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Quantitative sensory testing (QST) is used to systematically interrogate normal responding and alterations of nervous system function, including pain related central sensitization (CS). However, up to now QST of CS in human subjects has been mostly focused on temporal summation of second pain (TSSP), has been difficult to perform, and has been associated with low reliability. In contrast, slow ramp & hold (RH) procedures are simpler tests of temporal summation and easier to perform. We examined the usefulness of RH procedures as reliable generators of CS using two validated QST procedures: decay of pain aftersensations and wind-down. Twenty-seven pain-free subjects (74% female) were enrolled into the study. Trains of sensitivity adjusted TSSP or RH heat stimuli were applied to the hands of participants to achieve moderate temporal pain summation [50 NRS (0-100)]. Fifteen second aftersensations and 30s wind-down related to TSSP or RH were used for CS comparisons. Reliability of all test procedures was tested over 24 h. Use of sensitivity adjusted TSSP and RH heat stimuli resulted in average pain ratings of 48.2 and 49.6 NRS, respectively. Aftersensations or wind-down decay were not significantly different after either TSSP or RH, (all p > .05), indicating that each procedure achieved similar levels of short-term CS. Sensitivity adjusted RH stimuli were well tolerated and resulted in reliable pain increases of 50 NRS. The magnitude of short-term CS, determined by aftersensations and wind-down was similar after sensitivity-adjusted TSSP and RH stimuli (p > .05), suggesting that pain facilitation of healthy participants and likely chronic pain patients can not only be tested with TSSP but also with RH procedures. Perspective: This article examines the ability of RH procedures to generate similar central sensitivity augmentation than TSSP. The results suggest that RH is similarly well suited as TSSP to explore central pain mechanisms in healthy subjects and most likely also in chronic pain patients.
To assess the efficacy of three months of antibiotic treatment compared with placebo in patients with chronic low back pain, previous disc herniation, and vertebral endplate changes (Modic changes).
Opioids are prescribed more frequently than nonpharmacologic treatments for persistent musculoskeletal pain (MSP). We estimate the association between the supply of physical therapy (PT) and mental health (MH) providers and early nonpharmacologic service use with high-risk opioid prescriptions among Medicare beneficiaries with persistent MSP.
While much brain research on fibromyalgia (FM) focuses on the study of hyper-responsiveness to painful stimuli, some studies suggest that the increased pain-related brain activity often reported in FM studies may be in part explained by stronger responses to salient aspects of the stimulation rather than, or in addition to, its painfulness. We thus hypothesized that FM patients would demonstrate elevated brain responses to both pain onset and offset, two salient sensory events of opposing valences.
Primary somatosensory cortex (S1) is involved in pain processing and thus its suppression using neuromodulatory techniques such as continuous theta burst stimulation (cTBS) might be a potential pain management strategy in patients with neuropathic pain. cTBS over S1 is known to elevate pain threshold in young adults. However, the time course of this after-effect is unknown. Furthermore, the effect of cTBS over S1 on pain threshold might be confounded by changes in the excitability of primary motor cortex (M1), an area known to be involved in pain processing, due to spread of current. Therefore, whether S1 plays a role in pain processing independent of M1 also remains unknown. The corticospinal excitability (CSE) can provide a measure of M1 excitability because cTBS over M1 is known to reduce CSE. Here, we studied the time-course of the effects of MRI-guided cTBS over S1 on electrical pain threshold and CSE. Ten healthy young adults received cTBS over S1 and sham stimulation in counterbalanced sessions at least 5 days apart. Electrical pain threshold (EPT) and CSE were recorded before and following cTBS over S1. We assessed each measure once before stimulation and then every 10 min starting immediately after stimulation until 40 min. cTBS over S1 elevated EPT compared to sham stimulation with the after-effect lasting for 40 min. We observed no change in CSE following cTBS and sham stimulation. Our findings suggest that cTBS over S1 can elevate EPT for 40 minutes without altering M1 excitability.
This is a small pilot study to evaluate the effectiveness of an intravenous (IV) valproate sodium therapy protocol for migraine prevention in a population of patients with chronic migraine refractory to multiple preventive medications.
Native Americans (NAs) have a higher prevalence of chronic pain than other U.S. racial/ethnic groups, but there have been few attempts to understand the mechanisms of this pain disparity. This study used a comprehensive battery of laboratory tasks to assess peripheral fiber function (cool/warm detection thresholds), pain sensitivity (eg, thresholds/tolerances), central sensitization (eg, temporal summation), and pain inhibition (conditioned pain modulation) in healthy, pain-free adults (N = 155 NAs, N = 150 non-Hispanic Whites [NHWs]). Multiple pain stimulus modalities were used (eg, cold, heat, pressure, ischemic, and electric), and subjective (eg, pain ratings and pain tolerance) and physiological (eg, nociceptive flexion reflex) outcomes were measured. There were no group differences on any measure, except that NAs had lower cold-pressor pain thresholds and tolerances, indicating greater pain sensitivity than NHWs. These findings suggest that there are no group differences between healthy NAs and NHWs on peripheral fiber function, central sensitization, or central pain inhibition, but NAs may have greater sensitivity to cold pain. Future studies are needed to examine potential within-group factors that might contribute to NA pain risk.
EpiFibro (Brazilian Epidemiological Study of Fibromyalgia) was created to study patients with fibromyalgia (FM). Patients were included since 2011 according to the classification criteria for FM of the American College of Rheumatology of 1990 (ACR1990).
Inconsistent findings from migraine neuroimaging studies have limited attempts to localize migraine symptomatology. Novel brain network mapping techniques offer a new approach for linking neuroimaging findings to a common neuroanatomical substrate and localizing therapeutic targets. In this study, we attempted to determine whether neuroanatomically heterogeneous neuroimaging findings of migraine localize to a common brain network. We used meta-analytic coordinates of decreased grey matter volume in migraineurs as seed regions to generate resting state functional connectivity network maps from a normative connectome (n = 1000). Network maps were overlapped to identify common regions of connectivity across all coordinates. Specificity of our findings was evaluated using a whole-brain Bayesian spatial generalized linear mixed model and a region of interest analysis with comparison groups of chronic pain and a neurologic control (Alzheimer's disease). We found that all migraine coordinates (11/11, 100%) were negatively connected (t ≥ ±7, P < 10-6 family-wise error corrected for multiple comparisons) to a single location in left extrastriate visual cortex overlying dorsal V3 and V3A subregions. More than 90% of coordinates (10/11) were also positively connected with bilateral insula and negatively connected with the hypothalamus. Bayesian spatial generalized linear mixed model whole-brain analysis identified left V3/V3A as the area with the most specific connectivity to migraine coordinates compared to control coordinates (voxel-wise probability of ≥90%). Post hoc region of interest analyses further supported the specificity of this finding (ANOVA P = 0.02; pairwise t-tests P = 0.03 and P = 0.003, respectively). In conclusion, using coordinate-based network mapping, we show that regions of grey matter volume loss in migraineurs localize to a common brain network defined by connectivity to visual cortex V3/V3A, a region previously implicated in mechanisms of cortical spreading depression in migraine. Our findings help unify migraine neuroimaging literature and offer a migraine-specific target for neuromodulatory treatment.
This study aimed to analyze the associations among depressive/anxiety and pain symptoms in patients diagnosed with chronic pain.