Document 068YXO6Db7Jej9EbByZ1BYrbR

ox Eradication. No. 493, Geneva, e smallpox eradl'1 end global cerit SME/78.21, Ge lt: Towards the . 19 May I960. , World Health rland JOURNAL Of HYGIENE, EPIDEMIOLOGY. MICROBIOLOGY AND IMMUNOLOGY ZS, 1991, No. 3. 233--243 _! J JAN 21 ',982 Cc // A'WJo t ft*. AID NEUROLOGICAL CHANGES IN VINYL CHLORIDEEXPOSED WORKERS V, STtBLOVA', V, LAMSL*, 0. CHUMCAf, V. KELLEROVA', v. paskova1. j. viiovcovA', l. Uai< M Department of Neurology, Medical Faculty of Hygiene, Charles University, Prague 2) Outpatient Clinic of Occupational Health, District Centre of National Health, MSlnlk, Czechoslovakia . Vinyl chloride (VCJ toxicity for the human organism is not still fully clear. The occupational exposure to VC is linked with the development of liver hemangiosarcomas, or with other malignant processes of varying locality. Some authors diagnose changes in terms of scleroderma, universally are described roentgenologically detected lesions of interphalangaal Joints and zonal osteoly sis. They are described in association with Raynaud's syndrome (12, ID, 1, 4, 5 and others). Lange with his colleagues (12) describes angiologlcally detect able constriction of digital arteries, stenosis or partial occlusion of phalangeal blood vessels. Described are also various types of dysesthesia in fingers, parti cularly cold and numbness sensations. Also Byczkowska (3) reports frequent occurrence 'of finger paresthesia, whitening of fingers, but also of palms and soles, and other symptoms of peripheral vasomotor disorders. Neurological manifestations are described only sporadically. Spirtas and colleagues (16) emphasize particularly the narcotic action of VC at higher peak exposure concentrations. This manifests itself by vertigo, nausea and hea dache pains. Mentioned are also hand paresthesiae (prlnckllng, formication). Langauer-Lewowtcka (11) analyzes also the clinical symptoms In her group of 200 examinees who showed most frequently signs of cerebellar symptomato logy. She 'recorded frequent occurrence of headaches and sleep disorders, but : also trigeminal neuralgia. i Because of a lack of more detailed neurological studies among the VC-ex- ; posed persons, we conducted field investigations among the occupationally ex* t posed workers In a plant where there was six years before put into operation a workshop with a considerable VC hazard. ,, *_ sviu. u IKil cteaassdI!s8ai For Distribution by CMA SPECIAL PROGRAMS DIVISION 233 Rsf. No. (Jh far-, Je. Ph a j-e -EZZj Data_. Zebr-uicir^ ^ CMA 101864 r ' u MATERIAL AND METHODS The group of examinees consisted of 293 workers (263 males and 30 females], age 18--58 years, mean age 32.8 years. Of these *6 % were below 40. The average time of exposure was 2.8 years (range from 2 months to 6 years}. After consultations with plant physician and plant toxicologist the group was divided Into two subgroups ac cording to the level of exposure. The subgroup of high-risk workers, in which the ten- i tatively established maximum allowable concentration of 10 mg.m-3 had been fre quently and sometimes highly exceeded, involved polymerization workqr^. and some maintenance workers (a total of 109 persons]. The subgroup of lower-risk category of workers included those engaged in drying and bagging operations, but even here they were sometimes exposed to high peak exposure concentrations during cleaning and sampling operations, and those from the other plant workshops -- combustion, compres sors, cracking, chlorination, regeneration -- where the exposure risk was relatively low (a total of 184 persons). All the workers were examined neurologically, some of them repeatedly. A more detailed analysis of subjective complaints was performed on the basis of EOD and No questionnaire surveys. Electroencephalographic examination with photostimulation was made in 232 persons (255 recordings). The group of controls consisted of 4S persons without exposure to toxic substances. RESULTS An overview of subjective complaints is presented in Table 1. Headaches occur frequently, but they are less frequent than in the control group. The