Pub Date : 2025-10-03DOI: 10.1016/j.eplepsyres.2025.107675
Umair Ul Haq, Neha Majeed, Nisha Kumari, Anushe Saleh, Amna Tariq, Saad Masood, Junaid Imran, Safa Siddique Ali ansari, Hamzah Naushad Siddiqui, Muhammad Wasey Arshad, Muhammad Aamir, Abdul Rehman Shah Syed, Satesh Kumar, Mahima Khatri, Maria Rasheed
{"title":"Phenobarbital versus valproate for generalized convulsive status epilepticus in adults. An updated systematic review and meta-analysis","authors":"Umair Ul Haq, Neha Majeed, Nisha Kumari, Anushe Saleh, Amna Tariq, Saad Masood, Junaid Imran, Safa Siddique Ali ansari, Hamzah Naushad Siddiqui, Muhammad Wasey Arshad, Muhammad Aamir, Abdul Rehman Shah Syed, Satesh Kumar, Mahima Khatri, Maria Rasheed","doi":"10.1016/j.eplepsyres.2025.107675","DOIUrl":"10.1016/j.eplepsyres.2025.107675","url":null,"abstract":"","PeriodicalId":11914,"journal":{"name":"Epilepsy Research","volume":"217 ","pages":"Article 107675"},"PeriodicalIF":2.0,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145231822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-25DOI: 10.1016/j.eplepsyres.2025.107668
Haoyu Liu , Qiannan Song , Jiayi Jin , Hong Chen
<div><h3>Background</h3><div>cAMP response element-binding protein 3-like transcription factor 4 (CREB3L4) serves as an important transcriptional regulatory factor and plays a crucial role in neurological diseases, however, its specific mechanism in epilepsy pathogenesis remains unclear. This study aims to investigate the role of the CREB3L4-Sirtuin 4 (SIRT4) regulatory axis in epilepsy pathogenesis and its effects on γ-aminobutyric acid GABA/glutamate balance and mitochondrial function.</div></div><div><h3>Methods</h3><div>A classical epilepsy animal model was established, and quantitative real-time PCR, Western blot, and immunofluorescence staining techniques were employed to detect the expression changes of CREB3L4 and SIRT4 in the epilepsy model. CREB3L4 expression levels were modulated through lentivirus-mediated gene overexpression and RNA interference techniques to observe their effects on epileptic behavioral manifestations. ELISA was used to detect GABA and glutamate contents in brain tissues, and the GABA/glutamate ratio was calculated.</div></div><div><h3>Results</h3><div>CREB3L4 expression was downregulated 3.2-fold in the epilepsy model (1.026 ± 0.051–0.325 ± 0.028, p < 0.001), with 1.8-fold decreased GABA/glutamate ratio (1.065 ± 0.063–0.581 ± 0.046, p < 0.001). CREB3L4 overexpression upregulated SIRT4 mRNA 3.5-fold (0.185 ± 0.051–0.643 ± 0.039, p < 0.01) and reduced seizure frequency 2.0-fold (67.6 ± 3.1–34.4 ± 2.4 seizures, p < 0.001) and severity 2.2-fold (4.3 ± 0.3–2.0 ± 0.3 grade, p < 0.001). Conversely, CREB3L4 silencing exacerbated epilepsy progression, increasing seizure frequency 1.4-fold (58.7 ± 2.7–79.3 ± 4.2 seizures, p < 0.001) and severity 1.3-fold (3.7 ± 0.3–4.7 ± 0.2 grade, p < 0.001), with 2.2-fold decreased GABA/glutamate ratio (0.639 ± 0.051–0.288 ± 0.041, p < 0.001). Mechanistic studies demonstrated that CREB3L4 overexpression improved mitochondrial function through SIRT4 upregulation, thereby maintaining mitochondrial homeostasis. Meanwhile, activation of the CREB3L4-SIRT4 axis effectively increased brain tissue GABA content, improved the GABA/glutamate ratio, and restored neurotransmitter balance. Rescue experiments demonstrated that SIRT4 silencing (3.1-fold knockdown) significantly attenuated CREB3L4's neuroprotective effects, increasing seizure severity 1.6-fold (3.0 ± 0.5–4.8 ± 0.2 grade, p < 0.01), frequency 1.7-fold (43.2 ± 3.1–74.7 ± 4.2 seizures, p < 0.001), and reducing GABA/glutamate ratio 1.6-fold (1.81 ± 0.05–1.12 ± 0.05, p < 0.001), confirming SIRT4 as the key downstream mediator.</div></div><div><h3>Conclusion</h3><div>This study elucidates the important role of the CREB3L4-SIRT4 regulatory axis in epilepsy pathogenesis, revealing the molecular mechanism by which CREB3L4 transcriptionally activates SIRT4, subsequently regulates GABA/glutamate balance and maintains mitochondrial homeostasis, ultimately suppressing seizures and associated pathophysiological damage.</
{"title":"CREB3L4 upregulates SIRT4 expression to increase GABA/glutamate ratio and mitochondrial homeostasis for epilepsy suppression","authors":"Haoyu Liu , Qiannan Song , Jiayi Jin , Hong Chen","doi":"10.1016/j.eplepsyres.2025.107668","DOIUrl":"10.1016/j.eplepsyres.2025.107668","url":null,"abstract":"<div><h3>Background</h3><div>cAMP response element-binding protein 3-like transcription factor 4 (CREB3L4) serves as an important transcriptional regulatory factor and plays a crucial role in neurological diseases, however, its specific mechanism in epilepsy pathogenesis remains unclear. This study aims to investigate the role of the CREB3L4-Sirtuin 4 (SIRT4) regulatory axis in epilepsy pathogenesis and its effects on γ-aminobutyric acid GABA/glutamate balance and mitochondrial function.</div></div><div><h3>Methods</h3><div>A classical epilepsy animal model was established, and quantitative real-time PCR, Western blot, and immunofluorescence staining techniques were employed to detect the expression changes of CREB3L4 and SIRT4 in the epilepsy model. CREB3L4 expression levels were modulated through lentivirus-mediated gene overexpression and RNA interference techniques to observe their effects on epileptic behavioral manifestations. ELISA was used to detect GABA and glutamate contents in brain tissues, and the GABA/glutamate ratio was calculated.