基于静息态功能磁共振成像探索慢性特发性耳鸣中枢机制的文献研究

doi:10.12114/j.issn.1007-9572.2023.0523

中国全科医学 ›› 2026, Vol. 29 ›› Issue (22): 3175-3181.DOI: 10.12114/j.issn.1007-9572.2023.0523

基于静息态功能磁共振成像探索慢性特发性耳鸣中枢机制的文献研究

李柏洁, 张雪婷, 付渊博^*(), 刘慧林, 陈鹏, 倪雨彤, 曾宇涵

100010　北京市，首都医科大学附属北京中医医院神经内科

收稿日期:2025-06-12 修回日期:2026-09-05 出版日期:2026-08-05 发布日期:2026-07-08
通讯作者: 付渊博
作者贡献：
李柏洁负责文章的构思与设计、研究资料的收集与整理、论文撰写；张雪婷负责文章资料的收集；付渊博负责论文的修订、文章质量控制与审校、对文章整体负责、监督管理；刘慧林、陈鹏负责文章的修订、审校；倪雨桐、曾宇涵负责表格的编辑与整理。
基金资助:
2021年度"扬帆"计划重点医学专业（重点扶持专业）——中西医结合康复项目(ZYLX202140)

Research on the Central Mechanism of Chronic Idiopathic Tinnitus Based on rs-fMRI

LI Baijie, ZHANG Xueting, FU Yuanbo^*(), LIU Huilin, CHEN Peng, NI Yutong, ZENG Yuhan

Department of Neurology, Beijing Hospital of Traditional Chinese Medicine, Beijing 100010, China

Received:2025-06-12 Revised:2026-09-05 Published:2026-08-05 Online:2026-07-08
Contact: FU Yuanbo

摘要/Abstract

摘要： 背景特发性耳鸣因其病因和机制的复杂性，尚缺乏有效的治疗方法，且随着病程的迁延，对患者的生活质量造成严重影响。近年来，静息态功能磁共振成像（rs-fMRI）技术快速发展，被广泛应用于慢性特发性耳鸣的病理机制研究，越来越多的研究认为，慢性特发性耳鸣涉及多个大脑中枢脑区的可塑性改变。目的分析总结近10年rs-fMRI在慢性特发性耳鸣中枢机制领域的研究现状，梳理慢性特发性耳鸣中枢重塑机制，为塑造慢性特发性耳鸣的中枢模型夯实基础。方法检索2013-01-01—2023-01-01中国知网（CNKI）、万方数据知识服务平台、维普期刊资源整合服务平台（VIP）、PubMed中收录的与特发性耳鸣中枢机制及rs-fMRI相关的研究，纳入8项研究探讨慢性特发性耳鸣脑区功能活动的改变，其余7项研究探讨大脑网络功能连接的改变。结果本研究发现与健康受试者相比，慢性特发性耳鸣患者听觉中枢兴奋-抑制失衡，并与杏仁核、海马、额叶-纹状体环路等边缘系统脑区发生异常耦合；在脑网络方面，听视网络、默认网络、执行控制网络、突显网络、注意网络及皮层下-小脑网络均发生功能连接的异常。结论本文总结目前慢性特发性耳鸣中枢机制的rs-fMRI研究，发现慢性特发性耳鸣可能是听觉通路、边缘系统及多个大脑功能网络神经重塑的结果。

关键词: 耳鸣, 慢性特发性耳鸣, 静息态功能磁共振成像, 中枢机制, 文献研究

Abstract:

Background

Due to the complexity of its etiology and mechanisms, idiopathic tinnitus still lacks effective treatments. As the condition persists, it significantly impairs patients' quality of life. In recent years, with the rapid development of resting-state functional magnetic resonance imaging (rs-fMRI), this technique has been widely applied to investigate the pathological mechanisms of chronic idiopathic tinnitus. A growing body of research suggests that chronic idiopathic tinnitus involves plastic changes across multiple central brain regions.

Objective

This study aims to analyze and summarize the research progress over the past decade on the central mechanisms of chronic idiopathic tinnitus using rs-fMRI, clarify the mechanisms of central neural remodeling, and lay a solid foundation for constructing a central model of chronic idiopathic tinnitus.

Methods

Retrieval of studies related to the central mechanism of idiopathic tinnitus and rs-fMRI included in China National Knowledge Infrastructure (CNKI), Wanfang Data Knowledge Service Platform, VIP Journal Resource Integration Service Platform (VIP), and PubMed from January 1, 2013 to January 1, 2023, eight studies were included to explore alterations in functional activity in brain regions, while another seven studies investigated changes in functional connectivity within brain networks.

