Aberrant Functional and Causal Connectivity in Acute Tinnitus With Sensorineural Hearing Loss

Yuexin Cai,Mingwei Xie,Liping Lan,Zhaopeng Tong,Xiaoyan Wu,Yun Su,Jiahong Li,Yiqing Zheng,Wenchao Xu,Guisheng Chen,Caiping Dang,Jun Shen,Fei Zhao

doi:10.3389/fnins.2020.00592

Abstract

PurposeThe neural bases in acute tinnitus remains largely undetected. The objective of this study was to identify the alteration of the brain network involved in patients with acute tinnitus and hearing loss.MethodsAcute tinnitus patients (n = 24) with hearing loss and age-, sex-, education-matched healthy controls (n = 21) participated in the current study and underwent resting-state functional magnetic resonance imaging (fMRI) scanning. Regional homogeneity and amplitude of low-frequency fluctuation were used to investigate the local spontaneous neural activity and functional connectivity (FC), and Granger causality analysis (GCA) was used to analyze the undirected and directed connectivity of brain regions.ResultsCompared with healthy subjects, acute tinnitus patients had a general reduction in FC between auditory and non-auditory brain regions. Based on FC analysis, the superior temporal gyrus (STG) revealed reduced undirected connectivity with non-auditory brain regions including the amygdala (AMYG), nucleus accumbens (NAc), the cerebellum, and postcentral gyrus (PoCG). Using the GCA algorithm, increased effective connectivity from the right AMYG to the right STG, and reduced connectivity from the right PoCG to the left NAc was observed in acute tinnitus patients with hearing loss. The pure-tone threshold was positively correlated with FC between the AMYG and STG, and negatively correlated with FC between the left NAc and the right PoCG. In addition, a negative association between the GCA value from the right PoCG to the left NAc and the THI scores was observed.ConclusionAcute tinnitus patients have aberrant FC strength and causal connectivity in both the auditory and non-auditory cortex, especially in the STG, AMYG, and NAc. The current findings will provide a new perspective for understanding the neuropathophysiological mechanism in acute tinnitus.

Highlights

Tinnitus is defined as the perception of a phantom sound in the absence of an internal or external sound source (Chen et al, 2017c; Cai et al, 2018; Vanneste et al, 2019)
There was no significant difference in the regional homogeneity (ReHo) value and the fractional ALFF (fALFF) value between idiopathic sudden sensorineural hearing loss (ISSNHL) patients and the healthy controls in any brain region (p > 0.05, threshold-free cluster enhancement (TFCE) with family-wise error (FWE) correction)
The reduced functional connectivity (FC) was observed between the right superior temporal gyrus (STG) and the right CERCRU2_R, AMYG, postcentral gyrus (PoCG), the left CER8, CER6, MOG, ITG, and the PCL (p < 0.05, TFCE with FWE correction; Table 3 and Figure 1)

Summary

Introduction

Tinnitus is defined as the perception of a phantom sound in the absence of an internal or external sound source (Chen et al, 2017c; Cai et al, 2018; Vanneste et al, 2019). It is widely accepted that tinnitus in caused by peripheral cochlear impairment, and the aberrant activity in the central nervous system (Chen et al, 2017b; Cai et al, 2018). A large number of neuroimaging studies have reported that abnormality of central activities are involved in both auditory and non-auditory brain regions for chronic tinnitus (Chen et al, 2017c; Vanneste et al, 2019)

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