颅内电极皮层电刺激皮层后放电的抑制规律研究

目的:通过对后放电(AD)进行脉冲刺激抑制的研究,为皮层电刺激(ECS)治疗癫(痫)摸索合理的刺激参数.方法:回顾性研究2011～2012年行癫(痫)颅内电极埋置术并接受ECS病人的脑电图(EEG)资料共10例,如患者反复出现AD,即在相同位置给予相同参数的短暂脉冲刺激(BPS),有时可终止AD,对皮层AD的抑制规律进行分析.结果:对64个点重复刺激后可重复出现AD触点45个(70％),对这45个AD点给予BPS,其中13个(29％)在刺激后2s内AD终止,对比不同的AD波形、频率、部位、时相、累及范围、是否远隔、刺激潜伏期与BPS干预效果相关.结论:当在AD波形的负相峰及下降期,AD波形表现为棘慢波及节律性波,BPS潜伏期越短时,BPS干预AD更加有效.     

慢性酒精刺激对大鼠伏核EEG及脑电功率谱的影响

观察慢性酒精刺激过程中大鼠伏核EEG及功率谱的变化,探索酒精依赖的神经机制.在伏核埋植记录电极后,给大鼠饮用6%酒精水溶液30 d.用脑电图机及计算机信号采集系统记录及分析饮酒期间及停饮后的伏核EEG及功率谱.结果表明:在慢性饮酒过程中,d节律明显减小,散在的高幅慢活动δ波和θ波逐渐增多,功率谱分析表明δ频段功率百分比明显增加,而θ频段功率百分比明显减少,总功率减少.停饮后,出现棘波和棘慢综合波,并持续增多,δ频段功率百分比逐渐减少,而θ和α频段功率百分比逐渐增加,总功率增加,约在停饮9～10 d,脑电逐渐恢复正常.提示:伏核EEG和脑电功率谱的变化在一定程度上可反映慢性酒精刺激及撤除刺激对神经系统的影响.     

慢性酒精刺激对大鼠伏核EEG及脑电功率谱的影响

观察慢性酒精刺激过程中大鼠伏核EEG及功率谱的变化 ,探索酒精依赖的神经机制。在伏核埋植记录电极后 ,给大鼠饮用 6 %酒精水溶液 30d。用脑电图机及计算机信号采集系统记录及分析饮酒期间及停饮后的伏核EEG及功率谱。结果表明 :在慢性饮酒过程中 ,α节律明显减小 ,散在的高幅慢活动δ波和θ波逐渐增多 ,功率谱分析表明δ频段功率百分比明显增加 ,而θ频段功率百分比明显减少 ,总功率减少。停饮后 ,出现棘波和棘慢综合波 ,并持续增多 ,δ频段功率百分比逐渐减少 ,而θ和α频段功率百分比逐渐增加 ,总功率增加 ,约在停饮 9～ 10d ,脑电逐渐恢复正常。提示 :伏核EEG和脑电功率谱的变化在一定程度上可反映慢性酒精刺激及撤除刺激对神经系统的影响。     

电刺激构建大鼠皮层网络癫痫的海马细胞电生理特征

本文旨在探讨急性强直电刺激右后背海马（hippocampus，HPC）诱导出现双侧皮层网络癫痫的前背HPC神经元电生理机制。实验共用雄性SD大鼠35只，急性强直电刺激（60Hz，2s，0．4-0．6mA）大鼠右侧后背HPC（a—cute tetanization of the right posterior dorsal hippocampus，ATPDH）诱发癫痫模型。四通道同步记录双侧皮层电图（electrocorticogram，ECoG）或前背HPC深部电图和双侧前背HPC单位放电。结果显示，ATPDH可以引起以下效应：（1）双侧皮层癫痫样电活动起源于同侧HPC单位后放电，继而引起对侧HPC单位后放电，最终形成对侧和同侧皮层电图癫痫发作样电振荡；（2）增强双侧皮层4—10Hz节律性电振荡或诱发双侧HPCI00—250Hz电振荡，与此同时双侧HPC神经元均表现为非对称性电活动；（3）双侧HPC神经元锋电位间期（interspike interval，ISI）点呈现非规则性环状分布。同侧HPC爆发式单位放电IsI点分布的环状分层较规则、发生率较高，并与同侧HPC电振荡最大振幅的正弦式波动形成明显的时间对应关系。结果表明：ATPDH可诱导双侧皮层和HPC电图形成癫痫电网络。当皮层或HPC癫痫网络重建过程中，HPC神经元放电具有特征性ISI点环状分布等编码形式。     

