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Diagnosis

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The diagnosis of neurotoxic disease is not easy. The errors are usually of two types: either it is not recognized that a neurotoxic agent is the cause of neurological symptoms, or neurological (and especially neurobehavioural) symptoms are erroneously diagnosed as resulting from an occupational, neurotoxic exposure. Both of these errors can be hazardous since an early diagnosis is important in the case of neurotoxic disease, and the best treatment is avoiding further exposure for the individual case and the surveillance of the condition of other workers in order to prevent their exposure to the same danger. On the other hand, sometimes undue alarm can develop in the workplace if a worker claims to have serious symptoms and suspects a chemical exposure as the cause but in fact, either the worker is mistaken or the hazard is not actually present for others. There is practical reason for correct diagnostic procedures, as well, since in many countries, the diagnosis and treatment of occupational diseases and the loss of working capacity and invalidity caused by those diseases are covered by insurance; thus the financial compensation may be disputed, if the diagnostic criteria are not solid. An example of a decision tree for neurological assessment is given in Table 1.


Table 1. Decision tree for neurotoxic disease

I. Relevant exposure level, length and type

II. Appropriate symptoms insidiously increasing central (CNS) or peripheral (PNS) nervous system symptoms

III. Signs and additional tests CNS dysfunction: neurology, psychology tests PNS dysfunction: quantitative sensory test, nerve conduction studies

IV. Other diseases excluded in differential diagnosis


Exposure and Symptoms

Acute neurotoxic syndromes occur mainly in accidental situations, when workers are exposed short-term to very high levels of a chemical or to a mixture of chemicals generally through inhalation. The usual symptoms are vertigo, malaise and possible loss of consciousness as a result of depression of the central nervous system. When the subject is removed from the exposure, the symptoms disappear rather quickly, unless the exposure has been so intense that it is life-threatening, in which case coma and death may follow. In these situations recognition of the hazard must occur at the workplace, and the victim should be taken out into the fresh air immediately.

In general, neurotoxic symptoms arise after short-term or long-term exposures, and often at relatively low-level occupational exposure levels. In these cases acute symptoms may have occurred at work, but the presence of acute symptoms is not necessary for diagnosis of chronic toxic encephalopathy or toxic neuropathy to be made. However, patients do often report headache, light-headedness or mucosal irritation at the end of a working day, but these symptoms initially disappear during the night, weekend or vacation. A useful checklist can be found in Table 2.

Table 2. Consistent neuro-functional effects of worksite exposures to some leading neurotoxic substances

 

Mixed organic solvents

Carbon disulphide

Styrene

Organophos-
phates

Lead

Mercury

Acquisition

+




+


Affect

+


+


+


Categorization

+






Coding

+

+



+

+

Colour vision

+


+




Concept shifting

+






Distractibility





+


Intelligence

+

+


+

+

+

Memory

+

+

+

+

+

+

Motor coordination

+

+

+


+

+

Motor speed

+

+

+


+

+

Near visual contrast sensitivity

+






Odour perception threshold

+






Odour identification

+




+


Personality

+

+




+

Spatial relations

+

+



+


Vibrotactile threshold

+



+


+

Vigilance

+

+



+


Visual field





+

+

Vocabulary





+


Source: Adapted from Anger 1990.

Assuming that the patient has been exposed to neurotoxic chemicals, the diagnosis of neurotoxic disease starts with symptoms. In 1985, a joint working group of the World Health Organization and the Nordic Council of Ministers discussed the matter of chronic organic solvent intoxication and found a set of core symptoms, which are found in most cases (WHO/Nordic Council 1985). The core symptoms are fatigability, memory loss, difficulties in concentration, and loss of initiative. These symptoms usually start after a basic change in personality, which develops gradually and affects energy, intellect, emotion and motivation. Among other symptoms of chronic toxic encephalopathy are depression, dysphoria, emotional lability, headache, irritability, sleep disturbances and dizziness (vertigo). If there is also involvement of the peripheral nervous system, numbness and possibly muscular weakness develop. Such chronic symptoms last for at least a year after the exposure itself has ended.

