PO009 Nitrous oxide induced myeloneuronopathy

Abstract

Nitrous oxide (NO) is an increasingly used recreational drug amongst the young. Six patients presented to our unit with varying neurological presentations ranging from acute AIDP to a pure cord syndrome, mostly with a mixture of peripheral and central elements (myeloneuropathy). Some patients did not admit to taking it initially. Therefore a high index of clinical suspicion is needed. Most of the patients responded well to aggressive parenteral Vitamin B12 administration. This case series highlights the need to keep NO abuse in mind in younger patients who present with an acute cord syndrome or AIDP. Homocysteine and methylmalonic acid levels can be useful in suspected cases, even when abuse is denied by the patient.

Factors affecting the topography of nitrous oxide‐induced neurological complications

“…Of note, these patients were admitted via the emergency department of the university hospital of Marseille and probably reflect the most severe spectrum of N 2 O‐related neurological complications. Hence, the daily amount of N 2 O use was larger than that previously reported [1–3, 6]. This high level of consumption was probably enabled by the development in the past years of larger N 2 O cylinders of ~600 g that are easily available in numerous shops in Marseille.…”

“…Our study was limited by its monocentric aspect, which explains the small sample size. Moreover, although a 3‐month follow‐up consultation was scheduled for each patient, 40% failed to attend, which limited the possibility of collecting follow‐up data as described in other cohorts [1].…”

“…In the past few years, the heavy misuse of nitrous oxide (N 2 O) as a recreational drug has led to the admission in the emergency departments of numerous patients presenting acute or subacute sensorimotor deficits due to axonal polyneuropathy and/or myelopathy [1–9]. However, little is known about the factors affecting the topography and severity of nervous system injuries associated with N 2 O abuse and, in particular, why some patients predominantly present spinal cord involvement and others peripheral neuropathy.…”

What biological markers could be used for diagnosis and monitoring of nitrous oxide abuse?

“…Clinical symptoms of N 2 O exposure are related to the functional inactivation of vitamin B12 by oxidation of its cobalt ion [2]. This oxidation prevents the formation of methylcobalamin, resulting in a decrease in methionine synthase activity which converts homocysteine into methionine.…”

Longitudinal follow‐up and prognostic factors in nitrous oxide‐induced neuropathy

“…More recently, the widespread misuse of N 2 O as a recreational drug has resulted in an influx of patients to emergency and neurology departments, presenting with acute or subacute sensorimotor tetraparesis due to N 2 O‐induced neuropathy (N 2 On). These severe presentations, at times accompanied by a loss of walking ability, may be partly attributed to a change in consumption patterns, particularly with the availability of larger containers that enable higher daily intake 6 …”