Aquaporin-4- und Myelin-Oligodendrozyten-Glykoprotein-Antikörper-assoziierte Optikusneuritis: Diagnose und Therapie

Zusammenfassung

Die Optikusneuritis (ON) ist vielfach die erste Manifestation einer AQP4-Antikörper-vermittelten NMOSD (AQP4: Aquaporin-4, NMOSD: Neuromyelitis-optica-Spektrum-Erkrankung, Engl.: neuromyelitis optica spectrum disorders) oder einer Myelin-Oligodendrozyten-Glykoprotein-Antikörper-assoziierten Enzephalomyelitis (MOG-EM; auch MOG antibody associated disorders, MOGAD). Für beide Erkrankungen wurden in den vergangenen Jahren internationale Diagnosekriterien und Empfehlungen zu Indikation und Methodik der serologischen Testung vorgelegt. Seit Kurzem liegen zudem Ergebnisse aus 4 großen, internationalen Phase-III-Studien zur Behandlung der NMOSD vor. Mit dem den Komplementfaktor C5 blockierenden monoklonalen Antikörper Eculizumab wurde 2019 erstmalig ein Medikament zur Langzeitbehandlung der NMOSD, die bislang vornehmlich Off-Label mit Rituximab, Azathioprin und anderen Immunsuppressiva erfolgt, auf dem europäischen Markt zugelassen. Für die erst vor wenigen Jahren erstbeschriebene MOG-EM stehen inzwischen Daten aus mehreren retrospektiven Studien zur Verfügung, die eine Wirksamkeit von Rituximab und anderen Immunsuppressiva in der Schubprophylaxe auch in dieser Indikation nahelegen. Viele der zur Therapie der MS zugelassenen Medikamente sind entweder unwirksam oder können, wie z. B. Interferon-β, eine Verschlechterung des Krankheitsverlaufes bewirken. Beide Erkrankungen werden im Akutstadium mit hochdosierten Glukokortikoiden und Plasmapherese oder Immunadsorption behandelt. Diese Behandlung sollte möglichst rasch nach Symptombeginn eingeleitet werden. Insbesondere die MOG-EM ist durch eine oft ausgeprägte Steroidabhängigkeit gekennzeichnet, die ein langsames Ausschleichen der Steroidtherapie erfordert, und schließt viele Fälle der bislang meist als „idiopathisch“ klassifizierten „chronic relapsing inflammatory optic neuropathy“ (CRION) ein. Unbehandelt kann sowohl die NMOSD- als auch die MOG-EM-assoziierte ON zu schweren, persistierenden und oft bilateralen Visuseinschränkungen bis hin zur Erblindung führen. Beide Erkrankungen verlaufen meist relapsierend. Neben den Sehnerven sind häufig das Myelon sowie der Hirnstamm und, vor allem bei NMO-Patienten, das Dienzephalon betroffen; supratentorielle Hirnläsionen im kranialen MRT sind, anders als früher gedacht, kein Ausschlusskriterium, sondern häufig. In der vorliegenden Arbeit geben wir einen Überblick über Klinik, Diagnostik und Therapie dieser beiden wichtigen Differenzialdiagnosen der MS-assoziierten und idiopathischen ON.

