损伤性癫痫模型大鼠海马和额叶突触蛋白的动态表达

Objective To observe the time course of changes in synaptophysin (P38) expression in the cortex and hippocampus of rats with posttraumatic epilepsy (PTE), and explore the role of synaptic plasticity in the epileptogenesis of PTE. Methods Thirty-seven male Sprague-Dawley rats were randomized into normal control group (n=5), sham-operated group (n=12) with intracortical saline injection, and PTE model group (n=20) with stereotactic FeCl<,2> injection (0.1 mol/L, 10 μ1) into the motor cortex. The expression of P38 in the brain cortex and hippocampus of the rats was detected immunohistochemically at 1 h and 7, 14 and 30 days after the injections. Results Most of the rats with FeCl<,2> injection developed isolated epileptiform discharges soon alter the injection. Compared with the sham-operated groups, the rats in PTE group showed significantly decreased P38 expression in the right frontal cortex at all the time points of measurement (P<0.05). At 1 h after FeCl<,2> injection, P38 expression in the polymorphic layer, stratum lacunosum and stratum radiatum of the right hippocampai CA3 area and DG molecular layer underwent no significant changes (P>05), but at 7 days, the expression increased significantly in all the stratum regions of the right hippocampal CA3 area, and this high expression level was maintained till 30 days after the injection. Conclusion Synaptic plasticity alterations in relation to P38 expression changes in the cortex and hippocampus may play an important role in the epileptogenesis of PTE in this rat model.     

损伤性癫痫模型大鼠海马和额叶突触蛋白的动态表达

Objective To observe the time course of changes in synaptophysin (P38) expression in the cortex and hippocampus of rats with posttraumatic epilepsy (PTE), and explore the role of synaptic plasticity in the epileptogenesis of PTE. Methods Thirty-seven male Sprague-Dawley rats were randomized into normal control group (n=5), sham-operated group (n=12) with intracortical saline injection, and PTE model group (n=20) with stereotactic FeCl<,2> injection (0.1 mol/L, 10 μ1) into the motor cortex. The expression of P38 in the brain cortex and hippocampus of the rats was detected immunohistochemically at 1 h and 7, 14 and 30 days after the injections. Results Most of the rats with FeCl<,2> injection developed isolated epileptiform discharges soon alter the injection. Compared with the sham-operated groups, the rats in PTE group showed significantly decreased P38 expression in the right frontal cortex at all the time points of measurement (P<0.05). At 1 h after FeCl<,2> injection, P38 expression in the polymorphic layer, stratum lacunosum and stratum radiatum of the right hippocampai CA3 area and DG molecular layer underwent no significant changes (P>05), but at 7 days, the expression increased significantly in all the stratum regions of the right hippocampal CA3 area, and this high expression level was maintained till 30 days after the injection. Conclusion Synaptic plasticity alterations in relation to P38 expression changes in the cortex and hippocampus may play an important role in the epileptogenesis of PTE in this rat model.     

手术治疗顽固性癫痫初探（25例临床分析）

随访观察开颅手术治疗顽固性癫痫２５例，病程平均８．４年。术前平均服抗痫药治疗５．２年。皮质电图监测下行颞叶前份＋杏仁核切除１２例；颞叶外皮层痫灶切除３例；病灶＋周围皮层痫灶切除９例；胼胝前部切开１例。无明确病因者占６４％。痫灶光镜和电镜检查（１１例）结果符合癫痫的病理改变。随访结果，痊愈及显效者占８４％，总有效率９６％，无效４％。无手术死亡。     

IFN-γ和热干预对U251胶质瘤细胞的MHC-I类分子和HSP70表达的影响

目的 观察重组人干扰素-γ(IFN-γ)和热干预对人多形胶质母细胞瘤(GBM)U251细胞胞膜主要组织相容性抗原复合体-I(MHC-I)类分子和热休克蛋白70(HSP70)分子表达的影响.方法 将U251细胞分为3个干预组:IFN干预组(IFN-γ500 U/ml诱导48h),热干预组(43℃热休克2h).联合干预组(IFN-γ500U/ml诱导48h+43℃热休克2h),分别行相应诱导干预.流式细胞仪(FCM)检测不同干预因素处理后的U251细胞胞膜MHC-I类分子和HSP70表达情况.结果 IFN干预组、热干预组、联合干预组U251细胞胞膜MHC-I及HSP70表达率分别为(89.92±3.45)%和(5.11±1.89)%、(78.89±2.02)%和(42.18±3.85)%、(96.00.4±2.63)%和(53.61±4.24)%.结论 双因素(IFN-γ500 U/ml诱导48 h+43℃热休克2 h)联合干预是U251细胞胞膜MHC-I类分子和HSP70双高表达的最佳体外诱导方案.     

