Pain
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Activation of glial cells and neuro-glial interactions are emerging as key mechanisms underlying chronic pain. Accumulating evidence has implicated 3 types of glial cells in the development and maintenance of chronic pain: microglia and astrocytes of the central nervous system (CNS), and satellite glial cells of the dorsal root and trigeminal ganglia. Painful syndromes are associated with different glial activation states: (1) glial reaction (ie, upregulation of glial markers such as IBA1 and glial fibrillary acidic protein (GFAP) and/or morphological changes, including hypertrophy, proliferation, and modifications of glial networks); (2) phosphorylation of mitogen-activated protein kinase signaling pathways; (3) upregulation of adenosine triphosphate and chemokine receptors and hemichannels and downregulation of glutamate transporters; and (4) synthesis and release of glial mediators (eg, cytokines, chemokines, growth factors, and proteases) to the extracellular space. ⋯ Glial activation also occurs in acute pain conditions, and acute opioid treatment activates peripheral glia to mask opioid analgesia. Thus, chronic pain could be a result of "gliopathy," that is, dysregulation of glial functions in the central and peripheral nervous system. In this review, we provide an update on recent advances and discuss remaining questions.
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Individuals with spinal cord injury (SCI) often have chronic pain, which may have a major impact on their quality of life. The purpose of this article is to present an update on the classification of SCI pain, recent advances in the understanding of underlying mechanisms, and current evidence-based treatment of SCI pain. ⋯ We need to improve preclinical assessment of pain-like behavior in central pain models, and improve the clinical assessment of pain and our understanding of the interaction with cognitive, emotional, and social factors. In future studies on mechanisms and treatment, we need to acknowledge the different phenotypes of chronic SCI pain.
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Radiographic knee osteoarthritis (OA) is a highly prevalent condition that has been the focus of a number of studies identifying factors that are prognostic of continued or worsening pain and function. Although prior prognostic studies have identified a number of demographic, physical, and psychological factors that are predictive of outcome, minimal focus has been placed on pain coping skills as prognostic factors, despite cross-sectional evidence suggesting that pain coping skills are associated with pain and function in knee OA. The present study reports on the use of pain coping skills as prognostic factors for changes in pain and/or function over a 1-year period. ⋯ Data from the Coping Strategies Questionnaire were compared against 1-year change in pain, function, or both, using established criteria for defining whether the patient got better, worse, or stayed the same over the 1-year period. Results revealed a significant effect for praying/hoping, increased behavioral activities, and pain catastrophizing as prognostic of pain outcomes; ignoring pain and praying/hoping were prognostic of function outcomes; and increased behavioral activities and pain catastrophizing were prognostic of a combined pain and function outcome. The findings provide important new evidence regarding the potential clinical relevance of a number of pain coping responses hypothesized to influence future pain and function in persons with arthritis.
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Observational Study
Longitudinal Relationships between Anxiety, Depression, and Pain: Results from a Two Year Cohort Study of Lower Extremity Trauma Patients.
Previous studies have shown that pain, depression, and anxiety are common after trauma. A longitudinal relationship between depression, anxiety, and chronic pain has been hypothesized. Severe lower extremity trauma patients (n = 545) were followed at 3, 6, 12, and 24 months after injury using a visual analog "present pain intensity" scale and the depression and anxiety scales of the Brief Symptom Inventory. ⋯ The results suggest that in the early phase after trauma, pain predicts anxiety and depression, but the magnitude of these relationships are smaller than the longitudinal relationship from anxiety to pain over this period. In the late (or chronic) phase after injury, the longitudinal relationship from anxiety on pain nearly doubles and is the only significant relationship. Despite missing data and a single item measure of pain intensity, these results provide evidence that negative mood, specifically anxiety, has an important role in the persistence of acute pain.
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Patients with low back pain (LBP; N = 102), fibromyalgia (FM; N = 100), and headache (HA; N = 100) were asked to describe their pain in their own words, and the words and phrases they used were then classified into 7 global domains (eg, Pain Quality, Pain Magnitude) and as many specific subdomains as needed to capture all of the ideas expressed (eg, under Pain Quality, subdomains such as sharp, achy, and throbbing). Fifteen pain quality subdomains were identified as most common. Nine of these demonstrated significant between-group differences in frequency. ⋯ The findings are generally consistent with a study that used similar procedures in other patient samples to identify the most common words patients use to describe pain, supporting their generalizability. The findings also support the use of pain quality measures for discriminating between chronic pain conditions. Finally, the findings have important implications for evaluating and modifying pain quality measures as needed.