Document DM3EKxkaX1qpr56ZM9zdzyrEa

'c' ' poJ^^adicction. Jo. 433, Geneva, smallpox eradlaad global cer- SME/7S-21, Ge'i; Towards tbe 19 Mar 1930. World Health and . i.A **Vr P*'JO' JOURNAL or HYGIENE, B^D^.vTo j. 0 Sr| AND IMHUNOLTJ C'THfs^hMCJilCa, aa=TV 1 i0L00Y i -- j u9 w U .' '-wV. # JAN 2'i 1982 Environmental Affairs /;y/x o-'s/sr^ ~ *. t- r '? NEUROLOGICAL CHANGES IN VINYL CHLORIDEEXPOSED WORKERS V. STlBLOVA', V. IAMBI*, 0. CHUMCAt', V. SEUEKOVJl', V. PaSKOVA1. J, VlIOVCOV*', L. SLAB' l) Department ol Neurology, Medical Faculty of Hygiene, Charles University, Prague 3) Outpatient Clinic of Occupational Health, District Centre of National Health, MSlnlk, Czechoslovakia Vinyl chloride (VC) toxicity lor 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 interphalangeal joints and zonal osteoly sis. They are described In association with Raynaud's syndrome (12, 10, 1, 4, 5 and others). Lange with his colleagues [12] describes anglologically 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-Lewowlcka (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. 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 hazard. * For Distribution by CMA SPECIAL PROGRAMS DIVISION 233 Ref. No.. Date___ sagsas _L SL 027356 41. in <!-a & y-Z^.-^s^LCs - MATERIAL AND METHODS The group of examinees consisted of 293 workers (263 males and 30 females], age 18--58 years, mean age 32.6 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, in which the ten- t tatively established maximum allowable concentration of 10 mg. m~3 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 cleenmg and sampling operations, end 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 mote detailed analysis of subjective complaints was performed on the basis of EOD and N5 questionnaire surveys. Electroencephalographic examination with photostimulatlon was made in 232 persons (255 recordings). The group of controls consisted of 46 persons without exposure to toxic substances. A- 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 o comparison with controls Complaints Headache Sleep disorders GIT disorders Vertigo Psvchic disturbadon Dviesthesia Palpitations Total number of examinees VC -- exposed number /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 2JZ 1 0 0.0 1 2J 0 .0.0 44 _ 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 lncidenc^-of headaches and Table 2. Overvie Complai Headache Sleep disorder! CIT disorder* Vertigo Psychic disturber: Dysesthesia Palpitations Total number of e gastrointestinal was observed e In persons wit! ches was doub' more than 4 y psychic disturb Table 3. Overvi Complai Headache Sleep disorders GIT disorders Vertigo Psychic disturbs Dysesthesia Palpitations Total number of c posed workers showed a sign cent of more s Graph 1 p syndromes det lesion of perip : 8.7 %]. Diagn or loss of tend 234 ales}, age ;e time of :ioos with :roups acn the tenbeen freand some itegorv of here they ining and . comprestively low f. A more D and N5 ation was 5 persons sadaches . The in 's (palpli in con- -,ed to vi- s of exThe sub* :hss 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* GIT disorder* Vertigo Psvehic disturbation Dysesthesia Palpitations Total number of examinees Total number % 46 13.7 16 20 6.9 3 1.0 13 4.5 9 3.1 14 4.8 293 100.0 More exposed number 0<7o ' 19 7 11 2 6 7 S 109 17.4 6.4 10.1 1.8 5.5 6.4 4.6 100.0 Less exposed Uttiobcf 0/ tO 27 14.7 9 4.9 9 4.9 1 0.5 7 3.8 ft 1.1 9 4.9 184 100.0 gastrointestinal disorders, and furthermore, of dysesthesia of extremities. There was observed else 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 disorder* GIT disorder* Vertigo Psychic disturb*tion