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.     

美解眠诱发试验在颞叶癫痫术前脑电图监测中的应用

目的 研究美解眠诱发试验对颞叶癫痫患者癫痫发作和脑电图的影响.方法 回顾性分析60例颞叶癫痫患者行前颞叶切除术的术前视频脑电图(VEEG)监测情况,其中美解眠诱发组与对照组各30例,比较两组的VEEG监测时间、监测到的癫痫发作次数、形式和术后癫痫无发作率.同时比较诱发组诱发前后脑电图变化.结果 VEEG监测时间分别为诱发组35 h,对照组56 h,差异有统计学意义.诱发组药物诱发后VEEG监测到99次癫痫发作,包括注药后5 min内71次(71.7%)、6-60 min 18次(18.2%),其中10次(10.1%)诱发后出现与惯常发作不一致的癫痫发作;而对照组记录到102次癫痫发作,其中4次(3.9%)与惯常发作不一致,两组差异无统计学意义.诱发组注药后发作间期痫性放电明显增加,主要放电部位没有明显变化.诱发的发作期脑电图起源部分仍以单侧颞叶为主,与自然发作差异无统计学意义.结论 美解眠诱发不影响颞叶癫痫灶的定位,可用于颞叶癫痫的术前VEEG监测,可明显减少监测时间.     

电视录像脑电图在癫痫及其他发作性疾病中的诊断价值探讨

目的：评价电视脑电图（Video-EEG)监测在癫痫及其他发作性疾病临床诊断中的应用价值。方法：对216例具有各种发作性症状的患者进行连续24h的包括清醒、睡眠及诱发试验的Video-EEG监测。结果：216例患者中130例（60．2％）监测到临床发作，其中53例伴有发作期痫样放电，证实为癫痫性发作；73例发作期及发作间期均无痫样放电，为非癫痫性发作。216例患者中共80例监测到了痫样放电，其中64例通过发作期的脑电－临床表现和（或）发作间期的EEG特征，结合有关病史资料确定了癫痫的发作类型，27例监测后发作分类得到了修正。结论：Video-EEG可提高痫样放电的检出率，有助于癫痫发作与非癫痫发作的鉴别及癫痫的分型。     

低、高频闭环电刺激对氯化铁癫痫模型大鼠治疗作用的比较

目的探讨低、高频闭环电刺激对氯化铁癫痫模型大鼠的治疗效果。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,建立癫痫模型,分别给予低频刺激(1Hz)和高频刺激(100Hz),同时给予8小时脑电监测。分析大鼠8小时内发作总次数和发作总时间。结果低频和高频电刺激均能抑制大鼠的癫痫发作,而高频与低频刺激在治疗效果上无明显统计学差异。结论低频刺激为较佳的刺激方式。     

SPECT、EEG、MRI在癫痫发作期发作间期对癫痫灶的定位价值

目的:顽固性癫痫Г-刀治疗的关键在于定位,比较15例顽固性癫痫SPECT(single photon emission compu-ted tomography,SPECT)EEG,MRI在癫痫发作期、发作间期对癫痫灶的定位价值。方法:发作间期做SPECT、EEG、MRI,而后用0.25％美解眠诱发癫痫临床下发作记录发作期SPECT。结果:发作间期致痫灶SPECT 10人,EEG7人,MRI 3人;发作期SPECT 3人。结论:发作间期癫痫灶检出率SPEC:T66.67％,EEG44.67％,MRI 20％;发作期为20％。三项检查分别从代谢、电活动和结构对癫痫灶进行定位。SPECT阳性检出率最高;EEG在癫痫分类和定侧(左或右半球)具有优势;而MRI在癫痫灶定性方面有帮助。三者相结合可提高癫痫灶的准确性。     

探讨儿童部分性癫痫发作发作间期脑电图及与影像学的关系

目的探讨儿童部分性癫痫发作发作间期EEG及与影像学的关系。方法对67例部分性发作的癫痫患儿行长程录像脑电监测(VEEG)及影像学检查,分析发作间期EEG及与影像学的关系。结果与发作间期EEG正常的患儿比较,EEG异常患儿影像学正常率显著降低,影像学异常率显著增高(χ2=5.154,P=0.023)。发作间期异常放电51例患者中,42例(82.4%)间期放电与发作期部位一致,其中20例(47.6%)影像学检查正常,22例(52.4%)影像学检查异常,两者相比差异无统计学意义(P=0.726)。结论发作间期EEG异常部分性癫痫患儿,影像异常率高,大多数患儿发作间期放电与发作期起始放电部位一致。     

青霉素致大鼠急性癫痫模型全身性放电起源的实验研究

目的 探讨青霉素致大鼠急性癫痫模型全身性放电起源的定位特征.方法 给10只SD大鼠各铺设皮层、海马和杏仁核电极共7对,用青霉素300万U·kg-1腹腔注射建立急性全身性癫痫模型,同时脑电记录,观察全身性癫痫样放电起始阶段的脑电特征.结果 脑电显示全身性癫痫样放电起始阶段杏仁核最早出现连续性棘波.结论 青霉素诱导的急性全身性癫痫大鼠模型癫痫样放电并非完全同步化,杏仁核为癫痫易感区,可能参与放电起源.     

