首页 | 本学科首页   官方微博 | 高级检索  
相似文献
 共查询到20条相似文献,搜索用时 312 毫秒
1.
目的分析儿童颅脑损伤后癫痫猝死的相关因素及防治方法。方法总结了11例病例的年龄、性别、发病过程等临床资料及影像学资料。结果11例患儿因脑外伤后癫痫发作,经抗癫痫等治疗无效引起猝死。结论对儿童颅脑损伤患者应常规行首诊脑电图检查,采用口服抗癫痫药物及对症治疗,防治脑外伤后癫痫引起的猝死。  相似文献   

2.
目的探讨轻、中度闭合性颅脑损伤患者脑电图临床治疗前后的变化。方法对我院脑外科100例轻、中型颅脑损伤患者,临床治疗前后进行脑电图(EEG)检查比较。结果 100例颅脑损伤患者中,脑电图异常52例,治疗后与治疗前比较差异具有统计学意义(P〈0.05)。结论早期治疗可改善脑损伤后EEG异常,对于外伤性癫痫诊断及预后均能起到重要作用。  相似文献   

3.
目的为颅脑外伤术后癫痫的早期预防和治疗提供依据。方法回顾性分析166例颅脑损伤行开颅手术患者的临床资料,重点分析显微开颅手术、人工硬脑膜的应用以及预防性应用抗癫痫药物等因素与外伤性癫痫的关系。将所选择病例随机分为3组作为研究(每组又分为治疗组和对照组),治疗组分别采用显微镜下开颅手术、人工硬脑膜减张修补硬脑膜缺损、手术后预防性应用抗癫痫药物。对照组采用非显微开颅手术,无硬脑膜修补,术后无系统预防癫痫治疗。结果显微手术组患者癫痫发生率为6.66%,其对照组癫痫发生率为22.50%;硬脑膜修补组癫痫发生率为0,其对照组癫痫发生率为11.36%;药物预防癫痫组癫痫发生率为8.88%,对照组癫痫发生率为25.64%。各组之间对比差异有统计学意义(0.01〈P〈0.05)。结论显微手术、硬脑膜减张修补以及开颅术后预防性应用抗癫痫药物对减少术后癫痫发作有重要作用。  相似文献   

4.
54例眩晕型癫痫临床分析   总被引:1,自引:1,他引:0  
目的:分析眩晕型癫痫临床特征、脑电图、神经影像学、治疗效果及预后。方法:回顾性分析54例眩晕型癫痫患者的资料。结果:脑电图及颅脑影像学检查阳性率较高,病变主要位于额、颞、顶区,抗癫痫药物有效。结论:对于长期反复发作性眩晕,行脑电图等相关检查,可提高眩晕型癫痫的诊断率。  相似文献   

5.
脑卒中与癫痫的临床分析   总被引:1,自引:0,他引:1  
目的 探讨脑卒中后癫痫的临床表现、特点及发病机制。方法对(940例)例脑卒中病例中继发性癫痫患者的临床资料进行回顾性分析研究。结果卒中后癫痫发生率10%,早期癫痫发生7.66%,晚期癫痫发生2.43%。卒中后癫痫的发生率与病灶部位(皮质下/皮质)差异有统计学意义(P〈0.05)。结论脑卒中是癫痫发作的重要原因,皮质病变易导致癫痫发作,卒中急性期继发癫痫者预后较差,积极控制发作可改善预后,应给予正规抗癫痫治疗。  相似文献   

