Analysis of pain cognition by neuro-imaging

我们证明了解剖区域的非伤害性刺激触发的脑激活在一个单一的患者异常性疼痛使用功能性MRI评价。用非伤害性刺激测量疼痛的右脚和健康的左脚的大脑激活。3个月后进行相同的测量，确认后，alludynia触发的活动增加的主要和第二躯体感觉区，下顶叶，颞叶，内侧前额叶皮层，前扣带皮层和辅助运动区，而刺激健康侧只导致在活动的主要躯体感觉区和下顶叶。三个月后，在异常性疼痛的症状消失后，同样的刺激右脚，只显示第一和第二躯体感觉区的激活减少。异常性疼痛是继发于神经损伤或组织损伤。异常性疼痛如何被感知的机制基本上是未知的。在我们的病例中，患者出现符合CRPS I型标准的体征。虽然这些症状自然消失，但我们患者的异常性疼痛与CRPS I型相同。我们相信我们的发现对于理解CRP I型异常性疼痛的病理生理学有重要意义。

We demonstrated the anatomical area of cerebral activation triggered by non-nociceptive stimulation in a single patient with allodynia using functional MRI evaluations. Cerebral activation with non-nociceptive stimulus was measured for both the painful right foot and the healthy left foot. The same measurements were carried out 3 month later, after confirming that the alludynia triggered an increase in activity in the primary and second somatosensory area, inferior parietal lobe, insula, medial prefrontal cortex, anterior cingulated cortex and supplementary motor area, whereas stimulation to the healthy side only resulted n activity in the primary somatosensory area and inferior parietal lobe. Three months later, after the symptoms of allodynia had disappeared, the same stimuli to the right foot showed a decrease in activation of only the primary and second somatosensory area.Allodynia is secondary to nerve injury or tissue damage. The mechanism of how allodynia is perceived is essentially unknown. In our case the patient presented signs which fit the criteria for CRPS type I. Although these symptoms ceased naturally, the allodynia seen in our patient was common to that of CRPS type I. We believe that our findings are significant for understanding the pathophysiology of allodynia seen in CRP type I.