Vitamin B12 (Cobalamin) deficiency is a well-known cause of central and peripheral nervous system dysfunction, including sensorimotor peripheral neuropathy. Methylmalonate CoA mutase and homocysteine methyltransferase are cobalamin dependent enzymes. In cobalamin deficiency, the metabolic reactions catalysed by these enzymes are inhibited, resulting in the accumulation of methylmalonic acid (MMA) and homocysteine in the blood. High plasma levels of MMA and homocysteine indicate functional (organic) B12 deficiency in individuals with normal renal function and normal or low B12 level. Nitrous oxide (N₂O) is a poorly recognised cause of vitamin B12 deficiency and subsequent neuropathy/myelopathy. We present a case of 27 year old male who was diagnosed with a functional (psychogenic) right lower limb focal dystonia. His severely painful right leg paroxysmal spasms were treated on more than fifty occasions with Entonox (50:50 n₂O and oxygen mixture) over the five years. He developed an axonal sensorimotor neuropathy and was diagnosed with a functional (organic) B12 deficiency related to N₂O administration. His pre-treatment vitamin B12 levels were normal. However, levels of MMA and homocysteine were high. He was advised complete cessation of N₂O, B12 injections and cognitive behavioural therapy for the functional limb dystonia. Post-treatment, his sensory symptoms resolved and MMA and homocysteine levels normalised.