</div></div><div><h3>Results</h3><div>CREB3L4 expression was downregulated 3.2-fold in the epilepsy model (1.026 ± 0.051–0.325 ± 0.028, p < 0.001), with 1.8-fold decreased GABA/glutamate ratio (1.065 ± 0.063–0.581 ± 0.046, p < 0.001). CREB3L4 overexpression upregulated SIRT4 mRNA 3.5-fold (0.185 ± 0.051–0.643 ± 0.039, p < 0.01) and reduced seizure frequency 2.0-fold (67.6 ± 3.1–34.4 ± 2.4 seizures, p < 0.001) and severity 2.2-fold (4.3 ± 0.3–2.0 ± 0.3 grade, p < 0.001). Conversely, CREB3L4 silencing exacerbated epilepsy progression, increasing seizure frequency 1.4-fold (58.7 ± 2.7–79.3 ± 4.2 seizures, p < 0.001) and severity 1.3-fold (3.7 ± 0.3–4.7 ± 0.2 grade, p < 0.001), with 2.2-fold decreased GABA/glutamate ratio (0.639 ± 0.051–0.288 ± 0.041, p < 0.001). Mechanistic studies demonstrated that CREB3L4 overexpression improved mitochondrial function through SIRT4 upregulation, thereby maintaining mitochondrial homeostasis. Meanwhile, activation of the CREB3L4-SIRT4 axis effectively increased brain tissue GABA content, improved the GABA/glutamate ratio, and restored neurotransmitter balance. Rescue experiments demonstrated that SIRT4 silencing (3.1-fold knockdown) significantly attenuated CREB3L4's neuroprotective effects, increasing seizure severity 1.6-fold (3.0 ± 0.5–4.8 ± 0.2 grade, p < 0.01), frequency 1.7-fold (43.2 ± 3.1–74.7 ± 4.2 seizures, p < 0.001), and reducing GABA/glutamate ratio 1.6-fold (1.81 ± 0.05–1.12 ± 0.05, p < 0.001), confirming SIRT4 as the key downstream mediator.</div></div><div><h3>Conclusion</h3><div>This study elucidates the important role of the CREB3L4-SIRT4 regulatory axis in epilepsy pathogenesis, revealing the molecular mechanism by which CREB3L4 transcriptionally activates SIRT4, subsequently regulates GABA/glutamate balance and maintains mitochondrial homeostasis, ultimately suppressing seizures and associated pathophysiological damage.</","PeriodicalId":11914,"journal":{"name":"Epilepsy Research","volume":"218 ","pages":"Article 107668"},"PeriodicalIF":2.0,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145154691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-25DOI: 10.1016/j.eplepsyres.2025.107669
Giovanni Battista Dell’Isola , Margherita Siciliano , Gianluca D’Onofrio , Pietro Ferrara , Pasquale Striano , Marco Carotenuto , Alberto Verrotti
Neurological and neuropsychiatric disorders, particularly drug-resistant epilepsies and rare genetic syndromes such as CDKL5 deficiency disorder, pose significant therapeutic challenges. Ganaxolone (GNX), a synthetic neurosteroid and positive allosteric modulator of GABA-A receptors, has emerged as a promising treatment option due to its unique pharmacological properties. This review explores GNX's pharmacokinetic profile, preclinical evidence, and clinical applications. Preclinical studies have demonstrated its efficacy in reducing seizure frequency and severity across various epilepsy models, including amygdala kindling and status epilepticus, as well as its neuroprotective effects in hypoxic-ischemic encephalopathy. Clinical trials have confirmed GNX's benefits, particularly in CDD, where it significantly reduces seizure frequency, leading to its FDA and EMA approval. Additionally, GNX has shown potential in focal epilepsy, status epilepticus, and other drug-resistant epilepsies, although with variable results. Beyond epilepsy, GNX's modulation of GABAergic signaling suggests potential applications in neuropsychiatric conditions. Its favorable safety profile further supports its therapeutic value.
{"title":"Ganaxolone in Epilepsy: Insights into a Neurosteroid-Based Therapy","authors":"Giovanni Battista Dell’Isola , Margherita Siciliano , Gianluca D’Onofrio , Pietro Ferrara , Pasquale Striano , Marco Carotenuto , Alberto Verrotti","doi":"10.1016/j.eplepsyres.2025.107669","DOIUrl":"10.1016/j.eplepsyres.2025.107669","url":null,"abstract":"<div><div>Neurological and neuropsychiatric disorders, particularly drug-resistant epilepsies and rare genetic syndromes such as CDKL5 deficiency disorder, pose significant therapeutic challenges. Ganaxolone (GNX), a synthetic neurosteroid and positive allosteric modulator of GABA-A receptors, has emerged as a promising treatment option due to its unique pharmacological properties. This review explores GNX's pharmacokinetic profile, preclinical evidence, and clinical applications. Preclinical studies have demonstrated its efficacy in reducing seizure frequency and severity across various epilepsy models, including amygdala kindling and status epilepticus, as well as its neuroprotective effects in hypoxic-ischemic encephalopathy. Clinical trials have confirmed GNX's benefits, particularly in CDD, where it significantly reduces seizure frequency, leading to its FDA and EMA approval. Additionally, GNX has shown potential in focal epilepsy, status epilepticus, and other drug-resistant epilepsies, although with variable results. Beyond epilepsy, GNX's modulation of GABAergic signaling suggests potential applications in neuropsychiatric conditions. Its favorable safety profile further supports its therapeutic value.</div></div>","PeriodicalId":11914,"journal":{"name":"Epilepsy Research","volume":"218 ","pages":"Article 107669"},"PeriodicalIF":2.0,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145205979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-19DOI: 10.1016/j.eplepsyres.2025.107665
Ahmed Ameen Fateh , Abla Smahi , Muhammad Hassan , Cristina Cañete-Massé , Adam A.Q. Mohammed , Feng Yue , Zhanqi Hu , Hongwu Zeng
Background
Self-Limited Epilepsy with Centrotemporal Spikes (SeLECTs) is a dominant childhood epilepsy form characterized by seizures originating from the brain’s centrotemporal region. Crucially, unlocking the neural dynamics and mechanisms underlying SeLECTs paves the way for potent diagnostic and therapeutic strategies. Our work investigates dynamic functional connectivity (dFC) variability in the thalamocortical circuit in SeLECTs individuals, thereby shedding light on the temporal dynamics and anomaly in connectivity patterns tied to seizure occurrence and propagation.
