Abstract
A 51-year-old welder (nonsmoker) developed subacute lower paresthesias and progressive spastic paraplegia and ataxia. Symptoms appeared 10 days after the first zinc exposure in the yacht construction site (8-hour day/40 days in a confined space with face shield only). Examination revealed loss of vibratory sensation, spasticity, hyperreflexia, and sensory ataxia. Serum heavy metals (Cu 1 mg/L and Pb 4,22 μg/L), B-complex vitamins, and paraneoplastics on serum and CSF were unremarkable. The elevated zinc level (137 μg/dL) was found. Spinal MRI showed combined degeneration (Figure). Myelopathy in zinc smelter workers was reported in the 19th century1 and recently rediscovered in excessive zinc ingestion. Copper secondary deficiency is hypothesized even if the normal copper serum level is reported.2 Two months later, copper became low (0.8 mg/L), a time-dependent process might explain late copper deficiency in our case. Symptoms ameliorated 4 months later with normalization of serum zinc/copper levels.
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