Human Studies

Slow brushing over the skin activates C-tactile nerve fibers that transmit pleasant tactile experiences in healthy subjects, leading to an inverted U-shaped velocity dependence of ratings: C-tactile optimal stroking stimulations are rated as more pleasant than slower or faster stimulations. Chronic pain diseases such as postherpetic neuralgia (PHN) and complex regional pain syndrome show altered C-fiber innervation density, sensory loss, and pain sensitization.

Evidence supports but is inconclusive that sensitization contributes to chronic pain in some adults with sickle cell disease (SCD). We determined the prevalence of pain sensitization among adults with SCD pain compared with pain-free healthy adults. In a cross sectional, single session study of 186 African American outpatients with SCD pain (age 18-74 years, 59% female) and 124 healthy age, gender, and race matched control subjects (age 18-69 years, 49% female), we compared responses to standard thermal (Medoc TSA II) and mechanical stimuli (von Frey filaments). Although we observed no significant differences in thermal thresholds between controls and patients, patients with SCD had lower pain thresholds to mechanical stimuli and reported higher pain intensity scores to all thermal and mechanical stimuli at a non-painful body site. Compared with controls, about twice as many patients with SCD showed sensitization: 12% versus 23% at the anterior forearm site (p=.02), and 16% versus 32% across three tested sites (p=.004). Among patients with SCD, 18% exhibited some element of central sensitization. Findings indicate that persistent allodynia and hyperalgesia can be part of the SCD pain experience and should be considered when selecting therapies for SCD pain. Perspective: Compared with matched healthy controls, quantitative sensory testing in adults with pain and sickle cell disease (SCD) demonstrates higher prevalence of sensitization, including central sensitization. The findings of allodynia and hyperalgesia may indicate neuropathic pain and could contribute to a paradigm shift in assessment and treatment of SCD pain.

Evidence from genome-wide and candidate gene association studies, familial aggregation and linkage analyses demonstrate the genetic contribution to fibromyalgia (FM) disease. This study aimed to identify genetic biomarkers of FM and its related comorbid disorders, by exploring 41 polymorphisms potentially involved in FM pathogenesis in families with at least one patient with FM.

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).

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.

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).