Traumatic brain injury pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
Unlike most forms of traumatic death, a large percentage of the people killed by brain trauma do not die right away but rather days to weeks after the event.<ref>Sauaia A, Moore FA, Moore EE, Moser KS, Brennan R, Read RA, and Pons PT. 1995. Epidemiology of trauma deaths: a reassessment. ''Journal of Trauma'', Volume 38, Issue 2, Pages 185-193. PMID 7869433</ref> Rather than improving after being hospitalized, some 40% of TBI patients deteriorate.<ref>Narayan RK, Michel ME, Ansell B, Baethmann A, Biegon A, Bracken MB, Bullock MR, Choi SC, Clifton GL, Contant CF, Coplin WM, Dietrich WD, Ghajar J, Grady SM, Grossman RG, Hall ED, Heetderks W, Hovda DA, Jallo J, Katz RL, Knoller N, Kochanek PM, Maas AI, Majde J, Marion DW, Marmarou A, Marshall LF, McIntosh TK, Miller E, Mohberg N, Muizelaar JP, Pitts LH, Quinn P, Riesenfeld G, Robertson CS, Strauss KI, Teasdale G, Temkin N, Tuma R, Wade C, Walker MD, Weinrich M, Whyte J, Wilberger J, Young AB, Yurkewicz L. 2002. Clinical trials in head injury. ''Journal of Neurotrauma'', Volume 19, Issue 5, Pages 503-557. PMID 12042091</ref> Primary injury (the damage that occurs at the moment of trauma when tissues and blood vessels are stretched, compressed, and torn) is not adequate to explain this degeneration. Rather, the deterioration is caused by secondary injury, a complex set of [[biochemical cascade]]s that occur in the minutes to days following the trauma<ref>Xiong Y, Lee CP, and Peterson PL. 2001. Mitochondrial dysfunction following traumatic brain injury. In ''Head Trauma: Basic, Preclinical, and Clinical Directions''. Miller LP and Hayes RL, eds. Co-edited by Newcomb JK. 2001, John Wiley and Sons, Inc. New York. Pages 257-280.</ref> and contribute a large amount to morbidity and mortality from TBI.<ref>Sullivan PG, Rabchevsky AG, Hicks RR, Gibson TR, Fletcher-Turner A, and Scheff SW. 2000. Dose-response curve and optimal dosing regimen of cyclosporin A after traumatic brain injury in rats. ''Neuroscience'', Volume 101, Issue 2, Pages 289-295. PMID 11074152</ref> | *Unlike most forms of traumatic death, a large percentage of the people killed by brain trauma do not die right away but rather days to weeks after the event.<ref>Sauaia A, Moore FA, Moore EE, Moser KS, Brennan R, Read RA, and Pons PT. 1995. Epidemiology of trauma deaths: a reassessment. ''Journal of Trauma'', Volume 38, Issue 2, Pages 185-193. PMID 7869433</ref> Rather than improving after being hospitalized, some 40% of TBI patients deteriorate.<ref>Narayan RK, Michel ME, Ansell B, Baethmann A, Biegon A, Bracken MB, Bullock MR, Choi SC, Clifton GL, Contant CF, Coplin WM, Dietrich WD, Ghajar J, Grady SM, Grossman RG, Hall ED, Heetderks W, Hovda DA, Jallo J, Katz RL, Knoller N, Kochanek PM, Maas AI, Majde J, Marion DW, Marmarou A, Marshall LF, McIntosh TK, Miller E, Mohberg N, Muizelaar JP, Pitts LH, Quinn P, Riesenfeld G, Robertson CS, Strauss KI, Teasdale G, Temkin N, Tuma R, Wade C, Walker MD, Weinrich M, Whyte J, Wilberger J, Young AB, Yurkewicz L. 2002. Clinical trials in head injury. ''Journal of Neurotrauma'', Volume 19, Issue 5, Pages 503-557. PMID 12042091</ref> Primary injury (the damage that occurs at the moment of trauma when tissues and blood vessels are stretched, compressed, and torn) is not adequate to explain this degeneration. Rather, the deterioration is caused by secondary injury, a complex set of [[biochemical cascade]]s that occur in the minutes to days following the trauma<ref>Xiong Y, Lee CP, and Peterson PL. 2001. Mitochondrial dysfunction following traumatic brain injury. In ''Head Trauma: Basic, Preclinical, and Clinical Directions''. Miller LP and Hayes RL, eds. Co-edited by Newcomb JK. 2001, John Wiley and Sons, Inc. New York. Pages 257-280.</ref> and contribute a large amount to morbidity and mortality from TBI.<ref>Sullivan PG, Rabchevsky AG, Hicks RR, Gibson TR, Fletcher-Turner A, and Scheff SW. 2000. Dose-response curve and optimal dosing regimen of cyclosporin A after traumatic brain injury in rats. ''Neuroscience'', Volume 101, Issue 2, Pages 289-295. PMID 11074152</ref> | ||
