■在85%的慢性下腰痛(CLBP)患者中,无法确定具体的病理解剖原因。除了后腰内的主要外围驱动器,脊髓或脊柱上的致敏过程可能导致患者疼痛。
■本研究将非特异性CLBP患者的最疼痛区域(MP)概念化为主要受累区域,并评估外周体征,脊柱,在MP中使用定量感觉测试(QST)和脊柱上致敏,与MP(AD)相邻的无痛区域,还有一个遥控器,无痛控制区(CON)。
■59名CLBP患者(51岁,SD=16.6,22名女性患者)和35名无痛对照参与者的年龄分别匹配,性别,和测试领域(49年,SD=17.5,19名女性参与者)在MP中接受了完整的QST方案,并在AD和CON中评估了降低的QST方案。定量感官测试措施,除了矛盾的热感和动态机械性异常疼痛(DMA),将Z转化为匹配的对照参与者,并使用Z检验(α=0.001)测试显著性。使用Fisher精确检验(α=0.05)比较了队列之间的矛盾热感和DMA发生情况。用高疼痛和低疼痛CLBP子样品(50%分位数)进行相同的分析。
■患者在MP中表现为寒冷和振动感觉减退(所有Ps<0.001),在AD中表现为机械性痛觉过敏(P<0.001)和更频繁的DMA(P=0.044)。结果主要由高痛CLBP子样本驱动。在CON,没有观察到感觉改变。
■机械痛觉过敏和DMA与MP相邻但不在MP内,据说主要受影响的地区,可能反映了CLBP患者脊髓致敏引起的继发性痛觉过敏。
UNASSIGNED: In 85% of patients with chronic low back pain (CLBP), no specific pathoanatomical cause can be identified. Besides primary peripheral drivers within the lower back, spinal or supraspinal sensitization processes might contribute to the patients\' pain.
UNASSIGNED: The present study conceptualized the most painful area (MP) of patients with nonspecific CLBP as primarily affected area and assessed signs of peripheral, spinal, and supraspinal sensitization using quantitative sensory testing (QST) in MP, a pain-free area adjacent to MP (AD), and a remote, pain-free control area (CON).
UNASSIGNED: Fifty-nine patients with CLBP (51 years, SD = 16.6, 22 female patients) and 35 pain-free control participants individually matched for age, sex, and testing areas (49 years, SD = 17.5, 19 female participants) underwent a full QST protocol in MP and a reduced QST protocol assessing sensory gain in AD and CON. Quantitative sensory testing measures, except paradoxical heat sensations and dynamic mechanical allodynia (DMA), were Z-transformed to the matched control participants and tested for significance using Z-tests (α = 0.001). Paradoxical heat sensations and DMA occurrence were compared between cohorts using Fisher\'s exact tests (α = 0.05). The same analyses were performed with a high-pain and a low-pain CLBP subsample (50% quantile).
UNASSIGNED: Patients showed cold and vibration hypoesthesia in MP (all Ps < 0.001) and mechanical hyperalgesia (P < 0.001) and more frequent DMA (P = 0.044) in AD. The results were mainly driven by the high-pain CLBP subsample. In CON, no sensory alterations were observed.
UNASSIGNED: Mechanical hyperalgesia and DMA adjacent to but not within MP, the supposedly primarily affected area, might reflect secondary hyperalgesia originating from spinal sensitization in patients with CLBP.