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Optical coherence tomography in myelin-oligodendrocyte-glycoprotein antibody-seropositive patients: a longitudinal study.
J Neuroinflammation. 2019 Jul 25; 16(1):154.JN

Abstract

BACKGROUND

Serum antibodies against myelin-oligodendrocyte-glycoprotein (MOG-IgG) are detectable in a proportion of patients with acute or relapsing neuroinflammation. It is unclear, if neuro-axonal damage occurs only in an attack-dependent manner or also progressively. Therefore, this study aimed to investigate longitudinally intra-retinal layer changes in eyes without new optic neuritis (ON) in MOG-IgG-seropositive patients.

METHODS

We included 38 eyes of 24 patients without ON during follow-up (F/U) [median years (IQR)] 1.9 (1.0-2.2) and 56 eyes of 28 age- and sex-matched healthy controls (HC). The patient group's eyes included 18 eyes without (EyeON-) and 20 eyes with history of ON (EyeON+). Using spectral domain optical coherence tomography (OCT), we acquired peripapillary retinal nerve fiber layer thickness (pRNFL) and volumes of combined ganglion cell and inner plexiform layer (GCIP), inner nuclear layer (INL), and macular volume (MV). High-contrast visual acuity (VA) was assessed at baseline.

RESULTS

At baseline in EyeON-, pRNFL (94.3 ± 15.9 μm, p = 0.36), INL (0.26 ± 0.03 mm3, p = 0.11), and MV (2.34 ± 0.11 mm3, p = 0.29) were not reduced compared to HC; GCIP showed thinning (0.57 ± 0.07 mm3; p = 0.008), and VA was reduced (logMAR 0.05 ± 0.15 vs. - 0.09 ± 0.14, p = 0.008) in comparison to HC. Longitudinally, we observed pRNFL thinning in models including all patient eyes (annual reduction - 2.20 ± 4.29 μm vs. - 0.35 ± 1.17 μm, p = 0.009) in comparison to HC. Twelve EyeON- with other than ipsilateral ON attacks ≤ 6 months before baseline showed thicker pRNFL at baseline and more severe pRNFL thinning in comparison to 6 EyeON- without other clinical relapses.

CONCLUSIONS

We observed pRNFL thinning in patients with MOG-IgG during F/U, which was not accompanied by progressive GCIP reduction. This effect could be caused by a small number of EyeON- with other than ipsilateral ON attacks within 6 months before baseline. One possible interpretation could be a reduction of the swelling, which could mean that MOG-IgG patients show immune-related swelling in the CNS also outside of an attack's target area.

Authors+Show Affiliations

Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine and Charité - Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Robert-Rössle-Straβe 10, 13125, Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Charitéplatz 1, 10117, Berlin, Germany.Department of Neurology and Neuroradiology, Roger Salengro Hospital, University of Lille, INSERM 1171, Avenue du Professeur Emile Laine, 59037, Lille, France.Department of Neurology, Klinikum Rechts der Isar, Technische Universität München, Ismaninger Straβe 22, 81675, Munich, Germany.Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine and Charité - Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Robert-Rössle-Straβe 10, 13125, Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Charitéplatz 1, 10117, Berlin, Germany.Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine and Charité - Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Robert-Rössle-Straβe 10, 13125, Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Charitéplatz 1, 10117, Berlin, Germany.Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine and Charité - Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Robert-Rössle-Straβe 10, 13125, Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Charitéplatz 1, 10117, Berlin, Germany.Department of Pediatric Neurology and Developmental Medicine, Dr. von Hauner's Children's Hospital, University of Munich, Lindwurmstraβe 4, 80337, Munich, Germany.Molecular Neuroimmunology Group, Department of Neurology, University of Heidelberg, Im Neuenheimer Feld 400, 69120, Heidelberg, Germany.Clinical Department of Neurology, Medical University of Innsbruck, Anichstraβe 35, 6020, Innsbruck, Austria.Department of Neurology, Charité - Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin, Institute of Health, Charitéplatz 1, 10117, Berlin, Germany.Institute of Clinical Neuroimmunology, Ludwig-Maximilians University, Marchioninistr. 15, 81377, Munich, Germany.Munich Cluster for Systems Neurology, Feodor-Lynen-Str 17, 81377, Munich, Germany. Institute of Clinical Neuroimmunology, Ludwig-Maximilians University, Marchioninistr. 15, 81377, Munich, Germany.Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine and Charité - Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Robert-Rössle-Straβe 10, 13125, Berlin, Germany. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Charitéplatz 1, 10117, Berlin, Germany. Department of Neurology, Charité - Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin, Institute of Health, Charitéplatz 1, 10117, Berlin, Germany.Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine and Charité - Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Robert-Rössle-Straβe 10, 13125, Berlin, Germany. alexander.brandt@charite.de. NeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Charitéplatz 1, 10117, Berlin, Germany. alexander.brandt@charite.de. Department of Neurology, University of California Irvine, 30, 101 The City Dr S, Orange, CA, 92868, USA. alexander.brandt@charite.de.Institute of Clinical Neuroimmunology, Ludwig-Maximilians University, Marchioninistr. 15, 81377, Munich, Germany.Institute of Clinical Neuroimmunology, Ludwig-Maximilians University, Marchioninistr. 15, 81377, Munich, Germany. Data Integration for Future Medicine consortium (DIFUTURE), Ludwig-Maximilians University, Marchioninistr. 15, Munich, 81377, Germany.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

