Polyneuropathy induced by chronic carbon disulphide exposure

A 48 year old man worked at a viscose rayon plant as a fibre cutter for 23 years. In June 1992, he developed progressive numbness of both feet which then ascended to both knees, and was associated with muscle weakness. Two months later, numbness and clumsiness of both hands were noted and he was unable to perform his job. On evaluation, his muscle strength was diminished in all four limbs and he could not walk on his toes or heels and had difficulty climbing stairs. His handgrip was weak and there was a generalised absence of tendon reflexes. Impairment of light touch, pinprick, temperature, position, and vibration sensory modalities was evident in a glove and stocking distribution. Study of nerve conduction velocities (NCV) disclosed a prolonged distal latency (DL), decreased amplitudes of compound muscle and sensory nerve action potentials, and slowing of NCVs in median, ulnar, peroneal, tibial and sural nerves suggesting a mixed axonal and demyelinating polyneuropathy. There was no sign of diabetes mellitus, porphyria, Guillain- Barré syndrome or radiculopathy. He had consumed alcohol socially for 10 years.

His occupational history showed that he had worked in a poorly ventilated room with exposure to relatively high concentrations of carbon disulphide. Gloves and respirators were not routinely used during the operation. Several of his co-workers had similar symptoms of numbness and weakness in distal limbs; polyneuropathy due to occupational exposure to carbon disulphide was suspected. During the three year follow-up, motor deficits resolved slowly. One year later he was able to walk on toes and heels, however three years later 'tightness' of both legs still persisted. Tendon reflexes were absent in his lower limbs but present in upper limbs, and sensory impairment was only minimally improved (Chu et al., 1995).

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Diabetes 2

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