Figure 3

Functional deficits associated with dysfunction of the cognitive control network (CCN) in chronic tinnitus (n = 15) compared to healthy controls (n = 15). (A) Neurocognitive network dysfunction: Boxplots highlight significantly attenuated activation of the posterior right middle frontal gyrus (rMFG) during the n-back task in chronic tinnitus; significantly lower baseline connectivity between the right anterior insula (rAI) node of the salience network and the affected CCN node (rMFG) in chronic tinnitus; and significantly higher baseline connectivity between the affected CCN node (rMFG) and nodes of autobiographical memory network (AMN), including the left posterior cingulate cortex (PCC, illustrated here) and the left medial prefrontal cortex (mPFC). (B) Engagement of neurocognitive networks. Illustration of large-scale neurocognitive network functioning in healthy controls (left) and chronic tinnitus (right) with nodes of the CCN (red), SN (green) and AMN (blue). Here, while healthy controls show higher SN-CCN baseline connectivity associated with greater CCN activation, people experiencing chronic tinnitus show lower SN-CCN baseline connectivity and decreased CCN activation. This may underpin less proficient network switching, characterized by higher CCN-AMN baseline connectivity in chronic tinnitus, associated with difficulty switching attention away from the auditory environment (e.g. scanner noise), **p < 0.01; *p < 0.05.