皮层注射氯化亚铁建立外伤性癫痫动物模型

目的建立外伤性癫痫模型,观察症状、脑电图(EEG)和病理改变,探讨病理及致痫机制。方法立体定向注射不同剂量氯化亚铁(FeCl2)于大鼠右侧运动皮层或杏仁体致痫,设立正常对照组、生理盐水对照组。连续30 d行为学评分、EEG记录,HE染色、普鲁士蓝和腾氏蓝反应及Nissl染色行病理学观察。结果 1 000 nmol氯化亚铁皮层注射后平均经过(60±18)s的潜伏期,大鼠EEG表现出多种形式的癫痫样放电波形,大鼠症状及EEG呈典型癫痫变化,该组模型成功率87．5％,其行为学评分与对照组及其他各组之间比较有显著性差异(P<0．01)。氯化亚铁皮层注射组大体外观见右额叶萎缩,明显棕黄色,为含铁血黄素沉着。氯化亚铁右杏仁体注射组亦可见边缘系统含铁血黄素沉着。普鲁士蓝和腾氏蓝反应证实含铁化合物的沉积。皮层及杏仁体氯化亚铁注射部位、实验侧海马CA3区神经元减少,核固缩,胶质增生明显。结论含铁化合物在大鼠的皮层和边缘结构的沉积可以导致慢性的、自发性发作的癫痫灶形成。皮层注射1 000 nmol氯化亚铁建立的外伤性癫痫动物模型比杏仁体注射铁离子建立的模型更接近人类的外伤性癫痫临床与病理改变。     

急性氯化铁癫痫模型大鼠美解眠诱发放电的实验研究

目的 探讨急性氯化铁癫痫模型大鼠在发作间期美解眠诱发试验中的放电特征.方法 给予SD大鼠头颅额、顶、枕部铺设硬膜外电极6枚,用立体定向方法在大鼠感觉运动皮质区注入氯化铁溶液,建立急性癫痫模型,记录脑电24小时,观察在发作间期给予急性氯化铁癫痫模型大鼠腹腔注射美解眠后诱发癫痫发作的脑电情况.结果 美解眠诱发试验中,出现两种不同类型的癫痫发作期脑电,其中一种与急性氯化铁模型的发作期放电相同,另一种与美解眠自身所致癫痫的发作期放电相似.结论 急性氯化铁癫痫模型大鼠在美解眠诱发试验中能够产生原有癫痫发作,但是假阳性率较高;氯化铁致痫大鼠对美解眠的反应性较正常大鼠高.     

伽玛刀对癫痫大鼠模型的治疗作用及机制研究

目的 研究伽玛刀照射对癫痫大鼠的放射生物学作用,探讨伽玛刀治疗癫痫的作用机制.方法 制备海人酸大鼠癫痫模型,利用自行设计的伽玛刀动物定向头架,分别应用100Gy和20Gy的伽玛射线对癫痫大鼠海马组织进行照射,观察大鼠行为学、脑电图、MRI及超微结构、脑组织氨基酸含量及GABA能神经元表达变化.结果 伽玛刀照射后大鼠癫痫发作次数明显减少.100Gy组照射后2个月MRI表现为靶区高信号,20Gy组5个月MRI未见改变.伽玛刀照射后兴奋性氨基酸含量显著低于癫痫组,GABA能神经元表达低于正常,但高于癫痫组.结论 伽玛刀照射对癫痫大鼠具有治疗作用,高剂量伽玛射线(100Gy)对致痫灶有毁损作用.低剂量伽玛射线(20Gy)通过抑制兴奋性神经元释放兴奋性氨基酸使癫痫发作减少.     

