Cerebral damage following a single high exposure to carbon disulphide

The patient was a 48 year old man, previously healthy and employed as the head of a petrochemical laboratory. He had no history of trauma to the head, CNS infection or abuse of drugs or alcohol. His work was almost exclusively administrative, and there had been no previous exposure of importance to carbon disulphide or other neurotoxic agents.

In February 1979 a fire started in a galvanised bucket, which contained 100-150 ml of carbon disulphide and during the fire carbon disulphide fumes were evolved. The patient kicked the burning bucket along the floor for 20 minutes to get it out of the building, he was in the room for approximately 20 minutes and it was calculated that he was exposed to a minimum concentration of 400 ppm and a maximum concentration of 470,000 ppm carbon disulphide. He lost consciousness for approximately 10 minutes and was subsequently observed for 24 hours in a hospital, but no objective findings were recorded.

After a few asymptomatic days he then had progressive complaints of anxiety, nightmares, intermittent blurred vision lasting a few seconds, reduced memory and concentration, and headache, resulting in absences from work 2-3 times a week. Precordial pain and impotence occurred, symptoms which the patient had never previously experienced. As the symptoms progressed the patient was referred to an occupational medicine clinic. Neuropsychological examination established dementia in the form of reduced ability to learn and memorise, reduced rate in simple reaction time as well as in more complex tasks, and a reduction in abstract thinking. There were no focal neurological signs.

In a subsequent examination one year later no signs of progression were found. He had a slight decrease in strength in the left arm and leg, slightly decreased coordination in the left-sided finger-nose test, and a mild reduction of vibration sense in the left leg. Regional cerebral blood flow showed reduced cortical flow in the sensory-motor area on the right side. The left hemispheric flow was considered to be normal. CT scanning presented slight cortical atrophy of the cerebrum, and a slight, but significant, right central atrophy. Ocular symptoms were suggestive of optic neuritis, but at the time of the examination there were no objective ocular findings. Twenty-one months after the accident the symptoms were still present and, in spite of treatment, the patient was unable to manage his previous work and was forced to retire (Kruse et al., 1982).

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