Methods
Utilizing resting-state functional magnetic resonance imaging (rs-fMRI) data from 45 SeLECTs patients and 55 healthy controls (HCs), dynamic changes in functional connectivity (FC) across various brain regions were examined over time. We selected 16 thalamic seeds to delve into dFC variability using a sliding window approach. We also evaluated clinical data from both groups to discern its correlation with dFC variability. As a final step, a Support Vector Machine (SVM) was employed for classification analysis to demonstrate the potential use of dFC variability as a distinguishing feature between SeLECTs patients and HCs.
Results
t-test analysis manifested significant variances in dFC variability between SeLECTs and HCs groups related to thalamus seeds, also showing a correlation between VCI and certain areas. Out of 16 thalamus seeds, significant variances emerged in 9 seeds. Specifically, an increase in dFC variability was observed between the right occipital thalamus seed and the right precentral gyrus in SeLECTs patients, implying a positive connectivity alteration. On the other hand, a lowered dFC was observed between the right inferior prefrontal thalamus seed and the left cuneus, reflecting a reduction in their connectivity strength.
Conclusion
Our study underscores the significance of dFC variability within the thalamocortical circuit in SeLECTs individuals. The noticeable aberrant connectivity patterns enrich our understanding of temporal dynamics linked to SeLECTs seizure occurrence and propagation, thereby contributing to understanding SeLECTs pathophysiology. These insights may steer the development of precise diagnostic and therapeutic strategies for this widespread childhood epilepsy.
{"title":"Dynamic functional connectivity variability in the thalamocortical circuit: Insights from Self-Limited Epilepsy with Centrotemporal Spikes (SeLECTs)","authors":"Ahmed Ameen Fateh , Abla Smahi , Muhammad Hassan , Cristina Cañete-Massé , Adam A.Q. Mohammed , Feng Yue , Zhanqi Hu , Hongwu Zeng","doi":"10.1016/j.eplepsyres.2025.107665","DOIUrl":"10.1016/j.eplepsyres.2025.107665","url":null,"abstract":"<div><h3>Background</h3><div>Self-Limited Epilepsy with Centrotemporal Spikes (SeLECTs) is a dominant childhood epilepsy form characterized by seizures originating from the brain’s centrotemporal region. Crucially, unlocking the neural dynamics and mechanisms underlying SeLECTs paves the way for potent diagnostic and therapeutic strategies. Our work investigates dynamic functional connectivity (dFC) variability in the thalamocortical circuit in SeLECTs individuals, thereby shedding light on the temporal dynamics and anomaly in connectivity patterns tied to seizure occurrence and propagation.</div></div><div><h3>Methods</h3><div>Utilizing resting-state functional magnetic resonance imaging (rs-fMRI) data from 45 SeLECTs patients and 55 healthy controls (HCs), dynamic changes in functional connectivity (FC) across various brain regions were examined over time. We selected 16 thalamic seeds to delve into dFC variability using a sliding window approach. We also evaluated clinical data from both groups to discern its correlation with dFC variability. As a final step, a Support Vector Machine (SVM) was employed for classification analysis to demonstrate the potential use of dFC variability as a distinguishing feature between SeLECTs patients and HCs.</div></div><div><h3>Results</h3><div>t-test analysis manifested significant variances in dFC variability between SeLECTs and HCs groups related to thalamus seeds, also showing a correlation between VCI and certain areas. Out of 16 thalamus seeds, significant variances emerged in 9 seeds. Specifically, an increase in dFC variability was observed between the right occipital thalamus seed and the right precentral gyrus in SeLECTs patients, implying a positive connectivity alteration. On the other hand, a lowered dFC was observed between the right inferior prefrontal thalamus seed and the left cuneus, reflecting a reduction in their connectivity strength.</div></div><div><h3>Conclusion</h3><div>Our study underscores the significance of dFC variability within the thalamocortical circuit in SeLECTs individuals. The noticeable aberrant connectivity patterns enrich our understanding of temporal dynamics linked to SeLECTs seizure occurrence and propagation, thereby contributing to understanding SeLECTs pathophysiology. These insights may steer the development of precise diagnostic and therapeutic strategies for this widespread childhood epilepsy.</div></div>","PeriodicalId":11914,"journal":{"name":"Epilepsy Research","volume":"218 ","pages":"Article 107665"},"PeriodicalIF":2.0,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145104430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-19DOI: 10.1016/j.eplepsyres.2025.107667
Noora Puhakka , Mette Heiskanen , Xavier Ekolle Ndode-Ekane , Idrish Ali , Cesar Santana-Gomez , Shalini Das Gupta , Meheli Banerjee , Pedro Andrade , Riikka Immonen , Pablo Casillas-Espinosa , Gregory Smith , Rhys D. Brady , Juliana Silva , Emma Braine , Matthew R. Hudson , Glen R. Yamakawa , Nigel C. Jones , Sandy R. Shultz , Neil G. Harris , David K. Wright , Asla Pitkänen
Objective
To analyze the success of harmonization and standardization of plasma miRNA biomarker discovery and validation for post-traumatic epilepsy (PTE) in the EpiBioS4Rx international multicenter project.