in cidence of gastrointestinal disorders and other neurovegetative disorders (palpi tations, retrosternal pressure sensations) are significantly higher than in con trols. Psychic disturbances were observed only in those exposed. Table 1. Overview of subjective complaints in workers occupationally exposed to vi nyl chloride, in a comparison with controls Complaints Headache Sleep disorders GIT disorder* Vertigo Psvchic disturbation Dvsesthesia Palpitations Total number of VC -- exposed number 0/o/ 46 15.7 16 5.5 20 6.9 3 1.0 13 4.5 9 3.1 14 4.8 293 100.0 Controls number 0/O/ 9 19.6 2 4.4 1 2.2 1 2.2 0 0.0 1 2.2 0 0.0 46, 100.0 Significant differences were observed between the two subgroups of ex posed workers divided according to the level of exposure (Table 2). The sub group of more exposed workers showed a higher lncidence-of headaches and 234 Table 2. Overview Complaint Headache Sleep disorders GIT disorders Vertigo Psychic distorbatioi Dysesthesia Palpitations Total number of exi gastrointestinal < was observed el; In persons with ches was double more than 4 yei psychic disturba: Table 3. Overviet Complaint Headache Sleep disorders GIT disorders Vertigo Psychic disrurbat1 Dysesthesia Palpitations Total number of posed worker: showed a sigi cent of more set Graph 1 pre syndromes detec lesion of periphE : 8.7 %). Diagno: or loss of tendoi ales), age tge time of itioas with groups ac:h the ten- been Ireand some category of here they waning and i, compresatively low :y. A more 3D and N5 iation was 46 persons leadaches i. The inrs [palpin in con- ised to vi- 19.6 4.4 :.2 2.2 0.0 2.2 o!o 100.0 ?s of exThe subches and Table 2. Overview of subjective complaints in workers occupationally exposed to vi nyl chloride, relation to the level of exposure Complaints Headache Sleep disorder* CIT disorders Vertigo Psvchic disturbation Dysesthesia Palpitations Total number of examinees Total number O,0' 46 IS.7 16 5.5 20 6.9 3 1.0 13 4.5 9 3.1 14 4.8 293 100.0 More exposed number % ' 19 7 11 2 6 7 S 109 17.4 6.4 10.1 1.8 3.S 6.4 4.6 100.0 Less exposed number 0/O/ 27 14.7 9 4.9 9 4.9 1 O.S 7 3.8 2 1.1 9 4.9 184 100.0 gastrointestinal disorders, and furthermore, of dysesthesia of extremities. There was observed also a certain correlation with the length of exposure [Table 3), In persons with the exposure time longer than 4 years, the incidence of heada ches was double the incidence in the group with a shorter time of exposed for more than 4 years. Sleep disorders, gastrointestinal complaints, vertigo and psychic disturbances were also more frequent in those with a longer time of ex- Table 3. Overview of subjective complaints in workers occupationally exposed to vinyl chloride, relation to the length of exposure Complaints Headache Sleep disorders GIT disorders Vertigo Psychic disturbation Dvsefthesia Palpitations Total number of examinees To tal number O' 0 46 15.7 16 5.5 20 6.9 3 1.0 13 4.5 9 3.1 14 4.8 293 100.0 Exposure longer than 4 years number | % 24 23.8 8 7.9 9 8.9 3 3.0 8 7.9 8 7.9 4 4.0 101 100.0 Exposuze shorter than i years number O/o' 22 11.0 8 4.2 11 5.7 0 0.0 5 2.6 i O.S 10 5.2 192 100.0 posed workers is characterized in Table 4. The group of more exposed workers showed a significantly lower per cent of normal findings and a higher per cent of more severe findings than the group of less exposed workers. 'Graph 1 presents Incidence of the most frequent, objectively diagnosed syndromes detected In exposed and control groups. The most'frequent was the lesion of peripheral neurons, either motor or sensory, or both of them [16.8 % : :8.7%), Diagnosed were Impairments of muscle tonus or trophiclty, reduction or loss of tendon and bone reflexes, abnormal sensitivity. Compared to controls. Table 4. Severity of objectively diagnosed changes in workers occupationally exposed to vinyl chloride in relation to the level of exposure Severity of change* * To ud More exposed number 0/o number | % Less exposed number | % Normal Light change* Manifest change* Total number of examinee* 163 57.0 112 3S.0 16 5.0 293 100.0 50 46.0 49 45.0 10 9.0 109 100.0 115 62.5 34.2 6 3.3 184 100.0 the group of exposed workers showed also more frequently the symptomatology of peripheral neurovegetative disorders (12 % : 4.4 % ], specifically acrohypo* thermy, acrohyperhidrosis or whitening of fingers, associated with dysesthesia. 