Division of Clinical Psychology and Psychotherapy, Philipps University of Marburg, Germany.
J Affect Disord. 2011 Jun;131(1-3):143-9. doi: 10.1016/j.jad.2010.11.017. Epub 2010 Dec 16.
There is robust evidence that altered neural-immune interactions including increased levels of proinflammatory cytokines are involved in both the pathogenesis of depression and altered pain processing. Proinflammatory cytokines induce sickness behavior, a constellation of symptoms that bears a strong similarity to those of depression. A feature of sickness behavior is enhanced pain sensitivity and it has been suggested that proinflammatory cytokines interact with pain processing directly and via several neurobiological pathways. Previous research indicates that depression and pain are closely related. We investigated the association between proinflammatory cytokines and experimental pain in major depression.
Psychopathological variables, pressure pain thresholds (PPT) and concentrations of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) were measured in 37 outpatients with major depression and 48 healthy controls.
Compared with controls, depressed patients exhibited significantly higher levels of TNF-α and significantly decreased PPT indicating enhanced pain sensitivity. The group differences were robust when adjusting for sex and body mass index, although sex was significantly related to PPT. No group difference was observed in IL-6. PPT correlated significantly with TNF-α in women but not in men.
Because of the cross-sectional design, causality of the relation between TNF-α and pain cannot be determined. Results should be considered preliminary given the small sample size.
The present findings suggest that increased pain sensitivity in depression may be linked to increased TNF-α concentration. The absence of this association in men is discussed in terms of pain-related psychobiological sex differences.
有强有力的证据表明，改变的神经-免疫相互作用，包括增加的促炎细胞因子水平，参与了抑郁症和改变的疼痛处理的发病机制。促炎细胞因子引起疾病行为，这是一组症状，与抑郁症的症状非常相似。疾病行为的一个特征是增强的疼痛敏感性，有人认为促炎细胞因子通过几种神经生物学途径直接与疼痛处理相互作用。先前的研究表明，抑郁症和疼痛密切相关。我们研究了促炎细胞因子与重度抑郁症患者的实验性疼痛之间的关系。
在 37 名重度抑郁症门诊患者和 48 名健康对照者中测量了心理病理变量、压力疼痛阈值（PPT）以及肿瘤坏死因子-α（TNF-α）和白细胞介素-6（IL-6）的浓度。
与对照组相比，抑郁患者的 TNF-α水平显著升高，PPT 显著降低，表明疼痛敏感性增强。当调整性别和体重指数时，组间差异仍然显著，尽管性别与 PPT 显著相关。IL-6 组间无差异。在女性中，PPT 与 TNF-α显著相关，但在男性中则不相关。
由于横断面设计，TNF-α 和疼痛之间的关系的因果关系无法确定。由于样本量小，结果应被视为初步结果。
本研究结果表明，抑郁症患者的疼痛敏感性增加可能与 TNF-α浓度增加有关。男性中不存在这种关联，这与疼痛相关的心理生物学性别差异有关。
