Subacute combined degeneration of the cord secondary to nitr
An 18-year-old right-handed male roofer attended the emergency department with a short history of progressive sensory disturbance, distal limb weakness, and gait dysfunction. He complained of pins and needles starting in his fingers and toes and spreading proximally over a two-week period in which he developed associated numbness, distal weakness, and difficulty with his balance. He did not have bowel or bladder involvement.

His past medical history was unremarkable; his vaccination history was complete; he was a non-smoker who took no regular medication and denied recent foreign travel or illness. He reported an alcohol intake of 20–30 units per week and habitual N2O inhalation from ‘whippits’ (whipped cream dispenser canisters). Two weeks prior to admission he reported inhaling over 30 whippets at a social event with symptom onset several days later.

Neurological examination was remarkable for bilateral distal vibration and proprioceptive sensory loss more pronounced in the lower limbs, mild distal limb weakness, and pronounced sensory ataxia. The patella deep tendon reflexes were preserved but the ankle reflexes were absent. He had bilateral flexor plantar responses. There were no cerebellar signs, no cranial nerve abnormalities and cognitive function were normal. Nutritional causes of myeloneuropathy were considered including serum copper, folic acid, and vitamin E deficiencies, although vitamin B12 deficiency was suspected early due to the history of N2O use. Guillain-Barré Syndrome was also favored initially due to the prominent ascending peripheral neuropathy despite the lack of antecedent illness. Other aetiologies including metabolic, toxic, infective, inflammatory (transverse myelitis), and paraneoplastic disorders were also considered. Unenhanced MRI of the cervical spine demonstrated bilateral symmetric high T2 signal within the dorsal columns extending from the level of C2 to T2, with minimal cord expansion. Bilateral high T2 signal within the posterior funiculus gave rise to the inverted ‘V’ sign,1 which is described in SCDC. Brain MRI revealed normal appearances of the parenchyma, ventricles, and cerebrospinal fluid spaces.

On the second day of admission, the patient commenced 1000 mcg intramuscular hydroxocobalamin injections on alternative days for 2 weeks, followed by 1000 mcg every 2 months for a year. He was discharged after 3 days of admission at which time his weakness had improved but sensory disturbance persisted. Outpatient nerve conduction (NCS) and electromyography (EMG) studies were performed following discharge. NCS showed a length-dependent, predominantly motor axonal neuropathy in the lower limbs with some slowing of sensory conduction velocities. The EMG revealed corresponding acute denervation changes in the distal leg musculature. These findings are consistent with the peripheral neuropathy seen in vitamin B12 deficiency. The clinical team did not feel that a follow-up MRI was indicated because it would not have changed management. Six months following his admission symptoms had fully resolved and he had made a complete recovery.