20-1 y V. 7] / / 10- / A / / / A 7] p / --/ /' BC < n_ (/h D E F G* Graph 1: Objectively diagnosed changes in VC-exposed workers in a comparison to controls. X-axis -- objectively diagnosed changes: A -- peripheral neuron lesions, B -- peripheral neurovegetative symptomatology, C -- cerebellar symptomatology, D -- vestibular symptomatology, F -- extrapyramidal symptomatology, G -- disperse central symptomatology. Blank column -- group of controls, hatched column -- group of VC- -exposed. Y-axis -- % of examinees Graph 2 shows objectively diagnosed symptoms In relation to the level of exposure. A marked difference is in the incidence of peripheral neuron lesions: more exposed workers are affected more than twice as often (25.6% : 11.8 %). Celebellar and vestibular syndrome Is also more frequent (10%: 7.6% and 6.4 % : 3.3 %, respectively). There are also certain Indications of a correlation with the length of exposure, see Graph 3: those with more than 4 years of ex posure have more frequently peripheral neuron lesions 122.8 %: 13.6 %) and cerebellar impairments (13.9 %: 5.7 %). Frequency of the vestibulocerebellar syndrome is also higher (5 % : 0.5 %) In these persons. The results of EEG examinations of exposed and 81 non-exposed control workers are compared in Table 5. The per cent of abnormal EEG recordings In the group of exposed workers is higher than lq the conical group; the EEG abnormities detected in the controls were always least severe. Abnormities 236 < diagnosed In VC-e bined with the dl abnormities. Rela 46.5 % Of cases). Graph 2: Objective! of exposure. X-axis lower exposure lev a higher degree ferences were ot only in 40 % of wards beta and tl The addition, were used to in Graph 3: Objective of exposure. X-e> column -- expos: than 4 y CMA101867 * y exposed exposed 62.5 34.2 3.3 100.0 omatology acrohypoysesthesia. diagnosed in VC-exposed workers were predominantly episodic, In 5 cases com bined with the diffuse abnormity. Three EEG recordings revealed only diffuse abnormities. Relatively frequent was also the presence of sleep waves [in 46.5 % of cases). In 16 % of workers the sleep activity manifestations were of ^parlson to kn lesions, 5logy, D -- ;rse central oup of VC- ie level of ;n lesions: > : 11.8 %]. 7.6 /o and correlation ;ars of ex.6 %) and cerebellar id control ordlngs in the EEG bnormlties Graph 2: Objectively diagnosed changes In VC-exposed workers in relation to the level of exposure. X-axis abjecdvely diagnosed changes: A*D see Greph 1. Blank column -- lower exposure levels, hatched column -- higher exposure levels. Y-axis -- % of the total number of exposed subjects. a higher degree of severity [2c to 3, according to Roth (13)). Significant dif ferences were observed also in the photostimulation reaction that was normal only In 40 Vo of cases. The most frequent was extension of photic driving to wards beta and theta waves [in 43.4 ao of cases). The additionally conducted N5 and EOD (6, 7, 8, 9) questionnaire surveys were used to improve analysis of subjective complaints and to complement Graph 3: Objectively diagnosed changes in VC*exposed workers In relation to the length of exposure. X-axis -- objectively diagnosed changes: A-D see Graph 1. Blank column -- exposure shorter than 4 years, hatched column -- exposure longer then 4 years, Y-axis -- /o of the total number of exposed subjects. <= 237 '*i*>*&*W-:.J*e . i* *&*?'"