Case report: Recreational nitrous oxide abuse triggered peripheral neuropathy possibly through the immune-mediated pathogenesis

Abstract

Nitrous oxide (N2O), commonly known as laughing gas, is widely used in clinical practice and food industry. However, an increasing number of young people have been abusing N2O for recreational purpose, resulting in many functional disorders and sometimes irreversible nerve damage. We present the case of a 20-year-old N2O abuser who gradually developed peripheral neuropathy after continuously inhaling N2O for 2 months. The neurological symptoms of the patient had kept exacerbation for the next 2 months until she came for medical care sitting in a wheelchair. We suggested the patient halting N2O intake and supplementing methylcobalamine according to the standardized protocol. Her symptoms had partly recovered during the following 2 weeks but remained unchanged in another 2 weeks. Antibodies against ganglioside complexes were detected and anti-GM1 IgM antibodies were positive in both cerebrospinal fluid and serum. Intravenous immunoglobulin was given as an additional treatment and the patient's symptoms had significantly recovered further. The patient discharged walking by herself. Then she has been continuously followed up in outpatient department for the next 4 months and taking steroid hormone as well as methylcobalamine. Her symptoms gradually disappeared and all the electrophysiological parameters significantly improved. With this case we were able to show that N2O-related peripheral neuropathy is not only a metabolic disorder but also an immune-mediated disease. N2O intake can trigger a mimic Guillain-Barré syndrome.

Neurological Manifestations Induced by Nitrous Oxide Abuse

“…Neurological symptoms have developed over a median of 21 days, in line with previous data 14,32,37,48,62,65 . The clinical manifestations extracted from the literature confirmed that impaired proprioception and coordination and decreased superficial sensation were the most prevalent manifestations 20 . Classically, spinal cord MRI is characterized by the inverted V-sign on T2-weighted images and the absence of contrast enhancement 69,70 .…”

“…14,32,37,48,62,65 The clinical manifestations extracted from the literature confirmed that impaired proprioception and coordination and decreased superficial sensation were the most prevalent manifestations. 20 Classically, spinal cord MRI is characterized by the inverted V-sign on T2-weighted images and the absence of contrast enhancement. 69,70 Only a few cases reported in the literature have shown a minimal contrast enhancement 15,17,18,51 due to the breakdown of the blood-brain barrier related to inflammation and perivascular demyelination.…”

“…We identified 154 patients meeting our inclusion criteria after reviewing the literature 5–68 . There was a predominance of males (n=94, 61%), and the median age was 22 [19 to 26] years.…”

The prevalence, risks, and detection of driving under the influence of nitrous oxide

“…The excessive use of N 2 O can lead to considerable demyelination of peripheral axons, and subsequently to muscle weakness and even paralysis, especially in the lower limbs (van Amsterdam et al, 2015). There is no conventional definition of what is considered excessive use, but some case reports state use patterns of over a 500 metal bulbs/balloons per day (Lewis et al, 2021), although the occurrence of peripheral neuropathy has also been reported after the use of 10 bulbs per day (Cartner et al, 2007; Dong et al, 2022). It is not clear if comparatively modest usage patterns also significantly introduce the risk of peripheral demyelination.…”

Mechanisms and recent advances in the diagnosis and treatment of nitrous oxide-induced peripheral neuropathy: a narrative review

“…Furthermore, fatalities resulting from N₂O inhalation have been documented (9). Currently, only a limited number of studies have focused on the peripheral neuropathy caused by abusive inhalation of nitrous oxide (10)(11)(12), highlighting a lack of awareness regarding the toxicity associated with N₂O abuse. Therefore, this study aims to comprehensively outline the clinical characteristics, mechanisms, and management strategies for N₂O-associated peripheral neuropathy.…”