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Copper deficiency myelopathy secondary to overuse of zinc supplementation 2012

General Spine

AJAY, AGARWAL, MD
Suresh, C, Patel, MD, Non ASSR Member

Poster

Purpose

1.To describe the clinical and imaging features of copper deficiency myeloneuropathy. 2.To discuss the potential etiologies and the neurological manifestations of this deficiency state.

Methods & Materials

A 74-year-old, right-handed man presented with progressive numbness and weakness in both legs beginning 2 to 3 months ago. The patient also noted pain in his legs and feet for the past 3 to 4 months, which he describes as a painful tingling. On neurological examination, the patient had marked decreased in position, vibration, pin and light touch sensation in both lower extremities, less marked in the upper extremities. On laboratory evaluation, he was found to have a normal serum Vit B12 and serum folate. The serum zinc level was high while the serum copper level was very low. MRI of the cervical spine demonstrated a long segment of high signal intensity extending from approximately C2-C6 present within the dorsal columns. On further inquiry, the patient revealed history of taking 50 mg of zinc supplement everyday for the last 2 years as a prophylaxis for flu on his own. Zinc was discontinued and the patient was started on oral copper supplement, 8 mg of copper per day. The patient improved clinically in a couple of weeks and a follow up MRI performed after 2 months showed complete resolution of previously seen abnormal signal seen in the dorsal column.

Results

Discussion We believe that our patient developed copper deficiency myeloneuropathy secondary to overuse of zinc supplements. Both copper and zinc are absorbed in the stomach and proximal duodenum. Excess zinc levels cause an upregulation of metallothionein production in the enterocytes. Copper has a higher affinity for metallothionein than zinc, so it displaces zinc from metallothionein. Copper then remains in the enterocytes and is sloughed off into the intestinal tract and eliminated leading to copper deficiency state.

Conclusion

Unrecognized copper deficiency appears to be a common cause of idiopathic myelopathy in adults. The clinical and the radiological picture bear striking similarities to the syndrome of subacute combined degeneration associated with vitamin B12 deficiency. Early recognition and copper supplementation may prevent neurologic deterioration.

References/Financial Disclosures

Financial Disclosure : None

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