Traumatic brain injury pathophysiology: Difference between revisions

Jump to navigation Jump to search
 
(One intermediate revision by the same user not shown)
Line 2: Line 2:
{{Traumatic brain injury}}
{{Traumatic brain injury}}


{{CMG}} '''Associate Editor-in-Chief''' : Deekshitha Manney, MD
{{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

Traumatic brain injury Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Traumatic Brain Injury from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Neurocognitive Disorder due to Traumatic Brain Injury

Diagnosis

Diagnostic study of choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X Ray

Echocardiography and Ultrasound

CT

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Interventions

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Traumatic brain injury pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Traumatic brain injury pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Traumatic brain injury pathophysiology

CDC on Traumatic brain injury pathophysiology

Traumatic brain injury pathophysiology in the news

Blogs on Traumatic brain injury pathophysiology

Directions to Hospitals Treating Traumatic brain injury

Risk calculators and risk factors for Traumatic brain injury pathophysiology

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

  1. 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
  2. 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
  3. 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.
  4. 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


Template:WikiDoc Sources