• Christian Maihöfner, Hermann O Handwerker, and Frank Birklein.
• Department of Neurology, Institute for Experimental Physiology and Pathophysiology, University of Erlangen-Nuremberg, Erlangen, Germany. maihoefner@physiologie1.uni-erlangen.de
• Neurology. 2006 Mar 14;66(5):711-7.

ObjectiveTo investigate cerebral activations underlying touch-evoked pain (dynamic-mechanical allodynia) in patients with neuropathic pain.MethodsfMRI was used in 12 patients with complex regional pain syndromes (CRPSs). Allodynia was elicited by gently brushing the affected CRPS hand. Elicited pain ratings were recorded online to obtain pain-weighted predictors. Both activations and deactivations of blood oxygenation level-dependent signals were investigated.ResultsNonpainful stimulation on the nonaffected hand activated contralateral primary somatosensory cortex (S1), bilateral insula, and secondary somatosensory cortices (S2). In contrast, allodynia led to widespread cerebral activations, including contralateral S1 and motor cortex (M1), parietal association cortices (PA), bilateral S2, insula, frontal cortices, and both anterior and posterior parts of the cingulate cortex (aACC and pACC). Deactivations were detected in the visual, vestibular, and temporal cortices. When rating-weighted predictors were implemented, only few activations remained (S1/PA cortex, bilateral S2/insular cortices, pACC).ConclusionsAllodynic stimulation recruits a complex cortical network. Activations include not only nociceptive but also motor and cognitive processing. Using a covariance approach (i.e., implementation of rating-weighted predictors) facilitates the detection of a neuronal matrix involved in the encoding of allodynia. The pattern of cortical deactivation during allodynia may hint at a shift of activation from tonically active sensory systems, like visual and vestibular cortices, into somatosensory-related brain areas.

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