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Mr. FALLOWS (London) read a paper on (1) a case ofPolypoid Growth from a Meibomian Gland, and (2) the Useof Fluorescin in the Form of Tabloids in the Diagnosis ofCorneal Abrasions.Mr. H. E. JONES (Liverpool) read a paper on Irrigation
for the Nasal Duct.Mr. JuLER and Dr. GEORGE MACKAY remarked on the
instrument.Mr. JONES replied that he used boric solution. He did
not use corrosive sublimate owing to its effect upon thecanaliculus.
Mr. CHARLES WRAY (London) read a paper on
Extraction of Transparent Lens in High Myopia. Up to
August last over 2000 patients with myopia over 10 D. hadbeen submitted to operation. The immediate results weregood but the ultimate results were bad.
Mr. JOHN GRIFFITHS related particulars of a case of AcuteExophthalmic Goitre.
Dr. GEORGE MACKAY described a case upon which he hadoperated.
Dr. A. HILL GRIFFITH mentioned a similar case in whichhe had used thymus extract.
Mr. MARCUS GUNN stated that electricity had been founduseful.
Dr. A. BRONNER read a paper on Crystals of Cocaine inpreference to Solution.
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LARYNGOLOGY AND OTOLOGY.
FRIDAY, JULY 29TH.Dr. JOBSON HORNE (London) read a paper upon
The Pathogenesis and Earlier Clinical Evidence of LaryngealTuberculosis.
He said that it would not be possible for him to do morethan touch upon the threshold of the disease and endeavourto demonstrate what appeared to him to be the portal ofinfection, the beginning and progress of tuberculous destruc-tion, the origin and formation of the giant cell, and brieflyindicate the clinical counterparts of the early pathological
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changes which he had learnt to regard as the earliest signsand symptoms, not only of laryngeal tuberculosis, but also ofpulmonary tuberculosis. A lantern demonstration was givenof photographs of microscopic sections on which the con-clusions were based and some of the more important sectionswere shown under microscopes. The pathogenesis of thedisease had been studied in larynges which post mortempresented to the naked eye none of the usual signs of
laryngeal tuberculosis, but which had been removed frombodies of persons who had died undoubtedly from tubercu-losis. In the examination of these larynges films were firstprepared from the contents of the ventricles and stainedfor tubercle bacilli and the larynx was afterwards examinedmicroscopically throughout. Dr. Horne dwelt upon the
importance of the ventricle as a harbour for tubercle bacilli.The earliest changes noted in the lymphatics were a pro-liferation of the parenchyma of the acini and efferent ductsand the formation of masses of small round cells distendingand choking the ducts and obliterating the glands, theadjacent and superficial structures remaining intact. These
changes had been noted in the lymphatics situated in thewalls of the ventricles when a careful microscopic examina-tion of the entire larynx had failed to reveal changes in thelymphatics in other parts. The nature of this cell prolifera-tion was next considered. Was it to be regarded as
nothing more than an outcome of a traumatism or ofsome simple catarrhal process perhaps peculiar to tuberculoussubjects ? or was it to be attributed to one specific cause-namely, the presence of the tubercle bacillus ? Dr. Hornesaid that although he was not prepared altogether to acceptor reject the theory that these lymphoid masses were dueto a simple catarrhal process, he was now able to demonstratethe tubercle bacilli in the midst of some of them and wasof the opinion that once having gained an entry into thelymphatic ducts they acted as an irritant and caused a cell pro-liferation. Thefons et origo of the giant cell in tuberculosisnext came under consideration and by a series of lanternphotographs of microscopic specimens its development fromthe wall of a lymph space was demonstrated. The seriesshowed first the tubercle bacilli lying amongst the endo-thelial cells forming the wall of the lymph space ; secondly,the division and fusion of the adjacent and divided cells;and thirdly, the separation off of this plasmodial massas a giant cell. Reference was made to the researches onlepra laryngis by Dr. Paul Bergengrun of Riga, in which he
had shown that the so-called ’’ globi were bacillarythrombi lying in dilated lymphatics and that the lepra giantcell developed from the lymphatic endothelium. If, then, aewould appear to be the case from the foregoing, the tuber-culous process commenced in the lymphatics it would benatural to suppose that those parts which were rich iulymphatics would be the more common sites for infiltra-tion and ulceration, while such parts as were withoutglands would escape ulceration except by continuity. Thiswas clinically verified. The inter-arytenoid region, the’posterior third of the cord, the ventricular band, andthe epiglottis, especially the petiolus, were the parts morerichly endowed with glands and these were the parts morecommonly ulcerated in laryngeal tuberculosis. The cord, thefunctionally more important part of the cord,-namely, thatpart lying between the two small cartilaginous bodies-beingfree from glands escaped ulceration excepting superficialerosion and by continuity. A proliferation of the sub-
