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KMID : 0359719920100020136
Journal of the Korean Neurological Association
1992 Volume.10 No. 2 p.136 ~ p.142
A Clinical Study on chronic Carbon Disulfide(CS2) Intoxication.



Abstract
Carbon disulfide (CS2) a volatile solvent, has been widely used in the manufacture of the artificial silk because of its highly fat-soluble property. It has been accepted that CS2 is mostly absorbed to the human beings by inhalation and does
harms
mainly to the central and peripheral nervous systems and the cardiovascular sysem. But it is controversial whether the pathologic changes are due to the direct toxic effects of the CS2 or to the secondary effects of the Cs2-induced
arteriosclerosis.
Recently the authors have oserved the six patients of viscose rayon worker with a longstanding exposure to the CS2 and obtained the results as follows:
The ages of onset in the 6 subjects (5 males and one female) were ranged from 41 to 53 years (mean; 47.1) and the duration of exposure from 11 to 18 years (mean; 14.50.
Three of them had no hypertension.
Neurologically they showed headache, dizziness, general malaise, gait difficulty, visual and memory disturbances, paresthesia of distal extremities, dementia, parkinsonian features, pseudobubar palsy, spastic gait, dysarthria, hyperreflexia, and
reduced
or bsent ankle jerks.
Nerve conduction studies (N=4) revealed that three of them had polyneuropathy of axonal type.
MRI (N=6) revealedthe diffuse or patched high signal intensities in the periventricular white matter (6), in bothbasal ganglia (5), in both thalami (2), and in the corpus callosum (1). Five of them showed diffuse cerebral atrophy and one of them
had
previous hemorrhage in the left putamen also.
According to the above findings, CS2 seems to affect both central and peripheral nervous sustems. All the MRI findings are very similar to those of Binswanger's disease induced by hypertension, which has to be discriminated from our cases by the
gap of
the age of onset (usually over 65 years in the Binswanger's disease), and seem to be derived from the secondary effects of the CS2 but both the lack of hypertension (3 of 60 and the axonal polyneuropathy (3 of 4) might prefer the direct toxic
effects of
it.
In conclusion, CS2 seems to afet both the central nervous system more secondarily, and the peripheral nervous system more directly. Therefore, the widespread and systematic study will be necessary to verify the mechanisms of action of the CS2 on
the
nervous system.
KEYWORD
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