Dysesthesia Palpitation* Total number of examinees Total number O70' 46 15.7 16 53 20 6.9 3 1.0 13 4.5 9 3.1 14 4.8 293 100.0 Exposure longer ibAa 4 number yeaon/O/ 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 number 4 yeaO/rO'* 22 11.0 8 4.2 11 5,7 0 0.0 5 2.6 1 0.5 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 trophicity, reduction or loss of tendon and bone reflexes, abnormal sensitivity. Compared to controls, ' 235 SL 027358 3^ m pet j mu m m, & K-A SAS 'a**--' HI :/?,<?ji #4 TrTi-i ; : . >* T7V Table 4. Severity of objectively diagnosed changes Is workers occupationally exposed to vinyl chloride is relation to the level of exposure Seventy of change* Rormil Light change* Manifest chances Total number of examinees Total Dumber 0.0/ 165 57.0 112 38.0 16 5.0 293 100.0 More exposed number % so 46.0 49 45.0 10 9.0 109 100.0 Less exposed number 0to/ IIS 63, 6* 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 acrohypotherray, acrohyperhidrosis or whitening of fingers, associated with dysesthesia. diagnosed in VC-t bined with the d abnormities. ReL 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, hatched column -- group of VC- -exposed, y-axls -- % 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 % :11.6 %). 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 yeart of ex posure have more frequently peripheral neuron lesions ( 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 central group; the EEG abnormities detected in the controls were always least severe. Abnormities 236 < SL 027359 Graph 2: Objective of exposure. X-axi lower exposure lr a higher ^^ree lerences o: only in 4^% of wards beta and * The additior were used to ir Graph 3: Objectlvt of exposure. X-e column -- expo: than 4 y ed exposed II /o 62.5 54.2 3.3 100.0 matology icrohyposesthesia. ...... r',7' -- ------ - t-'*--- -- s'*' 1^. - -'- diagnosed In VC-exposed workers were predominantly episodic, in 5 cases com bined with the dllluse 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 logy, D -- se central up of VC- level of : lesions: : 11.8 %). 5 % and Trelatlon rs ol es %) and erebellar I control 'dings In the ZEG lomities > L.-J . -il-L-., Graph 2: Objectively diagnosed changes In VC-exposed workers in relation to the level of exposure. X-axis objectively diagnosed changes: A-D see Graph 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 % 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 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 than 4 years. Y-axis -- % of the total number of exposed subjects. 237 SL 027360 A rrAr-i. `555?' '.`v ** * - ~'fi0Zp 1 i?S*3> r* v-c:--^ *- EsjewEsfog tjC; -yy-r wtesms. A'- 3" i* .-VAkuiri. s ^'^h'w^*4F dCV-- Z*''* v+ Sftfc: vjffc `if SES* *?a ;^:V'r. .. 5< ,-*: 1 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 ol questionnaire were suggestive oi 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 Exp<>sed number O'O' 148 63.8 48 20.7 30 12.9 6 2.6 36 15.5 232 100.0 Controls number | % 37 70.4 19 23.4 5 6.2 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 hyperhidrosis was also very high (73 %). The Eyseneck perso nality questionnaire examines neurotictsm. 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 NS, 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 (16J, 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 bernene. 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 ro literature data 238 Aand to d^pbwr. naud's syndrom in terms of ste: lesions diagnos; ed by a direct companying me The narcot changes in the irreversible che ves In EEG re> firmed in a rei nees as well t solvents (19, 21 more serious a conical brain diffuse abnonn ment with the This leads us t cenxrations, a structures. VC*induce manifest them of changed hj authors on tin with ou^Adir We^rao t exposed worki damage. Comp in persons exp 1) Expose teratuxe, also these neurolo of exposure. 