityphlitis in a man inwhom there was a board-like hardness of the caecal region,and it was desirable for the man’s good that an examinationshould be made under chloroform in order that the hardnessof muscular action might be got rid of. After returning to con-sciousness the man experienced the most intense agony, anddied in nineteen hours from peritonitis, the result of ruptureof the intestine. This case led him to consider the value ofthe protective agency of the motor parts of the body, andmade him very recognitive of the degree in which readysensitiveness helps a patient. These natural medicativepowers beiug absent, he thought that. an ex9ggera.ted irrita-tive, severe, and strange disorder of joint might arise. Thephenomenon of the discussion on Chal cot’s disease was not anisolated ca-e. It was no new thing for a mysterious originto be claimed for a local manifestation. Fifteen or twentyyears ago the occurrence of auricular hæmatoma, or hæma-

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toma auris, was assigned to a mysterious disorder of thenervous system. But the divine madness of youth, such ashas been confessed to in the height of a scrimmage at foot-ball, may be accompanied by the formation of a bteb ofblood in the external ear of a hsematoma. auris. A literarygentleman had informed him that the evidences of shrunkenb<enatoma9 auris were to be seen in statuary representingGreek boxers, so that this affection could not be looked uponas a development or twig of modern civilisation. There wasa tendency, in the absence of proved direct causes, to appealto the nervous system, as if the disease were a kind ofspecial product. There used to be moderation in these viewsuntil the trophic nervous system was invented. By this sys-tem was meant a kind of Providence that supplied daily food tothe joints, a sort of Secretary of State of the Joint Department ;not that the nervous system actually found the material, butit should be remembered that Providence always uses means.Why should such a frightful, tenacious, unsparing cata-strophe afflict one joint when it was no greater sinner thanthe rest? No one had shown that the nerves going to thediseased joints were diseased. (Sir Andrew Clark herereferred Dr. Moxon to some observations by Charcot’s pupils.)Until it were proved that the neural changes were primaryand obvious, both destructive and irritative, he for onewould not be content to allow that the nerves caused thearthritic affection. He had examined cervical ganglia inlarge numbers, and never made much out; there might be alittie pinkness, a yellowness, or what not. Again, thefragile state of the bones used to be attributed to the stateof the nervous system in the inhabitants of those vast hotelsof not very critical guests. And recently a case of fractureo’ the ribs and sternum had been reported in the LANCET,and he dared say that the bones were soft. This fragility ofbone became startliog only when the conditions were

mystic. The tendency to bring in the vague and generaland to avoid measuring the force of the direct and measurablecauses must be deprecated. So it was with th6 unilateralbedsore of cases of hemiplegia. He was not ready to admitthe influence of trophic nerves in this connexion. Herethere was tendency of the body to roll upon the paralysed sideby the continuous action of the still active limbs. In this con-nexion Dr. Moxon referred to the manner in which the per-forating arteries of the thigh were protected as they run

_ under a tunnel of fibrous tissue, which in the contraction ofthe muscle was kept open so that the arteries were not con-stricted. It was the duty of a muscle to hold open its ownarterial channels. When a muscle is paralysed thevascular supply suffers, and as the vessels of the gluteusmaximus pass through the muscle before supplying the skinwhat was the wonder that the skin sloughed ? The play ofgenius of M. Charcot showed itself in the introduction of themarvellous to explain clinical phenomena. He was re-

minded of a time ten years ago when one of his colleaguesnow practising gynassotogy&mdash;a word, by the way, whichetymologically seemed to imply the most ambitious of all thesciences with the doubtful exception of theology-drew hisattention to a case of what others diagnose as hysteria.There was profound anaesthesia of one side, and he foundhis ambitious colleague hard at work with sovereigns andshillings producing what he believed was called a trans-ference of total insensibility. He was not quite sure what itwas all about, but it was very obscure. However, potatoparings cut into circles seemed to be endowed with thevirtues of the noble metals. He concluded by saying thatno one had ever brought so proud an imagination to hisscience, and no scientific imagination ever had a better powerof observation subordinated to it than had M. Charcot.Mr. HENRY MORRIS said that after the witty and

