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<p>This case report describes a 24-year-old male who developed subacute combined degeneration (SCD) as a result of chronic recreational nitrous oxide (N₂O) abuse over a six-month period. The patient presented with a two-week history of progressive paresthesias, initially affecting the feet and subsequently extending to the hips, along with lower limb numbness. Neurological examination revealed ataxia, hypoesthesia, impaired proprioception, and hyperreflexia, while muscle strength remained intact. Cerebrospinal fluid analysis showed mild protein elevation, and laboratory tests indicated macrocytic anemia with low vitamin B12 and elevated methylmalonic acid (MMA) levels. Homocysteine levels were within normal limits, likely due to the interval between the last use of N₂O and the blood test. MRI revealed T2-weighted hyperintensities in the spinal cord, consistent with SCD due to vitamin B12 deficiency. The patient had been using 100–200 canisters of N₂O daily but ceased use 10&#xa0;days prior to hospitalization. After initiating vitamin B12 supplementation, he showed mild improvement. The patient underwent a three-month rehabilitation program, along with continued cyanocobalamin treatment, regaining the ability to walk independently. Follow-up MRI demonstrated a reduction in spinal cord lesions. This case highlights the increasing prevalence of nitrous oxide abuse; to date, this is the first documented case of SCD due to recreational N₂O use registered in Italy. Timely diagnosis and treatment, including vitamin B12 supplementation, are critical in preventing long-term neurological sequelae.</p>

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Spinal cord syndrome: uncovering the risks of nitrous oxide abuse

  • 期刊论文

  • 发表日期：

    2026年3月2日

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  • Laura Ludovica Grassi,
  • Francesco Favruzzo,
  • Francesco Rossato,
  • Chiara Briani,
  • Andrea Fortuna

摘要

This case report describes a 24-year-old male who developed subacute combined degeneration (SCD) as a result of chronic recreational nitrous oxide (N₂O) abuse over a six-month period. The patient presented with a two-week history of progressive paresthesias, initially affecting the feet and subsequently extending to the hips, along with lower limb numbness. Neurological examination revealed ataxia, hypoesthesia, impaired proprioception, and hyperreflexia, while muscle strength remained intact. Cerebrospinal fluid analysis showed mild protein elevation, and laboratory tests indicated macrocytic anemia with low vitamin B12 and elevated methylmalonic acid (MMA) levels. Homocysteine levels were within normal limits, likely due to the interval between the last use of N₂O and the blood test. MRI revealed T2-weighted hyperintensities in the spinal cord, consistent with SCD due to vitamin B12 deficiency. The patient had been using 100–200 canisters of N₂O daily but ceased use 10 days prior to hospitalization. After initiating vitamin B12 supplementation, he showed mild improvement. The patient underwent a three-month rehabilitation program, along with continued cyanocobalamin treatment, regaining the ability to walk independently. Follow-up MRI demonstrated a reduction in spinal cord lesions. This case highlights the increasing prevalence of nitrous oxide abuse; to date, this is the first documented case of SCD due to recreational N₂O use registered in Italy. Timely diagnosis and treatment, including vitamin B12 supplementation, are critical in preventing long-term neurological sequelae.