Clinical Examination and Testing

The clinical examination should include a neurological examination, where attention should be paid to impairment of higher nervous functions, such as memory, cognition, reasoning and emotion; to impaired cerebellar functions, like tremor, gait, station and coordination; and to peripheral nervous functions, especially vibration sensitivity and other tests of sensation. Psychological tests can provide objective measures of higher nervous system functions, including psychomotor, short-term memory, verbal and non-verbal reasoning and perceptual functions. In individual diagnosis the tests should include some tests that give a clue as to the person’s premorbid intellectual level. History of school performance and previous job performance as well as possible psychological tests administered previously, for example in connection with military service, can help in the evaluation of the person’s normal level of performance.

The peripheral nervous system can be studied with quantitative tests of sensory modalities, vibration and thermosensibility. Nerve conduction velocity studies and electromyography can often reveal neuropathy at an early stage. In these tests special emphasis should be on sensory nerve functions. The amplitude of the sensory action potential (SNAP) decreases more often than the sensory conduction velocity in axonal neuropathies, and most toxic neuropathies are axonal in character. Neuroradiological studies such as computed tomography (CT) and magnetic resonance imaging (MRI) usually do not reveal anything pertinent to chronic toxic encephalopathy, but they may be useful in the differential diagnosis.

In the differential diagnosis other neurological and psychiatric diseases should be considered. Dementia of other aetiology should be ruled out, as well as depression and stress symptoms of various causes. Psychiatric consultation may be necessary. Alcohol abuse is a relevant confounding factor; excessive use of alcohol causes symptoms similar to those of solvent exposure, and on the other hand there are papers indicating that solvent exposure may induce alcohol abuse. Other causes for neuropathy also have to be ruled out, especially entrapment neuropathies, diabetes and kidney disease; also alcohol causes neuropathy. The combination of encephalopathy and neuropathy is more likely of toxic origin than either of these alone.

In the final decision the exposure should be evaluated again. Was there relevant exposure, considering the level, length and quality of exposure? Solvents are more likely to induce psycho-organic syndrome or toxic encephalopathy; hexacarbons, however, usually first cause neuropathy. Lead and some other metals cause neuropathy, although CNS involvement can be detected later on.

 

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Contents

Preface
Part I. The Body
Blood
Cancer
Cardiovascular System
Digestive System
Mental Health
Musculoskeletal System
Nervous System
Renal-Urinary System
Reproductive System
Respiratory System
Sensory Systems
Skin Diseases
Systematic Conditions
Part II. Health Care
Part III. Management & Policy
Part IV. Tools and Approaches
Part V. Psychosocial and Organizational Factors
Part VI. General Hazards
Part VII. The Environment
Part VIII. Accidents and Safety Management
Part IX. Chemicals
Part X. Industries Based on Biological Resources
Part XI. Industries Based on Natural Resources
Part XII. Chemical Industries
Part XIII. Manufacturing Industries
Part XIV. Textile and Apparel Industries
Part XV. Transport Industries
Part XVI. Construction
Part XVII. Services and Trade
Part XVIII. Guides

Nervous System References

Amaducci, L, C Arfaioli, D Inzitari, and M Marchi. 1982. Multiple sclerosis among shoe and leather workers: An epidemiological survey in Florence. Acta Neurol Scand 65:94-103.

Anger, KW. 1990. Worksite neurobehavioral research: Result, sensitive methods, test batteries and the transition from laboratory data to human health. Neurotoxicology 11:629-720.

Anger, WK, MG Cassitto, Y Liang, R Amador, J Hooisma, DW Chrislip, D Mergler, M Keifer, and J Hörtnagel. 1993. Comparison of performance from three continents on the WHO-recommended neurobehavioral core test battery (NCTB). Environ Res 62:125-147.

Arlien-Søborg, P. 1992. Solvent Neurotoxicity. Boca Raton: CRC Press.
Armon, C, LT Kurland, JR Daube, and PC O’Brian. 1991. Epidemiologic correlates of sporadic amyotrophic lateral sclerosis. Neurology 41:1077-1084.