Abstract

Optic neuritis (ON) is a frequent manifestation of aquaporin-4 (AQP4) antibody-mediated neuromyelitis optica spectrum disorders (NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated encephalomyelitis (MOG-EM; also termed MOG antibody-associated disorders, MOGAD). The past few years have seen major advances in the diagnosis and treatment of these two relatively new entities: international diagnostic criteria for NMOSD and MOG-EM have been proposed, improved antibody assays developed, and consensus recommendations on the indications and methodology of serological testing published. Very recently, the results of four phase III trials assessing new treatment options for NMOSD have been presented. With eculizumab, a monoclonal antibody inhibiting complement factor C5, for the first time a relapse-preventing long-term treatment for NMOSD – which has so far mostly been treated off-label with rituximab, azathioprine, and other immunosuppressants – has been approved. Data from recent retrospective studies evaluating treatment responses in MOG-ON suggest that rituximab and other immunosuppressants are effective also in this entity. By contrast, many drugs approved for the treatment of multiple sclerosis (MS) have been found to be either ineffective or to cause disease exacerbation (e.g., interferon-β). Recent studies have shown that not only NMOSD-ON but also MOG-ON usually follows a relapsing course. If left untreated, both disorders can result in severe visual deficiency or blindness, though MOG-ON seems to have a better prognosis overall. Acute attacks are treated with high-dose intravenous methylprednisolone and, in many cases, plasma exchange (PEX) or immunoadsorption (IA). Early use of PEX/IA may prevent persisting visual loss and improve the long-term outcome. Especially MOG-ON has been found to be frequently associated with flare-ups, if steroids are not tapered, and to underlie many cases of “chronic relapsing inflammatory optic neuropathy” (CRION). Both NMOSD-ON and MOG-ON are often associated with simultaneous or consecutive attacks of myelitis and brainstem encephalitis; in contrast to earlier assumptions, supratentorial MRI brain lesions are a common finding and do not preclude the diagnosis. In this article, we review the current knowledge on the clinical presentation, epidemiology, diagnosis, and treatment of these two rare yet important differential diagnoses of both MS-associated ON und idiopathic autoimmune ON.

Schlüsselwörter

Optikusneuritis - Sehnervenentzündung - Neuromyelitis optica - Neuromyelitis-optica-Spektrum-Erkrankungen (NMOSD) - Myelin-Oligodendrozyten-Glykoprotein (MOG) - Aquaporin-4 (AQP4) - Antikörper - Myelitis

Key words

optic neuritis - neuromyelitis optica - neuromyelitis optica spectrum disorders (NMOSD) - myelin oligodendrocyte glycoprotein (MOG) - Aquaporin-4 (AQP4) - antibodies - myelitis

