We report five cases of anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis. Five women (27-38 years), Who-presented with psychiatric symptoms, neurological complications, and decreased consciousness, were diagnosed with anti-NMDAR encephalitis after testing positive for serum anti-NMDAR antibodies. The mean（±SD）for hospitalization duration was 272.4（±144.8)days. All patients presented with respiratory failure due to central hypoventilation and required mechanical ventilation for 50.2（±13.1）days on average. Four patients showed no abnormal findings upon brain MRI, one showed high intensity lesions in the right temporal cortex and bilaterally in the hippocampus on T2 weighted images. Higher brain function assessment revealed an overall decrease in intelligence, attention, memory, and executive function in all patients. Temporal assessments revealed progressive improvement in these dysfunctions over several years. Four patients presented with deep venous thrombosis, articular contracture, ectopic ossification, and compression paralysis during the first immobility episode. Two had severely impaired communication and ability to perform activities of daily living when admitted for rehabilitation. However, eventually all the patients attained a premorbid state.
　Anti-NMDAR encephalitis possibly results from reversible synaptic dysfunction；therefore, it has a better functional prognosis compared with classical limbic encephalitis and other paraneoplastic neurologic syndromes. Previous studies found abnormalities in the limbic area on MRI in about 25％ of patients, although other findings were non-specific. Prevention of disuse syndrome due to prolonged immobility is important in acute phase rehabilitation. Our study shows that long-term temporal assessments of higher brain function are necessary and useful in the chronic stage.

A 56-year-old man was admitted to our hospital for the purpose of rehabilitation. Because this patient developed apallic syndrome 21 days after he recovered from his first coma, he was diagnosed with the interval form of carbon monoxide (CO) poisoning. On admission, he showed paralysis of all limbs, motor dysfunction due to joint contractures, pain, and higher brain dysfunction. These symptoms were consistent with magnetic resonance imaging (MRI) findings that the frontal white matter was mainly affected while the involvement in the basal ganglion was mild. Rehabilitation was continued, and his motor dysfunction was improved in a few months, although the higher brain dysfunction needed a longer term to improve. An interruption of his rehabilitation resulted in the exacerbation of the motor dysfunction. Subsequent complications of CO poisoning have been reported to be linked to the areas of the involvement revealed by MRI. Since CO poisoning can show various symptoms, a diversity of rehabilitation is required, according to the patients' symptoms. We think that rehabilitation is the most effective therapy for the subsequent complications of CO poisoning. Since the symptoms require a long time to improve, it is difficult to deal with them within the application of the existing health insurance and nursing care support regulations. We consider that rehabilitation for motor dysfunction and higher brain dysfunction are important, in addition to hyperbaric oxygen therapy in the acute stage of CO poisoning.