SCI
Alexa Malik, MD
Resident Physician
University of Missouri-Columbia PM&R Program
Columbia, Missouri, United States
Casey A. Sevy, DO
Associate Professor of Clinical Physical Medicine and Rehabilitation
University of Missouri Department of PM&R
Columbia, Missouri, United States
Alexa Malik, MD
University of Missouri Health System
Columbia, Missouri, United States
L2 AIS C spinal cord injury due to copper deficiency myeloneuropathy
Case Description:
A 71-year-old previously active woman presented with 3 moths of progressive, painless bilateral lower limb weakness and numbness, eventually requiring a wheelchair. On ED presentation, she had weakness in hip flexion, knee extension, and ankle dorsiflexion, with decreased sensation to the knees. MRI brain was normal, but MRI spine showed cord signal changes between T4–T10. EMG revealed bilateral sensorimotor polyneuropathy, leading to a diagnosis of myeloneuropathy. Plasmapheresis was started for suspected autoimmune etiology but was halted due to worsening symptoms. Labs revealed elevated zinc with low copper and ceruloplasmin, linked to long-term denture cream and zinc supplement use. She received IV then oral copper replacement. On admission to inpatient rehab, she showed mild gains and was diagnosed with L2 AIS C spinal cord injury. At discharge, she was functionally independent at the wheelchair level but remained nonambulatory. Four months later, she was beginning to walk with a walker.
Discussions:
Copper deficiency myeloneuropathy (CDM) is rare, and most cases occur in individuals with risk factors such as prior gastric surgery, excessive zinc intake, or malabsorption syndromes. CDM can be a difficult clinical diagnosis as presentation mimics other causes of myelopathy such as cord compression, immune-mediated pathologies, and subacute combined degeneration due to vitamin B12 deficiency. Prognosis is relatively poor, with only about 24–33% of patients showing neurological improvement, and fewer than 5–10% achieve full recovery, even with appropriate copper supplementation.
Conclusions: This case illustrates the importance of recognizing copper deficiency as a reversible cause of myeloneuropathy. Early intervention is crucial for optimal outcomes, and misdiagnosis can delay appropriate treatment, as seen here with ineffective plasmapheresis. Clinicians should routinely assess micronutrient levels in unexplained myelopathies, particularly in older adults with risk factors for zinc excess or malabsorption.
