British Journal of Industrial Medicine 1990;47:189-198

Delpech and the origins of occupational psychiatry

R R O'Flynn, H A Waldron

AbstractAuguste-Louis Delpech (1818-80) has beenremembered principally as the author of thefirst detailed description of the serious con-sequences of exposure to carbon disulphide. Aclose reading of his work suggests that hisreputation has been seriously undervalued.The subsequent development of occupationalpsychiatry, with its emphasis on the distinctionbetween the organic and the functional, may betraced through publications on carbon disul-phide. It is argued that a contemporaryapproach to occupational psychiatry is longoverdue.

On peut dire que le sulfure asassine; il tue l'homme, il luifait perdre toute dignite tout respect de soi meme.

Patient Monsieur B quoted by Delpech'

In the practice of occupational psychiatry one of thecentral problems is to relate toxic exposures to thedevelopment of psychological symptoms. We areeven now unable to understand the psychopatho-logical connections between "intoxication" and thephenomena of confusional states whereas for manyoccupational physicians "functional" disturbancesof bodily function are virtually equivalent todeliberate malingering.

Psychiatry has always been engaged in controversyto such an extent that historical arguments areforgotten and lessons once learnt must be relearnt.The quite opposing views of Delpech and Charcotthat form the basis of this paper are expressed evennow in discussions of the relative importance of"organic" and functional factors in the aetiology ofoccupational disease.

Charcot is well known as one of the major figures inthe development of neurology whereas Delpech isremembered, if at all, for his work on the adverseeffects of carbon disulphide.

Department of Psychiatry, Guy's Hospital, LondonSE1 9RTR R O'FlynnOccupational Health Department, St Mary's Hospi-tal, London W2 INYH A Waldron

Auguste-Louis DelpechDelpech was born in Paris on 3 August 1818, the sonof a doctor in the Falbourg St Germain. He qualifiedin medicine from the faculty in 1840 having been apupil of Trousseau. By an irony that will becomeevident later, his doctoral thesis, which was acceptedin 1846, was entitled "Des spasmes musculairesidiopathiques et de la paralysie nerveuse essentielle"and was apparently concerned with what would laterbe described as hysteria. He became a professor in thefaculty of medicine in 1847 with a work on thenosology of fevers. At the age of 29 he was appointedchef de clinique at L'Hotel Dieu and in 1852physician to the Central Paris Hospitals.Between 1856 and 1863 he published his work on

carbon disulphide that is discussed below. His laterwork included reports on trichinosis and porkbutchery, industrial diseases associated withchromates, and accounts of public health during thesiege of Paris in 1870.As Zeldin has pointed out, the medical profession

in France throughout the nineteenth century exer-cised considerable political power.2 Delpech was thusfollowing a tradition in becoming a city councillor in1876 having been awarded the Legion d'Honneur in1866. He died of angina pectoris (or a stroke) whilehunting on 5 September 1880.3As a professor in the University of Paris he

occupied the central ground of the profession:throughout the nineteenth century the Paris Schoolvigorously propounded scientific rationalism (par-ticularly detailed experimental observations) asopposed to the school of Montpellier which espouseda philosophical vitalist attitude to medicine.2 Thework on carbon disulphide admirably demonstratesthe former approach.

Carbon disulphide and vulcanisationCarbon disulphide was used first in medicine fortreating various illnesses, as a local and generalanaesthetic, and as a solvent in the compounding ofmedicines. Its main industrial uses since the middleof the nineteenth century, however, have been in twoprocesses, the vulcanisation of rubber and the xan-thation of viscose rayon.Rubber had been used in the new world for many

years, moulded into household objects or for water-proofing cloth. After its introduction into Europe itremained essentially a curiosity since uncured rubberhardens and cracks at low temperature and decom-

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poses and perishes in sunlight or heat. Its widespreaduse was made possible when Charles Goodyeardeveloped vulcanisation in 1841: after considerableexperimentation he demonstrated that if rubber washeated when mixed with flowers of sulphur it wasrendered resistant not only to temperature but also tosolvents that could dissolve the gum in its nativestate. Thomas Hancock in 1842 introduced analternative system of hot curing in which the rubberwas immersed in molten sulphur.These processes are suitable for manufacturing

large or solid items but small articles and thin stripsof rubber tended to char. Alexander Parkes in apatent of 1846 described a novel method which hecalled cold curing: rubber was exposed to sulphurchloride in a dilute solution in either naphtha orcarbon disulphide. The latter was generally adoptedas it produced further swelling of the rubber, thusspeeding up the process. Until the 1880s this processwas used to produce a wide variety of productsincluding gloves, balloons,4 and what Delpech des-cribes as "ce produit . .. industriellement consacrede preservatif, indique suffisamment l'usage"'-thatis, condoms.

In 1890 the method ofmaking artifical silk (viscoserayon) from the cellulose of wood pulp wasintroduced. The central process in this is the reactionbetween cellulose and carbon disulphide to formcellulose xanthate which takes place in sealed vesselsand generates considerable heat. Subsequently theviscose thus produced is extruded and woven intofabric.The hazards to health are, of course, quite dif-

ferent. In the early rubber industry large vats of thecuring mixture were open to the environment toallow the rubber to be dipped in, initially by hand. Inthe rayon process it is the cleaning out of the churnsand the further processing of the viscose that exposethe worker to the solvent. In the first the concentra-tion of vapour was, one assumes, constantly high,varying little during the day whereas in the secondhigh exposures occurred infrequently in the workingday. Common to both industries was the risk of fire.According to Hunter, Payan directed attention to

the danger to workers in 1851,' but it was Delpech'spapers of 1856 and 1863 that represented the firstdetailed account of the consequences to health ofoccupational exposure to carbon disulphide. Thiswas less than five years after the widespread use ofthesolvent in large scale industry.

