# French guidelines for the diagnostic and management of MOG antibody-associated disease.

L. Giorgi, R. Marignier, J. Pique, H. Maurey, C. Papeix, J. Ciron, N.

Collongues, E. Cheuret, Helene Zorphir, P. Meyer, et al.

► To cite this version:

L. Giorgi, R. Marignier, J. Pique, H. Maurey, C. Papeix, et al. French guidelines for the diagnostic and management of MOG antibody-associated disease. Revue Neurologique, 2025, Rev Neurol (Paris), 10.1016/j.neurol.2025.04.012. hal-05303403

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Practice guidelines

# French guidelines for the diagnosis and management of MOG antibody-associated disease ☆

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L. Giorgi<sup>a,\*</sup>, R. Marignier<sup>b</sup>, J. Pique<sup>b</sup>, H. Maurey<sup>a</sup>, C. Papeix<sup>c</sup>, J. Ciron<sup>d</sup>, N. Collongues<sup>e</sup>, E. Cheuret<sup>f</sup>, H. Zephyr<sup>g</sup>, P. Meyer<sup>h</sup>, S. Vukusic<sup>b</sup>, M. Doret-Dion<sup>i</sup>, M.-T. Abi Warde<sup>j</sup>, A.-L. Poulat<sup>k</sup>, E. Barreau<sup>l</sup>, R. Deschamps<sup>c</sup>, B. Audoin<sup>m</sup>, I. Mannes<sup>n</sup>, E. Yver<sup>o</sup>, C. Lattaud<sup>p</sup>, E. Maillart<sup>q</sup>, K. Deiva<sup>a</sup> on behalf of MIRCEM network<sup>1</sup>

<footnote><sup>a</sup>Service de neurologie pédiatrique, AP-HP, Hôpitaux Universitaires Paris-Saclay, site Bicêtre, 78, avenue du Général Leclerc, 94270 Le Kremlin Bicêtre, France</footnote>

<footnote><sup>b</sup>Service de neurologie, Hospices Civils de Lyon, Lyon, France</footnote>

<footnote><sup>c</sup>Service de neurologie, Fondation Rothschild, Paris, France</footnote>

<footnote><sup>d</sup>Service de neurologie, CHU de Toulouse, Toulouse, France</footnote>

<footnote><sup>e</sup>Service de neurologie, CHRU Strasbourg, Strasbourg, France</footnote>

<footnote><sup>f</sup>Service de neuropédiatrie, CHU de Toulouse, Toulouse, France</footnote>

<footnote><sup>g</sup>Service de neurologie, CHU de Lille, Lille, France</footnote>

<footnote><sup>h</sup>Service de neuropédiatrie, CHU de Montpellier, Montpellier, France</footnote>

<footnote><sup>i</sup>Service de gynécologie-obstétrique Hospices Civils de Lyon, Lyon, France</footnote>

<footnote><sup>j</sup>Service de neuropédiatrie, CHU de Strasbourg, Strasbourg, France</footnote>

<footnote><sup>k</sup>Service de neuropédiatrie, CHU de Lyon, Lyon, France</footnote>

<footnote><sup>l</sup>Service d'ophtalmologie, AP-HP, Hôpitaux Universitaires Paris-Saclay, site Bicêtre, Le Kremlin-Bicêtre, France</footnote>

<footnote><sup>m</sup>Service de neurologie, CHU de Marseille, Marseille, France</footnote>

<footnote><sup>n</sup>Service de radiopédiatrie, AP-HP, Hôpitaux Universitaires Paris-Saclay, site Bicêtre, Le Kremlin-Bicêtre, France</footnote>

<footnote><sup>o</sup>AP-HP, Hôpitaux Universitaires Paris-Saclay, site Bicêtre, Le Kremlin-Bicêtre, France</footnote>

<footnote><sup>p</sup>CHU de Pitié Salpêtrière, Pitié Salpêtrière, France</footnote>

<footnote><sup>q</sup>Service de neurologie, CHU de Pitié Salpêtrière, Pitié Salpêtrière, France</footnote>

<footnote>Given their role as Associate Editors, the authors Caroline Papeix and Hélène Zephyr had no involvement in the peer-review process of this article, nor did they have access to any information regarding this process. They did not participate in the decision-making regarding the article.</footnote>

<footnote>* Corresponding author.</footnote>

<footnote>E-mail address: laetitia.giorgi@aphp.fr (L. Giorgi).</footnote>

<footnote n="1">¹ You can find more information about the MIRCEM NETWORK at the link in the “Acknowledgements” section at the end of the article. https://doi.org/10.1016/j.neurol.2025.04.012</footnote>

<footnote>0035-3787/© 2025 The Authors. Published by Elsevier Masson SAS. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).</footnote>
## INFO ARTICLE

Article history:

Received 18 February 2025
Received in revised form
22 April 2025
Accepted 24 April 2025
Available online 9 June 2025

Keywords:

Myelin oligodendrocyte glycoprotein
antibody associated disease
Acute disseminated
encephalomyelitis
Optic neuritis
Therapeutic management

## ABSTRACT

MOG antibody-associated disease (MOGAD) is a new entity within the spectrum of autoimmune inflammatory diseases of the central nervous system. It is distinct from multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD). Although they share certain clinical characteristics, these 3 diseases differ in terms of their pathophysiology, disease course and response to treatment. MOGAD is a rare disease affecting both adults and children, with a higher frequency in the latter. The clinical presentation of MOGAD varies depending on age: in children under the age of 10, presentations of acute disseminated encephalomyelitis (ADEM) are frequently described, whereas in children over the age of 10 and in adults, unilateral or bilateral optic neuritis or acute myelitis is more often observed. Other, rarer presentations have also been reported, including encephalitic presentations with seizures. Radiologic findings can sometimes help guide the diagnosis: extensive anterior optic nerve involvement, perineuritis, extensive lesions of the spinal cord with involvement of the conus medullaris, and involvement of the pons, for example. Diagnosis is confirmed by measuring anti-MOG antibodies in the serum. In case of diagnostic doubt, the result must be confirmed in a reference laboratory (currently available in Lyon and Le Kremlin Bicêtre in France). The disease course is usually monophasic in children, but relapses are possible. In adults, the frequency of relapses seems higher than in children, estimated at more than 40% after 5 years. Visual, bladder/sphincter, cognitive and, to a lesser extent, motor sequelae may occur, but much less frequently than in NMOSD. In children and adults, attacks are treated with high-dose IV corticosteroids, which are often very effective, followed by an oral taper. In certain situations, long-term immunoactive therapy may be proposed, particularly when a relapse occurs, after discussion with a reference or expert center for Inflammatory diseases of the central nervous system. Long-term follow-up is proposed at the reference/expert center at least once a year. In between these appointments, follow-up with the referring pediatric neurologist, pediatrician, treating physician or referring neurologist is carried out every 6 months. It is important to check for the occurrence of a new attack and the onset of complications but also, in the case of long-term therapy, adherence to and tolerance of the treatment. Multidisciplinary management is essential and involves a variety of healthcare professionals (neurologist or pediatric neurologist, ophthalmologist, physiatrist, physiotherapist, speech therapist, occupational therapist, psychologist and social worker).

