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It is now widely accepted that cognitive control depends on the integrated operation of large-scale distributed brain networks. Recent methodological advances allow both structural and functional connectivity (FC) within these networks to be studied non- invasively in vivo. These approaches hold the promise of dramatically extending our understanding of the impact of traumatic brain injury (TBI) on cognitive control, which has the potential to help determine strategic targets for the rehabilitation of individuals with TBI. In the current thesis, structural and functional magnetic resonance imaging is combined to test the general hypothesis that cognitive deficits after TBI arise from functional disconnection within brain networks that mediate cognitive functions. Of particular interest are the interactions between two brain networks known as the Salience Network (SN) and the Default Mode Network (DMN). These networks are thought to be important for cognitive control however, how these networks interact during cognitive control is limited. This thesis largely investigates the effect of TBI on network interactions that accompany changing motor control. Functional MRI of the Stop Signal Task (SST) is initially used to study response inhibition. In healthy subjects, 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 TBI patients with impaired cognitive control. Furthermore, the amount of damage to the underlying white matter tract negatively correlated with the strength of FC between the networks. These findings are confirmed in a second group of TBI patients. In the second group, 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. I also replicate this pattern of structure-function in a group of elderly participants who demonstrate similar cognitive control impairments as the TBI group. The findings show that FC between the rAI and DMN increases with cognitive control, and that the ability to efficiently regulate the FC between the rAI and DMN can be predicted by the structural integrity within a remote brain network previously proposed to be involved in switching between internally and externally directed attention. This work provides 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. It also identifies DMN dysfunction as underlying various cognitive deficits after TBI, and confirms the relevance of white matter damage in the development of brain dysfunctions after TBI.