Une note sure les accidents qui d6veloppechez les ouvriers on caoutchouc, l'inhalationde sulfure de carbone6In his presentation to the Academie de Medecine on15 January 1856 Delpech noted that every bodilysystem could be affected in some way by carbondisulphide, although the commonest symptoms were

psychological:Troubles intellectuels-Affaiblissement de la memoire;vague et confusion dan les idees. Access alternatifs degaiete folle et d'emportement maniaque. Insomnie;agitation plus ou moins vives; reives penibles; reveils ensursant la nuit. Lejour, somnolence, abattement, etat detorpeur et d'inertie.The patients experienced constant headaches,

dizziness, and itching. Occasionally loss of sensationor analgesia developed. Delpech had, rarely,observed increased sexual desire but frequentlycomplete impotence developed. Affected individualswere prone to cramps and shaking of the limbs andoften developed paralysis and atrophy; the muscles,however, continued to contract when electricallystimulated. He emphasised the disturbances of themusculoskeletal system, especially of the legs.The workers were so saturated in the solvent that

their breath and urine smelt of it strongly.2 If theywere not removed from the source of it they wouldbecome so weak and anaemic that their lives werethreatened. Delpech further considered the actionsthat might prevent or combat the poisoning. Only achange of work could help the afflicted workers,combined with personal "sobriety." For prevention,he advocated well ventilated factories in whichworkers would not eat or sleep, greater separation ofthe various processes from one another, and theprovision of a largely meat diet for the healthyworkers.

Accidens (sic) que developpe chez les ouvriersen caoutchouc l'inhalation du sulfure decarbone en vapeur7Whereas the communications to the Academie deMedecine served to establish carbon disulphidepoisoning as an entity, Delpech's own success wouldhave depended on his report reaching the widestpossible number of colleagues: this was possibleusing the newspapers regularly directed at the mem-bers of the medical profession.A longer account of his findings was published

"from the proofs" of a paper in L'Union Medicale inMay 1856. It starts with an account of the illness ofVictor Delacroix then aged 27 who had been workingin the cold curing room ofa rubber works since 1853.In the three months before his admission to hospitalhe had developed several disabling symptoms withtrembling and shaking of the limbs and deafness sopronounced that people shouted into his ears to makehim hear. His memory had failed so completely thathe lost items put down only moments before. As wasoften observed, his sleep was grossly disturbed byterrible dreams. His digestion was ruined and he hadlost all sexual drive and function; his wife had left himeven though she herself was ill.On examination Delpech found him to be

prematurely aged, walking with a stick, his legs

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wasted and weak. The extensors, particularly of theleg, were more affected than the flexors but neitherwas spared; the contraction in response to a galvaniccurrent was unimpaired.He was given electrotherapy, sulphur baths, and

medications containing iron and nox vomica thatgradually restored him so that he was able torecuperate in the country far from his work. Only hisheadaches and his impotence did not improve sub-stantially.

Repeatedly throughout the account, and in thesynopsis that follows it, Delpech emphasised that thepoisoning produced by carbon disulphide resulted ingross disruption of all the bodily symptoms; indeedthe more closely he examined his patients, the morehe found in their symptoms.

In this work he formulated the course and thesymptomatology ofthe disease in terms ofexcitementsucceeded by suppression of each physiological sys-tem. In the late 1850s, however, his views underwenta change: indeed this might account for the delaybetween his preliminary communications and thepublication of the famous monograph. His earlierview appears to have been that the solvent dimini-shed the operation of the body. He therefore foundanalogies with other toxic substances such as lead andalcohol rather than boldly claiming that a uniqueillness had been described: the change of view leddirectly to the title of the 1863 monograph (l'intoxi-cation sp&iale).

Recherches sur l'intoxication speciale quedetermine le sulfure de carbonelDelpech's major review, the monograph to whichmost other authors have since referred, was derivedfrom a communication to the Academie Imperiale deMedecine in 1861. In it Delpech attempted toproduce a synthetic account of the effects of thesolvent in one particular group of workers in theinflated rubber industry, drawing on clinicalaccount, the results of animal experiments, andtherapeutic advances. The account is illustrated with23 histories of men, women, and children showingvarious aspects of carbon disulphide poisoning.These are vivid, often dramatic vignettes, rangingfrom a few sentences to several pages.Delpech chose the inflated rubber industry

because it allowed him to test his previous observa-tions. It had the other advantage that each workertended to be employed at different times in differentaspects of the trade.

Quantities of rubber were placed in large vesselsand were blown into shapes either directly by theworker using a small tube or by special machines.They were dried, often in the same rooms or nearbyin currents of air until all the solvent had evaporated.The workers were thus exposed to carbon disulphidethroughout the day. The process also involved

smaller quantities of sulphur chloride and the talcumpowder in which the condoms were dipped. Therewere hundreds of such factories in Paris, in all ofwhich most of the workers were ill.

