Psychological stress as a modulator of functional recovery following spinal cord injury.
Psychological stress as a modulator of functional recovery following spinal cord injury.
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DOI：
10.3389/fneur.2014.00044
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发表时间：
2014
影响因子：
3.4
通讯作者：
Hook MA
中科院分区：
文献类型：
--
作者：
Maldonado Bouchard S;Hook MA
有强有力的证据表明，社会环境触发了心理应激反应和糖皮质激素受体功能的变化。相当多的文献将压力弹性的后续变化与身体健康联系起来。在这里，汇聚的证据慢性心理应激在脊髓损伤（SCI）后的恢复过程中的调节作用。尽管SCI研究取得了相当大的进展，但我们仍然无法确定患者受伤后恢复变化的原因。我们认为，个人过去和现在的生活经历（以压力暴露的形式）可能会显着调节患者的SCI后的结果。我们提出了一个理论模型来解释慢性心理压力对身心恢复的负面影响。在SCI之前的生活中经历的压力以及作为创伤性损伤的结果，可能会损害糖皮质激素受体的敏感性和功能，并导致SCI后高水平的炎症和凋亡，减少损伤部位残留的组织并破坏功能的恢复。应激诱导的糖皮质激素抵抗和应激诱导的糖皮质激素受体的表观遗传变化都可以调节核因子-κ B调节的炎症通路和Bcl-2调节的凋亡通路。该模型不仅有助于对损伤后恢复过程的理论理解，而且为未来的研究提供了具体的可检验的假设。
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.
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DOI：
10.1073/pnas.1118355109
发表时间：
2012-04-17
影响因子：
11.1
作者：
Cohen, Sheldon;Janicki-Deverts, Denise;Turner, Ronald B.
通讯作者：
Turner, Ronald B.
组蛋白脱纤酶抑制结合行为疗法可增强脑外伤后的学习和记忆。
影响因子：
3.3
作者：
Dash, P. K.;Orsi, S. A.;Moore, A. N.
通讯作者：
Moore, A. N.
DOI：
10.1111/j.1526-4637.2012.01488.x
发表时间：
2012-11
期刊：
Pain medicine (Malden, Mass.)
影响因子：
--
作者：
Buchheit T;Van de Ven T;Shaw A
通讯作者：
Shaw A
影响因子：
158.5
作者：
BRACKEN, MB;SHEPARD, MJ;WINN, HR
通讯作者：
WINN, HR
影响因子：
120.7
作者：
Bracken, MB;Shepard, MJ;Young, W
通讯作者：
Young, W