Document 2wp4o0NwKM9e7J6gKzX4Q85L

-v - r '>&.. i- *01 Eradication, o. 493, Geneva, smallpox eradiand global cerSME/78.21, Ge* i: Towards the 19 May 1980. World Health and et. 0 journal orwycitNE, A4^A5t^4lT-V'IJf:1?(*,B*otoclt AND I M MONO AcT^>r6C1dr'3.H3-=7 J'YSJe, r Jtn- JAM 2'11982 Livironmsntal Affairs ry/ ^ '7/Z'ZU'<'- NEUROLOGICAL CHANGES IN VINYL CHLORIDEEXPOSED WORKERS ' V. STtBLOVA1. V. IAMBI1, O. CKUMCAL1, V. KEUtBOVl1, V. FaSKOVA1, [. VlTOVCOVA', L. 2 L A M Department of Neurology, Medical faculty ot Hygiene. Charles University, Prague J] Outpatient Clinic ot Occupational Health, District Centre ot National Health, MSlnDc, Czechoslovakia . Vinyl chloride (VC) toxicity tor the human organism is not still fully claar. 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 tnterphalangeal joints and zonal osteolysis. They are described in association with Raynaud's syndrome (12, 10, 1, 4, 5 and others). Lange with his colleagues (12) describes angiologically detect able constriction of digital arteries, stenosis or partial occlusion of phalangeal blood vessels. Described ere 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 ot peripheral vasomotor disorders. Neurological manifestations are described only sporadically. Spirtas and colleagues (16) emphasize particularly the narcotic action of VC etbigher peak exposure concentrations. This manifests itself by vertigo, nausea and hea dache pains. Mentioned are also hand parestheslae (prlnckllng, formication). Langauer-Lewowicka (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 ot headaches and sleep disorders, but also trigeminal neuralgia. Because of a lack of more detailed neurological studies among the VC-ex* posed persons, we conducted field Investigations among the occupationally ex posed workers in a plant where there was six years before put Into operation a workshop with a considerable VC bazard. ,, SL 041514 For Distribution by CMA SPECIAL PROGRAMS DIVISION Ref. No__L Date____ _ 233 jo &.-Vsi.Jm.-V ' *kS^rJ 'Si ::-p&ftpfi:l 38 -acSj 'r MATERIAL AND METHODS The group of examinees consisted at 233 workers [263 males and 30 females), age 18--SS years, mean age 32.8 years. Of these 76 % 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, tn which the ten tatively established maximum allowable concentration of 10 mg. m~] had been fre quently and sometimes highly exceeded, involved polymerization worker^, 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 neurologicaily, some of them repeatedly. A more detailed analysis of subjective complaints was performed on the basis of EOD and N5 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 neurovegetatlve 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 Complaint* Headache Sleep disorder* GIT disorder* Vertigo Psvchic disturb*tion Dvesthe*i* Palpitation* 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 Control* number O/O/ 9 19.6 2 4.4 1 2.2 1 12 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 lncldence_of headaches and 234 SL 041515 Table 2, Overview Complain*. Headache Sleep disorders C1T disorders Vertigo Psychic disturbatioi Dysesthesia Palpitation* Total number of ex: gastrointestinal ( was observed eh In persons with ches was double more than 4 ye_: psychic disturba; Table 3. Overview Complaint Headache Sleep disorders GIT disorder* Vertigo Psychic disturbatioi Dysesthesia Palpitation* Total number of ex: posed workers is showed a signlf cent of more set Graph 1 pre syndromes detec lesion of periphe : 8.7 %}. Diagnos or loss of tender ales). a;e ie time of ions with roups ac.1 the tenbeen freand some itegory of here they iniog and compresnvely low . A more 0 and N5 ation was 5 persons aadaches . The ins (palpii in con ed to VI o0/ 19,6 4q#,,4a4i 22 0.0n 0.0 00.0 s of exThe subuhas and Table 2. Overview of subjective complaints in workers occupationally exposed to vlnyl chloride, relation to the level of exposure Complaint* Headache