Abstract
Tinnitus (ringing in the ears) is a common auditory sensation that can become a chronic debilitating health condition with pervasive effects on health and wellbeing, substantive economic burden, and no known cure. Here we investigate if impaired functioning of the cognitive control network that directs attentional focus is a mechanism erroneously maintaining the tinnitus sensation. Fifteen people with chronic tinnitus and 15 healthy controls matched for age and gender from the community performed a cognitively demanding task known to activate the cognitive control network in this functional magnetic resonance imaging study. We identify attenuated activation of a core node of the cognitive control network (the right middle frontal gyrus), and altered baseline connectivity between this node and nodes of the salience and autobiographical memory networks. Our findings indicate that in addition to auditory dysfunction, altered interactions between non-auditory neurocognitive networks maintain chronic tinnitus awareness, revealing new avenues for the identification of effective treatments.
Highlights
Investigations of the neural correlates of chronic tinnitus have indicated involvement of non-auditory regions, including the prefrontal, anterior cingulate and insula cortices, the amygdala, and the hippocampal formation[4,5]
The increased cognitive control network (CCN)-autobiographical memory networks (AMN) connectivity between the right middle frontal gyrus (rMFG) and left posterior cingulate cortex (PCC) node was significantly correlated with higher ratings of scanner noise intrusion during task performance, r(30) = 0.43, p = 0.019, 95% BCa CI [0.07, 0.71]. These findings suggest that disrupted salience network (SN)-CCN and CCN-AMN connectivity may have a core role in perpetuating awareness of chronic tinnitus
Decreased SN-CCN connectivity may underpin dysfunction of the CCN and ineffective network-switching, characterised by increased CCN-AMN connectivity and the experience of greater difficulty engaging in goal-directed behavior (Fig. 3B)
Summary
Investigations of the neural correlates of chronic tinnitus have indicated involvement of non-auditory regions, including the prefrontal, anterior cingulate and insula cortices, the amygdala, and the hippocampal formation[4,5] This has led to the idea of a ‘tinnitus network’, typically characterized by altered auditory processing that generates the tinnitus sensation, which becomes associated with heightened attention and emotions (prefrontal cortex, anterior cingulate, insula, amygdala), consolidating memory of the sound (hippocampal region)[4,6]. By this account, the involvement of non-auditory brain regions in chronic tinnitus is viewed as a consequence or down-stream effect of the persistent tinnitus sensation, typically associated with its more pervasive effects on an individual’s psychosocial wellbeing[4]. 15 people with chronic tinnitus from the community and 15 healthy controls matched for age and gender performed a cognitively demanding task (the ‘n-back’ task), which is known to activate the CCN, while we measured blood oxygen level-dependent (BOLD) responses using functional magnetic resonance imaging (fMRI)
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