The journal of pain : official journal of the American Pain Society
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Migraine is characterized by an increased sensitivity to visual stimuli that worsens during attacks. Recent evidence has shown that feedforward volleys carrying incoming visual information induce high frequency (gamma) oscillations in the visual cortex, while feedback volleys arriving from higher order brain areas induce oscillatory activity at lower frequencies (theta/alpha/low-beta). We investigated visually induced high (feedforward) and low (feedback) frequency activations in healthy subjects and various migraine patients. ⋯ The presence of headache is associated with proportionally higher gamma (feedforward) activities. Perspective: This study provides an insight into the pathophysiology of migraine headache from the perspective of cortical sensory processing dynamics. Patients with migraine present alterations in feedback and feedforward visual signalling that differ with the presence of headache.
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Recent research has suggested that the magnitudes of analgesic treatment effects estimated in clinical trials have decreased over time. Implications of these findings for future sample size calculations and clinical trial research designs have not been addressed. In this article, we examine the standardized effect size (SES) for average pain intensity (API) and worst pain intensity (WPI) outcomes from randomized clinical trials (RCTs) of analgesic treatments shown to be efficacious for chronic low back pain, fibromyalgia, osteoarthritis pain, painful diabetic peripheral neuropathy, and postherpetic neuralgia that were published between 1980 and 2016. ⋯ Other methods to address the challenge of modest treatment effects by increasing trial efficiency and assay sensitivity are also briefly discussed. PERSPECTIVE: This article examines continuous pain intensity data obtained from analgesic treatment trials for chronic low back pain, fibromyalgia, osteoarthritis pain, painful diabetic peripheral neuropathy, and postherpetic neuralgia. Numerical declines in standardized effect sizes (SESs) were observed, with SESs being approximately 0.30 in the most recent trials.
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The purpose of this article was to examine age-related changes in conditioned pain modulation (CPM) and temporal summation of pain (TS) using meta-analytic techniques. Five electronic databases were searched for studies that compared measures of CPM and TS between healthy, chronic pain-free younger, middle-aged, and older adults. Eleven studies were included in the final review for TS and 11 studies were included in the review of CPM. ⋯ In summary, the data provided strong quantitative evidence of a general age-related decline in endogenous pain modulatory function as measured by TS and CPM. PERSPECTIVE: This review compared conditioned pain modulation and temporal summation of pain between younger, middle-aged, and older adults. These findings enhance our understanding of the decline in endogenous pain modulatory function associated with normal aging.
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Despite growing evidence of significant racial disparities in the experience and treatment of chronic pain, the mechanisms by which these disparities manifest have remained relatively understudied. The current study examined the relationship between past experiences of racial discrimination and pain-related outcomes (self-rated disability and depressive symptomatology), and tested the potential mediating roles of pain catastrophizing and perceived injustice related to pain. Analyses consisted of cross-sectional path modeling in a multiracial sample of 137 individuals with chronic low back pain (Hispanics N=43; Blacks N=43; Whites N=51). ⋯ Future research is needed to investigate temporal and causal mechanisms suggested by the model through longitudinal and clinical intervention studies. PERSPECTIVE: More frequent prior experiences of racial discrimination are associated with greater depressive symptomatology and pain-related disability in individuals with chronic low back pain. These associations are explained by the degree of injustice perception related to pain, but not pain catastrophizing, and were stronger among Black and Hispanic participants.
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Occupational exposure to mechanical vibration can produce the Hand-Arm Vibration Syndrome (HAVS), whose most disabling symptom is persistent muscle pain. Unfortunately, the pathophysiology of HAVS pain is still poorly understood, precluding the development of mechanism-based therapies. Since interleukin 33 (IL-33) is essential for inflammation and recovery that follows skeletal muscle injury, we explored its role in muscle pain in a model of HAVS, in adult male rats. ⋯ Together these data support the suggestion that IL-33 plays a central role in vibration-induced muscle pain by action, at least in part, on skeletal muscle nociceptors. PERSPECTIVE: Our findings provide evidence of the contribution of IL-33, acting on its canonical receptor, in nociceptors, to muscle pain induced by ergonomic vibration. This suggests that targeting IL-33/ST2 signaling may be a useful strategy for the treatment of muscle pain in hand-arm vibration syndrome.