惊恐障碍患者抑制性控制缺陷的事件相关电位研究

目的 探讨惊恐障碍患者抑制性控制缺陷的神经电生理机制.方法 采用视觉事件相关电位Go/Nogo实验方式,对16例惊恐障碍患者(PD)和13名健康对照(NC)进行研究.任务为随机出现的等概率双英文字母和单英文字母,要求被试者对双英文字母进行按键反应(Go),单英文字母不按键(Nogo),记录行为学数据和32导脑电数据.结果 惊恐障碍患者和止常对照组均产生了明显的额中央区Nogo-N2(PD组:F1,30=8.00,P=0.08;NC组:F1,24=4.60,P=0.042)和Nogo-P3效应(PD组:F1,30=7.85,P=0.09;NC组:F1,24=13.57,P=0.000),但是惊恐障碍患者的Nogo-N2和Nogo-P3波幅明显低于正常对照组(Fz:F=9.135,P=0.005;F=8.511,P=0.006),潜伏期差异无统计学意义.结论 惊恐障碍患者脑信息加工过程特定时间窗抑制性控制障碍,为进一步揭示惊恐障碍的发病机制提供了新的脑电生理证据.

Inhibitory control deficit in patients with panic disorder: an event-related potentials study

Objective To investigate the electrophysiological evidence of inhibitory control deficit in panic disorder patients using a visual simple Go/Nogo task. Methods Sixteen patients with panic disorder and 13 healthy volunteers received a visual simple Go/Nogo task. The stimuli were single or double English letters and appeared with equal probability. The subjects were instructed to press a button as quickly as possible when the double letter was presented (I. E. , GO), but make no response to the single letter (I. E. ,Nogo). 32 channel EEG data were recorded. Result All subjects displayed a distinct Go/Nogo effect in the N2 component (PD group: F1,30= 8.00, P = 0.008 ; NC group: F1,24 = 4.60, P = 0.042) and P3 component (PD group:F1,30 = 7.85,P =0.009; NC group:F1,24 = 13.57,P =0.000) at frontocentral sites, but the amplitudes of Nogo-N2 and Nogo-P3 were significantly reduced in panic disorder patients as compared to the healthy subjects (Fz: F = 9.135, P = 0.005 ; F = 8.511, P = 0.006, respectively). There was no significant differences between the latencies of Nogo-N2 and Nogo-P3. Conclusion Panic disorder may consist inhibitory control deficit which may assist in of fering new objective evidence to understand the etiology of panic disorder.