Carbon disulfide vasculopathy: A small vessel disease

Citation
Cc. Huang et al., Carbon disulfide vasculopathy: A small vessel disease, CEREB DIS, 11(3), 2001, pp. 245-250
Citations number
25
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
CEREBROVASCULAR DISEASES
ISSN journal
10159770 → ACNP
Volume
11
Issue
3
Year of publication
2001
Pages
245 - 250
Database
ISI
SICI code
1015-9770(2001)11:3<245:CDVASV>2.0.ZU;2-P
Abstract
We present the clinical manifestations of 4 male patients with acute stroke -like symptoms and polyneuropathy after long-term exposure to carbon disulf ide (CS2) in a viscose rayon plant. The ages of onset of polyneuropathy ran ged from 42 to 45 years with a duration of CS2 exposure between 6 and 21 ye ars. 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 sm oking 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 t omography (CT) scans showed low-density lesions in the basal ganglia in 2 p atients, cortical atrophy in 1 and normal in 1. Brain magnetic resonance im age (MRI) study disclosed multiple lesions in the corona radiata and basal ganglia on T-2-weighted images in 3 patients and cortical atrophy in 1. Aft er the diagnosis, they left their jobs for a CS2-free environment, and impr ovement of the working conditions was noted. During 5 years follow-up perio d, another 2 patients also developed an acute episode of stroke with hemipa resis. Brain CT and/or MRI follow-up studies in these 2 patients revealed new lesi ons in the basal ganglia and corona radiata. Intriguingly, a patient with p revious stroke also developed new lesions in the bilateral thalami and brai nstem. Carotid Doppler scan, transcranial Doppler scan and/or cerebral angi ography did not show any prominent stenosis or occlusion in the major intra cranial large arteries. We conclude that encephalopathy may occur in patien ts after long-term CS2 exposure, probably due to impaired cerebral perfusio n. 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. Theref ore, we suggest that CS2 exposure may be a risk factor for stroke. Copyrigh t (C) 2001 S.KargerAG, Basel.