2) Some tion of VC, sr locerebellar s 3) Amon, tion is, no do bination with motor chang< SL 027361 ;estive of chloride. o-o 70.4 23.4 6 J2 0.0 6.2 100.0 i by anamnolence Irequent thermore, :k persoicies that :y. In the fr(|^^he :nanges t.: .aints, irj. the ction of rebellar . tas and .5] end revious nenzene incidence :zene. We :~e cases peripheral mre 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 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 "elf 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 % 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 Rouskovd (14) in persons exposed to other toxic agents. CONCLUSIONS 1) Exposure to VC may lead, besides to other changes described in tbe li terature, also to lesions of tbe 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 ( - --* -- -*I*/***,*. r^r`r ^ -.'KSESSSfe * !* sagses''JlMlJs ? -T - ^V*.' -JvtS- y* u- -* y: * j ! ' '.J.-* '-7- ^ ' : ' > ./--. , *-.. = -VX .:. ^v. -Tr- ~_-v V3t- -!-\* more severe lesions of peripheral blood vessels. Equally Important are the ge neral neurovegetatlve manifestations [gastrointestinal and cardiovascular dis orders, hyperhldrosis, 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 end 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 in 293 workers occupationally exposed to vinyl chloride. Subjective complaints were evaluated on the background ot N5 and EOD quest!onnare survey analysis, EEG examinations, including pbotostimulation, 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 irequent subjective complaints were headache, neurovegetatlve disorders and dysesthesiae, among objective findings dominated cerebellar and/or vestibulocerebellar syndrome, lesions of peripheral neurons and peripheral neurovege tatlve 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 ebnormelity. 48J % 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 bave confirmed that vinyl cloride has a considerable impact on tbe 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. 240 < St ? b1 ov Vi, V,, Vito cblorure de vie II a 6tg it posts au chlcr & l'aide des tx flcatif produit imposition sui Les trouhl g Statlfs et dys tame vestibule pdrlph4rlque v xique direct p ayant lieu lors Des donni sujets dimont. (cbez 15,5 %) attelnte des s Les sujets jour, aux exar dans ce ces, sues de l'EEG S t ? b 1 O' vl, V., Vlt rid exponierte Man beot Vlaylchlorid < mlt Hllte de; Elnwirkung ' Exposition ab Die bfiuf: tome und Dy zerebellarsys: ren vegetatlv wobl als dlrs bei perlpbere !n dem EE test, die die Aktlvftlt (be dureh Affekt gen erkliren Die Vlny giseben Star sh 027363 w . "O. ----- - - *- ***-<-*. * the geoil^^ilar dismrovegetative lesions caushajjisms. i the assumed 2s), It occurs 22} and may :al structures 1 be ascribed 3ns accompa;tent changes accentuated rkers at risk essary to enrkers. Of the both for preostimulation. naily exposed d<1 of N5 and oul^^n, were je^^Rverage eurovegetative aellar and/or ai neurovegeto depend on inantly episoxosed showed episodic EEG o changes in -pact on the system and beral symptoj.isequence of ie systematic on the as- tory. Suppie- : ?V,v -- -.-r -- .j.T ; !