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Sensorimotor Peak Alpha Frequency Is a Reliable Biomarker of Prolonged Pain Sensitivity.

Previous research has observed that the speed of alpha band oscillations (8-12 Hz range) recorded during resting electroencephalography is slowed in chronic pain patients. While this slowing may reflect pathological changes that occur during the chronification of pain, an alternative explanation is that healthy individuals with slower alpha oscillations are more sensitive to prolonged pain, and by extension, more susceptible to developing chronic pain. To test this hypothesis, we examined the relationship between the pain-free, resting alpha oscillation speed of healthy individuals and their sensitivity to two models of prolonged pain, Phasic Heat Pain and Capsaicin Heat Pain, at two visits separated by 8 weeks on average (n = 61 Visit 1, n = 46 Visit 2). We observed that the speed of an individual's pain-free alpha oscillations was negatively correlated with sensitivity to both models and that this relationship was reliable across short (minutes) and long (weeks) timescales. Furthermore, the speed of pain-free alpha oscillations can successfully identify the most pain sensitive individuals, which we validated on data from a separate, independent study. These results suggest that alpha oscillation speed is a reliable biomarker of prolonged pain sensitivity with potential for prospectively identifying pain sensitivity in the clinic.

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An Initial Psychometric Evaluation of the Pain Concepts Questionnaire in a Low-SES Setting.

The examination of pain beliefs for chronic pain assessment and treatment has been a growing area of interest. A variety of questionnaires have been developed to assess pain beliefs, however, these questionnaires often require high levels of literacy and education. The Pain Concepts Questionnaire (PCQ) was developed with literacy-adaptations to better evaluate pain beliefs in a low socioeconomic (SES) population. This study is an initial exploratory evaluation of the PCQ in a sample of patients with chronic pain and multiple disparities as part of the Learning About My Pain (LAMP) trial, a randomized controlled trial comparing literacy-adapted psychosocial treatments for chronic pain. All data were collected at pre-treatment. Exploratory factor analysis (EFA) was performed to examine the underlying factor structure of the PCQ and cross-sectional correlational analyses examined relationships between pain beliefs with sociodemographic factors and chronic pain-related variables. Results suggested a 2-factor solution with a Biopsychosocial factor and Biomedical factor. Consistent with the literature, correlational analyses highlighted racial and SES disparities in pain beliefs and the importance of beliefs in pain- and cognitive/affective-related functioning. The study emphasizes the importance of pain beliefs in chronic pain management and recommends future research to further examine additional psychometric properties of the PCQ.

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JTC-801 alleviates mechanical allodynia in paclitaxel-induced neuropathic pain through the PI3K/Akt pathway.

Chemotherapy-induced peripheral neuropathy is a serious adverse effect of chemotherapeutic agents such as paclitaxel. JTC-801, a nociceptin/orphanin FQ opioid peptide (NOP) receptor antagonist, has been reported to attenuate neuropathic pain in several pain models. However, the therapeutic significance and function of JTC-801 in chemotherapy-induced peripheral neuropathy remain unclear. In this study, we determined the effect of JTC-801 on neuropathic pain induced by paclitaxel, and we explored the potential mechanism in the dorsal root ganglion (DRG). The behavioral test showed that single or multiple systemic administrations of JTC-801 significantly alleviated mechanical allodynia in paclitaxel-treated rats. Using Western blot analysis and immunohistochemistry, we found that paclitaxel increased the expression of phosphatidylinositol 3-kinase (PI3K) and phospho-Akt (p-Akt) in the DRG. Double immunofluorescence staining indicated that p-Akt was expressed in neurons in the DRG. Multiple injections of JTC-801 significantly inhibited the activation of Akt and decreased the expression of inflammatory cytokines. The data suggest that JTC-801 alleviates mechanical allodynia associated with paclitaxel-induced neuropathic pain via the PI3K/Akt pathway.

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A systematic review highlights the need to improve the quality and applicability of trials of physical therapy interventions for low back pain.

To review and assess the methodological quality of randomised controlled trials that test physical therapy interventions for low back pain.

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The effect of sex on motor function, lesion size, and neuropathic pain after contusion spinal cord injury in mice.

