Abstract
Vitamin B12 deficiency-associated myeloneuropathy is a combination of subacute combined degeneration of the spinal cord and peripheral neuropathy. There are various causes of vitamin B12 deficiency, including diet mistakes, gastrointestinal diseases, genetic disorders, and medication intake. We present a clinical case of a 20-year-old male with myeloneuropathy due to vitamin B12 deficiency. The symptoms had been developing for four to five months, and upon admission to our clinic, the patient was presented with superficial and deep sensation deficit, distal paresthesia, muscle weakness, spastic-paretic gait, and the feeling of incomplete emptying of the bladder after urinating. The MRI revealed hyperintense lesions in cervical and thoracic areas of the spinal cord, and the electroneurogram indicated decreased conduction speed and severe axonal damage of the peripheral nerves. The patient admitted about transitional abdominal pain for years and chronic overuse of nitrous oxide (laughing gas) before symptom onset. Treatment with intramuscular vitamin B12 was started. The patient was also diagnosed with chronic gastritis and treated with antibiotics for 10 days and a proton pump inhibitor for 30 days. After a nine-month treatment course with vitamin B12, the patient significantly improved, although some mild symptoms persisted. The clinical case demonstrates the importance of taking into consideration vitamin B12 deficiency when diagnosing myelopathy and/or peripheral neuropathy. Vitamin B12 deficiency-associated neurological conditions are easy to treat and potentially fully reversible if diagnosed on time.