--- RESUME S t f b 1 o v 4, V., L a m b 1. V., Chumchal, 0., Kellerovd, V,, PaSkovi, V,, V f t o v c o v 4, ]., 2 1 a b, L.: L'image nenrologiqne chei Jes sujets exposts an chlorore de vinyls II a tit ttudit d'une manure complexe 1'image neuroiogique chez 293 sujets ex posts au chlcrure de vinyle. Des troubles subjectlfs ont ttt analysts au plan dttaillt 4 i'aide des anquttes EOD et N5. II a ttt mis en tvidence un effet neurotoxique signi ficant produit par Chlorure de vinyle qui dtpend de la qualitt et de la quaniltt de 1'exposltion suble. Les troubles subjectifs renconirts le plus souvant: maux de ttt&^yraptOmes vt* gttatifs et dysesthtsie. Les donntes objectives ttmoignent pour une affection du systtme vestibuloctrtbelleux et pour celle du neurone ptripbtrique et de J'lnnervation ptriphtrlque vtgttative. La symptomatology ptriphtrlque peut rtsulter de J'effet toxique direct produit par chlorure de vinyle aussi bien que du mtcanlsme d'bypoxie eyant lieu lors des changements vasomoteurs ptriphtriques. Des donnts Issues de l'EEG ttmoignant une activitt de sommeil chez 46,5 % de sujets dtmontrent un effet narcotique du chlorure de vinyle. L'activitt tpisodique (Chez 15,5%] associte parfois 4 1'enomalie de diffusion pourrait s'expliquer par une attelnie des structures mtdlobasales, mtme lite aux changements du cortex. Les sujets exposts 4 l'influence du chlorure de vinyle ne se soumettent, jusqu`4 ce jour, aux examens systtmatiques au plan neuroiogique. 11 est ntcessaire de poursulvre, dans ce cas, une prophylaxie neuroiogique ttudtant 1'image clinique, les donntes is sues de l'EEG ou mtme de l'EMG. II est utile d'employer les anquttes EOD et N5. 2CSAMMENFASSUN0 S t y b 1 o v 4, V., L a m b l, V,, Chumchal. 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., 2 1 a b, L.: Neurologisches Bild bei den dem Vinylchlo- rid exponierten Arbeitenden Man beobachtete kompiexerweise das neurologische Bild bel 293 Arbeitenden, die Vinylchlorld exponiert waren. Subjektive Schwierigkeiten anelysierte man elngehender mit HHfe der EOD- und N 5-Fragebogen. Dabel hat man eine signlfikante seurotoxische Elnwlrkung von Vinylchlorid nachgewiesen, die von der IntensitBt und Dauer der Exposition abhangig 1st. Die htufigsten subjektiven Schwierlgkeiten waren Kopfschmerzen vegetative Symptome und Dysesth&sle. Der objekttve Sefund zeugt von der Affektion des Vestlbularzerebellarsystems. ferner von der Affektion des perlpheren Neurons und der pertpheren vegetativen Innervation. Die periphere Symptomatology kann man erklfiren sowohl als dlrekte Elnwlrkung yon Vinylchlorld, als euch den bypoxiscben Mechanlsmus bel perlpheren vesomotortschen Verlnderungea. In dem EEG-Befund stellte man bef 46,5 % Tiele der Gesamtheit die Seblafaktivitat fest, die die narkotiscbe Elnwlrkung von Vinylchlorld dokumentiert. Die episodische Aktlvttat (bei 15,5%] manchma! in Verbindung mlt Dlffusionsabnormitat kOnnte man durch Affektion von mediobasalen Strukturen, gegebenenfels" durch Kortexveranderungen erklSren. Die Vinylchlorid exponierten Arbeitenden werden bisber systematisch vom neurologiscben Standpunkt nicht beobachtet. Die Verlasser balten die gezielte neurologische Ss 241 SL 027364 IS *T * ' IK 4, ***.? * -7* i S3? z.+i** * t" v , * h - ,*, .V rfife -yir. ,`AV >'35 m. Vorbeugung in Verbindung mit Beobachtung des klinischen Bildes, des EEG- eventuell R., Me Michd L auch des EMG-Sefundes far notwendig. Sehr geeignet ist die Aowendung der EOO- und M.: Am. led. Hyg. N 5-Fragebogen. pp. 779--769. -- 17 I 16k. Vll, 1955, 5, ! SrfblovA, V.: ACta U: RESUMES' 12, I960, pp. 269--27 Cs. neurol. 26, 1963, S t f b 1 o v A, V., L a tn b 1, V.. Chumchal, 0., K e 11 e r o v 4, V., P a 3 k o v 4, V., V 11 o v c o v 4, V., 2 1 a b, L.: El cuadro nenroldgico an trabajadores ex- Received Moves puestos al vinilcloruro Se ha examinado globalmente el cuadro neuroldglco en 293 trabajadores expues- tos a! vinilcloruro. Las dificultades subjenvos se las analizd detalladamente mediante los cuestionarios EOD y N 5. Se mostrd el resultado neurotOxico marcado del vinilclo- ruro, el que dependia de la altura y duraciOn de la exposieidn. Las dificultades sub- jetivas mAs frecuentes eran los dolores de la cabeza, los slntomes vegetativos asl que la disestesia. 