Subacute combined degeneration of the cord secondary to nitrous oxide misuse: No laughing matter

Abstract

Nitrous oxide (N₂O) has several traditional uses as a surgical and dental anaesthetic, as well as in aerosol spray propellants. It is the combination of analgesic and euphoric qualities coupled with accessibility as an over-the-counter household item that lends N₂O to recreational use. Despite increasing evidence that prolonged use of N₂O both medically and as a drug of abuse can cause disabling neurological side-effects, it remains widely used. We present the case of an 18-year-old male who was diagnosed with subacute combined degeneration of the cord (SCDC) secondary to acute, heavy recreational use of N₂O. The patient presented with progressive paraesthesia affecting his hands and feet associated with distal weakness. MRI of the cervical spine revealed symmetric bilateral high T2 signal within the dorsal columns extending from the level of C2 to T2 with the inverted 'V' sign on axial T ₂-weighted slices indicative of SCDC. Although vitamin B12 levels were within normal range, marked elevation of methylmalonic acid and homocysteine support the diagnosis of B12 inactivation and functional B12 deficiency, which fully resolved with treatment.

Figure 1.

Sagittal T2 MRI cervical spine. There is high signal discretely involving the posterior column tracts with minimal cord expansion.

Figure 2.

Axial T2 MRI cervical spine. Arrow: bilateral high-intensity T2 signal within the posterior funiculus, resembling the appearance of an inverted letter ‘V’.

Figure 3.

Vitamin B12 is a cofactor in conversion of methylmalonyl coenzyme A to succinyl coenzyme A and of homocysteine to methionine. Elevated levels of the substrates methylmalonic acid and homocysteine can be used to identify vitamin B12 inactivation despite normal serum B12 concentrations. MS = methionine synthase, MCCoAM = methylmalonyl coenzyme CoA mutase.