We appreciate the interest and comments of Kumar and Ahlskog. We all agree that copper deficiency is the cause of neurologic deficit in our patients and that copper supplementation partially or completely reverses it. However, we significantly differ in the proposed pathogenesis of copper deficiency with hyperzincemia. We have suggested that idiopathic hyperzincemia is the primary problem and that the copper-deficient state is a secondary event, most likely due to impaired copper absorption in the intestine.1 Contrary to this theory, Kumar and Ahlskog and Prodan et al2 believe that a defect in copper metabolism, presumably impaired absorption, is the primary defect and that the elevation of plasma zinc levels is merely an epiphenomenon.
Hedera P, Brewer GJ. Myelopolyneuropathy Due to Copper Deficiency or Zinc Excess?—Reply. Arch Neurol. 2004;61(4):605. doi:10.1001/archneur.61.4.605-a
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