幼年大鼠癫痫持续状态后电生理和行为学的研究

目的观察幼年大鼠发生癫痫持续状态(status epilepticus,SE)后的电生理和行为学改变,并判断其表现是否符合Lennox-Gastaut综合征(Lennox-Gastaut syndrome,LGS)的电临床特点。方法 3周龄雄性Wistar大鼠50只,随机分为模型组(n=30)与对照组(n=20),模型组幼鼠腹腔注射氯化锂-匹鲁卡品诱发SE,对照组幼鼠用等量生理盐水代替匹鲁卡品。1周后,采用改进的颅内电极方法进行2周长程视频脑电监测,观察分析幼鼠脑电图背景活动、癫痫放电、癫痫发作及其相应症状学改变情况。脑电监测结束后,进行Morris水迷宫认知功能测试,观察记录幼鼠在水迷宫中寻找水下平台的潜伏期及游泳距离。结果共26只模型组幼鼠成功诱发SE并存活,对照组(n=20)表现正常。长程视频脑电监测期间,对照组幼鼠脑电背景活动正常,未见癫痫发作。模型组幼鼠发作间期癫痫放电显著增多,睡眠期可见弥漫性慢棘-慢波活动;共监测到3种癫痫发作类型:不典型失神发作、强直发作和肌阵挛发作。在水迷宫测试中,模型组幼鼠的潜伏期及游泳距离明显长于对照组(P0.05)。结论模型组幼鼠在发生SE后出现多种类型癫痫发作、异常脑电图表现及认知功能减退,该动物模型的电临床表现符合LGS的临床特征。     

视频脑电图监测对癫痫的诊断价值

目的探讨视频脑电图(Video-EEG)对癫痫的诊断价值.方法对252例发作性疾病患者进行连续12～24小时监测,其中包括清醒、睡眠及诱发试验,分析临床发作和异常放电的关系,异常放电出现的时相,癫痫分型与异常放电的关系,临床发作前脑电图的改变以及临床发作间期和发作期异常脑电图的不同表现.结果252例监测到临床发作142例,其中同时伴异常放电者为111例;252例检出异常放电187例,其中出现于睡眠期者146例;确诊的111例中103例确定了发作类型,其中25例修正了发作类型;确诊的111例监测到发作前脑电图的异常改变,表现为背景脑电波频率和波幅的改变,或者出现痫样放电;111例不同发作类型癫痫患者发作间期和发作期有不同的异常脑电图表现.结论视频脑电图可提高痫样放电的检出率,有助于癫痫的诊断及分型,有利于观察癫痫患者发作间期及发作期脑电图的表现.     

脑电监测癫痫患者的护理及干预

目的：为癫痫患提供在脑电监测癫痫发作过程的安全护理。保证脑电监测质量，确定致痫灶，为手术提供准确定位。方法：脑电监测前对患进行心理评估，对患应用抗癫痫药物进行干预，做好脑电监测过程中癫痫发作时各种抢救工作及护理安全措施。结果：42例癫痫患在脑电监测癫痫发作、美解眠诱发癫痫发作，在抢救工作准备充分，护理措施得当，监测医生和护士密切配合，即描记到致痫灶波形，又安全度过癫痫发作过程，无一例意外发生。结论：脑电监测癫痫波是确定致痫灶一种主要检查项目，是为选择手术方式提供科学依据一种主要手段。在脑电监测患癫痫发作期间，监测医生与护士进行密切配合，做好各项抢救及护理措施准备，是患平安度过脑电监测癫痫发作期的重要保证。     

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。     

痫性放电实现异体间转道并致痫动物的研究报道

目的观察青霉素癫痫模型痫性放电能否被引导电极转道至异体大鼠脑内并致痫。方法实验大鼠海马局部注射青霉素建立癫痫模型,通过引导电极拟将痫性放电导入异体大鼠同侧海马,观察实验大鼠的行为学、脑电图变化。结果致痫组、痫能导出组12只大鼠全部点燃,痫能导入组6只大鼠亦出现痫性发作,痫能导出组痫性发作时程缩短,致痫组、痫能导出组、痫能导入组大鼠脑电图均可记录到痫性波;对照组、电极组无痫性发作。结论实验性痫性放电可通过引导电极在异体大鼠脑组织间传导,脑内痫性放电有可能被电极导出。     

Focal akinetic seizures as documented by electroencephalography and video recordings.