epithelial blood-vessels was described as taking place side byside with this cell proliferation. With regard to the muscles,changes were described as occurring at an early stagein the fibres and as being clinically brought into evidence’by an early functional failure which was mainly myopathic,The earlier clinical evidence of laryngeal tuberculosis, thE’:clinical counterparts of these early pathological changes,.were next described. Whilst clinically investigating these it!.was necessary, inasmuch as only slight departures from thenormal were being looked for, to retain a control mentalimage of a normal larynx. This was done by constantlyexamining a large number-some hundreds in all wereexamined-of larynges in healthy subjects or at least pre-sumably free from tuberculosis. And it was whilst insearch of normal larynges that some important aids twothe present research were stumbled upon. The larynxhad been examined in 359 consecutive cases of pul-monary tuberculosis or cases in which there were reasonsfor suspecting pulmonary disease. The points to whichattention was mainly directed were the following a(1) disturbances of sensation, hypæsthesia, hyperasstbesia,paræsthesia; (2) colour changes, anæmia, hyperasmia; x(3) functional disturbances ; (4) impaired movements ofvocal cords apart from paralysis ; and (5) changes inthe contour of the larynx due to slight cedema. Inasmuchas disturbances of sensation were subjective too much signifi-cance could readily be attached to them if taken alone as aclue to pulmonary tuberculosis, but in regarding them onlyas evidence of I hysteria" " one was apt to miss importantclues to pulmonary tuberculosis. Hypagsthesia, was not
infrequently associated with anæmia of the soft palate,,and it might be stated that unless the subject was wilfullyhostile to laryngoscopy the more pallid the soft palatethe greater the tolerance to laryngoscopy. And whenin the course of the pulmonary condition the anaemiapassed off the tolerance often went with it. Anagmia ofthe laryngeal mucosa was noted as present in varying;degrees in 157 out of 359 cases. At times it was universal ; pwhen patchy it was confined to points where the mucosa.was more easily exposed to tension, occasioned by a slight,oedema in association with the proliferation of subepithelialvessels. It was as frequently met with in men as in women-Hyperasmia was noted in 117 out of 359 cases and rathermore frequently in males. This hyperæmia must be regarded)as a feature distinct from and not amounting to acute
laryngitis. Acute laryngitis did not occur so frequently asone might previously have anticipated. The hyperasmia was.often transient, within a few days giving way to pallor ; but,at times it was most persistent. These phenomena were.also attributed to the proliferation of subepithelial vessel’s.Disturbances in the vocal function were most frequently metwith, often transient, not amounting to more than a weaknessof voice or loss of tone. The production of voice called fora greater effort, there was a forgetfulness of office, a
sluggishness of one or both cords to act, so that there wasphonatory waste before voice was produced, and in connexionwith this required effort might be mentioned that in earlytuberculosis when the speaking voice was weak the singingvoice was quite clear. Then the singing voice might suddenlygo; this caused the patient to seek advice, and the possi-bility of commeneing tuberculosis should not be forgotten.Transient dysphonia. was more commonly met with amongstwomen, and especially young married women, duringpregnancy. Not infrequently in cases of so-called " hys-terical aphonia" thoracic signs of pulmonary tuberculosishad been subsequently made out, and it was as well to bearin mind the possibility of diagnosing "hysterical aphoiaia "’
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im the presence of pulmonary tuberculosis. Impairedmovement of the vocal cords apart from paralysis was- described and considered to be myopathic in origin anddue to the changes noted in the muscle fibres. With regardto transient oedema of the laryngeal mucosa, the contourin a large number of larynges in early pulmonary tuber-culosis when compared with that existing in a normal
larynx was found to be partially lost, more particularly in theEnter-arytenoid and arytenoid regions along the ventricularbands, and at the base of the epiglottis. A fine crenating orfringing occurs upon the folds of mucous membrane in theinter-arytenoid space, not sufficient to be called an ex-