Publikationsverlauf

Eingereicht: 04. Juni 2020

Angenommen: 30. Juni 2020

Artikel online veröffentlicht:
17. November 2020

• Literatur

• 1 Kale N. Optic neuritis as an early sign of multiple sclerosis. Eye Brain 2016; 8: 195-202 doi:10.2147/EB.S54131
• 2 Deutsche Ophthalmologische Gesellschaft e.V. (DOG); Berufsverband der Augenärzte Deutschlands e.V. (BVA). Beisse F, Bertram B, Claessens D. et al. Optikusneuritis, S2e-Leitlinie von DOG (Deutsche Ophthalmologische Gesellschaft e.V.) und BVA (Berufsverband der Augenärzte Deutschlands e.V.), 2018. Im Internet (Stand: 07.05.2020): https://www.awmf.org/uploads/tx_szleitlinien/045-010l_S2e_Optikusneuritis_2018-04.pdf
• 3 Jarius S, Wildemann B. Aquaporin-4 antibodies (NMO-IgG) as a serological marker of neuromyelitis optica: a critical review of the literature. Brain Pathol 2013; 23: 661-683 doi:10.1111/bpa.12084
• 4 Jarius S, Paul F, Weinshenker B. et al. Neuromyelitis optica. Nat Rev Dis Primers 2020;
• 5 Jarius S, Wildemann B. The history of neuromyelitis optica. J Neuroinflammation 2013; 10: 8 doi:10.1186/1742-2094-10-8
• 6 Jarius S, Wildemann B. The history of neuromyelitis optica. Part 2: ‘Spinal amaurosis’, or how it all began. J Neuroinflammation 2019; 16: 280 doi:10.1186/s12974-019-1594-1
• 7 Wingerchuk DM, Hogancamp WF, OʼBrien PC. et al. The clinical course of neuromyelitis optica (Devicʼs syndrome). Neurology 1999; 53: 1107-1114 doi:10.1212/wnl.53.5.1107
• 8 Wingerchuk DM, Banwell B, Bennett JL. et al. International consensus diagnostic criteria for neuromyelitis optica spectrum disorders. Neurology 2015; 85: 177-189 doi:10.1212/WNL.0000000000001729
• 9 Wingerchuk DM, Lennon VA, Pittock SJ. et al. Revised diagnostic criteria for neuromyelitis optica. Neurology 2006; 66: 1485-1489 doi:10.1212/01.wnl.0000216139.44259.74
• 10 Jarius S, Ruprecht K, Wildemann B. et al. Contrasting disease patterns in seropositive and seronegative neuromyelitis optica: a multicentre study of 175 patients. J Neuroinflammation 2012; 9: 14 doi:10.1186/1742-2094-9-14
• 11 Jarius S, Probst C, Borowski K. et al. Standardized method for the detection of antibodies to aquaporin-4 based on a highly sensitive immunofluorescence assay employing recombinant target antigen. J Neurol Sci 2010; 291: 52-56 doi:10.1016/j.jns.2010.01.002
• 12 Matiello M, Lennon VA, Jacob A. et al. NMO-IgG predicts the outcome of recurrent optic neuritis. Neurology 2008; 70: 2197-2200 doi:10.1212/01.wnl.0000303817.82134.da
• 13 Weinshenker BG, Wingerchuk DM, Vukusic S. et al. Neuromyelitis optica IgG predicts relapse after longitudinally extensive transverse myelitis. Ann Neurol 2006; 59: 566-569 doi:10.1002/ana.20770
• 14 Jarius S, Wildemann B. AQP4 antibodies in neuromyelitis optica: diagnostic and pathogenetic relevance. Nat Rev Neurol 2010; 6: 383-392 doi:10.1038/nrneurol.2010.72
• 15 Jarius S, Paul F, Franciotta D. et al. Mechanisms of disease: aquaporin-4 antibodies in neuromyelitis optica. Nat Clin Pract Neurol 2008; 4: 202-214 doi:10.1038/ncpneuro0764
• 16 Pache F, Wildemann B, Paul F. et al. [Neuromyelitis optica]. Fortschr Neurol Psychiatr 2017; 85: e1 doi:10.1055/s-0035-1567186
• 17 Jarius S, Ruprecht K, Kleiter I. et al. MOG-IgG in NMO and related disorders: a multicenter study of 50 patients. Part 2: Epidemiology, clinical presentation, radiological and laboratory features, treatment responses, and long-term outcome. J Neuroinflammation 2016; 13: 280 doi:10.1186/s12974-016-0718-0
• 18 Jarius S, Kleiter I, Ruprecht K. et al. MOG-IgG in NMO and related disorders: a multicenter study of 50 patients. Part 3: Brainstem involvement – frequency, presentation and outcome. J Neuroinflammation 2016; 13: 281 doi:10.1186/s12974-016-0719-z
