• Rajesh Verma, H N Praharaj, Vinay Kumar Khanna, Ravindra Kumar Garg, Maneesh Kumar Singh, and Hardeep Singh Malhotra.
• Department of Neurology, King George Medical University, Lucknow, U.P., India. drrajeshverma32@yahoo.com
• J. Neurol. Sci. 2013 Jun 15; 329 (1-2): 11-6.

BackgroundVitamin B12 deficiency is a well recognized cause of posterolateral myelopathy. In Indian subcontinent, it may coexist with nutritional copper deficiency producing partial response of patients to B12 supplementation. Hence the study was planned to look for association of hypocupremia and B12 deficiency.MethodsTwenty-three patients with posterolateral myelopathy (Romberg sign positive) were enrolled and investigated for levels of vitamin B12, copper and zinc and followed up for six months.ResultIn three patients, copper deficiency alone was found to be the cause. In another three, both copper and vitamin B12 were deficient. In all these six patients, ceruloplasmin and 24h urinary copper were found to be low suggesting dietary copper deficiency. Hyperzincemia was found in four of these patients. Magnetic resonance imaging of spine was normal in lone Cu deficient patients but showed T2 hyperintensity of posterior column in lone B12 or combined B12 and copper deficiency.ConclusionIn cases of B12 deficiency myelopathy not responding to supplementation, copper deficiency must be sought at the earliest to avoid and treat persistent neurological disability.Copyright © 2013 Elsevier B.V. All rights reserved.

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