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Comorbidity of chronic pain and depression: The hippocampus as a common denominator.

机译:慢性疼痛和抑郁症的合并症:海马是共同的分母。

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摘要

Patients who suffer from chronic pain are often afflicted with depressive illness as well, and vice versa. Antidepressants are common forms of treatment for both chronic pain and depression, but a definitive mechanism of action is still unknown. The hippocampus has been well accepted as a brain region involved in depressive illness and therapeutic action of antidepressant drugs, but it has yet to be accepted as a region that participates in pain processing. However, the pathogenesis of these two disease states share common neuromodulators and neurotransmitters acting within the hippocampus. Whereas the physiological and molecular basis for the coexistence of pain and depression is still being investigated, it is apparent that the hippocampus provides a viable anatomic link for these pathological disease states.;Chronic pain and depressive illness can act as chronic inescapable stressors. Each of these disorders has been shown to produce neuroplastic changes, i.e., atrophy, of the hippocampus, one of the primary regions regulating affect within the limbic system. Specifically, both disorders affect the hypothalamic-pituitary-adrenal (HPA) axis, causing an elevation in glucocorticoid (GCC) levels accompanied by a decrease in GCC responsiveness, which in turn damages brain structures involved in the regulation of the HPA axis, most notably the hippocampus.;Elevations in pro-inflammatory cytokines are routinely found in patients suffering from depression and chronic pain. GCCs are potent endogenous anti-inflammatory hormones; therefore, the reduced responsiveness that occurs during chronic pain and depressive illness causes a loss of GCC-mediated suppression of pro-inflammatory cytokine production. Pro-inflammatory cytokines also contribute to the increased production of the GCC. Thus, a vicious cycle is created, which results in elevated levels of cytokines and GCC. These cytokines also play a role in the turnover of monoamines within the hippocampus. For example, TNF-alpha inhibits the release of norepinephrine (NE), contributing to the overall insufficiency of NE that is commonly seen in depressive illness and chronic neuropathic pain.;Administration of tricyclic antidepressants, agents that increase the availability of monoamines and regulate the production of cytokines, can be effective treatments for both depression and chronic pain. Likewise, the increase in hippocampal neurogenesis that occurs following antidepressant drug administration also lends support that the hippocampus is a common brain region important in mediating analgesic and antidepressant effects.;The present review and investigation into the co-morbidity of depression and chronic pain will provide evidence that the hippocampus is a fundamental brain region involved in the development and maintenance of both disorders. The hypothesis that treatment and modification within the hippocampus would be advantageous to management of symptoms of chronic pain and major depressive disorders will be addressed.
机译:患有慢性疼痛的患者通常也患有抑郁症,反之亦然。抗抑郁药是治疗慢性疼痛和抑郁症的常见形式,但确切的作用机制仍未知。海马已被广泛接受为涉及抑郁症疾病和抗抑郁药治疗作用的大脑区域,但尚未被接受为参与疼痛处理的区域。但是,这两种疾病状态的发病机制共有共同的神经调节剂和在海马体内起作用的神经递质。尽管目前仍在研究疼痛和抑郁共存的生理和分子基础,但很明显海马为这些病理疾病提供了可行的解剖联系。慢性疼痛和抑郁症可以作为不可避免的慢性应激源。这些疾病中的每一种都已显示出产生海马神经塑性改变,即萎缩,这是调节边缘系统内影响的主要区域之一。具体而言,这两种疾病都会影响下丘脑-垂体-肾上腺(HPA)轴,导致糖皮质激素(GCC)水平升高,同时GCC响应度降低,进而损害涉及HPA轴调节的大脑结构。通常在患有抑郁症和慢性疼痛的患者中发现促炎性细胞因子升高。 GCC是有效的内源性抗炎激素;因此,在慢性疼痛和抑郁性疾病期间发生的反应性降低会导致GCC介导的促炎性细胞因子产生的抑制作用丧失。促炎细胞因子也有助于增加GCC的产生。因此,产生了恶性循环,其导致细胞因子和GCC水平升高。这些细胞因子在海马内单胺的转换中也起作用。例如,TNF-α抑制了去甲肾上腺素(NE)的释放,导致了NE的总体功能不全,这在抑郁症和慢性神经性疼痛中很常见。细胞因子的产生,可以有效治疗抑郁症和慢性疼痛。同样,抗抑郁药给药后海马神经发生的增加也支持海马是介导止痛和抗抑郁作用的重要大脑区域。本研究以及对抑郁症和慢性疼痛的合并症的研究将提供有证据表明海马是参与这两种疾病的发展和维持的基本大脑区域。将解决海马内的治疗和修饰对慢性疼痛和重度抑郁症的症状管理有利的假说。

著录项

  • 作者

    Fasick, Victoria R.;

  • 作者单位

    State University of New York at Buffalo.;

  • 授予单位 State University of New York at Buffalo.;
  • 学科 Biology Neuroscience.;Health Sciences Mental Health.;Health Sciences Pathology.
  • 学位 M.A.
  • 年度 2010
  • 页码 78 p.
  • 总页数 78
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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