© 2025 The Authors. Published by Elsevier Masson SAS. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

## 1. Abbreviations

<table><tr><td>ADEM</td><td>acute disseminated encephalomyelitis</td></tr><tr><td>ART</td><td>assisted reproductive technology</td></tr><tr><td>CBA</td><td>cell-based assay</td></tr><tr><td>CSF</td><td>cerebrospinal fluid</td></tr><tr><td>FLAMES</td><td>FLAIR-hyperintense lesions in MOG-Ab associated encephalitis with seizures</td></tr><tr><td>IG</td><td>immunoglobulin</td></tr><tr><td>IV</td><td>intravenous</td></tr><tr><td>IVIG</td><td>intravenous immunoglobulin</td></tr><tr><td>MDEM</td><td>multiphasic disseminated encephalomyelitis</td></tr><tr><td>MOG</td><td>myelin oligodendrocyte glycoprotein</td></tr><tr><td>MOG-Ab</td><td>MOG antibody</td></tr><tr><td>MOGAD</td><td>MOG antibody-associated disease</td></tr><tr><td>MRI</td><td>magnetic resonance imaging</td></tr><tr><td>MS</td><td>multiple sclerosis</td></tr><tr><td>NMDAR</td><td>N-methyl-D-aspartate receptor</td></tr><tr><td>NMOSD</td><td>neuromyelitis optica spectrum disorder</td></tr><tr><td>OCT</td><td>optical coherence tomography</td></tr></table>

<table><tr><td>ON</td><td>optic neuritis</td></tr><tr><td>PMR</td><td>physical medicine and rehabilitation</td></tr><tr><td>PNS</td><td>peripheral nervous system</td></tr><tr><td>STIR</td><td>short TI inversion recovery</td></tr><tr><td>VA</td><td>visual acuity</td></tr><tr><td>VEP</td><td>visual evoked potentials</td></tr></table>

## 2. Introduction

MOG antibody-associated disease (MOGAD) is a rare autoimmune inflammatory disease of the central nervous system, distinct from multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD) in terms of its pathophysiology, its clinical and radiological presentation, disease course and response to treatment [1-16].

Its exact incidence and prevalence remains unknown. A national study from the Netherlands calculated an average annual incidence across the country from 2015 to 2017 of 0.16/
100,000 in adults and 0.31/100,000 in children [17]. The sex ratio is close to 1 and the disease preferentially affects children and young adults [17].

### 3. Methodology

The methodology used to develop these guidelines was based on the 2012 recommendations of the Haute Autorité de Santé (HAS). (https://www.has-sante.fr/jcms/c_1340205/fr/methode-d-elaboration-des-protocoles-nationaux-de-diagnostic-et-de-soins-pnds). These guidelines were written in 2022.

### 4. Clinical presentation

The initial clinical phenotype of patients affected by MOGAD varies depending on age. In children under the age of 10, presentations of acute disseminated encephalomyelitis (ADEM) are frequently reported, whereas in children over the age of 10 and in adults, unilateral or bilateral optic neuritis or acute myelitis is more often observed [5,14,17-21]. The disease course also varies between patients, either with a monophasic course with a single attack or a relapsing one with a variable frequency of further attacks [2,5,16,17,22].

Banwell and al. [23], propose as diagnostic criteria: the association of a clinical presentation and clear positive MOG-IgG test results in serum. In case of clear positive MOG-IgG test results in serum or seronegative, additional MRI features are necessary.

#### 4.1. Optic neuritis

##### 4.1.1. Clinical picture

Optic neuritis (ON) is a frequent manifestation of MOGAD and the most common in adults and children over 10 years old [5,17,18,20,24-27]. It is characterized by a rapid decrease in visual acuity (VA) that develops within 24-72 hours, with the majority of cases being severe (VA of ≤ 1/10) and bilateral, as well as papilledema reported in 60-90% of cases. The loss of visual acuity is generally associated with, or preceded by eye pain that worsens with eye movement, sometimes described as headaches by the child and sometimes associated with true headaches that have nonspecific characteristics. There is also a reduction in contrast sensitivity, dyschromatopsia and, upon examination, a relative afferent pupillary defect (or Marcus Gunn sign) in cases of unilateral involvement, as well as visual field impairment [17,20,24,26-30].

Short-term prognosis is often good after high-dose intravenous corticosteroid therapy. However, functional sequelae or optic atrophy may be observed [16,17,26,30,31].

#### 4.1.2. MRI

Orbital MRI often confirms optic nerve involvement, showing generally extensive hyperintensity of the optic nerve in 80% of cases, and in half of the cases, the presence of optic perineuritis, characterized by poorly defined contrast enhancement of the nerve sheath and infiltration of the periorbital fat.

The optic nerves are frequently enlarged, particularly in the retrobulbar segment, with the optic chiasma and optic tracts usually spared. The involvement is bilateral in more than 50% of patients [5,8,20,25,26,29,30,32-37].

##### 4.1.3. Ophthalmologic exams

##### 4.1.3.1. Optical coherence tomography (OCT).
In the acute phase, optic disc edema will present as an increase in peripapillary nerve fiber layer thickness while the ganglion cell layer remains normal.

As the disease progresses, a thinning of the ganglion cell layer occurs within less than a month and optic nerve atrophy, which is usually global, becomes apparent within 2 to 3 months [17,18,29,38]. Retrospectively, OCT is a good way of confirming the past occurrence of clinically undetected anterior damage, especially when only the temporal fascicle is involved, which does not result in true optic atrophy on fundus examination.

There are no specific visual field abnormalities. There may be an enlargement of the blind spot associated with papilledema when the inflammation is located in the optic nerve sheath (perineuritis). When there is a severe decrease in visual acuity, the visual field often reveals a deep central or cecocentral scotoma. Visual evoked potentials (VEPs) are not useful in routine practice.

The disease course is most often favorable.

In the face of visual impairment, it is important to exclude other optic neuropathies of infectious or metabolic origin (Fig. 1).

