Traumatic brain injury: Symptoms to systems in the 21st century

创伤性脑损伤 神经科学 医学 心理学 医疗急救 精神科
作者
Geoffrey P. Dobson,Jodie L. Morris,Hayley L. Letson
出处
期刊:Brain Research [Elsevier BV]
卷期号:1845: 149271-149271 被引量:3
标识
DOI:10.1016/j.brainres.2024.149271
摘要

Severe traumatic brain injury (TBI) is a devastating injury with a mortality of ∼ 25-30 %. Despite decades of high-quality research, no drug therapy has reduced mortality. Why is this so? We argue two contributing factors for the lack of effective drug therapies include the use of specific-pathogen free (SPF) animals for translational research and the flawed practice of single-nodal targeting for drug design. A revolution is required to better understand how the whole body responds to TBI, identify new markers of its progression, and discover new system-acting drugs to treat it. In this review, we present a brief history of TBI, discuss its system's pathophysiology and propose a new research strategy for the 21st century. TBI progression develops from injury signals radiating from the primary impact, which can cause local ischemia, hemorrhage, excitotoxicity, cellular depolarization, immune dysfunction, sympathetic hyperactivity, blood brain barrier breach, coagulopathy and whole-body dysfunction. Metabolic reprograming of immune cells drives neuroinflammation and secondary injury processes. We propose if sympathetic hyperactivity and immune cell activation can be corrected early, cardiovascular function and endothelial-glycocalyx-mitochondrial coupling can be restored, and secondary injury minimized with improved patient outcomes. The therapeutic goal is to switch the injury phenotype to a healing phenotype by restoring homeostasis and maintaining sufficient tissue O
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