Methods
Adult male Sprague-Dawley rats were randomized to lateral fluid-percussion-induced traumatic brain injury (TBI) or sham operation at three study sites (Finland, Australia, USA). Video-electroencephalogram (vEEG) was performed in the 7th post-injury month to detect spontaneous seizures. Tail vein plasma was collected at baseline and 48 h after TBI for microRNA (miRNA) analysis. Common data elements were generated to document and monitor pre-analytic activities, including housing conditions, post-injury care, blood sampling, plasma preparation, plasma quality, storage, and shipping. miRNA analysis was performed using droplet digital PCR (ddPCR) at one study site (Finland) with on-site standardized procedures.
Results
The 2-day miRNA levels were successfully measured in 85 % (209/245) of the rats included in the final analysis cohort. Exclusions were related to small sample volume, hemolysis, and failed RNA extraction for ddPCR. Most of the pre-analytical factors leading to sample exclusions were related to non-optimal plasma pipetting. We also recognized gaps in data entry and monitoring of personnel training.
Conclusions
Our study demonstrates that conducting a successful plasma miRNA biomarker analysis requires procedural harmonization between laboratories, protocol standardization, inclusion and analysis of quality controls, training of researchers, and continuous monitoring of adherence to pre-agreed protocols.
{"title":"Standardization of preclinical methodologies for discovery and validation of circulating microRNA biomarkers for post-traumatic epileptogenesis – Lessons learned from the EpiBioS4Rx Project 1","authors":"Noora Puhakka , Mette Heiskanen , Xavier Ekolle Ndode-Ekane , Idrish Ali , Cesar Santana-Gomez , Shalini Das Gupta , Meheli Banerjee , Pedro Andrade , Riikka Immonen , Pablo Casillas-Espinosa , Gregory Smith , Rhys D. Brady , Juliana Silva , Emma Braine , Matthew R. Hudson , Glen R. Yamakawa , Nigel C. Jones , Sandy R. Shultz , Neil G. Harris , David K. Wright , Asla Pitkänen","doi":"10.1016/j.eplepsyres.2025.107667","DOIUrl":"10.1016/j.eplepsyres.2025.107667","url":null,"abstract":"<div><h3>Objective</h3><div>To analyze the success of harmonization and standardization of plasma miRNA biomarker discovery and validation for post-traumatic epilepsy (PTE) in the EpiBioS4Rx international multicenter project.</div></div><div><h3>Methods</h3><div>Adult male Sprague-Dawley rats were randomized to lateral fluid-percussion-induced traumatic brain injury (TBI) or sham operation at three study sites (Finland, Australia, USA). Video-electroencephalogram (vEEG) was performed in the 7th post-injury month to detect spontaneous seizures. Tail vein plasma was collected at baseline and 48 h after TBI for microRNA (miRNA) analysis. Common data elements were generated to document and monitor pre-analytic activities, including housing conditions, post-injury care, blood sampling, plasma preparation, plasma quality, storage, and shipping. miRNA analysis was performed using droplet digital PCR (ddPCR) at one study site (Finland) with on-site standardized procedures.</div></div><div><h3>Results</h3><div>The 2-day miRNA levels were successfully measured in 85 % (209/245) of the rats included in the final analysis cohort. Exclusions were related to small sample volume, hemolysis, and failed RNA extraction for ddPCR. Most of the pre-analytical factors leading to sample exclusions were related to non-optimal plasma pipetting. We also recognized gaps in data entry and monitoring of personnel training.</div></div><div><h3>Conclusions</h3><div>Our study demonstrates that conducting a successful plasma miRNA biomarker analysis requires procedural harmonization between laboratories, protocol standardization, inclusion and analysis of quality controls, training of researchers, and continuous monitoring of adherence to pre-agreed protocols.</div></div>","PeriodicalId":11914,"journal":{"name":"Epilepsy Research","volume":"218 ","pages":"Article 107667"},"PeriodicalIF":2.0,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145108996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-19DOI: 10.1016/j.eplepsyres.2025.107666
Cristiana Santos , Daniel Filipe Borges , Joana Isabel Soares
Background
Drug-resistant epilepsy often requires invasive monitoring. Although simultaneous scalp EEG and stereo EEG are increasingly used together, their added value for preoperative evaluation and surgical planning remains uncertain and warrants systematic investigation.
Methods
We systematically searched PubMed, Scopus and Web of Science for English- or Portuguese-language studies in which patients with drug-resistant epilepsy were simultaneously monitored with scEEG and SEEG. Reports lacking primary data, systematic reviews, conference abstracts, case reports and studies limited to scEEG with electrocorticography were excluded. Two reviewers independently screened all records, extracted data and assessed methodological quality. The protocol was registered in PROSPERO (CRD42024590432) and conducted in accordance with PRISMA-P guidelines.
Results
From 9750 records, 16 articles underwent full-text analysis, and eight retrospective observational studies met the inclusion criteria. These eight studies - evenly split between the United States and Europe - included 250 patients. Data on diagnostic yield and postoperative outcomes were inconsistent. Key findings included (i) detailed mapping of seizure onset and propagation across cortical and subcortical regions, (ii) typical latency intervals between scEEG and SEEG detection, and (iii) concordance rates in localizing the epileptogenic zone.
Conclusions
Simultaneous scEEG-SEEG provides complementary cortical and mesial findings that sharpen the delineation of the epileptogenic zone and allow for targeted surgery. SEEG captures the deep generators, while scEEG provides the broader context for electrode placement. Current evidence is limited to small, methodologically heterogeneous series. Standardized protocols, larger multicenter cohorts and multimodal co-registration are needed to confirm the diagnostic gain and anchor this two-layered approach in routine clinical care.
