A 70-year-old man developed a slowly progressive cerebellar syndrome after having been exposed to carbon disulfide (CS2) in a viscose rayon plant for 27 years. Ataxia, dysmetria, dysarthria and adiadochokinesia appeared 7 years after retirement from work (at age 54), and were later accompanied by cognitive deterioration, dysmnesia, spatio-temporal disorientation, emotional lability, and paranoid-obsessive disturbances. Brain computed tomography (CT) and magnetic resonance imaging (MRI) showed advanced global cerebellar atrophy, and a picture of less severe cerebrocortical atrophy. The case illustrates the possibility of chronic toxic encephalopathy among patients with previous long-term exposure to CS2. In such instances, cerebellar damage may develop as an exceptional, delayed manifestation of neurotoxicity: brain imaging techniques can significantly contribute to the diagnosis and follow-up, in addition to occupational anamnesis and neuropsychiatric evaluation. The patient presented also serves as a remainder that neurodegenerative disorders of apparently unknow origin sometimes derive from occupational toxic exposures suffered in the past. The clinical manifestations may appear several years after retirement from work, when the effects of toxic damage combine with age-related neuronal loss to overcome the brain functional reserve.

Cerebellar atrophy as a delayed manifestation of chronic carbon disulfide Poisoning

CANDURA, STEFANO
2003-01-01

Abstract

A 70-year-old man developed a slowly progressive cerebellar syndrome after having been exposed to carbon disulfide (CS2) in a viscose rayon plant for 27 years. Ataxia, dysmetria, dysarthria and adiadochokinesia appeared 7 years after retirement from work (at age 54), and were later accompanied by cognitive deterioration, dysmnesia, spatio-temporal disorientation, emotional lability, and paranoid-obsessive disturbances. Brain computed tomography (CT) and magnetic resonance imaging (MRI) showed advanced global cerebellar atrophy, and a picture of less severe cerebrocortical atrophy. The case illustrates the possibility of chronic toxic encephalopathy among patients with previous long-term exposure to CS2. In such instances, cerebellar damage may develop as an exceptional, delayed manifestation of neurotoxicity: brain imaging techniques can significantly contribute to the diagnosis and follow-up, in addition to occupational anamnesis and neuropsychiatric evaluation. The patient presented also serves as a remainder that neurodegenerative disorders of apparently unknow origin sometimes derive from occupational toxic exposures suffered in the past. The clinical manifestations may appear several years after retirement from work, when the effects of toxic damage combine with age-related neuronal loss to overcome the brain functional reserve.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11571/133442
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