Nitrous oxide induced neuropathy correlated with MRI imaging

Abstract

The neurotoxic effects of Nitrous Oxide (N2O), a recreational drug also known as laughing gas, are well known. Despite its declining use in medical settings due to side effects, N2O abuse is on the rise, particularly among young people. Amongst the most serious side effects is neurotoxicity, caused by a reduction in the bioavailability of vitamin B12.

We report the case of a 27-year-old male who, after heavy recreational use of N2O, presented to the emergency department, complaining of bilateral paraesthesia in his arms and legs, leading to their hospitalisation. A blood test was performed, finding decreased vitamin B12 levels. An electromyography found a decreased conduction speed of the left sural nerve and an MRI revealed hyperintense zones in the dorsal column of the cervical spinal cord, compatible with N2O toxicity. The patient’s vitamin B12 deficiency was corrected, and they received physical therapy as an inpatient, before continuing to receive outpatient treatment once they were able to use a walking frame.

The neurotoxicity of N2O is linked to the induction of vitamin B12 deficiency, which can lead to demyelination. This diagnosis can be made despite the presence of normal serum vitamin B12 levels, probably due to a reduction in cellular bioavailability. Homocysteine levels may be elevated in N2O toxicity, providing a crucial diagnostic clue. Treatment is based on reversing the vitamin B12 deficiency, but no consistent regimen has been established. The prognosis varies but may be improved by prompt treatment with vitamin B12.