背景：耐药癫痫通常需要侵入性监测。虽然同时头皮脑电图和立体脑电图越来越多地一起使用，但它们在术前评估和手术计划中的附加价值仍然不确定，需要系统的研究。方法系统检索PubMed、Scopus和Web of Science中同时监测耐药癫痫患者scEEG和SEEG的英文或葡萄牙文研究。缺乏原始数据的报告、系统综述、会议摘要、病例报告和仅限于脑电图与皮质电图的研究被排除在外。两名审稿人独立筛选所有记录，提取数据并评估方法学质量。该方案已在PROSPERO注册（CRD42024590432），并按照PRISMA-P指南进行。结果9750份记录中，16篇文章进行了全文分析，8项回顾性观察性研究符合纳入标准。这8项研究——平均分布在美国和欧洲——包括250名患者。诊断率和术后结果的数据不一致。主要发现包括：(1)癫痫发作和在皮层和皮层下区域传播的详细图谱，(2)scEEG和SEEG检测之间的典型潜伏期间隔，以及(3)癫痫区定位的一致性率。结论：同时进行的scieg - seeg提供了补充的皮层和中膜的发现，可以清晰地描绘癫痫发生区，并允许有针对性的手术。SEEG捕获深层发电机，而scEEG为电极放置提供了更广泛的背景。目前的证据仅限于小的、方法学上不一致的系列。需要标准化的方案，更大的多中心队列和多模式联合登记来确认诊断收益并将这种双层方法固定在常规临床护理中。
{"title":"Bridging surface and depth: A systematic review of seizure patterns in simultaneous scalp and stereo-EEG","authors":"Cristiana Santos , Daniel Filipe Borges , Joana Isabel Soares","doi":"10.1016/j.eplepsyres.2025.107666","DOIUrl":"10.1016/j.eplepsyres.2025.107666","url":null,"abstract":"<div><h3>Background</h3><div>Drug-resistant epilepsy often requires invasive monitoring. Although simultaneous scalp EEG and stereo EEG are increasingly used together, their added value for preoperative evaluation and surgical planning remains uncertain and warrants systematic investigation.</div></div><div><h3>Methods</h3><div>We systematically searched PubMed, Scopus and Web of Science for English- or Portuguese-language studies in which patients with drug-resistant epilepsy were simultaneously monitored with scEEG and SEEG. Reports lacking primary data, systematic reviews, conference abstracts, case reports and studies limited to scEEG with electrocorticography were excluded. Two reviewers independently screened all records, extracted data and assessed methodological quality. The protocol was registered in PROSPERO (CRD42024590432) and conducted in accordance with PRISMA-P guidelines.</div></div><div><h3>Results</h3><div>From 9750 records, 16 articles underwent full-text analysis, and eight retrospective observational studies met the inclusion criteria. These eight studies - evenly split between the United States and Europe - included 250 patients. Data on diagnostic yield and postoperative outcomes were inconsistent. Key findings included (i) detailed mapping of seizure onset and propagation across cortical and subcortical regions, (ii) typical latency intervals between scEEG and SEEG detection, and (iii) concordance rates in localizing the epileptogenic zone.</div></div><div><h3>Conclusions</h3><div>Simultaneous scEEG-SEEG provides complementary cortical and mesial findings that sharpen the delineation of the epileptogenic zone and allow for targeted surgery. SEEG captures the deep generators, while scEEG provides the broader context for electrode placement. Current evidence is limited to small, methodologically heterogeneous series. Standardized protocols, larger multicenter cohorts and multimodal co-registration are needed to confirm the diagnostic gain and anchor this two-layered approach in routine clinical care.</div></div>","PeriodicalId":11914,"journal":{"name":"Epilepsy Research","volume":"218 ","pages":"Article 107666"},"PeriodicalIF":2.0,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145108995","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-12DOI: 10.1016/j.eplepsyres.2025.107663
Aditi Goyal , Shilpa Rao , Mariamma Philip , A. Arivazhagan , Jitender Saini , LG Vishwanathan , Ajay Asranna , Raghavendra K , RC Mundlamuri , Nishanth Sadashiva , RD Bharath , Karthik K , Sandhya M , Malla Bhaskara Rao , Sanjib Sinha , Anita Mahadevan
Background
Focal cortical dysplasia (FCD) is a common cause of focal epilepsy, however pathophysiology of epileptogenesis in FCD remains unresolved. Emerging evidence suggests that dysfunctional astrocytes are key players in epilepsy. Recently two phenotypes of astrocytes (A1/A2) and microglia (M1/M2) have been described in neurological diseases with neuroinflammatory and neuroprotective roles. We investigated astrocytic (A1/A2) and microglial (M1/M2) phenotypes in FCD and their role in epileptogenesis.
Material and Methods
Histologically confirmed cases of surgically resected FCD IIa (n = 10) and FCD IIb (n = 10) and age and region-matched post-mortem controls (n = 4) were evaluated by immunohistochemistry using C3d and GBP2 (A1-astrocytic markers), pSTAT3 (A2-astrocytes), CD14 (M1-microglia) and CD163 (M2-microglia), caspase 3 (for apoptosis) and phosphorylated-Tau and phosphorylated-neurofilament (for neuronal degeneration). Semi-quantitative assessment for glial phenotypes were correlated with clinical parameters.
Results
Compared to the control group, in FCDIIa, pSTAT3 + A2-astrocytes (mean-44.1 cells/mm2) predominated in absence of C3d/GBP2 + A1-astrocytes. In FCDIIb, A2-astrocytes were significantly higher than A1 (p-value=0.04) [A1 (C3d-15.79 cells/mm2; GBP2–13.67 cells/mm2); A2 (pSTAT3–78.24 cells/mm2)]. Balloon cells in FCDIIb strongly labelled with C3d and GBP2 (A1-phenotype). In both FCDIIa and IIb, pSTAT3 + A2 astrocytes were localised to subpial zone. Increase in both inflammatory CD14 + M1 and reparative CD163 + M2 microglia in perivascular region, was seen in the dysplastic cortex in both FCD IIa (M1- 11.9/mm2, M2- 12.4 cells/mm2) and FCD IIb (M1–27.9/mm2, M2–18.7/mm2) with M1 >M2 in FCD IIb, though not statistically significant (p-value>0.05). Mean densities of astrocytes (A1, A2) and microglia (M1, M2) did not correlate with any of the clinical parameters. Caspase 3 labelled reactive astrocytes and oligodendrocytes and occasional dysmorphic neurons in both, and BC in FCDIIb.
