| Pain is a major cause of suffering and multiple chronic pain disorders remain resistant to treatment. A major part of this problem arises from inadequate understanding of pain mechanisms exhibited in the cortex during the experience of pain. The aim of this thesis is to increase our knowledge about the cortical processing of acute and chronic pain.;In the first study we use functional and anatomical approaches to elucidate cortical mechanisms of acute pain perception. We differentiate the brain regions into two components, one involved in nociceptive-specific representation, and a second underlying general magnitude estimation localized within the insula and extending to parietal regions. We show that insula acts as the interface between the two non-overlapping networks, and plays a key role in the transformation of stimulus into perception.;In the second study, we characterize the cortical responses underlying chronic back pain (CBP). We show that it exhibits a unique spatial presentation different from that of acute pain, and is localized to the medial prefrontal cortex. We also show that activity in the medial prefrontal cortex and insula are related to clinical parameters of CBP, mainly intensity and duration.;In the third study, we further investigate the impact of CBP on the cortex. We show that default mode network (DMN) -- a network that is more active at rest and implicated in processing self-referential information is considerably disrupted in CBP patients. We find that the default-mode brain activity of CBP patients remains consistently more engaged than in controls, with a prominent reduction in the total area of de-activated cortex. |
