Lee Sang-Yeon, Choi Byung Yoon, Koo Ja-Won, De Ridder Dirk, Song Jae-Jin
Department of Otorhinolaryngology-Head and Neck Surgery, Seoul National University Bundang Hospital, Seongnam, South Korea.
Unit of Neurosurgery, Department of Surgical Sciences, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
Front Neurosci. 2020 Nov 27;14:596647. doi: 10.3389/fnins.2020.596647. eCollection 2020.
Just as the human brain works in a Bayesian manner to minimize uncertainty regarding external stimuli, a deafferented brain due to hearing loss attempts to obtain or "fill in" the missing auditory information, resulting in auditory phantom percepts (i.e., tinnitus). Among various types of hearing loss, sudden sensorineural hearing loss (SSNHL) has been extensively reported to be associated with tinnitus. However, the reason that tinnitus develops selectively in some patients with SSNHL remains elusive, which led us to hypothesize that patients with SSNHL with tinnitus (SSNHL-T) and those without tinnitus (SSNHL-NT) may exhibit different cortical activity patterns. In the current study, we compared resting-state quantitative electroencephalography findings between 13 SSNHL-T and 13 SSNHL-NT subjects strictly matched for demographic characteristics and hearing thresholds. By performing whole-brain source localization analysis complemented by functional connectivity analysis, we aimed to determine the as-yet-unidentified cortical oscillatory signatures that may reveal potential prerequisites for the perception of tinnitus in patients with SSNHL. Compared with the SSNHL-NT group, the SSNHL-T group showed significantly higher cortical activity in Bayesian inferential network areas such as the frontopolar cortex, orbitofrontal cortex (OFC), and pregenual anterior cingulate cortex (pgACC) for the beta 3 and gamma frequency bands. This suggests that tinnitus develops in a brain with sudden auditory deafferentation only if the Bayesian inferential network updates the missing auditory information and the pgACC-based top-down gatekeeper system is actively involved. Additionally, significantly increased connectivity between the OFC and precuneus for the gamma frequency band was observed in the SSNHL-T group, further suggesting that tinnitus derived from Bayesian inference may be linked to the default mode network so that tinnitus is regarded as normal. Taken together, our preliminary results suggest a possible mechanism for the selective development of tinnitus in patients with SSNHL. Also, these areas could serve as the potential targets of neuromodulatory approaches to preventing the development or prolonged perception of tinnitus in subjects with SSNHL.
正如人类大脑以贝叶斯方式工作以尽量减少关于外部刺激的不确定性一样，因听力损失而传入神经阻滞的大脑会试图获取或“填补”缺失的听觉信息，从而产生听觉幻像感知（即耳鸣）。在各种类型的听力损失中，突发性感音神经性听力损失（SSNHL）与耳鸣的关联已被广泛报道。然而，耳鸣在一些SSNHL患者中选择性发展的原因仍然难以捉摸，这促使我们推测，有耳鸣的SSNHL患者（SSNHL-T）和无耳鸣的患者（SSNHL-NT）可能表现出不同的皮质活动模式。在当前研究中，我们比较了13名SSNHL-T患者和13名SSNHL-NT患者静息态定量脑电图结果，这些患者在人口统计学特征和听力阈值方面严格匹配。通过进行全脑源定位分析并辅以功能连接分析，我们旨在确定尚未确定的皮质振荡特征，这些特征可能揭示SSNHL患者耳鸣感知的潜在先决条件。与SSNHL-NT组相比，SSNHL-T组在贝叶斯推理网络区域，如额极皮质、眶额皮质（OFC）和膝前扣带回前部皮质（pgACC），在β3和γ频段表现出显著更高的皮质活动。这表明，只有当贝叶斯推理网络更新缺失的听觉信息且基于pgACC的自上而下的守门系统积极参与时，耳鸣才会在突然听觉传入神经阻滞的大脑中发展。此外，在SSNHL-T组中观察到OFC和楔前叶之间γ频段的连接显著增加，进一步表明源自贝叶斯推理的耳鸣可能与默认模式网络相关，从而使耳鸣被视为正常。综上所述，我们的初步结果提示了SSNHL患者耳鸣选择性发展的一种可能机制。此外，这些区域可作为神经调节方法的潜在靶点，以预防SSNHL患者耳鸣的发生或长期感知。
