Seizures in myelin oligodendrocyte glycoprotein antibody-associated disorders and related immune factors

Liu, Kang; Sun, Suzhen; Cui, Jieyuan; Zhang, Lei; Zhang, Kai; Zhang, Lin

doi:10.1016/j.seizure.2021.09.011

Cited by 11 publications

(10 citation statements)

References 27 publications

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“…The most recent meta‐analysis including 14 papers in 2020 has shown that the prevalence of seizures in MOGAD is approximately 20.5% (95% CI = 13.7–30.7%), 20 which is much higher than that in MS and AQP4‐NMOSD. In addition, the incidence of seizures in MOGAD is 10.3–24.5% 15,47,48 . The exact probability of epilepsy in MOGAD remains unknown, with only one study reporting the incidence of epilepsy being approximately 22.0% in MOGAD with acute disseminated encephalomyelitis (ADEM)‐like phenotypes 49 .…”

Section: Epidemiologymentioning

confidence: 99%

“…The underlying mechanism of seizures/epilepsy in MOGAD is not yet understood. The higher incidence of seizures in MOGAD may be related to its frequent cortical involvement, in particular, extensive lesions involving unilateral cortical regions 48,66 . Remission of seizures along with the reduction in size and number of corresponding lesions after immunotherapy may indicate the potential association between seizures and demyelination/inflammation in MOGAD 14,67,68 .…”

Section: Pathology and Physiological Mechanismsmentioning

confidence: 99%

“…In addition, the aseptic meningitis phenotype has been anecdotally reported to be associated with seizures in MOGAD 86 . CCE is considered a distinct clinical phenotype in MOGAD, characterized by adult onset seizures, headaches, fever, and other cortical symptoms 14,48,66,87,88 . By contrast, seizures in children are more likely to be associated with ADEM‐like phenotypes 3,7 …”

Section: Clinical Featuresmentioning

confidence: 99%

“…In addition, the incidence of seizures in MOGAD is 10.3-24.5%. 15,47,48 The exact probability of epilepsy in MOGAD remains unknown, with only one study reporting the incidence of epilepsy being approximately 22.0% in MOGAD with acute disseminated encephalomyelitis (ADEM)-like phenotypes. 49 Apart from factors such as study design and sample size, an increased recognition of MOGAD may further contribute to the heterogeneity between studies.…”

Section: Seizures/epilepsy In Aqp4-nmosdmentioning

confidence: 99%

“…The higher incidence of seizures in MOGAD may be related to its frequent cortical involvement, in particular, extensive lesions involving unilateral cortical regions. 48,66 Remission of seizures along with the reduction in size and number of corresponding lesions after immunotherapy may indicate the potential association between seizures and demyelination/ inflammation in MOGAD. 14,67,68 Furthermore, the development of seizures is considered more relevant to the immune response rather than the MOG antibody itself, 48 given a similar frequency of seizures between MOG antibody-positive and -negative patients with the ADEM phenotype.…”

Section: Seizures/epilepsy In Mogadmentioning

confidence: 99%

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Seizures and epilepsy in multiple sclerosis, aquaporin 4 antibody‐positive neuromyelitis optica spectrum disorder, and myelin oligodendrocyte glycoprotein antibody‐associated disease

Zheng

Cai

et al. 2022

Epilepsia

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Seizure is one of the manifestations of central nervous system inflammatory demyelinating diseases, which mainly include multiple sclerosis (MS), aquaporin 4 antibody‐positive neuromyelitis optica spectrum disorder (AQP4‐NMOSD), and myelin oligodendrocyte glycoprotein antibody‐associated disease (MOGAD). Acute symptomatic seizures secondary to MS/AQP4‐NMOSD/MOGAD occur in the acute phase of the diseases, and are more frequent in MOGAD. In contrast, recurrent nonprovoked seizures, mainly attributed to autoimmune‐associated epilepsy, occur in the nonacute phase of the diseases. Seizures in MS/AQP4‐NMOSD/MOGAD mostly have a focal onset. MS patients with concomitant systemic infections, earlier onset, and greater disease activity are more likely to have seizures, whereas factors such as greater MS severity, the presence of status epilepticus, and cortical damage indicate a greater risk of developing epilepsy. In MOGAD, cerebral cortical encephalitis and acute disseminated encephalomyelitis (ADEM)‐like phenotypes (predominately ADEM and multiphasic disseminated encephalomyelitis) indicate a greater seizure risk. Multiple relapses with ADEM‐like phenotypes predict epilepsy in pediatrics with MOGAD. Pathophysiologically, acute symptomatic seizures in MS are associated with neuronal hyperexcitability secondary to inflammation and demyelination. Chronic epilepsy in MS is largely due to gliosis, neuronal dysfunction, and synaptic abnormalities. The mainstay of treatment for seizures secondary to MS/AQP4‐NMOSD/MOGAD consists of immunotherapy along with antiseizure medications. This critical review discusses the most‐updated evidence on epidemiology, clinical correlates, and inflammatory mechanisms underlying seizures and epilepsy in MS/AQP4‐NMOSD/MOGAD. Treatment cautions including drug‐drug interactions and the impact of treatments on the diseases are outlined. We also highlight pitfalls and challenges in managing such patients and future research perspectives to address unsolved questions.

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Section: Epidemiologymentioning

confidence: 99%

Section: Pathology and Physiological Mechanismsmentioning

confidence: 99%