The journal of pain : official journal of the American Pain Society
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Comparative Study
Salivary cortisol release and hypothalamic pituitary adrenal axis feedback sensitivity in fibromyalgia is associated with depression but not with pain.
Results on hypothalamicpituitary-adrenal (HPA) axis function in fibromyalgia are heterogeneous and studies that integrate psychological and biological mechanisms in the search for pathways to fibromyalgia are rare. The goal of the study was to evaluate cortisol release and HPA axis feedback regulation in fibromyalgia and its association with psychopathology and pain. Beneath assessment of pain thresholds and self-report of pain, salivary free cortisol release over the day before and after intake of 0.5 mg of dexamethasone was measured in 21 female patients with fibromyalgia and 26 control women. Depression was assessed by questionnaires and clinical interview. We found reduced feedback sensitivity and slightly enhanced cortisol release in patients with fibromyalgia compared with healthy control subjects. Post hoc analyses showed that these effects are exclusively found in those patients, who also had major depressive disorder. Patients with fibromyalgia had lower pain pressure threshold, whereas heat pain thresholds were comparable with control subjects. Pain pressure and heat pain thresholds were not associated with cortisol release. On the other hand measurements of affective pain experience and depression were positively correlated with salivary cortisol over the day. Our results support the hypotheses that HPA axis related alterations are associated with affective disturbances, for example, depression, in patients with fibromyalgia. ⋯ The presented data suggest depression to be an important factor in HPA axis-related dysfunction in fibromyalgia. This might be one explanation for equivocal findings in the literature.
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A cross-sectional, Internet-based survey was conducted in a nationally representative sample of United States (US) adults to estimate the point prevalence of chronic pain and to describe sociodemographic correlates and characteristics of chronic pain. The survey was distributed to 35,718 members (aged 18 years and older) of a Web-enabled panel that is representative of the US population, and 27,035 individuals responded. Crude and weighted prevalence estimates were calculated and stratified by age, sex, and type of chronic pain. The weighted point-prevalence of chronic pain (defined as chronic, recurrent, or long-lasting pain lasting for at least 6 months) was 30.7% (95% CI, 29.8-31.7). Prevalence was higher for females (34.3%) than males (26.7%) and increased with age. The weighted prevalence of primary chronic lower back pain was 8.1% and primary osteoarthritis pain was 3.9%. Half of respondents with chronic pain experienced daily pain, and average (past 3 months) pain intensity was severe (≥ 7 on a scale ranging from 0 to 10) for 32%. Multiple logistic regression analysis identified low household income and unemployment as significant socioeconomic correlates of chronic pain. Chronic pain is prevalent among US adults and is related to indicators of poorer socioeconomic status. ⋯ The results of this cross-sectional Internet-based survey suggest a considerable burden of chronic pain in US adults. Chronic pain, experienced by about a third of the population, was correlated with indicators of poorer socioeconomic status. Primary chronic pain was most commonly attributed to lower back pain, followed by osteoarthritis pain.
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The formalin test produces 2 well-known acute phases of nociceptive behavior. Recently, we have shown that this same formalin test produces a third phase of nociceptive behavior consisting of prolonged thermal and mechanical hyperalgesia beginning days after formalin injection and lasting for at least 3 weeks. Here we investigated the activity of 3 MAPKs (p38, ERK and JNK) in the spinal dorsal horn following 5% formalin injection into rat hind paw. The p38 MAPK was rapidly activated in the spinal microglia minutes after injection and the activation persisted for 1 hour. In addition, this same injury induced a secondary increase of phospho-p38 expression in spinal microglia that was maximal 3 to 7 days postinjection. Intrathecal administration of p38 inhibitor SB203580 not only inhibited the early acute spontaneous nociceptive behaviors, but also inhibited the long-term formalin injury-induced mechanical hyperalgesia. Our results suggest that peripheral formalin injection induces 2 stages of microglial activation, and p38 activation in spinal microglia plays key roles in central pain modulation in formalin test respectively for the early acute phases and the late secondary long-term pain state as well. ⋯ This article presents unique properties of spinal microglial activation in a pain animal model. This finding could potentially help clinicians to further understand the contributions of spinal microglia to acute and chronic pain state.
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Burn injury induces severe pain that can be refractory to existing pharmacotherapies. The underlying mechanism of burn pain remains unclear. We previously established an animal model and reported that unilateral burn injury induces chronic and bilateral mechanical allodynia, which is associated with central sensitization and microglial activation in the spinal cord dorsal horn. Modulation of the activity of microglia and p38 mitogen-activated protein kinase (MAPK) has been shown to ameliorate neuropathic pain in several nerve-injury pain models. In the present study, we show in this rat model that daily treatment with the microglial inhibitor minocycline (10 mg/kg), administered at the time of burn injury and for 7 days thereafter, significantly attenuates ipsilateral and contralateral allodynia as assessed up to 1 month following burn injury. These sensory changes are paralleled by significant suppression of evoked hyperexcitability of dorsal-horn neurons and of the expression of phosphorylated p38 (phospho-p38) in OX42+ microglial cells within the dorsal horn. Our results suggest that modulation of inflammation at early times after burn injury may have long-lasting effects, attenuating central neuropathic mechanisms which contribute to pain after burn injury. ⋯ We demonstrate, in a rodent model of burn-associated pain, that the microglial inhibitor minocycline, delivered at the time of burn injury and for 1 week thereafter, has long-lasting effects, attenuating microglial activation and neuronal hyperresponsiveness in the dorsal horns, and ameliorating allodynia for at least 1 month.
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This study examined characteristics associated with prescription drug use disorder (PDUD) in primary-care patients with chronic pain from a cross-sectional survey conducted at an urban academically affiliated safety-net hospital. Participants were 18 to 60 years old, had pain for ≥ 3 months, took prescription or nonprescription analgesics, and spoke English. Measurements included the Composite International Diagnostic Interview (PDUD, other substance use disorders (SUD), Posttraumatic Stress Disorder [PTSD]); Graded Chronic Pain Scale, smoking status; family history of SUD; and time spent in jail. Of 597 patients (41% male, 61% black, mean age 46 years), 110 (18.4%) had PDUD of whom 99 (90%) had another SUD. In adjusted analyses, those with PDUD were more likely than those without any current or past SUD to report jail time (OR 5.1, 95% CI 2.8-9.3), family history of SUD (OR 3.4, 1.9-6), greater pain-related limitations (OR 3.8, 1.2-11.7), cigarette smoking (OR 3.6, 2-6.2), or to be white (OR 3.2, 1.7-6), male (OR 1.9, 1.1-3.5) or have PTSD (OR 1.9, 1.1-3.4). PDUD appears increased among those with easily identifiable characteristics. The challenge is to determine who, among those with risk factors, can avoid, with proper management, developing the increasingly common diagnosis of PDUD. ⋯ This article examines risk factors for prescription drug use disorder (PDUD) among a sample of primary-care patients with chronic pain at an urban, academic, safety-net hospital. The findings may help clinicians identify those most at risk for developing PDUD when developing appropriate treatment plans.