脑皮质电刺激对癫痫大鼠脑皮质兴奋性的影响

目的 观察重复脑皮质电刺激对氯化铁诱发慢性癫痫大鼠模型脑皮质兴奋性的影响.方法 通过在运动感觉区脑皮质注射氯化铁建立慢性癫痫大鼠模型,给予脑皮质低频(1 Hz)低强度(0.1 mA)和低频(1 Hz)高强度(1.0 mA)、高频(100 Hz)低强度(0.1 mA)和高频(100 Hz)高强度(1.0 mA)不同的重复电刺激,检测电刺激前后脑皮质后放电阈值、后放电时程和行为学评分.假刺激慢性癫痫大鼠作为对照组.结果 后放电阈值低频低强度组(2.10±0.38)mA与对照组(1.50±0.33)mA相比差异有统计学意义(P＜0.05).行为学评分和后放电时程各组与对照组相比差异无统计学意义.行为学评分与后放电阈值的比值低频低强度组(1.88±0.60)和低频高强度组(2.18±0.38)与对照组(3.22±0.67)相比差异有统计学意义(P＜0.01和P＜0.05).结论 重复低频低强度脑皮质电刺激可以升高氯化铁诱发慢性癫痫大鼠模型的脑皮质后放电阈值,降低脑皮质兴奋性,提示合适参数的脑皮质电刺激对氯化铁诱发大鼠癜痫具有抑制作用.     

海马内注射内皮素-1导致大鼠痫性发作和海马硬化的初步研究

目的 观察大鼠海马内注射内皮素(endothelin,ET)-1是否导致大鼠痫性发作和海马硬化.方法 立体定位在成年大鼠海马CA3区内分别注射1 μL ET-1(200 pmol,15只)、海人酸(kainate,KA 5 pmol,15只)或磷酸盐缓冲液(PBS,0.01 mol,8只),观察大鼠行为学、脑电及对侧海马病理学改变.结果 海马注射PBS后大鼠未见痫性发作,脑电图呈10～15 Hz、150-200μV基本节律.注射ET-1或KA 2 h内大鼠出现不同程度的痫性发作和脑电图异常改变(尖波或尖慢波),KA组3-5级发作率高于ET-1组(86.67% vs 16.67%,P<0.05).部分ET-1和KA组大鼠在给药后2～3周可见癫痫样发作行为学改变.与PBS组比较,El-1和KA组给药后48 h对侧海马各区Nissl染色细胞数明显减少,GFAP表达增强(P<0.05);给药后30 d,对侧CA3区和门齿区苔藓纤维出芽评分高于PBS组(P<0.05).结论 海马注射ET-1可以导致大鼠癫痫样行为改变和海马硬化.     

MicroRNA-132拮抗剂两种不同注射方式在匹罗卡品诱导的幼年大鼠癫痫急性期的差异

目的探讨microRNA-132拮抗剂对氯化锂-匹罗卡品诱导的幼年SD大鼠内侧颞叶癫痫(mesial temporal lobe epilepsy,MTLE)模型急性期的影响。方法实验分为4组:microRNA-132拮抗剂侧脑室置管组;microRNA-132拮抗剂阴性对照置管组;microRNA-132拮抗剂直接注射组;microRNA-132拮抗剂阴性对照直接侧脑室注射组;实验各组药物干预在造模前24 h进行。利用氯化锂-匹罗卡品建立SD大鼠MTLE模型,通过行为学观察各组大鼠癫痫持续状态发作潜伏时长,Racine评分观察各组大鼠抽搐发作的严重程度,脑电图监测癫痫样放电的频率及波幅,并统计实验各组大鼠诱导SE的成功率及24 h后的死亡率。结果在实验各组中,建模成功率无显著性差异,microRNA-132拮抗剂直接注射组幼年SD大鼠造模以后达到SE的潜伏时较其阴性对照组明显延长、癫痫发作的Racine评分明显下降、脑电图结果显示痫样放电的幅度及频率显著下降,死亡率降低,结果有统计学意义(P0.05)。MicroRNA-132拮抗剂侧脑室置管注射组与microRNA-132拮抗剂侧脑室直接注射组结果无统计学差异(P0.05)。结论 microRNA-132拮抗剂预处理SD大鼠能明显延长氯化锂-匹罗卡品诱导的SD幼年大鼠癫痫发作的潜伏期,减轻急性期抽搐严重程度及大脑样痫放电,降低大鼠癫痫持续状态后的死亡率。提示microRNA-132拮抗剂对氯化锂-匹罗卡品诱导的幼年SD大鼠MTLE的发生具有抑制作用,抑制microRNA-132有可能成为癫痫持续状态药物治疗的潜在靶点和新方向。     

