Antibodies to myelin oligodendrocyte glycoprotein in idiopathic optic neuritis

Abstract

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.

MOG-IgG associated optic neuritis is not multiple sclerosis

“…As suggested by previous results (Table 3), MOG-IgG positive patients may present with a clinical diagnosis of idiopathic ON 9,11 or NMOSD 6,10 . The MOG-IgG patients frequently have recurrent or bilateral ON and the male predominance contrasts with the female predominance in MS.…”

Autoantibodies and pain

“…This showed not only a marked reduction in relapse rate, and AQP4-antibody titers, but also a reduction in pain severity scores [42 && ]. In addition it has been shown that, when compared with those NMO patients without either AQP4 or MOG antibodies, those with MOG autoantibodies also report a significantly higher level of pain [37]. These data suggest a link between pain and the inflammatory or neuropathological effect of autoantibodies in NMO.…”

“…In a large proportion of patients (around 70%) autoantibodies against the water channel aquaporin-4 (AQP4) are found [36]; a smaller proportion of those patients who are negative for AQP4-antibodies has antibodies against another molecule myelin oligodendrocyte glycoprotein (MOG) [37], but in these cases the disease is less longstanding. AQP4-antibody positive NMO patients can experience loss of vision and paralysis, but pain is a particularly common feature of NMO with more than 80% of sufferers experiencing this symptom, often persisting even when the disease is relatively quiescent and intractable to conventional pain killers [38 & ].…”

Anti-myelin Oligodendrocyte Glycoprotein Antibodies in a Patient with Recurrent Optic Neuritis Involving the Cerebral White Matter and Brainstem

“…Among anti-AQP4 antibody-seronegative NMO patients, 21.1% were reported to have anti-MOG antibodies (4). In a recent report of patients with idiopathic optic neuritis, 27.6% were positive for MOG antibodies and 3.4% were positive for AQP4; these patients often showed optic pain and high CSF levels of myelin basic protein (6). Although our patient showed cerebral involvement with contrast enhancement lesions, myelin basic protein was not elevated in her CSF, and no oligoclonal bands were present.…”

“…The pathomechanisms of these antibody-positive demyelinating disorders are unknown. Moreover, cerebral brain magnetic resonance imaging (MRI) abnormalities of patients with optic neuritis with anti-MOG antibodies occur less frequently than optic nerve lesions (6). We herein report the case of a patient who had optic neuritis with a long-term follow-up, anti-MOG antibodies, and abnormalities in the cerebral white matter and brainstem.…”