Myeloneuropathy Secondary to Nitrous Oxide Abuse: A Case Report

Case Diagnosis: Rehabilitation of myeloneuropathy secondary to recreational nitrous oxide use

Case Description or Program Description: A 23-year-old gentleman with no significant past medical history presents with a subacute onset of progressive, bilateral lower limb weakness and numbness and paraesthesia in both hands. There was no bowel or bladder involvement. On examination, he had flaccid symmetrical distal weakness in his lower limbs and bilateral foot drop. He had impaired sensation below his knees and impaired vibration and proprioception bilaterally in his lower limbs. He also had positive babinski reflex on the left and absent ankle jerks.

A magnetic resonance imaging (MRI) of the spine revealed increased T2 signal in the posterior columns bilaterally. A nerve conduction study revealed length-dependent mild axonal sensorimotor polyneuropathy. MRI brain and analysis of the cerebrospinal fluid was unremarkable. Vitamin B12 level homocysteines level were elevated. He later admitted to a 6-year history of daily nitrous oxide inhalation from pressurised metal canisters. He has however stopped the abuse 1.5 years ago and took Vitamin B12 supplements over the counter in an attempt to treat his own symptoms. He underwent extensive evaluation and was eventually diagnosed with myeloneuropathy secondary to nitrous oxide toxicity. HE was continued on high dose Vitamin B12 supplementation.

He then underwent intensive inpatient tertiary rehabilitation.

Setting: Inpatient tertiary rehabilitation

Assessment/Results: On admission, he was unable to ambulate due to the lower limb weakness and sensory loss. He underwent strength and gait training and was prescribed bilateral ankle foot orthoses (AFO). On discharge, he still had bilateral foot drop but could ambulate 130m with bilateral axillary crutches. The functional independence measure improved from 92 on admission to 109.

Discussion (relevance): Nitrous oxide irreversibly inactivates methylcobalamin, resulting in functional vitamin B12 deficiency. Nitrous oxide misuse is becoming more prevalent in young adults and can potentially cause detrimental neurological complications. It is therefore important for physicians to understand about this phenomenon.

Conclusions: This case highlights the neurological and functional sequelae of nitrous oxide misuse. This case also illustrates the importance of rehabilitation to improve functional outcomes.