Nitrous oxide induced spinal cord oedema with normal serum B12 level with high plasma homocysteine level

Nitrous Oxide (N2O) widely known as 'Laughing gas' is used as inhaled anaesthetic, analgesic in clinical practice [1]. Its abuse has increasingly common among adolescents and young adults. Although it can cause multi system damage, multiple cases of neurology system damage had been reported. [2] Through oxidation, nitrous oxide inactivated B12 and hence inactive B12 is unable to perform as a co-factor for methionine synthase and methylmalonyl coA mutase. A male patient in his early 20s presented to emergency department with tingling sensation, loss of fine movements and dexterity in both hands for 2 weeks. He was recently presented to emergency after being involved in minor road traffic accidents (Whip lash injury). He had satisfactory imaging with CT head and neck to rule out cervical cord injury at that time. His symptoms were slowly progressed during 2 weeks with no involvement of lower limbs. On detail and thorough history taking, he admitted taking Laughing gas occasional abuse. His upper limb examination showed loss of sensation but preserve motor function, muscle tone and loss of fine movements. His routine blood tests were unremarkable with normal MCV (mean corpuscular volume), normal HB (haemoglobin) and low normal B12 level with 200 (Normal 180–1,000 pg/mL). He had no previous history of B12, haematological conditions. He had an MRI of head and whole spine to rule out spinal cord pathology which was reported unremarkable. Neurological opinion was sought who correctly pointed out that clinical presentation and findings were suggestive of neurotoxicity due to Nitrous Oxide and suggested that serum B12 level was not reliable to rule out B12 deficiency and MRI was done only axial views. It was incomplete MRI study and suggested to add sagittal views which showed increased intramedullary signal intensity aeras on T2 weighted which consistent with spinal cord oedema. His plasma homocysteine level was 100 (normal 5–15 µmol/L). Empirical treatment with IM B12 injection started and advised to stop abusing Nitrous oxide and follow up clinic in 3 months. He reports symptoms were resolved and good recovery. His serum B12 level increased to 800. The previous road traffic injury was red herring for patient's presentation and good social, recreational abuse need to be asked thoroughly in history taking. Serum B12 level is not a very reliable test to rule out B12 deficiency especially in Nitrous oxide induce neurotoxicity. It is important to learn that all imaging modalities need to be done both axial and sagittal view to be able to appreciate pathology. Although, Nitrous oxide was not known to have serious addiction, it is not harmless and may cause irreversible neurotoxicity if not treated early.