Birznieks Ingvars, Burton Alexander R, Macefield Vaughan G
Prince of Wales Medical Research Institute, Barker Street, Randwick, NSW 2031, Sydney, Australia.
J Physiol. 2008 Jun 1;586(11):2713-23. doi: 10.1113/jphysiol.2008.151746. Epub 2008 Apr 10.
Animal studies have shown that noxious inputs onto gamma-motoneurons can cause an increase in the activity of muscle spindles, and it has been proposed that this causes a fusimotor-driven increase in muscle stiffness that is believed to underlie many chronic pain syndromes. To test whether experimental pain also acts on the fusimotor system in humans, unitary recordings were made from 19 spindle afferents (12 Ia, 7 II) located in the ankle and toe extensors or peronei muscles of awake human subjects. Muscle pain was induced by bolus intramuscular injection of 0.5 ml 5% hypertonic saline into tibialis anterior (TA); skin pain was induced by 0.2 ml injection into the overlying skin. Changes in fusimotor drive to the muscle spindles were inferred from changes in the mean discharge frequency and discharge variability of spindle endings in relaxed muscle. During muscle pain no afferents increased their discharge activity: seven afferents (5 Ia, 2 II) showed a decrease and six (4 Ia, 2 II) afferents were not affected. During skin pain of 13 afferents discharge rate increased in one (Ia) and decreased in two (1 Ia, 1 II). On average, the overall discharge rate decreased during muscle pain by 6.1% (P < 0.05; Wilcoxon), but remained essentially the same during skin pain. There was no detectable correlation between subjective pain level and the small change in discharge rate of muscle spindles. Irrespective of the type of pain, discharge variability parameters were not influenced (P > 0.05; Wilcoxon). We conclude that, contrary to the 'vicious cycle' hypothesis, acute activation of muscle or skin nociceptors does not cause a reflex increase in fusimotor drive in humans. Rather, our results are more aligned with the pain adaptation model, based on clinical studies predicting pain-induced reductions of agonist muscle activity.
动物研究表明，对γ运动神经元的有害输入可导致肌梭活动增加，有人提出，这会导致由梭内肌驱动的肌肉僵硬增加，而这被认为是许多慢性疼痛综合征的基础。为了测试实验性疼痛是否也作用于人类的梭内肌运动系统，对19名清醒人类受试者的踝关节和趾伸肌或腓骨肌中的梭传入纤维（12条Ia类、7条II类）进行了单纤维记录。通过向胫骨前肌（TA）内一次性肌内注射0.5 ml 5%高渗盐水诱发肌肉疼痛；通过向覆盖其上的皮肤注射0.2 ml诱发皮肤疼痛。根据放松肌肉中梭终末的平均放电频率和放电变异性的变化推断对肌梭的梭内肌运动驱动的变化。在肌肉疼痛期间，没有传入纤维增加其放电活动：7条传入纤维（5条Ia类、2条II类）放电减少，6条（4条Ia类、2条II类）传入纤维未受影响。在皮肤疼痛期间，13条传入纤维中，1条（Ia类）放电率增加，2条（1条Ia类、1条II类）放电率降低。平均而言，肌肉疼痛期间总体放电率下降了6.1%（P<0.05；Wilcoxon检验），但在皮肤疼痛期间基本保持不变。主观疼痛程度与肌梭放电率的微小变化之间没有可检测到的相关性。无论疼痛类型如何，放电变异性参数均未受影响（P>0.05；Wilcoxon检验）。我们得出结论，与“恶性循环”假说相反，肌肉或皮肤伤害感受器的急性激活不会导致人类梭内肌运动驱动的反射性增加。相反，我们的结果更符合疼痛适应模型，该模型基于临床研究预测疼痛会导致主动肌活动减少。