Sleep disorder* GIT disorder* Vertigo Psvchic disturbation Dysesthesia Palpitation* Total number of examinee* Total number % 46 15.7 16 d.d 20 6.9 3 1.0 13 4.5 9 34 14 4.3 293 100.0 More exposed number 010/ ' 19 7 n 2 6 7 5 109 17.4 6.4 10.1 1.8 5.5 6.4 4.6 100.0 Leu exposed number 0/o/ 27 14.7 9 4.9 9 4.9 1 0.5 7 3.8 2 W 14 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 exposad to vinyl chloride, relation to the length of exposure Complaint* Headache Sleep disorder* GIT disorder* Vertigo Psychic disturbation Dvsesthetia. Palpitation! Total number of examinees Total number O0' 46 15.7 16 5.5 20 6.9 3 1.0 13 4.5 9 34 14 4.8 293 100.0 Exposure longer than 4 veax* 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 Exposure shorter than 4 yean number O/o' 22 11.0 8 4.2 11 5.7 0 0.0 5 2.6 i 0.5 10 54 192 100.0 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 (18.8 % : :8.7%). Diagnosed were Impairments of muscle tonus or trophiclty, reduction or loss of tendon and bone reflexes, abnormal sensitivity. Compared to controls. 235 *- SL 041516  ` '-tc.iilrr.v.-ert *- :? 1 g$<| -t'rfTV ^--n 53KJ s5^i /P-*-Sr =.~4f _yzc*i \< Table 4. Severity of objectively diagnosed changes in workers occupationally exposed to vinyl chloride in relation to the level of exposure Severity of change* Normal Light changes Manifest chances Total number of examinees Total number % 165 57.0 112 3E.0 16 5.0 293 100.0 More exposed number O' O 50 46.0 49 45.0 10 9.0 109 100.0 Leas exposed number 0to/ 115 0* 184 62.5 34.2 3.3 100.0 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. diagnosed in vc bined with the abnormities. Re 46.5 % of cases 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 -- extrapyramldal symptomatology. G -- disperse central symptomatology. Blank column -- group of controls, batched 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 i 22.8 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 In the control group; the EEG abnormities detected in the controls were always least severe. Abnormities 236 _< oM-517 Graph 2: Objectlvi of exposure. X-ax lower exposure le a higher degree ferencesa*tfe o only in of wards beta and : The eddltio; were used to i: Graph 3: Objective of exposure. X-e column -- expo1 than 4 i A exposed ixpoied 6--5 34.2 3.3 100.0 matology icrohyposesthesta, "iw , - , .'wna--y*-: :frJ9K'.J *fe**^v. v < ... .fry* >r,v diagnosed In VC-exposed workers were predominantly episodic, in S 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 ;artson to lesions, S7. D -- se central jp ol VC- level of . lesions: 11.3 /o). 5 % and rrelatlon rs o! ex %) and erebellar ! control rdings in the EEG lormitles Graph 2: Objectively diagnosed changes in VC-exposed workers in relation to the level ot exposure, X-axis abjectlveiy diagnosed changes: A-D see Graph 1. Blank column -- lower exposure levels, hatched column -- higher exposure levels. V-axls -- % ot the total number ot 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 /o of cases. The most frequent was extension of photic driving to wards beta and theta waves (in 43.4 % of cases). The additionally conducted N5 and EOD (6, 7, 8, 9) questionnaire surveys were used to improve analysis ot 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 than 4 years. Y-axis -- % of the total number of exposed subjects. 237 -t# radios '-i&z-g'T*. ***,'*'* ' asr^- 0%Si MSS? m -T 5=V. --. Vi anamnestic data. The questionnaire N5 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 Abnormal Total slight medium total Exposed number ] % US 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 63 0 0.0 5 6.2 81 100.0 a higher frequency of sleep disorders (36%) than originally revealed by ana mnestic data, highly frequent (5 % 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 hyperhidrosls 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 (II), but also by Schwartzovd (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, IS, 20). Here we also observed a high Incidence of dysesthesia alter 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: according to literature data 238 and to our ov naud's syndro: in terms of st lesions diagno ed by a dlrec companylng c The narcc changes in tht irreversible c! ves in EEG r firmed In a r nees as well solvents (19, 2 more serious cortical brain diffuse abnon ment with thi This leads us centrations, c structures. VC-Lnducs nanifest then of changed h authors on th vith owMmd: wi^Ro exposed work damage. Com; 1) Expos terature, also these neurolo of exposure. 