Seizure incidence among neuromyelitis optica spectrum disorder patients

Etemadifar, Masoud; Sabeti, Fatemeh; Khorvash, Reza; Mirbagheri, M; Nouri, Hosein; Salari, Mehri

doi:10.1016/j.neurol.2020.08.011

Cited by 5 publications

(3 citation statements)

References 16 publications

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“…According to TSC models, K ir channels are functionally impaired for extracellular K + uptake, resulting in neuronal excitation and seizure generation in TSC (Jansen et al, 2005). In NMOSD, AQP4 damage may increase the risk of epilepsy (Etemadifar et al, 2021), whereas in pentylenetetrazole‐induced rat epilepsy model, AQP4 expression was increased. Epilepsy is suppressed by inhibiting AQP4 expression (Lei et al, 2020).…”

Section: Connections Among Neurological Disorders Astrocytes and Drugsmentioning

confidence: 99%

The function of astrocytes and their role in neurological diseases

Yuan,

Huang,

Jiang

et al. 2023

Eur J of Neuroscience

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Astrocytes have countless links with neurons. Previously, astrocytes were only considered a scaffold of neurons; in fact, astrocytes perform a variety of functions, including providing support for neuronal structures and energy metabolism, offering isolation and protection and influencing the formation, function and elimination of synapses. Because of these functions, astrocytes play an critical role in central nervous system (CNS) diseases. The regulation of the secretiory factors, receptors, channels and pathways of astrocytes can effectively inhibit the occurrence and development of CNS diseases, such as neuromyelitis optica (NMO), multiple sclerosis, Alzheimer's disease (AD), Parkinson's disease (PD) and Huntington's disease. The expression of aquaporin 4 in AS is directly related to NMO and indirectly involved in the clearance of Aβ and tau proteins in AD. Connexin 43 has a bidirectional effect on glutamate diffusion at different stages of stroke. Interestingly, astrocytes reduce the occurrence of PD through multiple effects such as secretion of related factors, mitochondrial autophagy and aquaporin 4. Therefore, this review is focused on the structure and function of astrocytes and the correlation between astrocytes and CNS diseases and drug treatment to explore the new functions of astrocytes with the astrocytes as the target. This, in turn, would provide a reference for the development of new drugs to protect neurons and promote the recovery of nerve function.

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Section: Connections Among Neurological Disorders Astrocytes and Drugsmentioning

confidence: 99%

The function of astrocytes and their role in neurological diseases

Yuan,

Huang,

Jiang

et al. 2023

Eur J of Neuroscience

View full text Add to dashboard Cite

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“…In addition, the presence of periodic lateral epileptic discharges in MS (Figure 6) may indicate the exacerbation of MS and signal a poor prognosis, often accompanied by aphasic SE, 101 primary generalized convulsive SE, 102 and FBTCSs such as secondary generalized convulsive SE 102–104 . However, no EEG abnormalities were reported to be predictive of the development of chronic epilepsy in MS/AQP4‐NMOSD/MOGAD 7,11,92,95,100,105 …”

Section: Paraclinical Examinationsmentioning

confidence: 99%

“…For AQP4-NMOSD, cortical or subcortical lesions may be associated with seizures. 4,15,95 Patients with chronic epilepsy were more likely to have cortical atrophy on MRI, 24 although radiological risk factors for epilepsy in AQP4-NMOSD remain unknown.…”

Section: Examinations 71 | Magnetic Resonance Imagingmentioning

confidence: 99%

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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