Skip to content

Neurophysiological Characteristics of Nitrous Oxide‐Induced Polyneuropathy: A Case Series

Tanya Elisabeth Bentley, Volker Limmroth, Maximilian Zimmermann, Johannes Fabian Holle

Journal of the Peripheral Nervous System September 1, 2026 DOI: 10.1111/jns.70156 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Retrospective case series Case report Peer reviewed
Sample size 12
Population Patients with acute neurological symptoms and a history of nitrous oxide abuse at a German tertiary care hospital
Measures nerve conduction studies, somatosensory evoked potentials (SSEPs), MRI, serum vitamin B12, methylmalonic acid (MMA)
Key findings Electrophysiological testing showed polyneuropathy in 8 of 12 patients with nitrous oxide abuse, most often a pure motor pattern (5 of 8), with no distinct clinical phenotype. All tested patients had elevated methylmalonic acid, while only 3 of 10 had low vitamin B12, suggesting MMA is a more reliable biomarker.

Abstract

ABSTRACT:

Background: Nitrous oxide (N 2 O) misuse is a growing health concern, with N 2 O‐induced neurological disorders increasingly reported across Europe. Among these, N 2 O‐induced polyneuropathy (PNP) can lead to permanent deficits, yet its neurophysiological characteristics remain inconsistently described. This retrospective case series aimed to characterize the electrophysiological pattern of N 2 O‐induced polyneuropathy.

Methods: We reviewed the records of 12 patients with acute neurological symptoms and a history of N 2 O abuse, all of whom underwent electrophysiological testing at a German tertiary care hospital between July 2023 and December 2024. Data were analyzed descriptively.

Results: Conduction studies revealed evidence of PNP in eight out of 12 patients and the most common pattern was pure motor (5/8). No distinct clinical phenotype could be identified for patients with electrophysiologically confirmed PNP or Pure‐Motor PNP. SSEPs were abnormal in all assessable patients, whereas signs of SCD on MRI were present in a smaller proportion. Only three of 10 tested patients had reduced vitamin B12 levels, while all showed elevated methylmalonic acid (MMA) levels. Mean MMA levels were higher in patients with PNP than in those without.

Interpretation: The reason why N 2 O leads to different patterns of PNP remains unclear and a distinct phenotype for N 2 O‐induced PNP or Pure‐Motor PNP was not found in this cohort. MMA represents a more reliable biomarker than serum vitamin B12 in the diagnostic workup of N 2 O‐induced neurotoxicity. These findings highlight the need for further research into additional neurotoxic properties of N 2 O and individual predisposing factors underlying the different electrophysiological patterns of N 2 O‐induced PNP.

Citations in the library