Inhalants spotlight: the B12 story behind the spinal cord damage

Inhalants are a category we keep returning to because the harm pattern is unusually unforgiving — fast, hard to reverse if missed, and concentrated in adolescents and young adults whose neurology is still developing. The recent science is sharpening on one specific mechanism: how nitrous oxide (“whippets,” “galaxy gas”) depletes vitamin B12, how that depletion damages the spinal cord, and how short the window is to repair the damage when it’s caught.

The biology

Nitrous oxide irreversibly oxidizes the cobalt center of vitamin B12, deactivating it as a cofactor for the methionine synthase pathway. The body relies on that pathway to maintain myelin — the insulating sheath that lets nerve signals travel quickly down the spinal cord. With sustained N2O exposure, B12 stores drop, methionine synthase activity falls, myelin breaks down, and the part of the cord most dependent on it — the dorsal columns — begins to fail. Clinically, that shows up first as numbness or tingling in the feet, then unsteady walking, then weakness. The pattern has a name in neurology: subacute combined degeneration of the spinal cord. It’s the same disease historically caused by untreated pernicious anemia. Recreational nitrous oxide use, often heavy and concentrated over weeks or months, can recreate that disease in someone whose B12 baseline was previously normal.

What’s new in the imaging evidence

In January 2026, researchers at the Royal College of Surgeons in Ireland published a 14-case retrospective in the American Journal of Neuroradiology — summarized in their public release here — documenting MRI-confirmed spinal cord damage in young people who had been using nitrous oxide recreationally. Median patient age: 20. All cases occurred between 2021 and the end of 2024, a sharp post-pandemic uptick. The paper’s contribution is to take a story that had been told in case reports and turn it into an imaging-grade case series with consistent radiological findings — a step that tends to change how clinicians think about a syndrome.

What the treatment evidence says

A clinical perspective published by Yale School of Medicine emphasizes the part of the story families need to hear most clearly: when caught early, the damage is reversible. High-dose B12 supplementation — typically intramuscular or oral cobalamin, paired with cessation of N2O use — can restore methionine synthase activity, allow remyelination, and resolve symptoms entirely in many patients. The window is measured in weeks to months, not days, but it’s not unlimited. Cases identified late, especially after persistent gait dysfunction has set in, can show only partial recovery. Roughly 96% of N2O-induced B12 deficiency cases involve neurological symptoms — meaning by the time the deficiency is recognized, neurological assessment is essentially always indicated.

Where the field disagrees

The clinical literature is converging. The policy literature is not. Some jurisdictions are pursuing supply-side restrictions on commercial nitrous oxide canisters — the U.K.’s 2023 ban, several U.S. states moving against “Galaxy Gas”-style flavored canisters — while others are emphasizing harm reduction and B12 surveillance among heavy users. The harm-reduction-first camp argues that supply restrictions push use toward less-regulated dispensers; the supply-side-first camp argues that the access ease, low price, and absence of legal friction are driving the trend. Both camps agree on one thing: the demographic most at risk is teens and young adults, and the Brain Injury Association of Arizona has been raising the local alarm for Phoenix-area families.

Resources and what to watch for

If you or someone you love uses nitrous oxide recreationally, the early warning signs that justify a clinical visit are: persistent numbness or tingling in the feet, a feeling of “walking on cotton,” unsteady gait, or new clumsiness. A B12 level, a methylmalonic acid level, and — if symptoms warrant — an MRI of the cervical and thoracic spine give clinicians the data they need. Treatment is usually outpatient.

A B12 level, a methylmalonic acid level, and — if symptoms warrant — an MRI of the cervical and thoracic spine give clinicians the data they need.

Rize Recovery can help connect you to providers familiar with inhalant-related neurology and the broader treatment landscape.

If you’re in crisis, call or text 988. If you suspect acute neurological symptoms in yourself or someone else, go to the nearest emergency department — early evaluation is the single biggest predictor of recovery.