Background: Nitrous oxide is a widely available anaesthetic agent whose chronic use causes irreversible inactivation of vitamin B12, leading to subacute combined degeneration of the spinal cord (SACD). While high‑dose intramuscular B12 replacement often halts disease progression, complete neurological recovery is not always achieved. Case presentation: A 19‑year‑old Chinese male with a three month history of nitrous oxide use presented to the emergency department with acute lower‑limb weakness and encephalopathy. Examination revealed mild upper‑limb paresis, diminished deep tendon reflexes, and minimal voluntary movement in the legs. Laboratory studies showed pancytopenia, undetectable serum vitamin B12, and markedly elevated homocysteine. MRI of the brain and spine demonstrated generalised cerebral atrophy with white‑matter foci and extensive hyperintensity throughout the upper spinal cord. Complications included bilateral pulmonary emboli and lower‑limb deep venous thrombosis, managed initially with intravenous heparin followed by enoxaparin and a 6‑month course of apixaban. The patient received high‑dose intramuscular B12, oral methionine, thiamine, and supportive care for skin lesions. After a period of intense multidisciplinary rehabilitation, functional independence was restored although not complete neurological recovery. Conclusion: This case illustrates that nitrous oxide–induced SACD can present with profound neurological dysfunction but responds favourably to prompt vitamin B12 replacement, combined with multidisciplinary rehabilitation.
Smith et al. (Mon,) studied this question.