• 19 Wynford-Thomas R, Jacob A, Tomassini V. Neurological update: MOG antibody disease. J Neurol 2019; 266: 1280-1286 doi:10.1007/s00415-018-9122-2
• 20 Mader S, Gredler V, Schanda K. et al. Complement activating antibodies to myelin oligodendrocyte glycoprotein in neuromyelitis optica and related disorders. J Neuroinflammation 2011; 8: 184 doi:10.1186/1742-2094-8-184
• 21 Reindl M, Jarius S, Rostasy K. et al. Myelin oligodendrocyte glycoprotein antibodies: how clinically useful are they?. Curr Opin Neurol 2017; 30: 295-301 doi:10.1097/WCO.0000000000000446
• 22 Cobo-Calvo A, Ruiz A, Maillart E. et al. Clinical spectrum and prognostic value of CNS MOG autoimmunity in adults: the MOGADOR study. Neurology 2018; 90: e1858-e1869 doi:10.1212/WNL.0000000000005560
• 23 Cobo-Calvo A, Sepulveda M, Rollot F. et al. Evaluation of treatment response in adults with relapsing MOG-Ab-associated disease. J Neuroinflammation 2019; 16: 134 doi:10.1186/s12974-019-1525-1
• 24 Mori M, Kuwabara S, Paul F. Worldwide prevalence of neuromyelitis optica spectrum disorders. J Neurol Neurosurg Psychiatry 2018; 89: 555-556 doi:10.1136/jnnp-2017-317566
• 25 de Mol CL, Wong Y, van Pelt ED. et al. The clinical spectrum and incidence of anti-MOG-associated acquired demyelinating syndromes in children and adults. Mult Scler 2020; 26: 806-814 doi:10.1177/1352458519845112
• 26 Rostasy K, Mader S, Hennes EM. et al. Persisting myelin oligodendrocyte glycoprotein antibodies in aquaporin-4 antibody negative pediatric neuromyelitis optica. Mult Scler 2013; 19: 1052-1059 doi:10.1177/1352458512470310
• 27 Duignan S, Wright S, Rossor T. et al. Myelin oligodendrocyte glycoprotein and aquaporin-4 antibodies are highly specific in children with acquired demyelinating syndromes. Dev Med Child Neurol 2018; 60: 958-962 doi:10.1111/dmcn.13703
• 28 Boesen MS, Jensen PEH, Born AP. et al. Incidence of pediatric neuromyelitis optica spectrum disorder and myelin oligodendrocyte glycoprotein antibody-associated disease in Denmark 2008–2018: a nationwide, population-based cohort study. Mult Scler Relat Disord 2019; 33: 162-167 doi:10.1016/j.msard.2019.06.002
• 29 Reindl M, Waters P. Myelin oligodendrocyte glycoprotein antibodies in neurological disease. Nat Rev Neurol 2019; 15: 89-102 doi:10.1038/s41582-018-0112-x
• 30 Kleiter I, Gold R. Present and future therapies in neuromyelitis optica spectrum disorders. Neurotherapeutics 2016; 13: 70-83 doi:10.1007/s13311-015-0400-8
• 31 Matiello M, Schaefer-Klein J, Sun D. et al. Aquaporin 4 expression and tissue susceptibility to neuromyelitis optica. JAMA Neurol 2013; 70: 1118-1125 doi:10.1001/jamaneurol.2013.3124
• 32 Pittock SJ, Lennon VA, Krecke K. et al. Brain abnormalities in neuromyelitis optica. Arch Neurol 2006; 63: 390-396 doi:10.1001/archneur.63.3.390
• 33 Pittock SJ, Weinshenker BG, Lucchinetti CF. et al. Neuromyelitis optica brain lesions localized at sites of high aquaporin 4 expression. Arch Neurol 2006; 63: 964-968 doi:10.1001/archneur.63.7.964
• 34 Saadoun S, Waters P, Bell BA. et al. Intra-cerebral injection of neuromyelitis optica immunoglobulin G and human complement produces neuromyelitis optica lesions in mice. Brain 2010; 133: 349-361 doi:10.1093/brain/awp309
• 35 Papadopoulos MC, Verkman AS. Aquaporin 4 and neuromyelitis optica. Lancet Neurol 2012; 11: 535-544 doi:10.1016/S1474-4422(12)70133-3
• 36 Levy M, Wildemann B, Jarius S. et al. Immunopathogenesis of neuromyelitis optica. Adv Immunol 2014; 121: 213-242 doi:10.1016/B978-0-12-800100-4.00006-4
