The journal of pain : official journal of the American Pain Society
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Editorial
New proposals for the International Classification of Diseases-11 revision of pain diagnoses.
The representation of pain diagnoses in current classification systems like International Classification of Diseases (ICD)-10 and Diagnostic and Statistical Manual of Mental Disorders (DSM)-IV does not adequately reflect the state of the art of pain research, and does not sufficiently support the clinical management and research programs for pain conditions. Moreover, there is an urgent need to harmonize classification of pain syndromes of special expert groups (eg, International Classification of Headache Disorders) and general classification systems (eg, ICD-11, DSM-V). Therefore, this paper summarizes new developments, and proposals for pain diagnoses in revised classification systems. A qualitative review of the literature concerning new proposals for classification of pain syndromes that are based on consensus groups was conducted. Selected proposals of national and international pain societies that are based on consensual processes are presented. These proposals can be condensed to be used in ICD-11 classification. The benefits of considering multidimensional and transdiagnostic processes for the classification process are also outlined. The manuscript provides options how to transform current pain-specific classification proposals to the revision of ICD-11. ⋯ Pain research and expertise must be more visible in the ICD-11 revision process. A general category for pain diagnoses as well as specific pain diagnoses under existing categories of organ-specific sections are needed.
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Timing of assessment of psychological construct is controversial and results differ based on the model of pain induction. Previous studies have not used an exercise-induced injury model to investigate timing of psychological assessment. Exercise-induced injury models may be appropriate for these investigations because they approximate clinical pain conditions better than other experimental stimuli. In this study we examined the changes of psychological constructs over time and determined whether timing of assessment affected the construct's association with reports of pain intensity and disability. One-hundred twenty-six healthy volunteers completed the Fear of Pain Questionnaire (FPQ-III), Pain Catastrophizing Scale (PCS), and Tampa Scale of Kinesiophobia (TSK) prior to inducing muscle injury to the shoulder. The PCS and TSK were measured again 48 and 96 hours postinjury induction. Pain intensity and disability were collected at 48 and 96 hours and served as dependent variables in separate regression models. Results indicated that the FPQ-III had the strongest prediction of pain intensity from baseline to 96 hours. After baseline the PCS and TSK were stronger predictors of pain intensity and disability, respectively. These data provide support for the use of psychological constructs in predicting outcomes from shoulder pain. However, they deviate from the current theoretical model indicating that fear of pain is a consequence of injury and instead suggests that fear of pain before injury may influence reports of pain intensity. ⋯ The current study provides evidence that fear of pain can be assessed prior to injury. Furthermore, it supports that after injury pain catastrophizing and kinesiophobia are independently associated with pain and disability. Overall these data suggest that timing of psychological assessment may be an important consideration in clinical environments.
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Understanding individual differences in the variability of fibromyalgia pain can help elucidate etiological mechanisms and treatment targets. Past research has shown that spatial extent of pain, negative mood, and aftersensation (pain ratings taken after experimental induction of pain) accounts for 40 to 50% of the variance in clinical pain. Poor sleep is hypothesized to have a reciprocal relationship with pain, and over 75% of individuals with fibromyalgia report disturbed sleep. We hypothesized that measures of sleep would increase the predictive ability of the clinical pain model. Measures of usual pain, spatial extent of pain, negative mood, and pain aftersensation were taken from 74 adults with fibromyalgia. Objective (actigraph) and subjective (diary) measures of sleep duration and nightly wake time were also obtained from the participants over 14 days. Hierarchical regression indicated that greater spatial extent (R(2) = .26), higher aftersensation ratings (R(2) = .06), and higher negative mood (R(2) = .04) accounted for 36% of the variance in clinical pain (average of 14 daily pain ratings). None of the sleep variables were significant predictors of clinical pain. Results replicate previous research and suggest that spatial extent of pain, pain aftersensation, and negative mood play important roles in clinical pain, but sleep disturbance did not aid in its prediction. ⋯ This study suggests that measures of sleep duration and nightly wake time do not predict fibromyalgia pain at the group level. Fibromyalgia patients may benefit from a 3-pronged approach to pain management: reducing pain's spatial extent, normalization of central nervous system hypersensitivity, and psychobehavioral therapies for negative mood.
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Comparative Study
Effects of the δ opioid receptor agonist SNC80 on pain-related depression of intracranial self-stimulation (ICSS) in rats.
The delta opioid receptor agonist SNC80 produces both antinociceptive and antidepressant effects in rodents. This profile suggests that SNC80 may also reverse prodepressant effects of pain. Accordingly, this study compared SNC80 effects in complementary assays of pain-stimulated and pain-depressed behavior in rats. Intraperitoneal injection of dilute acid served as an acute noxious visceral stimulus in rats to stimulate abdominal stretching (a pain-stimulated behavior) or depress intracranial self-stimulation of the medial forebrain bundle (ICSS; a pain-depressed behavior). When administered once per week to minimize acute tolerance, SNC80 (1-10 mg/kg IP) decreased acid-stimulated stretching but had little effect on acid-induced depression of ICSS. More frequent SNC80 administration produced tolerance to SNC80 effects on acid-stimulated stretching, but unmasked antinociception in the assay of acid-depressed ICSS. SNC80 did not facilitate ICSS in the absence of pain, and effects of SNC80 were not duplicated by ARM390, a reputed delta agonist congener of SNC80 that does not internalize delta receptors. These findings support continued consideration of delta agonists as candidate analgesics to treat prodepressant effects of pain and illustrate the potential for diametrically opposite effects of drug treatments on preclinical measures of pain-stimulated and pain-depressed behavior. ⋯ The delta opioid agonist SNC80 blocked pain-related depression of intracranial self-stimulation in rats, suggesting that delta agonists may be useful to treat prodepressant effects of pain. Repeated SNC80 produced tolerance to SNC80 antinociception in a conventional assay of pain-stimulated behavior but unmasked SNC80 antinociception in an assay of pain-depressed behavior.
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The amygdala contributes to generation of affective behaviors to threats. The prototypical threat to an individual is exposure to a noxious stimulus and the amygdaloid central nucleus (CeA) receives nociceptive input that is mediated by glutamatergic neurotransmission. The present study evaluated the contribution of glutamate receptors in CeA to generation of the affective response to acute pain in rats. Vocalizations that occur following a brief noxious tail shock (vocalization afterdischarges) are a validated rodent model of pain affect, and were preferentially suppressed by bilateral injection into CeA of the NMDA receptor antagonist D-2-amino-5-phosphonovalerate (AP5, 1 μg, 2 μg, or 4 μg) or the non-NMDA receptor antagonist 6-Cyano-7-nitroquinoxaline-2,3-dione disodium (CNQX, .25 μg, .5 μg, 1 μg, or 2 μg). Vocalizations that occur during tail shock were suppressed to a lesser degree, whereas spinal motor reflexes (tail flick and hind limb movements) were unaffected by injection of AP5 or CNQX into CeA. Unilateral administration of AP5 or CNQX into CeA of either hemisphere also selectively elevated vocalization thresholds. Bilateral administration of AP5 or CNQX produced greater increases in vocalization thresholds than the same doses of antagonists administered unilaterality into either hemisphere indicating synergistic hemispheric interactions. ⋯ The amygdala contributes to production of emotional responses to environmental threats. Blocking glutamate neurotransmission within the central nucleus of the amygdala suppressed rats' emotional response to acute painful stimulation. Understanding the neurobiology underlying emotional responses to pain will provide insights into new treatments for pain and its associated affective disorders.