Pain
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Randomized Controlled Trial Comparative Study
Spinal cord stimulation normalizes abnormal cortical pain processing in patients with cardiac syndrome X.
Cardiac syndrome X (CSX) is characterized by effort angina, ST-segment depression during stress tests and normal coronary arteries. Abnormal nociception was suggested in these patients by studies showing a reduced cardiac pain threshold; furthermore, we recently found a lack of habituation to pain stimuli using recording of laser evoked potentials (LEPs). In CSX patients with severe angina, spinal cord stimulation (SCS) was shown to improve symptoms. ⋯ Similar results were observed during right-hand stimulation. Our study shows that in CSX patients SCS is able to restore habituation to peripheral pain stimuli. This effect might contribute to restore the ability of CSX patients to better tolerate cardiac pain.
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Comparative Study
Psychological predictors of pain expression and activity intolerance in chronic pain patients.
Recent research suggests that communicative and protective pain behaviors represent functionally distinct subsystems of behavior associated with pain. The present research examined whether components of pain experience such as pain severity, catastrophizing and fear of pain were differentially associated with communicative and protective pain behaviors. It was predicted that pain severity would be associated with decreased physical tolerance and heightened expression of pain behavior. ⋯ This study provides additional evidence for the functional distinctiveness of different types of pain expression and provides preliminary evidence for the functional distinctiveness of pain expression and activity intolerance. Discussion addresses the processes by which psychological factors might influence the display of different types of pain behaviors. Discussion also addresses how different types of interventions might be required to specifically target the sensory and behavioral dimensions of the pain system.
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Comparative Study
Voltage-gated sodium channel expression in rat and human epidermal keratinocytes: evidence for a role in pain.
Keratinocytes are implicated in sensory transduction and can influence nociception, but whether these contribute to chronic pain is not known. In neurons, voltage-gated sodium channels (Na(v)) are involved in neuropathic pain and are activated by depolarization. Since keratinocytes can also show changes in membrane potential, we used RT-PCR, in situ hybridization, and immunohistochemistry to investigate the expression of sodium channels in these cells. ⋯ In contrast, painful skin from CRPS and PHN subjects displayed Na(v)1.1, Na(v)1.2, and Na(v)1.8 immunolabeling, in addition to substantially increased signal for Na(v)1.5, Na(v)1.6, Na(v)1.7. These observations lead us to propose that pathological increases in keratinocyte sodium channel expression may contribute to pain by increasing epidermal ATP release, resulting in excessive activation of P2X receptors on primary sensory axons. Consistent with this hypothesis, animal models of neuropathic pain exhibit increases in subcutaneous ATP release and activity of primary sensory neurons, and peripheral administration of P2X antagonists has been shown to reduce neuropathic pain in humans.
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Comparative Study
Characteristics of chronic ischemic pain in patients with peripheral arterial disease.
Chronic ischemic pain is a leading cause of pain in the lower extremities. A neuropathic component in ischemic pain has been shown. Neuropathic pain questionnaires are established as a common tool in pain research. ⋯ The results suggest that the character of ischemic pain changes from nociceptive pain in patients with CI to predominantly neuropathic pain in patients with CLI. A neuropathic pain component seems to be a serious aspect in CLI, while it is not in CI. Questionnaires might be a helpful tool to investigate and diagnose ischemic pain.
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Comparative Study
EphrinB-EphB receptor signaling contributes to neuropathic pain by regulating neural excitability and spinal synaptic plasticity in rats.
Bidirectional signaling between ephrins and Eph receptor tyrosine kinases was first found to play important roles during development, but recently has been implicated in synaptic plasticity and pain processing in the matured nervous system. We show that ephrinB-EphB receptor signaling plays a critical role is induction and maintenance of neuropathic pain by regulating neural excitability and synaptic plasticity in the dorsal root ganglion (DRG) and the spinal dorsal horn (DH). Intrathecal application of blocking reagents for EphB-receptors, EphB1-Fc and EphB2-Fc chimeras inhibits the induction and maintenance of nerve injury-induced thermal hyperalgesia and mechanical allodynia. ⋯ Western Blot analysis shows that nerve injury triggers an upregulation of the ephrinB1 and EphB1 receptor proteins in DRG and the spinal cord. These results indicate that, by regulating excitability of nociceptive-related neurons in DRG and DH and the synaptic plasticity at the spinal level, ephrinB-EphB receptor signaling contributes to neuropathic pain. This novel role for ephrinB-EphB receptor signaling suggests that these molecules may be useful therapeutic targets for treating pain after nerve injury.