• 37 Lennon VA, Kryzer TJ, Pittock SJ. et al. IgG marker of optic-spinal multiple sclerosis binds to the aquaporin-4 water channel. J Exp Med 2005; 202: 473-477 doi:10.1084/jem.20050304
• 38 Lucchinetti CF, Mandler RN, McGavern D. et al. A role for humoral mechanisms in the pathogenesis of Devicʼs neuromyelitis optica. Brain 2002; 125: 1450-1461 doi:10.1093/brain/awf151
• 39 Uzawa A, Mori M, Hayakawa S. et al. Expression of chemokine receptors on peripheral blood lymphocytes in multiple sclerosis and neuromyelitis optica. BMC Neurol 2010; 10: 113 doi:10.1186/1471-2377-10-113
• 40 Jarius S, Paul F, Franciotta D. et al. Cerebrospinal fluid findings in aquaporin-4 antibody positive neuromyelitis optica: results from 211 lumbar punctures. J Neurol Sci 2011; 306: 82-90 doi:10.1016/j.jns.2011.03.038
• 41 Takeshita Y, Obermeier B, Cotleur AC. et al. Effects of neuromyelitis optica-IgG at the blood-brain barrier in vitro. Neurol Neuroimmunol Neuroinflamm 2017; 4: e311 doi:10.1212/NXI.0000000000000311
• 42 Wang H, Wang K, Zhong X. et al. Cerebrospinal fluid BAFF and APRIL levels in neuromyelitis optica and multiple sclerosis patients during relapse. J Clin Immunol 2012; 32: 1007-1011 doi:10.1007/s10875-012-9709-9
• 43 Saadoun S, Waters P, Owens GP. et al. Neuromyelitis optica MOG-IgG causes reversible lesions in mouse brain. Acta Neuropathol Commun 2014; 2: 35 doi:10.1186/2051-5960-2-35
• 44 Spadaro M, Winklmeier S, Beltran E. et al. Pathogenicity of human antibodies against myelin oligodendrocyte glycoprotein. Ann Neurol 2018; 84: 315-328 doi:10.1002/ana.25291
• 45 Weber MS, Derfuss T, Metz I. et al. Defining distinct features of anti-MOG antibody associated central nervous system demyelination. Ther Adv Neurol Disord 2018; 11: 1756286418762083 doi:10.1177/1756286418762083
• 46 Höftberger R, Guo Y, Flanagan EP. et al. The pathology of central nervous system inflammatory demyelinating disease accompanying myelin oligodendrocyte glycoprotein autoantibody. Acta Neuropathol 2020; 139: 875-892 doi:10.1007/s00401-020-02132-y
• 47 Chen JJ, Pittock SJ, Flanagan EP. et al. Optic neuritis in the era of biomarkers. Surv Ophthalmol 2020; 65: 12-17 doi:10.1016/j.survophthal.2019.08.001
• 48 Chen JJ, Bhatti MT. Clinical phenotype, radiological features, and treatment of myelin oligodendrocyte glycoprotein-immunoglobulin G (MOG-IgG) optic neuritis. Curr Opin Neurol 2020; 33: 47-54 doi:10.1097/WCO.0000000000000766
• 49 Jurynczyk M, Messina S, Woodhall MR. et al. Clinical presentation and prognosis in MOG-antibody disease: a UK study. Brain 2017; 140: 3128-3138 doi:10.1093/brain/awx276
• 50 Jarius S, Paul F, Aktas O. et al. MOG encephalomyelitis: international recommendations on diagnosis and antibody testing. J Neuroinflammation 2018; 15: 134 doi:10.1186/s12974-018-1144-2
• 51 Jang Y, Kim SM, Yun YI. et al. Comparison between optic neuritis associated with antibody against myelin oligodendrocyte glycoprotein and presumed idiopathic optic perineuritis. Neurol Sci 2020;
• 52 Asseyer S, Schmidt F, Chien C. et al. Pain in AQP4-IgG-positive and MOG-IgG-positive neuromyelitis optica spectrum disorders. Mult Scler J Exp Transl Clin 2018; 4: 2055217318796684 doi:10.1177/2055217318796684
• 53 Jarius S, Ruprecht K, Kleiter I. et al. MOG-IgG in NMO and related disorders: a multicenter study of 50 patients. Part 1: Frequency, syndrome specificity, influence of disease activity, long-term course, association with AQP4-IgG, and origin. J Neuroinflammation 2016; 13: 279 doi:10.1186/s12974-016-0717-1
