Wang Jun, Mathalon Daniel H, Roach Brian J, Reilly James, Keedy Sarah K, Sweeney John A, Ford Judith M
Department of Psychiatry, University of Texas Southwestern, Dallas, TX 75390, USA.
San Francisco VA Medical Center, San Francisco, CA 94121, USA; Department of Psychiatry, University of California, San Francisco, CA 94121, USA.
Neuroimage. 2014 May 1;91:91-8. doi: 10.1016/j.neuroimage.2014.01.003. Epub 2014 Jan 11.
Across the animal kingdom, sensations resulting from an animal's own actions are processed differently from sensations resulting from external sources, with self-generated sensations being suppressed. A forward model has been proposed to explain this process across sensorimotor domains. During vocalization, reduced processing of one's own speech is believed to result from a comparison of speech sounds to corollary discharges of intended speech production generated from efference copies of commands to speak. Until now, anatomical and functional evidence validating this model in humans has been indirect. Using EEG with anatomical MRI to facilitate source localization, we demonstrate that inferior frontal gyrus activity during the 300ms before speaking was associated with suppressed processing of speech sounds in auditory cortex around 100ms after speech onset (N1). These findings indicate that an efference copy from speech areas in prefrontal cortex is transmitted to auditory cortex, where it is used to suppress processing of anticipated speech sounds. About 100ms after N1, a subsequent auditory cortical component (P2) was not suppressed during talking. The combined N1 and P2 effects suggest that although sensory processing is suppressed as reflected in N1, perceptual gaps may be filled as reflected in the lack of P2 suppression, explaining the discrepancy between sensory suppression and preserved sensory experiences. These findings, coupled with the coherence between relevant brain regions before and during speech, provide new mechanistic understanding of the complex interactions between action planning and sensory processing that provide for differentiated tagging and monitoring of one's own speech, processes disrupted in neuropsychiatric disorders.
在整个动物界，动物自身行为产生的感觉与外部来源产生的感觉的处理方式不同，自身产生的感觉会受到抑制。有人提出了一种前向模型来解释跨感觉运动领域的这一过程。在发声过程中，对自己语音的处理减少被认为是由于将语音与从说话命令的传出副本生成的预期语音产生的伴随放电进行比较的结果。到目前为止，在人类中验证该模型的解剖学和功能证据一直是间接的。我们使用脑电图结合解剖磁共振成像来促进源定位，结果表明，在说话前300毫秒期间，额下回的活动与语音开始后约100毫秒时听觉皮层中语音声音处理的抑制有关（N1）。这些发现表明，来自前额叶皮层语音区域的传出副本被传输到听觉皮层，在那里它被用来抑制对预期语音声音的处理。在N1之后约100毫秒，后续的听觉皮层成分（P2）在说话时没有受到抑制。N1和P2效应共同表明，尽管感觉处理如N1所示受到抑制，但感知间隙可能会像P2缺乏抑制所反映的那样得到填补，这解释了感觉抑制和保留的感觉体验之间的差异。这些发现，再加上说话前后相关脑区之间的连贯性，为动作计划和感觉处理之间的复杂相互作用提供了新的机制理解，这些相互作用为对自己的语音进行区分标记和监测提供了支持，而这些过程在神经精神疾病中会受到干扰。
