Subacute combined degeneration of the cord
Vitamin B12 deficiency → dorsal column + corticospinal tract demyelination
Overview
Demyelination of the DORSAL COLUMNS and CORTICOSPINAL TRACTS (and peripheral nerves) from vitamin B12 deficiency (or nitrous oxide abuse, which inactivates B12). A reversible cause of a mixed sensory/UMN picture — treat B12 promptly. The classic trap: giving folate first can precipitate it.
Recognise
- Symmetrical dorsal-column loss: tingling, impaired PROPRIOCEPTION and VIBRATION, sensory ataxia, positive Romberg
- Corticospinal: leg weakness, spasticity, brisk knees BUT absent ankle jerks + upgoing plantars (mixed UMN/LMN)
- Context: pernicious anaemia, vegan diet, gastrectomy, nitrous oxide ("laughing gas") abuse; macrocytic anaemia
Red flags
- Progressive disability if untreated; neurological damage may become irreversible
Differentials & how to tell them apart
Investigations
Serum B12 (low), FBC/film (macrocytic anaemia, hypersegmented neutrophils), intrinsic-factor antibodies (pernicious anaemia); MRI cord (dorsal-column signal); ask about nitrous oxide use.
Management
IM vitamin B12 replacement promptly (and before folate); treat the cause
- 1Replace B12 (IM hydroxocobalamin) promptly; identify the cause (pernicious anaemia, diet, gastrectomy, nitrous oxide).Gate: Replace B12 BEFORE (or with) folate — giving folate alone in B12 deficiency can precipitate or worsen subacute combined degeneration
- 2Lifelong B12 for pernicious anaemia/irreversible cause; stop nitrous oxide; monitor neurological recovery.
Key points
Dorsal-column signs (lost vibration/proprioception, Romberg) + mixed UMN/LMN legs (absent ankle jerks, upgoing plantars) + macrocytic anaemia = B12 SCD. B12 before folate. Ask about nitrous oxide.
Monitor & prognosis
B12 level, blood count, neurological recovery.
Reversible if treated early; permanent if late.
Source: BNF; NICE CKS (B12 deficiency)