6.
颅脑手术后抗癫痫药物预防癫痫疗效分析   总被引:2,自引:0,他引:2  
目的:分析抗癫痫药物在脑外科治疗中的使用情况,探讨抗癫痫药物在颅脑手术后癫痫的预防作用以及各种药物作用的强弱。方法:查阅2001~2007年医院神经外科住院患者的病例资料,利用spss软件分析术后使用抗癫痫药是否对术后癫痫的发生率产生影响,并比较4种常用抗癫痫药对术后癫痫的预防作用。结果:非癫痫患者有预防性用药的93例,术后无发作的89例,发作4例;未使用抗癫痫药物的38例,术后无发作的36例,发作2例。有预防性用药与无预防性用药的术后癫痫发生率分别为4.30%和5.26%(P〉0.05),两组无统计学差异。苯妥英钠、苯巴比妥钠、丙戊酸钠、卡马西平4种抗癫痫药对非癫痫患者术后癫痫的预防作用无统计学差异。结论:对于非癫痫手术的患者,预防性使用抗癫痫药效果并不理想。外科中常用的四种抗癫痫药物在预防作用方面比较并无统计学差异。  相似文献   

7.
目的探讨儿童植物神经性癫痫的临床特点及脑电图改变。方法对疑似植物神经性癫痫的患儿行多次脑电图检测,确诊病人给予药物治疗并随访观察。结果本组病例临床表现复杂多样,以腹痛、头痛型多见,临床误诊率高达45%,多次脑电图检查可确诊,发作24小时内检查阳性率78.57%,24小时后检查阳性率40.62%,差异有显著性(P〈0.05),异常脑电图表现形式以阵发性高波幅慢节律、散发性尖波或棘波、阵发性高波幅尖波或尖慢波、棘波或棘慢波为多见;抗癫痫药物治疗有效,其显效率达73.33%,临床控制发作先于脑电图的恢复。结论儿童植物神经性癫痫临床极易误诊;及时、反复脑电图检查可以提高本病的诊断率。规律、长效服药治愈率明显提高。  相似文献   

8.
添加托吡酯治疗癫痫的临床研究   总被引:1,自引:0,他引:1  
目的:观察新型抗癫痫药托吡酯(妥泰)添加治疗癫痫的临床疗效和脑电图(EEG)变化。方法:进行开放性自身对照临床试验,对47例经临床和EEG确诊的癫痫患者在原有抗癫痫药物治疗不变的基础上,添加妥泰治疗,初始剂量为50mg.d^-1,2周后为100mg.d^-1,分2次服用,维持剂量200-400mg.d^-1。以治疗前3个月的发作频度和EEG改变为基础,治疗3个6个月后,分别观察发作频度和EEG的变化,并与治疗前进行比较。结果:添加妥泰治疗3和6个月后,发作次数明显减少,尤以治疗6个月后显著(P<0.01),总有效率(显效+有效)分别为61.70%和82.98%,差异显著(P<0.01);EEG异常率(高度和中度不正常)也由原来的23.4%和25.5%变为治疗3和6个月后的17.0%和19.1%以及0和10.6%,总异常率由原来的70.2%下降至59.6%和29.8%,差异有显著性(P<0.01)/。结论:妥泰作为一种辅助抗癫痫药物,不仅能明显减少癫痫的发作频度,使EEG异常率显著降低,而且不良反应少,值得临床推广应用。  相似文献   

9.
目的分析总结脑梗死后并发继发性癫痫的临床特点。方法回顾性分析100例脑梗死后继发癫痫患者的临床资料,并对癫痫类型、发作时间、病灶构成情况及预后情况进行分析。结果脑梗死后并发继发性癫痫的发生率8.0%,以早发型、部分性发作多见,病灶位于皮质的癫痫占71.0%,显著高于皮质下的发生率(P〈0.05)。结论继发性癫痫发作病灶部位多见于脑皮层梗死者,早发型、部分性发作多见,癫痫早期应重点行抗惊厥、脱水治疗,迟发性癫痫还需长期给予口服抗癫痫药物治疗才能取得较好疗效。  相似文献   

10.
中西医结合治疗脑外伤后继发性癫痫24例   总被引:2,自引:0,他引:2  
外伤性癫痫是颅脑损伤的严重并发症之一,并且重度颅脑损伤癫痫发作明显高于轻中度者[1],药物治疗是目前控制癫痫的主要措施,而现代医学所用的抗癫痫药副作用大,用  相似文献   

