The journal of pain : official journal of the American Pain Society
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Central sensitization represents an enhancement in the function of neurons and circuits in nociceptive pathways caused by increases in membrane excitability and synaptic efficacy as well as to reduced inhibition and is a manifestation of the remarkable plasticity of the somatosensory nervous system in response to activity, inflammation, and neural injury. The net effect of central sensitization is to recruit previously subthreshold synaptic inputs to nociceptive neurons, generating an increased or augmented action potential output: a state of facilitation, potentiation, augmentation, or amplification. Central sensitization is responsible for many of the temporal, spatial, and threshold changes in pain sensibility in acute and chronic clinical pain settings and exemplifies the fundamental contribution of the central nervous system to the generation of pain hypersensitivity. Because central sensitization results from changes in the properties of neurons in the central nervous system, the pain is no longer coupled, as acute nociceptive pain is, to the presence, intensity, or duration of noxious peripheral stimuli. Instead, central sensitization produces pain hypersensitivity by changing the sensory response elicited by normal inputs, including those that usually evoke innocuous sensations. ⋯ In this article, we review the major triggers that initiate and maintain central sensitization in healthy individuals in response to nociceptor input and in patients with inflammatory and neuropathic pain, emphasizing the fundamental contribution and multiple mechanisms of synaptic plasticity caused by changes in the density, nature, and properties of ionotropic and metabotropic glutamate receptors.
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This study examined the occurrence of alcohol use to manage pain in community-dwelling adults with tooth pain, jaw joint/face pain, and arthritis. Race/ethnicity, sex, and age were examined to determine their associations with alcohol use for pain. Community-dwelling adults from South Florida with tooth pain (n = 1,767), jaw joint/face pain (n = 1,199), or arthritis pain (n = 1,355) completed a structured telephone interview. Logistic regression models indicted that, similar to population rates, nonHispanic whites and males were the most likely to use alcohol to manage pain. In addition, alcohol use for pain was highest in younger adults. Individuals who self-managed oral pain with alcohol were more likely to use prescription and over-the-counter pain medications, but this association was not found for arthritis. Additional characteristics of individuals who self-medicated regardless of pain condition included greater pain frequency, depression, and higher levels of education. Being married was protective against the use of alcohol to manage pain symptoms. Use of alcohol for pain should be assessed during treatment evaluation so that physicians and other health care providers are aware of their patient's concomitant use of alcohol and pain medication, assess for psychosocial impairment, and make the appropriate referrals and adjustment to treatment. ⋯ Self-medication of pain with alcohol is most common among younger nonHispanic white males and associated with pain frequency, depression, and use of pain medications. Alcohol use for pain needs to be assessed so that health care providers can make appropriate referrals and adjustments to treatment.
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Comparative Study
Comparison of health care use and costs in newly diagnosed and established patients with fibromyalgia.
In 2004, the American Pain Society (APS) issued evidence-based fibromyalgia treatment recommendations. The objective of this claims database analysis is to describe prescription and medical use in patients with newly diagnosed and established fibromyalgia. Privately insured patients with 2+ myalgia/myositis claims (1999 to 2005) were categorized as newly diagnosed or established; this dichotomy involves comparisons between prediagnosis (S1) and postdiagnosis (S2) stages in the newly diagnosed and between newly diagnosed (S2) and established patients (S3). Use of APS guideline medications increased across stages: selective serotonin reuptake inhibitors (SSRIs) (S1, S2, S3: 20.6%, 22.9%, 25.3%), serotonin norepinephrine reuptake inhibitors (SNRIs) (4.5%, 6.4%, 8.9%), pregabalin/gabapentin (5.4%, 7.4%, 8.8%), benzodiazepines (19.0%, 21.1%, 24.2%), non-benzodiazepine sedatives (9.1%, 11.5%, 13.7%) (all P < .0001), and opioids (39.5%, 43.3%, 43.9%; S1 vs S2, P < .0001; S2 vs S3, P = .2835). Use of multiple therapeutic classes also increased across stages: 3+ classes (7.1%, 9.6%, 11.8%) (all P < .0001). Office visits to providers increased, on average, after diagnosis: primary care (70.9%, 78.3%, 76.3%; all P < .0001), chiropractors (28.8%, 51.1%, 53.3%; all P < .0001), rheumatologists (4.2%, 9.9%, 10.5%; S1 vs S2, P < .0001; S2 vs S3, P = .0595), mental health (6.4%, 7.3%, 8.3%; S1 vs S2, P < .0001, S2 vs S3, P = .0003). Average health care costs rose after diagnosis in the newly diagnosed group (S1: $6555 vs S2: $8654, P < .0001). ⋯ This paper investigates prescription drug and medical care use with respect to stages of fibromyalgia diagnosis. Established fibromyalgia patients use more medical resources and have higher rates of concomitant medication use than newly diagnosed fibromyalgia patients. Findings can help educate providers regarding optimal drug treatment patterns in this population.