术中体感诱发电位监测联合直接皮层电刺激技术在脑功能区手术中的应用

目的:探讨皮层体感诱发电位(SEP)波形位相倒置、术中直接电刺激(DCES)联合监测定位脑功能区的方法及意义.方法:在对37例运动感觉功能区占位患者术中采用SEP波形翻转、DCES定位感觉区和运动区的前提下,手术切除病变.结果:34例病人成功引出SEP,其中25例记录到明确的SEP的位相倒置,藉此定位中央沟,其中23例患者成功引出运动诱发电位(MEP),定位出感觉、运动皮层.有3例既未引出SEP也未引出MEP.术后患者脑功能大部分好转,未出现永久性功能障碍.结论:颅内占位患者术中联合采用SEP波形位相倒置与DCES监测技术定位,能在最大限度切除肿瘤的同时有效保护运动功能.     

激活大鼠右侧尾壳核重建双侧海马癫痫网络的细胞机制

目的　 探讨强直电刺激大鼠右侧尾壳核 (rightcaudateputamen ,RCPu)重建双侧海马 (hippocampus,HPC)癫痫电网络的细胞机制。 方法　 实验共用雄性SD大鼠 10 1只 ,体重 2 0 0～ 2 5 0g。急性强直电刺激 (6 0Hz ,2s,0 .4～ 0 .6mA)RCPu (acutetetanizationoftherightcaudateputamen ,ATRC)或右背HPC(acutetetanizationoftherightdorsalhippocampus,ATRDH) ,同步记录双侧前背HPC神经元单位放电 ,比较激活RCPu或RHPC时 ,神经通路长度对HPC癫痫电网络重建过程中单个神经元电活动的影响。 结果　(1)ATRC和ATRDH均能明显地调制单个HPC神经元的紧张式放电成为节律性爆发式放电。 (2 )ATRC引起的HPC爆发式单位放电串放电时程长[(6 5 0 .738± 5 6 .4 19)ms ,n =12 0 ]、串间隔短 [(interburstinginterval,IBI ,(772 .6 0 0± 4 6 .6 6 5 )ms,n =90 ) ;相反 ,ATRDH引起HPC的爆发式单位放电特征是串放电时程短 [(2 70 .6 12± 19.917)ms,n =12 3](T =6 .35 3,P <0 .0 0 1)、IBI长 [(1373.6 6 3± 12 1.2 36 )ms,n =10 3](T =4 .6 2 7P <0 .0 0 1)。 (3)ATRC诱发的海马细胞单位后放电时程长 [(7.0 6± 0 .776 )s,n =10 4 ]、潜伏期长 [(8.77± 1.2 31)trains ,n =30 ],而ATRDH诱发的单位后放电时程短 [(3.93± 0 .6     

电刺激丘脑底核对大鼠杏仁核电点燃的抑制作用

目的 在大鼠杏仁核电点燃癫痫模型中研究丘脑底核高频深部电刺激对点燃的抑制作用及其对Glu、GABA浓度的影响.方法 建立大鼠杏仁核电刺激点燃模型,观察丘脑底核高频深部电刺激对点燃发作的抑制作用,应用高效液相色谱（HPLC）测定大鼠脑组织中Glu、GABA的浓度.结果 对丘脑底核高频深部电刺激（130 Hz,0.2 ms,5 V）能够有效抑制大鼠杏仁核电点燃（P＜0.05）;并可以降低纹状体内Glu浓度,升高纹状体内GABA浓度（P＜0.05）.结论 丘脑底核高频深部脑电刺激能有效抑制大鼠杏仁核电点燃,其作用机制可能与改变Glu、GABA浓度平衡有关.     

