Copper is an essential trace metal and plays key roles in the structure and function of the nervous system, vascular, and skeletal tissues and in hematopoiesis and catecholamine metabolism. Inherited copper deficiency (Menkes’ disease) results in intellectual deterioration, failure to thrive, seizures, abnormal hair, and connective tissue abnormalities. Due to the ubiquitous distribution of copper and the low daily requirement, acquired copper deficiency is extremely rare in humans. Ataxic myelopathy due to copper deficiency does occur in ruminants and is called swayback.1 The hematologic manifestations of acquired copper deficiency are well described,2 but the neurologic manifestations of acquired copper deficiency in humans are not widely appreciated. We describe a case of myelopathy that occurred in the setting of copper deficiency. A 65-year-old man was evaluated for a 5-year history of progressive gait difficulty. For 1 year prior to evaluation, he had been using a cane and had paresthesias involving the feet and hands. He had been taking 200 to 400 mg of zinc a day for cold prevention for 22 years (recommended daily allowance of zinc, 15 mg/day). Neurologic examination …
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Kumar et al. (2003) studied this question.
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