An Observational Study Comparing Fibromyalgia and Chronic Low Back Pain in Somatosensory Sensitivity, Motor Function and Balance

Fibromyalgia (FM) and chronic low back pain (CLBP) have shared pathophysiology and have a considerable impact on patients’ daily activities and quality of life. The main objective of this study was to compare pain impact, somatosensory sensitivity, motor functionality, and balance among 60 patients with FM, 60 patients with CLBP, and 60 pain-free controls aged between 30 and 65 years. It is essential to know the possible differences existing in symptomatology of two of the major chronic pain processes that most affect the population, such as FM and CLBP. The fact of establishing possible differences in sensory thresholds, motor function, and proprioceptive measures among patients with FM and CLBP could bring us closer to a greater knowledge of the chronic pain process. Through an observational study, a comparison was made between the three groups (FM, CLBP, and pain-free controls) evaluating functional performance, postural balance, kinematic gait parameters, strength, depression, fatigue, and sensitivity to pain and vibration. Patients with chronic pain showed worse somatosensory sensitivity (p < 0.001) and motor function (p < 0.001) than pain-free controls. Moreover, patients with FM showed greater pain impact (p < 0.001) and bigger somatosensory (p < 0.001) and motor deficiencies (p < 0.001) than patients with CLBP. Further research should explore the possible reasons for the greater deterioration in patients with FM in comparison with other chronic pain conditions. Our results, showing the multiple areas susceptible of deterioration, make it necessary to adopt interdisciplinary interventions focused both on physical and emotional dysfunction.

Estrogens influence female itch sensitivity via the spinal gastrin-releasing peptide receptor neurons

There are sex differences in somatosensory sensitivity. Circulating estrogens appear to have a pronociceptive effect that explains why females are reported to be more sensitive to pain than males. Although itch symptoms develop during pregnancy in many women, the underlying mechanism of female-specific pruritus is unknown. Here, we demonstrate that estradiol, but not progesterone, enhances histamine-evoked scratching behavior indicative of itch in female rats. Estradiol increased the expression of the spinal itch mediator, gastrin-releasing peptide (GRP), and increased the histamine-evoked activity of itch-processing neurons that express the GRP receptor (GRPR) in the spinal dorsal horn. The enhancement of itch behavior by estradiol was suppressed by intrathecal administration of a GRPR blocker. In vivo electrophysiological analysis showed that estradiol increased the histamine-evoked firing frequency and prolonged the response of spinal GRP-sensitive neurons in female rats. On the other hand, estradiol did not affect the threshold of noxious thermal pain and decreased touch sensitivity, indicating that estradiol separately affects itch, pain, and touch modalities. Thus, estrogens selectively enhance histamine-evoked itch in females via the spinal GRP/GRPR system. This may explain why itch sensation varies with estrogen levels and provides a basis for treating itch in females by targeting GRPR.

Drop homotopic effects of masseter-muscle pain on somatosensory sensitivity in healthy participants

Current pain classifications use 1.0-kg palpation of the masseter muscle to distinguish between “pain patients” and “healthy controls” but a thorough understanding of the normal physiological responses to various somatosensory stimuli is lacking. The aim of this study was to investigate somatosensory function of the skin over the masseter muscle in healthy participants that were divided into a masseter pain prone group (MPP) (n = 22) and non-MPP group (n = 22), according to the response to a 1.0-kg palpation. Quantitative sensory testing (QST) was performed at the skin above the right masseter muscle (homotopic). In an additional experiment, 13 individuals each from MPP and non-MPP received application of 60% topical lidocaine tape to the skin over the masseter muscle for 30 min. Immediately after, mechanical pain sensitivity (MPS), dynamic mechanical allodynia, and pressure pain threshold were tested. Homotopic MPS was significantly higher and PPTs significantly lower in MPP than in N-MPP (P < 0.05). Strikingly, no other differences in QST outcomes were observed between the groups (P > 0.05). After lidocaine application, no significant differences in homotopic MPS were observed between groups. The presence or absence of acute provoked pain in masseter muscle is exclusively associated with differences in homotopic MPS which is decreased following topical anesthesia.

Serum artemin is not correlated with sensitivity within dogs with naturally occurring osteoarthritis pain

Osteoarthritis (OA) pain is associated with peripheral and central sensitization in humans and results in widespread increased sensitivity across the body. Sensitization contributes to the OA-associated pain (OAP) state. We recently identified increased levels of an endogenous neurotrophic factor, artemin (ARTN), in dogs with OAP compared to healthy pain-free controls. Circulating ARTN released from damaged tissues in OA, may play a central role in widespread sensitivity and pain. However, the relationship between ARTN and somatosensory sensitivity remains unknown. The study aimed to assess the relationship between serum ARTN concentrations and measures of sensitivity in dogs with OAP using quantitative sensory testing. We hypothesized that there would be a positive association between circulating ARTN and increased sensitivity to mechanical and thermal stimuli in dogs with OAP. We used linear and logistic regression models to assess the relationship between ARTN, sensitization, and pain within a cohort of 43 dogs with spontaneous OAP. Serum ARTN was not associated with the degree of sensitization within dogs with OAP. Further, across dogs with varying OAP severity, we did not find any association between ARTN, and clinical measures of joint pain and disability. Although a relationship between ARTN and joint pain was not ruled out.