2) Some tion of VC, sv locerebellar : 3) Amon, tion is, no do bination with motor change vlA5& ' m' V*- _v traits as syndroc-called estive o . chloride. Oo' 70.4 :3.4 6.3 0.0 6.2 100.0 i by anamnolence Irequem -.hermore, zk perso'.ctes that :y. In the from the changes mpiaints, uring the action of :erebellar irtas and (15) and previous , benzene incidence .zene. We :me cases peripheral rare data and to our own experience these changes are frequently associated with Ray naud's syndrome and may presumably, lead to even more severe consequencles 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 In 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 (46.5%) of cases In our group exami 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 /o 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. VC-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 RouskovA (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 r.-* r. * 'ft.'priifpx le-. m :vM" ZSfsr* 1 .. *** r^sr*- -<ri -A*' ''ti -' rVf - <4 '* ^L- m'-.' 'vtVI ** 3 A ,w* -i. r-T: *>.% .jee^^-av'v* -*'-?r'*5..i- >""'*-*r SKrsi . W'cvf V-'' 'wsa.-.Td v"-w* r \.\ . a -v7^.^, I t-*- .-`-r more severe lesions of peripheral blood vessels. Equally important are the ge neral neurovegetatlve manifestations [gastrointestinal and cardiovascular dis orders, hyperhidrosis, etc.) that might result from the central neurovegetatlve 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, 21^2) 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 nacrotic 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 00, and electromyographic examination. SUMMARY Neurological examinations were conducted in 233 workers occupationally exposed to vinyl chloride. Subjective complaints were evaluated on the background of N5 and EOD questionnare survey analysis, EEG examinations, including pbotostimulatioa. 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 wes 6 years. Among the most frequent subjective complaints were headache, neurovegetatlve disorders and dvsesthesiae, among objective findings dominated cerebellar and/or vestibulocerebellar syndrome, lesions of peripheral neurons and peripheral neurovegetattve 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, sometlnmes 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 vigility 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 of N5 and EOD questionnaire surveys is highly.advisable. s 240 < 0 styblov vl, v, Vito chlornre de vi 11 a 6t4 posis au chic a l'atde des a: flcatlf prodult l'exposition $u Les troub gStatlfs et dy tame vestlbul pdriphlrique xique direct ; ayant lieu lor Des donm sujets ddmorn (chex 15,5%] atteinte des : Les sujets jour, aux exa: dans ce cas, sues de l'EEC v 4, V.. V11 rid txponiertE Man beot Vtnylchlorid mlt Hllfe der Einwlrkung Exposition ab Die bfiuf: tome und Dy xerebellarsyst ren vegetatlv wohl als dire bei perlphere In dem EE test, die die Aktivltat (be durcb Aifekt gen erkiaren Die Vioy gischen Star ---'IV Xw T.-i-- * ut are the geovascular dis:urovegetative lesions caus* nanisms. 1 the assumed 2S). It occurs 22] and may :a! structures n be ascribed jns accompa;tent changes accentuated alters at risk essary to enrkers. 