In three patients with focal epilepsies, focal akinetic seizures that were characterized by ictal paresis of the contralateral arm during preserved consciousness were recorded with EEG and video. MRI and ictal/interictal EEG revealed a frontal or central focus in all patients. Focal akinetic seizures are probably due to epileptic activation of negative motor areas.     

Tetanus toxin-induced seizures in infant rats and their effects on hippocampal excitability in adulthood

A new experimental model of developmental epilepsy is reported. Behavioral and EEG features of seizures produced by unilateral intrahippocampal injection of tetanus toxin in postnatal day 9–11 rats, are described. Within 24–72 h of tetanus toxin injection, rat pups developed frequent and often prolonged seizures which included combinations of repetitive wet dog shakes, and wild running-jumping seizures. Intrahippocampal and cortical surface EEG recordings showed that coincident with these behaviors, electrographic seizures occurred not only in the injected hippocampus, but also in the contralateral hippocampus and bilaterally in the neocortex. Analysis of the interictal EEG revealed multiple independent spike foci. One week following tetanus toxin injection, the number of seizures markedly decreased; however, interictal spiking persisted. After injection rats were allowed to mature some were observed to have unprovoked behavioral seizures and/or epileptiform EEG activity. Mature animals were also studied using in vitro slice techniques. Recordings from hippocampal slices demonstrated spontaneous epileptiform burst discharges in the majority of rats which had tetanus toxin induced seizures as infants. These events occurred in area CA3 and consisted of interictal spikes and intracellularly recorded paroxysmal depolarization shifts (PDSs). On rarer occasions, electrographic seizures were recorded. The use of the tetanus toxin model in developing rats may facilitate a better understanding of the unique features of epileptogenesis in the developing brain and the consequences early-life seizures have on brain maturation and the genesis of epileptic conditions in later life.     

EEG non-linear feature extraction using correlation dimension and Hurst exponent

In this work, we evaluated the differences between epileptic electroencephalogram (EEG) and interictal EEG by computing some non-linear features. Correlation dimension (CD) and Hurst exponent (H) were calculated for 100 segments of epileptic EEG and 100 segments of interictal EEG. A comparison was made between epileptic EEG and interictal EEG in those non-linear parameters. Results show that the mean values of CD are 2.64 for epileptic EEG and 4.55 for interictal EEG. We also calculated approximate entropy (ApEn) of those EEG signals. The mean values of ApEn are 0.90 for epileptic EEG and 4.55 for interictal EEG. The values of CD and ApEn of epileptic EEG are generally lower than those of interictal EEG, indicating less complexity of EEG signals during seizures. The mean values of Hurst exponent are 0.19 for epileptic EEG and 0.29 for interictal EEG. Hurst exponents for epileptic EEG and interictal EEG are both <0.5. This indicates that both epileptic and interictal EEGs show long-range anticorrelation. The value of Hurst exponent of epileptic EEG signals is lower than that of interictal EEG signals, showing that the degree of anticorrelation of epileptic EEG signals is larger than that of interictal EEG. Hence, the non-linear parameters such as CD and Hurst exponent can help interpret epileptic and interictal EEGs and their neurodynamics.     

Relationship between neuronal loss and interictal glucose metabolism during the chronic phase of the lithium-pilocarpine model of epilepsy in the immature and adult rat

The lithium-pilocarpine (Li-Pilo) model of epilepsy reproduces most of the features of human temporal lobe epilepsy. After having studied the metabolic changes occurring during the silent phase, in the present study, we explored the relationship between interictal metabolic changes and neuronal loss during the chronic phase following status epilepticus (SE) induced by Li-Pilo in 10-day-old (P10), 21-day-old (P21), and adult rats. Rats were observed and their EEG was recorded to detect the occurrence of spontaneous recurrent seizures (SRS). Local cerebral glucose utilization was measured during the interictal period of the chronic phase, between 2 and 7 months after SE, by the [(14)C]2-deoxyglucose method in rats subjected to SE at P10, P21, or as adults. Neuronal damage was assessed by cell counting on adjacent cresyl violet stained sections. When SE was induced at P10, rats did not become epileptic, did not develop lesions and cerebral glucose utilization was in the normal range 7 months later. When SE was induced in adult rats, they all became epileptic after a mean duration of 25 days and developed lesions in the forebrain limbic areas, which were hypometabolic during the interictal period of the chronic phase, 2 months after SE. When SE was induced in P21 rats, 24% developed SRS, and in 43% seizures could be triggered (TS) by handling, after a mean delay of 74 days in both cases. The remaining 33% did not become epileptic (NS). The three groups of P21 rats developed quite comparable lesions mainly in the hilus of the dentate gyrus, lateral thalamus, and entorhinal cortex; at 6 months after SE, the forebrain was hypometabolic in NS and TS rats while it was normo- to slightly hypermetabolic in SRS rats. These data show that interictal metabolic changes are age-dependent. Moreover, there is no obvious correlation, in this model, between interictal hypometabolism and neuronal loss, as reported previously in human temporal lobe epilepsy.     

