Abstract
Traumatic brain injury (TBI) is the leading cause of death and disability in the world’s population under 45 years of age. About 10% of cases of TBI are severe (Glasgow Coma Scale [GCS] score ≤ 8 points); in this subgroup, the incidence of poor neurological outcome (severe disability, vegetative state or death) still exceeds 55% inmany centers [2]. The endpoints in the early treatment of TBI are adequate and aggressive resuscitation and patient management in the neurointensive care unit is focused on the avoidance and treatment of high intracranial pressure (ICP). To date, no neuroprotective therapy has proven effective in controlled clinical trials involving severe TBI and the International Mission for Prognosis and Analysis of Clinical Trials inTBI (IMPACT) study showed that despite a significant reduction in mortality, neurological sequelae in TBI survivors have not changed significantly in the last 25 years [3].
“The lessons to be learnt, in both science and the law, are to question your assumptions, to be open to new evidence, and not to accept statements from witnesses until their reliability has been verified” (Ekert and Vaux, 2005) [1]
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Sahuquillo, J., Merino, MA., Airado, C. (2012). Mitochondrial Dysfunction after Traumatic Brain Injury. In: Vincent, JL. (eds) Annual Update in Intensive Care and Emergency Medicine 2012. Annual Update in Intensive Care and Emergency Medicine, vol 2012. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-25716-2_64
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DOI: https://doi.org/10.1007/978-3-642-25716-2_64
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