杏仁核电点燃癫(痫)模型与氯化锂-匹罗卡品大鼠癫(痫)模型的对比研究

目的:探讨不同类型癫(痫)大鼠在急性期和慢性期反复自发性发作时、发作前后脑电图(EEG)相应指标改变以及行为学改变.方法:选取雄性SD大鼠40只,随机分为A、B、C、D4组.A组10只为杏仁核电点燃癫(痫)模型(不作电刺激)对照组;B组:10只,为制作杏仁核电刺激点燃癫(痫)模型组;C组:10只,氯化锂-匹罗卡品癫(痫)模型(只注生理盐水)对照组;D组:10只,制作氯化锂-匹罗卡品癫(痫)模型组.结果:D组慢性期发作时EEG频率与急性期频率相比差异有统计学意义(P＜0.05),与B组各时期相比差异有统计学意义(P＜0.05);D组慢性期发作后3 min发作频率与B组急性期相比差异有统计学意义(P＜0.05);A组与C组在频率、波幅方面比较差异无统计学意义(P＞0.05).结论:B、D两种不同类型的癫(痫)大鼠不同时期EEG和行为学都会发生相应的改变.     

重症肌无力患者IgG脑室内注射对大鼠EEG及BAEP的影响

目的 观察重症肌无力(myasthenia gravis，MG)患者IgG(AChRAb)经大鼠脑室内注入对其脑电图(electroencephalography，EEG)及脑干听觉诱发电位(brain stem auditory evoked potential，BAEP)的影响，并探讨AChRAb影响大鼠中枢神经系统(CNS)的机制。方法将从确诊的、AChRAb阳性的MG患者血清中提纯的IgG(AChRAb)，注射到实验组大鼠侧脑室，对照组大鼠则注射健康人IgG，观察大鼠行为学、BAEP、EEG改变。结果实验组大鼠术后出现类似于实验性自身免疫性MG的行为学改变，部分大鼠出现癫痫发作BAEP峰间潜伏期(IPLs)延长EEG异常，即δ、θ增多与痫性波发放增加。结论 MGAChRAb可致大鼠CNS损害，AChRAb与大鼠CNS神经元型乙酰胆碱受体结合，可能是其病理生理机制。     

去势对戊四氮点燃大鼠癫痫模型的行为学表现

目的 研究去势对戊四氮点燃大鼠癫痫模型行为学表现的影响.方法 采用戊四氮腹腔注射制作癫痫大鼠模型,对照研究去势大鼠同正常大鼠的潜伏期及持续时间等行为学表现.结果 大鼠癫痫模型全部点燃,去势组平均潜伏期(8.09±0.89) min((-x)±SD)长于非去势组的(3.94±0.65) min((-x)±SD).发作时间也有所缩短,去势组(19.16 ±3.06) min((-x)±SD)略短于非去势组的(26.37±2.90) min((-x)±SD) (P ＜0.05).非去势组点燃时间明显短于去势组,非去势组平均点燃时间(20.83±6.15) d((-x)±s),而去势组平均点燃时间(24.6±5.64) d((-x)±SD).结论 戊四氮点燃大鼠致痫模型是一种成熟的、较为安全的癫痫模型.去势后,SD雄鼠较正常非去势SD雄鼠相比致痫潜伏期延长、持续时间缩短、发作频率及程度减轻,点燃时间也明显长于正常SD雄鼠.     

氯喹对戊四氮慢性致痫大鼠脑皮质及海马腺苷激酶表达的影响

目的 观察氯喹对戊四氮致痫大鼠皮质和海马区腺苷激酶(ADK)表达的影响,探讨ADK与癫痫发作的关系及氯喹在癫痫发生过程中的作用. 方法 30只健康雄性SD大鼠按照随机数字表法分为对照组、戊四氮(PTZ)致痫组和氯喹干预组,每组10只.观察大鼠行为学表现,记录其脑电改变,采用免疫组化法检测3组大鼠皮质和海马区ADK的表达. 结果 对照组大鼠无癫痫发作,PTZ致痫组大鼠出现Racine评分中Ⅳ～Ⅴ级严重发作,氯喹干预组大鼠出现Ⅰ～Ⅲ级发作,差异有统计学意义(P＜0.05).PTZ致痫组大鼠脑电记录呈频发高幅的痫样波,氯喹干预组大鼠脑电记录显示慢波、小棘波.PTZ致痫组大鼠脑内ADK表达明显增强,以海马区最为显著,与对照组相比差异均有统计学意义(P＜0.05).氯喹干预组大鼠脑内ADK表达降低,但距离正常水平仍有较大差距,与对照组相比差异有统计学意义(P＜0.05). 结论 癫痫脑组织中存在ADK的表达异常,氯喹可以抑制这种表达,有效控制癫痫发作.     