crescence, but met with sufficiently often in pulmonarytuberculosis as to be deserving of attention. An early buttransient loss of symmetry in the outline of the arytenoideminences occurred. The ventricles become less patentand this loss of patency was commonly associated withsome oedema, of the inner wall of the ventricular band,which was ascertained clinically in endeavouring to passa curved platinum loop into the ventricle in searchof tubercle bacilli. A slight oedema of this part of theventricular band, together with an enfeebled action of thecompressor sacculi laryngis, must effectually retain sputumladen with tubercle bacilli within the ventricle when once ithad been lodged there in the act of coughing. Moreover, itwas pointed out that the choking by a cell proliferation ofthe ducts of the muciparous glands opening into the ventricle,the closure of the ventricle by the cedema secondary to theproliferation of vessels, and the failure of the compressorsacculi laryngis through changes in the muscle fibres to
discharge its contents, all combine to deprive the cords ofthe mucus necessary for their lubrication. The cords losethat semi-translucent mother-o’-pearl sheen and present anopaque pallor more approaching a dead ivory-white. With in-sufficient lubrication superficial erosions occurred ; this didnot amount to ulceration as met with elsewhere in the larynxinasmuch as the essential element was absent-namely, thelymphatics. -
DERMATOLOGY.
THURSDAY, JULY 28TH.
Professor BOECK (Christiania) opened a discussion on theNature and Treatment of Lupus Erythematosus.
He first referred to the various forms in which the diseasemight be met with and then emphatically stated his beliefthat lupus erythematosus was a tuberculous disease. Outof a large number of cases which he had collected 28 hadpresented . some internal tuberculous manifestations, 8 haddeveloped uberculous glands in association with the disease,and 23 had presented enlarged glands in some part ofthe body. Only. one-third of the total number of cases
had not presented any tuberculous manifestation. Afterdescribing the various diseases for which lupus erythematosusmight be mistaken, he summed up the histological evidenceswhich he regarded as supporting the view that the disease wasof tuberculous origin, viz.—(1) the presence of giant cellsin the lesion; (2) the presence of small migratory cell
Enfiltration ; and (3) the destruction of the intercellulartissue. He also thought that the presence of peripheral nervedisturbance favoured this view.
Dr. UNNA (Hamburg) took an entirely opposite view. He
thought that the disease was wholly unconnected with tubercle,though clinically the condition had some superficial resem-blance to lupus vulgaris, which was universally admitted tobe a true tuberculous process. He emphasised the value ofthorough histological investigation of every case and adducedthe histological features as against the tuberculous view. Not
only had there never been found any evidences of tuberclebacilli in the lesion, but the characters of the process did notaccord with those of tuberculous lesions of the skin. The
overgrowth downwards of the horny processes of the
-epidermis should not, he said, be confused with comedones.There was a peculiar moisture which was quite characteristicof lupus erythematosus, accompanied by a cellular over-growth which was not found in dry scaly conditions, and it :
’was this which led him to prefer desiccating remedies. Asregards internal treatment he favoured alkalies, carbonateof ammonia, ichthyol, and salicylates, all of which were’useful but unable to cure without external remedies. OnBthe other hand, external remedies could often cure withoutinternal remedies. He exhibited a valuable table classifying external remedies in the treatment of lupus erythematosus.Group 1 consisted of desiccating remedies, such as powder
of oxide of zinc, powder of calamine, powder of bismuth,&c., or sulphur zinc paste or washes consisting of lead lotion,lime water, &c. These soothing remedies were very valuablebut were very tardy in their action. Group 2 consisted of com-pressing remedies for the removal of the œdema of the skin-collodion with ichthyol or salicylic acid, zinc, gelatin, com-pressing bandages, masks, &c. Group 3 consisted of anti-hyperaemic remedies such as plaster mulls or pastes of
chrysarobin, ichthyolsulfon, and mercury. Among these hehad tried pyraloxin, which he believed to be a very dangerousremedy. The micro-cautery (with tiny points) might beclassed in this group, and he recommended a platino-iridiumpoint in preference to a point of platinum. Group 4 consistedof necrotising remedies which were of two degrees : (a) peel-ing remedies such as salicylic soap, plaster mull, zinc,resorcin paste, &c., and (b) ulcerative remedies such as
pyrogalol in strong doses, sublimate, and the Pacquelincautery. Group 5 were inflammatory remedies. Of allthese the anti-hyperæmic remedies were, he believed, bestfor cure, the compressing remedies coming next in order,and the desiccating or soothing group being also valuable.
