Mechanisms of neuropathic pain following mild blast traumatic brain injury and chronic stress.
thesisposted on 13.08.2019, 17:35 by Marcela Cruz-Haces
The incidence of mild blast traumatic brain injuryhas risen due tothe increased use of improvised explosive devices (IEDs) in militaryconflicts. Mild blast TBI (mbTBI) is especially relevant due to its lack of acutely observable symptoms, and to its association with long-term neurodegenerative and neuropsychiatric disorders. Predominantly, TBI patients often suffer from chronic stress, neuropathic pain and headaches, which greatly compromise the health and quality of life of these individuals. Treatments for neuropathic pain have been empirically found and produce little effect in lessening neuropathic pain, likely due to the lack of targeted therapies. This highlights the need for better understanding of the molecular mechanisms underlying neuropathicpain, TBI and chronic stress that could lead to mechanistic therapeutic targets. Oxidative stress is an important mechanism of the pathophysiology of neuropathic pain, TBI and chronic stress. We hypothesize that acrolein, an endogenously formed neurotoxin, is able to stay active in the body for up to 10 days, is involved in the pathophysiology of neuropathic pain in TBI and chronic stress. This study aims to correlate acrolein elevation in the body with neuropathic pain, deepen the understanding of underlying mechanisms of pain in TBI and chronic stress, and mitigate this pain with acrolein scavenging. The ultimate goal of this research is to provide therapies for TBI and chronic stress patients that can eliminate pain and significantly improve their healthand quality of life