- tj>'> t*rL ' - ^ tr CMA 101868 anamnestic data. The questionnaire NT5 examines superficial personal traits as well as certain clinical symptomatology, particularly neurovegetative syndro me, neurasthenic, depressive and anxiety-phobic symptoms, and the so-called toxic syndrome. Data provided by this type of questionnaire were suggestive of Table 5. Severity of EEG changes in workers occupationally exposed to vinyl chloride. in a comparison to controls EEG changes Normal Suspect , slight Abnormal medium total Total Exposed number J % 148 63.8 48 20.7 30 12.9 6 2.6 36 15.3 232 100.0 Controls number i % 57 70,4 19 23.4 5 6.2 0 0.0 5 6.2 81 100.0 a higher frequency of sleep disorders (36 ^o] than originally revealed hy ana mnestic data, highly frequent [5 /o level of significance] was also somnolence (76%), which had not been also indicated in personal histories. More frequent were also feelings of bad performance, fear of loosing life or health. Furthermore, the frequency of hyperhidrosis was also very high (73 %). The Eyseneck perso nality questionnaire examines neuroticism. It reveals subjective tendencies that are evaluated by the examinee and confronted with the objective reality. In the examined group there were not detected any significant deviations from the norm; increased neuroticism could not be demonstrated. DISCUSSION Clinical examination of VC-exposed workers revealed significant changes predominantly in neurologic symptomatology. Some of the subjective complaints, such as headaches, vertigo, sleep disorders or increased sleepiness during the day, as revealed by questionnaire N5, are suggestive of the narcotic action of VC, similarly as the occurrence of the cerebellar and/or vestibulocerebellar symptomatology. These changes have been, already described by Spirtas and colleagues (16), Langauer-lewowicka (11), but also by SchwartzovA (15) and others. This characteristic symptomatology was also described in our previous studies concerned with the occupational exposure to trichloroethylene, benzene and other organic solvents (17, 18, 20). Here we also observed a high Incidence of dysesthesia after exposures to some solvents, particularly to benzene. We ascribed it either to peripheral vasomotor changes, or -- at least In some cases -- to initial phases of polyneuropathy. In case of VC the presence of peripheral vasomotor changes Is evidently very significant: accordln^to literature data 238 and to our own i naud's syndrome in terms of steno lesions diagnosed ed by a direct n companying mort The narcotic changes in the bi irreversible chan ves in EEG reco firmed in a relai nees as well as solvents (19, 21, more serious ancortical brain st diffuse abnormal ment with the. c This leads us to centrations, can structures. VC-induced manifest themse of changed hyp authors on the with our finding We also be', exposed worker, damage. Compai in persons expo: 1) Expo: terature, alsc these neural of exposure. 2) Some tion of VC, s locerebellar syi 3) Among tion Is, no dout bination with t motor changes | traits as R syndro- sc-oailed gestive of 1 chloride. o 70.4 23.4 6.2 0.0 6.2 100.0 d by anaimnolence 2 frequent thermore, Jck personcies that tty. In the _ from the t changes omplatnts, during the action of jcerebellar pirtas and . (15) and x previous e, ber.2ene : incidence nzene. We ;ome cases peripheral arure data and to our own experience these changes are frequently associated with Ray naud's syndrome and may presumably lead to even more severe consequencies in terms of stenosis or occlusion, as described by Lange (12). Peripheral nerve lesions diagnosed in our group of VC-exposed examinees oould be then explain ed by a direct neurotoxic action of VC, or as a consequence of hypoxia ac companying more severe vasomotor changes i#n the periphery. The narcotic action of VC can be either transitory. Inducing only reversible changes in the brain function, or persistent, causing more permanent, sometime Irreversible changes in the CNS. Slight functional changes manifest themsel ves in EEG recordings by waves typical for various stages of sleep, as con firmed in a relatively high per cent (45.5%) of cases in our groupexami nees as well as In some of the examined subjects exposed to other organic solvents (19, 21, 22). Detection of episodic or diffuse EEG abnormalities is rather more serious and may be indicative of chronic changes in mediobasal and/or cortical brain structures. In our group of examinees, the joint episodic and diffuse abnormality occurred in 15.6 % of workers. This