Department of Physiology and Experimental Pathophysiology, University of Erlangen-Nuremberg, Erlangen, Germany.
Eur J Pain. 2010 Jan;14(1):64-70. doi: 10.1016/j.ejpain.2009.02.007. Epub 2009 Apr 5.
Mechanical hyperalgesia may develop following tissue inflammation or nerve injury. Basically, peripheral sensitization leads to primary hyperalgesia at the site of injury, whereas secondary hyperalgesia occurs in the surrounding tissue and results from central sensitization. The present study focuses on the cerebral processing of secondary mechanical hyperalgesia. Primary (S1) and secondary (S2) somatosensory cortices and posterior parietal cortex (PPC) are thought to be involved in cerebral processing of noxious mechanical stimuli. However, their response pattern in the presence of mechanical hyperalgesia remains to be elucidated. Therefore, we investigated the cortical processing of secondary mechanical hyperalgesia using magnetoencephalography (MEG). In 12 healthy subjects mechanoinsensitive c-nociceptors were repetitively stimulated using transcutaneously applied high-current electrical stimulation. This procedure resulted in stable areas of secondary mechanical hyperalgesia. Pin-prick stimuli were applied inside and outside the hyperalgesic area. The corresponding cortical activations were detected and quantified using MEG. We found pin-prick-induced sequential activation of contralateral S1, PPC and S2 as well as activation of ipsilateral S2 during both pin-prick hyperalgesia and normal pin-prick pain. During pin-prick hyperalgesia significantly higher activation was detected in contralateral PPC and bilateral S2 but not in S1 compared to normal pin-prick pain. In contrast to PPC, we found a significant correlation between increases of magnetic field strengths within bilateral S2 with the increase of pain ratings during pin-prick hyperalgesia. We conclude that the S2 cortex may be involved for the processing of secondary mechanical hyperalgesia in the human brain. PPC activation may reflect higher attentional processing during mechanical hyperalgesia.
机械性痛觉过敏可能在组织炎症或神经损伤后发生。基本上，外周敏化导致损伤部位的原发性痛觉过敏，而继发性痛觉过敏发生在周围组织中，是由中枢敏化引起的。本研究重点关注继发性机械性痛觉过敏的大脑处理。初级（S1）和次级（S2）体感皮层和顶后皮层（PPC）被认为参与了有害机械刺激的大脑处理。然而，它们在存在机械性痛觉过敏时的反应模式仍有待阐明。因此，我们使用脑磁图（MEG）研究了继发性机械性痛觉过敏的大脑处理。在 12 名健康受试者中，使用经皮施加的高电流电刺激反复刺激机械感觉神经无敏感受器。该程序导致稳定的继发性机械性痛觉过敏区域。在痛觉过敏区域内和外部应用刺痛刺激。使用 MEG 检测和量化相应的皮层激活。我们发现，刺痛引起的对侧 S1、PPC 和 S2 的顺序激活，以及在刺痛痛觉过敏和正常刺痛疼痛期间同侧 S2 的激活。在刺痛痛觉过敏期间，与正常刺痛疼痛相比，对侧 PPC 和双侧 S2 的激活明显更高，但 S1 没有。与 PPC 不同，我们发现双侧 S2 内磁场强度的增加与刺痛痛觉过敏期间疼痛评分的增加之间存在显著相关性。我们的结论是，S2 皮层可能参与了人类大脑中继发性机械性痛觉过敏的处理。PPC 的激活可能反映了机械性痛觉过敏期间更高的注意力处理。
