Moisset Xavier, Bouhassira Didier
INSERM U-792, Centre de Traitement et d'Evaluation de la Douleur, CHU Ambroise Pare, 9, avenue Charles de Gaulle, 92100 Boulogne-Billancourt cedex, France.
Neuroimage. 2007;37 Suppl 1:S80-8. doi: 10.1016/j.neuroimage.2007.03.054. Epub 2007 Apr 10.
Many studies have focused on defining the network of brain structures involved in normal physiological pain. The different dimensions of pain perception (i.e., sensory discriminative, affective/emotional, cognitive/evaluative) have been shown to depend on different areas of the brain. In contrast, much less is known about the neural basis of pathological chronic pain. In particular, it is unclear whether such pain results from changes to the physiological "pain matrix". We review here studies on changes in brain activity associated with neuropathic pain syndromes-a specific category of chronic pain associated with peripheral or central neurological lesions. Patients may report combinations of spontaneous pain and allodynia/hyperalgesia-abnormal pain evoked by stimuli that normally induce no/little sensation of pain. Modern neuroimaging methods (positron emission tomography (PET) and functional MRI (fMRI)) have been used to determine whether different neuropathic pain symptoms involve similar brain structures and whether these structures are related to the physiological "pain matrix". PET studies have suggested that spontaneous neuropathic pain is associated principally with changes in thalamic activity and the medial pain system, which is preferentially involved in the emotional dimension of pain. Both PET and fMRI have been used to investigate the basis of allodynia. The results obtained have been very variable, probably reflecting the heterogeneity of patients in terms of etiology, lesion topography, symptoms and stimulation procedures. Overall, these studies indicated that acute physiological pain and neuropathic pain have distinct although overlapping brain activation pattern, but that there is no unique "pain matrix" or "allodynia network".
许多研究都聚焦于确定参与正常生理性疼痛的脑结构网络。疼痛感知的不同维度（即感觉辨别、情感/情绪、认知/评估）已被证明取决于大脑的不同区域。相比之下，对于病理性慢性疼痛的神经基础了解得要少得多。特别是，尚不清楚这种疼痛是否源于生理性“疼痛矩阵”的变化。我们在此回顾与神经性疼痛综合征相关的脑活动变化的研究——神经性疼痛综合征是一种与外周或中枢神经病变相关的慢性疼痛的特定类型。患者可能会报告自发痛和痛觉过敏/超敏反应的组合——由通常不会引起/只会引起很少疼痛感觉的刺激诱发的异常疼痛。现代神经成像方法（正电子发射断层扫描（PET）和功能磁共振成像（fMRI））已被用于确定不同的神经性疼痛症状是否涉及相似的脑结构，以及这些结构是否与生理性“疼痛矩阵”相关。PET研究表明，自发神经性疼痛主要与丘脑活动和内侧疼痛系统的变化有关，内侧疼痛系统优先参与疼痛的情感维度。PET和fMRI都已被用于研究痛觉过敏的基础。所获得的结果差异很大，这可能反映了患者在病因、病变部位、症状和刺激程序方面的异质性。总体而言，这些研究表明，急性生理性疼痛和神经性疼痛具有不同但重叠的脑激活模式，但不存在独特的“疼痛矩阵”或“痛觉过敏网络”。