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。     

颅脑外伤后意外发现颅内肿瘤9例

自1993～1998年我科收治颅脑外伤后在检查或手术治疗中意外发现颅内肿瘤9例,文献报告较少,现总结如下。1　临床资料本组男性6例,女性3例;年龄24～69岁,50岁以上4例。车祸致颅脑外伤4例,跌倒4例,他伤1例;外伤当时有人事不省6例,原发昏迷1小时以上3例。伤后均有头痛,外伤当时诊断为头皮裂伤3例,轻型颅脑外伤2例,脑挫裂伤1例,颅内血肿3例,其中2例脑疝,在行颅脑CT前无一例考虑合并有颅内肿瘤。所有病人经头颅CT,6例经颅脑MRI检查,7例手术病理检查。结果意外发现星形细胞瘤4例,3例伴出血坏死,1例伴囊变;脑膜瘤3例;少枝突胶质瘤1例;巨大骨瘤1例…     

高表达热休克蛋白70鼠脑胶质瘤细胞瘤苗的体内抗瘤作用

目的观察高表达热休克蛋白70（HSP70）鼠脑胶质瘤细胞（C6细胞）瘤苗在体内的抗瘤效应.方法以SD大鼠为动物模型,采用热休克、β榄香烯、丝裂霉素单独或联合诱导制备不同高表达HSP70表达率的细胞瘤苗.各实验组注射不同HSP70蛋白表达率的瘤苗进行免疫,对照组注射1640培养液;C6细胞皮下注射,观察皮下胶质瘤成瘤率及成瘤大鼠的生存期,分析HSP70蛋白表达率与抗瘤效应间的关系.结果经C6细胞瘤苗免疫大鼠较对照组皮下胶质瘤成瘤率下降,成瘤大鼠平均生存期明显延长,平均生存期与瘤苗的HSP70表达率呈正相关,应用单克隆抗体封闭瘤苗的HSP70表达则此作用消失.结论应用高表达HSP70的C6细胞瘤苗明显延长载瘤大鼠生存期.瘤苗免疫大鼠的抗瘤作用是由HSP70介导的.     

中枢神经细胞瘤的诊断和显微手术治疗

目的探讨中枢神经细胞瘤（CNC）诊断及治疗经验。方法回顾性分析16例CNC的诊断及显微手术治疗情况。采取纵裂-胼胝体-脑室入路5例,经皮质造瘘侧脑室入路9例,经枕下正中小脑蚓部入路1例,直接开颅切除1例。术后3例行放射治疗。结果术前误诊率62．5％。病理分级：WHOⅡ级7例,Ⅱ-Ⅲ级3例,Ⅲ级1例,未定级5例。病变全切除10例,次全切除4例,部分切除2例。除1例失访和1例复发外,其他病例恢复良好。结论CNC多数位于脑室系统,在影像学上有其特点。选择适当的手术入路行显微手术治疗预后良好。     

低颅压性脑积水6例临床分析

目的探讨低颅压性脑积水的临床诊断和治疗策略。方法回顾性分析我院2013-2019年收治的6例低颅压性脑积水患者的临床资料并结合文献进行分析。脑室腹腔分流术后4例,颅骨修补术后1例,外伤性脑脊液鼻漏1例。6例腰穿初始压和侧脑室内初始压均<70 mmH₂O,其中腰穿初始压最高60 mmH₂O,最低负压;侧脑室内初始压最高65 mmH₂O,最低为-20 mmH₂O,两者之间存在压力梯度差(5～20 mmH₂O)。6例均行额部钻孔Omaya囊置入侧脑室额角低压持续外引流,引流时间4～36周。结果临床症状消失4例,明显改善2例,CT平扫显示脑室系统恢复正常,脑沟脑回重现。无颅内感染、硬膜下出血等并发症。随访12～70个月,1例于出院6个月后因肝癌死亡;1例因脑肿瘤复发播散继发高压性脑积水再行脑室腹腔分流,术后6个月因原发病进展而死亡;1例于出院后5个月因常压性脑积水复发在外院再行脑室腹腔分流术;另3例治愈,生活自理,无再行脑室腹腔分流术。结论低颅压性脑积水的蛛网膜下腔与侧脑室内压力...