在整个动物王国,听觉皮层的神经反应在发声过程中受到抑制,人类也不例外。一个常见的假设是抑制增加了对听觉反馈的敏感性,能够检测发声错误。这一假设先前已在非人灵长类动物中得到证实,然而,听觉抑制和人类语音监测灵敏度之间的直接联系仍然难以捉摸。为了解决这个问题,我们获得了35名神经外科参与者在演讲过程中的颅内脑电图(iEEG)记录.我们首先描述了听觉抑制的详细地形,在上颞回(STG)中变化。接下来,我们执行了延迟听觉反馈(DAF)任务,以确定抑制部位是否也对听觉反馈改变敏感.的确,重叠的地点对反馈的反应增强,表明灵敏度。重要的是,听觉抑制程度和反馈灵敏度之间有很强的相关性,暗示抑制可能是语音监控的关键机制。Further,我们发现,当参与者产生同时听觉反馈的语音时,如果参与者参与DAF范式,则有选择地激活后STG,提示注意负荷的增加可以调节听觉反馈的灵敏度。
大脑降低了对我们自己产生的输入的反应,如移动或说话。本质上,当我们执行这些动作时,我们的大脑“知道”接下来会发生什么,因此不需要对意外事件做出强烈的反应。这就是为什么我们不能挠自己,以及为什么大脑对我们自己的声音的反应不如对别人的声音的反应。安静大脑的反应也使我们能够专注于新事物或重要事物,而不会被自己的动作或声音分散注意力。对非人类灵长类动物的研究表明,当动物发出声音时,听觉皮层(负责处理声音的大脑区域)中的神经元显示出抑制的活动水平。有趣的是,当灵长类动物听到自己声音的改变版本时,许多相同的神经元变得更加活跃。但目前还不清楚这是否也发生在人类身上。为了调查,Ozker等人.使用一种叫做脑电图的技术来记录参与者说话时人脑不同区域的神经活动。结果表明,当个体说话时,参与听觉处理的大脑大多数区域的活动受到抑制。然而,当人们听到自己声音的改变版本时,出现了意想不到的延迟,这些相同的区域显示出更多的活动。此外,Ozker等人.发现听觉皮层的抑制水平越高,这些领域对一个人说话的变化越敏感。这些发现表明,抑制大脑对自我生成语音的反应可能有助于检测语音生成过程中的错误。言语障碍在各种神经系统疾病中很常见,比如口吃,帕金森病,和失语症.Ozker等人.假设这些缺陷可能是因为个体无法抑制大脑听觉区域的活动,在检测和纠正自己讲话中的错误时引起了斗争。然而,需要进一步的实验来检验这一理论。
Across the animal kingdom, neural responses in the auditory cortex are suppressed during vocalization, and humans are no exception. A common hypothesis is that suppression increases sensitivity to auditory feedback, enabling the detection of vocalization errors. This hypothesis has been previously confirmed in non-human primates, however a direct link between auditory suppression and sensitivity in human speech monitoring remains elusive. To address this issue, we obtained intracranial electroencephalography (iEEG) recordings from 35 neurosurgical participants during speech production. We first characterized the detailed topography of auditory suppression, which varied across superior temporal gyrus (STG). Next, we performed a delayed auditory feedback (DAF) task to determine whether the suppressed sites were also sensitive to auditory feedback alterations. Indeed, overlapping sites showed enhanced responses to feedback, indicating sensitivity. Importantly, there was a strong correlation between the degree of auditory suppression and feedback sensitivity, suggesting suppression might be a key mechanism that underlies speech monitoring. Further, we found that when participants produced speech with simultaneous auditory feedback, posterior STG was selectively activated if participants were engaged in a DAF paradigm, suggesting that increased attentional load can modulate auditory feedback sensitivity.
The brain lowers its response to inputs we generate ourselves, such as moving or speaking. Essentially, our brain ‘knows’ what will happen next when we carry out these actions, and therefore does not need to react as strongly as it would to unexpected events. This is why we cannot tickle ourselves, and why the brain does not react as much to our own voice as it does to someone else’s. Quieting down the brain’s response also allows us to focus on things that are new or important without getting distracted by our own movements or sounds. Studies in non-human primates showed that neurons in the auditory cortex (the region of the brain responsible for processing sound) displayed suppressed levels of activity when the animals made sounds. Interestingly, when the primates heard an altered version of their own voice, many of these same neurons became more active. But it was unclear whether this also happens in humans. To investigate, Ozker et al. used a technique called electrocorticography to record neural activity in different regions of the human brain while participants spoke. The results showed that most areas of the brain involved in auditory processing showed suppressed activity when individuals were speaking. However, when people heard an altered version of their own voice which had an unexpected delay, those same areas displayed increased activity. In addition, Ozker et al. found that the higher the level of suppression in the auditory cortex, the more sensitive these areas were to changes in a person’s speech. These findings suggest that suppressing the brain’s response to self-generated speech may help in detecting errors during speech production. Speech deficits are common in various neurological disorders, such as stuttering, Parkinson’s disease, and aphasia. Ozker et al. hypothesize that these deficits may arise because individuals fail to suppress activity in auditory regions of the brain, causing a struggle when detecting and correcting errors in their own speech. However, further experiments are needed to test this theory.