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Secondary amines react with nitrous acid to form N-nitrosamines, as depicted in Figure 1. Nitrous acid, a weak and unstable acid, is formed in situ from an aqueous solution of sodium nitrite and strong acids, such as hydrochloric acid or sulfuric acid, in cold conditions. In the presence of an acid, the nitrous acid gets protonated. The subsequent loss of water results in the formation of the electrophile known as nitrosonium ion.
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Nondepolarizing neuromuscular blockers prevent the membrane depolarization of muscle cells and inhibit muscle contraction. These are usually administered with anesthetics to achieve complete muscle relaxation. Upon administration, these drugs first block the small, rapidly contracting muscles of the face and hands, followed by the larger muscles of the trunk and the intercostal muscles. The diaphragm is the last muscle to be affected.
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Nitrous oxide-induced myeloneuropathy.

Grace Swart1,2, Christopher Blair3,4, Zhong Lu5,6

  • 1Department of Neurology, St Vincent's Hospital, Sydney, New South Wales, Australia.

European Journal of Neurology
|August 24, 2021
PubMed
Summary

Nitrous oxide misuse can lead to severe myeloneuropathy by inactivating vitamin B12. Early diagnosis and treatment with vitamin B12 can improve neurological deficits, even in severe cases.

Keywords:
hydroxocobalaminmyelopathyneuropathynitrous oxidesubacute combined degenerationvitamin B12

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Area of Science:

  • Neurology
  • Toxicology
  • Nutritional Science

Background:

  • Nitrous oxide (N2O) misuse is a global health concern.
  • Prolonged N2O exposure leads to vitamin B12 inactivation.
  • This inactivation causes a characteristic myeloneuropathy.

Purpose of the Study:

  • To review cases of myeloneuropathy secondary to nitrous oxide misuse.
  • To identify diagnostic markers and assess treatment outcomes.
  • To understand the relationship between N2O use, vitamin B12 levels, and neurological deficits.

Main Methods:

  • Retrospective review of 20 patients with N2O-induced myeloneuropathy.
  • Analysis of clinical presentation, serum vitamin B12, homocysteine levels, and spinal MRI.
  • Assessment of neurological recovery following vitamin B12 treatment.

Main Results:

  • Patients presented with paresthesias and gait instability; 7/20 were bedbound.
  • Serum vitamin B12 levels were often normal, but homocysteine was elevated.
  • Spinal MRI revealed characteristic dorsal column T2 hyperintensities in all patients.
  • Intramuscular vitamin B12 treatment led to variable functional recovery, with some bedbound patients regaining ambulation.

Conclusions:

  • Nitrous oxide misuse causes a severe, potentially reversible subacute myeloneuropathy.
  • Elevated homocysteine and MRI findings are key diagnostic indicators.
  • Neurological deficits can improve with abstinence and B12 supplementation.