运动性失语发病机制探讨:附25例fMRI分析  

Investigation of Pathologic Mechanism of Motor Aphasia: An Analysis of 25 fMRI Cases

作　　者：周筠[1] 陈红燕[2] 王丽敏[1] 韩在柱[3] 王拥军[1] 

机构地区：[1]首都医科大学附属北京天坛医院神经内科,北京市100050 [2]北京市神经外科研究所神经放射中心,北京市100050 [3]北京师范大学认知科学与学习国家重点实验室,北京市100871

出　　处：《中国康复理论与实践》2006年第8期667-668,共2页Chinese Journal of Rehabilitation Theory and Practice

基　　金：北京市自然科学基金资助项目(No.7052035)

摘　　要：目的探讨运动性失语症可能的发病机制。方法对25例伴运动性失语的脑梗死患者,采用磁共振波谱分析(MRS)及磁共振灌注成像(PWI)分析对病变波及的Broca区进行检测,并与对侧镜像区进行对比。结果MRS显示,受累语言功能区的N已酰天门冬氨酸、胆碱的代谢较对侧镜像区降低(P<0.05);PWI显示,多数患者受累语言功能区的局部脑血容量、局部脑血流量较对侧明显减少(P<0.01),对比剂平均通过时间、达峰时间较对侧镜像区延长(P<0.05)。结论运动性失语症患者急性期语言功能区呈低灌注、低代谢表现,可能是运动性失语症的发病机制之一。Objective To investigate the pathologic mechanism of motor aphasia. Methods 25 patients with cerebral infarction and motor aphasia were examined by magnetic resonance spectroscopy （MRS） and perfusion weighted imaging （PWI） at Broca＇s areas, the results were compared with thai of the mirror side. Results MRS showed that the N-acetyl aspartate, choline in Broca＇s areas reduced than that of the mirror side （ P 〈0.05） ; while PWI showed that the regional cerebral blood volume and regional cerebral blood flow of damaged Broca＇s areas decreased significantly than that of the right hemisphere （ P 〈0.01）. Mean transit time and time to peak of damaged Broca＇s areas prolonged than that of mirror side （ P 〈0.05）. Conclusion Hypoperfusion and hypometabolism revealed in Broca＇s areas of patients with motor aphasia may be one of the mechanisms of motor aphasia.

关 键 词：运动性失语症 BROCA区 发病机制 功能磁共振检查 

分 类 号：R743.3[医药卫生—神经病学与精神病学]