Nitrous oxide toxicity

Nitrous oxide (N2O) toxicity has serious medical sequelae including encephalopathy, myelopathy, neuropathy and endovascular effects 1. This results from demyelination and gliosis due to selective inhibition of vitamin B12.

N2O is an established and widely used anaesthetic gas though also misused quite commonly for recreational purposes. Canisters of nitrous oxide, colloquially known as “whippets”, "nangs", or "bulbs" 5, used commercially as a propellant for whipped cream is commonly abused.

The classic neurological appearance of vitamin B12 deficiency is the so-called subacute combined degeneration of the cord manifested as damage to the dorsal columns of the spinal cord, responsible for the transmission of vibratory and proprioceptive input. Peripheral neuropathy, optic atrophy, and dementia can also occur.

Neurotoxicity is secondary to the selective inhibition of vitamin B12 (hydroxocobalamin), which serves as a cofactor for methionine synthase, which is an enzyme active in folate metabolism and the formation of myelin sheath phospholipids 2,4.

The end result of overexposure is demyelination and eventual gliosis, both within the central nervous system and to a lesser extent the peripheral nervous system. 

Radiographic features are identical to those of subacute combined degeneration of the cord.

  • T2: thoracic hyperintense signal involving the dorsal columns (inverted "V" sign), although less commonly lateral tracts of the spinal cord may also be affected; very rarely is there involvement of the anterior spinal cord

Treatment options include:

  • halting exposure to nitrous oxide
  • high dose of intramuscular vitamin B12, followed by oral supplementation
  • methionine supplementation has also been used 2

On imaging, the differential diagnosis includes: 

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Article information

rID: 30559
Synonyms or Alternate Spellings:
  • Nitrous oxide induced myeloneuropathy
  • Nitrous oxide toxicity myeloneuropathy

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