Sami S A K, Rössel P, Dimcevski G, Nielsen K Dremstrup, Funch-Jensen P, Valeriani M, Arendt-Nielsen L, Drewes A M
Center for Sensory-Motor Interactions, Department of Health Science and Technology, Aalborg University, Aalborg, Denmark.
Neuroscience. 2006 Jun 19;140(1):269-79. doi: 10.1016/j.neuroscience.2006.02.031. Epub 2006 Apr 21.
Topographical organization in the neocortex shows experience-dependent plasticity. We hypothesized that experimental sensitization of the esophagus results in changes of the topographical distribution of the evoked potentials and the corresponding dipole source activities to painful stimulation. An endoscopic method was used to deliver 35 electrical stimuli at the pain threshold to a fixed area of the mucosa in 10 healthy volunteer men and women. The stimulations were repeated after 30 min (reproducibility experiment), and after 60 min following perfusion of 200 ml 0.1 N hydrochloric acid (sensitization experiment). During stimulation the electroencephalogram was recorded from 64 surface electrodes. The sensitization resulted in a decrease in the pain threshold (F=6.2; P=0.004). The topographic distribution of the evoked potentials showed reproducible negative (N1, N2) and positive (P1, P2) components. After acid perfusion a reduced latency and a change in localization was seen for the P1 subdivided into frontal and occipital components (F=29.5, P<0.001; F=53.7, P<0.001). Furthermore the sensitization resulted in a reduction of the latency for P2 (F=6.2, P=0.009). The source analysis showed consistent dipolar activity in the bilateral opercular-insular cortex before and after acid perfusion. For the anterior cingulate dipole there was a reduction in latency (P=0.03) and a posterior shift (P=0.0002) following acid perfusion. The findings indicate that short-term sensitization of the esophagus results in central neuroplastic changes involving the cingulate gyrus, which also showed pathological activation in functional diseases of the gut, thus reflecting the importance of this region in visceral pain and hyperalgesia.
新皮层中的拓扑组织表现出经验依赖性可塑性。我们假设，食管的实验性致敏会导致诱发电位的拓扑分布以及对疼痛刺激的相应偶极源活动发生变化。采用内镜方法，在10名健康志愿者男性和女性的黏膜固定区域，以疼痛阈值给予35次电刺激。在30分钟后重复刺激（再现性实验），并在灌注200毫升0.1N盐酸60分钟后重复刺激（致敏实验）。刺激期间，从64个表面电极记录脑电图。致敏导致疼痛阈值降低（F = 6.2；P = 0.004）。诱发电位的拓扑分布显示出可重复的负性（N1、N2）和正性（P1、P2）成分。酸灌注后，P1分为额叶和枕叶成分，其潜伏期缩短且定位改变（F = 29.5，P < 0.001；F = 53.7，P < 0.001）。此外，致敏导致P2潜伏期缩短（F = 6.2，P = 0.009）。源分析显示，酸灌注前后双侧岛盖-岛叶皮质存在一致的偶极活动。对于前扣带回偶极，酸灌注后潜伏期缩短（P = 0.03）且向后移位（P = 0.0002）。这些发现表明，食管的短期致敏会导致涉及扣带回的中枢神经可塑性变化，扣带回在肠道功能性疾病中也显示出病理性激活，从而反映出该区域在内脏疼痛和痛觉过敏中的重要性。