01 the both lor pre* ostimulation. naiiy exposed ad of N3 and filiation, were jects. Average ;urcvegetative Bsliar and/or at neurovegeto depend on nantly episo>osed showed episodic ZtC o changes in pact on the system and teral symptonsequence of :e systematic on the as- tory. Supple- RESUME S t f b 1 o v 4, V., Limbi, V., Cbuschtl, 0-, K e 11 e r o v 4. V,, p a S k o v 4, V,, V11 o v c o v 4, J,, 2 1 a b, L: L'lmage nenrologtqae chez lee mjets exposes an chlornre de vinyle 11 a 6tfe etudli d'une manure complexe 1'lmagB neurologique chez 293 sujets ex poses au Chlorure de vinyle. Des troubles eubjectlfs ont 4t4 analyses au plan detailie 4 l'aide des anquetes EOD et N5. II a 4t4 mis en evidence un effet neuratoxique signi ficant produtt par chlorure de vinvle qui depend de la qualite et de la quantlte de 1'exposltion suble. Les troubles subjectlfs rencontres le plus souvanr: maux de teta^ymptdmes v4gitatlfs et dysesthesia. Les donsees objectives temoignent pour une affection du svsteme vestlbuloc4rebelleux et pour celle du neurone peripbertque et de I'lnnervatlon p4riphrlque vegetative. La symptamatologie perlphirique peut rfesulter de l'etfet toxique direct produit par chlorure de vinyle aussi bien que du mecanlsrae d'hypoxie ayant lieu lors des cbangements vasomoteurs periphertques. Des donnes issues de l'EEG temoignant une activite de sommeil chez 46,5 % de sujets ddmomrent un effet narcotique du chlorure de vinyle. L'activite episodique (chez 15,5%) assoctde partois 4 1'enomalie de diffusion pourrait s'expllquer par une atteinte des structures mediobasales, mSme tide aux changements du cortex. Les sujets exposes 4 l'influence du chlorure de vinyle ne se soumettent. jusqu'4 ce Jour, aux examens systematlques au plan neurologique. II est ndcessaire de poursulvre, dans ce cas. une prophylaxie neurologique etudiant l'image ciinique, les donndes is sues de l'EEG ou mfime de l'EMG. II est utile d'employer les anqugtes EOD et N5. ZUSAMMENFASSL'NG S t y b 1 o v 4, V., L a m b 1. V., C h u m c h a 1. 0., K e 11 e r o v 4, V,, P a i k o * v 4, V., V 11 o v c o v 4. V., 21 a b, L.: Neurologiscbes Bild bei den dem Vlnylehlorid exponierten Arbeltenden Man beobachtete kompiexerweise das neuroiogische Bild bei 293 Arbeltenden, die Vinylchlorld expomert waren. Subjektive Schwierigkelten enalysierte men eingehender mit Hllfe der EOD- und N 5-Fragebogen. Dabei hat man eine signlflkante neurotoxische Elnwirkung von Vinylchlorld nachgewtesen, die von der Intensitat und Dauer der Exposition abhanglg 1st. Die hBufigsten subjektiven Schwierlgkeiten waren Kopfschmerzen vegetative Symptome und Dysesthasie. Der objektive Befund zeugt von der Affektion des Vestibularzerebellarsystems. ferner von der Affektion des peripheren Neurons und der penpheren vegetativen Innervation. Die penphere Symptomatology kann man erkiaren sowohl ais dlrekte Elnwirkung von Vinylchlorld, als auch den hypoxiscben Mechanlsmus bei peripheren vssomotonschen Veranderungen. In dem EEG-Befund stelite man bei 46,5 % Tlele der Gesamtheit die Schlataktlvitat test, die die narkotische Elnwirkung von Vinylchlorld dokumentiert. Die epiaodische Aktivitat [bei 15,5%) manchmal in Verblndung mit Dlffusionsabnormitat kbnnte man durch Affektion von mediobasalen Strukturen, gegebenenfalf durch Kortexvertnderungen erkiaren. Die Vinylchlorld exponierten Arbeltenden werden bisher systematised vom neurologischen Siandpunkt nicht beobachtet. Die Verfasser halten die gezielte neuroiogische *5 241 s, XV,-*z'- jsiej*, s Visit -T**5^ at"* fm ^no, Vorbeugung in Verbindung mil Beobachtung des kllnlschen Blldes, des EEG- eventuell auch des EMG-Befundes IQr notwendig. Sehr geeignet is: die Anwendung der EOD- und N 5-Fragebogen. K., Me Michael, A. M.: Am. led. Hvg pp. 779-789. -- I 14k. VII, 1955, 5, Srfblo4, V.: Acta t RESUMEN 12, I960, pp. 269-- Cs. neurol. 