11.
Medical treatment and neuroprotection in traumatic brain injury   总被引:3,自引:0,他引:3  
The goal of this article is to give an overview about the established current treatment concepts of traumatic brain injury, as well as an outlook on possible future developments in pharmacological neuroprotection. Modern medical treatment modalities of traumatic brain injury (TBI), including the preclinical management of severely head-injured patients, are reviewed. Since an increased intracranial pressure represents the most common complication of severe traumatic brain injury, frequently associated with the development of secondary brain damage, special emphasis was given to an updated treatment algorithm for this important condition. New insight into the pathophysiology of severe traumatic brain injury, especially the realization that brain damage develops sequentially, initiated several new treatment approaches aiming at the interruption of pathophysiological mechanisms leading to secondary brain injury. A high number of pharmacological substances have been tested for their ability to ameliorate secondary damage after TBI, or are currently under clinical trial. Although no drug has achieved this goal so far, the most promising of these therapeutical approaches, glutamate receptor antagonists, calcium channel antagonists, free radical scavengers, and cyclosporin A will be discussed in this review. Although a "magical bullet" for the treatment of traumatic brain injury has not been developed yet, several of the currently investigated neuroprotective strategies seem to be encouraging. A promising future approach might be to evaluate treatment strategies that combine several pharmacological agents, and possibly other treatment modalities, such as mild hypothermia, "tailored" according to the special pathology of patient subgroups, or even to every single patient in order to achieve an improvement in outcome after TBI.  相似文献   

12.
目的:分析急性单发性创伤性颅脑损伤后血钠、血钾、血氯、血镁、血钙离子的变化情况,并探究多重离子紊乱与颅脑损伤之间的关系。方法回顾性分析2012年7月—2015年6月中国医科大学附属第一医院神经外科收治的符合研究标准的患者158例,根据其入院格拉斯哥评分( Glasgow Coma Scale,GCS)判定颅脑损伤程度分为3组:重度损伤(GCS 评分3~8分)78例,中度损伤(GCS 评分9~14分)33例,轻度损伤( GCS 评分15分)47例。分别收集患者急诊入院时即时血离子浓度。采用相应的统计学方法分析急性单发性创伤性颅脑外伤后离子降低的独立危险因素,不同组间离子浓度均数和不同离子类型的发生率分别同颅脑损伤严重程度的关系,以及不同组别中多重离子紊乱构成比的差异。结果损伤严重程度、CT 提示中线位移、脑组织挫伤、蛛网膜下腔出血及颞叶和小脑损伤是颅脑损伤后离子降低的危险因素( OR ﹥1,P ﹤0.05)。血钠、血钾、血氯、和血镁浓度在不同颅脑损伤组间存在差异(r s ﹤0,P ﹤0.05)。各组间离子紊乱发生率存在显著性差异( P ﹤0.05),其中对于多重离子紊乱,重度损伤组发生率与轻、中度损伤组存在明显差异(P ﹤0.05)。其中血钠、镁,血钠、氯、镁,血钠、氯以及血钠、钾、镁、氯同时降低这4类离子紊乱模式的发病率较高。结论颅脑损伤的程度与多重离子紊乱密切相关,多重离子紊乱既可以作为颅脑损伤严重程度的评价指标,又可加重颅脑损害。明确急性单发性创伤性颅脑损伤后离子变化情况对患者病情的诊断和治疗具有重要的指导意义。  相似文献   