Delpech's experience had led him to believe thatthere were two different courses in the developmentof carbon disulphide poisoning: one presentedrapidly, in some cases after only a few hours, theother was much slower to develop and more chronic.Delpech's main attention was on the slow form,largely because he could identify phases within itmore readily.He noted that the acute intoxication had two

phases: the first that of excitement followed invaria-bly by collapse in which state a proportion ofpatientsremained. Each bodily system went through thisperiod of stimulation followed by a decline of func-tion yet each did so at a different rate according, heassumed, to individual physiological variation, whichled to the bewildering number of clinical presenta-tions.The illness was always preceded by a headache that

came on initially after finishing work. It wouldoccasionally start suddenly with terrible burstingpain whereas on other occasions it had a crushingquality.The patients would then develop tingling (four-

millements) and itching, particularly of the scrotum.Eventually, however, mental excitement wouldbegin, often shown most notably in extreme talk-ativeness. As Madame A told him, "Quoique j'eussela plus grand difficulte a trouver les mots dont j'avaisbesoin, j'avais un flux de paroles intarissable. Je mesentais deraisonner sans pouvoir m'arreter." Withthe pressure of speech came violent fluctuations ofmood ranging from happiness and elation to anxiousforeboding. A few became frankly insane. One, forexample, was subject to "des terreurs sans raison, lacroyance a des crimes imaginaires dont il se seraitrendu coupable, des hallucinations de la vue et del'ouie, une agitation maniaque extreme."

Occasionally epileptiform convulsions formed aconsiderable part of the clinical picture. Only twocases discussed in the monograph had ever experi-enced convulsions and in both they had occurred foronly a short period in the most severe intoxicationand disappeared rapidly.The patients were subject to endless agitation,

insomnia, and absurd or terrifying dreams. Theirvision was often directly disturbed and they might behallucinated or experience macropsia or diplopia.The painful muscular cramps and tremblings that

Delpech noted in 1856 could now be seen to formpart of the widespread stimulation of the musculo-skeletal system: some patients, for example,developed contractures of the hand much likewriters' cramp that Delpech presumably thought tobe a direct effect of mixing the solvent in the vats.

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The organs that above all were most predictablydisturbed were the genitals: Delpech now refined hisviews considerably, finding that they too werefrequently subject to excitation. "La stimulation desfonctions generatrices dans l'origine des accidentsd'intoxication est un caractere remarkable sur lequelil est necessaire d'insister. Chez un grand nombred'ouvriers en caoutchouc souffle, ce sympt6me s'estreproduit avec un intensite et une persistanced'ailleurs tr&s variable. [Un] jeune homme de vingtans, etait poursuivi par des erections constantes etdes besoins exageres. II se levant au milieu de la nuitet aller au loin chercher, dans des raprochementssexuels, la fin de cette obsession."Such a state of affairs might only last for a short

time or might more rarely persist throughout theillness. He had seen so few women workers that hewas unsure if a similar process occurred in them:certainly their menstrual periods were muchincreased, so much so that some were unable to workat all during their periods.The period of decline that followed the initial

excitement represented the depression of the func-tions originally so stimulated. "Les maladies sonttristes, decourages, livres a une indifferance absolue.Ils sont, disent-ils, comme heb&es. Ceux qui avaientquelque distinction quelque elegance, la perdent et sesentent en memes tomber dans l'abrutissement."Memory failed so dramatically that many would

forget even the simplest instructions. One workerpathetically told Delpech, "J'avais un reputation deraconter d'une maniere amusant, je ne puis plus lefaire maintenant ma langue tourne moins bienqu'autrefois."The patients lost sensation in many parts of the

body especially in the legs, indeed two men becamecompletely anaesthetised over the entire surface ofthe body so that they were able to bathe in a cold riverin November without complaint. Eyesight failed andpatients were troubled by perceiving everything in agrey fog; in most cases only blanching of the opticdisc could be observed, although a few patients alsohad corneal ulcers.The increased sexual desire was replaced by almost

universal impotence. So well known was this that nomarried man could be persuaded to take upemployment in one large factory. When erections didoccur they subsided so rapidly that coitus, let aloneejaculation, was impossible. Delpech speculated thatthe men were also sterile. One man talking of thisreported, "J'etais tres ardent, tres coureur, avantd'entrer a l'atelier, moins rapidement je me mis a fuirles occasions tout par absence de desir que parconscience de ma faiblesse."

Children exposed to carbon disulphide experien-ced major disruption of their sexual maturation. Aboy of 12 employed in the industry never experiencedany sexual desire whereas a man of 20 who had

worked in a factory since the age of 10 had a normalsized penis but atrophic testes. Women experiencedlack of desire and occasional complete sexual anaes-thesia so that many were abandoned by their hus-bands. None ever had full term pregnancies.Delpech discusses only briefly the paralyses that

developed in this phase. It might well affect only onemuscle or one group in ways not observed in otherpoisonings-for example, the left side of theabdomen was especially affected. Almost all the casereports detail paralyses; almost half the patientsbecame hemiplegic or paraplegic at some stageduring their illness.These observations led Delpech to speculate on

the underlying aetiology. Superficially the courseresembled that of other poisonings, of anaestheticagents, and of alcohol, particularly the phase ofexcitement preceding decline and collapse. In carbondisulphide intoxication, however, one strikingfeature was that functions might resist suppressionfor longer periods than others: this suggested aconstitutional factor on which the "poison" worked.Some symptoms could be most readily explained

as the direct effects of contact with carbon disul-phide. When a small amount was placed on the skinthere was first a sensation of unpleasant coldnesssucceeded by a feeling of heat followed by burningand extreme pain. Perhaps the vapour hanging nearthe floor first affected the legs in a similar way.Certainly when carbon disulphide was mixed withblood it reacted strongly to remove phosphorus fromit and bound itself to fat globules. Delpech used thisinsight to construct his treatment regime of adminis-tering phosphorus, reasoning that it was its loss fromthe blood that caused the anaemia and from the brainthat led to the mental depression.The most important observation made by Delpech

was that death was never an outcome of poisoningalone. Only one of his reported cases died and thiswas as a result of rupture ofan aortic aneurysm. Thiswas the only such outcome of which Delpech knew.One other patient, Madame L "se suicida sans motifapparent ... son intelligence s'etait alteree progres-sivement dupuis son entr&e a l'atelier. On pensaqu'elle s'etait asphyxiee dans un acces d'alienationmentale."For the most part cure or at least partial cure could

be effected by moving the patients from their work.Indeed, if they returned to it they tended to becomeill more quickly than before.

