Background: Nitrous oxide is a colourless, odourless gas that has been used in medicine for more than 150 years for its anaesthetic and analgesic properties. Its first recorded use as a recreational drug was in early 19th century Britain at 'laughing gas parties', where it was used to provide short-lived euphoria to the bored upper class. A recent resurgence of its abuse among Australian youth has led to marked neurological morbidity.
Objective: The aim of this article is to provide an overview of the clinical presentation, differential diagnosis, investigation and treatment of patients presenting with neurotoxicity due to recreational nitrous oxide abuse.
Discussion: Nitrous oxide exerts its neurotoxicity through vitamin B12 inactivation, which disrupts myelin sheath maintenance, leading to peripheral and central nervous system demyelination. Importantly, patients often present with non-specific sensorimotor signs and symptoms with normal serum vitamin B12 levels. Early recognition and treatment are crucial to limit long-term neurological sequelae.