Abstract
Purpose: The anterior cingulate cortex (ACC) has been suggested to be involved in chronic subjective tinnitus. Tinnitus may arise from aberrant functional coupling between the ACC and cerebral cortex. To explore this hypothesis, we used resting-state functional magnetic resonance imaging (fMRI) to illuminate the functional connectivity (FC) network of the ACC subregions in chronic tinnitus patients.Methods: Resting-state fMRI scans were obtained from 31 chronic right-sided tinnitus patients and 40 healthy controls (age, sex, and education well-matched) in this study. Rostral ACC and dorsal ACC were selected as seed regions to investigate the intrinsic FC with the whole brain. The resulting FC patterns were correlated with clinical tinnitus characteristics including the tinnitus duration and tinnitus distress.Results: Compared with healthy controls, chronic tinnitus patients showed disrupted FC patterns of ACC within several brain networks, including the auditory cortex, prefrontal cortex, visual cortex, and default mode network (DMN). The Tinnitus Handicap Questionnaires (THQ) scores showed positive correlations with increased FC between the rostral ACC and left precuneus (r = 0.507, p = 0.008) as well as the dorsal ACC and right inferior parietal lobe (r = 0.447, p = 0.022).Conclusions: Chronic tinnitus patients have abnormal FC networks originating from ACC to other selected brain regions that are associated with specific tinnitus characteristics. Resting-state ACC-cortical FC disturbances may play an important role in neuropathological features underlying chronic tinnitus.
Highlights
Tinnitus is an auditory phantom perception like ringing, roaring, or buzzing in ears in the absence of any objective external sounds (Jastreboff, 1990; Lockwood et al, 2002; Wegger et al, 2017)
The increased functional connectivity (FC) between the rostral ACC (rACC) and left precuneus was positively correlated with the Tinnitus Handicap Questionnaires (THQ) score (r = 0.507, p = 0.008) (Figure 4A)
The increased FC between the dorsal ACC (dACC) and right superior temporal gyrus (STG) was positively correlated with the tinnitus duration (r = 0.527, p = 0.006) (Figure 4B)
Summary
Tinnitus is an auditory phantom perception like ringing, roaring, or buzzing in ears in the absence of any objective external sounds (Jastreboff, 1990; Lockwood et al, 2002; Wegger et al, 2017). Previous studies have suggested that the central nervous system (CNS) may play a major role in the pathophysiology of the tinnitus (Lockwood et al, 2002; Eggermont, 2005; Bartels et al, 2007; Chen et al, 2015a). On the basis of electrophysiological and neuroimaging studies, it has been proposed that tinnitus may be generated from the aberrant neuronal activity in the CNS by a variety of mechanisms such as dysfunctional noise canceling, up-regulation of spontaneous firing rates, increased neural synchrony, increase central noise, tonotopic map reorganization, and aberrant neural connectivity to structures within and/or outside the auditory pathway (Lockwood et al, 1998; Noreña and Eggermont, 2003; Kaltenbach et al, 2005; Noreña and Farley, 2013; Zeng, 2013). The exact neuropathological mechanism underlying tinnitus has not yet been fully elucidated
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