In the monograph Delpech emphasises the impor-tance ofavoiding contact with carbon disulphide: it isclear from the cases he reports, however, that prolon-ged contact, particularly among those aged over 40tended to leave the patient chronically disabled byimpaired memory.As he had explained in his preliminary commun-

ication, the most important concern was to ensure

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adequate standards of ventilation and hygiene toprevent intoxication. His patient Monsieur D fol-lowed his ideas so closely that he radically redesignedthe workshop. He divided up the factory into small"cupboards" fronted by glass. Holes were cut intothe boxes through which the workmen could placetheir arms and carbon disulphide was only handledinside. The process of vulcanising items was dividedinto components with a man performing a single task.Finally, all equipment and the articles themselveswere left to dry in the open air. Perhaps understanda-bly, his fellow workers and the factory owners treatedhis efforts derisively. His boxes were called "magiclanterns" and his initiative was ignored. Only thesimplest changes could ever be made withoutstatutory obligations.

Animal studiesDelpech's experiments on animals represent one ofthe earliest approaches to inhalational industrialtoxicology. They are also further evidence of the firmobservational basis of all his work on carbon disul-phide. The communications of 1856 and 1863 con-tain accounts of a series of careful experiments.Whereas the design of these experiments was vir-tually perfect, their execution was not and theaccount of their failure is a further testimony toDelpech's extraordinary honesty. Differences bet-ween the series also emphasise the development ofhisideas on the pathology and physiology of the intoxi-cation.

Accidents produit par l'inhalation de sulfurede carbone en vapeur experiences sur lesanimaux8For these experiments reported in 1856, a box wasconstructed with a capacity of 0 5 m3. It was firmlyjointed and covered with glass on its upper surface.Four hoses, each 1 5 cm in diameter, allowed whatDelpech thought to be a sufficient amount of air toenter the box. Two pigeons were placed in the boxand once they had survived happily for a few days atablespoon of carbon disulphide was placed in a glassin the box. After only eight hours one bird had diedand, following the introduction of a similar amount,the second succumbed also.Delpech noticed that the birds had certainly eaten

grain splashed by the solvent and had in fact probablydied from suffocation because insufficient air enteredthe box. Accordingly the box was modified with theaddition of a number of small holes in the sides andbottom, and a container was fixed to the sides to allowcarbon disulphide to be safely introduced withoutcontaminating the food.A rabbit was subsequently exposed to 4 g ofcarbon

disulphide and as doses were repeated it firstdeveloped convulsions and then weakness ofthe hindlegs leading eventually to paralysis. This allowed

Delpech to state, "Cette experience ne pouvait laiserde doute sur l'intensite des effects produits par cettesubstance chez les hommes et chez les animaux, etelle isolait bien nettement son action." He wasimpressed by the presenting disturbance of motilityand the primary effect on the hind quarters thatclosely resembled the complaints of exposed work-ers.The rabbit was allowed to recover and then

replaced in the box with 12 g of carbon disulphidewhereupon it gradually became incapacitated by adense hemiplegia that followed several convulsions.It eventually died despite Delpech's attempts torevive it with warmth and brandy.When examined, the lungs were obviously

inflamed and the heart filled with black, unorganisedclots. The liver was fatty and like the intestineshowed discoloration secondary to postmortemchanges. The urine smelt heavily of carbon disul-phide, was alkaline, and loaded with albumin.Delpech embarked on the experiments having

recognised that his descriptions of the human symp-toms were not specific to carbon disulphide but couldbe produced by toxic exposures to several chemicalsin the environment. The initial animal studies werean attempt to produce some specific signs that werecaused by carbon disulphide alone. Viewed objec-tively he failed in this, presumably because theanimals were exposed to huge concentrations and, infact, perished either of asphyxiation or of acuteintoxication.The animal experiments became of greater impor-

tance after his recognition of the excitatory andinhibitory phases. Furthermore, he recognised thatany specific role for carbon disulphide could beproved only by excluding effects from those due tointeractions with other substances-for example,sulphur chloride in the vulcanising mixture.

Second animal experiments'For the experiments reported in 1863, a much largerbox was made 1 metre high, 0 5 metres in length, and1 metre wide. The interior of the box could bedivided horizontally in two by a glass shelf thusallowing two animals to be exposed simultaneously todifferent concentrations. The solvent was introducedvia reservoirs so that the animals were undisturbedand larger holes in the side of the box improved thegeneral ventilation.

In the first experiment 30 g of sulphur chlorideevaporated in the box in six hours and a rabbitshowed no ill effects even after two days exposure.Subsequently, 30 g of carbon disulphide killed thesame animal which had developed paralysis havingbeen placed on the floor of the box for two days.Carbon disulphide was substantially more volatileand evaporated so rapidly that the concentrationmust, Delpech reasoned, be much higher than that of

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the sulphur chloride.On this basis, Delpech reasoned that sulphur

chloride alone could not produced all the adverseeffects. This confirmed the observations that he hadmade at the factories. The chemical could certainlyproduced headache and considerably irritate thebronchus (particularly if it decomposed to hydro-chloric acid) but it produced no long term harm inman or in animals.

In the succeeding experiments he took great painsto examine the effects of the mixture of sulphurchloride and carbon disulphide. In proportion of tenparts of sulphur chloride and 90 parts of carbondisulphide, a rabbit died rapidly, probably, as a post-mortem finding disclosed, from a combination ofsuffocation and the effects of the solvent.