Results

Compared with healthy subjects, patients with chronic idiopathic tinnitus exhibited an excitatory-inhibitory imbalance in the auditory cortex, along with aberrant coupling with limbic system regions such as the amygdala, hippocampus, and frontal-striatal circuit. In terms of brain networks, abnormal functional connectivity was observed in the auditory-visual network, default mode network, executive control network, salience network, attention network, and subcortical-cerebellar network.

Conclusion

This review summarizes current rs-fMRI research on the central mechanisms of chronic idiopathic tinnitus and suggests that the condition may result from neural remodeling involving the auditory pathway, limbic system, and multiple functional brain networks.

Key words: Tinnitus, Chronic idiopathic tinnitus, rs-fMRI, Central mechanism, Literature research

中图分类号:

R 764.45

李柏洁,张雪婷,付渊博,等. 基于静息态功能磁共振成像探索慢性特发性耳鸣中枢机制的文献研究[J]. 中国全科医学, 2026, 29(22): 3175-3181. DOI: 10.12114/j.issn.1007-9572.2023.0523.
LI Baijie,ZHANG Xueting,FU Yuanbo, et al. Research on the Central Mechanism of Chronic Idiopathic Tinnitus Based on rs-fMRI[J]. Chinese General Practice, 2026, 29(22): 3175-3181. DOI: 10.12114/j.issn.1007-9572.2023.0523.

图/表 2

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第一作者	样本量（患者组/健康组）（例）	rs-fMRI数据分析方法	左侧脑区改变	右侧脑区改变	耳鸣观察量表	耳鸣量表与rs-fMRI指标改变相关性分析
崔金娈^[7]	40/40	GCA	左侧NAc到左侧额中回、右侧NAc到左侧额下回、右侧颞中回到左侧NAc、右侧额中回到右侧NAc的有效连接均增强	—	THQ	左侧NAc至左侧额中回增强的有效连接与THQ得分呈正相关；右侧额中回至右侧NAc增强的有效连接与耳鸣病程呈正相关
韩祺^[8]	21/21	ReHo	右颞上回、颞中回和颞下回ReHo值增高	右眶部额中回和三角部额下回、左额中回及角回、小脑蚓部ReHo值降低	THI	右颞中回ReHo值与THI评分呈正相关
韩祺^[9]	25/25	ReHo、fALFF	右侧颞中回和楔叶ReHo值增高；右侧颞中回和楔叶fALFF值升高	右侧额中回、左侧小脑前叶ReHo值降低	THI	右侧颞中回ReHo值与THI评分呈正相关
Chen^[12]	26/23	GCA	杏仁核：左杏仁核到左颞上回、非听觉区域（包括左前扣带皮层、左楔前叶、右侧角回）；左、右小脑后叶有效连通性下降；右杏仁核到包括右颞上回、右前扣带皮层、右额中回和右缘上回有效连通性增强。右侧额中回、左侧颞中回、左侧额下回和左侧中央后回到左侧杏仁核的有效连通性增强；左侧前扣带皮层、左侧颞中回、左侧额中回、右侧额下回和右侧中央后回到右侧杏仁核的有效连通性增强	海马体：左海马到左颞中回、左中央后回的有效连通性增加，到左枕中回有效连通性下降；右海马到左颞横回、右颞中回和右中央后回有效连通性增加，在右枕中回中也检测到有效连通性降低。右侧额上回、左海马旁回和左岛叶到左海马的有效连通性增强；左右额中回、左颞中回和左角回到右海马的有效连通性增强	THQ	THQ评分与左杏仁核到左颞上回及右杏仁核到右颞上回的连通性增加呈正相关；耳鸣持续时间与右海马到左颞横回连通性增加呈正相关
Chen^[13]	28/30	VMHC	耳鸣患者颞横回、额中回和枕上回的VMHC明显增加	—	THQ	耳鸣持续时间与钩回VMHC呈正相关；颞横回、颞上回、中央前回和距状回VMHC与THQ呈正相关
Chen^[14]	39/41	ALFF、fALLF	右额上回、左额下回、右颞中回、右角回ALFF增加；双侧枕中回ALFF下降。右额上回、缘上回fALFF增加；双侧枕中回fALFF下降	—	THQ	右侧额上回ALFF、左侧额上回fALFF与THQ评分呈正相关；右侧额上回ALFF、左侧额上回fALFF与耳鸣持续时间呈正相关
Chen^[15]	31/32	ALFF	右侧颞中回、右侧额上回和右侧角回的ALFF增加	左楔叶、右枕中回和双侧丘脑ALFF降低	THQ	右侧颞中回和右侧额上回ALFF增加与THQ评分呈正相关；右侧额上回ALFF与耳鸣持续时间呈正相关
Lan^[18]	41/60	图论	慢性耳鸣患者左侧海马、杏仁核和颞叶DC增加	右侧颞下回的DC减少	THQ	慢性耳鸣组右侧颞下回DC与SAS评分呈正相关

