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Journal Article

Citation

Ladak AA, Enam SA, Ibrahim MT. World Neurosurg. 2019; ePub(ePub): ePub.

Affiliation

Medical College, Aga Khan University Hospital, Karachi, Pakistan.

Copyright

(Copyright © 2019, Elsevier Publishing)

DOI

10.1016/j.wneu.2019.07.039

PMID

31301445

Abstract

Traumatic Brain Injury (TBI) is referred to any insult to the brain resulting in primary (direct) and secondary (indirect) damages to the brain parenchyma. Secondary damages are often linked to the molecular mechanisms that occur post TBI and ensue excitotoxicity, neuroinflammation and cytokine damage, oxidative damage and eventual cell death as prominent mechanisms of cell damage. We present a review highlighting the relation of each of these mechanisms with TBI, their mode of damaging brain tissue and therapeutic correlation. We also mention the long-term sequelae and their pathophysiology in relation to TBI focusing on Parkinson's, Alzheimer's disease, Epilepsy and Chronic Traumatic Encephalopathy. Understanding of the molecular mechanisms is important to realize the secondary and long-term sequelae that follow primary TBI and devise targeted therapy for quick recovery accordingly.

Copyright © 2019 Elsevier Inc. All rights reserved.


Language: en

Keywords

Traumatic Brain Injury; cell death; excitotoxicity; molecular mechanisms; neuroinflammation; secondary brain injury

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