The finding of augmented stimulation-evoked pain, assessed by patient self-report, has recently been corroborated by functional brain imaging techniques that allow the visualization of structures that are potentially involved in pain processing. These methods infer increased neural activity from highly localized increases in regional cerebral blood flow that are produced in response to anticipated metabolic demands. These methods can involve infusion of radioactive tracers or, in the case of functional magnetic resonance imaging (fMRI), the magnetic character of the level of oxygen in the blood is used as an indirect, intrinsic tracer. Functional imaging studies have shown that painful stimulation produces increased neural activity in structures involved in the processing of sensation, movement, cognition, and emotion. Functional imaging studies in chronic pain states that are characterized by hyperalgesia/allodynia have corroborated patients’ self-reports of mechanical hyperalgesia, identifying objective evidence of augmented responses to pressure stimuli (such as in the viscera and periphery in irritable bowel syndrome and FMS, respectively).
In a recent cross-sectional study of CLBP, we demonstrated that a simple laboratory measure of pressure-pain sensitivity was the best correlate of pain and functional status, exceeding the predictive value of any other demographic, psychological, or radiographic variable. In the present study, we have expanded on this work and performed both experimental pain testing and functional imaging in a cohort of patients with CLBP. This particular cohort was specifically identified to have idiopathic CLBP, i.e., individuals without evidence of any anatomic abnormalities on MRI or plain radiographs that could explain these symptoms. These patients were compared with both a normal healthy control group and a cohort of individuals with FMS.