Seizures in Cerebral Amyloid Angiopathy: A Systematic Review and Meta-Analysis.

IF 2.3 Q3 CLINICAL NEUROLOGY

Neurology. Clinical practice Pub Date : 2025-06-01 Epub Date: 2025-03-27 DOI:10.1212/CPJ.0000000000200454

Brin E Freund, Md Manjurul Islam Shourav, Anteneh M Feyissa, James F Meschia, Amen Yonas, Kevin M Barrett, William O Tatum, Michelle P Lin

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Abstract

Purpose of review: Cerebral amyloid angiopathy (CAA) is a disease of the cerebral vasculature that can result in microhemorrhages, as well as intraparenchymal and subarachnoid hemorrhage, superficial siderosis (SS), and/or secondary infarct/inflammation. CAA may be encountered as an isolated pathology or with Alzheimer disease and has been demonstrated to be associated with an increased risk of seizures. However, the overall rates of seizures and specific pathologies related to CAA and their subsequent risk of seizures have not been elucidated.

Recent findings: Prior studies of CAA and seizures are predominantly case reports or small case series, and larger studies have focused primarily on smaller subgroups of patients with CAA. Only 2 prior studies assessed larger heterogeneous populations of patients with CAA. One study focused on long-term outcomes and evaluated the impact of seizures on cognitive and survival outcomes retrospectively, although it did not delineate the effects of acute and chronic seizure disorders (epilepsy) and did not find an association. Long-term prospective or retrospective studies on outcomes regarding seizures/epilepsy and CAA are therefore lacking.

Summary: A total of 1,376 articles were identified, with 48 (34 case reports/series and 14 cohort studies) included in this review. Acute symptomatic seizures (ASyS) and epilepsy were poorly defined, and the overall prevalence of seizures in cohort studies was 22.8%, with significant heterogeneity (I ² = 77%; p < 0.01). Epilepsy was diagnosed in 34.4% and ASyS in 10.6% of patients in heterogeneous cohorts. Most of the studies assessed seizures in specific subgroups of CAA with variable prevalence, including CAA with related inflammation (CAA-ri): 56.9%; lobar intracranial hemorrhage (ICH): 17.1%; and cortical SAH (cSAH) or SS: 8.7%. In heterogeneous cohorts, SS (p < 0.001 and p = 0.03, respectively) and CAA-ri (p = 0.005 and p = 0.04, respectively) were significantly associated with epilepsy/seizures. In 1 study, cSAH (p = 0.03) and acute lobar ICH (p = 0.002) were associated with seizures, likely related to inclusion of ASyS. Status epilepticus (14/125) and drug resistance (6/89) were infrequent. Clinical pathologic entities associated with a risk of seizures include cSAH, CAA-ri, SS, and acute ICH.

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脑淀粉样血管病的癫痫发作：系统回顾和荟萃分析。

回顾目的：脑淀粉样血管病（CAA）是一种脑血管疾病，可导致微出血，以及肝实质内和蛛网膜下腔出血，浅表性铁沉着（SS）和/或继发性梗死/炎症。CAA可能作为一种孤立的病理或与阿尔茨海默病一起出现，并已被证明与癫痫发作风险增加有关。然而，与CAA相关的总体癫痫发作率和特定病理及其随后的癫痫发作风险尚未阐明。最近发现：先前关于CAA和癫痫发作的研究主要是病例报告或小病例系列，而大型研究主要集中在CAA患者的小亚组上。只有2个先前的研究评估了较大的异质人群的CAA患者。一项研究侧重于长期结果，并回顾性地评估了癫痫发作对认知和生存结果的影响，尽管它没有描述急性和慢性癫痫发作障碍（癫痫）的影响，也没有发现两者之间的关联。因此，缺乏关于癫痫发作/癫痫和CAA预后的长期前瞻性或回顾性研究。摘要：本综述共纳入1376篇文献，其中48篇（34篇病例报告/系列和14篇队列研究）。急性症状性发作（ASyS）和癫痫的定义不明确，队列研究中癫痫发作的总体患病率为22.8%，具有显著的异质性(I 2 = 77%；P < 0.01)。在异质队列中，34.4%的患者被诊断为癫痫，10.6%的患者被诊断为自闭症。大多数研究评估了CAA发病率不同的特定亚组的癫痫发作，包括CAA伴相关炎症（CAA-ri）： 56.9%；大叶性颅内出血（ICH）： 17.1%；皮质性SAH （cSAH）或SS: 8.7%。在异质性队列中，SS（分别p < 0.001和p = 0.03）和CAA-ri（分别p = 0.005和p = 0.04）与癫痫/发作显著相关。在1项研究中，cSAH （p = 0.03）和急性脑叶性脑出血（p = 0.002）与癫痫发作相关，可能与ASyS的纳入有关。癫痫持续状态（14/125）和耐药（6/89）少见。与癫痫发作风险相关的临床病理实体包括cah、CAA-ri、SS和急性ICH。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Neurology. Clinical practice CLINICAL NEUROLOGY-

CiteScore

4.00

自引率

0.00%

发文量

期刊介绍： Neurology® Genetics is an online open access journal publishing peer-reviewed reports in the field of neurogenetics. The journal publishes original articles in all areas of neurogenetics including rare and common genetic variations, genotype-phenotype correlations, outlier phenotypes as a result of mutations in known disease genes, and genetic variations with a putative link to diseases. Articles include studies reporting on genetic disease risk, pharmacogenomics, and results of gene-based clinical trials (viral, ASO, etc.). Genetically engineered model systems are not a primary focus of Neurology® Genetics, but studies using model systems for treatment trials, including well-powered studies reporting negative results, are welcome.