Axelson, O. 1996. Where do we go in occupational neuroepidemiology? Scand J Work Environ Health 22: 81-83.

Axelson, O, M Hane, and C Hogstedt. 1976. A case-referent study on neuropsychiatric disorders among workers exposed to solvents. Scand J Work Environ Health 2:14-20.

Bowler, R, D Mergler, S Rauch, R Harrison, and J Cone. 1991. Affective and personality disturbance among women former microelectronics workers. J Clin Psychiatry 47:41-52.

Brackbill, RM, N Maizlish, and T Fischbach. 1990. Risk of neuropsychiatric disability among painters in the United States. Scand J Work Environ Health 16:182-188.

Campbell, AMG, ER Williams, and D Barltrop. 1970. Motor neuron disease and exposure to lead. J Neurol Neurosurg Psychiatry 33:877-885.

Cherry, NM, FP Labrèche, and JC McDonald. 1992. Organic brain damage and occupational solvent exposure. Br J Ind Med 49:776-781.

Chio, A, A Tribolo, and D Schiffer. 1989. Motorneuron disease and glue exposure. Lancet 2:921.

Cooper, JR, FE Bloom, and RT Roth. 1986. The Biochemical Basis of Neuropharmacology. New York: Oxford Univ. Press.

Dehart, RL. 1992. Multiple chemical sensitivity—What is it? Multiple chemical sensitivities. Addendum to: Biologic markers in immunotoxicology. Washington, DC: National Academy Press.

Feldman, RG. 1990. Effects of toxins and physical agents on the nervous system. In Neurology in Clinical Practice, edited by WG Bradley, RB Daroff, GM Fenichel, and CD Marsden. Stoneham, Mass: Butterworth.

Feldman, RG and LD Quenzer. 1984. Fundamentals of Neuropsychopharmacology. Sunderland, Mass: Sinauer Associates.

Flodin, U, B Söderfeldt, H Noorlind-Brage, M Fredriksson, and O Axelson. 1988. Multiple sclerosis, solvents and pets: A case-referent study. Arch Neurol 45:620-623.

Fratiglioni L, A Ahlbom, M Viitanen and B Winblad. 1993. Risk factors for late-onset Alzheimer’s disease: a population-based case-control study. Ann Neurol 33:258-66.

Goldsmith, JR, Y Herishanu, JM Abarbanel, and Z Weinbaum. 1990. Clustering of Parkinson’s disease points to environmental etiology. Arch Environ Health 45:88-94.

Graves, AB, CM van Duijn, V Chandra, L Fratiglioni, A Heyman, AF Jorm, et al. 1991. Occupational exposure to solvents and lead as risk factors for Alzheimer’s disease: A collaborative re-analysis of case-control studies. Int J Epidemiol 20 Suppl. 2:58-61.

Grönning, M, G Albrektsen, G Kvåle, B Moen, JA Aarli, and H Nyland. 1993. Organic solvents and multiple sclerosis. Acta Neurol Scand 88:247-250.

Gunnarsson, L-G, L Bodin, B Söderfeldt, and O Axelson. 1992. A case-control study of motor neuron disease: Its relation to heritability and occupational exposures, particularly solvents. Br J Ind Med 49:791-798.

Hänninen, H and K Lindstrom. 1979. Neurobehavioral Test Battery of the Institute of Occupational Health. Helsinki: Institute of Occupational Health.

Hagberg, M, H Morgenstem, and M Kelsh. 1992. Impact of occupations and job tasks on the prevalence of carpal tunnel syndrome. Scand J Work Environ Health 18:337-345.

Hart, DE. 1988. Neuropsychological Toxicology: Identification and Assessment of Human Neurotoxic Syndromes. New York: Pergamon Press.

Hawkes, CH, JB Cavanagh, and AJ Fox. 1989. Motorneuron disease: A disorder secondary to solvent exposure? Lancet 1:73-76.

Howard, JK. 1979. A clinical survey of paraquat formulation workers. Br J Ind Med 36:220-223.

