卒中后癫痫发作

讨论各种脑血管疾病相关性癫痫发作的病因、发病机制、诊断和治疗。     

卒中后抑郁的发病机制

抑郁是卒中的一种常见并发症,它与卒中互相影响,进一步降低了患者的生活质量。对于卒中后抑郁的发病机制尚无统一定论,可能与神经递质、颅内病变部位、炎性细胞因子和精神社会心理等因素有关。     

卒中后抑郁的发病机制

卒中后抑郁(PSD)是卒中的常见并发症,其发病机制复杂,主要包括神经生物学机制和社会心理学机制,国内外研究一直无一致结论.目前认为,PSD是各种神经生物学和社会心理学因素综合作用的结果,其发病符合生物-心理-社会医学模式.     

卒中后癫痫发作和卒中后癫痫

卒中可导致偏瘫、失语和认知损害,还会并发癫痫发作甚至癫痫.近年来,有关卒中后癫痫发作和卒中后癫痫的研究越来越多,但主要集中在危险因素方面.文章对卒中后癫痫发作和卒中后癫痫的危险因素、发病机制和治疗进行了综述.     

创伤后癫痫发病机制及治疗的研究进展

随着工业化、城镇化的快速发展,我国交通事业也取得了长足的发展,但因此而引起的意外人身伤害也呈上升趋势。在这些伤害事件中,颅脑创伤成为仅次于四肢骨折的疾病,其致死率、致残率高。而创伤后癫痫是颅脑损伤后的严重并发症,其发病率为1.9%～30.0%。目前颅脑创伤后癫痫的发病机制尚未完全明确,病程中各时段出现的癫痫发作机制不尽相同,给治疗方案的选择带来一定的挑战。本研究就颅脑创伤后癫痫的发病机制、诊治现状进行综述。     

颅脑损伤后癫痫发作的研究进展

颅脑损伤（TBI）后癫痫发作是严重TBI后常见的并发症,根据发作时间可分为即刻或早期的（≤7 d）TBI后抽搐发作和晚期的（>7 d）TBI后继发性癫痫。癫痫发作不仅导致TBI后早期并发症和死亡率升高,而且也是TBI后数年死亡的主要原因。许多对TBI后癫痫发作机制的研究取得了成果,但仍有很多等待解决的问题。药物预防主要用于早期癫痫发作,但对TBI后晚期癫痫几乎没有预防效果。对于TBI后药物难治性癫痫,可以考虑进行癫痫灶切除或神经调控手术。     

不同类型卒中后癫痫的发病特点

目的探讨不同类型卒中后癫痫的发病特点。方法回顾性收集2005年1月—2010年7月煤炭总医院神经内科就诊的卒中患者1322例的资料,其中115例发生卒中后癫痫,根据不同的卒中类型,分为脑梗死（CI）组79例、脑出血（CH）组26例,蛛网膜下腔出血（SAH）组10例。比较3组患者癫痫的发生时间、发生类型、异常脑电图、治疗结果的差异及脑梗死和脑出血发生的部位。结果①卒中后癫痫的发生率为8.7%（115/1322）,其中SAH组的癫痫发生率最高（16.1%）,CH组的发生率为11.5%,CI组最低（7.6%）,差异有统计学意义（χ2=7.911,P〈0.02）。②早发性癫痫的发生率（65.2%）高于迟发性癫痫（34.8%）,差异有统计学意义（U=3.260,P〈0.01）。卒中后癫痫发生的时间经Ridit分析,SAH后癫痫的发生最早,与CI组比较,差异有统计学意义。③3组患者卒中后癫痫的发生类型比较,差异有统计学意义（χ2=31.522,P〈0.01）。其中CI组患者以部分性发作为主,占58.2%（46/79）;CH组患者中部分性发作和全身性发作各占42.3%（11/26）;SAH组患者中80.0%为全身性发作,20.0%为癫痫持续状态。④卒中后癫痫患者的脑电图异常率高,达94.8%（109/115）,3组患者的脑电图异常发生率的比较,差异无统计学意义（χ2=0.847,P=0.655）。⑤经积极治疗后,103例患者的癫痫得到控制,12例患者死亡。SAH组患者的病死率最高（40.0%,4/10）;CI组最低（6.3%,5/79）,CH组的病死率为11.5%（3/26）,组间比较差异有统计学意义（χ2=11.071,P〈0.01）。结论 3种类型卒中患者中,SAH后癫痫的发生最早、发生率最高、病死率最高。经积极治疗卒中后癫痫患者的预后较好。     

卒中后抑郁的发病机制和治疗

抑郁（PSD）是脑血管疾病常见的并发症，抑郁也是卒中的独立危险因素，卒中与抑郁之间存在着双向性关系，治疗抑郁症是防治卒中的重要措施。     

卒中后肩关节疼痛发病机制和治疗的研究进展

肩关节疼痛（简称肩痛）是卒中后偏瘫患者的重要并发症之一，发病率约在21％-72％，通常在卒中后2-3个月内发生^[1]。肩痛患者的肱二头肌和冈上肌肌腱存在压痛，不仅在静止时，而且在被动活动时也存在疼痛，多在肩关节外旋、外展时疼痛明显。肩痛影响卒中的预后，可引起患者严重抑郁，影响夜间睡眠，妨碍日常生活护理，     

Disability in elderly patients with chronic neurological illness: stroke, multiple sclerosis and epilepsy

