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Jingdong book

脑血管疾病(第2版)

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脑血管疾病(第2版)

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脑血管疾病是严重威胁人类健康和生命的常见病、多发病,随着人口老龄化的增加,我国脑血管疾病在疾病死因顺位中已前移至第一、二位,而且脑血管病是致残、致痴呆的重要原因,因此防治脑血管病,是卫生部门的重要工作。
Author Description

女,1932年生于重庆市,1955年毕业于北京医学院医疗系,男,1932年生,1952年毕业于第三军医大学医疗系。
Catalogue

上篇 总论
第一章 脑血液循环
第一节 脑动脉系统
第二节 脑静脉系统
第二章 脑血液循环的生理
第三章 脑血液循环的病理生理
第一节 缺血性脑损伤的病理生理
第二节 侧支循环
第三节 脑血管储备功能
第四节 脑的微循环
第五节 缺血半暗区
第四章 脑血管疾病的生化
第一节 缺血性脑血管病的生化
第二节 出血性脑血管病的生化
第五章 脑血管疾病的病理
第一节 脑动脉硬化
第二节 脑梗死
第三节 脑出血
第四节 脑蛛网膜下腔出血
第五节 颅内动脉瘤
第六节 脑动脉栓塞
第七节 颅内静脉系统血栓
第六章 脑血管疾病的遗传学
第一节 与脑血管病有关的单基因病
第二节 多基因遗传所致的脑血管病
第七章 脑血管疾病的临床检查
第一节 意识障碍
第二节 昏迷时定位体征的发现
第三节 失语症、失用症、失认证
第四节 构音障碍
第五节 眼位异常及其临床意义
第六节 脑疝的临床症状与体征
第八章 脑血管疾病的实验室检查
第一节 脑脊液检查
第二节 血液流变学检查
第三节 生化及其他检查
第九章 脑血管疾病的影像学检查
第一节 CT扫描
第二节 磁共振检查
第三节 头颈部动脉超声检查
第四节 数字减影脑血管造影

下篇 各论
第十章 脑血管疾病的流行病学、危险因素及预防
第一节 脑血管疾病的流行病学
第二节 脑血管疾病的危险因素
第三节 脑血管疾病的预防
第十一章 脑出血
第一节 总论
第二节 壳核出血
第三节 丘脑出血
第四节 脑叶出血
第五节 尾状核出血
第六节 带状核出血
第七节 脑干出血
附1 继发性脑干出血
附2 脑干血肿
第八节 脑室出血
第九节 小脑出血
第十二章 蛛网膜下腔出血
附脊部蛛网膜下腔出血
第十三章 短暂性脑缺血发作
第十四章 脑梗死
第一节 动脉粥样硬化性脑梗死
附进展性脑卒中
第二节 分水岭脑梗死
第三节 腔隙性脑梗死
第四节 脑栓塞
第五节 脑干梗死及其常见综合征
第十五章 慢性脑供血不足
第十六章 脑动脉狭窄及其治疗
第一节 脑动脉狭窄的常见部位及临床表现
第二节 脑动脉狭窄的外科治疗
第三节 脑动脉狭窄的介入治疗
第十七章 高血压脑病
第十八章 脑内盗血综合征
第一节 锁骨下动脉盗血综合征
第二节 颈动脉盗血综合征
第三节 脑梗死后盗血综合征
第十九章 几种特殊的脑血管疾病
第一节 脑底异常血管网
第二节 颞动脉炎
第三节 大动脉炎
第四节 系统性红斑狼疮的脑血管病变
第五节 结节 性多动脉炎
第六节 血栓闭塞性脉管炎
第七节 淀粉样脑血管病
第八节 颈内动脉纤维肌肉发育不良症
第九节 脑常染色体显性遗传脑动脉病伴皮质下梗死及白质脑病
第十节 可逆性脑血管收缩综合征
第二十章 颅内静脉系统血栓形成
第一节 概述
第二节 上矢状窦血栓形成
第三节 海绵窦血栓形成
第四节 横窦和乙状窦血栓形成
第五节 大脑深静脉血栓形成
第二十一章 脑血管性痴呆
附轻度认知功能损害
第二十二章 颅内动脉瘤
第二十三章 脑血管畸形
第二十四章 慢性硬膜下血肿
第二十五章 脑血管病后癫痫
第二十六章 脑卒中后抑郁
附抑郁自评量表(SDS)
第二十七章 内科及其他科疾病与脑血管病
第一节 心脏病与脑血管病
第二节 糖尿病与脑血管病
第三节 肾脏疾病与脑血管病
第四节 血液病与脑血管病
第五节 肝性脑病
第六节 肺性脑病
第七节 一氧化碳中毒与脑血管病
第八节 放射性脑病
第九节 梅毒与脑血管病
第十节 妊娠与脑血管病
第十一节 垂体瘤卒中
第二十八章 脑血管疾病的康复治疗
第一节 脑卒中功能恢复的机制
第二节 运动障碍的恢复过程和异常动作模式
第三节 康复开始时机和病例的选择
第四节 功能障碍的评价
第五节 康复治疗程序及方法
第六节 脑卒中常见并发症的康复处置
Book Abstract

