袁翠平,张志强,王正阁,张浩,谭启富,陈光辉,卢光明.内侧颞叶癫痫自我参照加工受损的功能磁共振成像[J].中国医学影像技术,2011,27(3):495~499
内侧颞叶癫痫自我参照加工受损的功能磁共振成像
Impaired self-referential processing in medial temporal lobe epilepsy revealed with functional MRI
投稿时间:2010-07-29  修订日期:2010-08-15
DOI:
中文关键词:  癫痫,颞叶  磁共振成像  心理过程
英文关键词:Epilepsy, temporal lobe  Magnetic resonance imaging  Mental processes
基金项目:国家自然科学基金(30800264、30971019)、南京军区重点医药卫生项目(07z030)、南京军区南京总医院基金项目(Q2008063)、江苏省博士后基金项目(0801033)。
作者单位E-mail
袁翠平 南京军区南京总医院医学影像科,江苏 南京 210002  
张志强 南京军区南京总医院医学影像科,江苏 南京 210002  
王正阁 南京军区南京总医院医学影像科,江苏 南京 210002  
张浩 南京军区南京总医院医学影像科,江苏 南京 210002  
谭启富 南京军区南京总医院神经外科,江苏 南京 210002  
陈光辉 南京军区南京总医院神经内科,江苏 南京 210002  
卢光明 南京军区南京总医院医学影像科,江苏 南京 210002 luguangming@vip.163.com 
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中文摘要:
       目的 采用功能磁共振成像(fMRI)技术对内侧颞叶癫痫(mTLE)患者的自我参照功能受损状况进行评价。方法 12例伴有海马硬化的mTLE患者及15名健康志愿者纳入本研究。采用内向诱导与外向诱导任务,以内向诱导任务为刺激状态、外向诱导任务为控制状态,收集fMRI数据,观察mTLE患者自我参照加工相关脑区反应的改变。结果 与健康志愿者相比,mTLE患者的内侧前额叶、扣带回前部及后部等与自我参照加工相关的区域活动明显降低(P<0.01)。结论 mTLE患者以内侧前额叶为主的自我参照加工脑区活动降低,反映其与自我参照加工相关的高级脑认知功能损伤,是mTLE患者异常影像表现的病理生理学基础。
英文摘要:
      Objective To assess the extent of impairment of self-referential processing in medial temporal lobe epilepsy (mTLE) with functional magnetic resonance imaging (fMRI). Methods Twelve mTLE patients with hippocampal sclerosis and 15 healthy volunteers were enrolled. The self-reference activation was induced by contrast of the imternally cued condition and externally cued condition in a block-designed fMRI task. The fMRI data were acquired. The changes of self-referential processing relevant encephalic region in mTLE patients were observed. Results Compared with healthy volunteers, the mTLE patients showed decreased activation in the regions associated with the self-referential processing (P<0.01), such as the medial prefrontal cortex, anterior cingulate cortex and the posterior cingulate cortex. Conclusion The significantly decreased activation in the medial prefrontal cortex in mTLE patients reflects the impairment of advanced cognitive abilities relevant to self-referential processing, probably suggesting the physiopathologic mechanism of mTLE.
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