26, 195 I S t f b 1 o v 4. V., L a m b 1, V., Chumchal, 0., K e 11 e r o v 4, V., P a 5 k o v a, V., V 11 o v c o v 4, V., 2 l a b, L.: El cuadro nenroldgieo en trabaiadnres ex- Received Move: pnestos at vinilclornro Se ba examinado globalmente el cuadro neurolbgico en 293 trabajadores expuestos al vinilcloruro. Las dificultades subjer.vos se las analizd detalladamente mediants los cuestionarios EOD y N 5. Se mostrb el resultado neurotdxico marcado del vinilcloruro, el que dependia de la altura y duracion de la exposicibn. Las dificultades subjetivas mis frecuentes eran los dolores de la cabeza, los sintomas vegetativos asl que la disestesia. El hallazgo objettvo muestra la afectacidn del sistema vestlbulocerebelar, ast que la de la neurona vegetative perlf6rice y de a inervacidn vegetative perifdrica, La sintomatologla perifSrica la puede expllcar tanto por el efecto t&xico directo del vinilcloruro, como por el mecanismo hipbxico con los cambios vasomotdricos perifericos. Se balld en ballazgos electroencefalogr4fieos una actlvidad del suefio en el 46,5 p. c. del conjunto. Ip que prueba el resultado narcbtico del vinilcloruro. La actlvidad epizPdico (en el 15,5 p. c.], a veces en la combinaciO:. con la anormidad dlfusa podrla i, se expllcar por a'ectaciOn de las estructuras mediobasales, eventualmente por cambios de la epidermis. Los trabajadores expuestos al vinilcloruro no son ailn examinados neuroldglca- mente de manera sistematlca. Hace falta que se hava reallzado neuroldgtca prevencibn encamir.ada lnciuso el cuadro cllmco, el hallazgc electroencefalogrAfico, eventualmente el electromiogrdfico. Se recomienda usar los cuestionarios EID y N 5. REFERENCES 1. Angulescu, F., Otolu, m., Dobrooesca, E.: Med. Int. 4, 1969, pp. 473--460. -- 2. Basalajev, A. V., Vazin, A. N., Kocetkov, A. G.; Gig. truda 2, 1972, pp. 24--27. -- 3. Byczkowska, Z., et al.: Pol. tyg. lekar. 29, 1974, 26, pp. 1461--1464. -- 4. Dlnman, B. 0., Warren, A., Whitehonse, W. M.: Arch. Environ. Hlth. 22, 1971, 1, pp. 61--73. -- 5. Dodson, V. N., Bertram, D,, Dinman, B. D., Whitehonse, W. M.: Arch. Environ. Hlth. 22, 1971, 1, pp. S3--91. -- 6. Engelsmann, F.: Cs. psycbol. 3, 1960, pp. 322-- 337. -- 7. Engelsmenn, F,, Drdkov4, S.: Cs. psychol. 4, 1964, pp. 340--348. -- S. Engelsmann, F., Drdkov4, S,: ACtlv. nerv. sup. 2, 1959, pp. 108--118. -- 9. Eysanck, H. J,, Eysenck, S. G. B.: Manual ol the Eysenck Personality Inventory. Unlv. of London Press, London 24. 1964. -- 10. Harris, D. K-. Adams, W. G. M.: Brit. Med. I- 16, 1967, pp. 712--714. -- 11. Langauer-Lewowicka, H., Kurzbauer, H., Byczkowska, Z., Wocka-Marek, T.: Activ. nerv. sup. 21, 1974, 4, pp. 290. -- 12. Lange, C. IL, Jnhe, S., Stein, G., Veltman, C.: Int. Arch. Arbeitsmed. 32, 1974, pp. 1-32. - 13. Roth, B.: Narkolepsie a hypersomnie z hladiska fysiologie $p4nku. Praha, SZdN, 1957. -- 14. Roukovi, V.: Inn ArcIT. Arbeltsmed. 34, 1975. pp. 283--2SS. -- 13. Schwartzovd. K.: Neurologlckd a EEG ndlezy u chronickych prOmyslovych otrav nSkterfmi orgenickymi rozpouStddly. Plzeftsky 16k. sb. Suppl. 25, 1970, pp. 5--88. -- 16. Spirtas. 242 A*' 6V * keventuell b00- und P aSkoidnres ei* s eipuesmediame vinilcioades subs ast qua ,'locerebe* tlva peri:o directo jricos pe ri el 46,5 actividad sa podrla camblos iroldgica,-evensidn ualmenie JL, Me Michael, A. L, Gamble, J., Van Ert, M.: Am. Ind. Hyg. Ass. J. 36. 1975, 10, pp. 779--789. -- 17. Stfblovi, V,: Prac. 16k. VII, 1955, 5, pp. 260-263. -- IS. Stable**, V.: Acta Unlv. Carol. Med. Suppl. 12, 1950, pp. 269--274. -- 19. Stfblovi, V.: Cs. neural. 26, 1963, p. 399. -- 20. Stable- vi, V.: Diagnoza a prevence v prtimyslove neurologlL Praha. SZdN, 1968. -- 21. Stfblov6, V.: lot Arch. Occup. Environ. Hitt. 38, 1977, pp. 263--282. -- 22. Stfblovi, V, Holanovd, V.: Prac. 16k. 25, 1973, pp. 90-- 98f Received November 10, 1980 V. Stfblova Dept. Neurology, Medical Faculty ol Hygiene, Charles University, 5rob4rova*50, 142 Praha 10, Czechoslovakia London larria, D. id. J. 16, ;aaer-Lezkowska, sup. 21, E., Juhe, vrch. Ar12. Roth, hlediska 1237. -- ;med. 34, .zord, K.: chraaicml orga16k. sh. Spirtat, SL TN. -3- i.--awm-tweM... 243 sissas r-isrszr* .Vr--^ . ;-V,V VW-~ 1 i",~~ i &sJc-' mtim