Nitrous oxide-induced demyelination: Clinical presentation, diagnosis and treatment recommendations

Recreational use of nitrous oxide (NO) in the general public has led to increasing reports of NO-induced demyelination (NOID). We describe the varying clinical presentations and pathophysiology, and offer a treatment paradigm.

A literature search of MEDLINE and EMBASE resulted in 42 publications with 37 studies meeting the inclusion criteria, for a total of 51 patients. Our case series included 5 patients seen from 2014 to 2018 followed over 3-60 months.

Those with sensory symptoms and subjective weakness were categorized as having "mild" symptoms (25%). Symptoms indicating involvement outside the dorsal columns such as observer-graded weakness were categorized as "moderate" (61%). Patients with the aforementioned plus cognitive effects were categorized as "severe" (12%). There was no dose-dependent relationship between the amount of NO used and clinical impairment. There was a trend between the severity of neurologic impairment and serum levels of B12. Two patients were noncompliant. One initiated only oral therapy and did not improve. One received injections a month apart and worsened.

Patients with NOID tend to have worse symptoms when presenting with lower serum vitamin B12 levels and have good recovery rates when treated with intramuscular B12 and oral supplementation.