Clinical Value of Serum Neuroplasticity Mediators in Identifying the Central Sensitivity Syndrome in Patients With Chronic Pain With and Without Structural Pathology
Clinical Value of Serum Neuroplasticity Mediators in Identifying the Central Sensitivity Syndrome in Patients With Chronic Pain With and Without Structural Pathology
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DOI：
10.1097/ajp.0000000000000194
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发表时间：
2015-11-01
影响因子：
2.9
通讯作者：
Caumo, Wolnei
中科院分区：
文献类型：
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作者：
Deitos, Alicia;Dussan-Sarria, Jairo A.;Caumo, Wolnei
背景和目的：中枢敏感综合征（CSS）包括从持续性躯体伤害感受（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）的一系列结构病理学中具有重叠症状的疾病。方法：我们研究了无结构病理学改变的女性CSS患者的脑源性神经营养因子（BDNF）、肿瘤坏死因子-（TNF-）、白细胞介素6（IL-6）和IL-10（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]）;由于持续性躯体/内脏伤害性感受导致CSS结果：CSS患者的血清TNF-α水平高于对照组（骨关节炎[n= 27]和子宫内膜异位症[n = 32]）;（28.6112.74 pg/mL）和BDNF（49.87 +/- 31.86 ng/mL）高于持续躯体/内脏伤害感受的受试者（TNF-=17.35 +/- 7.38 pg/mL; BDNF=20.44 +/- 8.30 ng/mL）和对照组（TNF-=21.41 +/- 5.74 pg/mL，BDNF=14.09 +/- 11.80 ng/mL）。此外，缺乏结构病理学的CSS患者呈现较低的IL水平。接受者操作者特征分析显示BDNF具有筛选CSS的能力（无论是否存在结构性病理）（截止值=13.31 ng/mL，曲线下面积[AUC]=0.86，灵敏度= 95.06%，特异性=56.76%）;以及其在CSS患者经历中度-重度抑郁症状时识别持续性伤害感受的能力（AUC=0.81;临界值=42.83 ng/mL，灵敏度= 56.80%，特异性=100%）。当在视觉模拟量表上测量的疼痛水平为
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