### 4.2. Acute myelitis

#### 4.2.1. Clinical picture

Acute myelitis is the 2nd most frequent clinical manifestation of MOGAD in adults [18,19,21,39], and the 3rd most frequent in children [5,17,22,40]. It consists of motor, sensory and vesicospincter dysfunction. It may be isolated or associated with ON or ADEM in children [7,17,41]. The prognosis remains favorable due to its good response to corticosteroids, but this clinical manifestation carries the greatest risk of sequelae, in particular sphincter and erectile sequelae [1,16,18,19,42].

#### 4.2.2. MRI

MRI reveals spinal cord hyperintensity on T2 sequences (T2 Spin Echo, T2 STIR). In most cases of MOGAD it is longitudinally extensive myelitis, defined by the extension of hyperintensity (on sagittal T2 sequences) of the spinal cord over at least three consecutive vertebral segments [8,17,34,35,41-43]. However, short myelitis has also been reported, accounting for up to 40% of MOGAD-associated cases of myelitis [8,18,21].

In both cases, involvement is mainly in the central cord gray matter, explaining the “H sign” appearance in axial sequences and the linear sagittal hyperintensity in sagittal sequences. Contrast enhancement is less common and, when present, tends to have a patchy appearance [19,21,34,39].

Spinal cord lesions are most often found in the cervical or thoracic regions, but lesions of the conus are more common than in other causes of myelitis and should prompt consideration of this diagnosis [8].
<figure><img src="image_3.png" /><figcaption>Fig. 1 – Optic neuropathy decision tree.</figcaption></figure>

A while after the acute attack, spinal MRI may appear normal and spinal cord atrophy is rare in MOGAD [8,19,21].

The two main differential diagnoses of myelitis are MS and NMOSD, but other origins should be considered (Fig. 2).

## 4.3. Acute disseminated encephalomyelitis (ADEM)

### 4.3.1. Clinical picture

Although very rare in adults, it is the first most common initial presentation of MOGAD seen in children, particularly in those under the age of 10 [5,17]. It is characterized by the association of encephalitic signs (altered level of consciousness or behavioral changes) not explained by fever, multifocal neurologic deficits (motor, sensory, visual, etc.), and a suggestive brain MRI [7,17]. Relapses, defined by the appea-

rance of new neurologic symptoms within 3 months of the first episode of ADEM, can either be a new episode of ADEM (MDEM: multiphasic disseminated encephalomyelitis) or one or more episodes of optic neuritis (ADEM-ON) [17].

### 4.3.2. MRI

In MOGAD-associated ADEM, there are multiple, bilateral T2/FLAIR hyperintensities, with blurred margins, that are extensive (often > 2 cm) and found in the subcortical and deep white matter and the deep grey matter (less commonly the cortical grey matter). Thalamic lesions, as well as those in the middle cerebellar peduncles and pons, are common [7,8].

Contrast enhancement, which is less frequent than in MS or NMOSD, is often quite extended and diffuse.

<figure><img src="image_4.png" /><figcaption>Fig. 2 – Myelitis decision tree.</figcaption></figure>
## 4.4. Cortical encephalitis (FLAIR-hyperintense Lesions in MOG-Ab associated Encephalitis with Seizures (FLAMES))

### 4.4.1. Clinical picture

Cortical encephalitis with seizures (FLAMES: FLAIR-hyperintense lesions in MOG-Ab associated encephalitis with seizures) is rare. It manifests with epileptic seizures as the main feature (85% of patients), often preceded by headaches, behavioral or pseudo-psychiatric disorders, impaired alertness, and sometimes fever and cortical symptoms that vary according to the region involved, occurring either immediately or following the critical phase [17,44-46].

It is important to test for the presence of anti-N-methyl-D-aspartate receptor (NMDAR) and anti-glycine receptor antibodies, not only for the differential diagnosis but also due to reports of co-autoimmunity, even though cases like this appear to be rare [47].

### 4.4.2. MRI

MRI reveals a T2/FLAIR hyperintensity and diffusion restriction of the cortical ribbon, with an edematous appearance of the cortex and sometimes hyperintensities in the subarachnoid spaces, associated with leptomeningeal contrast enhancement. The involvement in most cases is unilateral [8,44,46].

## 4.5. Brainstem involvement

### 4.5.1. Clinical picture

The prevalence of brainstem involvement in patients with MOGAD is estimated to be between 10% and 30% in adult series, and 9% in the pediatric series [5,6,17,18,48]. It is rarely isolated and is most often associated with ON and/or acute myelitis [6,17]. Symptoms can vary: cerebellar syndrome, cranial nerve involvement and involvement of the lemniscal pathway. Area postrema syndrome is much rarer in patients with MOGAD than in those with NMOSD [6,48].

### 4.5.2. MRI

Lesions of the brainstem are often diffuse, extensive in the axial plane, or affecting several regions of the brainstem. The most affected structures are, respectively: the pons (35% and 85%), the medulla oblongata (14% and 57%), and the middle cerebellar peduncles (46%) [6,8,9,34,48].

## 4.6. Other phenotypes

The “leukodystrophy-like” phenotype with extensive, confluent and symmetrical lesions, which are atypical for ADEM, is described in patients with MOGAD, especially in children [17,49,50]. The initial presentation is one of encephalitis, with ataxia (100%), optic neuritis (71%) and/or epilepsy (43%). Only partial improvement is achieved with corticosteroids, with cognitive and behavioral problems occurring in 57% of cases, epilepsy in 43% and a relapsing course in 40% of patients [17,49,50].

Although the MOG protein is not present in the peripheral nervous system (PNS), rare cases of peripheral nervous system involvement have been described (cranial nerves, myeloradiculitis, and polyneuropathies), in both adults and children,

more or less associated with central nervous system involvement [17,51,52].

## 5. Confirming the diagnosis

Imaging support the diagnosis, confirming the suspected attack based on clinical data. They equally provide qualitative information to guide the etiological diagnosis towards MOGAD rather than another inflammatory disease of the central nervous system: extensive anterior optic nerve involvement, perineuritis, extensive lesions of the spinal cord with involvement of the conus, and involvement of the pons.

Much more rarely, the radiologic findings may mimic those of MS and meet the Barkhof criteria. Contrast enhancement is observed and is mainly nodular, but may also be open ring-like, similar to what is seen in MS. The absence of a “Dawson finger” pattern of lesions is a red flag for MS, and should prompt a search for the presence of MOG antibodies. The presence of black holes on T1-weighted imaging is very atypical and should raise suspicion of MS.

In the presence of a suggestive clinical picture and MRI findings typical of MS in adults, MOG antibody testing is not recommended, as there is a risk of false-positive results and of misdiagnosis.