frequency is in agree ment with the cited literature data as well as with our previous experience. This leads us to a conclusion that even VC, particularly at higher exposure con centrations, can produce neurotic changes in the above described brain structures. V'C-induced pathophysiological changes are believed by some authors to manifest themselves by the central neurovegetative dysregulation, as a result of changed hypothalamus functions (2). This localization, presumed by these authors on the basis of their experimental studies, seems to be in agreement with our findings of EEG episodic abnormalities. We also believe that even FS reaction changes, recorded in our group of exposed workers, may be of importance In the early diagnosis of VC-induced damage. Comparable FS reaction changes were also described by Rouskovd (14) in persons exposed to other toxic agents. CONCLUSIONS 1) Exposure to VC may lead, besides to other changes described In the li terature, also to lesions of the nervous system. The onset and development of these neurologic changes depend on the VC exposure level and on the length of exposure. 2) Some of the neurologic manifestations are caused by the narcotic ac tion of VC, such as certain subjective complaints and cerebellar and/or vestibu locerebellar syndrome. These symptoms can be transitory or persistent. 3) Among the Important manifestations that are characteristic for VC ac tion is, no doubt, the peripheral vasomotor symptomatology, sometimes in com bination with the Raynaud's syndrome described in the literature. These vaso motor changes in the periphery may further develop, leading consequently to 239 s &ir*4r ^ .-*."7 .- ? -~ ', ,-j * 4 -*L * -,\ .1 itiM -,-%'.v:X^.Sri'%'-V. ^V A`3.r-Jr".#<".-t;^SCt>.'`'''<^-i5*"t ' -*'"^-"Tv-*-.--v--*.*,>* ; .-v-.,.-_.r^> -"r*i-Wef<rv?-'W'^''.-r.?'.vijf, '->5,---v * iU-vT -", V^^Jt more severe lesions of peripheral blood vessels. Equally important are the ge neral neurovegetative manifestations (gastrointestinal and cardiovascular dis orders, hyperhldrosls, etc.) that might result from the central neurovegetative dysregulatlon. Important are also symptoms of peripheral neuron lesions caus ed by a direct neurotoxic action of VC or by hypoxia-related mechanisms. 4) Episodic abnormality in EEG recordings seems to agree with the assumed involvement of hypothalamic structures (Basalajev and colleagues). It occurs even at exposure to the other types of organic solvents [15, 19, 21^22) and may be Indicative of a more diffuse affliction of mediobasal and cortical structures of the brain. Less severe manifestations of EEG sleep activity can be ascribed to the nacrotlc action of VC, more pronounced sleep manifestations accompa nied with abnormal EEG changes may be suggestive of more persistent changes in the CNS. 5) Neurological changes have not been so far sufficiently accentuated in the professional literature and, therefore, the monitoring of workers at risk is not conducted systematically and by suitable methods. It Is necessary to en sure a neurological prevention In these occupationally exposed workers. Of the supplementary methods of examination there are recommendable, both for pre vention and research purposes, to use EEG examination with photostimulation, questionnaires N5 and EOD, and electromyographic examination. SUMMARY Neurological examinations were conducted m 293 workers occupationally exposed to vinyl chloride. Subjecnve complaints were evaluated on the background of N5 and EOD questionnare survey analysis. EEG examinations, including photostimulation. were performed in 232 persons. The control group comprised 46 nonexposed subjects. Average time of exposure was 2.8 years, the longest time of exposure was 6 years. Among the most frequent subjective complaints were headache, neurovegetative disorders and dysesthesiae, among objective findings dominated cerebellar and/or vestibulocerebellar syndrome, lesions ot peripheral neurons and peripheral neurovege tative symptomatology. Subjective and objective symptoms were found to depend on the exposure level and the time of exposure. EEG examinations confirmed in 15.5 % of cases abnormities, predominantly episo dic, sometinmes, combined with the diffuse abnormality. 