Pain
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Randomized Controlled Trial
The role of threat-expectancy in acute pain: effects on attentional bias, coping strategy effectiveness and response to pain.
The aims of this study were threefold. Firstly, to investigate the effect of increasing threat-expectancy on attentional biases towards pain-related words. Secondly, to determine the interaction between threat-expectancy and the effectiveness of two coping strategies on pain threshold and tolerance. ⋯ The present results provide support for the fear-avoidance model of pain [Vlaeyen JWS, Linton SJ. Fear-avoidance and its consequences in chronic musculoskeletal pain: a state of the art. Pain 2000;85:317-332] and confirm the importance of threat-expectancy in hypervigilance towards pain and fear avoidance.
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Clinical Trial
An experimental study of viscero-visceral hyperalgesia using an ultrasound-based multimodal sensory testing approach.
Widespread visceral hypersensitivity and the overlap of symptom complexes observed in functional gastrointestinal disorders may be related to central sensitization and neuroplastic changes. A multimodal and multi-segmental model was developed to evaluate viscero-visceral hyperalgesia induced by experimental esophageal sensitization in healthy volunteers. Twelve healthy subjects were studied using a double-blinded, placebo-controlled design. ⋯ The present method demonstrated a new approach to assess multimodal sensitivity to experimental sensitization of the esophagus and related viscero-visceral hyperalgesia. Central mechanisms can explain the remote hyperalgesia to mechanical visceral stimulation and the increase in referred pain areas. The present method may be used to explore pathophysiology and pharmacological interventions in patients with visceral hypersensitivity.
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Nitric oxide (NO) acts as a neurotransmitter or neuromodulator involving in the modulation of thermal and/or inflammatory hyperalgesia. The neuronal nitric oxide synthase (nNOS) is a key enzyme for NO production in normal neuronal tissues, but its functional role in chronic pain remains unclear. The present study combined a genetic strategy with a pharmacologic approach to address the role of nNOS in the central mechanism of complete Freund's adjuvant (CFA)-induced chronic inflammatory pain. ⋯ Finally, spinal cord nNOS (but not endothelial NOS or inducible NOS) expression was up-regulated at 24h after CFA injection, occurring mainly in the ipsilateral superficial dorsal horn. Together, these data indicate that spinal cord nNOS may be essential for the maintenance of mechanical pain hypersensitivity and that it may also be sufficient for the development of mechanical pain hypersensitivity and for the development and maintenance of thermal pain hypersensitivity after chronic inflammation. Our findings suggest that spinal cord nNOS might play a critical role in central mechanisms of the development and/or maintenance of chronic inflammatory pain.
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P2X3 and P2X2/3 receptors in dorsal root ganglia (DRG) appear to participate in producing nociceptive responses after nerve injury. However, the mechanisms underlying the receptor-mediated nociception in the neuropathic state remain unclear. Using spared nerve injury (SNI) rats, we found that allodynic and nocifensive (flinch) behavioral responses developed after injury can be reversed by P2X receptor antagonists, indicating an involvement of P2X receptors. ⋯ ATP-induced P2X3 receptor-mediated currents in DRG neurons is 2.5-fold larger after SNI. The expression of P2X3 receptors on the cell membrane is significantly enhanced while the total expression of P2X3 receptors remained unchanged. Thus, the enhancement of trafficking of P2X3 receptors is likely an important mechanism contributing to the increase in receptor function after nerve injury.
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Acrylamide was intraperitoneally administered to male Sprague-Dawley rats at four different doses (5, 10, 20 and 30 mg/kg) three times a week for 5 consecutive weeks. Because of motor dysfunction, the 30 mg/kg dose was not used for behavioral pain tests. Clinical status remained good throughout the experiment and no motor deficit was observed at the other doses. ⋯ Mechanical and thermal hyperalgesia appeared after higher cumulative doses (70-280 mg/kg), except for cold (4 degrees C) hyperalgesia (20-80 mg/kg). All the modifications persisted throughout all study, except the mechanical hyperalgia. All the cumulative doses tested were lower than those generally reported to induce motor dysfunction (CD>250 mg/kg), confirming that CD may be considered to be a suitable index in assessing neurological signs and suggesting that early detection of acrylamide neurotoxicity would be possible using the sensory tests, especially those for detecting allodynia thresholds.