Original Paper

Carbon Disulfide Vasculopathy: A Small Vessel Disease
Chin-Chang Huang^a, Chun-Che Chu^a, Nai-Shin Chu^a, Trong-Neng Wu<sup>b

a</sup>Department of Neurology, Chang Gung Memorial Hospital and University, and
^bDiseases Surveillance and Quarantine Service, Department of Health, Executive Yuan, Taipei, Taiwan

Address of Corresponding Author

Cerebrovasc Dis 2001;11:245-250 (DOI: 10.1159/000047646)

  Key Words

• Carbon disulfide
• Vasculopathy
• Encephalopathy
• Neurotoxic disease
• Risk factor

  Abstract

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.

Copyright © 2001 S. Karger AG, Basel

  Author Contacts

Chin-Chang Huang, MD
Department of Neurology, Chang Gung Memorial Hospital
199 Tung-Hwa N Road, Taipei, Taiwan (ROC)
Tel. +886 3 3281200, ext. 8413, Fax +886 3 3287226
E-Mail cch0537@adm.cgmh.com.tw

  Article Information

Received: Received: June 16, 2000
Accepted: September 11, 2000
Number of Print Pages : 6
Number of Figures : 1, Number of Tables : 2, Number of References : 25