Conclusions
This is the first study examining astrocytic and microglial phenotypes in FCD IIa and IIb. Identification of specific astrocytic and microglial phenotypes offers novel therapeutic targets for modulation of epileptogenesis, especially in drug resistant epilepsy.
{"title":"Astrocytic and microglial phenotypes in focal cortical dysplasia","authors":"Aditi Goyal , Shilpa Rao , Mariamma Philip , A. Arivazhagan , Jitender Saini , LG Vishwanathan , Ajay Asranna , Raghavendra K , RC Mundlamuri , Nishanth Sadashiva , RD Bharath , Karthik K , Sandhya M , Malla Bhaskara Rao , Sanjib Sinha , Anita Mahadevan","doi":"10.1016/j.eplepsyres.2025.107663","DOIUrl":"10.1016/j.eplepsyres.2025.107663","url":null,"abstract":"<div><h3>Background</h3><div>Focal cortical dysplasia (FCD) is a common cause of focal epilepsy, however pathophysiology of epileptogenesis in FCD remains unresolved. Emerging evidence suggests that dysfunctional astrocytes are key players in epilepsy. Recently two phenotypes of astrocytes (A1/A2) and microglia (M1/M2) have been described in neurological diseases with neuroinflammatory and neuroprotective roles. We investigated astrocytic (A1/A2) and microglial (M1/M2) phenotypes in FCD and their role in epileptogenesis.</div></div><div><h3>Material and Methods</h3><div>Histologically confirmed cases of surgically resected FCD IIa (n = 10) and FCD IIb (n = 10) and age and region-matched post-mortem controls (n = 4) were evaluated by immunohistochemistry using C3d and GBP2 (A1-astrocytic markers), pSTAT3 (A2-astrocytes), CD14 (M1-microglia) and CD163 (M2-microglia), caspase 3 (for apoptosis) and phosphorylated-Tau and phosphorylated-neurofilament (for neuronal degeneration). Semi-quantitative assessment for glial phenotypes were correlated with clinical parameters.</div></div><div><h3>Results</h3><div>Compared to the control group, in FCDIIa, pSTAT3 + A2-astrocytes (mean-44.1 cells/mm<sup>2</sup>) predominated in absence of C3d/GBP2 + A1-astrocytes. In FCDIIb, A2-astrocytes were significantly higher than A1 (p-value=0.04) [A1 (C3d-15.79 cells/mm<sup>2</sup>; GBP2–13.67 cells/mm<sup>2</sup>); A2 (pSTAT3–78.24 cells/mm<sup>2</sup>)]. Balloon cells in FCDIIb strongly labelled with C3d and GBP2 (A1-phenotype). In both FCDIIa and IIb, pSTAT3 + A2 astrocytes were localised to subpial zone. Increase in both inflammatory CD14 + M1 and reparative CD163 + M2 microglia in perivascular region, was seen in the dysplastic cortex in both FCD IIa (M1- 11.9/mm<sup>2</sup>, M2- 12.4 cells/mm<sup>2</sup>) and FCD IIb (M1–27.9/mm<sup>2</sup>, M2–18.7/mm<sup>2</sup>) with M1 >M2 in FCD IIb, though not statistically significant (p-value>0.05). Mean densities of astrocytes (A1, A2) and microglia (M1, M2) did not correlate with any of the clinical parameters. Caspase 3 labelled reactive astrocytes and oligodendrocytes and occasional dysmorphic neurons in both, and BC in FCDIIb.</div></div><div><h3>Conclusions</h3><div>This is the first study examining astrocytic and microglial phenotypes in FCD IIa and IIb. Identification of specific astrocytic and microglial phenotypes offers novel therapeutic targets for modulation of epileptogenesis, especially in drug resistant epilepsy.</div></div>","PeriodicalId":11914,"journal":{"name":"Epilepsy Research","volume":"218 ","pages":"Article 107663"},"PeriodicalIF":2.0,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145085068","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-12DOI: 10.1016/j.eplepsyres.2025.107664
Xinru Tan , Hailang Liu , Yan Li , Qiaoling Hu , Lisi Yan , Jin Chen , Siqi Hong , Li Jiang
Background
Sleep-related hypermotor epilepsy (SHE) is a focal epilepsy with nocturnal hypermotor seizures. Although SHE was redefined in 2014, comprehensive pediatric studies are still lacking for this disorder. To address this need, here we describe the clinical and electroencephalography (EEG) characteristics of children with SHE.
Methods
We retrospectively enrolled pediatric patients with SHE diagnosis who were hospitalized at our institution from August 1, 2021, to August 31, 2023.
Results
Among the 47 patients, 31.9 % and 42.6 % manifested as SP2 and SP3, respectively. A total of 57.4 % of the patients showed a focal discharge as diagnosed by interictal EEG, 36.2 % showed multifocal discharges, and 6.4 % did not have discharge. Ictal EEG revealed that 66.0 % of patients presented with frontal lobe onset, 10.6 % with temporal lobe onset, and 23.4 % with unknown onset. Further, 36.2 % of patients had a structural etiology, approximately 80 % of those patients had focal cortical dysplasia. Finally, 23 patients were diagnosed with refractory epilepsy, and 15 of them underwent surgery.