第一作者	样本量（患者组/健康组）（例）	rs-fMRI数据分析方法	左侧脑区改变	右侧脑区改变	耳鸣观察量表	耳鸣量表与rs-fMRI指标改变相关性分析
崔金娈^[7]	40/40	GCA	左侧NAc到左侧额中回、右侧NAc到左侧额下回、右侧颞中回到左侧NAc、右侧额中回到右侧NAc的有效连接均增强	—	THQ	左侧NAc至左侧额中回增强的有效连接与THQ得分呈正相关；右侧额中回至右侧NAc增强的有效连接与耳鸣病程呈正相关
韩祺^[8]	21/21	ReHo	右颞上回、颞中回和颞下回ReHo值增高	右眶部额中回和三角部额下回、左额中回及角回、小脑蚓部ReHo值降低	THI	右颞中回ReHo值与THI评分呈正相关
韩祺^[9]	25/25	ReHo、fALFF	右侧颞中回和楔叶ReHo值增高；右侧颞中回和楔叶fALFF值升高	右侧额中回、左侧小脑前叶ReHo值降低	THI	右侧颞中回ReHo值与THI评分呈正相关
Chen^[12]	26/23	GCA	杏仁核：左杏仁核到左颞上回、非听觉区域（包括左前扣带皮层、左楔前叶、右侧角回）；左、右小脑后叶有效连通性下降；右杏仁核到包括右颞上回、右前扣带皮层、右额中回和右缘上回有效连通性增强。右侧额中回、左侧颞中回、左侧额下回和左侧中央后回到左侧杏仁核的有效连通性增强；左侧前扣带皮层、左侧颞中回、左侧额中回、右侧额下回和右侧中央后回到右侧杏仁核的有效连通性增强	海马体：左海马到左颞中回、左中央后回的有效连通性增加，到左枕中回有效连通性下降；右海马到左颞横回、右颞中回和右中央后回有效连通性增加，在右枕中回中也检测到有效连通性降低。右侧额上回、左海马旁回和左岛叶到左海马的有效连通性增强；左右额中回、左颞中回和左角回到右海马的有效连通性增强	THQ	THQ评分与左杏仁核到左颞上回及右杏仁核到右颞上回的连通性增加呈正相关；耳鸣持续时间与右海马到左颞横回连通性增加呈正相关
Chen^[13]	28/30	VMHC	耳鸣患者颞横回、额中回和枕上回的VMHC明显增加	—	THQ	耳鸣持续时间与钩回VMHC呈正相关；颞横回、颞上回、中央前回和距状回VMHC与THQ呈正相关
Chen^[14]	39/41	ALFF、fALLF	右额上回、左额下回、右颞中回、右角回ALFF增加；双侧枕中回ALFF下降。右额上回、缘上回fALFF增加；双侧枕中回fALFF下降	—	THQ	右侧额上回ALFF、左侧额上回fALFF与THQ评分呈正相关；右侧额上回ALFF、左侧额上回fALFF与耳鸣持续时间呈正相关
Chen^[15]	31/32	ALFF	右侧颞中回、右侧额上回和右侧角回的ALFF增加	左楔叶、右枕中回和双侧丘脑ALFF降低	THQ	右侧颞中回和右侧额上回ALFF增加与THQ评分呈正相关；右侧额上回ALFF与耳鸣持续时间呈正相关
Lan^[18]	41/60	图论	慢性耳鸣患者左侧海马、杏仁核和颞叶DC增加	右侧颞下回的DC减少	THQ	慢性耳鸣组右侧颞下回DC与SAS评分呈正相关

