The salience network is recruited in response to attention-grabbing changes in the environment, and it is anchored by the dorsal anterior cingulate cortex and orbital frontoinsular cortices, with robust connections with subcortical and limbic structures. Conversely, the DMN is activated when current situational demands are insufficient to capture our attention (e.g., during monotonous tasks); it encompasses a distributed set of regions including the medial and lateral temporal cortices and inferior lateral parietal cortices, centered on midline “hubs,” including the dorsomedial prefrontal and posterior cingulate cortices.Jilka et al. have monitored the activity of these networks in control and TBI subjects while they carried out two cognitive control tasks: a stop signal task in which participants were shown either left or right arrows and asked to press the corresponding left or right keys - except when a red dot was shown; and a motor switching task in which participants learned to respond to blue targets with their left hand and red targets with their right hand - except when they were instructed to switch their response. Successful performance on both tasks correlated with increased functional connectivity between the right anterior insula node of the salience network and the DMN. Deficits in inhibition seen in TBI patients correlated with decreased functional connectivity. Here is their abstract:
Interactions between the Salience Network (SN) and the Default Mode Network (DMN) are thought to be important for cognitive control. However, evidence for a causal relationship between the networks is limited. Previously, we have reported that traumatic damage to white matter tracts within the SN predicts abnormal DMN function. Here we investigate the effect of this damage on network interactions that accompany changing motor control. We initially used fMRI of the Stop Signal Task to study response inhibition in humans. In healthy subjects, functional connectivity (FC) between the right anterior insula (rAI), a key node of the SN, and the DMN transiently increased during stopping. This change in FC was not seen in a group of traumatic brain injury (TBI) patients with impaired cognitive control. Furthermore, the amount of SN tract damage negatively correlated with FC between the networks. We confirmed these findings in a second group of TBI patients. Here, switching rather than inhibiting a motor response: (1) was accompanied by a similar increase in network FC in healthy controls; (2) was not seen in TBI patients; and (3) tract damage after TBI again correlated with FC breakdown. This shows that coupling between the rAI and DMN increases with cognitive control and that damage within the SN impairs this dynamic network interaction. This work provides compelling evidence for a model of cognitive control where the SN is involved in the attentional capture of salient external stimuli and signals the DMN to reduce its activity when attention is externally focused.