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MOG-IgG in NMO and related disorders: a multicenter study of 50 patients. Part 4: Afferent visual system damage after optic neuritis in MOG-IgG-seropositive versus AQP4-IgG-seropositive patients.
J Neuroinflammation. 2016 11 01; 13(1):282.JN

Abstract

BACKGROUND

Antibodies against myelin oligodendrocyte glycoprotein (MOG-IgG) have been reported in patients with aquaporin-4 antibody (AQP4-IgG)-negative neuromyelitis optica spectrum disorders (NMOSD). The objective of this study was to describe optic neuritis (ON)-induced neuro-axonal damage in the retina of MOG-IgG-positive patients in comparison with AQP4-IgG-positive NMOSD patients.

METHODS

Afferent visual system damage following ON was bilaterally assessed in 16 MOG-IgG-positive patients with a history of ON and compared with that in 16 AQP4-IgG-positive NMOSD patients. In addition, 16 healthy controls matched for age, sex, and disease duration were analyzed. Study data included ON history, retinal optical coherence tomography, visual acuity, and visual evoked potentials.

RESULTS

Eight MOG-IgG-positive patients had a previous diagnosis of AQP4-IgG-negative NMOSD with ON and myelitis, and eight of (mainly recurrent) ON. Twenty-nine of the 32 eyes of the MOG-IgG-positive patients had been affected by at least one episode of ON. Peripapillary retinal nerve fiber layer thickness (pRNFL) and ganglion cell and inner plexiform layer volume (GCIP) were significantly reduced in ON eyes of MOG-IgG-positive patients (pRNFL = 59 ± 23 μm; GCIP = 1.50 ± 0.34 mm3) compared with healthy controls (pRNFL = 99 ± 6 μm, p < 0.001; GCIP = 1.97 ± 0.11 mm3, p < 0.001). Visual acuity was impaired in eyes after ON in MOG-IgG-positive patients (0.35 ± 0.88 logMAR). There were no significant differences in any structural or functional visual parameters between MOG-IgG-positive and AQP4-IgG-positive patients (pRNFL: 59 ± 21 μm; GCIP: 1.41 ± 0.27 mm3; Visual acuity = 0.72 ± 1.09 logMAR). Importantly, MOG-IgG-positive patients had a significantly higher annual ON relapse rate than AQP4-IgG-positive patients (median 0.69 vs. 0.29 attacks/year, p = 0.004), meaning that on average a single ON episode caused less damage in MOG-IgG-positive than in AQP4-IgG-positive patients. pRNFL and GCIP loss correlated with the number of ON episodes in MOG-IgG-positive patients (p < 0.001), but not in AQP4-IgG-positive patients.

CONCLUSIONS

Retinal neuro-axonal damage and visual impairment after ON in MOG-IgG-positive patients are as severe as in AQP4-IgG-positive NMOSD patients. In MOG-IgG-positive patients, damage accrual may be driven by higher relapse rates, whereas AQP4-IgG-positive patients showed fewer but more severe episodes of ON. Given the marked damage in some of our MOG-IgG-positive patients, early diagnosis and timely initiation and close monitoring of immunosuppressive therapy are important.

