A Case of Idiopathic Hypocupric Myeloneuropathy

Copper deficiency myeloneuropathy is a rare but treatable cause of noncompressive myelopathy that can mimic subacutecombined degeneration (SACD) due to vitamin B12 deficiency. Risk factors include gastrointestinal surgery, zinc overload, and malabsorption syndromes; however, no etiology is identified in up to 20% of cases. We report a 21-year-old female with no significant comorbidities, presenting with progressive gait difficulty, lower limb stiffness, imbalance, and unaware footwear slippage over 1 year. Neurological examination, laboratory tests, magnetic resonance imaging (MRI), and nerve conduction studies were performed. Examination revealed lower limb hypertonia, power 4+/5, exaggerated deep tendon reflexes in upper and lower limbs with absent ankle jerks, extensor plantars, and positive Romberg's sign. MRI showed cervical cord T2 hyperintensity with an "inverted V sign." Hemoglobin was 10.4 g/dL with MCV 116 fL, but vitamin B12 was >2000 pg/mL. Serum copper was low (24 mg/dL) and serum zinc was elevated (224.8 mg/dL). Nerve conduction study demonstrated symmetrical sensory axonal neuropathy. The patient was started on oral copper 8 mg/day. This case highlights the importance of considering copper deficiency myeloneuropathy even in the absence of typical risk factors or B12 deficiency. Early recognition and copper supplementation may prevent irreversible neurological damage.