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Antibodies to myelin oligodendrocyte glycoprotein in idiopathic optic neuritis.

Nakajima H, Motomura M, Tanaka K, Fujikawa A, Nakata R, Maeda Y, Shima T, Mukaino A, Yoshimura S, Miyazaki T, Shiraishi H, Kawakami A, Tsujino A - BMJ Open (2015)

Bottom Line: 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.Although 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.

View Article: PubMed Central - PubMed

Affiliation: Unit of Translational Medicine, Department of Neurology and Strokology, Nagasaki University Hospital, Nagasaki, Japan.

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Patient enrolment flow chart. Ophthalmologists diagnosed ON with the disturbance of optic acuity, visual field, critical flicker frequency (CFF), brain MRI, optical coherence tomography (OCT) and fluorescein fundus angiography. ION, ischaemic optic neuropathy; LHON, Leber's hereditary optic neuropathy; MS, multiple sclerosis; NMO, neuromyelitis optica; NMOSD, neuromyelitis optica spectrum disorders; OAS, orbital apex syndrome; ON, optic neuritis; TAO, thyroid-associated ophthalmopathy; THS, Tolosa-Hunt syndrome; MOG, myelin oligodendrocyte glycoprotein.
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BMJOPEN2015007766F1: Patient enrolment flow chart. Ophthalmologists diagnosed ON with the disturbance of optic acuity, visual field, critical flicker frequency (CFF), brain MRI, optical coherence tomography (OCT) and fluorescein fundus angiography. ION, ischaemic optic neuropathy; LHON, Leber's hereditary optic neuropathy; MS, multiple sclerosis; NMO, neuromyelitis optica; NMOSD, neuromyelitis optica spectrum disorders; OAS, orbital apex syndrome; ON, optic neuritis; TAO, thyroid-associated ophthalmopathy; THS, Tolosa-Hunt syndrome; MOG, myelin oligodendrocyte glycoprotein.

Mentions: Between 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 at Nagasaki University Hospital, Japan. We excluded the patients who fulfilled the diagnostic criteria of NMO/NMOSD,9 MS McDonald's criteria,10 ischaemic optic neuropathies, orbital apex syndromes, Leber's hereditary optic neuropathies, tumours, trauma, thyroid-associated ophthalmopathy, pentazocine and alcohol-induced, Tolosa-Hunt syndrome, dissociated disorder and IgG4-related disease. Finally, we defined 29 patients with idiopathic ON as the study cohort (figure 1), and we retrospectively reviewed their clinical symptoms and results of their CSF examination, MRI studies and response to steroid therapies. We used ELISA for myelin basic protein (MBP) analysis, of which the cut-off level was 102 pg/mL. We prepared a standard protocol of steroid pulse therapy: methylprednisolone (mPSL) 1 g/day for three consecutive days per week for 1–5 weeks. We defined the terms to evaluate the responsiveness to steroid pulse therapies in the acute phase (before other treatments; eg, plasma exchange, fingolimod); ‘complete’ meant recovery to the patients’ original visual acuities, ‘good’ meant recovery to more than half of their original visual acuities, ‘not good’ meant less than ‘good’ within 1–5 courses of mPSL pulse therapies. All of the sera samples were obtained from the patients in an acute phase at their onset or recurrence. The range of follow-up period was 3–53 months (see online supplementary table).


Antibodies to myelin oligodendrocyte glycoprotein in idiopathic optic neuritis.

Nakajima H, Motomura M, Tanaka K, Fujikawa A, Nakata R, Maeda Y, Shima T, Mukaino A, Yoshimura S, Miyazaki T, Shiraishi H, Kawakami A, Tsujino A - BMJ Open (2015)

Patient enrolment flow chart. Ophthalmologists diagnosed ON with the disturbance of optic acuity, visual field, critical flicker frequency (CFF), brain MRI, optical coherence tomography (OCT) and fluorescein fundus angiography. ION, ischaemic optic neuropathy; LHON, Leber's hereditary optic neuropathy; MS, multiple sclerosis; NMO, neuromyelitis optica; NMOSD, neuromyelitis optica spectrum disorders; OAS, orbital apex syndrome; ON, optic neuritis; TAO, thyroid-associated ophthalmopathy; THS, Tolosa-Hunt syndrome; MOG, myelin oligodendrocyte glycoprotein.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4390681&req=5

BMJOPEN2015007766F1: Patient enrolment flow chart. Ophthalmologists diagnosed ON with the disturbance of optic acuity, visual field, critical flicker frequency (CFF), brain MRI, optical coherence tomography (OCT) and fluorescein fundus angiography. ION, ischaemic optic neuropathy; LHON, Leber's hereditary optic neuropathy; MS, multiple sclerosis; NMO, neuromyelitis optica; NMOSD, neuromyelitis optica spectrum disorders; OAS, orbital apex syndrome; ON, optic neuritis; TAO, thyroid-associated ophthalmopathy; THS, Tolosa-Hunt syndrome; MOG, myelin oligodendrocyte glycoprotein.
Mentions: Between 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 at Nagasaki University Hospital, Japan. We excluded the patients who fulfilled the diagnostic criteria of NMO/NMOSD,9 MS McDonald's criteria,10 ischaemic optic neuropathies, orbital apex syndromes, Leber's hereditary optic neuropathies, tumours, trauma, thyroid-associated ophthalmopathy, pentazocine and alcohol-induced, Tolosa-Hunt syndrome, dissociated disorder and IgG4-related disease. Finally, we defined 29 patients with idiopathic ON as the study cohort (figure 1), and we retrospectively reviewed their clinical symptoms and results of their CSF examination, MRI studies and response to steroid therapies. We used ELISA for myelin basic protein (MBP) analysis, of which the cut-off level was 102 pg/mL. We prepared a standard protocol of steroid pulse therapy: methylprednisolone (mPSL) 1 g/day for three consecutive days per week for 1–5 weeks. We defined the terms to evaluate the responsiveness to steroid pulse therapies in the acute phase (before other treatments; eg, plasma exchange, fingolimod); ‘complete’ meant recovery to the patients’ original visual acuities, ‘good’ meant recovery to more than half of their original visual acuities, ‘not good’ meant less than ‘good’ within 1–5 courses of mPSL pulse therapies. All of the sera samples were obtained from the patients in an acute phase at their onset or recurrence. The range of follow-up period was 3–53 months (see online supplementary table).

Bottom Line: 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.Although 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.

View Article: PubMed Central - PubMed

Affiliation: Unit of Translational Medicine, Department of Neurology and Strokology, Nagasaki University Hospital, Nagasaki, Japan.

Show MeSH
Related in: MedlinePlus