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Experimental studies showed that dopamine influences pain perception in healthy volunteers. Dopamine dysfunctions have been linked to the physiopathology of fibromyalgia (FM), which is associated with hyperalgesia and deficient pain inhibition. We sought to investigate the relationships between catecholamine-related polymorphisms [dopamine-D(3) receptor (DRD3) Ser9Gly and catechol-O-methyltransferase (COMT) Val158Met] and thermal pain measures in healthy subjects and FM patients. Seventy-three subjects (37 FM patients and 36 controls) participated in this study. Thermal pain thresholds (TPTs) were measured using a Peltier thermode. Inhibitory systems were elicited using a thermal tonic pain stimulation administered before and after activation of the diffuse noxious inhibitory controls (DNIC) by means of a cold-pressor test. Genetic analyses were performed using polymerase chain reaction. Regression analyses were performed across and within groups. FM was associated with lower TPTs and deficient pain inhibition. DRD3 Ser9Gly polymorphism predicted (1) DNIC efficacy across groups and (2) thermal TPTs in FM patients. COMT Val158Met and thermal pain measures were not related. These preliminary results suggest that the DRD3 Ser9Gly polymorphism influences DNIC efficacy and TPTs and that this latter relationship is present only in FM patients. Two core psychophysical features of FM appear to be significantly influenced by limbic dopamine functioning. ⋯ This experimental study is the first to relate DNIC and TPTs to a functional polymorphism of limbic dopamine-D3 receptors. As lowered pain thresholds and deficient pain inhibition are 2 core features of fibromyalgia, these preliminary results may help identify a subgroup of FM patients who require closer medical attention.
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Factor-analytic studies of the structure of posttraumatic stress disorder (PTSD) symptoms have yielded inconsistent results. One of the reasons for the inconsistency may be that PTSD is highly comorbid with other disorders; the observed factor structure might depend on the particular comorbid disorder. One such disorder is chronic pain. The goal of the present study was to investigate whether PTSD symptom structure differs between pain and pain-free patients scheduled to undergo major surgery. Four hundred and forty-seven patients who were approached 7 to 10 days prior to scheduled surgery completed the PTSD Checklist-Civilian (PCL-C) Version and the Current Pain and Pain History Questionnaire; the latter was used to divide patients into pain (N = 175) and pain-free (N = 272) groups. Results showed that in pain-free patients, PTSD symptoms were best expressed as 2 symptom clusters (re-experiencing/avoidance; emotional numbing/hyperarousal) accounting for 52.4% of the variance. In pain patients, PTSD symptoms were best expressed as a single symptom cluster accounting for 51.1% of the variance. These results suggest different interrelationships among PTSD symptoms in these 2 populations. Results reflect the need for (1) controlling for pain in studies looking at PTSD-symptom expression and (2) further research on PTSD-symptom expression in pain populations. ⋯ These results may have important implications for research on the comorbidity between PTSD and chronic pain, as well as for treatment of PTSD symptoms in patients presenting with pain problems.