Abstract
Tinnitus, or phantom sound perception, leads to increased spontaneous neural firing rates and enhanced synchrony in central auditory circuits in animal models. These putative physiologic correlates of tinnitus to date have not been well translated in the brain of the human tinnitus sufferer. Using functional near-infrared spectroscopy (fNIRS) we recently showed that tinnitus in humans leads to maintained hemodynamic activity in auditory and adjacent, non-auditory cortices. Here we used fNIRS technology to investigate changes in resting state functional connectivity between human auditory and non-auditory brain regions in normal-hearing, bilateral subjective tinnitus and controls before and after auditory stimulation. Hemodynamic activity was monitored over the region of interest (primary auditory cortex) and non-region of interest (adjacent non-auditory cortices) and functional brain connectivity was measured during a 60-second baseline/period of silence before and after a passive auditory challenge consisting of alternating pure tones (750 and 8000Hz), broadband noise and silence. Functional connectivity was measured between all channel-pairs. Prior to stimulation, connectivity of the region of interest to the temporal and fronto-temporal region was decreased in tinnitus participants compared to controls. Overall, connectivity in tinnitus was differentially altered as compared to controls following sound stimulation. Enhanced connectivity was seen in both auditory and non-auditory regions in the tinnitus brain, while controls showed a decrease in connectivity following sound stimulation. In tinnitus, the strength of connectivity was increased between auditory cortex and fronto-temporal, fronto-parietal, temporal, occipito-temporal and occipital cortices. Together these data suggest that central auditory and non-auditory brain regions are modified in tinnitus and that resting functional connectivity measured by fNIRS technology may contribute to conscious phantom sound perception and potentially serve as an objective measure of central neural pathology.
Highlights
Tinnitus, the phantom perception of sound, is highly prevalent with an estimated 10–15% of adults affected in the United States [1]
Since phantom sound perception may originate from changes in multiple synchronized brain networks [15] that may extend beyond dedicated central auditory pathways, we investigated Resting state functional connectivity (RSFC) within various human auditory and non-auditory cortical areas under intact and aberrant conditions
Networks uniquely identified in tinnitus suggest that aberrant patterns of RSFC involving auditory and non-auditory regions may be essential to the central pathophysiology [45]
Summary
The phantom perception of sound, is highly prevalent with an estimated 10–15% of adults affected in the United States [1]. The underlying etiology of tinnitus is not well defined, yet is largely associated with peripheral ear pathology leading to aberrant neural activity within central auditory circuits [2, 3]. Auditory cortex in animal models of tinnitus is one region that shows increased spontaneous neural firing rates and enhanced neural synchrony [4]. These putative physiologic correlates of tinnitus in animals have yet to be explored or translated in humans and it is not known whether comparable objective indicators exist and are measurable. The ability to identify and measure putative correlates of tinnitus in humans is vital to understanding aberrant brain regions and circuits that could objectify the disease, and thereby, direct and monitor efficacy of targeted therapies
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