“…Indeed, in the minutes, hours, and days post‐injury, the pathophysiology of brain injury is dominated by pathological levels of extracellular glutamate (Vespa et al, ), mitochondrial function (Verweij et al, ), cerebral blood flow (Martin et al, ), metabolic rates of glucose and oxygen (Hattori et al, ; Meyer, Kondo, Nomura, Sakamoto, & Teraura, ), and neurovascular coupling (del Zoppo & Mabuchi, ; Povlishock & Kontos, ) among others (Busl & Greer, ; Greve & Zink, ; Maas, Stocchetti, & Bullock, ; Werner & Engelhard, ). Furthermore, the timing of these dynamics may itself depend on a number of additional factors, including strain magnitude and strain rate, which have been shown in in‐vitro models of neuronal compression to affect the time of neuronal death and the pathomorphology and extent of neural population injury, respectively (Bar‐Kochba, Scimone, Estrada, & Franck, ). However, within a month post‐injury and independent of cognitive function, many of these processes are no longer as prominent (Bergsneider et al, ; Inoue et al, ; Vespa et al, ; Xiong, Gu, Peterson, Muizelaar, & Lee, ) and changes in neuronal connectivity as a consequence of these injuries are now the prevailing source (Adams et al, ; Graham, Adams, Murray, & Jennett, ; Graham, Maxwell, Adams, & Jennett, ; Lutkenhoff et al, , ).…”