Authors+Show Affiliations

NeuroCure Clinical Research Center (NCRC), Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany. Department of Neurology, Charité - Universitätsmedizin Berlin, Berlin, Germany.NeuroCure Clinical Research Center (NCRC), Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany. Department of Neurology, Charité - Universitätsmedizin Berlin, Berlin, Germany.NeuroCure Clinical Research Center (NCRC), Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany.NeuroCure Clinical Research Center (NCRC), Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany.NeuroCure Clinical Research Center (NCRC), Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany.NeuroCure Clinical Research Center (NCRC), Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany.NeuroCure Clinical Research Center (NCRC), Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany. Experimental and Clinical Research Center, Max Delbrück Center for Molecular Medicine and Charité - Universitätsmedizin Berlin, Berlin, Germany.Molecular Neuroimmunology Group, Department of Neurology, University of Heidelberg, Heidelberg, Germany.Molecular Neuroimmunology Group, Department of Neurology, University of Heidelberg, Heidelberg, Germany.Clinical Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.Division of Neurology, Children's Hospital of Philadelphia, Pennsylvania, USA.Department of Neurology, Vejle Hospital, Vejle, Denmark. Department of Neurobiology, Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark.Department of Neurology, Vejle Hospital, Vejle, Denmark. Department of Neurobiology, Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark.Department of Neurology, Medical Faculty, Heinrich Heine University, Düsseldorf, Germany.Department of Neurology, Medical Faculty, Heinrich Heine University, Düsseldorf, Germany.Department of Ophthalmology, Medical Faculty, University of Freiburg, Freiburg, Germany.Department of Neurology, University of Würzburg, Würzburg, Germany.Department of Ophthalmology, University of Würzburg, Würzburg, Germany.Department of Neurology, Charité - Universitätsmedizin Berlin, Berlin, Germany.NeuroCure Clinical Research Center (NCRC), Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany. Department of Neurology, Charité - Universitätsmedizin Berlin, Berlin, Germany. Experimental and Clinical Research Center, Max Delbrück Center for Molecular Medicine and Charité - Universitätsmedizin Berlin, Berlin, Germany.NeuroCure Clinical Research Center (NCRC), Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany. Alexander.Brandt@charite.de.No affiliation info available

Pub Type(s)

Journal Article
Multicenter Study
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