13.
目的探讨小脑幕切开术在救治重型颅脑损伤合并颞叶钩回疝复位的应用。方法对我科2001年10月-2008年8月收治的38例重型颅脑损伤合并颞叶钩回疝患者在清除颅内血肿大骨瓣减压的基础上进行小脑幕切开术,观察其临床效果及并发症。结果38例患者中良好13例(34%),中残12例(32%),重残5例(13%),死亡8例(21%)。术后并发症:脑积水3例,外伤性癫痫4例,消化道出血6例,脑梗塞4例。结论应用小脑幕切开术能有效使颢叶钩回疝复位,缓解脑疝引起的继发性脑干损伤,远期预后较理想。  相似文献   

14.
The potential effects of Cerebrolysin (EBEWE Pharma, Unterach, Austria), a peptide preparation with neurotrophic activity, on brain bioelectrical activity, cognitive performance and clinical outcome in postacute traumatic brain injury (TBI) patients, were investigated in an exploratory study. A decrease in slow electroencephalogram (EEG) activity and an increase in fast frequencies were observed after the administration of Cerebrolysin. This EEG-activating effect was not influenced by TBI time course or severity, nor by the chronic treatment with nootropic compounds. Cognitive performance, evaluated with the Syndrome Kurztest test, improved in TBI patients after Cerebrolysin treatment, independent of disease severity, time course or disability. A significant improvement in the patients' clinical outcome, only evident during the first year after brain trauma, was also found following Cerebrolysin infusions. No relevant changes in biological parameters nor drug-related adverse events were observed. These promising preliminary results suggest that Cerebrolysin might be a useful treatment to improve the recovery of patients with traumatic brain damage, and encourage the conduction of confirmatory clinical trials.  相似文献   

15.
The neuroinflammatory response induced by microglia plays a vital role in causing secondary brain damage after traumatic brain injury (TBI). Previous studies have found that the improved regulation of activated microglia could reduce neurological damage post-TBI. Phillyrin (Phi) is one of the main active ingredients extracted from the fruits of the medicinal plant Forsythia suspensa (Thunb.) with anti-inflammatory effects. Our study attempted to investigate the effects of phillyrin on microglial activation and neuron damage after TBI. The TBI model was applied to induce brain injury in mice, and neurological scores, brain water content, hematoxylin and eosin staining and Nissl staining were employed to determine the neuroprotective effects of phillyrin. Immunofluorescent staining and western blot analysis were used to detect nuclear factor-kappa B (NF-κB) and peroxisome proliferator–activated receptor gamma (PPARγ) expression and nuclear translocation, and the inflammation-related proteins and mRNAs were assessed by western blot analysis and quantitative real-time PCR. The results revealed that phillyrin not only inhibited the proinflammatory response induced by activated microglia but also attenuated neurological impairment and brain edema in vivo in a mouse TBI model. Additionally, phillyrin suppressed the phosphorylation of NF-κB in microglia after TBI insult. These effects of phillyrin were mostly abolished by the antagonist of PPARγ. Our results reveal that phillyrin could prominently inhibit the inflammation of microglia via the PPARγ signaling pathway, thus leading to potential neuroprotective treatment after traumatic brain injury.  相似文献   

16.
In industrialised countries, the mean per capita incidence of traumatic brain injury (TBI) that results in a hospital presentation is 250 per 100,000. In Europe and North America alone, this translates to > 2 million TBI presentations annually. Approximately 25% of these presentations are admitted for hospitalisation. Despite the significance of these figures, there is no single interventional pharmacotherapy that has shown efficacy in the treatment of clinical TBI. This lack of efficacy in clinical trials may be due, in part, to the inherent heterogeneity of the traumatic brain injury population. However, it is the multifactorial nature of secondary injury that also poses a major hurdle, particularly for those therapies that have been designed to specifically target an individual injury factor. It is now becoming increasingly recognised that any successful TBI therapy may have to simultaneously affect multiple injury factors, somewhat analogous to other broad spectrum interventions. Recent efforts in experimental TBI have therefore focussed on developing novel pharmacotherapies that may affect multiple injury factors and thus improve the likelihood of a successful outcome. While a number of interventions are noteworthy in this regard, this review will focus on three novel compounds that show particular promise: magnesium, substance P antagonists and cyclosporin A.  相似文献   

