BackgroundHuntington's disease (HD) is a fatal inherited neurodegenerative disease, caused by a

Hydrogen sulfide (H2S) poisoning involves a risk of hypoxic brain damage. Six patients who lost consciousness due to H2S poisoning are described. The symptoms varied from anosmia in the patient with the shortest but highest exposure to delayed neurological deterioration in the patient with the longest exposure. The two patients with the most serious symptoms developed pulmonary edema, which may have prolonged the hypoxia. The patients were reexaminated 5 years or more after the poisoning. The five patients who had been unconscious in H2S atmosphere for from 5 to 15-20 min showed persisting impairment at neurological and neuropsychological re-examination. Memory and motor function were most affected. One patient was seriously demented. Recent reports of large groups of H2S-poisoned workers probably underestimate the risk of sequelae, due to the inclusion of cases with exposure of short duration and lack of follow-up.

In Norway's only viscose rayon plant, carbon disulfide (CS2) concentrations in ambient air usually were between 30 and 50 mg/m3 during the first 23 years of production. From 1970/1971 until the factory was closed in 1982, corresponding values were 10-25 mg/m3. Through all of these years, high peak exposures of CS2 and H2S occurred. In 1986, 16 of the 24 men still at work in 1982 and with at least 10 years' experience in the spinning room agreed to participate in this study. Clinical neurological examination demonstrated abnormalities in 15; neuropsychological tests showed impairments of probable organic origin in 14. Thirteen had cerebral atrophy demonstrated by cerebral computed tomography (CT). Electromyography (EMG) was abnormal in six, neurography in 11. Regional cerebral blood flow measurements indicated flow asymmetries in eight, whereas Doppler investigation of the extracranial carotid and vertebral arteries, electroencephalography (EEG), and evoked response investigations were mostly normal. Based on these results and the exposure data, a diagnosis of CS2-induced encephalopathy was reached in eight workers; another six had an encephalopathy in which CS2 exposure was regarded as a partial cause. Correspondingly, seven had a neuropathy probably caused by CS2 exposure alone; in three others, CS2 was found to be the partial cause of a neuropathy. This indicates that long-term, relatively moderate exposure to CS2 in association with high peak exposures to CS2 and H2S involves a substantial risk of developing neurotoxic disease.

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Aaserud 0, Juntunen J, Matikainen E. Vibration sensitivity thresholds: methodological considerations. sense tests made in a semiquantitative way with a 128 stuning fork.

The risk of long-term damage to the CNS after exposure to mixed solvents in work environments is controversial. Thirty-six workers were studied who had been exposed to organic solvents for more than 10 years (mean 24 5 years) in a working environment. The workers and unexposed controls were studied with a battery of neuropsychological and cognitive tests. Significant group differences were observed for the Wechsler adult intelligence scale (WAIS) digit span and symbol digit substitution, and on paired associate learning and continuous word recognition. The results suggest that long-term work-related exposure to organic solvents may have chronic toxic effects.

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A randomized double blind study with iohexol (Omnipaque) and metrizamide (Amipaque) in cervical myelography was performed in 50 patients, 29 with iohexol and 21 with metrizamide. The myelographies were performed either with lumbar or with C1-C2 puncture in about equal groups, using 300 mg I/ml and 240 mg I/ml of the contrast media respectively. The image quality was equal with both contrast media, excellent in about 4/5 and good in 1/5 of the examinations. Subjective side effects were twice as frequent with metrizamide as with iohexol. The most frequent side effect was headache, occurring in 34% with iohexol and in 67% with metrizamide. Altogether 24% or the patients had EEG changes after iohexol as compared to 47% after metrizamide. All EEG changes were slight dysrythmia-except in three patients with spike activity after metrizamide. These were the only ones with mental reactions as well. It can be concluded that in this trial iohexol was better suited for cervical myelography than metrizamide.