31345223

Citation

Oertel, Frederike C., et al. "Optical Coherence Tomography in Myelin-oligodendrocyte-glycoprotein Antibody-seropositive Patients: a Longitudinal Study." Journal of Neuroinflammation, vol. 16, no. 1, 2019, p. 154.
Oertel FC, Outteryck O, Knier B, et al. Optical coherence tomography in myelin-oligodendrocyte-glycoprotein antibody-seropositive patients: a longitudinal study. J Neuroinflammation. 2019;16(1):154.
Oertel, F. C., Outteryck, O., Knier, B., Zimmermann, H., Borisow, N., Bellmann-Strobl, J., Blaschek, A., Jarius, S., Reindl, M., Ruprecht, K., Meinl, E., Hohlfeld, R., Paul, F., Brandt, A. U., Kümpfel, T., & Havla, J. (2019). Optical coherence tomography in myelin-oligodendrocyte-glycoprotein antibody-seropositive patients: a longitudinal study. Journal of Neuroinflammation, 16(1), 154. https://doi.org/10.1186/s12974-019-1521-5
Oertel FC, et al. Optical Coherence Tomography in Myelin-oligodendrocyte-glycoprotein Antibody-seropositive Patients: a Longitudinal Study. J Neuroinflammation. 2019 Jul 25;16(1):154. PubMed PMID: 31345223.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Optical coherence tomography in myelin-oligodendrocyte-glycoprotein antibody-seropositive patients: a longitudinal study. AU - Oertel,Frederike C, AU - Outteryck,Olivier, AU - Knier,Benjamin, AU - Zimmermann,Hanna, AU - Borisow,Nadja, AU - Bellmann-Strobl,Judith, AU - Blaschek,Astrid, AU - Jarius,Sven, AU - Reindl,Markus, AU - Ruprecht,Klemens, AU - Meinl,Edgar, AU - Hohlfeld,Reinhard, AU - Paul,Friedemann, AU - Brandt,Alexander U, AU - Kümpfel,Tania, AU - Havla,Joachim, Y1 - 2019/07/25/ PY - 2018/11/13/received PY - 2019/06/13/accepted PY - 2019/7/27/entrez PY - 2019/7/28/pubmed PY - 2019/7/28/medline KW - Myelin-oligodendrocyte-glycoprotein KW - Optic neuritis KW - Optical coherence tomography SP - 154 EP - 154 JF - Journal of neuroinflammation JO - J Neuroinflammation VL - 16 IS - 1 N2 - BACKGROUND: Serum antibodies against myelin-oligodendrocyte-glycoprotein (MOG-IgG) are detectable in a proportion of patients with acute or relapsing neuroinflammation. It is unclear, if neuro-axonal damage occurs only in an attack-dependent manner or also progressively. Therefore, this study aimed to investigate longitudinally intra-retinal layer changes in eyes without new optic neuritis (ON) in MOG-IgG-seropositive patients. METHODS: We included 38 eyes of 24 patients without ON during follow-up (F/U) [median years (IQR)] 1.9 (1.0-2.2) and 56 eyes of 28 age- and sex-matched healthy controls (HC). The patient group's eyes included 18 eyes without (EyeON-) and 20 eyes with history of ON (EyeON+). Using spectral domain optical coherence tomography (OCT), we acquired peripapillary retinal nerve fiber layer thickness (pRNFL) and volumes of combined ganglion cell and inner plexiform layer (GCIP), inner nuclear layer (INL), and macular volume (MV). High-contrast visual acuity (VA) was assessed at baseline. RESULTS: At baseline in EyeON-, pRNFL (94.3 ± 15.9 μm, p = 0.36), INL (0.26 ± 0.03 mm3, p = 0.11), and MV (2.34 ± 0.11 mm3, p = 0.29) were not reduced compared to HC; GCIP showed thinning (0.57 ± 0.07 mm3; p = 0.008), and VA was reduced (logMAR 0.05 ± 0.15 vs. - 0.09 ± 0.14, p = 0.008) in comparison to HC. Longitudinally, we observed pRNFL thinning in models including all patient eyes (annual reduction - 2.20 ± 4.29 μm vs. - 0.35 ± 1.17 μm, p = 0.009) in comparison to HC. Twelve EyeON- with other than ipsilateral ON attacks ≤ 6 months before baseline showed thicker pRNFL at baseline and more severe pRNFL thinning in comparison to 6 EyeON- without other clinical relapses. CONCLUSIONS: We observed pRNFL thinning in patients with MOG-IgG during F/U, which was not accompanied by progressive GCIP reduction. This effect could be caused by a small number of EyeON- with other than ipsilateral ON attacks within 6 months before baseline. One possible interpretation could be a reduction of the swelling, which could mean that MOG-IgG patients show immune-related swelling in the CNS also outside of an attack's target area. SN - 1742-2094 UR - https://www.unboundmedicine.com/medline/citation/31345223/Optical_coherence_tomography_in_myelin_oligodendrocyte_glycoprotein_antibody_seropositive_patients:_a_longitudinal_study_ L2 - https://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-019-1521-5 DB - PRIME DP - Unbound Medicine ER -