• Frank Seifert, Isabella Jungfer, Martin Schmelz, and Christian Maihöfner.
• Department of Neurology, University of Erlangen-Nuremberg, Schwabachanlage 6, 91054 Erlangen, Germany.
• Hum Brain Mapp. 2008 Dec 1;29(12):1327-42.

AbstractSurrogate 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.Copyright 2007 Wiley-Liss, Inc.

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