Dr. MORGAN DOCKRELL (London) expressed the opinionthat there was no evidence of lupus erythematosus beingtuberculous, and urged that the name was very misleading.The term "lupus," he thought, should be given up and aterm like "atrophic erythema" or "ul-erythema" used inits place. It was true that lupus erythematosus occurredsometimes on a tuberculous soil and led to a compound condi-tion, but he was persuaded of its non-tuberculous origin.In reference to the treatment of the condition he quitesupported Dr. Unna’s remarks on the value of the soothingtreatment, and found that he could always stamp out thedisease without the use of irritants.
Dr. EDDOWES (London) narrated a case of lupus ery-thematosus which he thought might have some tuberculousorigin on account of the circumstances under which it arose.He had taken pieces of skin from the patient and inocu-lated guinea-pigs in the laboratory at St. Bartholomew’s
Hospital, but with negative results. As regards the treat-ment he recommended lead and calamine lotion as a dailyapplication, and generally applied a solution of ethylate ofsodium to obstinate cases. Scarification was sometimesuseful and so was acid nitrate of mercury, though thiswas severe. These remedies were the best with whichhe was acquainted. Quinine, as recommended by Dr. Payne,was often very beneficial but apparently did no per-manent good.
Dr. MAAR (Copenhagen) mentioned the results of thetreatment suggested by Professor Finsen of Copenhagen,who had employed in the treatment of lupus vulgaris andlupus erythematosus the chemical rays of electric light orsunlight by the exclusion of heat rays. In the few cases inwhich that treatment had been tried a successful result hadbeen obtained by persevering with it for a long time.
Dr. LESLIE ROBERTS (Liverpool), Dr. STOPFORD TAYLOR(Liverpool), and others took part in the discussion.Mr. MALCOLM MORRIS (London) then opened a discussion
on
TVhat do we Understand by Eczema ?The nature of eczema, he said, was a subject which hadengaged the attention of dermatologists ever since the timeof Willan ; but although a great deal was known abouteczema they were not agreed as to what it really was. Wasit a special process following certain laws in its evolutionand manifesting itself by definite characters, or was it aclinical expression denoting results of several forms ofmorbid action ? His own conception of eczema was ex-
pressed in the following definition, which he had given fiveyears ago : A catarrhal inflammation of the skin originatingwithout visible external irritation and characterised in somestages of its evolution by serous exudation." The terms ofthis definition excluded all forms of artificial dermatitis-i.e., inflammation of the skin produced by chemical ormechanical irritants. Lesions due to such causes might beexactly like those of genuine eczema, but there was thefundamental difference that they appeared in response to avisible cause and began to disappear when the cause ceasedto operate. On the other hand, true eczema arose withoutobvious cause ; the skin might be healthy or there might besome pre-existing abnormal condition. The older derma-
tologists, following Bateman, regarded eczema as a vesiculareruption caused by an external irritation, "by the rays ofthe sun or the irritation of various substances applied to theskin, or by mercury taken internally, though it was found