Accepted Manuscript

Anti-myelin oligodendrocyte glycoprotein (MOG) antibodies in

patients with optic neuritis and seizures

Josef Maxwell Gutman, Mark Kupersmith, Steven Galetta, Ilya

Kister

PII: S0022-510X(18)30058-3
DOI: doi:10.1016/j.jns.2018.01.042
Reference: JNS 15768
To appear in: Journal of the Neurological Sciences
Received date: 13 November 2017
Revised date: 2 January 2018
Accepted date: 31 January 2018

Please cite this article as: Josef Maxwell Gutman, Mark Kupersmith, Steven Galetta, Ilya
Kister , Anti-myelin oligodendrocyte glycoprotein (MOG) antibodies in patients with optic
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for all authors. Please check if appropriate. Jns(2018), doi:10.1016/j.jns.2018.01.042

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 ACCEPTED MANUSCRIPT

Anti-Myelin Oligodendrocyte Glycoprotein (MOG) Antibodies in Patients with Optic Neuritis

and Seizures

Josef Maxwell Gutman, MDa* ; Mark Kupersmith, MDb; Steven Galetta, MDa; Ilya Kister, MDa

a: Department of Neurology, NYU Langone Health, New York, NY, USA

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b: Icahn School of Medicine at Mount Sinai and New York Eye and Ear Infirmary, New York,

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NY, USA

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*Corresponding Author:

Josef Maxwell Gutman, MD

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Present Address

NYU Comprehensive MS Care Center

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At Perlmutter Cancer Center-Huntington

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789 Park Ave, 2nd Floor

Huntington, NY 11743
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[email protected]
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631-386-3466

Fax 631-386-3459
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Title (character count with spaces): 102

Abstract: 165

Word Count: 1974

References: 13
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Figures: 1

Tables: 1

Disclosures:

Dr. Gutman has no conflicts of interest to disclose.

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Dr. Kupersmith receives compensation from Quark Pharmacueticals for the conduct of the

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QP1007 NAION treatment trial.

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Dr Galetta has served as a consultant for Biogen.

Dr. Kister served on the scientific advisory board for Biogen Idec and Genentech, and received

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research support from Guthy-Jackson Charitable Foundation, National Multiple Sclerosis Society
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(NMSS), Biogen Idec, Serono, Genzyme, and Novartis.
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This research did not receive any specific grant from funding agencies in the public, commercial,
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or not-for-profit sectors.
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ABSTRACT

We describe four patients who experienced optic neuritis (ON) and seizures and were found to

have antibodies to myelin oligodendrocyte glycoprotein (MOG) in serum. The index case was a

previously healthy 39-year-old man who developed steroid dependent ON and had a generalized

seizure when steroids were tapered. He tested positive for antibodies to MOG. We have reviewed

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the charts of all 11 anti-MOG antibody positive patients in our practice and found that 4 patients,

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all of whom had experienced one of more episodes of ON, also had a generalized seizure during

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the course of their illness. In two patients – including the index case - seizure occurred during

steroid taper and in 2 others at the time of an episode of acute disseminated encephalomyelitis

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(ADEM). Association of anti-MOG antibodies and relapsing demyelinating disorders of the
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central nervous system is increasingly recognized. Testing for anti-MOG antibodies should be

considered in patients with optic neuritis and seizures, especially in those with who also have a
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history of ADEM.
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Key Words: Myelin oligodendrocyte glycoprotein (MOG), optic neuritis, seizure

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1. INTRODUCTION

Optic neuritis can be idiopathic or part of a generalized disorder such as multiple sclerosis (MS),

neuromyelitis optica (NMO) or sarcoidosis, but it is not generally associated with seizures. We

describe 4 patients followed in our practice who manifested the unusual constellation of optic

neuritis and seizures. All of them tested positive for anti-myelin oligodendrocyte glycoprotein

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(MOG) antibodies in serum. MOG antibodies were originally investigated as an autoantigen in

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the experimental autoimmune encephalomyelitis model of MS [1]. Recent development of highly

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sensitive, cell-based, IgG1-directed anti-MOG assays have allowed for identification of a

number of demyelinating/inflammatory syndromes associated with this antibody that include

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acute (ADEM) and multiphasic (MDEM) disseminated encephalomyelitis [2,3], recurrent
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steroid-sensitive optic neuritis (ON) [4], transverse myelitis [5], ‘focal encephalitis’ [6], and

others. Seizure has increasingly been recognized as a possible manifestation of MOG-associated

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disease; seizures were observed in 14.7% of MOG antibody seropositive patients in a recent
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series[7]. Our cases further highlight co-occurrence of ON and seizures in patients with MOG

antibody disease. Our study suggests the need to test for anti-MOG antibodies in patients with
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who manifest both features.