Diagnosis is confirmed by measuring serum levels of MOG antibodies [23,53-55]. In case of diagnostic uncertainty, the result must be confirmed in a reference laboratory (in France there are two: one in Lyon and one at Bicêtre Hospital in Paris) with a cell-based assay, using live cells (live CBA), ideally before starting any immunoactive therapy [54,55]. The clinical relevance of testing CSF for MOG-Ab is still currently being evaluated.

In the event of a negative result and if the clinical presentation is suggestive, a new MOG-Ab assay is recommended.

CSF analysis reveals pleocytosis in almost half of all cases, with lymphocytic predominance. The presence of intrathecal synthesis (presence of unmatched oligoclonal bands) is very rare, unlike in MS [41,56-59].

## 6. Disease evolution

A relapse is defined as a recurrence after 28 days. A worsening of signs or the appearance of new clinical signs may occur during the initial attack after corticosteroid therapy is stopped, and in the absence of an oral corticosteroid taper, hence the one month necessary delay before considering the occurrence of a second actual attack.

In children, the disease course is usually monophasic but relapses are possible, mainly in the form of ON. Prognostic factors for relapse include an initial clinical presentation of ON, an older age and persistent MOG-Ab, especially at high titers (> 1:1280) [5,16,17,22,40,60,61].

In adults, the frequency of relapses appears to be higher than in children, estimated at more than 40% at five years, with the highest risk of relapse occurring in the first few years following the initial attack [2,18,22]. To date, no reliable factor has been identified to predict the risk of relapse in adults,
although the disappearance of antibodies during follow-up appears to be correlated with a lower risk of relapse, as it is in children. Male gender and spinal cord involvement during the initial attack also appear to be factors that reduce the risk of relapse.

Despite the severity of symptoms at the nadir of the attack, recovery is generally good after the first episode, and sequelae are more significant in the case of relapses [5,16,18,20,25,30,31,48,61]. Visual, bladder/sphincter, cognitive and, to a lesser extent, motor sequelae may occur, but much less frequently than in NMOSD. In patients presenting with ADEM, neurocognitive follow-up is essential as more than 40% of these children may potentially develop sequelae [5,16].

Radiologically, we can observe a complete disappearance of lesions in all anatomical regions: optic nerve, spinal cord, and brain. This evolution is highly specific to MOGAD [8,9,12,32,34,35,41,55]. Moreover, the accumulation of asymptomatic lesions over time, typical of MS, seems to be exceptional in MOGAD.

# 7. Therapeutic management

## 7.1. Treatment of the initial attack and/or relapses

In adults and children, treating an attack is an emergency, with first-line therapy consisting of high-dose IV methylprednisolone at a dose of 30 mg/kg/day (without exceeding 1 gram), for 3 to 5 days, depending on the severity of the attack and the degree of improvement reached by the 3rd day of treatment [40,62,63]. In the event of insufficient recovery, a 2nd series of corticosteroid pulses over 3 to 5 days is recommended [62,64]. Symptoms are usually highly responsive to corticosteroids.

Oral corticosteroids are then recommended at a dose of 1 mg/kg/day (maximum 60 mg/day) for one month, starting

immediately after cessation of intravenous corticosteroid therapy, followed by 0.5 mg/kg/day for one month, then a gradual tapering over one month, for a total of 3 months [62,65]. Associated measures (contraindication of live vaccines, balanced diet that maintains normal blood sugar and sodium levels, vitamin and calcium supplementation) must also be followed.

Intravenous immunoglobulin (IVIG) at a dose of 2 g/kg over 2 to 5 days and therapeutic apheresis (plasmapheresis and/or immunoadsorption) are 2nd-line treatments in the event of cortico-resistance and/or insufficient recovery [62,66]. They should be proposed quickly (before days 10-15) in severe forms at risk of sequelae (acute transverse myelitis in particular and sometimes optic neuritis), after consultation with an expert center.

In the event of poor recovery in children, induction treatment with rituximab may be proposed (Fig. 3).

## 7.2. Maintenance therapy

A maintenance treatment, aimed at reducing relapses and sequelae, is proposed in certain situations: when a relapse occurs or in case of poor recovery, assessed 1 to 3 months after the initial episode for example, following consultation with a reference or expert center specializing in rare inflammatory diseases of the brain and spinal cord [40,62,64].

Due to the risk of relapse, which seems to be highest in the initial years and decreases significantly thereafter, discontinuation of treatment should be discussed after two to three years of treatment, in the absence of a new clinical episode [40,62,64].

Azathioprine, mycophenolate mofetil and monthly IVIG infusions appear to be promising first-line therapies for MOGAD [40,62,64,67-71] (Fig. 2: Maintenance treatment in children).

<figure><img src="image_5.png" /><figcaption>Fig. 3 – Attack treatment in children.</figcaption></figure>
<figure><img src="image_6.png" /><figcaption>Fig. 4 – Maintenance treatment in children.</figcaption></figure>

The role of anti-CD20 therapy such as rituximab in adult patients is debated given its demonstrated lack of efficacy in certain case series or retrospective studies [25,64,72,73].

In the event of relapses while under therapy in children, we suggest switching to rituximab or monthly IVIG if the initial treatment was azathioprine or mycophenolate mofetil, or combining rituximab and IVIG if the initial treatment was one of the 2 [40,62]. New therapies, such as tocilizumab (anti-IL6) or anti-complement agents, can be considered after consultation with the reference center [57,62,74,75] (Fig. 4).

In adults, several treatments have been shown to be of interest in this situation, mainly anti-IL-6 receptor therapy and IVIG therapy [69,74,75].

In all cases, an expert opinion from a reference or expert center specializing in rare inflammatory diseases of the brain and spinal cord is required.

## 8. Follow-up

An annual follow-up consultation at a reference/expert center is recommended. In between, clinical follow-up by the referring neurologist/pediatric neurologist and the treating physician is carried out at least once every 6 months.

At each consultation, it is important to check for the occurrence of a new attack, to assess the impact of sequelae from previous attacks, and to evaluate adherence to and tolerance of treatments (maintenance or symptomatic) [5,16,18,31,63,76].

The value of monitoring MOG-Ab serologic status remains debated. Several studies suggest an association between persistent MOG-Ab positivity and the risk of relapse [53,60,77]. It is suggested that serum antibody levels be monitored every 6 months for the first 2 years, and then according to the clinical progression of the disease.

It is recommended to perform follow-up imaging on the same type of MRI machine and using the same acquisition protocol.

