Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2018;16(8):1224-1238.
doi: 10.2174/1570159X15666170613083606.

Recent Advances in Pathophysiology of Traumatic Brain Injury

Affiliations
Review

Recent Advances in Pathophysiology of Traumatic Brain Injury

Parmeet Kaur et al. Curr Neuropharmacol. 2018.

Abstract

Background: Traumatic brain injury (TBI) constitutes the primary reason for mortality and morbidity in persons worldwide below 45 years of age. 1.7 million Traumatic events occur yearly in the United States alone, considering for 50,000 deaths. In severe traumatic brain injury sufferers, a considerable achievement attained in treating short-term consequences; but till date, huge failures are occurring in researcher's capability to render severe traumatic brain injury sufferers to an elevated degree of performing.

Methods: Initial damage force results in Primary brain injury, causing tissue destruction and distortion in the early post-injury period. These secondary injuries from TBI cause changes in cell performance and dissemination of trauma via activities like free-radical generation, depolarization, and formation of edema, excitotoxicity, and disruption of blood brain barrier, calcium homeostasis, and intracranial hematoma. The expectation for developing effect in TBI sufferers is the best knowledge of these activities and enhancement of remedies that restrict secondary brain damage.

Results: The focal point of this study is on knowing the complex outburst of secondary impairments and studying the pathophysiology of TBI which provides alternative treatment benefits.

Conclusion: While injured persons demonstrate dissimilar levels of harm and every case is novel with specific recovery profiles, this article strengthens the recent pathophysiological sight of TBI mainly attention on oxidative stress, excitotoxicity, cerebral oxygenation and cerebral blood flow (CBF), development of edema, and inflammatory activities. For initial research acknowledgment of these recurring factors could permit clarification of possible beneficial targets.

Keywords: Traumatic brain injury; excitotoxicity; inflammation; oxidative stress; primary brain injury; secondary injury..

PubMed Disclaimer

Figures

Fig. (1)
Fig. (1)
Pathophysiology of Primary Brain Injury.
Fig. (2)
Fig. (2)
Contributing events in the pathophysiology of Secondary Brain Injury.
Fig. (3)
Fig. (3)
Free radical generation that leads to oxidative stress. (The color version of the figure is available in the electronic copy of the article).

References

    1. Langlois J.A., Rutland-Brown W., Wald M.M. The epidemiology and impact of traumatic brain injury: a brief overview. J. Head Trauma Rehabil. 2006;21(5):375–378. [http://dx.doi.org/10.1097/ 00001199-200609000-00001]. [PMID: 16983222]. - PubMed
    1. Thurman D. Traumatic Brain Injury in the United States: A Report to Congress. Centers for Disease Control and Prevention; 1999.
    1. Freire M.A. Pathophysiology of neurodegeneration following traumatic brain injury. West Indian Med. J. 2012;61(7):751–755. [PMID: 23620976]. - PubMed
    1. Thurman D.J., Alverson C., Browne D., Dunn K.A., Guerrero J., Johnson R., Johnson V., Langlois J., Pilkey D., Sniezek J.E.
    1. Nolan S. Traumatic brain injury: a review. Crit. Care Nurs. Q. 2005;28(2):188–194. [http://dx.doi.org/10.1097/00002727-200504000-00010]. [PMID: 15875448]. - PubMed