Cortical Oscillatory Signatures Reveal the Prerequisites for Tinnitus Perception: A Comparison of Subjects With Sudden Sensorineural Hearing Loss With and Without Tinnitus

Abstract

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.

The balance between Bayesian inference and default mode determines the generation of tinnitus from decreased auditory input: A volume entropy‐based study

“…The power spectra were compared (a) after visual artifact rejection only, and (b) after visual artifact and ICA component rejection. There was no statistically significant difference in the mean power of the delta (2–3.5 Hz), theta (4–7.5 Hz), alpha1 (8–10 Hz), alpha2 (10–12 Hz), beta 1 (13–18 Hz), beta2 (18.5–21 Hz), beta 3 (21.5–30 Hz), or gamma (30.5–44 Hz) frequency band (Han et al, 2018 ; Kim et al, 2016 ; Lee et al, 2019 ; Lee, Choi, Koo, De Ridder, & Song, 2020 ; Song et al, 2017 ; Vanneste, Song, & De Ridder, 2018 ) between the two approaches. Therefore, we reported the results of the two‐step artifact correction data.…”

Tinnitus and the Triple Network Model: A Perspective

“…It can be hypothesized that in chronic tinnitus the default mode network, which controls self-representational processing may become pathologically connected to tinnitus-provoking networks [ 89 ]. The significance of this finding is tremendous, as this may be a neurobiological rationale why in chronic tinnitus the sound becomes embodied—that is, an integral part of the self, the new normal default state [ 92 ]—thereby making treatments more difficult [ 93 ]. Furthermore, not only can tinnitus become an integral part of the self, but when suffering becomes chronic, fear can turn into anxiety and sadness into depression, all common comorbidities in tinnitus.…”

Preoperative Significance of Ipsilateral Manual Neck Compression in Patients With Pulsatile Tinnitus Secondary to Sigmoid Sinus Dehiscences and Diverticula

“…Tinnitus can be pulsatile or non-pulsatile depending on the characteristics of the perceived sound ( 1 ). Non-pulsatile tinnitus, often referred to as subjective tinnitus, is presumably caused by functional changes in the auditory and non-auditory cortices ( 2 , 3 ). Meanwhile, pulsatile tinnitus (PT) is caused by altered vascular hemodynamics, such as turbulent blood flow or vibration of a dehiscent vascular wall, or abnormal perception of the sound of normal flow, such as third-window lesions due to bony defects of the inner ear.…”