Conclusions
Patients mainly presented as SP3 and SP2. The focal discharges detected by interictal EEG accounted for approximately 57.4 % and the frontal lobe onset detected by ictal EEG accounted for approximately 66 %. Structural etiology (mainly focal cortical dysplasia) accounted for approximately 33 %, and surgery was an effective treatment for these patients.
{"title":"Clinical and EEG characteristics of sleep-related hypermotor epilepsy in children","authors":"Xinru Tan , Hailang Liu , Yan Li , Qiaoling Hu , Lisi Yan , Jin Chen , Siqi Hong , Li Jiang","doi":"10.1016/j.eplepsyres.2025.107664","DOIUrl":"10.1016/j.eplepsyres.2025.107664","url":null,"abstract":"<div><h3>Background</h3><div>Sleep-related hypermotor epilepsy (SHE) is a focal epilepsy with nocturnal hypermotor seizures. Although SHE was redefined in 2014, comprehensive pediatric studies are still lacking for this disorder. To address this need, here we describe the clinical and electroencephalography (EEG) characteristics of children with SHE.</div></div><div><h3>Methods</h3><div>We retrospectively enrolled pediatric patients with SHE diagnosis who were hospitalized at our institution from August 1, 2021, to August 31, 2023.</div></div><div><h3>Results</h3><div>Among the 47 patients, 31.9 % and 42.6 % manifested as SP2 and SP3, respectively. A total of 57.4 % of the patients showed a focal discharge as diagnosed by interictal EEG, 36.2 % showed multifocal discharges, and 6.4 % did not have discharge. Ictal EEG revealed that 66.0 % of patients presented with frontal lobe onset, 10.6 % with temporal lobe onset, and 23.4 % with unknown onset. Further, 36.2 % of patients had a structural etiology, approximately 80 % of those patients had focal cortical dysplasia. Finally, 23 patients were diagnosed with refractory epilepsy, and 15 of them underwent surgery.</div></div><div><h3>Conclusions</h3><div>Patients mainly presented as SP3 and SP2. The focal discharges detected by interictal EEG accounted for approximately 57.4 % and the frontal lobe onset detected by ictal EEG accounted for approximately 66 %. Structural etiology (mainly focal cortical dysplasia) accounted for approximately 33 %, and surgery was an effective treatment for these patients.</div></div>","PeriodicalId":11914,"journal":{"name":"Epilepsy Research","volume":"218 ","pages":"Article 107664"},"PeriodicalIF":2.0,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145079941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-10DOI: 10.1016/j.eplepsyres.2025.107661
Ioannis Karakis , Lidia MVR Moura , Nada Boualam , Martha Wetzel , David Howard
Objective
To provide updated estimates of the healthcare costs associated with epilepsy using large, state-based all-payer claims databases.
Methods
We conducted a retrospective cohort study using all-payer claims data from Colorado, Massachusetts, and Virginia for 2016–2019, including individuals enrolled in Medicare, Medicaid, and individual and small-group commercial plans. Individuals with epilepsy were identified using a validated claims-based algorithm and matched with non-epilepsy controls based on age and sex. The two groups' healthcare use and costs were compared using generalized linear regressions and adjusting for age, sex, insurance status, and comorbidities.
Results
The study included 150,808 adults with epilepsy in Colorado, 122,222 in Virginia, and 118,707 in Massachusetts. State-level estimates of annual costs for adults with epilepsy were between $28,000 and $34,000 (2021 U.S. dollars), whereas costs for matched controls were between $2900 and $6300. Adults with epilepsy incurred higher costs than matched controls across all types of care. Adjusted analyses revealed that costs attributable to epilepsy ranged from $12,000 to $31,000, depending on the covariates included.
Conclusion
Our study provides updated and comprehensive cost estimates for epilepsy from diverse U.S. states, demonstrating the utility of all-payer claims data to generate state-specific and aggregate estimates of epilepsy burden to guide interventions. This study confirms that epilepsy imposes a substantial economic burden on the healthcare system, with costs higher than previous estimates.
{"title":"The health care costs of epilepsy: Evidence from all-payer claims data","authors":"Ioannis Karakis , Lidia MVR Moura , Nada Boualam , Martha Wetzel , David Howard","doi":"10.1016/j.eplepsyres.2025.107661","DOIUrl":"10.1016/j.eplepsyres.2025.107661","url":null,"abstract":"<div><h3>Objective</h3><div>To provide updated estimates of the healthcare costs associated with epilepsy using large, state-based all-payer claims databases.</div></div><div><h3>Methods</h3><div>We conducted a retrospective cohort study using all-payer claims data from Colorado, Massachusetts, and Virginia for 2016–2019, including individuals enrolled in Medicare, Medicaid, and individual and small-group commercial plans. Individuals with epilepsy were identified using a validated claims-based algorithm and matched with non-epilepsy controls based on age and sex. The two groups' healthcare use and costs were compared using generalized linear regressions and adjusting for age, sex, insurance status, and comorbidities.</div></div><div><h3>Results</h3><div>The study included 150,808 adults with epilepsy in Colorado, 122,222 in Virginia, and 118,707 in Massachusetts. State-level estimates of annual costs for adults with epilepsy were between $28,000 and $34,000 (2021 U.S. dollars), whereas costs for matched controls were between $2900 and $6300. Adults with epilepsy incurred higher costs than matched controls across all types of care. Adjusted analyses revealed that costs attributable to epilepsy ranged from $12,000 to $31,000, depending on the covariates included.</div></div><div><h3>Conclusion</h3><div>Our study provides updated and comprehensive cost estimates for epilepsy from diverse U.S. states, demonstrating the utility of all-payer claims data to generate state-specific and aggregate estimates of epilepsy burden to guide interventions. This study confirms that epilepsy imposes a substantial economic burden on the healthcare system, with costs higher than previous estimates.</div></div>","PeriodicalId":11914,"journal":{"name":"Epilepsy Research","volume":"218 ","pages":"Article 107661"},"PeriodicalIF":2.0,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145060001","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-09DOI: 10.1016/j.eplepsyres.2025.107662
Manav Jain , Laurel Charlesworth , Helen Driver , Gavin P. Winston , Lysa Boissé Lomax , Garima Shukla
Introduction
Persons with epilepsy (PWE) frequently contend with disrupted sleep related to multiple seizure related as well as other factors like medications and comorbidities. Such disturbances often lead to fragmented sleep, which can adversely affect quality of life and compromise seizure management. Previous
Although previous research has addressed conditions like sleep apnea and insomnia among PWE, less attention has been paid to periodic limb movements (PLMs), a requirement for diagnosis of the periodic limb movement disorder and also commonly observed in restless legs syndrome (RLS) as well as other conditions. This study aims to determine the prevalence and specific features of PLMs in PWE and to explore how these movements correlate with objective sleep measurements.
