No evidence of impaired sensorimotor adaptation in Complex Regional Pain Syndrome

Abstract

AbstractSensorimotor conflict is theorised to contribute to the maintenance of some pathological pain conditions, such as Complex Regional Pain Syndrome (CRPS). We therefore tested whether sensorimotor adaptation is impaired in people with CRPS by characterising their adaption to lateral prismatic shifts in vision. People with unilateral upper limb CRPS Type I (n = 17), and pain-free individuals (n = 18; matched for age, sex, and handedness) completed prism adaptation with their affected/non-dominant and non-affected/dominant arm, in a counterbalanced order. We examined 1) the rate at which participants compensated for the optical shift during prism exposure (i.e. strategic recalibration), 2) endpoint errors made directly after prism adaptation (sensorimotor realignment) and their retention, and 3) kinematic markers associated with feedforward motor control and sensorimotor realignment. We found no evidence that strategic recalibration was different between people with CRPS and controls, including no evidence for differences in a kinematic marker associated with trial-by-trial changes in movement plans. Participants made significant endpoint errors in the prism adaptation after-effect phase, which are indicative of sensorimotor realignment. Overall, the magnitude of this realignment was not found to differ between people with CRPS and pain-free controls. However, people with CRPS made greater endpoint errors when using their affected hand than their non-affected hand, whereas no such difference was seen in controls. Taken together, these findings suggest that strategic control and sensorimotor realignment were not impaired for either arm in people with CRPS. In contrast, they provide some evidence that there is a greater propensity for sensorimotor realignment in CRPS, consistent with more flexible representations of the body and peripersonal space. Our study challenges the theory that sensorimotor conflict might underlie pathological pain that is maintained in the absence of tissue pathology.