• 54 Tumani H, Petereit H-F. Leitlinie Lumbalpunktion und Liquordiagnostik, S1-Leitlinie, 2019. In: Deutsche Gesellschaft für Neurologie, Deutsche Gesellschaft für Liquordiagnostik und Klinische Neurochemie, Hrsg. Leitlinien für Diagnostik und Therapie in der Neurologie Im Internet (Stand: 07.05.2020): https://www.dgn.org/images/red_leitlinien/LL_2019/PDFs_Download/030141_LL_Lumbalpunktion_und_Liquordiagnostik_2019.pdf
• 55 Jarius S, Eichhorn P, Franciotta D. et al. The MRZ reaction as a highly specific marker of multiple sclerosis: re-evaluation and structured review of the literature. J Neurol 2017; 264: 453-466 doi:10.1007/s00415-016-8360-4
• 56 Jarius S, Pellkofer H, Siebert N. et al. Cerebrospinal fluid findings in patients with myelin oligodendrocyte glycoprotein (MOG) antibodies. Part 1: Results from 163 lumbar punctures in 100 adult patients. J Neuroinflamm 2020; 17: 261 doi:10.1186/s12974-020-01824-2
• 57 Jarius S, Lechner C, Wendel EM. et al. Cerebrospinal fluid findings in patients with myelin oligodendrocyte gylcoprotein (MOG) antibodies. Part 2: Results from 108 lumbar punctures in 80 pediatric patients. J Neuroinflammation 2020; 17: 262 doi:10.1186/s12974-020-01825-1
• 58 Salama S, Khan M, Shanechi A. et al. MRI differences between MOG antibody disease and AQP4 NMOSD. Mult Scler 2020;
• 59 Ramanathan S, Prelog K, Barnes EH. et al. Radiological differentiation of optic neuritis with myelin oligodendrocyte glycoprotein antibodies, aquaporin-4 antibodies, and multiple sclerosis. Mult Scler 2016; 22: 470-482 doi:10.1177/1352458515593406
• 60 Dubey D, Pittock SJ, Krecke KN. et al. Clinical, radiologic, and prognostic features of myelitis associated with myelin oligodendrocyte glycoprotein autoantibody. JAMA Neurol 2019; 76: 301-309 doi:10.1001/jamaneurol.2018.4053
• 61 Sinnecker T, Clarke MA, Meier D. et al. Evaluation of the central vein sign as a diagnostic imaging biomarker in multiple sclerosis. JAMA Neurol 2019;
• 62 Siebert N, Paul F. Neuromyelitis-optica-Spektrum-Erkrankung. DGNeurologie 2019; 2: 280-284
• 63 Oertel FC, Kuchling J, Zimmermann H. et al. Microstructural visual system changes in AQP4-antibody-seropositive NMOSD. Neurol Neuroimmunol Neuroinflamm 2017; 4: e334 doi:10.1212/NXI.0000000000000334
• 64 Tian DC, Su L, Fan M. et al. Bidirectional degeneration in the visual pathway in neuromyelitis optica spectrum disorder (NMOSD). Mult Scler 2018; 24: 1585-1593 doi:10.1177/1352458517727604
• 65 Akaishi T, Sato DK, Nakashima I. et al. MRI and retinal abnormalities in isolated optic neuritis with myelin oligodendrocyte glycoprotein and aquaporin-4 antibodies: a comparative study. J Neurol Neurosurg Psychiatry 2016; 87: 446-448 doi:10.1136/jnnp-2014-310206
• 66 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: 282 doi:10.1186/s12974-016-0720-6
• 67 Neto SP, Alvarenga RM, Vasconcelos CC. et al. Evaluation of pattern-reversal visual evoked potential in patients with neuromyelitis optica. Mult Scler 2013; 19: 173-178 doi:10.1177/1352458512447597
• 68 Ringelstein M, Kleiter I, Ayzenberg I. et al. Visual evoked potentials in neuromyelitis optica and its spectrum disorders. Mult Scler 2014; 20: 617-620 doi:10.1177/1352458513503053
• 69 Vabanesi M, Pisa M, Guerrieri S. et al. In vivo structural and functional assessment of optic nerve damage in neuromyelitis optica spectrum disorders and multiple sclerosis. Sci Rep 2019; 9: 10371 doi:10.1038/s41598-019-46251-3
• 70 Ringelstein M, Harmel J, Zimmermann H. et al. Longitudinal optic neuritis-unrelated visual evoked potential changes in NMO spectrum disorders. Neurology 2020; 94: e407-e418 doi:10.1212/WNL.0000000000008684
• 71 Jarius S, Paul F, Aktas O. et al. [MOG encephalomyelitis: international recommendations on diagnosis and antibody testing]. Nervenarzt 2018; 89: 1388-1399 doi:10.1007/s00115-018-0607-0