Idiopathic generalised epilepsy of adult onset: clinical syndromes and genetics

OBJECTIVE: To study the clinical features and genetics of idiopathic generalised epilepsy (IGE) beginning in adult life. METHODS: Consecutive patients with IGE, defined as generalised seizures with spike or polyspike and wave on EEG, were studied in the setting of a first seizure clinic where an early postictal EEG record is part of the protocol. Patients were divided into two groups: "classical IGE" with onset before 20 years and inclusive of all the IGE subsyndromes recognised by the international classification; and "adult onset IGE", when seizure onset was at age 20 years or later. Seizure patterns, clinical features, and genetics of the adult onset group were examined. RESULTS: Of 121 patients with an electro-clinical diagnosis of IGE, 34 (28%) were diagnosed as adult onset IGE. The seizure patterns in these 34 cases were tonic-clonic seizures + absences (3), tonic-clonic seizures + myoclonus (6), and tonic-clonic seizures alone (25). Tonic-clonic seizures were often precipitated by alcohol or sleep deprivation. The proportion of affected first and second degree relatives did not differ between the classical and adult onset IGE groups. Twenty adult onset cases were treated with sodium valproate, four with other antiepileptic drugs, and 10 were untreated. Follow up of 32 of the 34 cases (for 31 (22) months (mean (SD)) showed that tonic-clonic seizures recurred in eight patients: five with identified provocative factors and three without. CONCLUSIONS: Adult onset IGE is a relatively frequent and benign disorder. Seizures are usually provoked and are easy to control. Patients in this age group may often be misdiagnosed as having non-lesional partial epilepsy. Early postictal EEG and sleep deprivation studies may improve the detection of these patients. Pedigree analysis suggests that adult onset IGE, like classical IGE, has a genetic aetiology.     

West syndrome in tuberous sclerosis complex

West syndrome occurs commonly in children with tuberous sclerosis complex and is associated with a grave prognosis for cognitive and seizure outcomes. We sought to determine the epilepsy outcome of children with tuberous sclerosis complex and West syndrome and whether EEG, MRI, or steroid therapy duration were different in those whose epilepsy improved compared with those with intractable seizures. Seventeen patients with tuberous sclerosis complex and West syndrome were identified. For each patient, two sets of clinical evaluations, EEG and MRI data, and treatment information separated by at least 12 months were obtained. The patients were divided into two seizure outcome groups. EEG, MRI, and treatment data were compared between the groups. The intellectual deficiency was either severe (76%) or moderate (24%). Seizure control improved in 10 and worsened in seven, without mortality (follow-up range = 12-216 months). No significant differences in EEG background, MRI findings, or steroid treatment duration were evident between the groups. The difference in EEG-sleep approached statistical significance (P = 0.06). Our findings did not confirm reports of high mortality and poor epilepsy outcome in intellectually deficient children with West syndrome and tuberous sclerosis complex. EEG sleep was the best indicator of seizure control and approached statistical significance. The duration of steroid therapy had no influence on seizure control.     

氯化铁致痫大鼠早期颅内电极脑电图的观察

目的探讨氯化铁(FeCl3)致痫大鼠早期颅内电极脑电图的特点。方法将40只SD大鼠随机分为正常组(n=6)、对照组(n=6)、模型组(n=28)。模型组大鼠采用皮层内注射FeCl3溶液建立癫痫模型,对照组注射等量生理盐水,正常组不注射任何液体。通过颅内电极连续记录建模过程中早期脑电图。结果模型组28只大鼠左侧大脑皮层内注FeCl36min后,颅内电极脑电图开始出现间断性痫样放电;12min后,25只大鼠观察到突出于背景的快节律、高波幅异常放电,以及痫样异常放电由左侧半球向右侧半球快速扩散,同时观察到大鼠全身发作时行为改变。正常组和对照组脑电图均未发现癫痫样放电。结论早期颅内电极脑电图可观察到建模过程中的痫样放电及急性发作时典型表现,为创伤后癫痫的深入研究提供了较好的实验平台。     

Seizures in juvenile Huntington's disease: Frequency and characterization in a multicenter cohort

