Seifert Frank, Jungfer Isabella, Schmelz Martin, Maihöfner Christian
Department of Neurology, University of Erlangen-Nuremberg, Schwabachanlage 6, 91054 Erlangen, Germany.
Hum Brain Mapp. 2008 Dec;29(12):1327-42. doi: 10.1002/hbm.20470.
Surrogate models of pain and hyperalgesia allow the investigation of underlying mechanisms in healthy volunteers. Here, we investigated brain activation patterns during mechanical and heat hyperalgesia in an inflammatory human pain model using functional magnetic resonance imaging. Heat and mechanical hyperalgesia were induced on the right forearm by UV-B application in 14 healthy subjects. All four conditions (nonsensitized heat and nonsensitized mechanical pain, sensitized heat and sensitized mechanical pain) were perceptually matched. A 2 x 2 factorial analysis was performed. Areas with main effect of sensitization were insula, anterior cingulate cortex (ACC), prefrontal cortices (PFC), parietal association cortices (PA), thalamus, and basal ganglia. A main effect of modality with more activation during heat hyperalgesia was found in primary somatosensory cortex (S1), ACC, PFC, and PA. A main effect of modality with more activation during mechanical hyperalgesia was found in secondary somatosensory cortices, posterior insula, and contralateral inferior frontal cortex (IFC). An interaction of sensitization and modality was found bilaterally in IFC. Areas with similar effects of sensitization in both stimulus modalities were ACC, bilateral anterior insula and bilateral IFC. We conclude that different types of hyperalgesia in a human surrogate model of inflammatory pain produce different brain activation patterns. This is partly due to a differential processing of thermal and mechanical pain and an interaction of sensitization and modality in the caudal portion of the IFC. Finally, the data provide evidence for the existence of a common "sensitization network" consisting of ACC, bilateral anterior insula, and parts of the IFC.
疼痛和痛觉过敏的替代模型有助于在健康志愿者中研究潜在机制。在此,我们使用功能磁共振成像,在炎症性人类疼痛模型中研究了机械性和热性痛觉过敏期间的脑激活模式。通过对14名健康受试者的右前臂进行UV - B照射来诱导热性和机械性痛觉过敏。所有四种情况(未致敏的热痛和未致敏的机械性疼痛、致敏的热痛和致敏的机械性疼痛)在感觉上相互匹配。进行了2×2析因分析。致敏的主要效应区域包括脑岛、前扣带回皮质(ACC)、前额叶皮质(PFC)、顶叶联合皮质(PA)、丘脑和基底神经节。在原发性体感皮质(S1)、ACC、PFC和PA中发现热痛觉过敏期间激活更多的模态主要效应。在继发性体感皮质、后脑岛和对侧额下回(IFC)中发现机械性痛觉过敏期间激活更多的模态主要效应。在IFC双侧发现致敏和模态的相互作用。在两种刺激模态中具有相似致敏效应的区域是ACC、双侧前脑岛和双侧IFC。我们得出结论,在炎症性疼痛的人类替代模型中,不同类型的痛觉过敏产生不同的脑激活模式。这部分是由于热痛和机械性疼痛的差异处理以及IFC尾部致敏和模态的相互作用。最后,数据为存在由ACC、双侧前脑岛和IFC部分组成的共同“致敏网络”提供了证据。