Abstract
There is strong evidence indicating that the social environment triggers changes to the psychological stress response and glucocorticoid receptor function. Considerable literature links the subsequent changes in stress resiliency to physical health. Here, converging evidence for the modulatory role of chronic psychological stress in the recovery process following spinal cord injury (SCI) is presented. Despite the considerable advances in SCI research, we are still unable to identify the causes of variability in patients’ recovery following injury. We propose that individuals’ past and present life experiences (in the form of stress exposure) may significantly modulate patients’ outcome post-SCI. We propose a theoretical model to explain the negative impact of chronic psychological stress on physical and psychological recovery. The stress experienced in life prior to SCI and also as a result of the traumatic injury, could compromise glucocorticoid receptor sensitivity and function, and contribute to high levels of inflammation and apoptosis post-SCI, decreasing the tissue remaining at the injury site and undermining recovery of function. Both stress-induced glucocorticoid resistance and stress-induced epigenetic changes to the glucocorticoid receptor can modulate the nuclear factor-kappa B regulated inflammatory pathways and the Bcl-2 regulated apoptosis pathways. This model not only contributes to the theoretical understanding of the recovery process following injury, but also provides concrete testable hypotheses for future studies.
Highlights
When individuals suffer an spinal cord injury (SCI), for example, placing them at high-risk of suffering from chronic psychological stress [95, 96], past exposure to a stressful environment resulting in epigenetic changes that compromise glucocorticoid receptor sensitivity and function would lead to high levels of inflammation and apoptosis post-SCI, decreasing the tissue remaining at the injury site and undermining recovery of function
We have reviewed one mechanism, via the function of the glucocorticoid receptor and the psychological stress response to the environment, which may account for a part of the unexplained variance found in patients’ recovery following SCI
Based on the current literature, two potential mechanisms involved are the processes of inflammation and apoptosis: the NF-κB and the B-cell CLL/lymphoma 2 (Bcl-2) pathway, respectively
Summary
The effects of stress on glucocorticoid receptor signaling and the downstream processes of inflammation and apoptosis, depend on whether such stress is acute or chronic. Contribute to high levels of inflammation and apoptosis, decreasing the tissue remaining at the injury site and undermining recovery of function post-SCI. There is strong evidence for the social environment triggering changes to the psychological stress response, and glucocorticoid receptor function, with considerable literature linking the subsequent changes in stress resiliency to physical health. When we are exposed to a homeostatic challenge, such as a sign of danger, the brain first reacts via the neural route. It activates the sympathetic nervous system, which prompts the adrenal glands to release catecholamines, namely epinephrine and norepinephrine. Glucocorticoids function in a negative neuroendocrine feedback loop; high plasma levels signal the hypothalamus to stop producing
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
