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Journal of Clinical Medicine
By Joseph Albou, Julien Fallouh, Bertrand Degos and 5 others.
Background/Objectives: Nitrous oxide is known to cause neurological damage. We investigated the potential effects of nitrous oxide (N2O) abuse on the optic nerve through comprehensive ophthalmological evaluation of patients diagnosed with N2O-related neurological disorders.
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This retrospective, monocentric case series included patients hospitalized for N2O-related neurological manifestations in the neurology department of a French tertiary care center. Suspected optic neuropathy was defined as abnormal retinal nerve fiber layer (RNFL) and ganglion cell layer (GCL) thickness according to age- and sex-adjusted normative values, in the presence or absence of visual field defects.
Ten patients (mean age: 22.2 ± 3.6 years) were assessed. They all presented with symptoms typical of N2O-induced neuropathy or myelopathy and elevated blood methylmalonic acid and total homocysteine levels, which are markers of vitamin B12 inactivation. Three patients showed decreased RNFL and GCL thickness. The cumulative exposure to N2O was higher (3220 ± 2801 kg vs. 165 ± 158 kg) and the consumption duration was longer (36 ± 32 vs. 8 ± 8 months) in these three patients compared to those without optic nerve involvement.
This preliminary case series suggests that massive and prolonged N2O exposure may be associated with subclinical optic neuropathy, possibly mediated by vitamin B12 inactivation. Given the growing prevalence of recreational N2O use, ophthalmological evaluation including OCT could be considered in patients with heavy or prolonged use and neurological symptoms. These findings are hypothesis-generating and require confirmation in larger prospective studies.
Published in Journal of Clinical Medicine. The abstract is shown as published and remains the work of its authors; read the full article at the source.
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