Nitrous oxide induced subacute combined degeneration of the spine cord: A case report

Abstract

Rationale: In recent years, recreational use of inhaled nitrous oxide (N2O) is on the increase among young people, accompanied by a corresponding rise in reports about its toxicity. Subacute combined degeneration of the spine cord (SCD) is the typical clinical picture of the nervous system disorder caused by N2O intoxication, as a result of metabolic disturbance of vitamin B12. Patient concerns, diagnoses, interventions and outcomes: We report a 28-year-old female of SCD due to prolonged use of N2O, presented with paresthesia and unsteady in walking progressing within 1 month. Symptoms gradually improved with the treatment of intramuscular injections of hydroxocobalamin combined with N2O abstinence, and the patient recovered completely with normal neurological examination after 4 months of follow-up. Lessons: Clinicians should be aware of the clinical features and pathogenesis of SCD caused by N2O intoxication in order to lead effective treatment as soon as possible. Recreational N2O use should always be considered as an etiology when dealing with patients presented with myelopathy and/or neuropathy suspected of vitamin B12 deficiency.

Nitrous Oxide as an Emerging Cause of Subacute Combined Degeneration and Polyneuropathy: A Two-Case Report

“…The clinical presentation of our cases is similar to that of cases previously described by other authors [3,10,11,13,14,18,19]. They exhibit certain characteristics that need to be highlighted.…”

“…Methionine synthase changes homocysteine into methionine, which is then converted into Sadenosylmethionine, an important methyl group donor that helps methylate myelin basic protein (MBP) [14]. A highly methylated MBP is critical for maintaining myelin integrity; therefore, a deficiency in its methylation can lead to demyelination [14]. This metabolic pathway is shown in Figure 3.…”

“…The failure of this pathway leads to the accumulation of methylmalonyl-CoA and propionyl-CoA, which retrogradely induces an increase in odd-chain and branched-chain fatty acids that accumulate in the lipids of the membranes of the nervous system. Changes in the fatty acid composition of myelin can alter its integrity and cause demyelination [5,11,13,14]. This metabolic pathway can be seen in detail in Figure 4.…”

“…Neurological complications such as subacute combined degeneration (SCD) and polyneuropathy, previously mentioned, could result from this [6,7,11,12]. In addition, neuropsychiatric symptoms may also occur [2,10,12,14]. This may include apathy, memory impairment, personality changes, emotional lability, and, in more severe cases, impulsive and aggressive behaviors, psychosis, and visual and auditory hallucinations [10].…”

“…The functional alteration of the aforementioned metabolic pathways leads to the accumulation and elevation of homocysteine (due to failure of methionine synthase) and methylmalonic acid (due to failure of methylmalonyl-CoA mutase) [13,14]. Furthermore, it has consequences for the function of the nervous system by generating alterations in the formation and maintenance of myelin sheaths and a deficit in energy production in the axons [1,11,13,14]. Neurological complications such as subacute combined degeneration (SCD) and polyneuropathy, previously mentioned, could result from this [6,7,11,12].…”