Methods
This investigation employed a retrospective chart review of consecutive adult patients diagnosed with epilepsy who underwent polysomnography at a tertiary-care sleep laboratory over a ten-year span. The control group consisted of individuals evaluated for possible obstructive sleep apnea, who were matched to cases based on age, sex, and the severity of sleep apnea. Patient records were initially identified using keywords related to “epilepsy” or “seizures.” Epilepsy diagnosis was confirmed through detailed chart review, which also yielded clinical details likety duration of epilepsy, seizure classification, and antiseizure medication usage. Sleep parameters such as sleep efficiency, spontaneous arousal index, periodic limb movement index, periodic limb movement with arousal index, and apnea-hypopnea index were extracted from archived polysomnography reports. The subsequent analysis was carried out using descriptive statistical methods using RStudio version 4.4.1.
Results
A total of 152 relevant patient records were found in the database. Of these, 61 patients with epilepsy (mean age 41.4 ± 17.2 years, including 31 females) met the inclusion criteria and were matched with 61 patients suspected for OSA. Within the epilepsy cohort, 43 patients experienced focal-onset epilepsy while 16 had generalized epilepsy. 25 patients were prescribed two or more antiseizure medications, and 12 were categorized as medically refractory. PLMs were detected in 23 % of patients with epilepsy compared to 26 % in the control group, with mean PLMI values of 6.1 ± 16.8 and 8.8 ± 20.7, respectively. The PLMAI was also similar between the two groups (0.5 ± 1.0 vs. 1.1 ± 2.4). Other sleep parameters, including the mean AHI (16.0 ± 20.0 in the epilepsy group vs. 19.7 ± 19.4 in the control group), did not exhibit significant differences between groups. Within the epilepsy cohort, the only factor linked to the presence of periodic limb movements was older age, with no observed association with seizure type, number of antiseizure medications, or seizure control.
{"title":"Periodic limb movements among persons with epilepsy: A retrospective polysomnographic study","authors":"Manav Jain , Laurel Charlesworth , Helen Driver , Gavin P. Winston , Lysa Boissé Lomax , Garima Shukla","doi":"10.1016/j.eplepsyres.2025.107662","DOIUrl":"10.1016/j.eplepsyres.2025.107662","url":null,"abstract":"<div><h3>Introduction</h3><div>Persons with epilepsy (PWE) frequently contend with disrupted sleep related to multiple seizure related as well as other factors like medications and comorbidities. Such disturbances often lead to fragmented sleep, which can adversely affect quality of life and compromise seizure management. Previous</div><div>Although previous research has addressed conditions like sleep apnea and insomnia among PWE, less attention has been paid to periodic limb movements (PLMs), a requirement for diagnosis of the periodic limb movement disorder and also commonly observed in restless legs syndrome (RLS) as well as other conditions. This study aims to determine the prevalence and specific features of PLMs in PWE and to explore how these movements correlate with objective sleep measurements.</div></div><div><h3>Methods</h3><div>This investigation employed a retrospective chart review of consecutive adult patients diagnosed with epilepsy who underwent polysomnography at a tertiary-care sleep laboratory over a ten-year span. The control group consisted of individuals evaluated for possible obstructive sleep apnea, who were matched to cases based on age, sex, and the severity of sleep apnea. Patient records were initially identified using keywords related to “epilepsy” or “seizures.” Epilepsy diagnosis was confirmed through detailed chart review, which also yielded clinical details likety duration of epilepsy, seizure classification, and antiseizure medication usage. Sleep parameters such as sleep efficiency, spontaneous arousal index, periodic limb movement index, periodic limb movement with arousal index, and apnea-hypopnea index were extracted from archived polysomnography reports. The subsequent analysis was carried out using descriptive statistical methods using RStudio version 4.4.1.</div></div><div><h3>Results</h3><div>A total of 152 relevant patient records were found in the database. Of these, 61 patients with epilepsy (mean age 41.4 ± 17.2 years, including 31 females) met the inclusion criteria and were matched with 61 patients suspected for OSA. Within the epilepsy cohort, 43 patients experienced focal-onset epilepsy while 16 had generalized epilepsy. 25 patients were prescribed two or more antiseizure medications, and 12 were categorized as medically refractory. PLMs were detected in 23 % of patients with epilepsy compared to 26 % in the control group, with mean PLMI values of 6.1 ± 16.8 and 8.8 ± 20.7, respectively. The PLMAI was also similar between the two groups (0.5 ± 1.0 vs. 1.1 ± 2.4). Other sleep parameters, including the mean AHI (16.0 ± 20.0 in the epilepsy group vs. 19.7 ± 19.4 in the control group), did not exhibit significant differences between groups. Within the epilepsy cohort, the only factor linked to the presence of periodic limb movements was older age, with no observed association with seizure type, number of antiseizure medications, or seizure control.</div></div><div><h3>Conclusions</h3><div>PLMs are a","PeriodicalId":11914,"journal":{"name":"Epilepsy Research","volume":"218 ","pages":"Article 107662"},"PeriodicalIF":2.0,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145085185","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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