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      Damage to the Salience Network and interactions with the Default Mode Network.

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          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.

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          Author and article information

          Journal
          J. Neurosci.
          The Journal of neuroscience : the official journal of the Society for Neuroscience
          1529-2401
          0270-6474
          Aug 13 2014
          : 34
          : 33
          Affiliations
          [1 ] Computational, Cognitive and Clinical Neuroimaging Laboratory, Centre for Neuroscience, Division of Experimental Medicine, Imperial College London, London, W12 0NN, United Kingdom, Department of Psychology, Goldsmiths College, University of London, SE14 6NW, United Kingdom.
          [2 ] Computational, Cognitive and Clinical Neuroimaging Laboratory, Centre for Neuroscience, Division of Experimental Medicine, Imperial College London, London, W12 0NN, United Kingdom.
          [3 ] Systems and Restorative Neurology, University of Cambridge Neurology Unit, Herchel Smith Building for Brain and Mind Sciences Robinson Way, Cambridge, CB2 0SZ, United Kingdom, and.
          [4 ] Department of Psychology, Goldsmiths College, University of London, SE14 6NW, United Kingdom.
          [5 ] Oxford University, Department of Experimental Psychology, Oxford, OX1 3UD, United Kingdom.
          [6 ] Computational, Cognitive and Clinical Neuroimaging Laboratory, Centre for Neuroscience, Division of Experimental Medicine, Imperial College London, London, W12 0NN, United Kingdom, MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital Campus, London, W12 0NN, United Kingdom.
          [7 ] Computational, Cognitive and Clinical Neuroimaging Laboratory, Centre for Neuroscience, Division of Experimental Medicine, Imperial College London, London, W12 0NN, United Kingdom, david.sharp@imperial.ac.uk.
          Article
          34/33/10798
          10.1523/JNEUROSCI.0518-14.2014
          25122883
          c62ce1ee-d433-424a-bfe8-9500dd8c111e
          Copyright © 2014 Jilka et al.
          History

          Default Mode Network,functional connectivity,psychophysiological interactions,salience network,traumatic brain injury

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