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JNNP Online First, published on March 6, 2015 as 10.1136/jnnp-2014-310206
LETTER
MRI and retinal abnormalities in isolated optic neuritis with myelin oligodendrocyte glycoprotein and aquaporin-4 antibodies: a comparative study INTRODUCTION Acute optic neuritis (ON) typically presents with ocular pain and low visual acuity (VA), and there is a risk of permanent vision loss if ON is not managed properly.1 ON may be the first symptom of inflammatory diseases of the central nervous system (CNS), such as multiple sclerosis and neuromyelitis optica spectrum disorder (NMOSD). Recently, we reported some distinct characteristics between seropositive antiaquaporin-4 (anti-AQP4) patients and seropositive antimyelin oligodendrocyte glycoprotein (anti-MOG) patients with NMOSD, using our in-house cell-based assays (CBA). However, patients with a single attack of unilateral ON were not included in our previous study. None of the previous studies of anti-MOG+ patients performed orbital MRI or optical coherence tomography (OCT) segmentation analyses, which may have diagnostic and prognostic implications. To address these issues, we evaluated the diagnostic utility of the anti-MOG assay and compared the MRI and OCT findings of anti-MOG+ and anti-AQP4+ patients with isolated ON.
PATIENTS AND METHODS Patients We investigated 28 affected ON eyes from 21 consecutive anti-AQP4 seronegative patients aged 12 years or older who presented with isolated ON (4 cases with
PostScript
simultaneous bilateral ON, 3 cases with relapsing unilateral ON, and 14 cases with a single attack of unilateral ON) and were admitted to Tohoku University Hospital between 2011 and 2013. We excluded patients with ON already associated with brain and/or spinal cord MRI lesions. We compared anti-MOG+ ON eyes with nine affected ON eyes from eight anti-AQP4+ patients with isolated ON (one simultaneous bilateral ON). Severe VA loss was set at 0.1 in the decimal Japanese chart (equivalent to 20/200).2
Statistical analysis
Orbital MRI
RESULTS Anti-MOG serological status and clinical recovery after treatment
All patients performed orbital imaging using a 1.5 T MRI. We measured the short τ inversion recovery (STIR) and/or T2-weighted image hyperintense lesions in anatomical segments of the optic nerve.3 We also evaluated the presence of contrast-enhancing lesions.
Spectral domain OCT Spectral domain OCT with automated retinal segmentation was performed using a three-dimensional OCT-2000 with system software V.8.11 (Topcon Corp, Tokyo, Japan) during the follow-up (6 months after ON episodes). We evaluated ganglion cell-inner plexiform layer (GCIPL) and retinal nerve fibre layer (RNFL) thickness.
Anti-MOG CBA Sera collected during acute ON attacks from the 21 idiopathic isolated ON patients were tested blindly for anti-MOG using our in-house CBA as previously reported with slight modifications.4 We used stably transfected full-length MOG-expressing cells and a goat antihuman Fc-specific IgG crossadsorbed secondary antibody (Pierce Biotechnology, Rockford, Illinois, USA) to reduce the risk of light chain cross-reactivity from other immunoglobulin subclasses.
Non-parametric tests (Wilcoxon tests) were used to compare the clinical data and CBA titres between patient groups. Categorical data from the study were analysed using Fisher’s exact test and p
JNNP Online First, published on March 6, 2015 as 10.1136/jnnp-2014-310206
LETTER
MRI and retinal abnormalities in isolated optic neuritis with myelin oligodendrocyte glycoprotein and aquaporin-4 antibodies: a comparative study INTRODUCTION Acute optic neuritis (ON) typically presents with ocular pain and low visual acuity (VA), and there is a risk of permanent vision loss if ON is not managed properly.1 ON may be the first symptom of inflammatory diseases of the central nervous system (CNS), such as multiple sclerosis and neuromyelitis optica spectrum disorder (NMOSD). Recently, we reported some distinct characteristics between seropositive antiaquaporin-4 (anti-AQP4) patients and seropositive antimyelin oligodendrocyte glycoprotein (anti-MOG) patients with NMOSD, using our in-house cell-based assays (CBA). However, patients with a single attack of unilateral ON were not included in our previous study. None of the previous studies of anti-MOG+ patients performed orbital MRI or optical coherence tomography (OCT) segmentation analyses, which may have diagnostic and prognostic implications. To address these issues, we evaluated the diagnostic utility of the anti-MOG assay and compared the MRI and OCT findings of anti-MOG+ and anti-AQP4+ patients with isolated ON.
PATIENTS AND METHODS Patients We investigated 28 affected ON eyes from 21 consecutive anti-AQP4 seronegative patients aged 12 years or older who presented with isolated ON (4 cases with
PostScript
simultaneous bilateral ON, 3 cases with relapsing unilateral ON, and 14 cases with a single attack of unilateral ON) and were admitted to Tohoku University Hospital between 2011 and 2013. We excluded patients with ON already associated with brain and/or spinal cord MRI lesions. We compared anti-MOG+ ON eyes with nine affected ON eyes from eight anti-AQP4+ patients with isolated ON (one simultaneous bilateral ON). Severe VA loss was set at 0.1 in the decimal Japanese chart (equivalent to 20/200).2
Statistical analysis
Orbital MRI
RESULTS Anti-MOG serological status and clinical recovery after treatment
All patients performed orbital imaging using a 1.5 T MRI. We measured the short τ inversion recovery (STIR) and/or T2-weighted image hyperintense lesions in anatomical segments of the optic nerve.3 We also evaluated the presence of contrast-enhancing lesions.
Spectral domain OCT Spectral domain OCT with automated retinal segmentation was performed using a three-dimensional OCT-2000 with system software V.8.11 (Topcon Corp, Tokyo, Japan) during the follow-up (6 months after ON episodes). We evaluated ganglion cell-inner plexiform layer (GCIPL) and retinal nerve fibre layer (RNFL) thickness.
Anti-MOG CBA Sera collected during acute ON attacks from the 21 idiopathic isolated ON patients were tested blindly for anti-MOG using our in-house CBA as previously reported with slight modifications.4 We used stably transfected full-length MOG-expressing cells and a goat antihuman Fc-specific IgG crossadsorbed secondary antibody (Pierce Biotechnology, Rockford, Illinois, USA) to reduce the risk of light chain cross-reactivity from other immunoglobulin subclasses.
Non-parametric tests (Wilcoxon tests) were used to compare the clinical data and CBA titres between patient groups. Categorical data from the study were analysed using Fisher’s exact test and p