第五节 缺血半暗区
在急性局灶性脑缺血的严重缺血部位和正常部位之间存在有一过渡区,称之为缺血半暗区。其CBF中等程度减少,处于电衰竭和离子衰竭阈值之间。缺血半暗区的细胞无电活动,同时有反复的一过性膜离子梯度和高能代谢产物的丧失。据认为这种状态下的细胞可引起临床症状;但仍能存活,并能对治疗产生反应。然而,关于缺血半暗区的稳定程度以及这种对动物所采用的病理生理学定义的情况是否也适用于人类急性脑卒中仍有激烈的争议。
已经明确,在体循环稳定情况下,梗死周边组织可以逐渐发展成脑梗死。脑和血管有许多内在的因素会影响到缺血半暗区的恶化。任何一个缺血半暗区CBF的情况取决于侧支血管的张力、数量和距缺血中心区的远近、血黏度以及CPP。其中CPP特别重要,其极易受到治疗的影响。CPP是动脉压和静脉压之差。由于脑组织和脑脊液的压力可以迅速传递,其变化能有效地传递到薄壁的脑静脉,因此通常CPP是用平均动脉压(MABP)和颅内压(ICP)之差来表示。CPP=MABP-ICP。
即使脑缺血时体循环MABP稳定,如果ICP全面增加或梗死局部压力增加引起了缺血半暗区的血流受阻,仍可使CPP降低。当CBF降至离子衰竭阈值以下,组织生存力丧失。有报道急性实验性缺血脑卒中常存在有大的局部组织压力梯度,范围在1.33-2.66kPa(10~20mmHg);但却未发现其对局部CBF有影响。另有人报道水肿组织确有CBF下降,但其中的关系很复杂,有可能是脑血管反应性和张力的改变,这些改变与组织压力本身无关。由于测定组织微血管CBF和氧运输较困难,进一步实验还无法进行。
对常见的缺血性脑卒中资料进行比较显示,水肿的机械压迫作用不可能对原发性缺血性脑损害及灌流压和CBF产生大的影响。原发性损害被认为是神经元的破坏和整合神经功能的能力丧失。传统上认为,原发性损害发生在进展性脑梗死之前,即发生在神经胶质细胞和内皮细胞破坏、白细胞浸润、血管崩溃和其他继发性过程之前。组织压力梯度的发展与组织继发性损害密切相关。继发过程所致损害在临床上的意义在于其对水肿形成、颅内压升高和脑疝的影响。然而继发过程发生在原发性神经元损害之后,为后期改变。
在特殊情况下,例如高温时缺血、严重缺血再灌注以及栓塞时发生的血-脑屏障内皮结构的早期崩溃、组织白细胞浸润和迅速发生的血管源性水肿的资料显示:早期形成的水肿与原发缺血性脑损害之间有因果关系。神经元发生的原发性病理改变和其他脑组织成分的继发性病理改变之间的区别是人为划分的。
值得注意的是,缺血半暗区的恶化不依赖于CBF的进一步减少。在许多脑卒中动物模型中梗死发展的整个时间里,CBF是比较稳定的或仅有非常缓慢的变化。这就排除了由于缺血进展导致梗死中心区增大的可能。然而常常可以观察到,随组织pH、糖酵解代谢产物、ATP浓度和组织学的改变,持续低灌注组织却逐渐形成了梗死。
……

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