At the time of the first inflammatory attack, or during a new attack, it is recommended to perform an MRI of the brain, optic nerves and the whole spinal cord, both without and with injection of contrast. In the event of an attack involving the spinal cord, it is recommended that whole spine MRI include the cauda equina.

In adults, it is recommended to perform an MRI scan with and without contrast 6 months after the relapse, focusing on the region affected during the last relapse, followed by a brain MRI (± optic nerves) and a whole spine MRI without contrast between 12 and 18 months after the relapse. Durand-Dubief and al. [78] propose that in the absence of clinical activity, a cerebral (± optic nerves) and spinal cord MRI should be performed without gadolinium injection every 3 years.

In children, MRI follow-up at 6 months (focusing on the region affected during the last attack), at 12 months, and then at 2 years is recommended. Intravenous gadolinium contrast should be administered during the initial assessment and repeated only in the event of clinical or radiological worsening [79].

Multidisciplinary management is essential, involving a range of healthcare professionals (neurologist or pediatric neurologist, ophthalmologist, physiotherapist, speech therapist, occupational therapist, psychologist and social worker).

Therapeutic patient education and connecting with a patient organization can help in improving the quality of life of patients and their families.

## 9. Pregnancy

Data show that the risk of relapses seems to decrease during pregnancy, compared with the year prior to pregnancy; however, it increases in the post-partum period [80-82].

It is recommended to consider the pregnancy planning of patients with MOGAD when choosing maintenance treatment [80]. Pregnancy planning should be favored during a period of MOGAD inactivity of at least 12 months.
A preconception consultation is recommended, if possible at a reference center for inflammatory diseases of the central nervous system (MIRCEM, CRC-SEP), to discuss the benefits and risks of discontinuing, continuing or switching maintenance therapy before conception, and to discuss the continuation, reduction or discontinuation of symptomatic treatments.

In the case of disabling sequelae, a physical medicine and rehabilitation (PMR) consultation is important in order to plan pregnancy, delivery and management of the disability with their child. A neuro-urology consultation is also important for the management of urinary and anorectal dysfunction.

The determination of mode of delivery should be based on obstetrical indications, regardless of the patient's disability. In patients with a significant disability, consultation between the neurologist, physiatrist and obstetrician is recommended.

Breastfeeding is not contraindicated in women with MOGAD. If treatment is resumed, the continuation of breastfeeding should be discussed on a case-by-case basis, depending on the molecules involved.

All types of assisted reproductive technology (ART) procedures can be offered to women with MOGAD, after consultation between the physician at the fertility clinic and the expert neurologist.

## 10. Conclusion

MOGAD is a rare disease that can affect people of all ages. Despite the variability seen in its clinical presentation, the availability of biologic diagnostic tests and the improved recognition of brain and spinal imaging signs enable an early diagnosis. Although the disease can be highly responsive to corticosteroids, relapses and sequelae are possible. New targeted therapies are currently being developed.

## Disclosure of interest

The authors declare that they have no competing interests.

## Acknowledgments

The authors thank BRAIN-TEAM network (https://brain-team.fr/les-membres/les-centres-de-reference/maladies-neuro-inflammatoires-de-lenfant/) and all the NOMADMUS, MIRCEM network, as well as Pr Caroline Froment Tilikete, Dr Marie-Caroline Pouget, Pr Sylvie Nguyen The Tich, Dr Bertrand Bourre, Pr Jérôme de Seze, patients, parents patients and members of the association NMO France for their support in the preparation of the manuscript, Mrs. Natasha Barr for translation.

## REFERENCES

[1] Absoud M, Greenberg BM, Lim M, Lotze T, Thomas T, Deiva K. Pediatric transverse myelitis. Neurology 2016;87(9_Supplement_2):S46-52.

[2] Akaishi T, Misu T, Fujihara K, Takahashi T, Takai Y, Nishiyama S, et al. Relapse activity in the chronic phase of anti-myelin-oligodendrocyte glycoprotein antibody-associated disease. J Neurol 2022;269(6):3136-46.

[3] Alshamrani F, Alnajashi H, Shosha E, Casserly C, Morrow SA. Case series: myelin oligodendrocyte glycoprotein-immunoglobulin g-related disease spectrum. Front Neurol 2020;11:89.

[4] Ambrosius W, Michalak S, Kozubski W, Kalinowska A. Myelin oligodendrocyte glycoprotein antibody-associated disease: current insights into the disease pathophysiology, diagnosis and management. Int J Mol Sci 2020;22(1):100.

[5] Armangue T, Olivé-Cirera G, Martínez-Hernandez E, Sepulveda M, Ruiz-Garcia R, Muñoz-Batista M, et al. Associations of paediatric demyelinating and encephalitic syndromes with myelin oligodendrocyte glycoprotein antibodies: a multicentre observational study. Lancet Neurol 2020;19(3):234-46.

[6] Banks SA, Morris PP, Chen JJ, Pittock SJ, Sechi E, Kunchok A, et al. Brainstem and cerebellar involvement in MOG-IgG-associated disorder versus aquaporin-4-IgG and MS. J Neurol Neurosurg Psychiatry 2020 [jnnp-2020-325121].

[7] Baumann M, Sahin K, Lechner C, Hennes EM, Schanda K, Mader S, et al. Clinical and neuroradiological differences of paediatric acute disseminating encephalomyelitis with and without antibodies to the myelin oligodendrocyte glycoprotein. J Neurol Neurosurg Psychiatry 2015;86(3):265-72.

[8] Baumann M, Bartels F, Finke C, Adamsbaum C, Hacohen Y, Rostásy K, et al. E.U. paediatric MOG consortium consensus: part 2 - Neuroimaging features of paediatric myelin oligodendrocyte glycoprotein antibody-associated disorders. Eur J Paediatr Neurol 2020;29:14-21.

[9] Baumann M, Grams A, Djurdjevic T, Wendel EM, Lechner C, Behring B, et al. MRI of the first event in pediatric acquired demyelinating syndromes with antibodies to myelin oligodendrocyte glycoprotein. J Neurol 2018;265(4):845-55.

[10] Bellinvia A, Pastò L, Razzolini L, Fratangelo R, Prestipino E, Fonderico M, et al. The clinical spectrum of anti-MOG associated acquired demyelinating disorders: three case-reports. Mult Scler Relat Disord 2019;33:51-4.

[11] Berzero G, Taieb G, Marignier R, Younan N, Savatovsky J, Leclercq D, et al. CLIPPERS mimickers: relapsing brainstem encephalitis associated with anti-MOG antibodies. Eur J Neurol 2018;25(2):e16-7.