brilliant speech of Dr. Moxon’s it would be tame forthe Society to come down to the level of a simple matter offact. He narrated two cases of Charcot’s disease. One wasthat of a man admitted in 1877 to Middlesex Hospital fordisease of the knee, which seemed to require amputation.The joint had the appearance of aggravated chronicrheumatic arthritis, but it had all the special characters ofCharcot’s disease. There was in addition a malignanttumour of the face which had been five times removed, andwas in fact a rodent ulcer. The limb was put up in aThomas’s splint. Six years bef"re being seen the man hadbeen working in water, and then felt pain of a rheumaticcharacter, which lasted twelve months before swelling of thejoint occurred. At the end of six years the le hung like atlail upon the thigh. The internal ligament of the knee wasossified. Eight weeks before death there was difficulty in

speaking, and blood was vomited a few days before death,The case was one of long-standing Charcot’s disease withoutataxic symptome, and improved under the rest obtained bymeans of the splint, though the movement continued to befree in many directions. The disease was of a rheumaticcharacter, and he agreed with Mr. Hutchinson that theinsensitive state of the joint largely contributed to thecausation of the disease. The other case was that of a manwith elephantiasis of one limb, and intestinal obstructiondue to an enormously thickened volvulus, in which thesac. like omentum was greatly thickened, and which must haveexisted a very long time; the man died from the obstructionafter having experienced severe sudden pain in the abdomenlasting but a shott time. In this case the ankle had lost allits normal characters ; the man walked on the inner borderof the foot, and there were perforating ulcers on the greattoes of each foot. The right foot had become diseasedtwenty-one years before, bone having been lost and suppura-tion set up. Fifteen yeara before the left ankle becameaffected, and the elephantoid condition of the kin had lastedten years. At the autopsy there was a saucer-like cavityabout the ankle, with thickening of bone around the tibiaand fibula, which were firmly united ; irregular thickening ofthe shafts of the bones also existed; the posterior tibialnerves of both sides were swollen, and sections made by Mr.Hudson showed changes in the nerves like those describedby Messrs. Savory and Butlin ; there was enormous thicken-ing of the epineurium, but little of the perineurium, and somethickening of the endoneurium. The sensory fibres werealmost absent. The painlessness of the disease, the longcontinuance, the profuse perspiration without ataxicsymptoms were noteworthy features.Mr. HERBERT PAGE spoke of the case of a man who had

had severe gastric crises, lightning pains, and in whom thetarsal bones of one foot were disorganised, the other footfollowing suit soon after. (Clinical Trans. 1883 ) The feetwere put up in plaster-of Paris and ankylosis obtained. Thefeet were extremely misshapen. There was little or no

ataxia in the case. In August, 1884, there was a recurrenceof the attack in one foot, the ankle and tarsal bones beinginvolved. If this were an exacerbation of rheumatism itwas strange that it should not have attacked the other foot.It was the clinical features on which Charcot established thedisease as a wholly distinct malady. The wearing away ofthe bone is rapid, and not like a rheumatoid change in whichfriction might play a part. Further, in the case above men-tioned other symptoms clearly referable to the nervous systemwere present, as, for example, the attacks of haematuria.Why should we not admit that irritative lesions of nervetrunks produced changes in the parts supplied wholly differentfrom those alterations which might result from mere removalof nervous influence, as in cases of simple section of nerves ?Further, in cases of irritative nerve lesion, as when a con-tractile scar irritated a nerve trunk, the changes induced ata distance ceased when the nerve was freed from the irritatingscar tissue. And if lesions of nerve trunks could set upchanges, why should not lesions of the central parts of thenervous system have the same influence ? He felt sure thatthe pathology of acute bedsores was of this nature. Withregard to the whole question, he thought that we were in acondition of what he termed mdividual belief. In his beliefCharcot’s disease was a distinctive affection of joints.In reply to Dr. MOXON, Mr. PAGE said that there was no

ataxy of gait, and that the recurrence of joint disease affectedonly one foot.

Dr. MoxoN then inquired whether rheumatism was lesscapable of acting on one side than locomotor ataxy ; was notataxy always of both sides ?

