Synopsis
Recognise vitamin B12-related posterior and lateral column injury even without anaemia, take cause-defining samples promptly and start replacement before neurological disability becomes fixed.
- Subacute combined degeneration is spinal-cord injury from functional vitamin B12 deficiency, predominantly affecting dorsal columns and lateral corticospinal tracts, often with peripheral neuropathy.
- Symptoms include symmetrical paraesthesia, impaired vibration and joint position, sensory ataxia, a positive Romberg sign, gait disturbance, weakness and later spasticity or extensor plantar responses.
- Peripheral nerve involvement can reduce ankle reflexes while cord involvement produces brisk knees or plantar responses, creating a mixed central and peripheral examination.
Key red flags
Vibration and joint position are impaired in the feet, stance worsens with eyes closed and gait becomes stamping or broad-based from sensory ataxia despite relatively preserved pain and temperature.
Investigation priorities
Provide the initial biochemical assessment in most people with compatible symptoms and risk factors before replacement.
Management branches
Progressive proprioceptive loss, sensory ataxia or pyramidal signs occur with plausible B12 deficiency.
- Take total or active B12, blood count, folate and cause-directed samples immediately, adding MMA or homocysteine for indeterminate results or suspected nitrous oxide exposure.
- Begin replacement before delayed results return when neurological injury is significant, generally using intramuscular hydroxocobalamin through BNF and local neurological loading guidance.
Key medicines
Intramuscular hydroxocobalamin loadingFor neurological involvement, BNF practice commonly uses 1 mg on alternate days until no further improvement.
Intramuscular hydroxocobalamin maintenanceNeurological maintenance is commonly 1 mg every two months when an irreversible cause persists.