惊恐障碍患者抑制性控制缺陷的事件相关电位研究

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

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正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。

Objective To investigate the electrophysiological evidence of inhibitory control deficit in panic disorder patients using a visual simple Go/ Nogo task. Method 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 offering new objective evidence to understand the etiology of panic disorder.