Dr. PvE SMITH said that there was no evidenca to show thatany disease was new. Cholera and diphtheria were not new,and cerebro-spinal insular sclerosis had only recently beenrecognised. With regard to the relation of Cbarcot’s diseaseto osteo-arthritis, he said there was no adequate evidencefor separating them. In osteo-arthritis there was great ex-cess of bony growths, whilst in Cbarcot’s disease there wasa great deal of wasting of cartilage and bone, yet if asunicienu number of specimens were examined, more or lessattempts at the production of new bone would be found.The age and duration of the disease allowed of the distin-

guishing of varieties in the large group of cases. A contrastwas drawn between the rheumatoid changes in a youngwoman and those in an old man. Acute rheumatism wasan entirely different disease. And yet occasionally cases ofacute rheumatism exhibited changes i!a the phalanges like

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those of osteo-arthritis. Brief mention was made of twosuch cases, both of which had valvular disease of the heart.Trophic nerves had now been allowed an existence byphysiologists, though Schiff’s early experiments and thoseof Danders were first interpreted otherwise. The evidencefor the existence of trophic nerves was so strong that therecould be no doubt on the matter. Mr. Hilton had observedhow lesions of the hand waxed and waned with pressure onthe ulnar nerve by an exostosis. Again, bedsores of rapidand violent production were best explained on theassumption of their existence. Zona followed the course ofthe nerves, yet nerve lesions could hardly have anything todo with Charcot’s disease, seeing that the anterior rootswerenot involved in tabes dorsalis. The whole pathology ofgout was so different from osteo-arthritis that confusion onthis score ought to be impossible. Irish disease was almosta synonym for osteo-arthritis. Gout is almost unknown inIreland and Vienna, so much so that when a specicaen ofgouty joint appeared it was long before the nature f thedisease was recognised in Vienna. The fetlock of a, horsesometimes showed an example of osteo-arthritis. Baskhad discovered osteo-arthritic lesions in bones found atGibraltar, which must have belonged to bears of the glacia,lperiod. And Flower had shown the cervical vertebrae ofa porpoise with similar lesions. Syphilis certainly hadnothing to do with these affections. Hutchinson had rescuedthe lesions of congenital syphilis from the group of scrofulousdiseases. Dr. Pye Smith considered that tabes was not anabsolutely fixe&ugrave; and definite entity. He differed from Dr.Wilks in believing that there was a real complex of symptomswhich might justly be said to come under the wide categoryof tabes dorsalis. He concluded by referring to the dictumwhich said that investigation was to be preferred to specula-tive imagination.

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MEDICAL SOCIETY OF LONDON.

Relapsing Pneu’Inonia.AN ordinary meeting of this Society was held on Monday

last, Mr. Arthur Durham, President, in the chair.Sir ANDREW CLARK read a paper on a case of Pelap,,4ing

Pneumonia in an aged person, an abstract of which will be;found on another page.

Dr. C. T. WILLIAMS said that he had always regardedacute croupous consolidation of the lungs, not as a localdisease, and not exactly as an inflammation, but as a case ofblood-poisoning. He put such cases in the class of fevers.He had seen somewhat similar cases, though the rdapse3were neither so frequent nor severe. Supporting treatmentwas all that was wanted.Dr. SANSOM asked whether there was any history of

the inhalation of vitiated air. He quoted a case in whichthere were rigors, with the accession of febrile symptomsand initial partial comsolidation of the right upper lobe ;delirium was very great indeed, and lasted a few days ;the illness was an extremely rapid one. A few day,s laterhe found the patient with precisely the same symptoms,which ran almost exactly the same course. In both casesthere were rusty sputa, but the patient had also severe

haemoptysis. Recovery took place by defervescence at theend of a week. He referred to another case of pharyngitiswith febrile acumosis on altarnate days for a week, in whicha severe attack of consolidation of the lungs was passedthrough. The etiology of this case was as conclusive as

anything could well be ; there was a large crack fin thesoil pipe, from which sewer gas found its way into the bed-room of the patient ; and, in fact, all the residents In thehouse suffered in some way or other.

Dr. DOUGLAS POWELL was a little disappointed that SirAndrew had not given his explanation of the case. H.ad thepatient been exposed to malarious influences? P,ee-urrentthrombosis suggested itself as a method of explanation, butthe clinical symptoms did not fit with this hypothesis. At thefag end of pneumonia, in some instances, the resolutioni-eems to take place too fast, and an overdose of morbidmaterial is taken into the circulation, and hectic phenomena.produced. He described such phenomena many yeais-ago.

