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Inhaled nitrous oxide-induced functional B12 deficiency.

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Recreational nitrous oxide (N₂O) misuse can cause spinal cord damage by depleting vitamin B12. Young users experiencing neurological symptoms like numbness and weakness should seek medical advice and stop N₂O use.

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Area of Science:

  • Neurology
  • Toxicology

Background:

  • Recreational nitrous oxide (N₂O) use is prevalent among young individuals due to accessibility and low cost.
  • Poor awareness exists regarding the severe neurological adverse effects associated with N₂O misuse.
  • N₂O inhalation can lead to spinal cord degeneration by interfering with DNA synthesis via cobalamin (vitamin B12) inactivation.

Observation:

  • A 19-year-old male presented with a 4-week history of progressive paresthesia in extremities and 2 weeks of limb weakness.
  • Clinical examination revealed an ataxic gait, reduced grip and ankle strength, and impaired lower limb sensation.
  • MRI confirmed myelopathy in the cervical and thoracic spinal cord.

Findings:

  • The patient reported recent recreational nitrous oxide (N₂O) inhalation.
  • Neurological symptoms significantly improved after cessation of N₂O use and initiation of B vitamin supplementation.
  • The case highlights a direct correlation between N₂O misuse and subacute combined degeneration of the spinal cord.

Implications:

  • Urgent need for public health education on the risks of recreational N₂O.
  • Clinicians should consider N₂O toxicity in young patients presenting with myelopathy symptoms.
  • Prompt diagnosis and management, including N₂O cessation and B12 repletion, are crucial for recovery.