Brain processing of capsaicin-induced secondary hyperalgesia - A functional MRI study
Brain processing of capsaicin-induced secondary hyperalgesia - A functional MRI study
复制标题
DOI：
10.1212/wnl.53.3.548
复制
发表时间：
1999-08-11
期刊：
影响因子：
9.9
通讯作者：
Roberts, TPL
中科院分区：
文献类型：
--
作者：
Baron, R;Baron, Y;Roberts, TPL
目的：目的：利用功能性磁共振成像（fMRI）研究辣椒素诱导的继发性机械性痛觉过敏疼痛成分激活的神经网络。背景：机械性痛觉过敏（即，对无害的触觉刺激的疼痛）是神经性疼痛综合征的令人痛苦的症状。动物实验表明，中枢疼痛处理的改变使触觉刺激能够激活中枢疼痛信号神经元。用辣椒素也可以在实验中产生类似的中枢致敏作用。研究方法：在9名健康人的大脑激活模式，在占主导地位的前臂皮肤无痛性机械刺激所造成的成像功能磁共振成像。在刺激部位附近注射辣椒素以诱导继发性机械性痛觉过敏。然后，在不改变刺激强度和位置的情况下，相同的机械刺激被感知为疼痛。这两种激活模式进行了比较，以隔离特定的疼痛相关的组成部分，机械痛觉过敏的触觉组件。结果如下：无痛性机械刺激的模式包括对侧初级感觉皮层（SI）和双侧次级感觉皮层（SII）的活动。在痛觉过敏过程中，对侧前额叶皮层的激活程度显著较高：中间（布罗德曼区域[BA] 6、8和9）和额下回（BA 44和45）。SI、SII和前扣带回皮质内无变化。结论：前额叶激活被解释为注意力、认知评估和对疼痛做出反应的运动行为计划的结果。前扣带回激活的缺乏与C-伤害感受器刺激后的生理性疼痛形成对比。这可能表明痛觉过敏和C-伤害感受器疼痛的处理差异，或者可能是由于与急性辣椒素疼痛相比，痛觉过敏期间情感感觉的习惯化。
Objective: To investigate, using functional MRI (fMRI), the neural network that is activated by the pain component of capsaicin-induced secondary mechanical hyperalgesia. Background: Mechanical hyperalgesia(i.e., pain to innocuous tactile stimuli) is a distressing symptom of neuropathic pain syndromes. Animal experiments suggest that alterations in central pain processing occur that render tactile stimuli capable of activating central pain-signaling neurons. A similar central sensitization can be produced experimentally with capsaicin. Methods: In nine healthy individuals the cerebral activation pattern resulting from cutaneous nonpainful mechanical stimulation at the dominant forearm was imaged using fMRI. Capsaicin was injected adjacent to the stimulation site to induce secondary mechanical hyperalgesia. The identical mechanical stimulation was then perceived as painful without changing the stimulus intensity and location. Both activation patterns were compared to isolate the specific pain-related component of mechanical hyperalgesia from the tactile component. Results: The pattern during nonpainful mechanical stimulation included contralateral primary sensory cortex (SI) and bilateral secondary sensory cortex (SII) activity. During hyperalgesia, significantly higher activation was found in the contralateral prefrontal cortex: the middle (Brodmann areas [BAs] 6, 8, and 9) and inferior frontal gyrus (BAs 44 and 45). No change was present within SI, SII, and the anterior cingulate cortex. Conclusions: Prefrontal activation is interpreted as a consequence of attention, cognitive evaluation, and planning of motor behavior in response to pain. The lack of activation of the anterior cingulate contrasts with physiologic pain after C-nociceptor stimulation. It might indicate differences in the processing of hyperalgesia and C-nociceptor pain or it might be due to habituation of affective sensations during hyperalgesia compared with acute capsaicin pain.