[12] Biotti D, Bonneville F, Tournaire E, Ayrignac X, Dallière CC, Mahieu L, et al. Optic neuritis in patients with anti-MOG antibodies spectrum disorder: MRI and clinical features from a large multicentric cohort in France. J Neurol 2017;264(10):2173-5.

[13] Biotti D, Lerebours F, Bonneville F, Ciron J, Clanet M, Brassat D. Late-onset neutropenia and neurological relapse, during long-term rituximab therapy in myelin oligodendrocyte glycoprotein-antibody spectrum disorder. Mult Scler Houndmills Basingstoke Engl 2018;24(12):1645-7.

[14] Bouzar M, Daoudi S, Hattab S, Bouzar AA, Deiva K, Wildemann B, et al. Neuromyelitis optica spectrum disorders with antibodies to myelin oligodendrocyte glycoprotein or aquaporin-4: clinical and paraclinical characteristics in Algerian patients. J Neurol Sci 2017;381:240-4.

[15] Brayo P, Hartsell FL, Skeen M, Morgenlander J, Eckstein C, Shah S. The clinical presentation and treatment of MOG antibody disease at a single academic center: A case series. J Neuroimmunol 2019;337:577078.

[16] Bruijstens AL, Breu M, Wendel EM, Wassmer E, Lim M, Neuteboom RF, et al. E.U. paediatric MOG consortium consensus: Part 4 - Outcome of paediatric myelin
oligodendrocyte glycoprotein antibody-associated
disorders. Eur J Paediatr Neurol 2020;29:32-40.

[17] Bruijstens AL, Lechner C, Flet-Berliac L, Deiva K, Neuteboom RF, Hemingway C, et al. E.U. paediatric MOG consortium consensus: Part 1 - Classification of clinical phenotypes of paediatric myelin oligodendrocyte glycoprotein antibody-associated disorders. Eur J Paediatr Neurol 2020;29:2-13.

[18] Deschamps R, Pique J, Ayrignac X, Collongues N, Audoin B, Zéphir H, et al. The long-term outcome of MOGAD: An observational national cohort study of 61 patients. Eur J Neurol 2021;28(5):1659-64.

[19] Dubey D, Pittock SJ, Krecke KN, Morris PP, Sechi E, Zalewski NL, et al. Clinical, radiologic, and prognostic features of myelitis associated with myelin oligodendrocyte glycoprotein autoantibody. JAMA Neurol 2019;76(3):301-9.

[20] Chen JJ, Flanagan EP, Jitprapaikulsan J, López-Chiriboga ASS, Fryer JP, Leavitt JA, et al. Myelin oligodendrocyte glycoprotein antibody-positive optic neuritis: clinical characteristics, radiologic clues, and outcome. Am J Ophthalmol 2018;195:8-15.

[21] Ciron J, Cobo-Calvo A, Audoin B, Bourre B, Brassat D, Cohen M, et al. Frequency and characteristics of short versus longitudinally extensive myelitis in adults with MOG antibodies: a retrospective multicentric study. Mult Scler Houndmills Basingstoke Engl 2020;26(8):936-44.

[22] Cobo-Calvo A, Ruiz A, Rollot F, Arrambide G, Deschamps R, Maillart E, et al. Clinical features and risk of relapse in children and adults with myelin oligodendrocyte glycoprotein antibody-associated disease. Ann Neurol 2021;89(1):30-41.

[23] Banwell B, Bennett JL, Marignier R, Kim HJ, Brilot F, Flanagan EP, et al. Diagnosis of myelin oligodendrocyte glycoprotein antibody-associated disease: International MOGAD Panel proposed criteria. Lancet Neurol 2023;22(3):268-82.

[24] Ducloyer JB, Caignard A, Aidaoui R, Ollivier Y, Plubeau G, Santos-Moskalyk S, et al. MOG-Ab prevalence in optic neuritis and clinical predictive factors for diagnosis. Br J Ophthalmol 2020;104(6):842-5.

[25] Etemadifar M, Abbasi M, Salari M, Etemadifar F, Tavakoli H. Comparing myelin oligodendrocyte glycoprotein antibody (MOG-Ab) and non MOG-Ab associated optic neuritis: clinical course and treatment outcome. Mult Scler Relat Disord 2019;27:127-30.

[26] Merabtene L, Vignal Clermont C, Deschamps R. Neuropathie optique dans le syndrome des anticorps anti MOG positif. J Fr Ophtalmol 2019;42(10):1100-10.

[27] Wendel EM, Baumann M, Barisic N, Blaschek A, Coelho de Oliveira Koch E, Della Marina A, et al. High association of MOG-IgG antibodies in children with bilateral optic neuritis. Eur J Paediatr Neurol 2020;27:86-93.

[28] Toanen V, Vignal-Clermont C. Neuropathies optiques inflammatoires. PubMed [Internet] 2016. www.em-premium.com/data/traites/op/21-71372. - Search Results. Disponible sur: https://pubmed.ncbi.nlm.nih.gov/?term=Toanen+V%2C+Vignal-Clermont+C+%282016%29+Neuropathies+optiques+inflammatoires.%2F%2Fwww.em-premium.com%2Fdata%2Ftraites%2Fop%2F21-71372. &filter=datesearch.y_10. [cité 28 mars 2025].

[29] Cheuret E, Meyer P, Varenne F, Leboucq N, Biotti D, Deiva K. Prise en charge de la neuropathie optique inflammatoire de l'enfant. J Pédiatrie Puériculture 2021;34(3):115-21.

[30] Jelcic I, Hanson JVM, Lukas S, Weber KP, Landau K, Pless M, et al. Unfavorable structural and functional outcomes in myelin oligodendrocyte glycoprotein antibody-associated optic neuritis. J Neuro-Ophthalmol 2019;39(1):3-7.

[31] Song H, Zhou H, Yang M, Xu Q, Sun M, Wei S. Clinical characteristics and outcomes of myelin oligodendrocyte

glycoprotein antibody-seropositive optic neuritis in varying age groups: a cohort study in China. J Neurol Sci 2019;400:83-9.

[32] Ramanathan S. Prelog K, Barnes EH, Tantsis EM, Reddel SW, Henderson APD, et al. Radiological differentiation of optic neuritis with myelin oligodendrocyte glycoprotein antibodies, aquaporin-4 antibodies, and multiple sclerosis. Mult Scler Houndmills Basingstoke Engl 2016;22(4):470-82.

[33] Shor N, Aboab J, Maillart E, Lecler A, Bensa C, Le Guern G, et al. Clinical, imaging and follow-up study of optic neuritis associated with myelin oligodendrocyte glycoprotein antibody: a multicentre study of 62 adult patients. Eur J Neurol 2020;27(2):384-91.

