====== Seizure after aneurysmal subarachnoid hemorrhage ====== {{rss>https://pubmed.ncbi.nlm.nih.gov/rss/search/1VwHIhVo4vdzrt-3c6bf_dhj3iLanKnTvb8hC841xQQvIs0EIe/?limit=15&utm_campaign=pubmed-2&fc=20230830024225}} ---- ---- ===== Epidemiology ===== Literature has reported [[seizure]] rates to be as high as 27% in this population ((Lin YJ, Chang WN, Chang HW, Ho JT, Lee TC, Wang HC, Tsai NW, Tsai MH, Lu CH. Risk factors and outcome of seizures after spontaneous aneurysmal subarachnoid hemorrhage. Eur J Neurol. 2008 May;15(5):451-7. doi: 10.1111/j.1468-1331.2008.02096.x. Epub 2008 Mar 5. PubMed PMID: 18325027. )). More recently published studies have found seizure rates to be significantly lower than previously described (1–10%) ((Rosengart AJ, Huo JD, Tolentino J, Novakovic RL, Frank JI, Goldenberg FD, Macdonald RL. Outcome in patients with subarachnoid hemorrhage treated with antiepileptic drugs. J Neurosurg. 2007 Aug;107(2):253-60. PubMed PMID: 17695377. )) ((Chumnanvej S, Dunn IF, Kim DH. Three-day phenytoin prophylaxis is adequate after subarachnoid hemorrhage. Neurosurgery. 2007 Jan;60(1):99-102; discussion 102-3. PubMed PMID: 17228257. )). ===== Risk factors ===== Paavola et al. examined data for 760 [[consecutive]] 12-month [[survivor]]s of [[aneurysmal subarachnoid hemorrhage]], born in [[1950]] or after, with a first aSAH from January 1, 1995, to December 31, 2018. Of the 760 patients (median age, 47 years; 53% females; median follow-up, 11 years), 111 (15%) developed [[epilepsy]] at a median of 7 months (interquartile range, 2-14 months) after admission for aSAH. Of the 2240 [[population]] controls and 4653 first-degree relatives of aSAH patients, 23 (0.9%) and 80 (1.7%) respectively developed epilepsy during the follow-up period. Among the 79 patients with epilepsy in first-degree relatives, 22 (28%) developed epilepsy after aSAH; in contrast, among the 683 patients with no epilepsy in first-degree relatives, 89 (13%) developed epilepsy after aSAH. Having at least one relative with epilepsy was an independent risk factor for epilepsy after aSAH (hazard ratio, 2.44; 95% confidence interval, 1.51-3.95). Cumulative 1-year rates by first-degree relationship were 40% with one or more children with epilepsy, 38% with one or more affected parents, 5% with one or more affected siblings, and 10% with no relatives with epilepsy. Patients who developed [[epilepsy]] after aSAH were significantly more likely to have first-degree relatives with epilepsy than those who did not develop epilepsy after the aSAH ((Paavola JT, Jokimäki J, Huttunen TJ, Fraunberg MVUZ, Koivisto T, Kämäräinen OP, Lång M, Jääskeläinen JE, Kälviäinen R, Lindgren AE, Huttunen J. Long-term Risk of Epilepsy in Subarachnoid Hemorrhage Survivors With Positive Family History: A Population-Based Follow-up Study. Neurology. 2023 Aug 29:10.1212/WNL.0000000000207737. doi: 10.1212/WNL.0000000000207737. Epub ahead of print. PMID: 37643884.)). ---- [[Epilepsy]] is a common and serious complication of [[subarachnoid hemorrhage]] (SAH), giving rise to increased [[morbidity]] and [[mortality]]. It's difficult to identify patients at high risk of epilepsy and the application of [[antiepileptic drug]]s (AEDs) following SAH is a controversial topic. Therefore, it's pressingly needed to gain a better understanding of the risk factors, underlying mechanisms, and the optimization of therapeutic strategies for epilepsy after SAH. [[Neuroinflammation]], characterized by [[microglia]]l activation and the release of inflammatory [[cytokine]]s has drawn growing attention due to its influence on patients with epilepsy after SAH. In a review, Wang et al. discussed the [[risk factor]]s for epilepsy after SAH and emphasize the critical role of microglia. Then they discussed how various [[molecule]]s arising from pathophysiological changes after SAH activates specific receptors such as [[TLR4]], [[NLRP3]], [[RAGE]], [[P2X7R]] and initiate the downstream inflammatory pathways. Additionally, they focused on the significant responses implicated in epilepsy including neuronal [[excitotoxicity]], the disruption of the [[blood-brain barrier]] (BBB), and the change of immune responses. As the application of AEDs for seizure prophylaxis after SAH remains controversial, the regulation of neuroinflammation targeting the key pathological molecules could be a promising therapeutic method. While neuroinflammation appears to contribute to epilepsy after SAH, more comprehensive experiments on their relationships are needed ((Wang J, Liang J, Deng J, Liang X, Wang K, Wang H, Qian D, Long H, Yang K, Qi S. Emerging Role of Microglia-Mediated Neuroinflammation in Epilepsy after Subarachnoid Hemorrhage. Mol Neurobiol. 2021 Jan 26. doi: 10.1007/s12035-021-02288-y. Epub ahead of print. PMID: 33501625.)). ===== Complications ===== Seizure activity has been associated with secondary neurologic injury including reduced [[cerebral blood flow]] and [[intracranial hypertension]] ((Rhoney DH, Tipps LB, Murry KR, Basham MC, Michael DB, Coplin WM. Anticonvulsant prophylaxis and timing of seizures after aneurysmal subarachnoid hemorrhage. Neurology. 2000 Jul 25;55(2):258-65. PubMed PMID: 10908901. )). ===== Prohylaxis ===== see [[Anticonvulsant in aneurysmal subarachnoid hemorrhage]]. ===== References =====