The persistence, intractability and apparent absence of peripheral disease to account for many chronic pain disorders has led to an increasing interest in the possibility of a central etiology. Functional imaging has revealed that brain activation in chronic pain patients generally looks similar to that of control subjects receiving experimental pain. Several reviews have suggested a generalized decrease in brain activation in patients with chronic pain from various sources with some studies demonstrating augmented response in the prefrontal or anterior cingulate cortices and reduced response in the thalamus. Most findings are interpreted as supporting dominant themes in the clinical understanding or interpretation of chronic pain, including hypersensitivity, hypervigilance, hyperalgesia, central sensitization, stress mediated dysfunction and, encompassing all these themes, the biopsychosocial model of pain. These interpretations provide a good descriptive account of chronic pain but do not amount to a mechanistic explanation that identifies causal relations. In our lab we have developed several techniques to create pain without injury to model one of the most pressing aspects of chronic pain, which is persistent pain despite the absence of objective biomedical causes. Using hypnosis, we have been able to generate pain without physical stimulation in normal pain free controls. Imaging has demonstrated that this hypnotic pain experience correlates with known pain related regions of the brain. One reasonable interpretation is that these regions can therefore generate pain without a typically noxious stimulus. We have also identified a group of people who respond to images of other people’s pain with pain of their own. This empathic pain often localizes to the region of observed pain and causes activation of brain areas associated with pain from a physically noxious source. We have also used fMRI with a group of fibromyalgia patients who controlled their own fibromyalgia pain with hypnotic suggestion. Functional imaging demonstrated significant association of pain related regions with changes in fibromyalgia pain. Psychological augmentation of sensory information via brain areas that typically process noxious information may therefore cause some chronic pain disorders directly. Alternatively, a failure of the brain to damp non-noxious sensory information may cause chronic allodynic or hyperalgesic pain. We have developed a technique to damp pain experience from a noxious source in normal volunteers and have demonstrated this damping to correlate with activation in the PAG region. We expect to extend this technique to chronic pain patients and hope that by augmenting and damping pain experience we can begin to address the factors that may cause pain without injury. Because brain responses are the final common representation of the processes underlying chronic pain we expect imaging to play a crucial part in developing understanding. This does not, however, necessarily mean that chronic pain is purely a brain problem. How information arrives at the brain matters and it might not always make sense to chase problems of diagnosis and existential psychosocial problems into the brain.