2019
DOI: 10.1007/978-3-030-04615-6_4
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Subarachnoid Hemorrhage-Related Epilepsy

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Cited by 5 publications
(6 citation statements)
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“…The analysis of the neuroradiological characteristics of the study population demonstrates that cSS, whether focal or disseminated, and CAA‐ri are predisposing factors for the development of epilepsy. Even if the pathogenetic mechanisms leading to the development of seizures in CAA are not known, it is conceivable that hemosiderin deposition at the cortical level (leading to cSS) could exert a proepileptogenic irritative effect 34,35 . Moreover, because CAA‐ri seems to be mediated by anti‐Aβ autoantibodies, 7,8 an immune‐mediated process responsible for the onset of seizures could be involved, similarly to autoimmune encephalitis 36 …”
Section: Discussionmentioning
confidence: 99%
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“…The analysis of the neuroradiological characteristics of the study population demonstrates that cSS, whether focal or disseminated, and CAA‐ri are predisposing factors for the development of epilepsy. Even if the pathogenetic mechanisms leading to the development of seizures in CAA are not known, it is conceivable that hemosiderin deposition at the cortical level (leading to cSS) could exert a proepileptogenic irritative effect 34,35 . Moreover, because CAA‐ri seems to be mediated by anti‐Aβ autoantibodies, 7,8 an immune‐mediated process responsible for the onset of seizures could be involved, similarly to autoimmune encephalitis 36 …”
Section: Discussionmentioning
confidence: 99%
“…Even if the pathogenetic mechanisms leading to the development of seizures in CAA are not known, it is conceivable that hemosiderin deposition at the cortical level (leading to cSS) could exert a proepileptogenic irritative effect. 34,35 Moreover, because CAA-ri seems to be mediated by anti-Aβ autoantibodies, 7,8 an immune-mediated process responsible for the onset of seizures could be involved, similarly to autoimmune encephalitis. 36 These data lead to further considerations.…”
Section: Discussionmentioning
confidence: 99%
“…As a severe complication of SAH, epilepsy increases mortality and disability rates ( 13 ). Although the underlying mechanisms of epilepsy after SAH remain unclear, several classes of risk factors have been reported to contribute to a greater risk of epilepsy after SAH, such as hemosiderin deposition, subarachnoid clot burden, hypertension, vasospasm, and acute hydrocephalus ( 3 , 14 , 15 ). Hemosiderin deposition in the brain and spinal cord due to hemorrhage into the subarachnoid space in some patients is considered to be a cause and key predictor of epilepsy after SAH ( 16 ).…”
Section: Discussionmentioning
confidence: 99%
“…Moreover, SAH combined with epilepsy leads to anxiety, depression, and other psychological problems, which may be worse than primary disease. However, the potential mechanisms of epilepsy secondary to SAH are still unclear (3)(4)(5).…”
Section: Introductionmentioning
confidence: 99%
“…Early seizures after SAH occur most commonly in the first 24 hours [26]. The actuarial risk of epilepsy after SAH was 18% by the first year, 23% by the second year, and 25% by the fifth year in the survivors of SAH [28]. Aneurysm location most associated with the development of SAH-related epilepsy is middle cerebral artery at the M1 branch and artery bifurcation [66].…”
Section: Subarachnoid Hemorrhagementioning
confidence: 99%