• 72 Wildemann B, Jarius S, Franz J. et al. MOG-expressing teratoma followed by MOG-IgG-positive optic neuritis. Acta Neuropathologica 2020;
• 73 Lee HJ, Kim B, Waters P. et al. Chronic relapsing inflammatory optic neuropathy (CRION): a manifestation of myelin oligodendrocyte glycoprotein antibodies. J Neuroinflammation 2018; 15: 302 doi:10.1186/s12974-018-1335-x
• 74 Wandinger KP, Stangel M, Witte T. et al. Autoantibodies against aquaporin-4 in patients with neuropsychiatric systemic lupus erythematosus and primary Sjögrenʼs syndrome. Arthritis Rheum 2010; 62: 1198-1200 doi:10.1002/art.27337
• 75 Aktas O, Kleiter I, Kümpfel T. et al. Praktische Aspekte der Diagnostik und Therapie der Neuromyelitis-optica-Spektrum-Erkrankungen. In: Kompetenznetz Multiple Sklerose e.V., Hrsg. Qualitätshandbuch MS/NMOSD Empfehlungen zur Therapie der Multiplen Sklerose und Neuromyelitis-optica-Spektrum-Erkrankungen für Ärzte, Ausgabe Januar 2020. München: Krankheitsbezogenes Kompetenznetz Multiple Sklerose e.V.; 2020. Im Internet (Stand: 08.10.2020): https://www.kompetenznetz-multiplesklerose.de/wp-content/uploads/2019/09/KKNMS_Qualitätshandbuch-MSNMOSD_2019_webfrei.pdf
• 76 Bonnan M, Valentino R, Debeugny S. et al. Short delay to initiate plasma exchange is the strongest predictor of outcome in severe attacks of NMO spectrum disorders. J Neurol Neurosurg Psychiatry 2018; 89: 346-351 doi:10.1136/jnnp-2017-316286
• 77 Kleiter I, Gahlen A, Borisow N. et al. Neuromyelitis optica: evaluation of 871 attacks and 1,153 treatment courses. Ann Neurol 2016; 79: 206-216 doi:10.1002/ana.24554
• 78 Kleiter I, Gahlen A, Borisow N. et al. Apheresis therapies for NMOSD attacks: A retrospective study of 207 therapeutic interventions. Neurol Neuroimmunol Neuroinflamm 2018; 5: e504 doi:10.1212/NXI.0000000000000504
• 79 Merle H, Olindo S, Jeannin S. et al. Treatment of optic neuritis by plasma exchange (add-on) in neuromyelitis optica. Arch Ophthal 2012; 130: 858-862 doi:10.1001/archophthalmol.2012.1126
• 80 Ramanathan S, Mohammad S, Tantsis E. et al. Clinical course, therapeutic responses and outcomes in relapsing MOG antibody-associated demyelination. J Neurol Neurosurg Psychiatry 2018; 89: 127-137 doi:10.1136/jnnp-2017-316880
• 81 Cree BAC, Bennett JL, Kim HJ. et al. Inebilizumab for the treatment of neuromyelitis optica spectrum disorder (N-MOmentum): a double-blind, randomised placebo-controlled phase 2/3 trial. Lancet 2019; 394: 1352-1363 doi:10.1016/S0140-6736(19)31817-3
• 82 Yamamura T, Kleiter I, Fujihara K. et al. Trial of satralizumab in neuromyelitis optica spectrum disorder. N Engl J Med 2019; 381: 2114-2124 doi:10.1056/NEJMoa1901747
• 83 Pittock SJ, Berthele A, Fujihara K. et al. Eculizumab in aquaporin-4-positive neuromyelitis optica spectrum disorder. N Engl J Med 2019; 381: 614-625 doi:10.1056/NEJMoa1900866
• 84 Traboulsee A, Greenberg BM, Bennett JL. et al. Safety and efficacy of satralizumab monotherapy in neuromyelitis optica spectrum disorder: a randomised, double-blind, multicentre, placebo-controlled phase 3 trial. Lancet Neurol 2020; 19: 402-412 doi:10.1016/S1474-4422(20)30078-8
• 85 Ayzenberg I, Wildemann B. Praktische Aspekte der Therapie mit Eculizumab. In: Qualitätshandbuch MS/NMOSD Empfehlungen zur Therapie der Multiplen Sklerose und Neuromyelitis-optica-Spektrum-Erkrankungen für Ärzte, Ausgabe Januar 2020. München: Krankheitsbezogenes Kompetenznetz Multiple Sklerose e.V.; 2020. Im Internet (Stand: 08.10.2020): https://www.kompetenznetz-multiplesklerose.de/wp-content/uploads/2019/09/KKNMS_Qualitätshandbuch-MSNMOSD_2019_webfrei.pdf