Traumatic brain injury pathophysiology: Difference between revisions
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{{Traumatic brain injury}} | {{Traumatic brain injury}} | ||
{{CMG}} '''Associate Editor-in-Chief''' : Deekshitha Manney | {{CMG}} '''Associate Editor-in-Chief''' : {{Deekshitha Manney}} | ||
==Overview== | ==Overview== | ||
The progression of traumatic brain injury usually involves the inflammatory response pathway. | The progression of traumatic brain injury usually involves the inflammatory response pathway. | ||
Latest revision as of 15:27, 23 December 2021
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor-in-Chief : Deekshitha Manney, M. D[2]
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 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. Cerebral edema can eventually lead to herniation of brain leading to death.
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