1 hallazgo objetivo muestra la afectacidn del sisiema vestlbulocerebe- lar, as! que la de la neurona vegetative perlfArica y de a inervacidn vegetatlva peri- fdrica. La sintomatologia perlfArica la puede explicar tanto por el efecto tdxico dlrecto del vinilcloruro, como por el mecanismo hipdxico con los cambios vasotnotOricos pe- 1 rif4ricos. Se halld en hallazgos electroencefalogr4flcos una actividad del suefio en el 46,5 p. c. del conjunto, lp que prueba el resultado narcdtlco del vinilcloruro. La actividad epizddica [en el 15,5 p. c.), a veces en la combinacid:. con la anormidad difusa podrla se explicar por afectacidn de las estructuras mediobasaies, eventualmente por cambios i| de la epidermis. Los trabajadores expuestos a! vinilcloruro no son adn exeminados neuroldgica- mente de manera sistem4tica. Hace falta que se haya realizado neurologies prevenciOn encamisada incluso el cuadro cllnico, el hallazgo elecrroencefalogrAfico, eventualmente el electromiogrAfico. Se recomienda usar los cuestionarios EID y N 5. REFERENCES 1. Angulescu, F., Otota, m., Dobronesca, 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. Dinman, B. D., Warren, A_, Whiiebouse, W. M.: Arch. Environ. Hlth. 22, 1971, 1, pp. 61--73. -- 5. Dodson. V. S., Bertram, ., Dinman, B. D., Wbitebousa, W. M.: Arch. Environ. Kith. 22. 1971, 1. pp. 63--91. -- 6. Engelsmann, F.: Cs. psychol. 3, 1960, pp. 322-- 337. -- 7. Engelsmann, F., DrdkovA, S.: Cs. psychol. 4, 1964, pp. 340--346. -- 6. Engelimsnn, F., DrdkovA, S-: Activ. nerv. sup. 2, 1959, pp. 108--11S. -- 9. Eysenck, H. Eysenck, S. G. B.: Manual of the Eysenck 242 Personality Inventory. Univ. of London Press, London 24. 1964. -- 10. Harris, D. K., Adams, W. G. M.: Brit. Med. J. 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. Juhe, S., Stein, G., Veltman, C-: Int. Arch. Ar* beitsoed. 32, 1974, pp. 1--32. -- 13. Roth. B.: Narkolepsie a hypersomnie z hlediska fysiologie spAnku. Praha, SZdN, 1957. -- 14. Rooskov6, V.: Int. Arch. Arbeitsmed. 34, 1975, pp. 263--299. -- 15. ScbwamovA, K.: NeurologickA a EEG n4lezy u chronickf'Ch pr6myslovch otrav nSkterymi organickyml rozpouStAdly. Pl2eflsky 16k. sb. Suppl. 25, 1970, pp. 5--68. -- 16. SpSrta*. ' SL 027365 i I, - V * EQ^^und Psikoldores ei- s expuesoedlante : viniiciDades sub>s asl que ilocerebetiva peri:o dlrecto j.-Scos pe- ii el 46,5 acrividad sa podrla - cambios lroldglcarevencihn :ua|^^ce London iarris, D. ad. ]. 16, ganer-Lazkowtka, sup. 21, E., Juhe, Irch, Ar12. Roth, hlediska 1237. -- ;med. 34, .zdvA, K.; chrontcmi orga14k. sb. Spirtas, R., Me Michael, A. L., Gamble, J., Van Ert, M.: Am. !nd. Hyg. Ass. J. 36,- 1275, 10, pp. 779--789. -- 17, Stfblovd, V.: Prac. 14k. VII, 1955, 5, pp. 260-- 263. -- 15. StfMoei, V.: Acta Unlv. Carol. Med. Suppl. 12, 1950, pp. 269--274. -- 19. Stfblovd, V.: Cs. neurol. 26, 1963, p. 399. -- 20. Stfblo- vA, V.: Diagnoza a prevence v prumyslove neurologiL Praha, SZdN, 1968. -- 21. Stfblov4, V.: Int. Arch. Occup. Environ. Hlth. 38, 1977, pp. 263--282. -- 22. StJblovA. V., HolanoTi, V.: Prac. 14k. 25, 1373, pp. 90-- 964 Received November 10, 1980 V. StyblovA, Dept. Neurology, Medical Faculty of Hygiene, Charles University, SrobArova^SO, 100 42 Praha 10, Czechoslovakia * - *- "' i-- *" "s^WvV's' 1 **&&7>?r** 'XTV " ci". "a^'^reS.* -: * '.'V17 ..-V; ~Viv' ; * --.vi 243 SL 027366 , *. * M, *>-'.%* " .-/ v a-*7 ! -7*^' f-" - r .L v-- ? V.