Marked increase in severe neurological disorders after nitrous oxide abuse: a retrospective study in the Greater Paris area.

BACKGROUND: Recreational nitrous oxide (N2O) use has become more widespread worldwide, leading to an increase in myelopathies and peripheral neuropathies. The aim of this study was to describe clinical and socioeconomical characteristics of severe N2O-induced (NI) neurological disorders (NI-NDs), to determine its incidence in the Greater Paris area and to compare it with that of similar inflammatory neurological disorders. METHODS: We performed a retrospective multicentric cohort study of all adult patients with severe NI-NDs in the neurology and general internal medicine departments of the Greater Paris area from 2018 to 2021. The incidence was compared with that of non-NI-myelitis and Guillain-Barré syndrome (GBS) using a sample of 91,000 hospitalized patients sourced from health insurance data. RESULTS: Among 181 patients, 25% had myelopathy, 37% had peripheral neuropathy and 38% had mixed disease. Most were aged between 20 and 25 years, lived in socially disadvantaged urban areas, and exhibited high rates of unemployment (37%). The incidence of NI-NDs increased during 2020 and reached a peak mid-2021. The 2021 incidence in 20-25-year-olds was 6.15 [4.72; 8.24] per 100,000 persons for NI-myelopathy and 7.48 [5.59; 9.37] for NI-peripheral neuropathy. This was significantly higher than for non-NI-myelitis (0.35 [0.02; 2.00]) and GBS (2.47 [0.64; 4.30]). The incidence of NI-NDs was two to three times higher in the most socially disadvantaged areas. CONCLUSION: The recent increase in recreational N2O use has led to a rise in the incidence of severe NI-NDs, particularly in young adults with low socioeconomic status for whom NI-NDs strongly outweigh similar neurological disorders.

Biomarkers for the diagnosis and monitoring of nitrous oxide intoxication: objectives and methodology of the SFBC Working Group.

The recreational use of nitrous oxide (N2O) is an emerging public health issue. Chronic N2O abuse may result in various clinical symptoms, encompassing neurological, psychiatric and cardiovascular outcomes. Despite the difficulties for the laboratory investigation of N2O intoxication, there is currently no guidelines in France to help both clinicians and biologists use appropriate biomarkers for the diagnosis and monitoring of patients with clinical symptoms potentially related to N2O intoxication. A multi-disciplinary Working Group, carried out under the auspices of the French Society of Clinical Biology (SFBC) and in collaboration with the French Societies of Emergency Medicine (SFMU), Analytical Toxicology (SFTA), Hemostasis and Thrombosis (SFTH), Vitamins and Biofactors (SFVB), and the French Federation of Neurology (FFN), was recently implemented to elaborate practical guidelines. The methodology of the Working Group is based on the critical analysis of the literature, and raising concerns and objectives are grouped into five working packages. The present manuscript primarily aims to expound upon the methodology and objectives of the ongoing SFBC Working Group on N2O.

Giant-cell arteritis related strokes: scoping review of mechanisms and rethinking treatment strategy?

Stroke is a rare and severe complication of giant cell arteritis (GCA). Although early diagnosis and treatment initiation are essential, the mechanism of stroke is often related to vasculitis complicated by arterial stenosis and occlusion. Its recurrence is often attributed to early steroid resistance or late GCA relapse, so immunosuppressive treatment is often reinforced. However, many questions concerning the mechanisms of stroke remain elusive, and no review to date has examined the whole data set concerning GCA-related stroke. We therefore undertook this scoping review. GCA-related stroke does not necessarily display general signs and inflammatory parameters are sometimes normal, so clinicians should observe caution. Ischemic lesions often show patterns predating watershed areas and are associated with stenosis or thrombosis of the respective arteries, which are often bilateral. Lesions predominate in the siphon in the internal carotid arteries, whereas all the vertebral arteries may be involved with a predominance in the V3-V4 segments. Ultrasonography of the cervical arteries may reveal edema of the intima (halo sign), which is highly sensitive and specific of GCA, and precedes stenosis. The brain arteries are spared although very proximal arteritis may rarely occur, if the patient has microstructural anatomical variants. Temporal artery biopsy reveals the combination of mechanisms leading to slit-like stenosis, which involves granulomatous inflammation and intimal hyperplasia. The lumen is sometimes occluded by thrombi (<15%), suggesting that embolic lesions may also occur, although imaging studies have not provided strong evidence for this. Moreover, persistence of intimal hyperplasia might explain persisting arterial stenosis, which may account for delayed stroke occurring in watershed areas. Other possible mechanisms of stroke are also discussed. Overall, GCA-related stroke mainly involves hemodynamic mechanisms. Besides early diagnosis and treatment initiation, future studies could seek to establish specific preventive or curative treatments using angioplasty or targeting intimal proliferation.