Conclusion: At equal levels of pressure, patients with CLBP or fibromyalgia experienced significantly more pain and showed more extensive, common patterns of neuronal activation in pain-related cortical areas. When stimuli that elicited equally painful responses were applied (requiring significantly lower pressure in both patient groups as compared with the control group), neuronal activations were similar among the three groups. These findings are consistent with the occurrence of augmented central pain processing in patients with idiopathic CLBP.
Chronic low back pain (CLBP) is one of the most common and expensive musculoskeletal disorders in developed countries. Back pain in general affects 70–85% of all people at some time in their lives, but 90% of affected individuals recover, typically within 12 weeks. Recovery after 12 weeks is slow and uncertain, and this subset of patients with CLBP accounts for major expenses in the health care and disability systems.
Despite the magnitude of the problem, little is known about the precise cause of CLBP. There is often a mismatch between objective findings and symptoms. Despite advances in imaging, in most patients, it is impossible to determine whether identifiable structural or mechanical abnormalities are responsible for the symptoms. Moreover, even when anatomic abnormalities are detected, the significance is unclear, since bulging disks or annular tears are found in high percentages of asymptomatic individuals. This mismatch between anatomic abnormalities and symptoms has led to studies of the psychosocial factors that may contribute to CLBP. These studies suggest that increasing age, female sex, lower levels of formal education, depression, stress, job dissatisfaction, and disability/compensation issues may play some role in expression of symptoms and in chronicity. However, all of the known anatomic, demographic, and psychosocial factors that might cause CLBP do not explain the symptoms in a significant number of subjects. These individuals are sometimes referred to as having “idiopathic” or “nonspecific” CLBP.
Pain in other idiopathic chronic pain conditions, such as irritable bowel syndrome and fibromyalgia syndrome (FMS), appears to result from abnormalities in pain processing rather than from damage or inflammation of peripheral structures. A common finding in these and other “central” or “non-nociceptive” pain syndromes is increased tenderness to pressure, which can be classified as mechanical hyperalgesia (i.e., increased pain in response to normally painful stimuli) and/or mechanical allodynia (i.e., pain in response to normally nonpainful stimuli). These abnormalities are found even in the absence of any identifiable psychological or behavioral factors, thus implicating central mechanisms that exacerbate pain (e.g., “wind-up”) or that attenuate pathways that begin in the brain stem and normally inhibit the ascending transmission of pain-related activity.