46.5 % of the exposed showed presence of sleep activity as a consequence of VC narcotic action. The episodic EEG activity could be ascribed to lesions of mediobasal structures, or even to changes in brain cortex. Our data have confirmed that vinyl clorlde has a considerable impact on the human nervous system. Most frequent are lesions of vestibulocerebellar system and viglUty disorders due to VC narcotic action. Frequent occurrence of peripheral sympto matology can be explained by a direct neurotoxic action of VC, or as a consequence of hypoxia caused by peripheral vasomotor changes. As a rule, regular check-ups of VC-exposed workers do not include systematic neurological examinations. The systematic neurologic prevention, based on the as sessment of clinical, EEG and/or EMG examinations, should become obligatory. Supple mentary use ot N5 and EOD questionnaire surveys^ is highly .<asdvisable. 240 s t y blov< v4, V., Vltov chlarnxe de vin; II a 6t4 6ti posds au chlcrt 4 l'alde des ant ficatif produit l'exposltion sub Les trouble gfetatlfs et dysi time vestlbuloi pdriphfirlque vxique direct pi ayant lieu lors Des donn: sujets dfimontr (cher 15,5 % ] atteinte des s- Les sujets jour, aux exair dans ce css, > sues de l'EEG Styb1ov vi, V., VI t rid exponiert* Man beob Vinylchlorid e mit Hilfe der Elnwirkung v Exposition Die he tome und zerebellars ren vegeta wohl als d bei perlph. In dem test, die die Aktivitftt [be durch Affekt gen erklSren. Die Vlny glschen Stan s-v.;-7P -."i" ji,, "viu CMA 101871 Jit are the geSovascular dlsleurovegetative n lesions causchanisms. tb the assumed ues). It occurs I, 22) and may 'leal structures an be ascribed ions accompadstent changes y accentuated /orkers at risk icessary to enmrkers. Of the , both for preotostimulation. ionally exposed iund of N5 and imulation, were ects. Average neurovegetatlve reDellar and/or ;ral neurovege- to depand on minantly episoxposed showed i episodic EEG to changes in mpaet on the ar system and pheral symptoconsequence of -ide systematic :d on the as;atory. Supple- rni.. t " i niH RESUMS S t f b 1 o v A, V., L a m b 1, V.,' Chumchal, 0., Kellerovi, v,, P a 5 k o v A, V., V It o v c o v A, J., 2 ! a b, L.: L'imaga neurologique chex lea sujets exposAs an chlornra da vlnyle 11 a AtA AtudIA d'une manlAre complexe l'image neurologique chex 293 sujets ex posAs au chlorure de vlnyle. Des troubles cubjectifs ont Ate ar.alysAs au plan dAtaiUA A l'alde des anquAtes SOD et NS. 11 a AtA mis en Avidence un effet neurotoxique significatif prodult par chlorure de vlnyle qul depend de la quanta et de la quantitA de 1'exposltion suble, Les troubles subjectlfs rencontrAs la plus souvant: maux de tate^ymptOmes vAgStatlfs et dysesthAsle. Les donnAes objectives tAmolgnent pour une affection du systAme vestlbulocarabelleux et pour celle du neurone parlpharique et de l'innervatlon pArlpharique vAgAtative. La symptOmatologie pArlphArique peut rAsulter de 1'effet toxique direct prodult par chlorure de vlnyle aussi bien que du macanlsme d'hypoxie ayant lieu lors des ebangements vasomoteurs pAripbArtques. Des donnAs issues de l'EEG tAmoignant une activitA de sommeil chex 46,5 % de sujets dAmontrent un effet narcotique du chlorure de vinyte. L'actlvitA Aptsodlque (Chez 15,5%) associae parfois A 1'anomalie de diffusion pourrait s'expliquer par une attelnte des structures mAdiobasales, mAme liAe aux changements du cortex. Les sujets exposas A l'influence du chlorure de vinvle ne se soumettent, jusqu'A ce jour, aux examens systamatlques au plan neurologique. tl est nAcessaire de poursuivre, dans ce cas, une prophylaxie neurologique Atudiant l'image ciimque, les donnAes is sues de l'EEG ou mfime de I'EMG. II est utile d'employer les anquAtes EOD et N5. Z US A M M EN FAS S UN G S t y b 1 o v a, V., L a m b 1. V.. Chumchal. 