帕金森病的脑深部电刺激治疗

帕金森病(PD)是神经内、外科治疗的难题。药物治疗效果不好;立体定向损毁疗法有半数病人术后复发,二次损毁副作用大,效果较差;双侧损毁治疗风险更大,且效果不稳定。近年,国外应用脑深部电刺激(DBS)治疗帕金森病,取得了良好疗效。本文综合近年国外文献,对DBS治疗PD的概况作一介绍。     

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。     

中风病人的短潜伏期体感诱发电位与脑电地形图、脑电检查结果对比分析

本文对中风病人136例进行短潜伏期体感诱发电位检查(SSEP),其中75例同时作脑电地形图检查(BEAM)及同步脑电检查(EEG),全部病人均作头颅CT检查。根据临床表现与/或头颅CT显示的不同部位,将病人组分为8组。分析其SSEP与BEAM的特点。脑干病变多影响P_(14),额叶病变多影响P_(22),丘脑病变多影响N_(16),皮层下病变多影响N_(16)、N_(18)、N_(19),顶叶病变多影响N_(20)、P_(40),异常率为100％。同时作BEAM结果,异常率为97.3％,同步EEG异常率为88％,头颅CT10例阴性,异常率86.6％,四种检查异常有显著差异。     

A comparison between detectors of high frequency oscillations

Objective

High frequency oscillations (HFOs) are a biomarker of epileptogenicity. Visual marking of HFOs is highly time-consuming and inevitably subjective, making automatic detection necessary. We compare four existing detectors on the same dataset.

Methods

HFOs and baselines were identified by experienced reviewers in intracerebral EEGs from 20 patients. A new feature of our detector to deal with channels where baseline cannot be found is presented. The original and an optimal configuration are implemented. Receiver operator curves, false discovery rate, and channel ranking are used to evaluate performance.

Results

All detectors improve performance with the optimal configuration. Our detector had higher sensitivity, lower false positives than the others, and similar false detections. The main difference in performance was in very active channels.

Conclusions

Each detector was developed for different recordings and with different aims. Our detector performed better in this dataset, but was developed on data similar to the test data. Moreover, optimizing on a particular data type improves performance in any detector.

Significance

Automatic HFO detection is crucial to propel their clinical use as biomarkers of epileptogenic tissue. Comparing detectors on a single dataset is important to analyze their performance and to emphasize the issues involved in validation.     

Excess of high frequency electroencephalogram oscillations in boys with autism.

BACKGROUND: An elevated excitation/inhibition ratio has been suggested as one mechanism underpinning autism. An imbalance between cortical excitation and inhibition may manifest itself in electroencephalogram (EEG) abnormalities in the high frequency range. The aim of this study was to investigate whether beta and gamma range EEG abnormalities are characteristic for young boys with autism (BWA). METHODS: EEG was recorded during sustained visual attention in two independent samples of BWA from Moscow and Gothenburg, aged 3 to 8 years, and in age matched typically developing boys (TDB). High frequency EEG spectral power was analyzed. RESULTS: In both samples, BWA demonstrated a pathological increase of gamma (24.4-44.0 Hz) activity at the electrode locations distant from the sources of myogenic artefacts. In both samples, the amount of gamma activity correlated positively with degree of developmental delay in BWA. CONCLUSIONS: The excess of high frequency oscillations may reflect imbalance in the excitation-inhibition homeostasis in the cortex. Given the important role of high frequency EEG rhythms for perceptual and cognitive processes, early and probably genetically determined abnormalities in the neuronal mechanisms generating high frequency EEG rhythms may contribute to development of the disorder. Further studies are needed to investigate the specificity of the findings for autism.     

