Chronic Carbon Disulfide Encephalopathy

Huang, Chin‐Chang; Chu, Chun‐Che; Chen, Rou‐Shayn; Lin, Shinn-Kuang; Shih, Tung‐Sheng

doi:10.1159/000117294

Cited by 33 publications

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“…In the patient described, both CT and MRI showed a picture of diffuse and progressive encephalic atrophy which was particularly pronounced in the cerebellum, according with the clinical picture. Focal or diffuse brain atrophy in CT scans following chronic CS 2 exposure was also documented in previous reports 6,7,20,21) . A MRI study was performed by Peters et al 5) , who showed a pattern of central demyelinization in two out of four CS 2 -poisoned patients.…”

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“…A MRI study was performed by Peters et al 5) , who showed a pattern of central demyelinization in two out of four CS 2 -poisoned patients. Huang et al 21) described ten viscose rayon workers with polyneuropathy and neuropsychiatric disturbances: brain MRI abnormalities (mild cerebrocortical atrophy and/or multiple lesions of the basal ganglia and corona radiata) were present in seven of them. In the case reported by Frumkin 8) , MRI revealed advanced cerebellar atrophy and prominent atrophy in the posterior tracts and nuclei of the pons.…”

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Cerebellar Atrophy as a Delayed Manifestation of Chronic Carbon Disulfide Poisoning.

2003

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A 70-year-old man developed a slowly progressive cerebellar syndrome after having been exposed to carbon disulfide (CS 2 ) 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 CS 2 . 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 unknown 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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Cerebellar Atrophy as a Delayed Manifestation of Chronic Carbon Disulfide Poisoning.

2003

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“…Some also had chronic encephalopathy with abnormal computed tomography (CT) and magnetic resonance image (MRI) studies in the initial evaluation [21]. During the follow-up period, another 2 patients also developed an acute-onset stroke-like episode with hemiparesis and slurred speech.…”

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confidence: 99%

Carbon Disulfide Vasculopathy: A Small Vessel Disease

Huang

Chu²,

Chu³

et al. 2001

Cerebrovasc Dis

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We present the clinical manifestations of 4 male patients with acute stroke-like symptoms and polyneuropathy after long-term exposure to carbon disulfide (CS2) in a viscose rayon plant. The ages of onset of polyneuropathy ranged from 42 to 45 years with a duration of CS2 exposure between 6 and 21 years. The ages of onset of stroke were from 42 to 48 years. The risk factors for stroke including heart disease and diabetes were denied, except for smoking in 4, hyperlipidemia in 2 and hypertension in 1. At the initial visit in 1992, only 2 patients developed sudden onset of hemiparesis suggesting a lacunar stroke before the diagnosis of CS2 intoxication. Brain computed tomography (CT) scans showed low-density lesions in the basal ganglia in 2 patients, cortical atrophy in 1 and normal in 1. Brain magnetic resonance image (MRI) study disclosed multiple lesions in the corona radiata and basal ganglia on T₂-weighted images in 3 patients and cortical atrophy in 1. After the diagnosis, they left their jobs for a CS2-free environment, and improvement of the working conditions was noted. During 5 years follow-up period, another 2 patients also developed an acute episode of stroke with hemiparesis. Brain CT and/or MRI follow-up studies in these 2 patients revealed new lesions in the basal ganglia and corona radiata. Intriguingly, a patient with previous stroke also developed new lesions in the bilateral thalami and brainstem. Carotid Doppler scan, transcranial Doppler scan and/or cerebral angiography did not show any prominent stenosis or occlusion in the major intracranial large arteries. We conclude that encephalopathy may occur in patients after long-term CS2 exposure, probably due to impaired cerebral perfusion. The lesions tend to occur in the basal ganglia, corona radiata and even brainstem, particularly involving the small-sized vessels. In addition, the cerebral lesions may progress even after cessation of CS2 exposure. Therefore, we suggest that CS2 exposure may be a risk factor for stroke.

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“…In the study by Hageman et al [14], the brain MRI showed diffuse white matter hyperintensities, cerebral cortical atrophy, and mild enlargement of the ventricular system in 1 patient with long-term CS 2 exposure. In our previous studies [11, 12], multiple lacunar infarcts were noted in the subcortical white matter, basal ganglion, and even in the brain stem. Therefore, chronic encephalopathy with a small vessel disease was suggested [12].…”

Section: Discussionmentioning

confidence: 95%

“…The central toxicity of CS 2 can be characterized by cognitive dysfunction, emotional lability, parkinsonian features, cerebellar dysfunction, acute stroke-like symptoms, and atherosclerosis with dyslipidemia [8, 9, 10, 11, 12]. Brain computed tomography (CT) and magnetic resonance images (MRI) show focal or diffuse brain atrophy, and multiple brain lesions in the basal ganglia and subcortical white matter [8, 11, 12]. The data may indicate a small vessel disease.…”

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confidence: 99%

Diffuse White Matter Lesions in Carbon Disulfide Intoxication: Microangiopathy or Demyelination

Huang

Kuo

et al. 2003

Eur Neurol

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Long-term exposure to carbon disulfide (CS₂) may induce diffuse encephalopathy with parkinsonism, pyramidal signs, cerebellar ataxia, and cognitive impairments, as well as axonal polyneuropathy. The pathogenic mechanisms of diffuse encephalopathy are unclear, although vasculopathy and toxic demyelination have been proposed. Recently, we have encountered a patient who developed headache, limb tremors, gait disturbance, dysarthria, memory impairment, and emotional lability after long-term exposure to CS₂. The brain magnetic resonance images (MRI) showed diffuse hyperintensity lesions in T₂-weighted images in the subcortical white matter, basal ganglia, and brain stem. The brain computed tomography perfusion study revealed a diffusely decreased regional cerebral blood flow and prolonged regional mean transit time in the subcortical white matter and basal ganglion. To our knowledge, there have been few reports demonstrating diffuse white matter lesions in chronic CS₂ encephalopathy using brain MRI. In addition, the ^99mTc-TRODAT-1 single photon emission computed tomography showed a normal uptake of the dopamine transporter, indicating a normal presynaptic dopaminergic pathway. We conclude that diffuse white matter lesions may develop after chronic exposure to CS₂, possibly through microangiopathy. In addition, CS₂ poisoning can be considered as one of the causes of chronic leukoencephalopathy.

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Chronic Carbon Disulfide Encephalopathy

Cited by 33 publications

References 0 publications

Cerebellar Atrophy as a Delayed Manifestation of Chronic Carbon Disulfide Poisoning.

Cerebellar Atrophy as a Delayed Manifestation of Chronic Carbon Disulfide Poisoning.

Carbon Disulfide Vasculopathy: A Small Vessel Disease

Diffuse White Matter Lesions in Carbon Disulfide Intoxication: Microangiopathy or Demyelination

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