Pain
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Migraine is one of the most common and most disabling disorders. Between attacks, migraine patients are otherwise normal but are sensitized to nonnoxious events known as triggers. The purpose of these studies was to investigate whether a headache-like event causes sensitization, or priming, to subsequent subthreshold events. ⋯ Finally, hind paw IL-6 produced paw allodynia but not priming to paw injection of pH 7.0 at 72 hours demonstrating differences in priming depending on location. These data indicate that afferent input from the meninges produces BDNF-dependent priming of the dural nociceptive system. This primed state mimics the interictal period of migraine where attacks can be triggered by normally nonnoxious events and suggests that BDNF-dependent plasticity may contribute to migraine.
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The rostral ventromedial medulla (RVM) has a well-documented role in pain modulation and exerts antinociceptive and pronociceptive influences mediated by 2 distinct classes of neurons, OFF-cells and ON-cells. OFF-cells are defined by a sudden pause in firing in response to nociceptive inputs, whereas ON-cells are characterized by a "burst" of activity. Although these reflex-related changes in ON- and OFF-cell firing are critical to their pain-modulating function, the pathways mediating these responses have not been identified. ⋯ Few of these neurons expressed calcitonin gene-related peptide, suggesting that the RVM projection from PB is distinct from that to the amygdala. These data show that a substantial component of "bottom-up" nociceptive drive to RVM pain-modulating neurons is relayed through the PB. While the PB is well known as an important relay for ascending nociceptive information, its functional connection with the RVM allows the spinoparabrachial pathway to access descending control systems as part of a recurrent circuit.
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Review Meta Analysis
A Systematic Review with Meta-analysis of Childhood and Adolescent Risk and Prognostic Factors for Musculoskeletal Pain.
A variety of factors may be involved in the development and course of musculoskeletal (MSK) pain. We undertook a systematic review with meta-analysis to synthesize and evaluate the quality of evidence about childhood and adolescent factors associated with onset and persistence of MSK pain, and its related disability. Studies were identified from searches of electronic databases (PubMed, EMBASE, PsycINFO, CINAHL, and Web of Science), references of included studies, and the Pediatric Pain mail list. ⋯ However, moderate-quality evidence also suggests that high body mass index, taller height, and having joint hypermobility are not risk factors for onset of MSK pain. We found other risk and prognostic factors explored were associated with low or very low quality of evidence. Additional well-conducted primary studies are needed to increase confidence in the available evidence, and to explore new childhood risk and prognostic factors for MSK pain.
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Review
Transmission of risk from parents with chronic pain to offspring: an integrative conceptual model.
Offspring of parents with chronic pain are at increased risk for pain and adverse mental and physical health outcomes (Higgins et al, 2015). Although the association between chronic pain in parents and offspring has been established, few studies have addressed why or how this relation occurs. Identifying mechanisms for the transmission of risk that leads to the development of chronic pain in offspring is important for developing preventive interventions targeted to decrease risk for chronic pain and related outcomes (eg, disability and internalizing symptoms). ⋯ Our proposed model highlights 5 potential mechanisms for the relation between parental chronic pain and pediatric chronic pain and related adverse outcomes: (1) genetics, (2) alterations in early neurobiological development, (3) pain-specific social learning, (4), general parenting and family health, and (5) exposure to stressful environment. In addition, the model presents 3 potential moderators for the relation between parent and child chronic pain: (1) the presence of chronic pain in a second parent, (2) timing, course, and location of parental chronic pain, and (3) offspring's characteristics (ie, sex, developmental stage, race or ethnicity, and temperament). Such a framework highlights chronic pain as inherently familial and intergenerational, opening up avenues for new models of intervention and prevention that can be family centered and include at-risk children.