Ringler R, Greiner M, Kohlloeffel L, Handwerker O H, Forster C
Institute of Physiology and Experimental Pathophysiology, University of Erlangen/Nuernberg, Universitätsstrasse 17, D-910547 Erlangen, Germany.
Pain. 2003 Oct;105(3):445-453. doi: 10.1016/S0304-3959(03)00258-6.
The contribution of four cortical areas (S1, S2, insular cortex and gyrus cinguli) to pain processing was assessed by functional magnetic resonance imaging (fMRI). Phasic (mechanical impact) and tonic stimuli (squeezing) were applied to the back of a finger, both at two different strengths. Stimuli were adjusted to inflict weak and strong pain sensations. It had been shown before that stronger noxious mechanical stimuli induce a weaker input from myelinated mechanoreceptors, but a more vigorous input from nociceptive primary afferents, and vice versa. Sizes of activation clusters and percent increase of the blood oxygenation level dependent (BOLD) signal during activation were compared in the areas of interest. Phasic stimulus patterns were more closely reflected in the time course of the MR signal in S1, S2 and the cingulate than tonic patterns, since the tonic stimuli tended to induce slow MR signal increase also during the resting periods which is in parallel to the persisting character of the tonic pain sensations. In S1 only the contralateral side was activated in most cases, and the more painful stimuli did not induce greater BOLD responses compared to the less painful stimuli in this area. Paradoxically, more painful stimuli produced smaller activation clusters in S1, both in tonic and phasic stimulus trials. In contralateral S2 more painful phasic stimuli induced significantly stronger BOLD responses than the weaker stimuli. The responses to tonic stimuli did not differentiate painfulness and were significantly smaller than the phasic. Activation clusters in this area were also smaller for tonic stimuli. In the gyrus cinguli more painful phasic stimuli induced stronger BOLD responses, but no difference was seen between tonic stimulation of different strength. Though the insular cortex was often bilaterally activated, no significant differences between stimulus quality or intensity were found. Our results provide evidence for a contribution of the S2 projection area and of the cingulate cortex to the processing of the intensity dimension of phasic mechanical pain. Such evidence was not found for the S1 area, which probably receives dominant input from non-nociceptive mechanoreceptors.
通过功能磁共振成像（fMRI）评估了四个皮质区域（初级体感皮层、次级体感皮层、岛叶皮层和扣带回）对疼痛处理的贡献。向手指背部施加阶段性（机械冲击）和持续性刺激（挤压），两种刺激均采用两种不同强度。刺激强度经调整以引发微弱和强烈的疼痛感。此前研究表明，更强的有害机械刺激会使有髓机械感受器的输入减弱，但伤害性初级传入神经的输入更强烈，反之亦然。比较了感兴趣区域激活簇的大小以及激活过程中血氧水平依赖（BOLD）信号的百分比增加情况。与持续性刺激模式相比，阶段性刺激模式在初级体感皮层、次级体感皮层和扣带回的磁共振信号时间进程中体现得更为紧密，因为持续性刺激在静息期也往往会导致磁共振信号缓慢增加，这与持续性疼痛感觉持续存在的特点相符。在初级体感皮层，多数情况下仅对侧被激活，与该区域中疼痛较轻的刺激相比，疼痛更强烈的刺激并未引发更大的BOLD反应。矛盾的是，在持续性和阶段性刺激试验中，疼痛更强烈的刺激在初级体感皮层产生的激活簇更小。在对侧次级体感皮层，疼痛更强烈的阶段性刺激比较弱刺激引发的BOLD反应显著更强。对持续性刺激的反应无法区分疼痛程度，且明显小于对阶段性刺激的反应。该区域中持续性刺激的激活簇也更小。在扣带回中，疼痛更强烈的阶段性刺激引发更强的BOLD反应，但不同强度的持续性刺激之间未观察到差异。尽管岛叶皮层常常双侧激活，但在刺激性质或强度方面未发现显著差异。我们的研究结果为次级体感皮层投射区域和扣带回皮层在阶段性机械性疼痛强度维度处理中的作用提供了证据。在初级体感皮层未发现此类证据，该区域可能主要接收来自非伤害性机械感受器的输入。