Accordingly, Delpech considerably decreased theamount of solvent that he introduced into the box, atthe same time decreasing the proportion of sulphurchloride to carbon disulphide to one part in a

hundred. Over the succeeding three days anotherhealthy young rabbit was exposed to repeated dosesof the mixture, becoming increasingly agitated.Indeed, one night its cries were so loud that someonewho lived 60 yards away complained that his sleepwas disturbed. This animal too eventually perished.

Further experiments showed that rabbits rapidlybecame paralysed by carbon disulphide but had no

substantial symptoms when exposed only to sulphurchloride even when the fumes of the sulphur chloridewere so dense as to resemble a fog. Furthermore,careful analysis of the results of mixing the solventand the sulphur chloride showed no evidence of anychemical reaction that might be responsible forproducing a third toxic compound.The animal experiments did not, by 1863,

represent an attempt to reproduce in the rabbit signsidentical with those demonstrable in man. Delpechseems to have accepted that the development ofparalysis of the hind legs was an equivalent of thehuman weakness and tremor so pronounced in thelegs. This allowed him to move beyond simplyexposing the animals and observing their behaviourto testing complicated hypotheses with paralysis as a

recognised end point.Delpech introduced into his practice the use of

phosphorus in the treatment of the intoxication notonly because of its stimulation of the organism inother diseases but also because of his aetiologicaltheories. In all cases there was a generalimprovement, particularly in the restoration of sex-

ual potency and function.

"Carbon disulphide neurosis"In his discussion of the mode of action, Delpech saw

clearly that the direct effects of carbon disulphidewere similar to those of alcohol and of the generalanaesthetics (indeed, before the introduction of

chloroform, carbon disulphide had been suggested asan alternative agent). The period of excitementoccurred initially followed by a progressive depres-sion of function. He pursued the analogy of thecentral effects of the anaesthetics into a direct effecton the peripheral nervous system of carbon disul-phide vapours. He was thus able to account for thesymmetry ofthe distal weakness and loss of sensationand its pronounced effects on the legs.His accounts ofthe psychological manifestations of

the intoxication remain vivid largely because he didnot speculate on them from within the framework ofcontemporary psychiatry. It is striking, for example,that most of the phenomena he described were thosethat were being vigorously debated in French psy-chiatric publications in the 1840s and 1850s.9 Byplacing his discussion firmly within the organic heavoided controversy, albeit unwittingly. It seemslikely that his work on carbon disulphide was accep-ted as authoritative until Charcot's critique becauseit was read largely by physicians rather than byalienists. Charcot's contribution is largely misunder-stood because the audience reading it now ispredominantly interested in carbon disulphide andnot in "hysteria": for example, Braceland suggeststhat he "beclouded" the issue and this has been thetraditional view of this contribution.'0

Intoxication par le sulfure de carbone"In his demonstration of 6 November 1888 Charcotdisplayed a man who had been admitted to hospitalwith carbon disulphide poisoning. In his introduc-tion he pointed out that between 1856 and 1863Delpech had changed his views to suggest thatcarbon disulphide caused a specific identifiable dis-ease rather than causing symptoms common toseveral other intoxicants. Charcot's examination ofthis patient led him to no such conclusion; indeed, heasserted, playing on the contemporary confusion,that Delpech's "carbon disulphide neurosis" wasnothing but a simple case of "vulgar neurosis."

Charcot's patient was a previously healthy andvigorous 60 year old man of a sober disposition nevergiven to excesses: like all carbon disulphide workershe was forbidden to drink alcohol. There was noneuropathic trait in his family which included severalcentenarians. Since 1872 he had worked as a generallabourer and in a vulcanising factory. In the fourmonths before the illness he had been working in afactory cleaning out the vats that contained thevulcanising mixture.

Quite suddenly one afternoon he collapsed uncon-scious "comme frappe d'apoplexie." He had sud-denly been overcome by a feeling of suffocation and aburning pain in the scrotum. He was rescued by hisfriends who thought him suffocated and he remainedunconscious for half an hour. Confused and bewil-dered he was taken back to his bed where he remained

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for two days. On the third day he noticed that hisright arm felt heavy and by the evening it wascompletely paralysed. Gradually his right leg becameheavy and weak; he could walk only with difficulty.The case closely resembled those described by Del-pech.

Charcot demonstrated the neurological findings tohis audience offering a commentary at the same time.It is an interesting observation that despite thefrequency with which the paper is quoted, its contin-ual confusion between right and left, caused by faultyproof reading, has not been previously noted.The man dragged his leg behind him as if it were

inert and lifeless: he made no attempt to move it nordid he circumduct the limb when he was walking aswould be the case "dans un hemiplegie ancienne decause organique." The right arm was supple,undeformed, and without rigidity. The hand,however, was deformed, being held with the fingersat right angles to the palm so strongly as to resistmovement. Charcot pointed out that usually inorganic paralyses the fingers were folded over orhooked ("en crochet"). The reflexes were not exag-gerated in either limb. There was complete loss ofsensation down the right side (sparing, according tothe published illustration, part of the abdomen andthe flexor surface of the arm); this also extended tothe underlying structures. It was important to noticethat while sensation was completely abolished, motorfunction was not. This differed from the example oflesions in the posterior limb of the interior capsule.More remarkably the face was not affected by themotor loss. One could readily note a frequent twitch-ing of the angle of the right side of the mouthdownwards and to the right. Charcot had describedin his previous work all these features as beingclassically found only in hysteric paralyses, par-ticularly the mismatch between motor and sensoryloss and the "spasme glosso-labiale." The specialsenses were all directly affected on the right side. Thevisual field of the right eye was greatly diminished aswas hearing and the sense of taste on the right side ofthe tongue.The man's mental state was particularly worthy of