27802824

Citation

Pache, Florence, et al. "MOG-IgG in NMO and Related Disorders: a Multicenter Study of 50 Patients. Part 4: Afferent Visual System Damage After Optic Neuritis in MOG-IgG-seropositive Versus AQP4-IgG-seropositive Patients." Journal of Neuroinflammation, vol. 13, no. 1, 2016, p. 282.
Pache F, Zimmermann H, Mikolajczak J, et al. MOG-IgG in NMO and related disorders: a multicenter study of 50 patients. Part 4: Afferent visual system damage after optic neuritis in MOG-IgG-seropositive versus AQP4-IgG-seropositive patients. J Neuroinflammation. 2016;13(1):282.
Pache, F., Zimmermann, H., Mikolajczak, J., Schumacher, S., Lacheta, A., Oertel, F. C., Bellmann-Strobl, J., Jarius, S., Wildemann, B., Reindl, M., Waldman, A., Soelberg, K., Asgari, N., Ringelstein, M., Aktas, O., Gross, N., Buttmann, M., Ach, T., Ruprecht, K., ... Brandt, A. U. (2016). MOG-IgG in NMO and related disorders: a multicenter study of 50 patients. Part 4: Afferent visual system damage after optic neuritis in MOG-IgG-seropositive versus AQP4-IgG-seropositive patients. Journal of Neuroinflammation, 13(1), 282.
Pache F, et al. MOG-IgG in NMO and Related Disorders: a Multicenter Study of 50 Patients. Part 4: Afferent Visual System Damage After Optic Neuritis in MOG-IgG-seropositive Versus AQP4-IgG-seropositive Patients. J Neuroinflammation. 2016 11 1;13(1):282. PubMed PMID: 27802824.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - MOG-IgG in NMO and related disorders: a multicenter study of 50 patients. Part 4: Afferent visual system damage after optic neuritis in MOG-IgG-seropositive versus AQP4-IgG-seropositive patients. AU - Pache,Florence, AU - Zimmermann,Hanna, AU - Mikolajczak,Janine, AU - Schumacher,Sophie, AU - Lacheta,Anna, AU - Oertel,Frederike C, AU - Bellmann-Strobl,Judith, AU - Jarius,Sven, AU - Wildemann,Brigitte, AU - Reindl,Markus, AU - Waldman,Amy, AU - Soelberg,Kerstin, AU - Asgari,Nasrin, AU - Ringelstein,Marius, AU - Aktas,Orhan, AU - Gross,Nikolai, AU - Buttmann,Mathias, AU - Ach,Thomas, AU - Ruprecht,Klemens, AU - Paul,Friedemann, AU - Brandt,Alexander U, AU - ,, Y1 - 2016/11/01/ PY - 2016/04/01/received PY - 2016/09/09/accepted PY - 2016/11/3/pubmed PY - 2017/10/7/medline PY - 2016/11/3/entrez KW - Devic syndrome KW - Myelin oligodendrocyte glycoprotein antibodies (MOG-IgG) KW - NMO-IgG KW - aquaporin-4 antibodies (AQP4-IgG) KW - neuromyelitis optica KW - neuromyelitis optica spectrum disorders (NMOSD) KW - optic neuritis KW - optical coherence tomography KW - retinal neuro-axonal damage KW - visual acuity KW - visual evoked potentials SP - 282 EP - 282 JF - Journal of neuroinflammation JO - J Neuroinflammation VL - 13 IS - 1 N2 - BACKGROUND: Antibodies against myelin oligodendrocyte glycoprotein (MOG-IgG) have been reported in patients with aquaporin-4 antibody (AQP4-IgG)-negative neuromyelitis optica spectrum disorders (NMOSD). The objective of this study was to describe optic neuritis (ON)-induced neuro-axonal damage in the retina of MOG-IgG-positive patients in comparison with AQP4-IgG-positive NMOSD patients. METHODS: Afferent visual system damage following ON was bilaterally assessed in 16 MOG-IgG-positive patients with a history of ON and compared with that in 16 AQP4-IgG-positive NMOSD patients. In addition, 16 healthy controls matched for age, sex, and disease duration were analyzed. Study data included ON history, retinal optical coherence tomography, visual acuity, and visual evoked potentials. RESULTS: Eight MOG-IgG-positive patients had a previous diagnosis of AQP4-IgG-negative NMOSD with ON and myelitis, and eight of (mainly recurrent) ON. Twenty-nine of the 32 eyes of the MOG-IgG-positive patients had been affected by at least one episode of ON. Peripapillary retinal nerve fiber layer thickness (pRNFL) and ganglion cell and inner plexiform layer volume (GCIP) were significantly reduced in ON eyes of MOG-IgG-positive patients (pRNFL = 59 ± 23 μm; GCIP = 1.50 ± 0.34 mm3) compared with healthy controls (pRNFL = 99 ± 6 μm, p < 0.001; GCIP = 1.97 ± 0.11 mm3, p < 0.001). Visual acuity was impaired in eyes after ON in MOG-IgG-positive patients (0.35 ± 0.88 logMAR). There were no significant differences in any structural or functional visual parameters between MOG-IgG-positive and AQP4-IgG-positive patients (pRNFL: 59 ± 21 μm; GCIP: 1.41 ± 0.27 mm3; Visual acuity = 0.72 ± 1.09 logMAR). Importantly, MOG-IgG-positive patients had a significantly higher annual ON relapse rate than AQP4-IgG-positive patients (median 0.69 vs. 0.29 attacks/year, p = 0.004), meaning that on average a single ON episode caused less damage in MOG-IgG-positive than in AQP4-IgG-positive patients. pRNFL and GCIP loss correlated with the number of ON episodes in MOG-IgG-positive patients (p < 0.001), but not in AQP4-IgG-positive patients. CONCLUSIONS: Retinal neuro-axonal damage and visual impairment after ON in MOG-IgG-positive patients are as severe as in AQP4-IgG-positive NMOSD patients. In MOG-IgG-positive patients, damage accrual may be driven by higher relapse rates, whereas AQP4-IgG-positive patients showed fewer but more severe episodes of ON. Given the marked damage in some of our MOG-IgG-positive patients, early diagnosis and timely initiation and close monitoring of immunosuppressive therapy are important. SN - 1742-2094 UR - https://www.unboundmedicine.com/medline/citation/27802824/MOG_IgG_in_NMO_and_related_disorders:_a_multicenter_study_of_50_patients__Part_4:_Afferent_visual_system_damage_after_optic_neuritis_in_MOG_IgG_seropositive_versus_AQP4_IgG_seropositive_patients_ L2 - https://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-016-0720-6 DB - PRIME DP - Unbound Medicine ER -