The aim of the study was to evaluate disability in patients with elderly stroke, multiple sclerosis (MS) and epilepsy, and to analyze its relationship with demographic characteristics. We conducted a cross-sectional study involving 113 patients with neurological diseases. The data were collected with a Personal Information Form, the Rivermead Mobility Index (RMI), and the Brief Disability Questionnaire (BDQ) were used. The data were evaluated using percentage, variance analysis, the Kruskal-Wallis test and the Pearson correlation analysis. The study results demonstrate that among three disorders, the severity of disability increased in patients with stroke, epilepsy and MS, respectively. It was also found that in patients with stroke, MS and epilepsy experiencing disability in mobility, 32.7% had experienced moderate physical-social disability, and 63.3% had experienced severe physical-social disability, and that there was a significantly high relationship between mobility disability and physical-social disability. The severity of disability was found to be higher for older age, low level education, self-employed and widows. Especially in stroke patients, disability is a common problem in patients with epilepsy and MS. Detecting the level of disability is very important for decreasing the limitation in elderly patients with neurological illness.     

肝源性糖尿病发病机制研究进展*

肝源性糖尿病是继发于慢性肝功能损伤后发生的糖尿病。近年来,多项研究表明胰岛素抵抗与肝源性糖尿病之间的关系密切,但肝源性糖尿病的发病机制尚未完全阐明,了解肝源性糖尿病发病机制有助于提高临床对肝源性糖尿病的认识和防治水平。本文阐述了胰岛素分泌与代谢障碍、肝炎病毒感染、肝纤维化和肝硬化引起的肝脏损害、血清胰岛素样生长因子-1、肿瘤坏死因子-α和游离脂肪酸等体液因子代谢紊乱、瘦素和脂联素等脂肪细胞因子的影响以及其他方面的最新研究发现。     

老年抑郁症病因及发病机制研究新进展

老年抑郁症是一种复杂的精神性疾病,其影响因素可有负性生活事件、年龄、性别、躯体疾病、经济状况、个人脆弱性、社会支持等,而这些因素构成的大脑背景更容易受到压力的影响,从而导致生理结构的病理改变,例如脑结构改变、血管损伤、炎症机制、神经内分泌改变等。本文旨在对老年抑郁症的病因及发病机制的研究新进展进行综述,以期为临床治疗和预防老年抑郁症提供参考。     

缺血性卒中后癫痫发作复发和耐药的预测因素

目的：探讨缺血性卒中后癫痫发作复发和耐药性的预测因素。方法回顾性纳入连续的缺血性卒中后首次癫痫发作患者的临床资料,计算癫痫发作复发率及耐药发生率,应用生存分析及 Cox 比例风险模型分析癫痫发作复发和耐药的预测因素。结果共纳入74例连续的缺血性卒中后首次癫痫发作患者,男性45例,女性29例,年龄（66.64±11.50）岁;早发性癫痫发作患者26例,迟发性癫痫发作患者48例。迟发性癫痫发作[优势比（odds ratio, OR）2.56,95％可信区间（confidence interval, CI）1.11~5.88;P =0.027]和部分性发作（OR 3.68,95％ CI 1.29~10.48;P =0.015）是缺血性卒中后癫痫发作复发的预测因素;早发性癫痫发作是耐药性的独立预测因素（OR 6.20,95％ CI 2.04~18.84;P =0.001）。结论迟发性癫痫发作和部分性发作患者易复发,早发性癫痫发作患者易产生耐药性。     

自身免疫性甲状腺疾病的遗传学发病机制进展

自身免疫疾病是遗传和环境相互影响的结果.免疫调节基因和甲状腺特异基因在自身免疫性甲状腺疾病的发病过程中起重要作用.     

卒中后癫痫:危险因素和病理生理学机制

近年来,卒中后癫痫(post-stroke epilepsy, PSD)发病率逐年增高,有关PSD的研究也日益增多.除卒中类型、部位和严重程度外,PSD的发生还与小血管病变、遗传因素等有关,但确切的病理生理学机制尚不十分清楚.文章对PSD危险因素和病理生理学机制进行了综述.     

Peripheral glucose metabolism is altered by epileptic seizures

The aim of the present study was to investigate the status of jejunal absorption and peripheral metabolism of glucose in Wistar Audiogenic Rats (WAR), a genetic model of epilepsy, after seizures induced by intensive sound exposure. The jejunal loop of rats was isolated and infused (0.5 mL min⁻¹) with Tyrode solution containing twice the normal concentrations of glucose, sodium, and potassium. Samples were taken at 5 or 10-min intervals over a 40-min period. At the end of the experiment, samples of liver and gastrocnemius muscle were taken to measure the levels of glycogen, glucose-6-phosphate, fructose-6-phosphate and glucose transporter-4 (GLUT4). Hepatic glucose-6-phosphate increased in WAR submitted to audiogenic seizure (21.90 ± 3.08) as compared to non-susceptible Wistar rats (8.12 ± 0.87) and to WAR not submitted to audiogenic stimulation (5.17 ± 0.97). In addition, an increase in hepatic fructose-6-phosphate, an intermediate metabolite of the glycolytic pathway, was observed in WAR submitted to audiogenic seizure (5.98 ± 0.99) compared to non-susceptible Wistar rats (2.38 ± 0.53). According to the present results, jejunal absorption of glucose was not changed by seizures. However, generalized tonic–clonic seizures produced by sound stimulation resulted in a decrease in muscle glycogen content. In addition, our results demonstrated that the concentration of GLUT4 in the gastrocnemius muscle of WAR was 1.6-fold higher than that observed in resistant rats and that the audiogenic stimulus led to decreased concentration of this receptor in the muscle of WAR animals.