Mechanical allodynia in neuropathic pain. Where are the brain representations located? A positron emission tomography (PET) study. (27th March 2013)

• Record Type: Journal Article
• Authors: Peyron, R.; Faillenot, I.; Pomares, F.B.; Le Bars, D.; Garcia‐Larrea, L.; Laurent, B.
• Is Part Of: European journal of pain. Volume 17:Number 9(2013)
• Page Start: 1327
• Page End: 1337
• Publication Date: 2013-03-27
• Subjects: Pain -- Periodicals; Pain -- Treatment -- Periodicals; Pain -- Physiological aspects -- Periodicals; 616.0472
• DOI: 10.1002/j.1532-2149.2013.00307.x
• Languages: English
• ISSNs: 1090-3801

Abstract

Abstract: Background: Brain areas involved in nociception have been repeatedly investigated. Therefore, brain responses to physiological pain conditions are well identified. The same is not true for allodynic pain in patients with neuropathic pain since the cortical reorganizations that are involved in the conversion of non‐noxious stimuli into painful sensations still remain unknown. Methods: The present positron emission tomography (PET) study enrolled 19 patients with dynamic mechanical allodynia to brushing or to cold rubbing of the skin. PET activations during allodynic stimulation were compared to those obtained with the same innocuous stimulation applied outside the neuropathic pain area (control). In a second comparison, they were compared with responses to a noxious heat stimulation applied outside the neuropathic pain area (experimental pain). Results: Common responses to allodynia and control stimulations were found in contralateral SI, SII and insula and in ipsilateral cerebellum. Not surprisingly, heat pain condition was associated with activations in contralateral prefrontal and SII cortices and, bilaterally, in the anterior insular cortices. Distinctive cortical responses between control and allodynic conditions were restricted to one activation within the contralateral anterior insula, a region also activated by experimental heat pain. Conclusions: The insular subdivision was inappropriately activated considering the innocuous nature of the stimulus, but adequately activated with regard to pain‐evoked sensation. Subcortically, the hypothesis of reorganization at any level of the somatosensory and pain pathways underlying such insular activity was supported by the observed shift of thalamic activation from a lateral‐posterior to an anterior‐medial position.