Changes in the Default Mode Network

From: <a id="null" class="null" href="https://jamanetwork.com/journals/jamaneurology/fullarticle/1688414">https://jamanetwork.com/journals/jamaneurology/fullarticle/1688414</a>

Previous studies investigating the DMN during the resting state in TBI have found alterations that reflect both decreases<a class="ref-link section-jump-link" href="https://jamanetwork.com/journals/jamaneurology/fullarticle/1688414#noi130036r11" data-tab-toggle=".tab-nav-references">11</a> and increases in functional connectivity.<a class="ref-link section-jump-link" href="https://jamanetwork.com/journals/jamaneurology/fullarticle/1688414#noi130036r12" data-tab-toggle=".tab-nav-references">12</a>The increases have been interpreted as compensatory or adaptive mechanisms because they were often positively correlated with cognitive outcome.<a class="ref-link section-jump-link" href="https://jamanetwork.com/journals/jamaneurology/fullarticle/1688414#noi130036r8" data-tab-toggle=".tab-nav-references">8</a>,<a class="ref-link section-jump-link" href="https://jamanetwork.com/journals/jamaneurology/fullarticle/1688414#noi130036r34" data-tab-toggle=".tab-nav-references">34</a> Another possible interpretation is that this increased connectivity, measured in voxels surrounding the DMN nodes, reflects a diffusion of the DMN nodes during recovery from TBI. This latter interpretation also may be supported by the fact that the white matter injury found in the cingulum in TBI precludes the functional inhibition of areas surrounding these nodes. We suggest that the increases found in frontal areas may reflect compensation because the amplitude of the fluctuations in these regions correlated with performance, but the increase in the spread of connectivity around the PPC may reflect a loss of directionality in the connectivity caused by the injury. On the other hand, Mayer et al<a class="ref-link section-jump-link" href="https://jamanetwork.com/journals/jamaneurology/fullarticle/1688414#noi130036r8" data-tab-toggle=".tab-nav-references">8</a> described a pattern of decreased long-distance functional connectivity between the nodes of the DMN (ie, between anterior and posterior nodes).Previous studies investigating the DMN during the resting state in TBI have found alterations that reflect both decreases<a class="ref-link section-jump-link" href="https://jamanetwork.com/journals/jamaneurology/fullarticle/1688414#noi130036r11" data-tab-toggle=".tab-nav-references">11</a> and increases in functional connectivity.<a class="ref-link section-jump-link" href="https://jamanetwork.com/journals/jamaneurology/fullarticle/1688414#noi130036r12" data-tab-toggle=".tab-nav-references">12</a>The increases have been interpreted as compensatory or adaptive mechanisms because they were often positively correlated with cognitive outcome.<a class="ref-link section-jump-link" href="https://jamanetwork.com/journals/jamaneurology/fullarticle/1688414#noi130036r8" data-tab-toggle=".tab-nav-references">8</a>,<a class="ref-link section-jump-link" href="https://jamanetwork.com/journals/jamaneurology/fullarticle/1688414#noi130036r34" data-tab-toggle=".tab-nav-references">34</a> Another possible interpretation is that this increased connectivity, measured in voxels surrounding the DMN nodes, reflects a diffusion of the DMN nodes during recovery from TBI. This latter interpretation also may be supported by the fact that the white matter injury found in the cingulum in TBI precludes the functional inhibition of areas surrounding these nodes. We suggest that the increases found in frontal areas may reflect compensation because the amplitude of the fluctuations in these regions correlated with performance, but the increase in the spread of connectivity around the PPC may reflect a loss of directionality in the connectivity caused by the injury. On the other hand, Mayer et al<a class="ref-link section-jump-link" href="https://jamanetwork.com/journals/jamaneurology/fullarticle/1688414#noi130036r8" data-tab-toggle=".tab-nav-references">8</a> described a pattern of decreased long-distance functional connectivity between the nodes of the DMN (ie, between anterior and posterior nodes).

Arenivas et al<a class="ref-link section-jump-link" href="https://jamanetwork.com/journals/jamaneurology/fullarticle/1688414#noi130036r11" data-tab-toggle=".tab-nav-references">11</a> studied connectivity within the nodes of the DMN (examined DMN functional connectivity in a cohort of patients 6 to 11 months after TBI), and found decreases in the core nodes of the DMN. We suggest that the increased connectivity in areas surrounding DMN nodes, which we found in the late chronic stage, might represent the brain’s attempt to compensate functionally for weaker connectivity within DMN nodes caused by structural damage after traumatic axonal injury.

Augmented functional connectivity in the anterior and posterior areas of the DMN.  Reductions within the fibers corresponding to the cingulum, and the FA of this bundle was correlated with the increased connectivity of the frontal node of the DMN. The cingulum is a long, medial associative bundle that runs within the cingulate gyrus all around the corpus callosum, connecting the medial frontal and parietal lobes.<a class="ref-link section-jump-link" href="https://jamanetwork.com/journals/jamaneurology/fullarticle/1688414#noi130036r36" data-tab-toggle=".tab-nav-references">36</a> This finding suggests that damage to this fascicle leads to functional reorganization consisting of increased local connectivity surrounding the nodes of the network, probably resulting from decreased interconnectivity between the frontal and parietal nodes.