Metabolic and toxic causes of myelopathy.

Abstract

This article provides an update on the various metabolic and toxic causes of myelopathy. The clinical features, laboratory findings, characteristic imaging and electrodiagnostic patterns, and approach to treatment are reviewed in depth. Vitamin B12 deficiency is a common condition, with prevalence rates that increase with age, and is particularly common in the elderly and in certain geographic areas. Nutritional surveys from the United States have suggested prevalence rates of approximately 6% in those 70 years of age or older, and prevalence rates were reported to be 10% in those older than 75 in the United Kingdom. Copper deficiency is a less common cause of myelopathy, but may result in clinical signs and symptoms indistinguishable from those of vitamin B12 deficiency. Recent reports highlight the importance of excessive zinc in the pathogenesis of copper deficiency and the importance of exogenous zinc cessation in the treatment of copper deficiency. A recent study reviewed previously reported cases of zinc myelopathy in zinc-smelter workers in the 1870s. These workers developed symptoms identical to those reported in the modern descriptive series of copper deficiency myeloneuropathy. Deficiencies of vitamin B12, folate, copper, and vitamin E may result in characteristic clinical, electrodiagnostic, and imaging features. Prompt recognition and treatment is critical to limit permanent neurologic impairment. Recognition of the toxic causes of myelopathy, including nitrous oxide exposure, heroin, radiation, various chemotherapeutic agents, liver disease, konzo, lathyrism, and zinc excess, is aided by understanding the typical clinical and imaging features associated with these agents.