Pain
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Despite the development of the IASP criteria, diagnosing complex regional pain syndrome (CRPS) remains a challenge because all symptoms vary interindividually, including the vascular abnormalities. Previous studies showed that skin temperature asymmetries between the affected and contralateral extremity around 2 degrees C are useful for diagnosing CRPS. However, they were either assessed only at one single point in time or during specific investigations including controlled thermoregulatory modulation of sympathetic activity which limits their practicability. ⋯ However, both patient groups differed significantly in parameters characterizing the skin temperature dynamics. A sum score (2 *Q Oscill +r2 id +DeltaT2) allowed diagnosing CRPS with a specificity of 67% vs. patients with other painful diseases and 79% vs. healthy controls (sensitivity: 73%, respectively, 94%) and reflected the severity of the dysfunction in CRPS better than the mean skin temperature side differences alone. The applied skin temperature analysis can be easily applied in the clinical settings and serves as a further facet in the difficult diagnosis of CRPS.
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P2X receptors on dorsal root ganglion (DRG) neurons have been strongly implicated in pathological nociception after peripheral nerve injuries or inflammation. However, nothing is known of a role for purinergic receptors in neuropathic pain produced by a chronic compression of DRG (CCD) - an injury that may accompany an intraforaminal stenosis, a laterally herniated disc or other disorders of the spine leading to radicular pain. In a rat model of DRG compression, hyperexcitable neurons retain functioning axonal connections with their peripheral targets. ⋯ These currents were accompanied by the generation of action potentials - but only in the CCD neurons. U0126, a specific inhibitor of the MEK1/2, greatly down-regulated the enhanced current. Taken together, these observations suggest that enhanced purinergic responses after CCD are mediated by P2X 3 receptors.
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Operant conditioning mechanisms have been demonstrated to be important in the development of chronic pain. Most experimental studies have investigated the operant modulation of verbal pain reports with extrinsic reinforcement, such as verbal reinforcement. Whether this reflects actual changes in the subjective experience of the nociceptive stimulus remained unclear. ⋯ Results demonstrated that sensitization to prolonged heat-pain stimulation was enhanced by operant learning within 1h. The extent of sensitization was directly dependent on the received magnitude of reinforcement. Thus, operant learning mechanisms based on intrinsic reinforcement may provide an explanation for the gradual development of sustained hypersensitivity during pain that is becoming chronic.
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Various mechanisms at peripheral, spinal and/or supraspinal levels may underlie neuropathic pain. The nervous system's capacity for long-term reorganisation and chronic pain may result from abnormalities in RVM facilitatory On cells. Hence, via brainstem injections of the toxic conjugate dermorphin-saporin, which specifically lesions facilitatory cells expressing the mu-opioid receptor (MOR), we sought to determine the influence of these cells in normal and spinal nerve-ligated (SNL) rats. ⋯ During the early stages of nerve injury, or following medullary MOR cell ablation, PGB is ineffective at inhibiting spinal neuronal responses possibly due to quiescent spinal 5HT(3) receptors. This can however be overcome, and PGB's efficacy restored, by pharmacologically mimicking the descending drive at the spinal level with a 5HT(3) receptor agonist. Since RVM facilitatory neurones are integral to a spino-bulbo-spinal loop that reaches brain areas co-ordinating the sensory and affective components of pain, we propose that activity therein may influence painful outcome following nerve injury, and responsiveness to treatment.
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Multicenter Study
Severity of acute pain after childbirth, but not type of delivery, predicts persistent pain and postpartum depression.
Cesarean delivery rates continue to increase, and surgery is associated with chronic pain, often co-existing with depression. Also, acute pain in the days after surgery is a strong predictor of chronic pain. Here we tested if mode of delivery or acute pain played a role in persistent pain and depression after childbirth. ⋯ Women with severe acute postpartum pain had a 2.5-fold increased risk of persistent pain and a 3.0-fold increased risk of postpartum depression compared to those with mild postpartum pain. In summary, cesarean delivery does not increase the risk of persistent pain and postpartum depression. In contrast, the severity of the acute pain response to childbirth predicts persistent morbidity, suggesting the need to more carefully address pain treatment in the days following childbirth.