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2. CASE REPORTS
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2.1 Case 1:

A 39-year-old man was evaluated for new onset headaches and acute binocular visual loss. Initial

neuro-ophthalmological examination revealed visual acuity of 20/100-3 in the right eye with

pinhole correction to 20/70-3 and 20/30-2 in the left eye. With effort he was able to see all

Ishihara color plates with each eye. MRI of the brain and orbits showed bilateral enhancement
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and edema of the optic nerves and normal brain (Figure 1A-1B). He was given a course of IV

steroids followed by an oral steroid taper. Vision improved on steroid taper to 20/20 in both eyes

within 1 month. As prednisone was tapered to less than 10 mg daily, however, his headaches

recurred and visual acuity worsened in the left eye to 20/40-1. The prednisone dose was

increased, with resolution of symptoms, and a slower prednisone taper was prescribed with a

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total course of treatment of three months. One week following discontinuation of steroids, the

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patient developed headaches, mild confusion, and had a single generalized seizure. He was

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started on levetiracetam and oral prednisone. EEG at the time of hospitalization demonstrated

asymmetry with slowing in the left hemisphere as well as a single generalized sharp wave. MRI

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brain at that time showed a FLAIR hyperintense lesion in the left subinsular region (Figure 1C),
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and no evidence of optic nerve abnormalities. Cerebrospinal fluid analysis was significant for 39

leukocytes/mm3 (mixed neutrophil and lymphocyte), normal glucose, protein slightly elevated at
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50 mg/dL, no oligoclonal bands, and mildly elevated myelin basic protein at 22 ng/mL.
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Aquaporin-4 (AQP4) antibody testing in serum and CSF was negative, but he tested positive for

anti-MOG antibodies in serum at Mayo Neuroimmunology Laboratory (Rochester, MN). MRI

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one month after the seizure revealed resolution of the left subinsular hyperintensity with
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development of a cortical hyperintensity in the right parietal region (Figure 1D). He was initiated

on rituximab and has not had recurrence of neurologic symptoms during 1 year of follow up with
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slow prednisone taper. He was tapered off of levetiracetam after being seizure free for 6 months

and having normalization of EEG.

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FIGURE 1

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Figure 1: Magnetic Resonance Imaging, Case 1. 1A – Axial postcontrast imaging during initial

episode of optic neuritis shows enhancement of both optic nerves but no other enhancing lesions.
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1B – Coronal T2 sequence from same episode shows increased signal of the bilateral optic

nerves more prominent on the left and absence of other brain parenchymal lesions. 1C -

Axial FLAIR sequence taken at the time of seizure, several months after the initial episode,

shows hyperintense lesion in the left subinsular region. 1D- Coronal FLAIR sequence taken one

month after the seizure shows a new hyperintensity in the right medial parietal region; the left

subinsular hyperintensity had resolved (not shown).

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2.2 Case 2:

A 12-year-old girl experienced acute-onset weakness and encephalopathy followed by a seizure.

MRI revealed multifocal white matter enhancing lesions and leptomeningeal enhancement. CSF

studies, done at an outside hospital, were described as ‘consistent with an inflammatory process’.

She recovered completely after treatment with oral steroids. She developed right-sided optic

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neuritis 8 years after the initial episode and was treated with IV steroids. MRI at that time

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revealed a few nonspecific subcortical white matter changes and enhancement of the right optic

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nerve. AQP4 antibody testing was negative, and anti-MOG antibody testing via cell based assay

at Mayo Neuroimmunology Laboratory (Rochester, MN) was positive. At present she is

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receiving mycophenylate mofetil and has been relapse free for 1.5 years.
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2.3 Case 3:
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An 8-year-old girl presented to the hospital with malaise, headaches, and seizures. During the
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hospitalization she developed hemiparesis and bowel and bladder dysfunction as well as severe

bilateral vision loss. MRIs revealed multifocal white matter changes consistent with ADEM. She
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was treated with steroids and IVIg. Ten years later she developed transverse myelitis shortly
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after receiving the H1N1 flu vaccine. She received steroids, but experienced ON as steroids were

tapered off. Over the following two years optic neuritis would recur whenever steroid doses were
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tapered below prednisone 20 mg daily. Treatment with mycophenylate, azathioprine, and

rituximab as steroid sparing agents failed to prevent recurrences of optic neuritis. She was

subsequently started on tocilizumab, a monoclonal antibody against the interleukin-6 (IL-6)

receptor, and remains free of further relapses for approximately 18 months, even while

prednisone dose has been decreased to 5 mg daily. She has tested negative for AQP4 antibodies
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on multiple occasions, but positive for serum anti-MOG antibodies using cell-based assay (Prof.

