卒中后失语症中支持发声听觉反馈控制的功能性神经活动与连接缺陷：一项fMRI研究
Functional neural activity and connectivity deficits underlying vocal auditory feedback control in post-stroke aphasia: An fMRI study.
文献信息
| PMID | 42913270 |
|---|---|
| 原文 | 在 PubMed 查看原文 ↗ |
| 发表日期 | 2026 |
| 作者 | Roozbeh Behroozmand |
| 作者单位 | Speech Neuroscience Lab, Department of Speech Language and Hearing, Callier Center for Communication Disorders, School of Behavioral and Brain Sciences, The University of Texas at Dallas, Richardson, TX, USA. Electronic address: roozbeh.behroozmand@utdallas.edu. |
| 期刊 | Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology |
| SCI 分区 | Q2 |
| IF | 4.6 |
| 研究类型 | 临床研究 · 临床 |
| 所属专科 | 咽喉科 |
中文摘要
目的： 本研究探讨卒中后失语症中发声产生和运动控制缺陷背后感觉运动整合受损的功能性神经活动与连接相关因素。
方法： 采集15名失语症参与者和15名对照参与者在随机±100音分音高偏移刺激改变听觉反馈条件下发语音元音时的fMRI数据。
结果： 我们发现失语症中卒中所致脑损伤与左半球背侧流网络激活减弱相关，包括前运动皮层和运动皮层、后颞上区域及缘上回。功能连接分析显示，失语症中后颞上回（pSTG）与背侧和腹侧中央前回言语区（dPSA和vPSA）之间的左半球耦合降低，提示听觉-运动整合受损。失语症参与者对音高偏移听觉反馈的跟随性和相反性（即代偿性）发声反应均减弱，反映快速前馈和较慢反馈控制机制均受损。此外，发声代偿行为受损与pSTG和左侧背侧中央前回言语区（dPSA）以及右侧背侧喉运动皮层（dLMC）之间的功能连接降低相关，提示这些网络在发声产生过程中基于听觉反馈的喉运动控制中的关键作用及其在失语症中由卒中导致的损害。
结论： 我们的数据提供了失语症中听觉-运动整合受损以及背侧流网络内神经通信受损的汇聚性证据。
意义： 这些发现强调，失语症治疗的临床干预受益于靶向支持发声听觉反馈处理和控制的感觉运动机制。强化感觉运动整合通路的个性化干预可能进一步促进流畅言语交流的恢复。
英文摘要
OBJECTIVE: This study investigated the functional neural activity and connectivity correlates of disrupted sensorimotor integration underlying vocal production and motor control deficits in post-stroke aphasia.
METHODS: fMRI data were acquired from 15 aphasia and 15 control participants during vocalization of speech vowel sounds under altered auditory feedback with randomized ± 100-cents pitch-shift stimuli.
RESULTS: We found that stroke-induced brain damage in aphasia was associated with diminished activation within left-hemisphere dorsal stream networks, including premotor and motor cortices, posterior superior temporal regions, and supramarginal gyrus. Functional connectivity analysis revealed reduced left-hemisphere coupling between posterior superior temporal gyrus (pSTG) and dorsal and ventral precentral speech areas (dPSA and vPSA) in aphasia, indicating disrupted auditory-motor integration. Aphasia participants exhibited reduced following and opposing (i.e., compensatory) vocal responses to pitch-shifted auditory feedback, reflecting impairments in both rapid feedforward and slower feedback-based control mechanisms. In addition, impaired vocal compensatory behavior was associated with reduced functional connectivity between pSTG and the left dorsal precentral speech areas (dPSA) as well as the right dorsal laryngeal motor cortex (dLMC), suggesting the critical role of these networks in auditory-feedback-based laryngeal motor control during vocal production and their stroke-induced impairment in aphasia.
CONCLUSIONS: Our data provide converging evidence of disrupted auditory-motor integration and impaired neural communications within dorsal stream networks in aphasia.
SIGNIFICANCE: These findings emphasize that clinical interventions for aphasia therapy benefit from targeting sensorimotor mechanisms supporting vocal auditory feedback processing and control. Personalized interventions that strengthen sensorimotor integration pathways could further enhance recovery of fluent verbal communication.