Abstract
Acquired copper deficiency constitutes an under-recognised cause of myelopathy. Aim of the study was to describe the clinical and imaging features at admission and after copper supplementation of a patient with acquired copper deficiency myeloneuropathy. A 73-year-old woman presented with anaemia and signs of posterior column dysfunction. Somatosensory evoked potentials showed impaired central pathway conduction. Serum copper and caeruloplasmin levels were low. Nerve conduction assessment revealed axonal polyneuropathy. Spinal magnetic resonance imaging (MRI) showed posterior column hyperintensity. Diffusion tensor imaging disclosed decreased fractional anisotropy (FA) corresponding to the hyperintensity. Copper supplementation normalised the haematological picture, whereas vibratory sensitivity was only slightly improved. Control MRI revealed a slight hyperintensity at C1-C2 level; FA values normalised. In conclusion, in acquired copper-deficiency-associated myelopathy, correction of blood and MRI alterations precedes that of neurological manifestations, which may remain suboptimal.
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