The important role of operant learning in chronic pain is widely recognized. However, the precise mechanisms mediating between nociceptive processing, operant consequences and altered pain perception remain being unclear. The general aim of the three studies contained in this thesis was to clarify the latter. For this purpose, experimental operant learning tasks were employed that were independent of subjective pain report, in order to avoid the risk of solely changing response crite-ria. Further, intrinsic reinforcement—within the nociceptive system by reductions in nociceptive input—was applied. In contrast to extrinsic reinforcement—external to the nociceptive system e.g. by monetary reinforcement—intrinsic reinforcement directly affects pain perception. In study 1, a continuous operant conditioning procedure for enhancing pain sensitivity with different magnitudes of reinforcement and different schedules of reinforcement was implemented in healthy participants. The results indicated a dose-dependency of the operant learning. Further, enhanced pain sensitivity was the result of underlying learning rather than immediate (unconditioned) effects of reinforcement (pain relief). Together with a previous study, the independence of the operant learning mechanism from the experimental procedure was demonstrated. Thus, operant learning of pain sensitivity was demonstrated to be a valid and robust mechanism. In order to demonstrate operant learning to be implicit—i.e. learning without awareness—study 2 employed a discrete-trial operant learning procedure in healthy participants similar to a previously implemented operant learning procedure. Awareness was tested with a behavioral task (prediction of reinforcement) and a standardized interview, addressing different levels of processing. The results demonstrated that operant learning of altered pain sensitivity was implicit; neither verbalization of the operant contingencies (the relationships between behavior and stimuli associated with reinforcement) nor behavioral discrimination was necessary for successful operant learning. Study 3 repeated the same paradigm as study 2 in chronic pain patients with fibromyalgia with and without comorbid irritable bowel syndrome for testing the vulnerability of these patients to operant learning of altered pain sensitivity. In contrast to a hypothesized heightened vulnerability, operant learning was impaired in these patients compared to healthy participants. Moreover, fibromyalgia patients with and without irritable bowel syndrome respond differentially to the operant conditioning: While fibromyalgia patients with irritable bowel syndrome showed no signs of operant learning, fibromyalgia patients without irritable bowel syndrome displayed enhanced perceptual sensitization, but this enhancement was paradoxically more pronounced in the habituation learning condition than in the sensitization learning condition. Thus, parameters of operant learning of altered pain sensitivity differentiated between healthy participants and chronic pain patients as well as between different groups of chronic pain patients. In addition, a dissociation of physical stimulus intensities and subjective pain reports was observed, indicating that overt reporting is not the adequate representation level of pain perception relevant for learning altered pain sensitivity. Taken together, these studies demonstrated (1) operant learning to a be powerful, pathogenetically relevant mechanism, producing gross changes in pain sensitivity without the persons’ knowledge and (2) the necessity of behavioral discrimination paradigms that do not depend on subjective measures of pain expe-rience in the first place. The proposed implicit operant learning mechanism of altered pain sensitivity with intrinsic reinforcement provides an explanation for the gradual development of hypersensitivity in pain that is becoming chronic. These results have implications for a wide range of applications ranging from diagnostic procedures to therapeutical interventions in chronic pain