note. Charcot had taught that female hysterics failedto respond to their disabilities in a "normal" manner:they all reacted with "belle indifference" (or as hegraphically expresses it here "brio morbide").Among men, particularly of the working class, thesituation differed; they were always "gens sombres,melancholiques, deprimes, descourages."The present patient was no different. Whereas he

had never been jolly he had always responded to life'sdifficulties without complaint. He was not utterlyinconsolable. Since the accident he had experiencedthe most terrifying dreams; he was chased by lions,wolves, or fantastic creatures or he took refuge from aflood only to see the water covering the mountain on

which he stood. This was so different from hysteria,at least superficially, that some authors had sugges-ted that the condition ought to be called "neurosetraumatique." But all the symptoms were entirelycharacteristic of hysteria caused by trauma or intox-ication. Indeed, almost all the symptoms discussedby Delpech similarly fitted into the same category.Only some isolated nerve lesions, just like thoseobserved in lead or alcohol poisoning, seemed toresult from poisoning by carbon disulphide itself.

Sulfure de carbone et hysteria"2In 1888, three days after Charcot's demonstration,Marie read a paper to the Societe Medicale desHospitaux in which he continued the attack onDelpech. He presented the same patient as Charcotand a man of 36 with almost identical symptoms.Marie elaborated the theoretical links between

carbon disulphide poisoning and the development ofhysteria. All the cases of neurological symptomspresented by Delpech were, as Charcot had shown,understandable only as functional disorders. Del-pech had ignored the strict demarcation of the loss ofsensation and the curious distribution of the motordeficits. When paralyses occurred they never led tocontractures nor were the muscles flaccid. Occasion-ally all four limbs might be paralysed in ways rarelyseen in organic illnesses. It was strange, he remarked,that so many of the symptoms of the reportedpoisonings occurred on the right side of the body.Finally, the disturbance of sexual functioning oftenfirst manifested by increased desire was only seen inhysteria.

Marie's conclusion was similar to Charcot's: theperipheral neuropathy that could be demonstratedclinically was one manifestation ofcarbon disulphideintoxication and the "toxic hysteria" was the other.

Charcot and hysteriaIn conventional accounts of carbon disulphidepoisoning, authors almost always mention the workof Charcot and Marie either in a neutral, perhapsembarrassed tone4 or in a dismissive one'0 whereasDelpech is presented as describing the significantfeatures of carbon disulphide poisoning. As early as1905, Jump and Cruice reinterpreted all the clinicalsigns in Marie's cases as resulting from isolatedperipheral neuropathies.'3 They ignore the fact thatCharcot and Marie themselves had emphasised thatneuropathies could easily be shown by objectiveclinical investigations-for example, by elec-trogalvanic stimulation. Jump and Cruice and manyother authors practised in a neurology radicallyaltered by the successes of Charcot and HughlingsJackson, one in which the functional disturbanceoccurring without structural abnormality was unreal,fabricated, or psychological.

Unfortunately a reading ofDelpech, who practised

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before the "invention" of modern neurology, bythose after its creation, paradoxically makes himseem a contemporary and makes Charcot seemmisguided. A more careful consideration must takeinto account the theoretical practices of both men.Delpech, as we have noted above, operated within

the tradition of careful, painstaking observation ofpatients and of attempts to define relations betweendifferent pathological entities. The nosologiesderived were as elegant and complicated as theLinnean classification of species (on which, indeed,they were based). The reference points for carbondisulphide intoxication were the acute effects of theanaesthetics and the symptoms of chronic leadpoisoning. Between 1856 and 1863 Delpech hadidentified a series of closely related diseases differingfrom one another according to their severity andduration as much as their outcome.

In general Delpech shows no great interest in themorbid processes causing the symptoms (probablydue in part to the absence of postmortem material).Such an attitude, labelled by Lopez-Pinero andothers as the physiopathological view,"4 developedout of the failure of anatomy and pathology com-pletely to described many diseases, particularly thelarge group designated then as neuroses. Delpech,with his emphasis on precise changes in function andhis repeated use of "excitation" and "suppression,"follows a tradition derived from Broussais and Rochewriting more than 20 years earlier. Accordingly, hiscontinued references to anatomical structures do nothave the same significance as those by Charcot.Delpech would hold that function, the result ofderanged physiology, was the only way of under-standing the intoxication whereas Charcot alwayssought an anatomical lesion. Even the animalexperiments that so closely resemble those ofcontemporary toxicology have a different purpose:Delpech was clearly trying to replicate the form oftheillness, not its pathology.By 1882 the anatomicoclinical method had trium-

phed over the approach that concentrated on func-tion. Charcot's own work, which correlated theclinical presentation of multiple sclerosis with brainchanges, was central to this as was his concept of the"lesion." His work on hysteria, described as his"crowning moment and denoument"14 was anattempt to explore the area of the neuroses, thenunderstood as abnormalities of nervous function.

