Willman J, Kurian AL, Lucke-Wold B. Mechanisms of vascular injury in neurotrauma: A critical review of the literature. World J Meta-Anal 2024; 12(3): 95417 [DOI: 10.13105/wjma.v12.i3.95417]
Corresponding Author of This Article
Jonathan Willman, MD, College of Medicine, University of Florida, 1600 SW Archer Road, Gainesville, FL 32610, United States. jonathanwillman@ufl.edu
Research Domain of This Article
Neurosciences
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Meta-Anal. Sep 18, 2024; 12(3): 95417 Published online Sep 18, 2024. doi: 10.13105/wjma.v12.i3.95417
Mechanisms of vascular injury in neurotrauma: A critical review of the literature
Jonathan Willman, Annu Lisa Kurian, Brandon Lucke-Wold
Jonathan Willman, College of Medicine, University of Florida, Gainesville, FL 32610, United States
Annu Lisa Kurian, College of Medicine, Florida State University, Tallahassee, FL 32304, United States
Brandon Lucke-Wold, Department of Neurosurgery, University of Florida, Gainesville, FL 32611, United States
Co-corresponding authors: Jonathan Willman and Brandon Lucke-Wold.
Author contributions: Willman J worked with the other authors in conceptualization. He planned the structure of the paper, orchestrated the first draft, and wrote significant portions of the first draft. He was a co-corresponding author and the primary editor; Kurian AL contributed to the conceptualization and wrote significant portions of the first draft; Lucke-Wold B contributed to the conceptualization and helped orchestrate the project. He was a co-corresponding author. He provided senior oversight and quality review.
Conflict-of-interest statement: All authors declare no conflict of interest.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Jonathan Willman, MD, College of Medicine, University of Florida, 1600 SW Archer Road, Gainesville, FL 32610, United States. jonathanwillman@ufl.edu
Received: April 9, 2024 Revised: July 20, 2024 Accepted: July 29, 2024 Published online: September 18, 2024 Processing time: 156 Days and 15.3 Hours
Abstract
One in every two individuals will experience a traumatic brain injury in their lifetime with significant impacts on the global economy and healthcare system each year. Neurovascular injury is a key aspect of neurotrauma to both the brain and the spinal cord and an important avenue of current and future research seeking innovative therapies. In this paper, we discuss primary and secondary neurotrauma, mechanisms of injury, the glymphatic system, repair and recovery. Each of these topics are directly connected to the vasculature of the central nervous system, affecting severity of injury and recovery. Consequently, neurovascular injury in trauma represents a promising target for future therapeutics and innovation.
Core Tip: Primary neurotrauma is an initial mechanical insult to the central nervous system. Secondary neurotrauma involves metabolic and cellular derangements that occur days to months after the initial insult. Together, this neurotrauma disrupts cerebral autoregulation and neurovascular coupling, leading to derangements in neurovascular flow and blood-brain barrier dysfunction. Similarly, the glymphatic system, responsible for clearing waste products through the perivascular space, becomes impaired following neurotrauma, leading to increased protein deposition and cognitive decline. Emerging therapeutics focus on reducing neuroedema, decreasing blood-brain barrier dysfunction, and promoting neuroregeneration.