Carbon disulfide neurotoxicity: Taiwan experience.

Carbon disulfide (CS2) intoxication may induce peripheral neuropathy, encephalopathy, and cardiovascular diseases. In our studies, abnormalities of the peripheral nerves including clinical symptoms and electrophysiological findings were still present 3 years after cessation of CS2 exposure. The data indicate that CS2 neuropathy may persist for a period of time. The involvement of central nervous system may continue even longer. Brain magnetic resonance images usually show multiple high signal intensities in the basal ganglia and subcortical white matter suggesting a vascular event particularly in the small vessels. In addition, a patient with diffuse demyelination in the cerebral hemispheres also showed a diffuse decrease of regional cerebral blood flow indicating a microangiopathy. Therefore, CS2 exposure should be considered as a risk factor for strokes and one of the causes for diffuse leucoencephalopathy. Because CS2 may induce parkinsonian features, a differential diagnosis between CS2 parkinsonism and idiopathic parkinsonism is important. In our study, dopamine transporter with 99mTc-TRODAT-1 brain single photon emission computed tomography showed a normal uptake in the corpus striatum. The data suggest a normal presynaptic dopaminergic pathway function and provide useful information in differentiation. The involvement of cardiovascular systems may be due to thrombotic effects rather than atherogenic effects. In addition, absorption of CS2 through skin is also significant particularly in workers with skin lesions.