Evidence of augmented central pain processing in idiopathic chronic low back pain

Abstract

Objective. For many individuals with chronic low back pain (CLBP), there is no identifiable cause. In other idiopathic chronic pain conditions, sensory testing and functional magnetic resonance imaging (fMRI) have identified the occurrence of generalized increased pain sensitivity, hyperalgesia, and altered brain processing, suggesting central augmentation of pain processing in such conditions. We compared the results of both of these methods as applied to patients with idiopathic CLBP (n ‫؍‬ 11), patients with widespread pain (fibromyalgia; n ‫؍‬ 16), and healthy control subjects (n ‫؍‬ 11).Methods. Patients with CLBP had low back pain persisting for at least 12 months that was unexplained by MRI/radiographic changes. Experimental pain testing was performed at a neutral site (thumbnail) to assess the pressure-pain threshold in all subjects. For fMRI studies, stimuli of equal pressure (2 kg) and of equal subjective pain intensity (slightly intense pain) were applied to this same site.Results. Despite low numbers of tender points in the CLBP group, experimental pain testing revealed hyperalgesia in this group as well as in the fibromyalgia group; the pressure required to produce slightly intense pain was significantly higher in the controls (5.6 kg) than in the patients with CLBP (3.9 kg) (P ‫؍‬ 0.03) or the patients with fibromyalgia (3.5 kg) (P ‫؍‬ 0.006).When equal amounts of pressure were applied to the 3 groups, fMRI detected 5 common regions of neuronal activation in pain-related cortical areas in the CLBP and fibromyalgia groups (in the contralateral primary and secondary [S2] somatosensory cortices, inferior parietal lobule, cerebellum, and ipsilateral S2). This same stimulus resulted in only a single activation in controls (in the contralateral S2 somatosensory cortex). When subjects in the 3 groups received stimuli that evoked subjectively equal pain, fMRI revealed common neuronal activations in all 3 groups.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 3 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 (1,2). 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 (3). 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 (2,4).Despite the magnitude of the problem, little is known about the precise cause of CLBP. There is often a mismatch between objectiv...

Low pressure pain thresholds are associated with, but does not predispose for, low back pain

“…This was found to be the case in cross-sectional observations at both baseline and 8-year follow-up and corroborates previous findings [5,7,22]. The study by Jensen et al [15] reported a correlation between number of tender points and intensity of LBP in a population of sub-acute and CLBP with 4-12 weeks of sick-listing.…”

“…generalized hyperalgesia) and a range of chronic or long-lasting pain conditions, including chronic low back pain (CLBP) [5,7,14,15,22]. Such generalized hyperalgesia may be maintained by nociception and may be modulated by changes in the afferent barrage [19,26].…”

Concurrent activation of the somatosensory forebrain and deactivation of periaqueductal gray associated with diabetes-induced neuropathic pain

“…In addition, noxious stimulation of the nerve damaged hindpaw also produced higher levels of discharge in S1, which lasted for extended periods following the termination of the stimulus (Guilbaud, et al, 1992). Furthermore, neuroimaging studies in patients with chronic low back pain, fibromyalgia and peripheral nerve injury have also reported increased activity in somatosensory cortices , Giesecke, et al, 2004.…”

Chronic Back Pain Is Associated with Decreased Prefrontal and Thalamic Gray Matter Density

“…Thus, DLPFC atrophy may lead to a disruption of its control over orbitofrontal activity, which in turn is critical in the perception of negative affect in general (Small, 2002;Goel and Dolan, 2003) and particularly in pain states (Price, 2000;Apkarian et al, 2004b). Thalamic atrophy in CBP is important, because it is a major source of nociceptive inputs to the cortex (although the peak decrease in gray matter seems more anterior than the medial thalamic target of spinothalamic terminations), and damage to this region may be a reason for the generalized sensory abnormalities commonly associated with chronic pain (Moriwaki and Yuge, 1999;Rommel et al, 2001;Fishbain et al, 2003;Giesecke et al, 2004). Moreover, the thalamic atrophy that we observe provides an explanation for repeated reports of decreased baseline and stimulus-evoked activity and for abnormal chemistry within the thalamus for diverse chronic pain states (Apkarian et al, 2004b).…”