17.
In industrialised countries, the mean per capita incidence of traumatic brain injury (TBI) that results in a hospital presentation is 250 per 100,000. In Europe and North America alone, this translates to > 2 million TBI presentations annually. Approximately 25% of these presentations are admitted for hospitalisation. Despite the significance of these figures, there is no single interventional pharmacotherapy that has shown efficacy in the treatment of clinical TBI. This lack of efficacy in clinical trials may be due, in part, to the inherent heterogeneity of the traumatic brain injury population. However, it is the multifactorial nature of secondary injury that also poses a major hurdle, particularly for those therapies that have been designed to specifically target an individual injury factor. It is now becoming increasingly recognised that any successful TBI therapy may have to simultaneously affect multiple injury factors, somewhat analogous to other broad spectrum interventions. Recent efforts in experimental TBI have therefore focussed on developing novel pharmacotherapies that may affect multiple injury factors and thus improve the likelihood of a successful outcome. While a number of interventions are noteworthy in this regard, this review will focus on three novel compounds that show particular promise: magnesium, substance P antagonists and cyclosporin A.  相似文献   

18.
目的: 研究右美托咪定对脑外伤(traumatic brain injury,TBI)后小鼠认知功能和脑组织损伤的影响,揭示右美托咪定(Dex)治疗脑外伤的可能作用机制。方法: 将60只小鼠随机分为假手术组(Sham组)、模型组(TBI组)和右美托咪定治疗组(Dex+TBI组)。采用神经损伤严重程度评分(NSS)和旋转实验(Rotarod test)评价各组小鼠在TBI后24 d的神经功能;采用行为学实验评估TBI后小鼠运动依赖的学习记忆能力损害;HE染色观察脑组织体积损伤,TUNEL染色分析神经元细胞死亡,蛋白印迹实验分析突触相关蛋白pre-BDNF、BDNF、GAP43、Synaptophysin和Synapsin表达。结果: 与TBI组相比,TBI+Dex组小鼠神经损伤恢复水平和认知能力均提高,差异有统计学意义(P<0.01);脑组织体积损伤减小(P<0.01),TUNNEL阳性细胞数量显著增加(P<0.01);突触相关蛋白表达显著增加(P<0.01)。结论: 右美托咪定对脑外伤后小鼠认知功能和脑组织损伤具有保护作用,其机制可能是增加了突触相关蛋白的表达。  相似文献   

19.
目的:探讨含有人碱性成纤维细胞生长因子的缓释性生物蛋白海绵在脑外伤患者术中的临床应用方法。方法:回顾性分析58例存活脑外伤患者术中使用生物蛋白海绵的临床资料。结果:术后3~7天均不同程度出现头皮下或硬膜下薄层积液,但无持续性增加;术后3~6个月继发性癫痫的发病率为13%,术后无颅内感染、脑积水发生。结论:含有人碱性成纤维细胞生长因子的缓释性生物蛋白海绵在脑外伤患者术中的临床应用广泛,使用简单,如果注意使用方法,在脑皮层表面先直接覆盖一层,再用普通明胶海绵覆盖一层,然后缝合硬膜或敞开硬膜减压,就能取得更好疗效,减少并发症。  相似文献   

20.
创伤性脑损伤(TBI)发生时,外力立即造成神经系统损害。这种原发性损伤触发了体内生化级联以及新 陈代谢和细胞变化在内的继发性神经损害,称为继发性脑损伤。TBI后的神经炎症是持续的神经元损伤的关键因 素。神经炎症涉及损伤后细胞和分子调控机制,包括神经胶质(小胶质细胞和星形胶质细胞)的激活,引起脑内的炎 症介质的释放,导致周围免疫细胞的募集。了解 TBI炎症病理生理学的最新进展对于制定更有效的治疗策略至关 重要。  相似文献   

设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号