Graven-Nielsen T, Babenko V, Svensson P, Arendt-Nielsen L
Center for Sensory-Motor Interaction, Laboratory for Experimental Pain Research, Aalborg University, Aalborg, Denmark.
Brain Res. 1998 Mar 23;787(2):203-10. doi: 10.1016/s0006-8993(97)01480-7.
The ability of muscle pain to generate somatosensory sensibility changes is controversial. Thus, in the present study, tonic infusion of hypertonic saline (5%, 7.1 ml administered over 15 min) into the tibialis anterior (TA) muscle was used as an experimental model to induce local and referred pain. The sensibility to high-intensity pressure stimuli applied to the local pain area, referred pain area and an arm was assessed in 14 healthy volunteers. Infusion of isotonic (0.9%) saline into the other leg served as control. The subject continuously scored the pain intensity on an electronic visual analogue scale (VAS). Pressure pain threshold (PPT) was determined on the TA muscle (2 cm and 10 cm from the infusion site), at the frontal aspect of the ankle (area of referred pain) and on the arm. To minimise the skin component of the PPT, the skin covering the assessment sites was anaesthetised with an anaesthetic creme. The PPTs were obtained before and after cutaneous analgesia, 1 min and 10 min after infusion start and 10 min after the pain had disappeared. Infusion of hypertonic saline caused significantly (P<0. 05) higher VAS scores than infusion of isotonic saline. A significant (P<0.04) increase of the PPT (i.e., decreased sensibility) was found at the ankle and on the arm during muscle pain compared to the control condition. No significant differences in PPTs on the TA muscle were found during saline-induced muscle pain compared to the infusion of isotonic saline. The decrease in deep sensibility at the heterotopic sites (referred pain area and arm), but not at homotopic sites (TA muscle), probably reflected the phenomenon of diffuse noxious inhibitory control (DNIC). The inhibitory mechanism during muscle pain was shown to be effective for the deep tissue sensibility in healthy subjects. Thus, a pathologically disturbed inhibitory mechanism may result in widespread deep hyperalgesia in muscle pain patients.
肌肉疼痛产生躯体感觉敏感性变化的能力存在争议。因此，在本研究中，将高渗盐水（5%，15分钟内注入7.1毫升）持续输注到胫骨前肌（TA）中作为实验模型，以诱导局部和牵涉痛。在14名健康志愿者中评估了施加于局部疼痛区域、牵涉痛区域和手臂的高强度压力刺激的敏感性。向另一条腿输注等渗（0.9%）盐水作为对照。受试者在电子视觉模拟量表（VAS）上持续对疼痛强度进行评分。在TA肌肉（距输注部位2厘米和10厘米处）、踝关节前部（牵涉痛区域）和手臂上测定压力痛阈（PPT）。为了将PPT的皮肤成分降至最低，用麻醉乳膏对覆盖评估部位的皮肤进行麻醉。在皮肤镇痛前后、输注开始后1分钟和10分钟以及疼痛消失后10分钟获取PPT。与输注等渗盐水相比，输注高渗盐水导致VAS评分显著更高（P<0.05）。与对照情况相比，在肌肉疼痛期间，踝关节和手臂处的PPT显著增加（即敏感性降低）（P<0.04）。与输注等渗盐水相比，在盐水诱导的肌肉疼痛期间，TA肌肉上的PPT没有显著差异。异位部位（牵涉痛区域和手臂）而非同位部位（TA肌肉）深部敏感性的降低可能反映了弥漫性伤害性抑制控制（DNIC）现象。肌肉疼痛期间的抑制机制对健康受试者的深部组织敏感性有效。因此，病理上紊乱的抑制机制可能导致肌肉疼痛患者出现广泛的深部痛觉过敏。