[34] Shor N, Deschamps R, Cobo Calvo A, Maillart E, Zéphir H, Ciron J, et al. MRI characteristics of MOG-Ab associated disease in adults: An update. Rev Neurol (Paris) 2021;177(1-2):39-50.

[35] Salama S, Khan M, Levy M, Izbudak I. Radiological characteristics of myelin oligodendrocyte glycoprotein antibody disease. Mult Scler Relat Disord 2019;29:15-22.

[36] Lotan I, Brody J, Hellmann MA, Bialer O, Ganelin-Cohen E, Michaeli N, et al. Myelin oligodendrocyte glycoprotein-positive optic neuritis masquerading as pseudotumor cerebri at presentation. J Neurol 2018;265(9):1985-8.

[37] Lopez-Chiriboga AS, Van Stavern G, Flanagan EP, Pittock SJ, Fryer J, Bhatti MT, et al. Myelin oligodendrocyte glycoprotein antibody (MOG-IgG)-positive optic perineuritis. Neuro-Ophthalmol Aeolus Press 2020;44(1):1-4.

[38] Korobelnik JF. OCT en ophtalmologie: rapport 2019. Issy-les-Moulineaux: Elsevier Masson; 2019.

[39] Chien C, Scheel M, Schmitz-Hübsch T, Borisow N, Ruprecht K, Bellmann-Strobl J, et al. Spinal cord lesions and atrophy in NMOSD with AQP4-IgG and MOG-IgG associated autoimmunity. Mult Scler Houndmills Basingstoke Engl 2019;25(14):1926-36.

[40] Hacohen Y, Wong YY, Lechner C, Jurynczyk M, Wright S, Konuskan B, et al. Disease course and treatment responses in children with relapsing myelin oligodendrocyte glycoprotein antibody-associated disease. JAMA Neurol 2018;75(4):478-87.

[41] Loos J, Pfeuffer S, Pape K, Ruck T, Luessi F, Spreer A, et al. MOG encephalomyelitis: distinct clinical, MRI and CSF features in patients with longitudinal extensive transverse myelitis as first clinical presentation. J Neurol 2020;267(6):1632-42.

[42] Taieb G, Labauge P. Anti-MOG antibodies with longitudinally extensive transverse myelitis preceded by CLIPPERS. Neurology 2015;85(14):1262-3.

[43] Transverse Myelitis Consortium Working group. Proposed diagnostic criteria and nosology of acute transverse myelitis. Neurology 2002;59(4):499-505.

[44] Budhram A, Mirian A, Le C, Hosseini-Moghaddam SM, Sharma M, Nicolle MW. Unilateral cortical FLAIR-hyperintense Lesions in Anti-MOG-associated Encephalitis with Seizures (FLAMES): characterization of a distinct clinico-radiographic syndrome. J Neurol 2019;266(10):2481-7.

[45] Tao R, Qin C, Chen M, Yu HH, Wu LJ, Bu BT, et al. Unilateral cerebral cortical encephalitis with epilepsy: a possible special phenotype of MOG antibody-associated disorders. Int J Neurosci 2020;130(11):1161-5.

[46] Ogawa R, Nakashima I, Takahashi T, Kaneko K, Akaishi T, Takai Y, et al. MOG antibody-positive, benign, unilateral, cerebral cortical encephalitis with epilepsy. Neurol Neuroimmunol Neuroinflammation 2017;4(2):e322.

[47] Ramberger M, Bsteh G, Schanda K, Höftberger R, Rostásy K, Baumann M, et al. NMDA receptor antibodies: a rare
association in inflammatory demyelinating diseases. Neurol Neuroimmunol Neuroinflammation 2015;2(5):e141.

[48] Jarius S, Kleiter I, Ruprecht K, Asgari N, Pitarokoili K, Borisow N, 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(1):281.

[49] Yazbeck E, Maurey H, Leroy C, Horellou P, Napuri S, Lali M, et al. Progressive leukodystrophy-like demyelinating syndromes with MOG-antibodies in children: a rare under-recognized phenotype. Neuropediatrics 2021;52(4):337-40.

[50] Hacohen Y, Rossor T, Mankad K, Chong W, 'Kling', Lux A, Wassmer E, et al. 'Leukodystrophy-like' phenotype in children with myelin oligodendrocyte glycoprotein antibody-associated disease. Dev Med Child Neurol 2018;60(4):417-23.

[51] Cobo-Calvo A, Ayrignac X, Kerschen P, Horellou P, Cotton F, Labauge P, et al. Cranial nerve involvement in patients with MOG antibody-associated disease. Neurol Neuroimmunol Neuroinflammation 2019;6(2):e543.

[52] Shen Y, Cheng Z, Zhou C. Bilateral trigeminal root entry zone enhancement in MOG-IgG-associated brainstem encephalitis. Neurol Sci 2019;40(5):1083-5.

[53] Armangue T, Capobianco M, de Chalus A, Laetitia G, Deiva K. E.U. paediatric MOG consortium. E.U. paediatric MOG consortium consensus: Part 3 - Biomarkers of paediatric myelin oligodendrocyte glycoprotein antibody-associated disorders. Eur J Paediatr Neurol 2020;29:22-31.

[54] Reindl M, Schanda K, Woodhall M, Tea F, Ramanathan S, Sagen J, et al. International multicenter examination of MOG antibody assays. Neurol Neuroimmunol Neuroinflammation 2020;7(2):e674.

[55] Tzartos JS, Karagiorgou K, Tzanetakos D, Breza M, Evangelopoulos ME, Pelidou SH, et al. Deciphering anti-MOG IgG antibodies: clinical and radiological spectrum, and comparison of antibody detection assays. J Neurol Sci 2020;410:116673.

[56] Kaneko K, Sato DK, Nakashima I, Ogawa R, Akaishi T, Takai Y, et al. CSF cytokine profile in MOG-IgG+ neurological disease is similar to AQP4-IgG+ NMOSD but distinct from MS: a cross-sectional study and potential therapeutic implications. J Neurol Neurosurg Psychiatry 2018;89(9):927-36.

[57] Horellou P, Wang M, Keo V, Chrétien P, Serguera C, Waters P, et al. Increased interleukin-6 correlates with myelin oligodendrocyte glycoprotein antibodies in pediatric monophasic demyelinating diseases and multiple sclerosis. J Neuroimmunol 2015;289:1-7.

[58] Kothur K, Wienholt L, Tantsis EM, Earl J, Bandodkar S, Prelog K, et al. B Cell, Th17, and neutrophil related cerebrospinal fluid cytokine/chemokines are elevated in MOG antibody associated demyelination. PloS One 2016;11(2):e0149411.

