Copper deficiency as a treatable cause of poor balanceBMJ 2010; 340 doi: https://doi.org/10.1136/bmj.c508 (Published 12 April 2010) Cite this as: BMJ 2010;340:c508
- Zhaleh Khaleeli, neurology registrar1,
- Daniel G Healy, consultant neurologist2,
- Anthony Briddon, prinicipal clinical scientist3,
- Michael P Lunn, consultant neurologist 2,
- Mary M Reilly, consultant neurologist 2,
- John Land, consultant in clinical biochemistry3,
- Gavin Giovannoni, neurology professor 4
- 1Department of Neurology, National Hospital for Neurology and Neurosurgery, London WC1N 3BG
- 2MRC Centre for Neuromuscular Diseases, National Hospital for Neurology and Neurosurgery, Queen Square, London, WC1N 3BG
- 3Neurometabolic Unit, National Hospital for Neurology and Neurosurgery, London WC1N 3BG
- 4Department of Clinical Neurosciences, Barts and the London School of Medicine and Dentistry, London E1 2AT
- Correspondence to: G Giovannoni
- Accepted 8 December 2009
Patients presenting with a neurological syndrome typical of B-12 deficiency may actually be manifesting symptoms of copper deficiency, as has been recognised over the past decade.1 Most commonly, they have a progressive spinal cord syndrome resulting in poor balance due to loss of proprioception. The cases we report show that copper deficiency, which has various causes, is more common than previously realised and often goes undiagnosed. Increased awareness of this condition is vital because early diagnosis and treatment can prevent severe disability.
A 65 year old man presented in 2006, having fallen in the shower on closing his eyes; he had burning and tightness affecting his feet and had recently lost weight. Over six months he became bedbound due to poor balance. He had undergone partial gastrectomy in 1973 for a duodenal ulcer. Three years before the neurological symptoms developed, he was diagnosed with asymptomatic B-12 deficiency, which was successfully treated.
Initial examination showed a positive Romberg test and an inability to walk heel-to-toe. Cranial nerve examination was unremarkable. Tone and power were normal, ankle jerks were depressed, and one plantar reflex was extensor. Over six months he developed spastic weakness in his legs (hip flexion MRC grade 4), hyper-reflexia, and bilateral extensor plantar reflexes. Sensory disturbance suggested greater abnormality in the posterior columns; vibration sense was reduced to the costal margins, proprioception to the ankle, and pinprick to mid-foot level.
Magnetic resonance imaging showed T2 signal abnormality in the posterior cervical cord at C2-4 (figure ⇓). Electrophysiology found lower limb motor abnormalities consistent with a motor neuronopathy, but sensory nerve action potentials were normal. Central motor conduction to the limbs (a method for examining the central motor pathways, in which the difference between the latency of motor evoked potentials …
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