Abstract
Nitrous oxide (N(2)O) has been thought to be a harmless recreational substance by public perception, but it has been linked to subacute combined degeneration (SACD) due to induction of a functional vitamin B12 deficiency via oxidation and inactivation of the cobalt ion in its molecular structure. N(2)O has been rising in popularity due to several factors including accessibility, low cost, and low perceived risk, leading otherwise healthy people to develop what used to be a neurological disease experienced by select patient populations with dietary restrictions or medical conditions leading to low levels of vitamin B12. Vitamin B12 plays a crucial role in many cellular processes, and loss of functional vitamin B12 cannot be detected by measuring it directly. Substrates from its metabolic pathways such as homocysteine and methylmalonic acid must be measured to check its functional status. Vitamin B12 deficiency also leads to a hypercoagulable state due to the build-up of homocysteine in the blood. We present the case of a 26-year-old male who had reportedly used N(2)O for six months leading to SACD and a popliteal deep vein thrombosis. The options for treatment are abstaining from substance use and vitamin B12 supplementation; however, full recovery after SACD develops is unlikely and patients may be left with permanent neurological dysfunction from N(2)O use.