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1.
目的探讨脑源性神经营养因子(BDNF)和其特异性受体TrkB的表达与颞叶癫痫(TLE)之间的关系。方法选取52例难治性TLE患者术中切除的颞叶、海马及癫痫灶组织,用免疫组化SP法对其组织中BDNF及TrkB含量进行检测,并与12例对照组进行比较研究。结果(1)在难治性TLE患者中,BDNF、TrkB在颞叶、海马及癫痫灶组织中含量较对照组明显增加(均P〈0.05)。(2)BDNF、TrkB两者的表达呈正相关(r=0.545,P〈0.01)。结论难治性TLE患者的颞叶、海马及癫痫灶组织中BDNF及TrkB含量显著增高,且两者的表达呈正相关,提示其可能对TLE的发作、持续及终止起重要作用。  相似文献   

2.
目的探讨脑源性神经营养因子(BDNF)和其特异性受体TrkB的表达与颞叶癫痫(TLE)之间的关系。方法选取52例难治性TLE患者术中切除的颞叶、海马及癫痫灶组织,用免疫组化SP法对其组织中BDNF及TrkB含量进行检测,并与12例对照组进行比较研究。结果(1)在难治性TLE患者中,BDNF、TrkB在颞叶、海马及癫痫灶组织中含量较对照组明显增加(均P〈0.05)。(2)BDNF、TrkB两者的表达呈正相关(r=0.545,P〈0.01)。结论难治性TLE患者的颞叶、海马及癫痫灶组织中BDNF及TrkB含量显著增高,且两者的表达呈正相关,提示其可能对TLE的发作、持续及终止起重要作用。  相似文献   

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4.
目的观察鞘氨醇激酶1(SphK1)在难治性颞叶癫痫(TLE)患者及匹罗卡品诱导的TLE大鼠模型中的表达,探讨其在TLE发病中的作用机制。方法收集TLE患者手术切除的皮质标本,纳入癫痫组(n=16)。收集脑外伤患者切除的颞叶皮质标本,纳入对照组(n=10)。将72只雄性SD大鼠按随机数字表法分为模型对照组(MC组,n=32)和匹罗卡品组(PILO组,n=40),PILO组根据匹罗卡品诱导癫痫持续状态(SE)后的观察时间随机分为4个亚组:E6h组、E1d组、E3d组和E7d组(n=8)。采用免疫组化染色法检测SphK1在TLE患者颞叶皮质中的表达变化;运用Western blotting法检测SphK1在大鼠海马中的表达变化;采用免疫荧光染色法观察在人颞叶皮质和大鼠海马中星形胶质细胞(AST)活化增生情况和SphK1在AST中的表达。结果癫痫组人颞叶皮质中SphK1的阳性细胞数及AST细胞数均明显多于对照组(均P0.05)。E6h组、E1d组、E3d组和E7d组大鼠海马SphK1表达水平均明显高于MC组(均P0.05);PILO组AST细胞数明显多于MC组(P0.05)。免疫荧光染色结果显示,在癫痫组患者颞叶皮质中,SphK1主要在活化的AST的胞质中表达;而在PILO组大鼠海马中,SphK1主要在活化的AST的胞核中表达。结论 SphK1在TLE患者颞叶皮质和TLE大鼠海马中的表达明显增加,SphK1参与了TLE的发病。  相似文献   

5.
目的研究胶质纤维酸性蛋白(GFAP)及谷氨酸-胱氨酸转运体(GLAST)、神经胶质谷氨酸转运体(GLT-1)在颞叶癫痫患者海马区的表达情况。方法取40例难治性颞叶内侧癫痫患者在手术中切除的海马组织,根据在光镜下观察到的神经元丢失情况,分为海马硬化组(A组)23例和海马非硬化组(B组)17例,通过免疫组化法检测两组GFAP、GLAST、GLT-1的表达情况。结果A组GFAP的表达与B组比较,总海马区域、CA1区、CA2区、齿状回表达增加(P<0.01)。A组GLAST的表达与B组比较,海马总区域、齿状回差异无显著性(P>0.05)、CA1区减少(P<0.05)、CA2区则增加(P<0.05)。A组GLT-1的表达与B组比较,总海马区域、CA1区减少(P<0.01)、CA2区增加(P<0.01),齿状回差异无显著性(P>0.05)。结论颞叶内侧癫痫患者海马各区GFAP表达增加,GLAST、GLT-1在海马CA1区减少、CA2区表达增加,提示癫痫发作后海马区谷氨酸转运体重新分布可能是难治性癫痫发病机制之一。  相似文献   

