Rehabilitation Considerations for Coexistent Copper and Vitamin B12 Deficiency Myelopathy: A Case Report

Case Diagnosis: A 68-year-old male with lower extremity weakness and gait instability attributed to copper deficiency myelopathy with concurrent vitamin B12 deficiency.

Case Description or Program Description: Patient acutely admitted for progressive weakness requiring ambulation assistance following an extended trip to Haiti. He was previously independent for self-care and mobility. Workup showed decreased serum copper level, normal B12 level and mild T2 flair hyperintensity in the dorsal columns on MRI of thoracic spine. He was admitted again 6 months later for further functional decline with undetectable copper levels, decreased B12 level, and normal signal of spinal cord on MRI of cervical and thoracic spine. The patient received parenteral treatment followed by oral copper and B12 supplementation. He was discharged to acute inpatient rehabilitation (AIR).

Setting: University-affiliated Acute Inpatient Rehabilitation

Assessment/Results: Patient received intensive physical, occupational, and speech therapy during 18-day admission to AIR. On initial evaluation, he required maximal assistance for ambulation with significant proprioception deficits including erratic steppage pattern and difficulty sequencing steps. Patient demonstrated progress throughout stay with improved gait distance and decreased assist levels. Lower extremity proprioception continued to limit safety with gait and transfers. He is expected to continue benefiting from skilled therapy services in the outpatient setting.

Discussion (relevance): Vitamin B12 deficiency is the most prevalent cause of subacute combined degeneration (SCD). Similarly, copper deficiency myelopathy presents as subacute gait disturbance with prominent sensory ataxia and/or spasticity, reflecting involvement of the dorsal columns of the spinal cord. A high level of suspicion is essential for an accurate and timely diagnosis. In this patient, the coexistent deficiencies of copper, more notably, and B12, secondarily, led to an extremely rare diagnosis and management plan. Copper and B12 supplementation generally prevent worsening of neurologic symptoms, but there is limited research on the functional recovery of affected patients.

Conclusions: Neurorehabilitation can help patients overcome residual deficits from copper deficiency myelopathy.