.U1’. ROGERS Fp()ke of the case of a gentleman seventyyeajs of sgc, who went through six relapses of pneumonia.’hwelve Fars ago he had rheumatic fever with valvular

affection. There was a history of gout in the family. Hewas attending the patient for rheumatic gout ; a rigor setin, the temperature rose, and the signs of consolidation ofthe middle lobe of the left lung were made out. There wasno cough and no expectoration. Delirium set in suddenly.There were frequent changes in the patient’s state, verymuch as happened in Sir Andrew’s case. He believed therewas some poison at work in the system. Eczema broke outin the course of the case. There was something more thaninflammation in pneumonia.Dr. T. H. GREEN said he still felt somewhat in the dark

as to the nature of the case under discussion. He consideredthat "pneumonia" was a general fever with a local mani.festation in the lungs. He would separate Sir Andrew’s casefrom those of acute pneumonia. It seemed to him that thecase was more likely to be due to some septic influence.Dr. SmnMS inquired into the family history of the case,

especially as regards rheumatism and gout, The relapses atregular intervals suggested such an etiology. Cases hadbeen recorded by Dr. Johnson, in which there was no ex.pectoration, and in a case under his care there had been noexpectoration whatever; these cases were probably of agouty or rheumatic nature.Dr. S. COUPLAND thought the case must be placed more

in the category of septic pneumonia than anything else.With regard to the histological nature of pneumonia, hereferred to the views of Hamilton of Aberdeen, who believedthat pneumonia was not an inflammation, but was due to aprofound circulatory disturbance. That view had not beenaccepted by the majority of histologists. The lung mightbe ’best compared to a serous membrane where there werefibrinous exudations in inflammation. An inflammatorychange was almost ’solely a vascular change, and so wherewe had to do with congestion and rupture of vessels it waspossible for the mind to perceive a distinction without adifference in the views which had been propounded respect.ing the histological nature of pneumonia. He himself pre-ferred not to teach his pupils the view of Sir Andrew andHamilton.Sir ANDREW CLARK, in reply, said the expectoration was

very minute in quantity. It was no rare thing for him tosee cases without expectoration, and he ventured to say thatone-third of the cases at the London Hospital had no ex-pectoration. He thought that there was no evidence of cellproliferation or cell advancement, but as the whole aspectwas one of regression, and, further, since there was a wantof close organic union between the exudation and thealveolar wall, and no sign in the alveolus of any texturalchange, that he was justified in the views he held. Theproducts of inflammation of the pleura were totally unlikethose of pneumonia. Textural changes may be observed inpneumonia when the alveolar wall is excited to action by thepresence of foreign material. He was quite familiar withthe cases of relapsing pneumonia due to too rapid absorptionfrom a resolving consolidation, as well as with those due toperityphlitis, pelvic cellulitis, or phlebitis. He believedthat a malarial influence might have been at work in thiscase. Gout was also a possibility. He had seen at least adozen such cases as the one recorded, and had made twopost-mortem examinations which seemed conclusive ofthe presence of pneumonia. The intimate nature ofdisease could not be determined by anatomical alterations.Mr. DURHAM showed the Cervical Cyst of a boy whom

he bad exhibited at the Society two weeks ago.Dr. RADCLIFFE CROCKER showed a case of Gangrenous

Ulceration of the Groin in a child ; the disease began threeweeks after the measles.

OPHTHALMOLOGICAL SOCIETY.

Unilateral Irido-Choroiditis.&mdash;Retinitis Albuminurica.&mdash;Vesicle of Cornea.&mdash;Hyphcemia.&mdash;Hysterical Deviation.&mdash;Cocaine.&mdash;Ophthalmic Models.A MEETING of this Society was held on Dec. litb, Mr. J.

Hutchinson, F.R.S., President, in the chair.Mr. MARCUS GUNN showed a child, aged eight years, the

subject of Unilateral Choroiditis. Some years before thischild’s birth the mother had suffered from syphilis. Twoyea.-rs ago the child had a feverish attack, probably due tomeningitis. Mr. Gunn found that there were numeroussynechiae in the right eye; the optic disc was occluded by a