ObjectivesTo investigate the differences of clinical features, cerebrospinal fluid (CSF), MRI findings and response to steroid therapies between patients with optic neuritis (ON) who have myelin oligodendrocyte glycoprotein (MOG) antibodies and those who have seronegative ON.SettingWe recruited participants in the department of neurology and ophthalmology in our hospital in Japan.MethodsWe retrospectively evaluated the clinical features and response to steroid therapies of patients with ON. Sera from patients were tested for antibodies to MOG and aquaporin-4 (AQP4) with a cell-based assay.ParticipantsBetween April 2009 and March 2014, we enrolled serial 57 patients with ON (27 males, 30 females; age range 16–84 years) who ophthalmologists had diagnosed as having or suspected to have ON with acute visual impairment and declined critical flicker frequency, abnormal findings of brain MRI, optical coherence tomography and fluorescein fundus angiography at their onset or recurrence. We excluded those patients who fulfilled the diagnostic criteria of neuromyelitis optica (NMO)/NMO spectrum disorders (NMOSD), MS McDonald's criteria, and so on. Finally we defined 29 patients with idiopathic ON (14 males, 15 females, age range 16–84 years).Results27.6% (8/29) were positive for MOG antibodies and 3.4% (1/29) were positive for AQP4. Among the eight patients with MOG antibodies, five had optic pain (p=0.001) and three had prodromal infection (p=0.179). Three of the eight MOG-positive patients showed significantly high CSF levels of myelin basic protein (p=0.021) and none were positive for oligoclonal band in CSF. On MRIs, seven MOG-positive patients showed high signal intensity on optic nerve, three had a cerebral lesion and one had a spinal cord lesion. Seven of the eight MOG-positive patients had a good response to steroid therapy.ConclusionsAlthough not proving primary pathogenicity of anti-MOG antibodies, the present results indicate that the measurement of MOG antibodies is useful in diagnosing and treating ON.

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A 63-year-old Japanese woman with a 30-year history of systemic lupus erythematosus developed macrohematuria and massive proteinuria after seroconversion of myeloperoxidase anti-neutrophil cytoplasmic antibodies (MPO-ANCA). A renal biopsy indicated focal proliferative lupus nephritis (class III A/C) with a fibrous crescent formation. Methylprednisolone pulse therapy (500 mg, 3 successive days) was administered because of progressive proteinuria. Steroid therapy did not suppress the progressive proteinuria; therefore, tacrolimus was added as an alternative immunosuppressive therapy, resulting in the improvement of proteinuria and renal impairment. This case report suggests that MPO-ANCA might play a pathogenic role in the exacerbation of immune-complex-type lupus nephritis.

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A 79-year-old man presented to the emergency room with sudden onset of dysarthria followed by coma. Eight months before admission, he had undergone C1-C2 posterior fusion. Brain MRI showed multiple posterior circulation infarcts. He experienced resolution of symptoms after intravenous thrombolysis. CT angiography revealed the irregularity of the V3 segment of the right vertebral artery where the cervical screw contacted. Although the dual antiplatelet therapy with aspirin and clopidogrel had been started, he developed severe consciousness disturbance, quadriplegia, and decerebrate posturing to painful stimuli on the 24th hospital day. His eyes were fixed in the midline. Diffusionweighted imaging revealed a subtle hyperintense lesion in the pons, and MR angiography showed basilar artery occlusion. He underwent mechanical thrombectomy. Complete recanalization was achieved on the second attempt using a stent retriever, and the patient s condition recovered to pretreatment level. Heparin and cilostazol were started after the discontinuation of aspirin and clopidogrel. On the 52nd hospital day, the right vertebral artery sacrifice with coil embolization was performed to prevent recurrences. Cerebral infarction could occur as a long-term complication of C1-C2 posterior fusion. A vertebral artery injury at the site of cervical screw contact could be one of the causes of the complication. Endovascular parent artery occlusion should be considered in ischemic stroke patients who have vertebral artery legions after cervical spine surgery.