第一作者	样本量（患者组/健康组）（例）	rs-fMRI观察指标	左侧脑区改变	右侧脑区改变	耳鸣观察量表	耳鸣量表与rs-fMRI指标改变相关性分析
陈晓辉^[6]	31/33	FC	背侧前扣带回与双侧眶额皮层的FC增加，左侧前脑岛与左侧小脑VIIb叶的FC增加	背侧前扣带回与右侧中央前回和右侧顶下小叶的FC降低	THQ	背侧前扣带回-顶下小叶FC与耳鸣病程和THQ得分呈负相关；背侧前扣带回-中央前回FC与THQ得分呈负相关
刘圣华^[10]	31/40	ICA	前扣带回嘴部与左楔前叶、右中央后回、右壳核之间FC增加；前扣带回背部与右颞上回、右下顶叶、右眶额叶皮层、右额叶前回内侧FC增加	前扣带回嘴部与左矩状回FC减少；前扣带回背部与梭状回FC减少	THQ	前扣带回嘴部与左楔前叶FC增加与THQ评分正相关；前扣带回背部与右颞上回FC增加与耳鸣持续时间正相关；前扣带回背部与右下顶叶小叶FC增加与THQ评分正相关
马晓彦^[11]	60/36	ReHo、ALFF、FC	右颞上回ReHo升高；右颞上回到右颞极功能连接增强	—	THI	右颞上回到右颞极功能连接和THI正相关
Chen^[16]	29/30	ReHo、FC	双侧前脑岛、左额下回和右缘上回ReHo值升高。左前脑岛与左额中回、右前脑岛与右额中回、右颞下回与右楔前叶的FC增强	左楔叶ReHo降低	THQ	左前脑岛与左额中回的FC增强，右前脑岛与右额中回的FC增强与THQ呈正相关
Ddavies^[17]	12/11	ICA	右侧缘上回和左侧颞中回的FC增加，然而，在使用FWE校正后，这些功能连通性增强的区域没有存活下来	—	THQ、TCHQ	耳鸣组与对照组的平均双变量相关系数无显著差异
Lanting^[19]	20/20	ICA	—	视觉皮层、扣带回、DMN中FC降低	THI、TRQ 、TCSQ	—
Zhang^[20]	31/33	FC	左丘脑与右角回，右中扣带皮层，左小脑后叶FC增加；右丘脑与左后扣带皮层和双侧小脑后叶FC增加	左丘脑与右颞中回、右眶额中皮层、左额中回、右中央前回和双侧距状裂皮质FC下降；右丘脑与左颞上回、左杏仁核、右额上回、左中央前回、左枕中回FC下降	THQ	左丘脑与右颞中回FC与THQ评分呈负相关；右丘脑与左颞上回FC与耳鸣持续时间呈负相关

第一作者	样本量（患者组/健康组）（例）	rs-fMRI观察指标	左侧脑区改变	右侧脑区改变	耳鸣观察量表	耳鸣量表与rs-fMRI指标改变相关性分析
陈晓辉^[6]	31/33	FC	背侧前扣带回与双侧眶额皮层的FC增加，左侧前脑岛与左侧小脑VIIb叶的FC增加	背侧前扣带回与右侧中央前回和右侧顶下小叶的FC降低	THQ	背侧前扣带回-顶下小叶FC与耳鸣病程和THQ得分呈负相关；背侧前扣带回-中央前回FC与THQ得分呈负相关
刘圣华^[10]	31/40	ICA	前扣带回嘴部与左楔前叶、右中央后回、右壳核之间FC增加；前扣带回背部与右颞上回、右下顶叶、右眶额叶皮层、右额叶前回内侧FC增加	前扣带回嘴部与左矩状回FC减少；前扣带回背部与梭状回FC减少	THQ	前扣带回嘴部与左楔前叶FC增加与THQ评分正相关；前扣带回背部与右颞上回FC增加与耳鸣持续时间正相关；前扣带回背部与右下顶叶小叶FC增加与THQ评分正相关
马晓彦^[11]	60/36	ReHo、ALFF、FC	右颞上回ReHo升高；右颞上回到右颞极功能连接增强	—	THI	右颞上回到右颞极功能连接和THI正相关
Chen^[16]	29/30	ReHo、FC	双侧前脑岛、左额下回和右缘上回ReHo值升高。左前脑岛与左额中回、右前脑岛与右额中回、右颞下回与右楔前叶的FC增强	左楔叶ReHo降低	THQ	左前脑岛与左额中回的FC增强，右前脑岛与右额中回的FC增强与THQ呈正相关
Ddavies^[17]	12/11	ICA	右侧缘上回和左侧颞中回的FC增加，然而，在使用FWE校正后，这些功能连通性增强的区域没有存活下来	—	THQ、TCHQ	耳鸣组与对照组的平均双变量相关系数无显著差异
Lanting^[19]	20/20	ICA	—	视觉皮层、扣带回、DMN中FC降低	THI、TRQ 、TCSQ	—
Zhang^[20]	31/33	FC	左丘脑与右角回，右中扣带皮层，左小脑后叶FC增加；右丘脑与左后扣带皮层和双侧小脑后叶FC增加	左丘脑与右颞中回、右眶额中皮层、左额中回、右中央前回和双侧距状裂皮质FC下降；右丘脑与左颞上回、左杏仁核、右额上回、左中央前回、左枕中回FC下降	THQ	左丘脑与右颞中回FC与THQ评分呈负相关；右丘脑与左颞上回FC与耳鸣持续时间呈负相关

基于静息态功能磁共振成像探索慢性特发性耳鸣中枢机制的文献研究

Research on the Central Mechanism of Chronic Idiopathic Tinnitus Based on rs-fMRI

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