中文摘要：

目的：探讨焦虑症患者血氧水平依赖功能MR成像（BOLD．mRI）负激活特点及其神经病理机制。方法：焦虑症组10例、对照组10名受试者参加试验，先进行焦虑状态特质量表（STAI-T）测试，随后进行BOLD·fMRI，2次fMRI试验数据采集。采用组块设计刺激模式，刺激材料（情绪中性词及威胁词）通过听觉呈现。试验1为情绪中性词与无词空白对照交替，试验2为威胁词与情绪中性词交替，2次试验均要求受试者仔细听通过耳机传人的词语，并对其引起的主观情绪体验作出心理判断（愉快、不愉快或中性），空白对照不给任务。采用SPM99软件进行数据处理，先分析单个被试，然后行组间分析。主要观察焦虑症患者负激活脑区特点，数据处理时把静息期与任务期数据进行反减得到负激活图，对有关脑区的反应特性做进一步分析。结果：焦虑症组STAI-T分值（584-8）高于对照组（334-5），差异有统计学意义（t=8．3，P〈0．01）。fMRI试验1对照组与患者组均有负激活脑区，试验2仅有患者组出现负激活，正常对照组无负激活脑区，上述3组负激活脑区网络基本相同，主要包括MPFC（BA10、BA24／32）、PCC／楔前叶（BA31／30）、丘脑及两侧顶下小叶（BA39／40）等脑区。试验1MPFC（BA24／32）平均负激活强度（平均T值）正常人（5．1）强于患者（4．2）（t=4．8，P=0．006），而患者PCC平均T值（5．8）强于正常人（4．9）（t=2．4，P=0．026）。结论：焦虑症组MPFC及PCC存在功能异常，这种异常在其神经病理机制中具重要作用。

英文摘要：

Objective We used blood oxygenation level dependent-functional MR imaging （BOLD- fMRI） to explore the characteristics of deactivation patterns in patients with anxiety disorders and the underlying neural mechanism of this disease. Methods Ten patients and ten healthy controls participated the experiments. All subjects performed the trait portion of the State-Trait anxiety Inventory （STAI-T） prior to the fMRI scans. The subjects underwent noninvasive functional magnetic resonance imaging while listening actively to emotionally neutral words alternating with no words （experiment 1 ） and threat related-words alternating with emotionally neutral words （experiment2）. During fMRI scanning, subjects were instructed to closely listen to each stimuli word and to silently make a judgment of the word＇s valence. Data were analyzed with statistical parametric mapping （SPM 99 ）. Individual and group analysis were conducted. Results Mean STAI-T score was significantly higher for patients group than that of controls （58 ± 8 for patients group and 33±5 for controls,t = 8. 3 ,P 〈 0. 01 ）. Our fMRI data revealed sets of deactivation brain regions in Experimentl for patients and healthy controls, however, the deactivation can be found in experiment 2 only for patients. Interestingly, all the observed deactivation patterns were similar. The related areas compromise medial prefrontal cortex（ BA 10,BA 24/32 ）, posterior cingulate（ BA 31/30） and bilateral inferior parietal cortex（ MPFC ） （ BA 39/40 ）, which nearly overlapping with the organized default model network. Further more, the mean t values in the MPFC area（ BA 24/32） was significantly higher for control group than that of patient （5. 1 controls and 4. 2 for patients, t = 4. 8, P = 0. 006 ）, conversely, the mean t values in the posterior cingulate cortex（PCC） area was significantly higher for patients 1 than that of controls （4. 9 controls and 5.8 for patients, t = 2.4, P = 0. 026）. Conclusion Our observations suggest