6.
目的研究人难治性颞叶癫痫(TLE)颞叶组织中是否存在肿瘤坏死因子-α(TNF-α)转导的神经细胞凋亡。方法采用免疫组化SP染色法检测30例难治性TLE(TLE组)与10例脑外伤患者的正常颞叶组织(对照组)脑组织神经元、胶质细胞中肿瘤坏死因子受体相关死亡结构域蛋白(TRADD)、凋亡信号调节激酶1(ASK1)、天冬氨酸特异性半胱氨酸蛋白酶8(caspase 8)的表达并分析其表达差异。透射电镜下观察TLE痫灶神经元、胶质细胞超微结构改变。结果TLE组神经元和胶质细胞caspase 8表达较对照组增加(分别P<0.05,P<0.01)。两组神经元与胶质细胞中均未见TRADD、ASK1明显阳性表达。透射电镜观察见TLE组神经元具有细胞体积变小、核固缩、异染色质增多及边缘化、细胞及核膜边缘皱缩不齐、核分裂像、凋亡小体形成等凋亡特征,而胶质细胞则出现水肿现象。结论人难治性TLE病颞叶组织的神经元及胶质细胞中可能存在TNF-α转导的细胞凋亡。  相似文献   

7.
目的 探讨海马zif268mRNA及其蛋白的时空表达变化与颞叶癫痫脑损伤的关系. 方法 将雄性Wistar大鼠随机分为3组:其中正常组6只,假手术对照组(Sham组)和海人酸(KA)颞叶癫痫点燃组(TLE组)各36只,后两组按点燃后6h、24h、3d、7d、14d、21d时间点各分为6小组,每小组6只.采用KA杏仁核点燃建立经典颞叶癫痫模型,应用原位杂交和免疫组织化学方法分别检测海马神经元zif268mRNA及其蛋白的表达.结果 TLE组zif268mRNA表达在总体上和点燃后远期21d海马CA1、CA3区和齿状同(DG)均高于Sham组(P<0.05).TLE组Zif268蛋白表达在总体上和远期21d海马DG表达低于Sham组(P<0.05).回归分析提示颞叶癫痫与海马zif268mRNA表达呈正相关(β=0.286,P<0.001),与Zif268蛋白表达呈负相关(β=-0.153,P<0.001).结论 颞叶癫痫大鼠海马zif268mRNA及其蛋白的时空表达变化可能参与颞叶癫痫发病及其脑损伤过程.  相似文献   

8.
颞叶癫痫(temporal lobe epilepsy,TLE)是最常见的癫痫类型,大约占40%,且很大一部分为药物难治性癫痫,有统计表明难治性癫痫中70%为TLE,故是目前研究的热点。海马硬化是TLE的特征性病理改变,包括海马神经元丢失和异常苔藓纤维出芽,常常继发于最初的颅脑损伤,包括脑外伤、脑卒中、脑肿瘤、脑膜炎和脑炎、儿童时期的热性惊厥以及癫痫持续状态等,也有一部分病因不明。大量研究表明TLE的形  相似文献   

9.
目的 研究难治性颞叶癫痫患者颞叶新皮质中NCAM-140kDa(神经细胞粘附分子B)的表达,探讨其在难治性癫痫形成中的意义,并初步探讨颞叶新皮质的可塑性与难治性癫痫的关系.方法按随机化原则,在我们建立的难治性癫痫患者术后脑组织库中抽取15例患者的颞叶脑组织,用免疫组织化学、免疫荧光法分别检测其NCAM-140kDa的表达,并与对照组进行比较.结果免疫组化检测到的实验组和对照组的NCAM-140kDa平均光密度值分别为:0.2290±0.0427、0.1789±0.0258,两组比较差异有显著性(P<0.05).免疫荧光检测到的实验组和对照组的NCAM荧光强度分别为28.8345±3.2635、20.4513±2.2834,与对照组相比,差异有显著性(P<0.05).结论 NCAM-140kDa在难治性颞叶癫痫患者的颞叶新皮质中表达增加,提示其参与了难治性颞叶癫痫的形成及颞叶皮质神经细胞的可塑性改变与难治性癫痫的形成密切相关.  相似文献   