Interictal high‐frequency oscillations (HFOs) as predictors of high frequency and conventional seizure onset zones

We investigated the relationship between the interictal high‐frequency oscillations (HFOs) and the seizure onset zones (SOZs) defined by the ictal HFOs or conventional frequency activity (CFA), and evaluated the usefulness of the interictal HFOs as spatial markers of the SOZs. We analysed seizures showing discrete HFOs at onset on intracranial EEGs acquired at ≥1000‐Hz sampling rate in a training cohort of 10 patients with temporal and extratemporal epilepsy. We classified each ictal channel as: HFO+ (HFOs at onset with subsequent evolution), HFO‐ (HFOs at onset without evolution), CFA (1.6–70‐Hz activity at onset with evolution), or non‐ictal. We defined the SOZs as: hSOZ (HFO+ channels only), hfo+&‐SOZ (HFO+ and HFO‐ channels), and cSOZ (CFA channels). Using automated methods, we detected the interictal HFOs and extracted five features: density, connectivity, peak frequency, log power, and amplitude. We created logistic regression models using these features, and tested their performance in a separate replication cohort of three patients. The models containing the five interictal HFO features reliably differentiated the channels located inside the SOZ from those outside in the training cohort (p<0.001), reaching the highest accuracy for the classification of hSOZ. Log power and connectivity had the highest odds ratios, both being higher for the channels inside the SOZ compared with those outside the SOZ. In the replication cohort of novel patients, the same models differentiated the HFO+ from HFO‐ channels, and predicted the extents of the hSOZ and hfo+&‐SOZ (F1 measure >0.5) but not the cSOZ. Our study shows that the interictal HFOs are useful in defining the spatial extent of the SOZ, and predicting whether or not a given channel in a novel patient would be involved in the seizure. The findings support the existence of an abnormal network of tightly‐linked ictal and interictal HFOs in patients with intractable epilepsy.     

Graph index complexity as a novel surrogate marker of high frequency oscillations in delineating the seizure onset zone

ObjectiveTo investigate the Graph Index Complexity (uGIC) as a marker of high frequency oscillatory (HFO) activity, the seizure onset zone (SOZ), and surgical outcome.MethodsThe SOZ, rates of HFOs at two thresholds (broad, strict), and uGIC were determined using EEG data from 41 patients. The correlation between HFOs and uGIC were calculated. HFOs and uGIC were compared within and outside the SOZ. Postsurgical outcome was compared to the colocalization of HFOs and resected SOZ.ResultsThere was significant correlation between uGIC and both broad (r = 0.69, p < 0.0005) and strict HFOs (r = 0.48, p < 0.0005). All were significantly greater within the SOZ overall, but only in 17/41 (strict, uGIC) or 18/41 (broad) patients. HFO markers were significantly greater within the SOZ for 8/15 patients with positive postsurgical outcomes, but not for any patients with negative outcomes (0/5).ConclusionThe uGIC is a marker of HFO activity, while HFOs and uGIC are markers of the SOZ overall. Colocalization of HFOs and the SOZ has strong positive predictive value for postsurgical outcome, but poor negative predictive value.SignificanceThe uGIC is an objective surrogate marker of HFO activity independent of identifying discrete HFO events.     

Determination of neurotransmitter release into the caudate nucleus during convulsions induced by pentylenetetrazole using in vivo differential pulse voltammetry

In vivo differential pulse voltammetry using an electrochemically treated carbon fiber electrode was applied to the investigation of the in vivo release of indoleamine and catecholamine within the caudate nucleus of freely moving and immobilized rats during convulsions induced by pentylenetetrazole (PTZ). Two distinct oxidation peaks, on at 130 mV (3,4-dihydroxyphenylacetic acid (DOPAC] and the other at 300 mV (5-hydroxyindoleacetic acid), were observed in voltammograms obtained from the caudate nucleus. In the caudate nucleus of freely moving rats, the in vivo oxidation current that peaked at 300 mV showed almost no change during and after tonic convulsions induced by 60 mg/kg of PTZ i.p. During tonic convulsions, the amplitude of the DOPAC oxidation peak significantly decreased to 75% of the peak height recorded prior to the injection of PTZ, and the minimum lasted for about 30 min; then the mean curve slowly recovered to the control level within 60 min. These results suggest that the release of dopamine (DA) in the caudate nucleus of freely moving rats decreased during tonic convulsions induced by PTZ. In another experiment, the EEGs of immobilized rats were recorded simultaneously, and the changes in the EEG pattern were used as an index of convulsion. In voltammograms from the caudate nucleus of immobilized rat, the peak height of the 130-mV oxidation potential significantly increased during ictal seizures. The increase lasted for 3-6 min after the ictal seizures. The severe electrical activity of the brain during ictal seizures interfered with the recording of some voltammograms.(ABSTRACT TRUNCATED AT 250 WORDS)     

Value of ictal and interictal epileptiform discharges and high frequency oscillations for delineating the epileptogenic zone in patients with focal cortical dysplasia

Objectives

There are different neurophysiological markers of the Epileptogenic Zone (EZ), but their sensitivity and specificity for the EZ is not known in Focal Cortical Dysplasia (FCD) patients.

