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A positron emission tomography study of wind‐up pain in chronic postherniotomy pain
Author(s) -
Kupersl Ron,
Lonsdalel Markus Nowak,
Aasvangl Eske,
Kehletl Henrik
Publication year - 2011
Publication title -
european journal of pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.305
H-Index - 109
eISSN - 1532-2149
pISSN - 1090-3801
DOI - 10.1016/j.ejpain.2011.01.003
Subject(s) - neuropathic pain , medicine , secondary somatosensory cortex , chronic pain , allodynia , insula , anesthesia , positron emission tomography , hyperalgesia , anterior cingulate cortex , thalamus , neuroscience , psychology , nociception , physical therapy , receptor , cognition
Many neuropathic pain conditions are characterized by abnormal responses to noxious or innocuous mechanical stimulation, including wind‐up pain. Whereas previous brain imaging studies have explored the cerebral correlates of hyperalgesia and allodynia, no studies are available on mechanical‐induced wind‐up pain in neuropathic pain patients. We therefore used positron emission tomography (PET) to investigate the cerebral response pattern of mechanical wind‐up pain in a homogenous group of 10 neuropathic pain patients with long‐standing postherniotomy pain in the groin area. Patients were scanned in the following conditions: (1) rest; (2) wind‐up pain, induced by 2 Hz von Frey stimulation in the painful area; (3) non‐painful 2 Hz von Frey stimulation in the homologous contralateral area and (4) tonic pressure pain in the homologous contralateral area. A direct comparison between wind‐up pain and non‐painful von Frey stimulation revealed that the former more strongly activated contralateral secondary somatosensory cortex, insula, anterior cingulate cortex, right dorsolateral prefrontal cortex, thalamus and cerebellum. In addition, wind‐up pain also activated the sublenticular extended amygdala (SLEA) and the brain stem. A direct comparison between wind‐up pain and pressure pain revealed that both activated a largely overlapping network. Since no de novo brain areas were activated by wind‐up pain, our data suggest that the processes specific to wind‐up pain do not occur at the cerebral level.