全面性发作癫(癎)患者记忆功能与海马质子磁共振波谱改变的相关性分析

目的 探讨原发性癫(癎)全面性发作患者记忆功能损害的特征以及磁共振波谱(magnetic resonance spectroscopy,MRS)检查与记忆功能的关系.方法 对45例癫(癎)全面性发作的患者和20例健康对照组进行临床记忆量表的测量,双侧海马行1H-MRS检测及体积测量,比较2组间记忆量表的各项量表分、记忆商和1H-MRS的各项指标,并对记忆量表的结果与海马1H-MRS结果进行相关分析.结果 癫(癎)组包括服药组(指向记忆15.68±4.79,联想学习18.70±5.84,图像自由回忆13.19±6.22,人像特点回忆12.02±4.31)与未服药组(指向记忆17.19±5.86,联想学习20.00±6.77,图像自由回忆18.44±6.62,人像特点回忆13.19±6.62)以及不同发作频率组的多数项量表分及记忆商(服药组74.64 ±18.52,未服药组79.07±20.20,≥3次/月组78.10±21.22,<3次/月组73.81±17.72)显著低于对照组(t=4.794-10.224,P<0.01);且癫(癎)服药组和发作频率≥3次/月组的各项量表分及记忆商显著低于服药组和发作频率<3次/月组(t=3.267～6.537,P<0.01).癫(癎)组海马体积(左侧2.45±0.25,右侧2.56±0.31)、N-乙酰天门冬氨酸(NAA,左侧12.93±1.73,右侧11.88±1.69)及NAA/胆碱(Cho)+肌酸(Cr,左侧0.48±0.08,右侧0.39±0.07)显著低于对照组,Cho(左侧15.02±0.86,右侧14.94±0.96)、Cr(左侧11.86±0.71,右侧10.71±0.42)显著高于对照组(t=4.103～5.768,P<0.01);癫(癎)组的各项量表分及记忆商与左右侧NAA浓度、NAA/Cho+Cr均呈明显正相关(r=O.489～0.727,P相似文献   

托吡酯对癫痫大鼠认知功能及海马组织中NCAM的mRNA表达影响

目的研究托吡酯（TPM）对癫痫大鼠认知功能的影响以及使用TPM后大鼠海马组织中神经细胞粘附分子（NCAM）的mRNA表达变化。方法将大鼠随机分成生理盐水（NS）组、癫痫（EP）组、癫痫＋托吡酯治疗1周（TPM1周）组和癫痫＋托吡酯治疗4周（TPM4周）组,建立匹罗卡品诱导癫痫大鼠模型和TPM干预模型,观察大鼠的行为学改变,通过Morris水迷宫实验测试大鼠的学习记忆能力,并通过Real—TimePCR检测大鼠海马组织中NCAM的mRNA表达水平。结果EP组大鼠的逃避潜伏期大于NS组,原平台象限游泳时间百分比小于NS组,海马NCAM的mRNA表达水平高于NS组（P〈0．01）;TPM1周组和TPM4周组大鼠的逃避潜伏期大于EP组,原平台象限游泳时间百分比小于EP组,海马NCAM的mRNA表达水平低于EP组（P〈0.01）;TPM4周组大鼠的逃避潜伏期大于TPM1周组,原平台象限游泳时间百分比小于TPM1周组,海马NCAM的mRNA表达水平低于TPMI周组（P〈0.05）。结论大鼠产生癫痫持续状态后认知功能明显下降,海马NCAM的mRNA表达上调;使用大剂量TPM短期治疗后其认知功能进一步下降,海马NCAM的mRNA表达受抑,且下降与受抑程度与TPM的持续使用时间有关。     

癫痫患儿与正常儿童气质的差异性研究

目的探讨癫痫患儿与正常儿童气质的差别。方法随机入选2007-2008年我院儿科确诊的42名癫痫患儿及56名非癫痫正常儿童,进行气质测定。结果（1）癫疴组与正常儿童组气质类型分布存在显著性差异（χ2=6．417,P=0．040）;（2）癫痫患儿在活动水平、节律性、适应性、坚持性、情绪本质等气质维度的得分比正常儿童高,且具有统计学差异（P〈0．05）。结论癫痫疾病对儿童的气质特点具有显著的影响,使患儿的气质偏向消极。     

药物难治性癫痫外科治疗展望

癫痫是危害较大的神经系统疾病,其发病率在4‰～6‰.在我国有近600万癫痫患者,其中20%～30%患者对内科药物治疗效果不佳,是癫痫外科治疗的主要目标[1,2].近二十年来,随着神经电生理技术和神经影像学的飞速发展,药物难治性癫痫患者的术前定位和评估取得了明显的突破,外科手术已成为癫痫治疗的一种重要手段[2].同时,随着外科麻醉和手术技巧的不断改进,尤其是显微神经外科技术的应用,使癫痫的外科治疗越来越安全有效,外科治疗已成为治疗药物难治性癫痫患者的主要手段[2,3].     

