“…Returning to the biomechanical deformation effects reviewed above, long-coursing axons are going to be more vulnerable, particularly interhemispheric connections, especially the corpus callosum and anterior commissure (Cecil et al, 1998;Holshouser et al, 2006;Inglese et al, 2005b;Mathias et al, 2004;Wilde et al, 2006a;Wilde et al, 2006c). Thus, neuropsychological tasks that require interhemispheric integration and0or multiple intracortical connections often show differences in the form of slowed responding, even in those with mTBI (Mathias et al, 2004) So, the hypothesis put forth in this section is that the biomechanics of brain injury simultaneously disrupt neurological function in the upper brainstem, pituitaryhypothalamic axis, medial temporal lobe, and basal forebrain concomitant with irritative injury to the vasculature and meninges, which gives rise to the symptoms observed in the post-concussive state and the neuropsychological sequela associated with such an injury. How rapidly these neural, dural, and vascular areas return to homeostasis or recovery from some adaptive mechanism or do not recover, provides the biological basis for the symptoms expressed.…”