The journal of pain : official journal of the American Pain Society
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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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Chronic pain resulting from physical stressors is often accompanied by psychological disorders such as depression. Although depressive disorders are associated with changes in brain anatomy, it remains unknown if changes in brain anatomy associated with increased state depression levels also occur in patients with chronic pain. When individuals are experiencing physical stressors such as ongoing pain, depressive personality traits may predispose them to develop depressive states. The aim of this study was to use brain morphometry to determine the interaction among chronic pain, state and trait depression, and regional brain structure. We investigated regional gray matter volume in 42 chronic pain patients and 35 controls using voxel-based morphometry of T1-weighted anatomical images. Significant relationships between regional gray matter volume and state or trait depressive values were determined. In chronic pain patients, state depression scores were significantly correlated to subtle changes in the thalamus and the cingulate, dorsolateral prefrontal, and hippocampal cortices. These same brain regions were also significantly correlated to trait depressive scores. Unexpectedly, gray matter volumes in these regions were not correlated to trait depressive scores in healthy controls. Because trait depressive values were not correlated to gray matter in controls, but were so in chronic pain patients, these data strongly suggest that subtle changes in brain anatomy can evoke changes in individuals' trait depression values. If these regional gray matter changes are severe enough, changes in an individual's personality trait may result. ⋯ This study demonstrates anatomical brain alterations associated with both state and trait depression in chronic pain patients. Because our study reveals that trait depression is not correlated to the anatomy of these regions in healthy controls, ongoing pain itself may result in anatomical changes that in turn can alter an individual's personality.
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Previous studies have reported that the intrathecal (i.t.) administration of transforming growth factor β1 (TGF-β1) prevents and reverses neuropathic pain. However, only limited information is available regarding the possible role and effects of spinal TGF-β1 in neuropathic pain. We aimed to investigate the antinociceptive effects of exogenous TGF-β1 on chronic constriction injury (CCI)-induced neuropathic pain in rats. We demonstrated that sciatic nerve injury caused a downregulation of endogenous TGF-β1 levels on the ipsilateral side of the lumbar spinal dorsal gray matter, and that the i.t. administration of TGF-β1 (.01-10 ng) significantly attenuated CCI-induced thermal hyperalgesia in neuropathic rats. TGF-β1 significantly inhibited CCI-induced spinal neuroinflammation, microglial and astrocytic activation, and upregulation of tumor necrosis factor-α. Moreover, i.t. TGF-β1 significantly attenuated the CCI-induced downregulation of glutamate transporter 1, the glutamate aspartate transporter, and the excitatory amino acid carrier 1 on the ipsilateral side. Furthermore, i.t. TGF-β1 significantly decreased the concentrations of 2 excitatory amino acids, aspartate and glutamate, in the spinal dialysates in CCI rats. In summary, we conclude that the mechanisms of the antinociceptive effects of i.t. TGF-β1 in neuropathy may include attenuation of spinal neuroinflammation, attenuation, or upregulation of glutamate transporter downregulation, and a decrease of spinal extracellular excitatory amino acids. ⋯ Clinically, medical treatment is usually initiated after the onset of intractable pain. Therefore, in the present study, i.t. TGF-β1 was designed to be administered 2 weeks after the establishment of CCI pain. Compared to the continuous TGF-β1 infusion mode, single-dose administration seems more convenient and practical to use.
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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.