The journal of pain : official journal of the American Pain Society
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The current study tested whether the effectiveness of distraction using virtual reality (VR) technology in reducing cold pressor pain would maintain over the course of 8 weekly exposures. Twenty-eight adults, 18 to 23 years of age, underwent 1 baseline cold pressor trial and 1 VR distraction trial in randomized order each week. VR distraction led to significant increases in pain threshold and pain tolerance and significant decreases in pain intensity, time spent thinking about pain, and self-reported anxiety, relative to baseline. Repeated exposure did not appear to affect the benefits of VR. Implications for the long-term use of VR distraction as a nonpharmacological analgesic are discussed. ⋯ This article addresses the concern that the efficacy of virtual reality-assisted distraction from pain could potentially decrease with repeated exposure. The current finding that efficacy did not diminish over several repeated exposures provides support for the use of virtual reality as an adjuvant treatment of pain.
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People often respond with distress and avoidance to their own negative experiences, such as the physical, cognitive, and emotional aspects of depression or anxiety. When people with chronic pain respond this way, their overall level of distress may increase, they may struggle to avoid their emotional experiences, and their daily functioning may decrease. The purpose of this study was to examine the role of anxiety sensitivity (AS), or "fear of anxiety," in relation to these processes. It was predicted that those persons with chronic pain who report higher AS will also report higher emotional distress and greater disability caused by chronic pain. A second purpose was to examine whether therapeutic processes designed to reduce emotional avoidance, namely, acceptance, mindfulness, and values, could be demonstrated to reduce the role of AS in relation to this distress and disability based on a statistical model including these variables. Subjects were 125 consecutive adult patients (64.8% women) seeking services from a specialty pain service in the United Kingdom. All patients completed a standard set of measures of AS, acceptance of pain, mindfulness, and values-based action, as well as measures of pain, disability, and emotional functioning, at their initial consultation, and these data formed the basis for the current study. In correlation and regression analyses, AS was associated with greater pain, disability, and distress. In regression analyses, the 3 proposed therapeutic processes reduced the average variance accounted for by AS in patient functioning from DeltaR(2) = .21 to DeltaR(2) = .048. This means that when the 3 therapeutic variables are taken into account statistically, AS alone retained relatively little association with patient functioning. These results suggest that AS may amplify the impact of emotional distress on patient functioning in chronic pain and that processes of acceptance, mindfulness, and values-based action may reduce this effect. ⋯ Humans can fear and struggle to avoid their own emotional experiences, even when these cannot harm them. Data presented here show individuals with chronic pain have more distress and disability when they manifest more fear of anxiety symptoms, and behavior patterns of "acceptance" and "mindfulness" may reduce this effect.
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The parafascicular nucleus (nPf) of the intralaminar thalamus is implicated in the processing of pain affect in both animals and humans. Administration of morphine into nPf results in preferential suppression of the affective reaction to noxious tail shock in rats. The involvement of the ventrolateral periaqueductal gray in mediating the antinociceptive action of morphine injected into nPf was evaluated. Vocalizations that occur after tail shock offset (vocalization afterdischarges) are a validated rodent model of pain affect and were preferentially suppressed by injection of morphine into nPf. 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 morphine into nPf. Inactivation of the vPAG via the microinjection of muscimol (GABA(A) agonist) produced dose-dependent antagonism of morphine-induced increases in vocalization thresholds. The results demonstrate that a functional link between the nPf and vPAG in generating the antinociceptive action of morphine injected into nPf. ⋯ Microinjection of morphine into nucleus parafascicular preferentially suppressed rats' affective reaction to noxious stimulation. This affective analgesia was reversed by inactivation of the ventrolateral periaqueductal gray. Understanding the neurobiology underlying the suppression of pain affect will provide insights into new treatments for pain and its associated affective disorders.
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The facet joint is a common source of pain in both the neck and low back, and can be injured by abnormal loading of the spinal joints. Whereas a host of nociceptive changes including neuronal activation, neuropeptide expression, and inflammatory mediator responses has been reported for rat models of joint pain, no such responses have been explicitly investigated or quantified for painful mechanical injury to the facet joint. Two magnitudes of joint loading were separately imposed in a rat model of cervical facet joint distraction: Painful and nonpainful distractions. Behavioral outcomes were defined by assessing mechanical hyperalgesia in the shoulders and forepaws. Substance P (SP) mRNA and protein levels were quantified in the dorsal root ganglion (DRG) and spinal cord at days 1 and 7 following distraction. Painful distraction produced mechanical hyperalgesia that was significantly greater (P < .010) than that for a nonpainful distraction. Painful distraction significantly increased spinal SP mRNA (P = .048) and SP protein expression in the DRG (P = .013) at day 7 compared to nonpainful distraction. However, spinal SP protein for painful distraction was significantly less (P = .024) than that for nonpainful distraction at day 1. Joint distractions producing different behavioral outcomes modulate SP mRNA and protein in the DRG and spinal cord, suggesting that SP responses may be involved with different temporal responses in painful joint loading. ⋯ SP mRNA and protein in the DRG and spinal cord are quantified at 2 time points after cervical facet joint distractions that separately do or do not produce mechanical hyperalgesia. Studies describe a role for SP to contribute to pain produced by mechanical joint loading.
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Opiates are currently the mainstay for treatment of moderate to severe pain. However, prolonged administration of opiates has been reported to elicit hyperalgesia in animals, and examples of opiate-induced hyperalgesia have been reported in humans as well. Despite the potential clinical significance of such opiate-induced actions, the mechanisms of opiate-induced hypersensitivity remain unknown. The transient receptor potential vanilloid1 (TRPV1) receptor, a molecular sensor of noxious heat, acts as an integrator of multiple forms of noxious stimuli and plays an important role in the development of inflammation-induced hyperalgesia. Because animals treated with opiates show thermal hyperalgesia, we examined the possible role of TRPV1 receptors in the development of morphine-induced hyperalgesia using TRPV1 wild-type (WT) and knock-out (KO) mice and with administration of a TRPV1 antagonist in mice and rats. Administration of morphine by subcutaneous implantation of morphine pellets elicited both thermal and tactile hypersensitivity in TRPV1 WT mice but not in TRPV1 KO mice. Moreover, oral administration of a TRPV1 antagonist reversed both thermal and tactile hypersensitivity induced by sustained morphine administration in mice and rats. Immunohistochemical analyses indicate that sustained morphine administration modestly increases TRPV1 labeling in the dorsal root ganglia. In addition, sustained morphine increased flinching and plasma extravasation after peripheral stimulation with capsaicin, suggesting an increase in TRPV1 receptor function in the periphery in morphine-treated animals. Collectively, our data indicate that the TRPV1 receptor is an essential peripheral mechanism in expression of morphine-induced hyperalgesia. ⋯ Opioid-induced hyperalgesia possibly limits the usefulness of opioids, emphasizing the value of alternative methods of pain control. We demonstrate that TRPV1 channels play an important role in peripheral mechanisms of opioid-induced hyperalgesia. Such information may lead to the discovery of analgesics lacking such adaptations and improving treatment of chronic pain.