10.
目的 检测大鼠杏仁核点燃癫痫后不同脑区脑源性神经营养因子(BDNF)及其受体TrkB的表达与定位。方法 建立大鼠杏仁核点燃癫痫模型,应用免疫组化方法观察点燃鼠不同脑区不同点燃时程BDNF及TrkB的表达及含量。结果 点燃后大鼠颞叶及海马BDNF随着点燃次数的增加而升高,并持续至点燃后 49d;TrkB的表达也是随着点燃次数的增加而升高,并持续至点燃后7d(改变同BDNF),点燃1周后表达逐渐减少,至点燃后7周时基本恢复正常。结论 BDNF及TrkB直接参与癫痫的发生与发展。早期具有保护作用,但随着表达的进一步增加,又促进癫痫的发生发展,并一定程度上促进了癫痫发作后的神经细胞凋亡及脑损伤过程。  相似文献   

11.
颞叶癫痫脑电图分析及病灶超微结构观察   总被引:1,自引:0,他引:1  
目的 研究影像学检查无异常的颞叶癫痫患者,电生理异常与皮层棘波灶及海马超微病变的关系.方法 选择经CT或MRI检查未见异常的颞叶癫痫患者7例,术前做脑电图或24h视频脑电监测,术中在脑电监测下取颞叶大脑皮质棘波灶和海马组织,做电镜观察.结果 7例患者电生理检查均可见典型痫样放电.颞叶皮质痫灶和海马可见不同程度的神经元固缩,胶质细胞变性,胶质增生,突触数量及突触结构改变,血脑屏障破坏等改变.结论 影像学无异常的颞叶癫痫患者颞叶皮层痫灶和海马超微结构病理变化明显,特别是突触的变化,是导致癫痫患者脑电生理机能异常及癫痫反复自发性发作的形态学基础.  相似文献   

12.
目的:探讨 EEG、MR对颞叶癫癎(TLE)术前定位。方法:用 MR、EEG对 20例 TLE病例进行术前定位,与术中 EEG和术后随访结果比较。结果:20例病例中17例依据MR及EEG获得定位,主要在海马区域病变12例,前颞叶5例.另3例MR检查正常,依据多次EEG检查获得定位,随访疗效满意。结论:EEG是诊断TLE的重要手段,MR可对继发性TLE作出正确诊断,MR对海马硬化检查可协助EEG对TLE定位诊断。  相似文献   

13.
Abstract: The spatial relationship between a circumscribed lesion in the temporal lobe detected by MRI and an epibptogenic focus identified by ictal depth EEG along with a correlation, of the MRI lesion with neuropath logical findings were investigated in patients with medically intractable temporal lobe epilepsy but without any focal lesion on CT. Four parameters (an areal ratio of the temporal lobe against the hemisphere, area and calculated T1, T2 values of the hippocampus) were used to determine the abnormal MRI side. An agreement was reached in 67–72%, of 18 patients between the abnormal values of the hippocampus area and of calculated T1, T2 and the side of the epileptogenic focus. In 14 of 17 patients, typical hippocampus sclerosis was demonstrated in respected tissue in accordance with the MRI lesions (atrophy and/or prolonged T2 of hippocampus). These results imply: 1) MRI abnormality thus defined may, if not all, indicate the side of the epileptogenic focus, and 2) also the presence of hippocampal sclerosis. It was emphasized that the MRI lesion would be a usable instrument to explore the causal relationship of hippocampus sclerosis to a generation of epileptogenic lesions as well as for presurgical evaluation.  相似文献   

14.
Medically intractable temporal lobe epilepsy is a common disease typically associated with hippocampal damage (sclerosis) and synaptic remodelling. These changes could include increased glutamate receptor expression, enhancing excitability and the potential for neuronal injury. We directly assessed this hypothesis using quantitative in vitro receptor autoradiography to determine the densities of glutamate-, NMDA-, quisqualateh-amino-3-hydroxy-5-methyl-isoxazoleproprionic acid (AMPA)- and kainic acid-preferring binding sites in surgically removed hippocampi from patients with mesial temporal lobe epilepsy (sclerosis; MTLE) and patients with mass-associated temporal lobe epilepsy (no sclerosis: MaTLE), compared with autopsy material. Neuronal cell counts and in situ total protein densities were also obtained. In general, MaTLE and autopsy binding densities were indistinguishable. In contrast, some regions of MTLE hippocampi exhibited decreased receptor densities, with a corresponding loss of protein. In the hilus and CA1, however, ligand binding densities did not differ from the comparison groups in spite of markedly reduced protein content, consistent with increased glutamate receptor density. Kainate-preferring sites were distributed differently from the other glutamate subtypes and were uniformly decreased throughout the MTLE hippocampus, except for a unique expression within the outer dentate molecular layer. Along with increased NMDA and AMPA receptor densities in the hilus and CA1, this distinctive population of kainate receptors establishes that increased glutamate receptor expression is a feature of the remodelled MTLE hippocampus. These observations suggest that enhanced sensitivity to glutamate may be an important element in the pathophysiology of temporal lobe epilepsy.  相似文献   