Charcot had been interested in functionalneurological illness from the earliest phase in hiscareer, when he was an inteme at the Salpetriere. Onthe ward, caring for convulsive patients, he learnt todistinguish between those patients suffering fromepilepsy and those who were not. As he investigatedthe latter group he began to describe some whoseconvulsions formed part ofa hysterical crisis. In 1882he showed the similarity between the phases of these

hysterical crises and the stages of the hypnotic state.This suggested that similar processes were operatingin both groups.By 1884 he had observed that it was possible to

recreate the symptoms of hysterical paralyses(presenting after accidents, for example) using hyp-notic suggestion in susceptible subjects. A smallproportion of individuals seemed to live in a perman-ent somnambulistic state so that hypnotism was noteven necessary, whereas for others the state had to beinduced. He called the resulting paralyses "dyn-amic" and opposed them to the organic paralyses, theoutcome of direct damage to the nervous system.5 16

Freud, who studied under Charcot in the winter of1886-7, explained the process whereby a pos-traumatic paralysis could develop.'7 "We will takethe case of a person who is subjected to a traumawithout having been ill previously and perhapswithout even having any hereditary taint. Thetrauma must fulfil certain conditions. It must besevere-that is, it must be ofa kind involving the ideaof mortal danger. But it must not be severe in thesense of bringing physical activity to an end.Moreover, the trauma must have some relationshipto some part of the body. Let us suppose that a heavybillet of wood falls on a workman's shoulder. Theblow knocks him down, but he soon realises thatnothing has happened and goes home. After a fewweeks ... he wakes up one morning and notices thatthe arm that was subjected to the trauma is hangingdown limp and paralysed, though in the interval . .he has made perfectly good use of it ... The work-man was not in a state of hypnosis. Nevertheless wemay assume that he was in a special state of mindduring the trauma; and Charcot is inclined to equatethat effect with the artificially induced state ofhypnosis. This being so, the traumatic spontaneousparalysis is completely explained and brought intoline with the paralysis produced by suggestion, andthe genesis of the symptom is unambiguously deter-mined by the circumstances of the trauma."'"8

Freud's own development of Charcot's theory(which led on into psychoanalysis) had already, by1893, suggested to him that functional disorders hadtheir sources in psychological disorder.'9 Indeed afterCharcot's death almost all his work on hysteria fellinto disrepute; only his theories on posttraumaticneurosis continued to exercise influence.This has obscured the precise way in which

Charcot and Marie were using phrases such ashysteria and neurosis. They referred to the results oflesions too subtle or perhaps too short lived to bedetected in the brain at necropsy and were in someway related to the psychological state of the person atthe time oftheir origin. It was the continued failure ofall attempts to demonstrate the lesions and theobscurity of their causes that led to the failure of thetheory.

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Delpech and the origins of occupational psychiatry

Nevertheless, we may reconstruct the aetiologythat Charcot proposed for the effects of carbondisulphide. Because of its acute effects, the solventinduced a psychological state in the men, virtuallyidentical with that ofhypnosis, in which lesions coulddevelop in the central nervous system. These, notcaused by the carbon disulphide, could lead on to thehysterical paralyses observed. The entire clinicalpicture was a compound ofthe effects of these lesionsand the peripheral neuropathy. Marie could statewith obvious satisfaction "les neurites peripheriqueet 'hysteria toxique' sont functions des memes intoxi-cations. Peut-etre cette notion permettra-t-elle depenetrer plus avant dans les arcanes de l'hysteriapouvrant bien tirer, elle aussis, son origine de veri-table lesions des centres nerveaux.""2

Psychiatry of carbon disulphide poisoningafter CharcotFor most of this century hysteria and neurosis havehad as their causes psychological factors that produceno physical effects. In reports on carbon disulphide"functional disability" was increasingly ignored asincreasing attention was paid to other consequencesof poisoning, such as optic neuritis.20 Whereas Del-pech was honoured because of priority, Charcot'scontributions were cited perhaps because of his vastimportance in neurology.

In the 1880s the chiefuse ofcarbon disulphide wasin the viscose rayon industry. From the late 1880scold vulcanisation was performed using sulphurchloride vapour rather than a solution. In the churnrooms of the rayon process the ambient concentra-tion ofcarbon disulphide was much lower than in thevulcanisation sheds of the 1860s; the major dangeroccurred with the opening of the churns and theircleaning.Jump and Cruice reported the symptoms of two

men from the Artifical Silk Works in Philadelphia.'3In both, major disturbances of mood and behaviourdominated their mental state. Only one had abnormalfindings on neurological investigation; the other,complaining of vertigo and formication, had noobjective signs.The major feature of true carbon disulphide

poisoning was, in their view, that of a peripheralneuritis closely resembling that of alcoholic neuritis(now recognised as a symptom of thiaminedeficiency). They conclusively demolish Marie'sargument about his own cases while maintaining that"peculiar manifestations of hysteria" can beobserved with the neuritis. The psychiatric abnor-malities were, in their view, the direct toxic effects ofexposure to the solvent. Despite reviewing Delpech's1863 monograph they nowhere comment on his ideasof the two stages.While the neurology of carbon disulphide was

being classified, its psychiatry was becoming ob-

scure. According to Braceland,° an often unreliableauthority, Laudenheimer in a monograph of 1899suggested that carbon disulphide acted as "anexogenous poison that might initiate a psychosis." Inan uncited work Rodenacker was credited with theview that some personality types, particularly thosewith cyclothymic traits, were particularly susceptibleto its adverse effects whereas others were insensitive.Unnamed opponents by contrast suggested that thepsychotic symptoms were the direct effects of thesolvent, were specific to it, and differed in form fromfunctional psychosis.The synthesis of these views was produced in the

monograph of Bonhoeffer.2' Its publication in theGerman Monatschrift fur Psychiatrie und Neurologieensured that it has been forgotten by occupationalphysicians. His detailed examination of several casesled him to define several disease entities on the basisof the phenomenology and course.There was no doubt that even in small quantities

the solvent produced a peripheral neuropathy mostpronounced in the sensory modalities. Similar directeffect could be observed, he suggested, in the Parkin-sonian syndrome equally common among this groupof solvent workers. A toxic psychosis whose primarysymptoms were clouding and fluctuation of level ofconsciousness, impairment of memory, and mooddisturbance could be produced after repeatedexposure to high concentrations. In most cases thisresolved after a few months and certainly within ayear. Rarely, the acute psychosis was extremelysevere in which case the sufferer would be leftpermanently disabled with a "chronic psychosis ofthe Korsakoff type." Finally, in individuals predis-posed by heredity or habit to a functional psychosissuch as schizophrenia, carbon disulphide could has-ten its development even when a toxic psychosis didnot develop first. In such cases the prognosis was nodifferent from other causes of the same psychosis.This view was popularised by Braceland's 1941