Markus Reindl’s Laboratory, Medizinische Universität, Innsbruck, Austria).

2.4 Case 4 (This case is described in greater detail in a separate publication [8]):

A 4-year-old girl presented to the hospital with leg weakness. During the hospitalization she

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became encephalopathic. MRI revealed multiple brain and spine lesions consistent with ADEM.

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She was treated with IV steroids with improvement in her condition. During prednisone taper,

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she developed bilateral optic neuritis. She subsequently had three more episodes of unilateral

optic neuritis followed by a brainstem relapse with new onset nystagmus and associated with

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new MRI lesions in the cerebellum and thalamus for which she was treated with steroids. During
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steroid taper, she experienced a secondarily generalized seizure. She was started on antiepileptic

therapy and has not had any more seizures during 7 years of follow up, though she suffered from
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recurrent episodes of optic neuritis despite therapy with azathioprine and rituximab. Presently
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she has been in prolonged remission for over 2 years on combination of rituximab and monthly

intravenous immunoglobulin (IVIg). Multiple assays for AQP4 antibodies were negative, but
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retroactive testing of her specimens at Mayo Neuroimmunology Laboratory (Rochester, MN)

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demonstrated consistent high-titer positivity for anti-MOG antibodies via cell based assay over a

6 year period.
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We have summarized information about all patients’ presentations, courses, and treatments in

Table 1.
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TABLE 1

Clinical history of 4 patients with optic neuritis, seizure, and MOG antibodies

Age at Se ADE Optic Seizur Myeliti Therap Anti- Follo

Sympto x M Neuritis e s y MOG w Up
m Onset
Patien 39 M - + + - IVMP, Mayo 1 year
t1 (2 PRED,
episodes, RTX

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steroid

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dependent
)

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Patien 12 F + + + - IVMP, Mayo 8
t2 (w PRED, years
ADEM MM

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)
Patien 8 F + + + + IVMP, Innsbruc 13
t3 (Recurren (w IVIg, k years
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t, steroid ADEM PRED,
dependent ) MM,
) PLEX,
TOC
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Patien 4 F + + + + (w IVMP, Mayo 19

t4 (Recurren ADEM PRED, years
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t, some ) IVIg,
steroid AZA,
dependent RTX
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Legend:
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Therapies: IVMP (intravenous methylprednisolone), PRED (oral prednisone), RTX (rituximab),

MM (mycophenylate mofetil), IVIg (intravenous immune globulin), PLEX (plasma exchange),
TOC (tocilizumab), AZA (azathioprine)
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Bold indicates current therapy

Anti-MOG: Mayo – (Mayo Neuroimmunology Laboratory (Rochester, MN), Prof. Andrew
McKeon, personal communication), Innsbruck (Medizinische Universität Innsbruck, Prof
Markus Reindl, personal communication)

3 DISCUSSION
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The four patients in this study were all found to have anti-MOG antibodies via cell based assays

and all had one or more episodes of optic neuritis and a generalized seizure at some point during

their illness. Three of our patients have had more than 5 years of follow up with two having more

than 10 years of follow up. Two of our patients (cases 2 and 3) had long delays between the

index episode of ADEM and subsequent episode of optic neuritis. Case 4 has also had extensive

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follow up over many years though with further neurological events.

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Cases 1-3 had MOG antibodies tested only on one occasion; case 4 has had persistent MOG

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antibody positivity for several years.

