脑梗死伴短暂性脑缺血发作26例临床分析  被引量:9

脑梗死伴短暂性脑缺血发作26例临床分析

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作  者:赵建民[1] 

机构地区:[1]河南省新乡市中心医院,河南新乡453000

出  处:《中国医药导报》2006年第29期37-38,共2页China Medical Herald

摘  要:目的探讨短暂性脑缺血发作(TIA)的发病机制及在脑梗死中的临床意义。方法回顾性分析2001年6月~2004年9月本院的26例伴有TIA的脑梗死患者的临床资料(观察组),并随机对26例无TIA的脑梗死患者设为对照组。结果观察组基本痊愈6例,显著进步15例,进步5例,治愈率为80.76%。对照组基本痊愈2例,显著进步12例,进步8例,无变化4例,治愈率为53.84%。两组患者治愈率相比有显著差异(P<0.01),两组神经功能缺损评分相比有显著性差异(P<0.01)。结论TIA的发病机制可能与微栓子学说及脑血管痉挛有关。TIA诱导神经组织产生缺血耐受即缺血预处理,使大脑通过内源性或血管保护机制以对抗脑梗塞后的严重损害,起到神经保护作用。Objective The outbreak mechanism that study brief cerebral ischemia go into action Transient ischemic attack (TIA) and in brain obstruct of clinical meaning.Methods The review analyzes 2001-06~2004-09 26 companions of hospitalses contain clinical data(observe set) that the TIA brain obstructs the sufferer, and obstruct to 26 brains that have no the TIA with the machine the sufferer establish for matched control.Results Observe the set is basic to recover from illness 6 examples, the Very obvious progresses 15 examples, progress 5 examples, the cure rate is 80.76%.The matched control is basic to recover from illness 2 examples, the very obvious progresses 12 examples, progress 8 examples, have no change 4 examples, the cure rate is 53.84%.Two sufferer's cure rates compares the very obvious difference ( P<0.01), two nerves function defection and damage grade point compares the Very obvious difference( P<0.01). Conclusions the TIA outbreak mechanism may have something to do with tinyly bolting sub-theory and afferent spasm in brains. the TIA induces the nervous tissue creation lacks the blood bears to suffer to lack namely the blood prepares to handle, making the brain pass inside source or blood vessel protection mechanisms to resist the brain obstruct the behind serious damage, rising the nerve protect the function.

关 键 词:脑梗死 短暂性脑缺血发作 发病机制 缺血耐受性 缺血预处理 

分 类 号:R[医药卫生]

 

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