Little is known about the epilepsy that often occurs in the juvenile form of Huntington's disease (HD), but is absent from the adult‐onset form. The primary aim of this study was to characterize the seizures in juvenile HD (JHD) subjects with regard to frequency, semiology, defining EEG characteristics, and response to antiepileptic agents. A multicenter, retrospective cohort was identified by database query and/or chart review. Data on age of HD onset, primary HD manifestations, number of CAG repeats, the presence or absence of seizures, seizure type(s), antiepileptic drugs used, subjects' response to antiepileptic drugs (AEDs), and EEG results were assembled, where available. Ninety subjects with genetically confirmed JHD were included. Seizures were present in 38% of subjects and were more likely to occur with younger ages of HD onset. Generalized tonic‐clonic seizures were the most common seizure type, followed by tonic, myoclonic, and staring spells. Multiple seizure types commonly occurred within the same individual. Data on EEG findings and AED usage are presented. Seizure risk in JHD increases with younger age of HD onset. Our ability to draw firm conclusions about defining EEG characteristics and response to AEDs was limited by the retrospective nature of the study. Future prospective studies are required. © 2012 Movement Disorder Society     

Electroclinical features of epilepsy in patients with juvenile type dentatorubral-pallidoluysian atrophy

Purpose: To clarify the electroclinical characteristics of epileptic seizures in patients with juvenile type dentatorubral‐pallidoluysian atrophy (DRPLA). Methods: Seventeen patients with juvenile type DRPLA confirmed by genetic analysis were studied retrospectively. The clinical records of all 17  patients and the ictal video electroencephalography (EEG) recordings from 12 of the 17 patients were reviewed. Results: Electroclinical studies in 12 patients identified 11 habitual seizures in 6 patients as partial seizures on ictal video EEG recordings. Clinical manifestations composed mainly of versions of the head and loss of consciousness. These partial seizures were persistently recorded throughout the clinical course. Brief generalized seizures (atypical absence and myoclonic seizure) were observed in 6 of 12 patients at the early stage. In contrast, generalized tonic–clonic seizures (GTCS) were recorded in four advanced stage patients who were almost bedridden. Semiological studies in 17 patients showed that the prevalence of partial seizures was significantly higher in patients with younger epilepsy onset (below 10 years of age; χ² test, p < 0.05) and that the age of epilepsy onset was significantly lower in patients with partial seizures than in those without partial seizures (Mann‐Whitney U test, p = 0.02). However, the number of CAG repeats and age at clinical onset were not significantly different between two groups. Discussion: Partial seizure is one of the common epileptic features in juvenile type DRPLA, especially in patients with younger epilepsy onset. Seizure types may be affected in an age‐dependent manner and change evolutionally during progression of the clinical stage.     

Congenital destructive hemispheric lesions and epilepsy: clinical features and relevance of associated hippocampal atrophy

We studied the clinical, EEG and MRI findings in 19 patients with epilepsy secondary to congenital destructive hemispheric insults. Patients were divided in two groups: 10 with cystic lesions (group 1), and 9 with atrophic lesions (group 2). Seizure and EEG features, as well as developmental sequelae were similar between the two groups, except for the finding that patients of group 2 more commonly presented seizures with more than one semiological type. MRI showed hyperintense T2 signal extending beyond the lesion in almost all patients of both groups, and it was more diffuse in group 2. Associated hippocampal atrophy (HA) was observed in 70% of group 1 patients and 77.7% of group 2, and it was not correlated with duration of epilepsy or seizure frequency. There was a good concordance between HA and electroclinical localization. The high prevalence of associated HA in both groups suggests a common pathogenesis with the more obvious lesion. Our findings indicate that in some of these patients with extensive destructive lesions, there may be a more circumscribed epileptogenic area, particularly in those with cystic lesions and HA, leading to a potential rationale for effective surgical treatment.     

