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Clinical Value of Serum Neuroplasticity Mediators in Identifying the Central Sensitivity Syndrome in Patients With Chronic Pain With and Without Structural Pathology

机译:血清神经可塑性调节剂在识别慢性疼痛伴或不伴结构病理的中枢综合征中的临床价值

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Background and Objectives:Central sensitivity syndrome (CSS) encompasses disorders with overlapping symptoms in a spectrum of structural pathology from persistent somatic nociception (eg, osteoarthritis) to absence of tissue injury such as in fibromyalgia, chronic tension-type headache, and myofascial pain syndrome. Likewise, the spectrum of the neuroplasticity mediators associated with CSS might present a pattern of clinical utility.Methods:We studied the brain-derived neurotrophic factor (BDNF), tumor necrosis factor- (TNF-), and interleukins 6 (IL-6) and IL-10 in female patients with CSS absent of structural pathology (chronic tension-type headache [n=30], myofascial pain syndrome [n=29], fibromyalgia [n=22]); with CSS due to persistent somatic/visceral nociception (osteoarthritis [n=27] and endometriosis [n=32]); and in pain-free controls (n=37).Results:Patients with CSS absent of structural pathology presented higher serum TNF- (28.6112.74 pg/mL) and BDNF (49.87 +/- 31.86 ng/mL) than those with persistent somatic/visceral nociception (TNF-=17.35 +/- 7.38 pg/mL; BDNF=20.44 +/- 8.30 ng/mL) and controls (TNF-=21.41 +/- 5.74 pg/mL, BDNF=14.09 +/- 11.80 ng/mL). Moreover, CSS patients absent of structural pathology presented lower IL levels. Receiver operator characteristics analysis showed the ability of BDNF to screen CSS (irrespective of the presence of structural pathology) from controls (cutoff=13.31 ng/mL, area under the curve [AUC]=0.86, sensitivity=95.06%, specificity=56.76%); and its ability to identify persistent nociception in CSS patients when experiencing moderate-severe depressive symptoms (AUC=0.81; cutoff=42.83 ng/mL, sensitivity=56.80%, specificity=100%). When the level of pain measured on the visual analog scale was <5 and moderate-severe depressive symptoms were observed TNF- discriminated structural pathology in the chronic pain conditions (AUC=0.97; cutoff=22.11 pg/mL, sensitivity=90%, specificity=91.3%).Conclusion:Neuroplasticity mediators could play a role as screening tools for pain clinicians, and as validation of the complex and diffuse symptoms of these patients.
机译:背景与目的:中枢敏感性综合症(CSS)涵盖了从持续的躯体伤害(例如骨关节炎)到无组织损伤(如纤维肌痛,慢性紧张型头痛和肌筋膜疼痛综合征)的一系列结构病理中具有重叠症状的疾病。同样,与CSS相关的神经可塑性介体谱也可能呈现出临床效用模式。方法:我们研究了脑源性神经营养因子(BDNF),肿瘤坏死因子-(TNF-)和白介素6(IL-6)。女性没有结构病理的CSS患者(慢性紧张型头痛[n = 30],肌筋膜疼痛综合征[n = 29],纤维肌痛[n = 22])和IL-10。由于持续的躯体/内脏伤害感受(骨关节炎[n = 27]和子宫内膜异位[n = 32])而患有CSS;结果:无结构病理的CSS患者的血清TNF-(28.6112.74 pg / mL)和BDNF(49.87 +/- 31.86 ng / mL)高于持续性患者。体细胞/内脏伤害感受(TNF- = 17.35 +/- 7.38 pg / mL; BDNF = 20.44 +/- 8.30 ng / mL)和对照(TNF- = 21.41 +/- 5.74 pg / mL,BDNF = 14.09 +/- 11.80 ng / mL)。此外,没有结构病理的CSS患者的IL水平较低。接收者操作者特征分析显示,BDNF能够从对照中筛查CSS(无论是否存在结构病理)(临界值= 13.31 ng / mL,曲线下面积[AUC] = 0.86,灵敏度= 95.06%,特异性= 56.76%) );以及在出现中度至重度抑郁症状时能够识别CSS患者持续伤害感受的能力(AUC = 0.81;临界值= 42.83 ng / mL,敏感性= 56.80%,特异性= 100%)。当在视觉模拟量表上测得的疼痛水平<5且在慢性疼痛情况下观察到中度重度抑郁症状时,可辨别TNF的结构病理(AUC = 0.97;临界值= 22.11 pg / mL,敏感性= 90%,特异性= 91.3%)。结论:神经可塑性调节剂可以作为疼痛临床医生的筛查工具,并可以验证这些患者的复杂和弥散性症状。

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