review that preceded his own study of the effects ofthe solvent on a group of 90 rayon workers."0 Twooutcomes seemed to be common among these menworking in a factory manufacturing collars. Onegroup developed symptoms entirely characteristic ofa toxic psychosis after a briefprodromal illness; theygenerally recovered completely. A small proportion,however, developed mental disorders, not neces-sarily psychoses, that were perhaps functions of apre-existing disposition. Almost all his patients werehallucinated and deluded at least for a time afterleaving the churn rooms. In Braceland's view hys-teria was unlikely to account for any significant partof the symptoms, the effects being purely those ofintoxication.

In the past 20 years this constant theme of devalu-ing or ignoring the functional has become dominantin occupational psychiatry so much so that it has

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seemed to become an annex ofneurology. The recentconcerns about other solvents causing psychiatricdisease reflect this, resulting in some confusion whenpsychiatric symptoms do not coincide completelywith physical findings, generally signs of cerebralfailure. Yet any true occupational psychiatry mustfind such problems to be its true subject: it is in thesefunctional cases that the significant difficulties maybest be shown.One case of Delpech's series illustrates this par-

ticularly well. The man was admitted in December1860 with right sided paralysis after a sudden attackthat had been followed by seven days unconscious-ness. Delpech originally assumed that he hadsuffered from a left side cerebral haemorrhage. InFebruary 1862 he was readmitted with extensiveerysipelas. In the course of this illness the paralysislessened and he regained function of his hand and hisfoot. He was discharged "satisfaisant." One couldhave supposed, Delpech said, that the violent inflam-mation of the erysipelas had led to a resolution of thehaemorrhage. Perhaps a more modern explanationwould concentrate on the circumstances of the cure,both the powerful effect on a labourer of the eminentphysician's personal attention and the consequencesof successful litigation against an employer.Even in Delpech the elements of the patient's

symptoms seem to be an amalgam of the physical andthe psychological. In the 50 years since Bonhoeffer'spaper a crude organic model has persuadedoccupational psychiatrists that disorders of psy-chological functioning are identical with those ofbrain functioning and only recently has its failure as amodel been recognised as such.

Annales d'Hygiene Publique 1863;19:65-183.2 Zeldin T. France 1848-1945: ambition and love. Oxford: Oxford

University Press, 1979.3 Tournier SL. Auguste Louis Dominique Delpech. In: Dictiona-

ire de biographie Francais. Tom X. Paris: Libraire Letouzay etAne, 1965.

4 Pickles SS. The production and utilization of rubber. In: SingerC, Holmyard EJ, Hlal AR, Williams TL, eds. A history oftechnology. Vol 5. London: Oxford University Press, 1958.

5 Hunter D. The diseases ofoccupation. London: Churchill Living-stone, 1979.

6 Delpech ALD. Une note sur les accidents qui developpe chez lesouvriers en caout-chouc, l'inhalation de sulfure de carbone.Gazette Hebdomadaire de Medecine et Chirurgie 1856;3:40-2.

7 Delpech ALD. Accidens que developent chez les ouvriers encaoutchouc l'inhalation du sulfure de carbone en vapeur.L'Union Medicale 1856;1O:265-7.

8 Delpech ALD. Accidents produit par l'intoxication de sulfure decarbone en vapeur experience sur les animaux. GazetteHebdomadaire de Medecine et Chirurgie 1856;3:384-6.

9 Berrios GE. Delirium and confusion in the 19th century. Br JPsychiatry 1981;139:439-49.

10 Braceland FJ. Mental symptoms following carbon disulfideabsorption and intoxication. Ann Intern Med 1942;16:246-61.

1 1 Charcot JM. Intoxication par le sulfure de carbone. In: Les leconsdu mardi a la salpetriere 1887-1888. Paris: Delabage etLacarnier, 1887:43-53.

12 Marie P. Sulfure de carbone et hysterie. Societe Medicale desHopitaux 1888;6:445-54.

13 Jump HD, Cruice JM. Chronic poisoning from carbon disul-phide. University of Pennyslvania Medical Bulletin 1905;17:193-6.

14 Lopez-Pinero J. The concept of neurosis. Cambridge: CambridgeUniversity Press, 1986.

15 Ellenberger H. The discovery of the unconscious. New York: BasicBooks, 1970.

16 Drinka GF. The birth of neurosis. New York: Simon andSchuster, 1984.

17 Jones E. The life and work of Sigmund Freud. Vol 1. The youngFreud. London: Hogarth Press, 1972.

18 Freud S. The mechanism of hysterical phenomena. In: Thestandard edition of the complete psychological works of SigmundFreud. Vol II. Early psychoanalytic publications. London:Hogarth Press, 1975.

19 Critchley EMR, Cantor HE. Charcot's hysteria renaissant.BrMed J 1984;289:1785-8.

20 Frost A, Gunn, Nettleship. Report on poisoning by bisulphide ofcarbon and sulphur chloride. Lancet 1985;i:1 13.

21 Bonhoeffer K. Ueber die Neurologischen und PsychischenFolgerscheinungen der CS, Vergiftung. Monatschrift furPsychiatrie und Neurologie 1930;75:195-213.

I Delpech ALD. Industrie du caoutchouc souffle. Recherches surl'intoxication speciale que determine le sulfure de carbone. Accepted 28 June 1989

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