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We present a case of a 59-year-old female who had been treated for optic neuritis 2 years before being transferred to our hospital. She had been positive for anti-AQP4 antibodies. No cerebrospinal lesions were observed, and based on the diagnosis of neuromyelitis optica spectrum disorder (NMOSD), 5 mg/day oral prednisolone was continued for 2 years. Acute lower back pain and urinary retention appeared on day X. On day X + 1, consciousness disturbance (JCS level II) and paraplegia appeared, and she was transferred to our hospital. Neck stiffness, paraplegia, and urinary retention were present. A cerebrospinal fluid examination revealed mononucleosis-dominant pleocytosis (1,232 cells/μl). Brain magnetic resonance imaging (MRI) showed multiple lesions around the ventricles and corpus callosum, and spinal MRI revealed a longitudinally extensive transverse myelitis lesion (C2-Th5). A relapse of NMOSD was diagnosed and steroid pulse therapy was started, but the symptoms progressed and quadriplegia and coma occurred. Head MRI showed new deep white matter lesions around the ventricles. Plasma exchange was added after the second steroid pulse. The patient's consciousness gradually improved, and spontaneous movement of the left upper limb eventually appeared. We experienced a case of NMOSD that relapsed with multiple cerebrospinal lesions despite corticosteroid therapy, but plasmapheresis therapy was effective.

We report a 55 year old Japanese man with a history of alcohol abuse, who was in a near fasting state for the previous few days.He was admitted to our hospital with abrupt disturbance of consciousness. He presented disturbance of consciousness with extreme hypoglycemia and ketoacidosis with high β-hydroxybutyric acid concentration. Taking into account his living history, we diagnosed with alcoholic ketoacidosis (AKA). Symptoms ameliorated with glucose injection and fluid loading. AKA patients show abdominal pain, nausea or vomiting, but they are usually alert and lucid despite the severe acidosis. This case, however, presented comatose status caused by hypoglycemia. Poor oral intake of this patient was assumed to be the cause of hypoglycemia. Alcoholism may cause hypoglycemia accompanying with AKA, due to a low carbohydrate intake, the inhibition of gluconeogenesis, and reduced hepaticglycogen storage as seen in this case. Here, we report a case of AKA that demonstrated hypoglycemia with the literature review.