The journal of pain : official journal of the American Pain Society
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Observational Study
Pain sensitivity and autonomic factors associated with development of TMD: the OPPERA prospective cohort study.
Multiple studies report that individuals with chronic temporomandibular disorder (TMD) have enhanced sensitivity to experimental pain. Additionally, chronic TMD cases show altered autonomic function, including elevated heart rate and reduced heart rate variability. However, causal inferences regarding the association between TMD and pain sensitivity and autonomic function cannot be drawn from these cross-sectional observations. The prospective Orofacial Pain: Prospective Evaluation and Risk Assessment (OPPERA) study examines whether measures of pain sensitivity or cardiac autonomic function provide predictive value in TMD incidence. A cohort of 2,737 initially TMD-free participants was followed for up to 5.2 years, during which time 260 developed first-onset TMD. Fourteen of 39 experimental pain measures produced significant hazard ratios, such that greater pain sensitivity was associated with greater TMD incidence. A single autonomic measure-heart rate at rest-was also associated significantly with greater TMD incidence. In contrast, using the same measures of pain sensitivity and cardiac autonomic function, we previously reported a larger group of variables that was significantly associated with chronic TMD in the OPPERA case-control study. Future studies should investigate whether premorbid pain sensitivity or autonomic function more specifically predicts risk of developing chronic TMD than first-onset TMD. ⋯ Our previous case-control studies showed that associations with both pain sensitivity and cardiac autonomic function are profound in chronic TMD cases. Here we show that some measures of enhanced pain sensitivity contribute modestly to the risk of developing TMD whereas autonomic dysregulation appears to confer little or no risk for TMD incidence.
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Comparative Study
Comparative responsiveness of verbal and numerical rating scales to measure pain intensity in patients with chronic pain.
Verbal rating scale (VRS) and numerical rating scale (NRS) are regularly used to assess and monitor pain in chronic pain patients. Although the NRS has been generally preferred, limited comparative responsiveness evidence was reported. This study compared the responsiveness of VRS and NRS measuring current pain and investigated the influence of different references (ie, worst, least, average, and current pain or their composite) on the NRSs' responsiveness. Two hundred fifty-four chronic pain patients attended a 10-day pain self-management program and were assessed with two 6-point VRSs (assessing current pain) and four 11-point NRSs (assessing worst, least, average, and current pain) at pre- and posttreatment. A patient-reported rating of pain improvement was used as the criterion for standardized response mean and receiver operating characteristic curve analyses. Results showed that the VRSs and NRSs exhibited small responsiveness in all patients, but the magnitude of responsiveness became moderate to large in patients with improved pain. However, in patients with pain improvements, the NRS current pain item and composite score (made up of the 4 pain items) were found to have significantly larger responsiveness and greater discriminatory ability to detect the presence of improvement than other current pain VRSs and the NRSs assessing worst, least, and average pain. Potential implications for clinical practice are discussed. ⋯ This study shows that the current pain and composite NRSs were more responsive than the current pain VRSs and the NRSs measuring other individual pain references in patients with improved pain, undertaking a short-term, self-management program. The results help inform the selection of pain intensity measures in studies using similar types of intervention.
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The temporal dynamics of the blood oxygen level-dependent (BOLD) signal, especially for painful stimulations, is not completely understood. In this study, the BOLD signal response to a long painful electrical stimulation (a continuous painful stimulation of 2 minutes) is directly compared to that of a short painful stimulation (four 30-second periods of painful stimulation interleaved with 30-second rest) in an effort to further probe the relationship between the temporal dynamics of the BOLD signal during constant-intensity pain stimulation. Time course analysis showed that both stimulation protocols produced 3 similarly timed peaks in both data sets, suggesting an early and delayed BOLD response to painful stimulation initiation, and a response related to stimulus termination. Despite the continuous stimulation, the BOLD signal returned to baseline in the 2-minute task. Even with this signal discrepancy, however, the activation maps of the 2 pain tasks differed only slightly, suggesting that the bulk of the activation is determined by the sharp rise in BOLD signal with stimulus onset. These findings imply that the BOLD signal response time course is not directly reflective of pain perception. ⋯ This article demonstrates that the BOLD signal for a painful stimulation contains multiple peaks and does not maintain the constant level during stimulation that is assumed in typical analysis. Although these dynamics should be accounted for in future studies because of their ability to confound results, their presence did not significantly alter the overall group maps.
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Although joint pain is common, its mechanisms remain undefined, with little known about the spinal neuronal responses that contribute to this type of pain. Afferent activity and sustained spinal neuronal hyperexcitability correlate to facet joint loading and the extent of behavioral sensitivity induced after painful facet injury, suggesting that spinal neuronal plasticity is induced in association with facet-mediated pain. This study used a rat model of painful C6-C7 facet joint stretch, together with intrathecal administration of gabapentin, to investigate the effects of one aspect of spinal neuronal function on joint pain. Gabapentin or saline vehicle was given via lumbar puncture prior to and at 1 day after painful joint distraction. Mechanical hyperalgesia was measured in the forepaw for 7 days. Extracellular recordings of neuronal activity and astrocytic and microglial activation in the cervical spinal cord were evaluated at day 7. Gabapentin significantly (P = .0001) attenuated mechanical hyperalgesia, and the frequency of evoked neuronal firing also significantly decreased (P < .047) with gabapentin treatment. Gabapentin also decreased (P < .04) spinal glial fibrillary acidic protein expression. Although spinal Iba1 expression was doubled over sham, gabapentin did not reduce it. Facet joint-mediated pain appears to be sustained through spinal neuronal modifications that are also associated with astrocytic activation. ⋯ Intrathecal gabapentin treatment was used to investigate behavioral, neuronal, and glial response in a rat model of painful C6-C7 facet joint stretch. Gabapentin attenuated mechanical hyperalgesia, reduced evoked neuronal firing, and decreased spinal astrocytic activation. This study supports that facet joint pain is sustained through spinal neuronal and astrocytic activation.