15.
Summary: We performed a retrospective study of 30 patients with presumed intractable temporal lobe epilepsy (TLE) who underwent chronic intracranial EEG monitoring (CIEM). Multicontact depth electrodes were stereotactically implanted through the medial occipital lobe into amygdala and hippocampus. All patients had previously undergone extracranial ictal EEG monitoring that proved inadequate to localize the epileptogenic zone. No morbidity as associated with CIEM in the 30 patients. Twenty-five patients were shown to have exclusively or predominantly unilateral temporal lobe seizures, and 5 patients had bitemporal seizures without unilateral predominance; 24 patients subsequently underwent an anterotemporal lobe cortical resection. Twenty-one patients have been followed a minimum of 1 year postoperatively. Nine patients (43%) had a class I outcome (seizure-free, auras only, or provoked seizures), 3 patients (14%) had a class I1 outcome (≥95% seizure reduction), 4 patients (19%) had a class III outcome (≥50% seizure reduction); and 5 patients (24%) had a class IV outcome (<50% seizure reduction or no change). A prolonged interhemispheric propagation time (p <0.01) and magnetic resonance imaging (MR1)-identified hippocampal atrophy (p <0.01) correlated with a favorable surgical outcome. Results of this study may prove useful in counseling patients who undergo CIEM before temporal lobe surgery.  相似文献   

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Summary: Purpose : Chromogranins are neuropeptide precursors stored in large dense core vesicles. Because physiological functions have been postulated for peptides originating from chromogranins, we investigated the distribution of chromogranins A and B and secretoneurin (a peptide derived from secretogranin II) in the control and epileptic hippocampus of humans and rats.
Methods : Chromogranin immunoreactivity (IR) was investigated in paraformaldehyde-fixed hippocampal specimens from 24 temporal lobe epilepsy patients with intractable seizures, postmortem from 15 patients deceased from nonneurological disorders, in rats 30 days after kainate-induced limbic seizures, and in control rats.
Results : In control rats and in humans, chromogranin A and B IR and secretoneurin IR were present in mossy fibers. In addition, chromogranin B IR was found in granule cells, and chromogranin A IR was found in granule and CA2 pyramidal cells in the human hippocampus. In both species, chromogranin B and secretoneurin were unevenly distributed in the molecular layer of the dentate gyrus. The most intriguing change seen in human temporal lobe epilepsy specimens and in the kainic acid model of the rat was the prominent staining of the inner molecular layer, indicating storage of chromogranins A and B and secretoneurin in terminals of reorganized mossy fibers, from which they may be released upon nerve stimulation.
Conclusion : Chromogranins A and B and secretoneurin are valid markers for hippocampal neurons and delineate epilepsy-induced reorganization of mossy fibers.  相似文献   

18.
We studied auditory event-related potentials (ERPs) in 11 surgically treated patients with intractable temporal lobe epilepsy (TLE) pre- and postoperatively. ERPs through sphenoidal electrodes (Sp1-T3, Sp2-T4) provided clinically relevant and correctly lateralizing electrophysiologic evidence of temporal lobe dysfunction in 9 of 11 patients, confirmed by EEGs, electrocorticograms, neuroradiologic, and neuropsychological results, and clinical follow-up. Lateralizing asymmetries were noted in P300 amplitude, but latencies were prolonged bilaterally. Sphenoidal ERPs might serve as a new functional indicator of temporal lobe dysfunction in patients evaluated for epilepsy surgery.  相似文献   

19.
目的:研究术前对颞叶癫癎不同定位手段的综合应用。方法:采用EEG、PET、MRI、MRS对24例顽固性颞叶癫癎患者进行术前定位。结果:结合EEG,MRI,MRS,PET对83%,79%,85%病例作出定位;EEG结合MRI与MRS,可对92%病例作出定位;EEG结合MRI,MRS,PET,可对96%的病例作出定位。结论:结合EEG,综合采用MRI,MRS,PET等手段可提高对颞叶癫癎术前定位的准确率。  相似文献   

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