Spinal cord injury (SCI) causes neurodegeneration, impairs locomotor function, and impacts the quality of life particularly in those individuals that develop neuropathic pain. Whether the time course of neurodegeneration, locomotor impairment, or neuropathic pain varies with sex, however, remains understudied. Therefore, the objective of this study in male and female C57BL/6 mice was to evaluate the following outcomes for six weeks after a 75-kdyn thoracic contusion SCI: locomotor function using the Basso Mouse Scale (BMS); spinal cord tissue sparing and rostral-caudal lesion length; and mechanical allodynia and heat hyperalgesia using hindpaw application of Von Frey filaments or radiant heat stimuli, respectively. Although motor function was largely similar between sexes, all of the males, but only half of the females, recovered plantar stepping. Rostral-caudal lesion length was shorter in females than in males. All animals, regardless of sex, developed mechanical allodynia and heat hyperalgesia after SCI; there were no differences in pain outcomes between sexes. We conclude that contusion SCI yields subtle sex differences in mice depending on the outcome measure but no significant differences in behavioral signs of neuropathic pain.

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Anxiety, depression, and opioid misuse among adults with chronic pain: the role of emotion dysregulation.

The opioid epidemic is a significant public health concern in the United States, particularly among adults with chronic pain. Considerable research suggests that people with mental health problems, including anxiety and depression, may experience more opioid-related problems in the context of chronic pain. Yet, little work has examined potential mechanisms underyling these relations. Emotion dysregulation is one mechanistic factor that may link anxiety and depression and opioid-related problems among persons with chronic pain. Therefore, the current study examined the explanatory role of emotion dysregulation in the cross-sectional relationship between anxiety and depression problems and current opioid misuse and severity of opioid dependence among 431 adults with chronic pain who reported currently using opioid medications (74% female, M=38.32 years, SD = 11.11). Results indicated that emotion dysregulation explained, in part, the relationship between anxiety and depression symptoms and opioid-related problems. These findings highlight the need to further consider the role of emotion dysregulation among adults with chronic pain who use prescription opioids and experience symptoms of anxiety or depression. Future prospective research will be needed to further establish emotion dysregulation as a mechanism in anxiety/depression-opioid misuse/dependence processes.

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A Comprehensive Review of the Treatment and Management of Myofascial Pain Syndrome.

Myofascial pain syndrome (MPS) is a musculoskeletal pain condition that stems from localized, taut regions of skeletal muscle and fascia, termed trigger points. The purpose of this comprehensive review is to provide updated information on prevalence, pathophysiology, and treatment modalities with a focus on interventional modalities in managing MPS.

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Composite Score Is a Better Reflection of Patient Response to Chronic Pain Therapy Compared With Pain Intensity Alone.

The pain Numeric Rating Scale (NRS) score became standard when pain was introduced as the fifth vital sign in the 1990s. Although plagued with issues, it remains the basis for primary outcome measures in clinical trials for chronic pain therapies. Multidimensional composite scoring that considers all aspects of the chronic pain experience may provide a more meaningful response measure. Herein we propose a multidimensional responder index.

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A Randomized Sham-Controlled Cross-Over Study on the Short-Term Effect of Non-Invasive Cervical Vagus Nerve Stimulation on Spinal and Supraspinal Nociception in Healthy Subjects.

The aim of the present study was to test the effects of vagus nerve stimulation (VNS) on the descending pain inhibition, quantified by the nociceptive flexor (RIII) reflex and the conditioned pain modulation (CPM) paradigm, and on supraspinal nociceptive responses, assessed by pain intensity and unpleasantness ratings and late somatosensory evoked potentials (SEPs), in healthy subjects.

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Early exposure to environmental enrichment protects male rats against neuropathic pain development after nerve injury.

Because environmental elements modify chronic pain development and endogenous mechanisms of pain control are still a great therapeutic source, we investigated the effects of an early exposure to environmental enrichment (EE) in a translational model of neuropathic pain. Young male rats born and bred in an enriched environment, which did not count on running wheel, underwent chronic constriction injury (CCI) of sciatic nerve. EE abolished neuropathic pain behavior 14 days after CCI. Opioid receptors' antagonism reversed EE-analgesic effect. β-endorphin and met-enkephalin serum levels were increased only in EE-CCI group. Blockade of glucocorticoid receptors did not alter EE-analgesic effect, although corticosterone circulating levels were increased in EE animals. In the spinal cord, EE controlled CCI-induced serotonin increase. In DRG, EE blunted the expression of ATF-3 after CCI. Surprisingly, EE-CCI group showed a remarkable preservation of sciatic nerve fibers compared to NE-CCI group. This work demonstrated global effects induced by an EE protocol that explain, in part, the protective role of EE upon chronic noxious stimulation, reinforcing the importance of endogenous mechanisms in the prevention of chronic pain development.

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