脑梗塞患者血清脂蛋白（a）测定及其临床意义

应用酶标法测定58例脑梗塞患者和56例健康对照者血清脂蛋白(a)[LP(a)]含量,并同时测定了其他脂代谢指标,对其中26例脑梗塞患者还测定了血浆纤维蛋白溶解(简称纤溶)指标。结果表明脑梗塞组存在显著的脂代谢和纤溶功能紊乱。LP(a)含量增高,与所测脂代谢、纤溶指标无显著相关,是脑梗塞发病独立的危险因素。     

Cell volume regulation: a review of cerebral adaptive mechanisms and implications for clinical treatment of osmolal disturbances: II

Cerebral cell volume regulatory mechanisms are activated by sustained disturbances in plasma osmolality. Acute hypernatremia causes a predictable shrinkage of brain cells due to the sudden imposition of a plasma-to-cell osmolal gradient. However, during chronic hypernatremia cerebral cell volume is maintained close to the normal range as a result of the accumulation of electrolytes and organic osmolytes including myo-inositol, taurine, glutamine, glycerophosphorylcholine, and betaine. The increased cytosolic level of these molecules is generally accomplished via increased activity of sodium (Na⁺)-dependent cotransport systems. The slow dissipation of these additional osmotically active solutes from the cell during treatment of hypernatremia necessitates gradual correction of this electrolyte abnormality. Acute hyponatremia leads to cerebral cell swelling and severe neurological dysfunction. However, prolonged hyponatremia is associated with significant reductions in brain cell electrolyte and organic osmolyte content so that cerebral cell volume is restored to normal. While acute hyponatremia can be treated with the administration of moderate doses of hypertonic saline in order to control seizure activity, chronic hyponatremia should be corrected slowly in order to prevent subsequent neurological deterioration. If the rate of correction exceeds 0.5 mmol/l per hour, or if the total increment in serum [Na⁺] exceeds 25 mmol/l in the first 48 h of therapy, then there is an increased risk of the development of cerebral demyelinating lesions. Chronic hyperglycemia activates the brain cell volume regulatory adaptations in the same manner as hypernatremia. Therefore, during the treatment of diabetic ketoacidosis, it is imperative to restore normoglycemia gradually in order to prevent the occurrence of cerebral edema. It is possible that excessive administration of electrolyte-free solutions and high doses of insulin may increase the risk of this complication. While there are some data to suggest that brain cell size is disturbed during acute uremia, additional work is necessary to clarify the role of cerebral cell volume regulation during acute and chronic uremia.     

Clinical impact of CCM mutation detection in familial cavernous angioma

Introduction and background A 3-year-old Bosnian girl with a large symptomatic brainstem and multiple supratentorial cavernous angiomas, who underwent neurosurgical treatment, is presented. As multiple cavernomas are more common in familial cases, genetic analyses and neuroradiological imaging were performed in the patient and her parents to see whether there was any evidence for inheritance. This information is important for genetic counseling and provision of medical care for at-risk relatives. Currently, no recommendation is available on how to manage these cases.Results Genetic analyses demonstrated a novel CCM1 frameshift mutation (c.1683_1684insA; p.V562SfsX6) in the child and the asymptomatic 27-year-old mother. Sensitive gradient-echo magnetic resonance imaging of the mother revealed multiple supratentorial lesions, whereas analogous imaging of the father showed no pathological findings.Conclusion This case exemplifies that seemingly sporadic cases with multiple lesions might well be hereditary and that presymptomatic genetic testing of family members may identify relatives for whom clinical and neuroradiological monitoring is indicated.     

脑动静脉畸形实验动物模型的建立

脑动静脉畸形是一种比较常见的严重威胁人们生命安全和生存质量的脑血管疾病，目前人们主要是通过尸体解剖以及CT、MRI等影像学的方法认识。近年来，学者们应用各种动物模型来研究脑动静脉畸形的血流动力学，病理生理学以及脑动静脉畸形栓塞材料的评估，栓塞后临床疗效评价，放射照射剂量对脑动静脉畸形的影响等。本文就脑动静脉畸形实验动物的常用种类，动物模型的建立方法以及动物模型的实际应用进行了综述。     

高压氧对大鼠局灶性脑缺血再灌注时神经元特异性烯醇化酶的影响

目的研究高压氧(HBO)对大鼠局灶性脑缺血再灌注(IR)时．大鼠脑梗塞体积．脑组织病理改变及神经元特异性烯醇化酶(NSE)含量的影响。方法用线栓法制备阻断大脑中动脉(MCA)的局灶性脑IR模型。Wistar大鼠30只，随机分为5组：正常对照组(N组n=-6)，缺血再灌注2h 常压空气组(Rt组,n=-6)，缺血再灌注24h 常压空气组(R2组，n=-6)，缺血再灌注2h HBO组(H1组，n=-6)，缺血再灌注24h HBO组(H2组，n=-6)。R1、R2、H1、H2组缺血时间均为2h。R1、R2组暴露于常压空气，H1、H2组暴露于2．5MPa氧气。病理切片用HE染色，用Swanson方法测定脑梗塞体积，用酶联免疫法测定NSE含量。结果H1、H2组与R1、R2组相比，神经元缺血性损害较轻，脑梗塞体积缩小，NSE含量明显下降，差异有统计学意义。结论HBO能减轻缺血性脑损害，保护脑组织。     