Hutchinson, LJ, RW Amsler, JA Lybarger, and W Chappell. 1992. Neurobehavioral Test Batteries for Use in Environmental Health Field Studies. Atlanta: Agency for Toxic Substances and Disease Registry (ATSDR).

Johnson, BL. 1987. Prevention of Neurotoxic Illness in Working Populations. Chichester: Wiley.

Kandel, ER, HH Schwartz, and TM Kessel. 1991. Principles of Neural Sciences. New York: Elsevier.

Kukull, WA, EB Larson, JD Bowen, WC McCormick, L Teri, ML Pfanschmidt, et al. 1995. Solvent exposure as a risk factor for Alzheimer’s disease: A case-control study. Am J Epidemiol 141:1059-1071.

Landtblom, A-M, U Flodin, M Karlsson, S Pålhagen, O Axelson, and B Söderfeldt. 1993. Multiple sclerosis and exposure to solvents, ionizing radiation and animals. Scand J Work Environ Health 19:399-404.

Landtblom, A-M, U Flodin, B Söderfeldt, C Wolfson and O Axelson. 1996. Organic solvents and multiple sclerosis: A synthesis of the cement evidence. Epidemiology 7: 429-433.

Maizlish, D and O Feo. 1994. Alteraciones neuropsicológicas en trabajadores expuestos a neurotóxicos. Salud de los Trabajadores 2:5-34.

Mergler, D. 1995. Behavioral neurophysiology: Quantitative measures of sensory toxicity. In Neurotoxicology: Approaches and Methods, edited by L Chang and W Slikker. New York: Academic Press.

O’Donoghue, JL. 1985. Neurotoxicity of Industrial and Commercial Chemicals. Vol. I & II. Boca Raton: CRC Press.

Sassine, MP, D Mergler, F Larribe, and S Bélanger. 1996. Détérioration de la santé mentale chez des travailleurs exposés au styrène. Rev epidmiol med soc santé publ 44:14-24.

Semchuk, KM, EJ Love, and RG Lee. 1992. Parkinson’s disease and exposure to agricultural work and pesticide chemicals. Neurology 42:1328-1335.

Seppäläinen, AMH. 1988. Neurophysiological approaches to the detection of early neurotoxicity in humans. Crit Rev Toxicol 14:245-297.

Sienko, DG, JD Davis, JA Taylor, and BR Brooks. 1990. Amyotrophic lateral sclerosis: A case-control study following detection of a cluster in a small Wisconsin community. Arch Neurol 47:38-41.

Simonsen, L, H Johnsen, SP Lund, E Matikainen, U Midtgård, and A Wennberg. 1994. Evaluation of neurotoxicity data: A methodological approach to classification of neurotoxic chemicals. Scand J Work Environ Health 20:1-12.

Sobel, E, Z Davanipour, R Sulkava, T Erkinjuntti, J Wikström, VW Henderson, et al. 1995. Occupations with exposure to electromagnetic fields: A possible risk factor for Alzheimer’s disease. Am J Epidemiol 142:515-524.

Spencer, PS and HH Schaumburg. 1980. Experimental and Clinical Neurotoxicology. Baltimore: Williams & Wilkins.

Tanner, CM. 1989. The role of environmental toxins in the etiology of Parkinson’s disease. Trends Neurosci 12:49-54.

Urie, RL. 1992. Personal protection from hazardous materials exposures. In Hazardous Materials Toxicology: Clinical Principles of Environmental Health, edited by JB Sullivan and GR Krieger. Baltimore: Williams & Wilkins.

World Health Organization (WHO). 1978. Principles and Methods of Evaluating the Toxicity of Chemicals, Part 1 and 2. EHC, No. 6, Part 1 and 2. Geneva: WHO.

World Health Organization and Nordic Council of Ministers. 1985. Chronic Effects of Organic Solvents On the Central Nervous System and Diagnostic Criteria. EHC, No. 5. Geneva: WHO.

Zayed, J, G Ducic, G Campanella, JC Panisset, P André, H Masson, et al. 1990. Facteurs environnementaux dans l’étiologie de la maladie de Parkinson. Can J Neurol Sci 17:286-291.