Secondary injury events are poorly understood but are thought to include [[cerebral edema|brain swelling]], alterations in [[cerebral blood flow]], a decrease in the tissues' [[pH]], [[free radical]] overload, and [[excitotoxicity]]. These secondary processes damage neurons that were not directly harmed by the primary injury. | *Secondary injury events are poorly understood but are thought to include [[cerebral edema|brain swelling]], alterations in [[cerebral blood flow]], a decrease in the tissues' [[pH]], [[free radical]] overload, and [[excitotoxicity]]. These secondary processes damage neurons that were not directly harmed by the primary injury. | ||
==References== | ==References== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
The progression of traumatic brain injury usually involves the inflammatory response pathway.
Pathophysiology
- Unlike most forms of traumatic death, a large percentage of the people killed by brain trauma do not die right away but rather days to weeks after the event.[1] Rather than improving after being hospitalized, some 40% of TBI patients deteriorate.[2] Primary injury (the damage that occurs at the moment of trauma when tissues and blood vessels are stretched, compressed, and torn) is not adequate to explain this degeneration. Rather, the deterioration is caused by secondary injury, a complex set of biochemical cascades that occur in the minutes to days following the trauma[3] and contribute a large amount to morbidity and mortality from TBI.[4]
- Secondary injury events are poorly understood but are thought to include brain swelling, alterations in cerebral blood flow, a decrease in the tissues' pH, free radical overload, and excitotoxicity. These secondary processes damage neurons that were not directly harmed by the primary injury.
References
- ↑ Sauaia A, Moore FA, Moore EE, Moser KS, Brennan R, Read RA, and Pons PT. 1995. Epidemiology of trauma deaths: a reassessment. Journal of Trauma, Volume 38, Issue 2, Pages 185-193. PMID 7869433
- ↑ Narayan RK, Michel ME, Ansell B, Baethmann A, Biegon A, Bracken MB, Bullock MR, Choi SC, Clifton GL, Contant CF, Coplin WM, Dietrich WD, Ghajar J, Grady SM, Grossman RG, Hall ED, Heetderks W, Hovda DA, Jallo J, Katz RL, Knoller N, Kochanek PM, Maas AI, Majde J, Marion DW, Marmarou A, Marshall LF, McIntosh TK, Miller E, Mohberg N, Muizelaar JP, Pitts LH, Quinn P, Riesenfeld G, Robertson CS, Strauss KI, Teasdale G, Temkin N, Tuma R, Wade C, Walker MD, Weinrich M, Whyte J, Wilberger J, Young AB, Yurkewicz L. 2002. Clinical trials in head injury. Journal of Neurotrauma, Volume 19, Issue 5, Pages 503-557. PMID 12042091
- ↑ Xiong Y, Lee CP, and Peterson PL. 2001. Mitochondrial dysfunction following traumatic brain injury. In Head Trauma: Basic, Preclinical, and Clinical Directions. Miller LP and Hayes RL, eds. Co-edited by Newcomb JK. 2001, John Wiley and Sons, Inc. New York. Pages 257-280.
- ↑ Sullivan PG, Rabchevsky AG, Hicks RR, Gibson TR, Fletcher-Turner A, and Scheff SW. 2000. Dose-response curve and optimal dosing regimen of cyclosporin A after traumatic brain injury in rats. Neuroscience, Volume 101, Issue 2, Pages 289-295. PMID 11074152