脑囊虫病患者脑脊液中一氧化氮及肿瘤坏死因子α水平研究

目的　探讨脑囊虫病患者各期脑脊液中的一氧化氮 (NO)、肿瘤坏死因子α(TNF α)的变化规律及它们在脑囊虫病中的作用机制。方法　检测 4 9例明确诊断并依据MR分期 ,单发脑实质内囊虫的脑囊虫病患者和 2 0名对照者脑脊液中NO、TNF α水平。结果　NO在脑囊虫病的Ⅰ期显著降低而TNF α水平呈显著升高 ,NO、TNF α于Ⅱ期、Ⅲ期 (整个退变死亡期 )均表现为高水平 ,Ⅳ期恢复正常 ,NO和TNF α存在高度正相关关系。结论　在单发脑实质内囊虫病中NO、TNF α可能参与杀虫作用 ,其免疫调节与杀虫机制存在着动态平衡 ,参与感染控制     

动脉硬化性脑白质病的CT表现与临床分析

目的 :探讨动脉硬化性脑白质病的临床与CT表现特点。方法 :收集 10 0例动脉硬化性脑白质病的临床与CT资料进行综合分析。结果 :10 0例的CT表现为 :弥漫性脑白质低密度改变 ,主要分布在双侧脑室旁及半卵圆中心白质区 ,病灶多呈条带状及月晕状。合并脑萎缩 90例 ;脑梗塞 76例 ,其中 2 5例有大的梗塞灶 ,其余为腔隙性梗塞 ;脑出血 9例 ,其中位于壳核 5例 ,丘脑 3例 ,小脑 1例 ;有 15例伴发基底节区软化灶。增强扫描 8例 ,显示病灶无明显增强。结论 :动脉硬化性脑白质病是发生于老年人的缺血性脑血管病 ,高血压动脉硬化是其主要发病因素。     

凋亡诱导因子在实验性脑卒中后高温状态下的表达

目的探讨caspase非依赖途径在卒中后高温的神经元损伤环节中是否发挥重要作用。方法应用SD大鼠局灶性脑缺血模型,分别设立缺血后高温、缺血后正常温度和假手术组,每组8只。观察动物行为学评分、梗死体积和凋亡诱导因子(AIF)在海马的表达。利用PC12细胞培养缺氧及高温处理后,观察荧光双染AIF在细胞内的表达变化,及流式细胞仪技术检测细胞凋亡水平。结果缺血后高温组的行为学评分和梗死体积明显增加,AIF表达增高。PC12缺氧及高温培养后AIF从30min开始在胞核内表达,且随时间延长逐渐增多,细胞凋亡率随时间延长和温度增高而增加,且不被caspase广谱抑制剂所抑制。结论AIF在卒中后高温的过程中发生由胞浆到胞核的转移,caspase非依赖途径由此发挥重要作用。     

不同脑保护方法中炎症反应对脑组织的影响

目的 通过观察体外循环中采用不同脑保护方法时脑组织中各种炎性细胞因子的变化，探讨脑保护对炎症反应的影响。方法 将18只健康成年杂种犬随机均分为3组：常温体外循环组（normothermic cardiopulmonary bypass，NCPB组），深低温停循环组（deep hypothermic circulatory arrest，DHCA组），深低温停循环＋间断选择性顺行性脑灌注组（intermittent selective antegrade cerebral perfusion，ISACP，DHCA＋ISACP组）。术后检测犬脑组织的含水量，分离并取出海马，制备脑组织匀浆，采用放射免疫法测定白细胞介素-1β（IL-1β）和肿瘤坏死因子-α（TNF—α）的含量。在透射电子显微镜（TE）下检测海马脑组织的细胞形态学变化。结果 DHCA组的IL-1β和TNF—α含量明显高于NCPB组和DHCA＋ISACP组（P〈0．01），但NCPB组与DHCA＋ISACP组间比较差别无统计学意义（P〉0．05）；TNF—α和IL-1β含量与脑水肿的程度呈正相关（r=0．987，0．942；P〈0．01）。TE检查显示DHCA组超微结构破坏较严重，而NCPB组和DHCA＋ISACP组破坏较轻。结论 长时间DHCA会造成脑损伤，DHCA＋ISACP有一定的脑保护作用，IL-1β和TNF—α在长时间DHCA中对脑损伤起一定的作用。     

经皮血管内栓塞颅内动静脉畸形（附38例治疗效果观察）

经皮血管内采用氰基丙烯酸异丁脂（ＩＢＣＡ）栓塞治疗３８例颅内动静脉畸形（ＡＶＭ）病人。其中８例达到１００％完全栓塞，栓塞面积大于７５％的１０例，大于５０％者１１例；余下９例栓塞面积小于５０％，１９例以出血为首发症状，１１例以癫痫为首发症状，６例神经功能障碍，２例以头痛为主要症状。栓塞术后发生并发症５例，占１３％，无死亡病例。本文讨论了超选插管技术问题、Ａｍｙｔａｌ试验假阴性、导管粘连及正常灌注压突破。