Forelimb dyskinesia mediated by high‐frequency stimulation of the subthalamic nucleus is linked to rapid activation of the NR2B subunit of N‐methyl‐d‐aspartate receptors

Dyskinesia is a major side‐effect of chronic l ‐DOPA administration, the reference treatment for Parkinson’s disease. High‐frequency stimulation of the subthalamic nucleus (STN‐HFS) alleviates parkinsonian motor symptoms and indirectly improves dyskinesia by decreasing the l ‐DOPA requirement. However, inappropriate stimulation can also trigger dyskinetic movements, in both human and rodents. We investigated whether STN‐HFS‐evoked forelimb dyskinesia involved changes in glutamatergic neurotransmission as previously reported for l ‐DOPA‐induced dyskinesias, focusing on the role of NR2B‐containing N‐methyl‐d ‐aspartate receptors (NR2B/NMDARs). We applied STN‐HFS in normal rats at intensities above and below the threshold for triggering forelimb dyskinesia. Dyskinesiogenic STN‐HFS induced the activation of NR2B (as assessed by immunodetection of the phosphorylated residue Tyr¹⁴⁷²) in neurons of the subthalamic nucleus, entopeduncular nucleus, motor thalamus and forelimb motor cortex. The severity of STN‐HFS‐induced forelimb dyskinesia was decreased in a dose‐dependent manner by systemic injections of CP‐101,606, a selective blocker of NR2B/NMDARs, but was either unaffected or increased by the non‐selective N‐methyl‐d ‐aspartate receptor antagonist, MK‐801.     

The nitric oxide system modulates the in vivo release of acetylcholine in the nucleus accumbens induced by stimulation of the hippocampal fornix/fimbria-projection

Nerve signals from the hippocampus to the nucleus accumbens (NAc) are transmitted through a glutamatergic pathway via the fornix/fimbria fibres. The aim of the present study was to investigate whether cholinergic neurons are activated by this projection and whether the nitric oxide (NO) system is also involved in the signal transduction within this nucleus. For this purpose, the NAc of urethane-anaesthetized rats was superfused, by the push-pull technique, with compounds that influence the NO system while the fornix/fimbria was electrically stimulated for short periods. The amount of acetylcholine (ACh) released in the superfusate was then determined. Electrical stimulation of the fornix/fimbria increased the ACh output in the NAc. This effect was abolished by superfusion with tetrodotoxin and decreased by superfusion with the glutamate receptor antagonists AP-5 and DNQX indicating the involvement of action potentials and glutamate. Superfusion with the inhibitor of neuronal NO synthase, NS 2028 also diminished stimulation-evoked ACh release. The NO donor PAPA/NO increased basal release. Simultaneous application of PAPA/NO and electrical stimulation led to an over-additive increase of ACh release. The effect of PAPA/NO on stimulation-evoked release was also abolished by NS 2028. The selective inhibitor of phosphodiesterase type 5 (PDE 5), 5-[2-ethoxy-5-(morpholinylacetyl)phenyl]-1,6-dihydro-1-methyl-3-propyl-7H-pyrazolo[4,3-d]pyrimidin-7-one methanesulphanate monohydrate also enhanced stimulation-induced release of ACh. Our findings indicate, that action potentials propagated by the fornix/fimbria to the NAc release glutamate which increases ACh release predominantly via NMDA receptors. In addition, nitrergic neurons are activated to enhance NO synthesis. The released NO seems to exert, via cGMP, a potent facilitatory role in the transduction and processing of signals from the hippocampus within the NAc, while the PDE 5 decreases the effects of NO.