Objective: Patients with complex regional pain syndrome (CRPS) suffer from continuous regional limb pain and from hyperesthesia to touch and pain. To better understand the pathophysiological mechanisms underlying the hyperesthesia of CRPS patients, we investigated their cortical processing of touch and acute pain.
Methods: Cortical responses to tactile stimuli applied to the thumbs, index and little fingers (D1, D2, and D5) and nociceptive stimuli delivered to dorsa of the hands were recorded with a whole-scalp neuromagnetometer from eight chronic CRPS patients and from nine healthy control subjects.
Results: In the patients, primary somatosensory (SI) cortex activation to tactile stimulation of D2 was significantly stronger, and the D1-D5 distance in SI was significantly smaller for the painful hand compared to the healthy hand. The PPC activation to tactile stimulation was significantly weaker in the patients than in the control subjects. To nociceptive stimulation with equal laser energy, the secondary somatosensory (SII) cortices and posterior parietal cortex (PPC) were similarly activated in both groups. The PPC source strength correlated with the pain rating in the control subjects, but not in the patients.
Conclusions: The enhanced SI activation in hyperesthetic CRPS patients may reflect central sensitization to touch. The decreased D1-D5 distance implies permanent changes in SI hand representations in chronic CRPS. The defective PPC activation could be associated with the neglect-like symptoms of the patients. As the SII and PPC responses were not enhanced in the CRPS patients, other brain areas are likely to contribute to the observed hyperesthesia to pain.
Significance: Our results indicate changes of somatosensory processing at cortical level in CRPS.