以癫为首发症状的幕上星形细胞瘤的诊疗体会

目的 探讨癫癎与星形细胞瘤的关系及影响术后癫癎控制的因素.方法 回顾性分析35例以癫癎为首发症状的星形细胞瘤患者,运用SPSS 15.0对术中肿瘤切除程度和术前癫癎病程分别与术后6个月癫癎控制情况进行卡方检验.结果 35例病人全切25例,次全切6例,部分切除4例;病理诊断(WHO)Ⅰ～Ⅱ26例,Ⅲ～Ⅳ9例;术前癫癎病程1～6个月13例,＞6个月～2年17例,2年以上5例.分别与术后6个月癫癎控制情况行卡方检验,P值分别为0.016、0.039,差异均有统计学意义.结论 以癫癎为首发症状的脑星形细胞瘤多为低级别肿瘤,手术全切及术前癫癎病程短者术后癫癎较易控制.     

Identification of epileptogenic foci from causal analysis of ECoG interictal spike activity

ObjectiveIn patients with intractable epilepsy, the use of interictal spikes as surrogate markers of the epileptogenic cortex has generated significant interest. Previous studies have suggested that the cortical generators of the interictal spikes are correlated with the epileptogenic cortex as identified from the ictal recordings. We hypothesize that causal analysis of the functional brain networks during interictal spikes are correlated with the clinically-defined epileptogenic zone.MethodsWe employed a time-varying causality measure, the adaptive directed transfer function (ADTF), to identify the cortical sources of the interictal spike activity in eight patients with medically intractable neocortical-onset epilepsy. The results were then compared to the foci identified by the epileptologists.ResultsIn all eight patients, the majority of the ADTF-calculated source activity was observed within the clinically-defined SOZs. Furthermore, in three of the five patients with two separate epileptogenic foci, the calculated source activity was correlated with both cortical sites.ConclusionsThe ADTF method identified the cortical sources of the interictal spike activity as originating from the same cortical locations as the recorded ictal activity.SignificanceEvaluation of the sources of the cortical networks obtained during interictal spikes may provide information as to the generators underlying the ictal activity.     

Clinical neurophysiology of the episodic ataxias: Insights into ion channel dysfunction in vivo

Clinical neurophysiology has become an invaluable tool in the diagnosis of muscle channelopathies, but the situation is less clear cut with neuronal channelopathies. The genetic episodic ataxias are a group of disorders with heterogeneous phenotype and genotype, but share in common the feature of intermittent cerebellar dysfunction. Episodic ataxia (EA) types 1 and 2 are the most widely recognised of the autosomal dominant episodic ataxias and are caused by dysfunction of neuronal voltage-gated ion channels. There are central and peripheral nervous system manifestations in both conditions, and they are therefore good models of neuronal channelopathies to study neurophysiologically. To date most work has focussed upon characterising the electrophysiological properties of mutant channels in vitro. This review summarises the role of voltage-gated potassium and calcium channels, mutations of which underlie the main types of episodic ataxia types 1 and 2. The clinical, genetic and electrophysiological features of EA1 and EA2 are outlined, and a protocol for the assessment of these patients is proposed.     

Predictors of refractoriness in a Turkish status epilepticus data bank

Refractory status epilepticus (RSE) is known to constitute approximately 10–50% of all cases of status epilepticus (SE) and is associated with significant morbidity and mortality. In the present study, data from a prospectively collected SE database were analyzed. Patients with RSE (defined as a SE episode requiring a second line of intravenous treatment following intravenous phenytoin) were compared with patients with nonrefractory SE (NRSE); 290 episodes of SE were identified, of which 108 (38%) were defined as RSE. Univariate analysis revealed that age, female gender, SE type, SE duration, and acute etiology were associated with refractoriness, whereas electroencephalographic patterns were not. Nonconvulsive SE, which is probably associated with delays in treatment initiation, was a predictor of RSE, although it was not retained as a predictor in multivariate analysis. In the latter analysis, female gender (odds ratio: 1.815, 95% CI: 1.053–3.126) and acute etiology (odds ratio: 0.619, 95% CI: 0.429–0.894) were shown to be the only significant independent predictors of refractoriness.     

Incidence of atypical handedness in epilepsy and its association with clinical factors

The incidence of atypical handedness (left-handedness and ambidexterity) in patients with epilepsy, particularly its association with major clinical factors, is not well established. We evaluated a full range of clinical variables in 478 patients with epilepsy from the United States and Korea. With the Edinburgh Handedness Inventory, handedness was established as both a categorical variable (right-handed, left-handed, ambidextrous) and a continuous variable. Seizures were classified as complex or simple partial, primary generalized, or generalized tonic–clonic. The relationship between handedness and a range of clinical findings was explored. The overall incidence of atypical handedness in our patients was higher than in the general population (13.6%) and significantly higher in the U.S. patient group (17.6%) than in the Korean patients (8.8%). Handedness was not associated with sex; age; seizure type; age at onset; type, side, or site of EEG or brain imaging abnormalities; family history of seizures; refractory epilepsy; or history of epilepsy surgery.