Delta oscillation underlies the interictal spike changes after repeated transcranial direct current stimulation in a rat model of chronic seizures

BackgroundTranscranial direct current stimulation (tDCS) provides a noninvasive polarity-specific constant current to treat epilepsy, through a mechanism possibly involving excitability modulation and neural oscillation.ObjectiveTo determine whether EEG oscillations underlie the interictal spike changes after tDCS in rats with chronic spontaneous seizures.MethodsRats with kainic acid-induced spontaneous seizures were subjected to cathodal tDCS or sham stimulation for 5 consecutive days. Video-EEG recordings were collected immediately pre- and post-stimulation and for the subsequent 2 weeks following stimulation. The acute pre-post stimulation and subacute follow-up changes of interictal spikes and EEG oscillations in tDCS-treated rats were compared with sham. Ictal EEG with seizure behaviors, hippocampal brain-derived neurotrophic factor (BDNF) protein expression, and mossy fiber sprouting were compared between tDCS and sham rats.ResultsInterictal spike counts were reduced immediately following tDCS with augmented delta and diminished beta and gamma oscillations compared with sham. Cathodal tDCS also enhanced delta oscillations in normal rats. However, increased numbers of interictal spikes with a decrease of delta and theta oscillations were observed in tDCS-treated rats compared with sham during the following 2 weeks after stimulation. Resuming tDCS suppressed the increase of interictal spike activity. In tDCS rats, hippocampal BDNF protein expression was decreased while mossy fiber sprouting did not change compared with sham.ConclusionsThe inverse relationship between the changes of delta oscillation and interictal spikes during tDCS on and off stimulation periods indicates that an enhanced endogenous delta oscillation underlies the tDCS inhibitory effect on epileptic excitability.     

EEG non-linear feature extraction using correlation dimension and Hurst exponent

Abstract

In this work, we evaluated the differences between epileptic electroencephalogram (EEG) and interictal EEG by computing some non-linear features. Correlation dimension (CD) and Hurst exponent (H) were calculated for 100 segments of epileptic EEG and 100 segments of interictal EEG. A comparison was made between epileptic EEG and interictal EEG in those non-linear parameters. Results show that the mean values of CD are 2·64 for epileptic EEG and 4·55 for interictal EEG. We also calculated approximate entropy (ApEn) of those EEG signals. The mean values of ApEn are 0·90 for epileptic EEG and 4·55 for interictal EEG. The values of CD and ApEn of epileptic EEG are generally lower than those of interictal EEG, indicating less complexity of EEG signals during seizures. The mean values of Hurst exponent are 0·19 for epileptic EEG and 0·29 for interictal EEG. Hurst exponents for epileptic EEG and interictal EEG are both <0·5. This indicates that both epileptic and interictal EEGs show long-range anticorrelation. The value of Hurst exponent of epileptic EEG signals is lower than that of interictal EEG signals, showing that the degree of anticorrelation of epileptic EEG signals is larger than that of interictal EEG. Hence, the non-linear parameters such as CD and Hurst exponent can help interpret epileptic and interictal EEGs and their neurodynamics.     

Coexistence of symptomatic focal and absence seizures: Video-EEG and EEG-fMRI evidence of overlapping but independent epileptogenic networks

The distinction between typical absences and hypomotor seizures in patients having frontal lesions is difficult. In focal epilepsy, generalized-like interictal discharges can reflect either a coexistent generalized epileptic trait or a secondary bilateral synchrony. Using combined measures of the EEG and blood oxygenation level dependent (BOLD) activity, we studied a 50-year-old patient with both absence-like and symptomatic focal motor seizures. Focal activity induced activation in the lesional area and deactivation in the contralateral central cortex. Generalized spike-and-wave discharges (GSWDs) resulted also in perilesional activation, and multifocal symmetrical cortical and thalamic activations, and deactivation in associative cortical areas. Although the central cortex was involved during both types of epileptic activity, electroencephalography (EEG)–functional magnetic resonance imaging (fMRI) revealed distinct neuronal networks at the time of the focal or generalized discharges, allowing a clear-cut differentiation of the generators. Whether the patient had distinct epileptic syndromes or distinct electrographic patterns from the lesional trigger remains debatable.