[59] Jarius S, Lechner C, Wendel EM, Baumann M, Breu M, Schimmel M, et al. Cerebrospinal fluid findings in patients with myelin oligodendrocyte glycoprotein (MOG) antibodies. Part 2: results from 108 lumbar punctures in 80 pediatric patients. J Neuroinflammation 2020;17(1):262.

[60] López-Chiriboga AS, Majed M, Fryer J, Dubey D, McKeon A, Flanagan EP, et al. Association of MOG-IgG serostatus with relapse after acute disseminated encephalomyelitis and proposed diagnostic criteria for MOG-IgG-associated disorders. JAMA Neurol 2018;75(11):1355-63.

[61] Waters P, Fadda G, Woodhall M, O'Mahony J, Brown RA, Castro DA, et al. Serial anti-myelin oligodendrocyte glycoprotein antibody analyses and outcomes in children with demyelinating syndromes. JAMA Neurol 2020;77(1):82-93.

[62] Bruijstens AL, Wendel EM, Lechner C, Bartels F, Finke C, Breu M, et al. E.U. paediatric MOG consortium consensus: part 5 - Treatment of paediatric myelin oligodendrocyte glycoprotein antibody-associated disorders. Eur J Paediatr Neurol 2020;29:41-53.

[63] Jarius S, Ruprecht K, Kleiter I, Borisow N, Asgari N, Pitarokoili K, 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(1):280.

[64] Cobo-Calvo A, Sepúlveda M, Rollot F, Armangué T, Ruiz A, Maillart E, et al. Evaluation of treatment response in adults with relapsing MOG-Ab-associated disease. J Neuroinflammation 2019;16(1):134.

[65] Chen JJ, Flanagan EP, Bhatti MT, Jitprapaikulsan J, Dubey D, Lopez Chiriboga ASS, et al. Steroid-sparing maintenance immunotherapy for MOG-IgG associated disorder. Neurology 2020;95(2):e111-20.

[66] Padmanabhan A, Connelly-Smith L, Aqui N, Balogun RA, Klingel R, Meyer E, et al. Guidelines on the use of therapeutic apheresis in clinical practice - evidence-based approach from the writing committee of the american society for apheresis: the eighth special issue. J Clin Apheresis 2019;34(3):171-354.

[67] Li S, Ren H, Xu Y, Xu T, Zhang Y, Yin H, et al. Long-term efficacy of mycophenolate mofetil in myelin oligodendrocyte glycoprotein antibody-associated disorders: a prospective study. Neurol Neuroimmunol Neuroinflammation 2020;7(3):e705.

[68] Montcuquet A, Collongues N, Papeix C, Zephir H, Audoin B, Laplaud D, et al. Effectiveness of mycophenolate mofetil as first-line therapy in AQP4-IgG, MOG-IgG, and seronegative neuromyelitis optica spectrum disorders. Mult Scler Houndmills Basingstoke Engl 2017;23(10):1377-84.

[69] Lu Q, Luo J, Hao H, Liu R, Jin H, Jin Y, et al. Efficacy and safety of long-term immunotherapy in adult patients with MOG antibody disease: a systematic analysis. J Neurol 2021;268(12):4537-48.

[70] Ramanathan S, Mohammad S, Tantsis E, Nguyen TK, Merheb V, Fung VSC, et al. Clinical course, therapeutic responses and outcomes in relapsing MOG antibody-associated demyelination. J Neurol Neurosurg Psychiatry 2018;89(2):127-37.

[71] Tsantes E, Curti E, Siena E, Granella F. Successful intravenous immunoglobulin treatment in relapsing MOG-antibody-associated disease. Mult Scler Relat Disord 2019;32:27-9.

[72] Whittam DH, Cobo-Calvo A, Lopez-Chiriboga AS, Pardo S, Gornall M, Cicconi S, et al. Treatment of MOG-IgG-associated disorder with rituximab: an international study of 121 patients. Mult Scler Relat Disord 2020;44:102251.

[73] Durozard P, Rico A, Boutiere C, Maarouf A, Lacroix R, Cointe S, et al. Comparison of the response to rituximab between myelin oligodendrocyte glycoprotein and aquaporin-4 antibody diseases. Ann Neurol 2020;87(2):256-66.

[74] Lotan I, Charlson RW, Ryerson LZ, Levy M, Kister I. Effectiveness of subcutaneous tocilizumab in neuromyelitis optica spectrum disorders. Mult Scler Relat Disord 2020;39:101920.

[75] Rigal J, Pugnet G, Ciron J, Lépine Z, Biotti D. Off-label use of tocilizumab in neuromyelitis optica spectrum disorders and MOG-antibody-associated diseases: a case-series. Mult Scler Relat Disord 2020;46:102483.

[76] Clinical characteristics and outcomes of myelin oligodendrocyte glycoprotein antibody-seropositive optic neuritis in varying age groups: A cohort study in China. PubMed [Internet], 2019. doi: 10.1016/j.jns.2019.03.014. [cité 28 mars 2025] Disponible sur: https://pubmed.ncbi.nlm.nih.gov/30904690/.
[77] Hennes EM, Baumann M, Schanda K, Anlar B, Bajer-Kornek B, Blaschek A, et al. Prognostic relevance of MOG antibodies in children with an acquired demyelinating syndrome. Neurology 2017;89(9):900-8.

[78] Durand-Dubief F, Shor N, Audoin B, Bourre B, Cohen M, Kremer S, et al. MRI management of NMOSD and MOGAD: proposals from the French Expert Group NOMADMUS. J Neuroradiol J Neuroradiol 2025;52(1):101235.

[79] Gulani V, Calamante F, Shellock FG, Kanal E, Reeder SB. International society for magnetic resonance in medicine. Gadolinium deposition in the brain: summary of evidence and recommendations. Lancet Neurol 2017;16(7):564-70.

[80] Collongues N, Alves Do Rego C, Bourre B, Biotti D, Marignier R, da Silva AM, et al. Pregnancy in patients with AQP4-Ab, MOG-Ab, or double-negative neuromyelitis optica disorder. Neurology 2021;96(15):e2006-15.

[81] Wang L, Zhou L, ZhangBao J, Huang W, Chang X, Lu C, et al. Neuromyelitis optica spectrum disorder: pregnancy-related attack and predictive risk factors. J Neurol Neurosurg Psychiatry 2020;92(1):53-61.

[82] Vecchio D, Virgilio E, Naldi P, Comi C, Cantello R. MOG-antibody demyelinating diseases: a case of post-partum severe rhombencephalitis and transverse myelitis. Mult Scler Relat Disord 2018;21:9-10.