Psychiatric comorbidities in a young man with subacute myelopathy induced by abusive nitrous oxide consumption: a case report.
Falk Mancke, Gintarė Kaklauskaitė, Jennifer Kollmer, Markus Weiler
Substance abuse and rehabilitation January 1, 2016 DOI: 10.2147/sar.s114404 via PubMed
Summary
AI-generated from the abstractA 35-year-old man with MRI-confirmed subacute myelopathy from nitrous oxide (N2O) use also had cannabinoid and nicotine dependence and abused amphetamines, cocaine, LSD, and ketamine. A transient psychotic and depressive episode from synthetic cannabinoid abuse preceded these findings. The case highlights that N2O toxicity can cause irreversible neurological damage if untreated for months, making it essential to consider N2O in patients with substance use disorders who develop new neurological deficits.
Study at a glance
| Characteristics | Case study Case report Peer reviewed |
|---|---|
| Sample size | 1 |
| Population | 35-year-old male with N2O-induced subacute myelopathy and comorbid substance use disorders |
| Topics | Addiction |
| Keywords | Addictive disorders Laughing gas Subacute combined degeneration Vitamin b12 deficiency |
| Key finding | N2O consumption can cause subacute myelopathy that may become irreversible if untreated for months, and clinicians should routinely exclude N2O toxicity in patients with substance use disorders and new neurological deficits. |
Abstract
Nitrous oxide (N2O), a long-standing anesthetic, is known for its recreational use, and its consumption is on the rise. Several case studies have reported neurological and psychiatric complications of N2O use. To date, however, there has not been a study using standardized diagnostic procedures to assess psychiatric comorbidities in a patient consuming N2O. Here, we report about a 35-year-old male with magnetic resonance imaging confirmed subacute myelopathy induced by N2O consumption, who suffered from comorbid cannabinoid and nicotine dependence as well as abuse of amphetamines, cocaine, lysergic acid diethylamide, and ketamine. Additionally, there was evidence of a preceding transient psychotic and depressive episode induced by synthetic cannabinoid abuse. In summary, this case raises awareness of an important mechanism of neural toxicity, with which physicians working in the field of substance-related disorders should be familiar. In fact, excluding N2O toxicity in patients with recognized substance-related disorders and new neurological deficits is compulsory, as untreated for months the damage to the nervous system is at risk of becoming irreversible.