Although little is known about the natural history of headache after TBI, it has been reported that TBI-attributed headache was persistent over five years or longer after TBI [12, 14, 26, 27].
Although alcohol use increases the risk of experiencing TBI, it remains unclear whether outcomes in alcohol-impaired TBI patients are different from those of unimpaired patients.
In an experimental model of diffuse TBI, it was recently shown that Epo, administrated intravenously up to 30 minutes after TBI, not only reverses cerebral edema but also significantly restores brain tissue oxygenation to normal levels [55].
In evaluating the effectiveness of clinical interventions for TBI it is important to measure disability accurately.
While this argument might be advanced when considering severe TBI, it does not seem plausible in cases of mild TBI.
Since analysis was restricted to mild and moderate TBI, it is unclear whether these findings also apply to severe TBI.
Although rehabilitation therapy is considered important for TBI, it is anticipated that regenerative therapy will soon be available as a promising treatment for these patients.
As neuroscientists and clinician researchers initiate programs to meet the growing demand to understand and effectively treat TBI, it is important to consider engineering principles in the selection of the most appropriate preclinical model to use.
20 ROS are key mediators of secondary cell damage after a neurological insult, including TBI; it is therefore unsurprising that a less tightly coupled ETC may confer a cell survival advantage after injury.
These experimental data have shown that although propofol has neuroprotective effects on TBI, it is not as effective as magnesium, and it attenuates the neuroprotective effects of magnesium sulphate on secondary injury factors following traumatic brain injury.
In an experimental model of diffuse TBI, it was recently shown that Epo, administrated intravenously up to 30 minutes after TBI, not only reverses cerebral edema but also significantly restores brain tissue oxygenation to normal levels [ 55].
