Since Descartes’ time, pain is traditionally seen as the consequence of an increase in pain input. Also in chronic pain this mechanism is still commonly accepted, maintained via peripheral pathological triggers. In 1965 Melzack and Wall proposed a new theory of pain, which has revolutionized the way pain physicians and researchers look at pain. It basically suggested that pain was the result of a balance problem in pain input in the spinal cord, in which large fibers do not sufficiently suppress activity of the pain transmitting and C-fibers. We here show using multimodal imaging techniques that chronic pain is not only the result of an imbalance in increased spinal pain input, but a consequence of an imbalance in the brain between pain input and pain suppressing areas, resulting from a dysfunctional communication between the main hubs controlling pain input and pain suppression. In view of the analogy between pain, tinnitus, Parkinson’s disease, and depression it can be proposed to use a similar approach to study these brain disorders, and in view of the common neurological core for physical and psychological pain, this approach could benefit the study of psychological pain as well. It is of interest that the same mechanism might be involved in obesity, suggesting that the imbalance between stimulus input and stimulus suppression might be non-specific and more universally applicable.