There was also substantial phenotypic variation among our patients - three patients were young

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girls at disease onset while the index case was a man who developed his first symptom, optic
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neuritis, in his late 30s. The seizures were observed in two clinical contexts – either during an

episode of ADEM (patients 2 and 3) or as oral steroids were tapered off (patients 1 and 4). This
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observation suggests that seizure may be a distinct clinical manifestation of MOG antibody
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disease in addition to commonly recognized demyelinating relapses such as ON, transverse

myelitis, or ADEM. The two patients who had seizures outside of ADEM episodes were started
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on antiepileptic medications; no patients had any seizure recurrence and all have been off of
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antiepileptics for at least several months. None of our patients were found to have other systemic

diseases after extensive workup and long follow up in some cases (up to 19 years in case 4).
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Seizures have been increasingly described in anti-MOG syndromes. In a large case series of 50

anti-MOG antibody positive patients, only one patient was reported to have a seizure in the

setting of sinus venous thrombosis, which was thought to have been provoked by high dose

steroid therapy [5]. However, in a pediatric series, 5 out of 26 (19%) anti-MOG positive patients
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had a seizure [3]; it was not specified how many of them also had ON. A case report from Japan

describes an 8-year-old boy with a steroid-dependent optic neuritis who developed seizures

during a steroid taper [9] and was found to have anti-MOG antibodies in serum, which bears

close similarity to our patient 1, except for the age for onset.

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An interesting case series from Japan presented four patients with anti-MOG antibodies,

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unilateral ‘focal encephalitis’ and seizures associated with cortical T2/FLAIR hyperintense

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lesions during the acute phase; two of the four patients also had optic neuritis [6]. Our patient 1

showed a left subcortical lesion during an episode of confusion and generalized seizure that

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resolved on 3 month follow up scan (Fig. 1C-1D), which is similar to MRI findings in some of
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the ‘focal encephalitis’ patients in the Japanese case series with unilateral cortical signal changes.

More recently Hamid et al. found that in their cohort of 34 patients with MOG antibodies, 5
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patients had seizures, which was a much higher rate than in AQP4-positive NMO patients [7].
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Four of the 5 patients also had optic neuritis during the course of illness, which was recurrent in

3 patients, and some patients demonstrated symptom recrudescence with steroid taper similar to
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our patient #1[7]. All of the patients with seizures in Hamid et al. series demonstrated
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“inflammatory cortical brain lesions” that were sometimes quite extensive but could also be

localized to small area of the cortex or brainstem[7]. Four of five patients in the cohort had
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encephalopathy during the episode of seizure [7] as did 2 out of 4 patients in our series (cases 2-

3).

Three patients in our series (patients 1, 3, and 4) fit broadly into the category of chronic relapsing

inflammatory optic neuropathy (CRION) with recurrent episodes of steroid dependent optic
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neuritis in the absence of other systemic or inflammatory disease such as sarcoidosis [10].

CRION is a phenotypic description of a syndrome that quite possibly represents a heterogeneous

group of patients with varying underlying immunologic phenotypes including a subset that will

be found to have MOG antibodies as has already been recognized in several cohorts [4,11].

Huppke et al and Baumann et al both describe pediatric patients with ADEM and optic neuritis

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which in some cases was recurrent in patients with anti-MOG antibodies [12,13]; intervals

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between ADEM and optic neuritis was up to 2 years in these series, while in our cohort there was

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delay up to 10 years.

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More specific MOG antibody testing has only become available recently and therefore it is not
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possible to correlate titers with symptoms in these patients though case 4 has demonstrated

persistent MOG antibody positivity over the past several years. These cases highlight the
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importance of revisiting the diagnosis of patients with atypical demyelinating syndromes as new
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antibodies are discovered. ADEM and optic neuritis, even with events separated over many years,

should prompt testing for MOG antibodies as this may have implications for prognosis and
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optimal treatment.
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Anti-MOG antibodies have been associated with a wide spectrum of presentations, and the
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spectrum is likely to expand further as commercial testing for anti-MOG antibodies using highly

sensitive cell-based IgG1-directed assays has recently become available at Mayo Clinic

Laboratory. While the mode of pathogenesis of these antibodies is not known, several cases have

been found with lesions exhibiting inflammatory demyelination with MS type II pathology [1].
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While there is no definitive therapy for MOG related disease at this time, it is probable that more

targeted therapies may be available in the future.

Our cases highlight that MOG antibody testing should be considered in patients with recurrent,

steroid-dependent optic neuritis who test negative for other common etiologies such as MS,

AQP4 positive NMOSD, or sarcoidosis, especially if the patient develops seizure during steroid

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taper or during an ADEM-like episode.

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Highlights
 Four patients with optic neuritis and seizure were MOG antibody seropositive.
 Episodes of seizure and optic neuritis were separated by up to ten years.
 Seizures occurred either in the setting of ADEM or during steroid taper.
 Seizure in a patient with prior optic neuritis should prompt MOG antibody testing.

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