Maihöfner Christian, Ringler Ralf, Herrndobler Franz, Koppert Wolfgang
Department of Neurology, Schwabachanlage 6, D91054 Erlangen, University Hospital Erlangen, Germany.
Eur J Neurosci. 2007 Sep;26(5):1344-56. doi: 10.1111/j.1460-9568.2007.05733.x.
One of the most distressing symptoms of many neuropathic pain syndromes is the enhanced pain sensation to tactile or thermal stimulation (hyperalgesia). In the present study we used functional magnetic resonance imaging (fMRI) and explored brain activation patterns during acute impact pain and mechanical hyperalgesia in the human ultraviolet (UV)-B model. To investigate pharmacological modulation, we examined potential differential fMRI correlates of analgesic and antihyperalgesic effects of two intravenous cyclooxygenase inhibitors, i.e. parecoxib and acetylsalicylic acid (ASA). Fourteen healthy volunteers participated in this double-blinded, randomized and placebo-controlled crossover study. Tactile stimuli and mechanical impact hyperalgesia were tested at the site of a UV-B irradiation and acute mechanical pain was tested at a site distant from the irradiated skin. These measurements were conducted before and 30 min after a 5-min intravenous infusion of either saline (placebo), parecoxib 40 mg or ASA 1000 mg. Acute mechanical pain and mechanical hyperalgesia led to widespread activations of brain areas known to comprise the human pain matrix. Analgesic effects were found in primary (S1) and secondary (S2) somatosensory cortices, parietal association cortex (PA), insula, anterior parts of the cingulate cortex and prefrontal cortices. These brain areas were also modulated under antihyperalgesic conditions. However, we observed a greater drug-induced modulation of mainly PA and inferior frontal cortex during mechanical hyperalgesia; during acute mechanical pain there was a greater modulation of mainly bilateral S2. Therefore, the results of the present study suggest that there is a difference in the brain areas modulated by analgesia and antihyperalgesia.
许多神经性疼痛综合征最令人痛苦的症状之一是对触觉或热刺激的痛觉增强(痛觉过敏)。在本研究中,我们使用功能磁共振成像(fMRI),探索了人类紫外线(UV)-B模型中急性冲击性疼痛和机械性痛觉过敏期间的脑激活模式。为了研究药物调节作用,我们检查了两种静脉注射环氧化酶抑制剂(即帕瑞昔布和乙酰水杨酸(ASA))镇痛和抗痛觉过敏作用的潜在fMRI差异相关性。14名健康志愿者参与了这项双盲、随机、安慰剂对照的交叉研究。在UV-B照射部位测试触觉刺激和机械冲击性痛觉过敏,在远离照射皮肤的部位测试急性机械性疼痛。这些测量在静脉输注生理盐水(安慰剂)、40mg帕瑞昔布或1000mg ASA 5分钟之前和之后30分钟进行。急性机械性疼痛和机械性痛觉过敏导致已知构成人类疼痛矩阵的脑区广泛激活。在初级(S1)和次级(S2)体感皮层、顶叶联合皮层(PA)、岛叶、扣带回皮层前部和前额叶皮层发现了镇痛作用。这些脑区在抗痛觉过敏条件下也受到调节。然而,我们观察到在机械性痛觉过敏期间,主要是PA和额下回皮层受药物诱导的调节作用更大;在急性机械性疼痛期间,主要是双侧S2受调节作用更大。因此,本研究结果表明,镇痛和抗痛觉过敏调节脑区存在差异。