Doménech-García Víctor, Palsson Thorvalur S, Boudreau Shellie A, Bellosta-López Pablo, Herrero Pablo, Graven-Nielsen Thomas
Center for Neuroplasticity and Pain (CNAP), SMI, Department of Health Science and Technology, Faculty of Medicine, Aalborg University, Aalborg, Denmark.
Universidad San Jorge, Campus Universitario, Villanueva de Gállego, Zaragoza, Spain.
Pain Med. 2020 Nov 1;21(11):2850-2862. doi: 10.1093/pm/pnaa228.
Nociception caused by injuries may sensitize central mechanisms causing expanded pain areas. After recovery, the status of such pain distribution and sensitivity mechanisms is unknown. The present study investigated whether individuals who have fully recovered from a distal radius fracture demonstrate increased pain sensitivity and expanded distribution of pressure-induced pain.
Cross-sectional single-blinded study.
Clinical setting.
Twenty-three pain-free individuals with a history of painful distal radius fracture and 22 nonfractured, age/gender-matched controls participated in two experimental sessions (day 0, day 1) 24 hours apart.
Pressure pain thresholds (PPTs) were recorded bilaterally at the extensor carpi radialis longus (ECRL), infraspinatus, and gastrocnemius muscles. Spatial distribution of pain was assessed following 60-second painful pressure stimulation at the ECRL (bilateral) and the infraspinatus muscles on the fractured or dominant side. Participants drew pain areas on a body map. After day 0 assessments, prolonged pain was induced by eccentric exercise of wrist extensors on the fractured/dominant side.
Compared with controls, pressure-induced ECRL pain in the fracture group referred more frequently toward the distal forearm (P < 0.005) on day 0. Both groups showed larger pain areas on day 1 compared with day 0 (P < 0.005), although the fracture group showed a larger relative change between days (P < 0.005). The fracture group showed larger pain areas on the fracture side compared with the contralateral side on both days (P < 0.005).
Prolonged pain and recovered prior painful injuries like fractures may sensitize pain mechanisms manifested as expanded pain distribution. Pressure-induced referred pain can be a simple pain biomarker for clinical use.
损伤引起的伤害感受可能会使中枢机制敏感化,导致疼痛区域扩大。恢复后,这种疼痛分布和敏感机制的状态尚不清楚。本研究调查了桡骨远端骨折已完全康复的个体是否表现出疼痛敏感性增加以及压力诱发疼痛的分布范围扩大。
横断面单盲研究。
临床环境。
23名有桡骨远端骨折疼痛病史且无痛的个体以及22名年龄/性别匹配的未骨折对照者参加了相隔24小时的两次实验 session(第0天、第1天)。
双侧记录桡侧腕长伸肌(ECRL)、冈下肌和腓肠肌的压力痛阈值(PPTs)。在ECRL(双侧)和骨折侧或优势侧的冈下肌进行60秒的疼痛压力刺激后,评估疼痛的空间分布。参与者在人体图上画出疼痛区域。在第0天评估后,通过骨折侧/优势侧腕伸肌的离心运动诱发持续性疼痛。
与对照组相比,骨折组在第0天由压力诱发的ECRL疼痛更频繁地向远端前臂放射(P < 0.005)。与第0天相比,两组在第1天的疼痛区域均更大(P < 0.005),尽管骨折组在两天之间的相对变化更大(P < 0.005)。在两天中,骨折组骨折侧的疼痛区域均大于对侧(P < 0.005)。
持续性疼痛以及既往如骨折等疼痛性损伤的恢复可能会使疼痛机制敏感化,表现为疼痛分布范围扩大。压力诱发的牵涉痛可作为一种简单的临床疼痛生物标志物。