“…In that case, the asymptomatic performance of the two groups with individual lesions could be explained in terms of a shift towards an alternative neural substrate that efficiently masked the impairment created by the prefrontal lesion. We have previously argued [Mogensen, 2011a[Mogensen, , 2011b[Mogensen, , 2012a[Mogensen, , 2012b[Mogensen, , 2014[Mogensen, , 2015Mogensen and Malá, 2009] that posttraumatically, the neural substrate of task mediation is reorganized in such ways that within the preserved regions of the brain a given structure can demonstrate either an increased or decreased contribution to the mediation of the task. In support of that, we have reported findings suggesting that during posttraumatic recovery of task performance on certain tasks, there is a mutual interdependence between the prefrontal cortex and the hippocampus [Mogensen et al, 2004a[Mogensen et al, , 2005[Mogensen et al, , 2007.…”