0., K e 11 e r o v A, V.. F a 5 k o va, V., VI to vc ova, V., 2 1 a b, L.: Neurologisches Bild be! den dem Vinylchlorid exponierten Arbeltendan Man beobachtete kompiexerweise das neurologische Bfid bel 293 Arbeaenden, die Vlnylchlorid exponiert waren, Subjektive Schwierigkelten analyslerte man eingehender mit Hllfe der EOD- und N 5-Fragebogen. Dabei bat men eine signlfikante neurotoxische Elnwlrkung von Vlnylchlorid nachgewiesen, die von der Intensitat und Dauer der Exposition abhanglg 1st. Die hAufigsten subjektlven Schwlerlgkeiten waren Kopfschmerzen vegetative Symptome und DysesthAsle. Der objekttve Befund zeugt von der Affektlon des Vesttbularzerebellarsysteras, ferner von der Affektlon des perlpheren Neurons und der penpheren vegetatlven Innervation. Die periphere Symptomatologle kann man erkliren sowohl els dlrekte Elnwlrkung von Vlnylchlorid, als auch den hypoxischen Mechanlsmus bel perlpheren vasomotorischen VerAnderungen. In dem EEG-Befund stellte man bel 46,5 % Tiele der Gasamtheit die ScblafaktlvitAt fest, die die narkotische Einwtrkung von Vlnylchlorid dokumentlert. Die episodische AktlvltAt (bel 15,5%} manchtna! in Verblndung mit Dlffustonsabnormitat kbnnte man durch Affektlon von mediobasalen Strukturen, gegebenenfals" durch Kortexverfinderungen erklAren. Die Vlnylchlorid exponierten Arbeltenden werden blsher systematisch vom neurologiseben Standpunkt nlcht beobaebtet. Die Verlasser balten die gezielte neurologische e&i >t*% --rXj-*lA/e'.-'-' WJr+f.-t -c 'A,- IT, . 6' 1 SV 1^1-- ii-'AUkil.J. Vorbeugung in Verbmdung mit Beobachtung des klinischen Bildes, des EEG- eventuell auch des EMG-Befundes Iflr notwendig. Sehr geeignet ist die Anwendung der EQD- und N 5-Fragebogan. RESUMEN S t y b 1 a v A, V., L a m b 1, V,, Churachal, 0., K e 11 e r o v a. V., P a 5 k o v 4, V., V 11 o v c o v 4, V., 2 I a t>, L.: El cuadro nenrolflgico en traba(adores expuestos at vinilcloruro R., Me Michael, A. L., M.: Am. Ind. Hyg. , pp. 779-789. - 17. 14k. VII, 1955, 5, f Stfblovl, V.: Acta Uni 12, I960, pp. 269--274 Cs. neuroi. 26, 1S63, j Received Kovemb> Se ha exammado globalmente el cuadro neuroldgico en 293 trabajadores expuestos al vinilcloruro. Las diticultades subjettvos se ias aDalizd detalladamente mediante los cuestionarios SOD y N 5. Se mostrd el resultado neurotbxico marcado del vinilclo }: ruro, el que dependla de la altura y duracidn de la exposicidn. Las dlficultades sub- jetivas m4s frecuentes eran los dolores de la cabeza, los sintomas vegetativos ast que la disestesia. El hallazgo objetivo muestra la afectacidn del sistema vestibulocerebelar, asl que la de la neurona vegetative perifgrica y de a inervacidn vegetativa perlf4rica. La sintomatologla perifSrica la puede explicar tanto por el efecto tdxico directo i 5el vinilcloruro, como por el mecamsmo hipOxico con los cambios vasomotOricos pe- i nfdncos. Se balld en hallazgos electroencefalogr4icos una actividad del suefio en el 46,5 p. c. del conjunto, io que prueDa el resultado narcOtico del vinilcloruro. La actividad epizbdica (en el 15,5 p. c.), a veces en la combmacid:. con la anormidad dtfusa podrla n se explicar por afectacidn de las estructuras mediobasales, eventualtnente por cambios 1 i! de la epidermis. Los trabajadores expuestos al vinilcloruro no son aiin examinados neuroldglca- mente de manera sistem4t;ca. Hace falta que se haya realizado neuroldgica prevenciOn encammada incluso el cuadro cllmco, el hallazgo eiectroencefalogr4fico, eventualmenie el electromiogr4fico. Se recomienda usar los cuestionarios EID y N 5. ) i REFERENCES 1. Angulescu, F., Otoin, m., Dobronescn, E.: Med. Int. 4, 1969, pp. 473--480. -- 2. Basalajev, A. V., Vazin, A. 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Hlth. 38, 1977, pp. 263-- 282. -- 22. Stfblovi, V., Holanovi, V.: Prac. 16k. 25, 1973, pp. 90-- 9SP P.ecelved November 10, 1980 V. Styblovd, Dept. Neurology, Medical Faculty of Hygiene. Charles University, Srobdrova^SO, 100 42 Praha 10, Czechoslovakia rr-yirv-''** r-jffaSSSW v - .. \ 'vor ji ..V'bS.V' >f London Harris, D. led. J. 16. oganar-Leczkowska, v. sup. 21, . E., Juhe, Arch. Ar- 12. Roth, z hlediska , 1957. -- tsmed. 34, rtiovi, K.: i chronicymi o:ga- 16k. sb. i. Spirtai, .*.*`*^ ' "*7 - 243 *V :`:r t' Jt -- %i t- ' "v V"T CMA 101874