The journal of pain : official journal of the American Pain Society
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With the increasing societal awareness of the prevalence and impact of acute pain, there is a need to develop an acute pain classification system that both reflects contemporary mechanistic insights and helps guide future research and treatment. Existing classifications of acute pain conditions are limiting, with a predominant focus on the sensory experience (eg, pain intensity) and pharmacologic consumption. Consequently, there is a need to more broadly characterize and classify the multidimensional experience of acute pain. ⋯ Significant numbers of patients still suffer from significant acute pain, despite the advent of modern multimodal analgesic strategies. Mismanaged acute pain has a broad societal impact as significant numbers of patients may progress to suffer from chronic pain. An acute pain taxonomy provides a much-needed standardization of clinical diagnostic criteria, which benefits clinical care, research, education, and public policy. For the purposes of the present taxonomy, acute pain is considered to last up to seven days, with prolongation to 30 days being common. The current understanding of acute pain mechanisms poorly differentiates between acute and chronic pain and is often insufficient to distinguish among many types of acute pain conditions. Given the usefulness of the AAPT multidimensional framework, the AAAPT undertook a similar approach to organizing various acute pain conditions.
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Review Meta Analysis
Analgesic effects of alcohol: A systematic review and meta-analysis of controlled experimental studies in healthy participants.
Despite the long-standing belief in the analgesic properties of alcohol, experimental studies have produced mixed results. This meta-analysis aimed to clarify whether alcohol produces a decrease in experimentally-induced pain and to determine the magnitude of any such effect. PubMed, PsycINFO, and Embase databases were searched from inception until April 21, 2016 for controlled studies examining the effect of quantified dosages of alcohol on pain response to noxious stimulation. Eighteen studies involving 404 participants were identified providing alcohol versus no-alcohol comparisons for 13 tests of pain threshold (n = 212) and 9 tests of pain intensity ratings (n = 192). Random effects meta-analysis of standardized mean difference (SMD) provided robust support for analgesic effects of alcohol. A mean blood alcohol content (BAC) of approximately .08% (3-4 standard drinks) produced a small elevation of pain threshold (SMD [95% CI] = .35 [.17-.54], P = .002), and a moderate to large reduction in pain intensity ratings (SMD [95% CI] = .64 [.37-.91], P < .0001), or equivalently, a mean reduction of 1.25 points on a 0- to 10-point pain rating scale. Furthermore, increasing BAC resulted in increasing analgesia, with each .02% BAC increment producing an increase of SMD = .11 for pain threshold and SMD = .20 for reduced pain intensity. Some evidence of publication bias emerged, but statistical correction methods suggested minimal impact on effect size. Taken together, findings suggest that alcohol is an effective analgesic that delivers clinically-relevant reductions in ratings of pain intensity, which could explain alcohol misuse in those with persistent pain despite its potential consequences for long-term health. Further research is needed to corroborate these findings for clinical pain states. ⋯ This meta-analysis provides robust evidence for the analgesic properties of alcohol, which could potentially contribute to alcohol misuse in pain patients. Strongest analgesia occurs for alcohol levels exceeding World Health Organization guidelines for low-risk drinking and suggests raising awareness of alternative, less harmful pain interventions to vulnerable patients may be beneficial.
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Vestibulodynia is a form of provoked vulvodynia characterized by profound tenderness, hyperinnervation, and frequently inflammation within well-defined areas of the human vestibule. Previous experiments in animal models show that inflammatory hypersensitivity and hyperinnervation occur in concert with establishment of a local renin-angiotensin system (RAS). Moreover, mechanical hypersensitivity and sensory axon sprouting are prevented by blocking effects of angiotensin II on angiotensin II receptor type 2 (AT2) receptors. This case-control study assessed whether a RAS contributes to hyperinnervation observed in human vestibulodynia. Vestibular biopsies from asymptomatic controls or patients' nontender areas showed moderate innervation and small numbers of inflammatory cells. In women with vestibulodynia, tender areas contained increased numbers of mechanoreceptive nociceptor axons, T-cells, macrophages, and B-cells, whereas mast cells were unchanged. RAS proteins were increased because of greater numbers of T cells and B cells expressing angiotensinogen, and increased renin-expressing T cells and macrophages. Chymase, which converts angiotensin I to angiotensin II, was present in constant numbers of mast cells. To determine if tender vestibular tissue generates angiotensin II that promotes axon sprouting, we conditioned culture medium with vestibular tissue. Rat sensory neurons cultured in control-conditioned medium showed normal axon outgrowth, whereas those in tender tissue-conditioned medium showed enhanced sprouting that was prevented by adding an AT2 antagonist or angiotensin II neutralizing antibody. Hypersensitivity in provoked vestibulodynia is therefore characterized by abnormal mechanonociceptor axon proliferation, which is attributable to inflammatory cell-derived angiotensin II (or a closely related peptide) acting on neuronal AT2 receptors. Accordingly, reducing inflammation or blocking AT2 represent rational strategies to mitigate this common pain syndrome. ⋯ This study provides evidence that local inflammation leads to angiotensin II formation, which acts on the AT2 to induce nociceptor axon sprouting in vulvodynia. Preventing inflammation and blocking AT2 therefore present potential pharmacological strategies for reducing vestibular pain.
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Randomized Controlled Trial
TRPA1 and TRPV1 antagonists do not inhibit human acidosis-induced pain.
Acidosis occurs in a variety of pathophysiological and painful conditions where it is thought to excite or contribute to excitation of nociceptive neurons. Despite potential clinical relevance the principal receptor for sensing acidosis is unclear, but several receptors have been proposed. We investigated the contribution of the acid-sensing ion channels, transient receptor potential vanilloid type 1 (TRPV1) and transient receptor potential ankyrin type 1 (TRPA1) to peripheral pain signaling. ⋯ A continuous intraepidermal injection of pH 4.3 was used to counter the buffering capacity of tissue and generate a prolonged painful stimulation. In this model, addition of A-967079, BCTC or amiloride did not reduce the reported pain. In conclusion, target-validated antagonists, applied locally in human skin, have excluded the main hypothesized targets and the mechanism of the human acidosis-induced pain remains unclear.
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Randomized Controlled Trial
Validity of Simplified Versus Standard Self-Report Measures of Pain Intensity in Preschool-Aged Children Undergoing Venipuncture.
There are inadequate age-specific data to support the use of current self-report pain scales in 3- and 4-year-old children. Most preschool-aged children also lack the necessary cognitive development to use standard scales. We aimed to evaluate the validity and feasibility of 2 novel simplified scales (Simplified Faces Pain Scale, S-FPS; Simplified Concrete Ordinal Scale, S-COS) for preschool-aged children. These simplified scales used a 2-step self-report method: children were first asked whether they have pain (yes/no); only if yes, then pain intensity was self-reported using a 3-point scale with visual aids signifying mild/moderate/severe. ⋯ Correlation with Face Legs Activity Cry Consolability was moderate to strong and cooperation rates were similar for all self-report scales. The simplified scales can improve and simplify pain assessment for 4-year-olds. Quantitative pain rating remains challenging for 3-year-olds.