癫痫动物模型脑中神经肽Y的动态含量变化及意义

目的:探讨匹罗卡品(PILO)诱发的癫痫大鼠模型脑组织中神经肽Y(Neuropeptide Y,NPY)含量的动态变化及意义,进一步明确NPY与癫痫的关系,为抗癫痫治疗,研制抗癫痫药物提供新途径。方法:健康成年雄性SD大鼠120只,随机分为两组:单纯腹腔注射匹罗卡品组(癫痫模型组);单纯腹腔注射生理盐水组(对照组);注射后根据Racine制定的标准判定是否有癫痫发作,并行脑电图检查,观察有无癫痫样波(棘波,尖波,棘慢波,尖慢波)发放。两组大鼠分别于给药后1h,3h,6h,24h,3d,7d,15d,30d,60d将大鼠麻醉,取出脑组织,对脑组织中的NPY含量进行测定。结果:癫痫模型组60只大鼠中,2只死于癫痫持续状态,其余大鼠可观察到边缘发作行为表现,脑电图有典型的癫痫样波发放,对照组无癫痫发作及癫痫样波发放。癫痫模型组脑NPY含量与对照组相比,差异有显著性P<0.05;癫痫模型组急性期(1h-7d)与慢性期(15d-60d)比较差异有显著性P<0.05,对照组差异无显著性;癫痫模型组与对照组脑中的NPY含量在12h,24h,15d,30d,60d.差异有显著性P<0.05或P<0.01,癫痫模型组脑中的NPY含量各组(各时间段)比较有差异有显著性P<0.05,对照组差异无显著性,癫痫模型组大鼠Ⅳ-Ⅴ级发作与Ⅱ-Ⅲ级发作,脑NPY含量比较,差异有显著性P<0.05。结论:1.神经肽Y与癫痫密切相关,癫痫发作后?     

Development of later life spontaneous seizures in a rodent model of hypoxia-induced neonatal seizures

Purpose: To study the development of epilepsy following hypoxia‐induced neonatal seizures in Long‐Evans rats and to establish the presence of spontaneous seizures in this model of early life seizures. Methods: Long‐Evans rat pups were subjected to hypoxia‐induced neonatal seizures at postnatal day 10 (P10). Epidural cortical electroencephalography (EEG) and hippocampal depth electrodes were used to detect the presence of seizures in later adulthood (>P60). In addition, subdermal wire electrode recordings were used to monitor age at onset and progression of seizures in the juvenile period, at intervals between P10 and P60. Timm staining was performed to evaluate mossy fiber sprouting in the hippocampi of P100 adult rats that had experienced neonatal seizures. Key Findings: In recordings made from adult rats (P60–180), the prevalence of epilepsy in cortical and hippocampal EEG recordings was 94.4% following early life hypoxic seizures. These spontaneous seizures were identified by characteristic spike and wave activity on EEG accompanied by behavioral arrest and facial automatisms (electroclinical seizures). Phenobarbital injection transiently abolished spontaneous seizures. EEG in the juvenile period (P10–60) showed that spontaneous seizures first occurred approximately 2 weeks after the initial episode of hypoxic seizures. Following this period, spontaneous seizure frequency and duration increased progressively with time. Furthermore, significantly increased sprouting of mossy fibers was observed in the CA3 pyramidal cell layer of the hippocampus in adult animals following hypoxia‐induced neonatal seizures. Notably, Fluoro‐Jade B staining confirmed that hypoxic seizures at P10 did not induce acute neuronal death. Significance: The rodent model of hypoxia‐induced neonatal seizures leads to the development of epilepsy in later life, accompanied by increased mossy fiber sprouting. In addition, this model appears to exhibit a seizure‐free latent period, following which there is a progressive increase in the frequency of electroclinical seizures.     

Spike frequency is dependent on epilepsy duration and seizure frequency in temporal lobe epilepsy.

OBJECTIVES: We wanted to investigate factors that are associated with frequency of interictal epileptiform discharges by investigating 303 patients with temporal lobe epilepsy (TLE). METHODS: We included all patients who consecutively underwent the adult presurgical evaluation program at our center and who had intractable, medial TLE with complex partial seizures due to unilateral medial temporal lobe lesions. The interictal EEG samples were automatically recorded and stored on computer. The location and frequency of interictal epileptiform discharges were assessed by visual analysis of interictal EEG samples of 2-minute duration every hour. RESULTS: There were 303 patients (aged 16-63) who met the inclusion criteria. The median interictal epileptiform discharge frequency was 15 IED/h, the median seizure frequency was 4 seizures/month. According to univariate analyses, we found that age at monitoring, epilepsy duration, and higher seizure frequency were associated with higher interictal epileptiform discharge frequency. In the logistic regression analysis, we found that higher seizure frequency (p < 0.001) and longer epilepsy duration (p = 0.007) were independently associated with higher spike frequency, while the age at monitoring was not. CONCLUSIONS: Seizure frequency and epilepsy duration (years of patient's life with seizure activity) were independently associated with IED frequency, suggesting that IED are modulated by seizures.