Pain
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The prefrontal cortex may be a promising target for transcranial magnetic stimulation (TMS) in the management of pain. It is not clear how prefrontal TMS affects pain perception, but previous findings suggest that ventral lateral and medial prefrontal circuits may comprise an important part of a circuit of perceived controllability regarding pain, stress, and learned helplessness. Although the left dorsolateral prefrontal cortex is a common TMS target for treating clinical depression as well as modulating pain, little is known about whether TMS over this area may affect perceived controllability. ⋯ Although it is not clear whether this cortical area is directly involved with modulating perceived controllability or whether downstream effects are responsible for the present findings, it appears possible that left dorsolateral prefrontal TMS may produce analgesic effects by acting through a cortical perceived-control circuit regulating limbic and brainstem areas of the pain circuit. Despite evidence that prefrontal TMS can have analgesic effects, fast left prefrontal TMS appears to acutely suppress analgesia associated with perceived-control. This effect may be limited to the emotional dimension of pain experience.
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Despite some other known psychiatric adverse effects, ziconotide is recommended for intrathecal pain treatment with a good efficacy and safety. Although some hints in previous studies are apparent, a higher suicidality has not been accepted as a treatment risk of ziconotide treatment by the investigators in the former randomized controlled trials so far. We present two cases supporting the suspicion of ziconotide-induced suicidality. ⋯ The patient, who has completed suicide, had earlier given rise to discuss a potential depressive disorder, however, this diagnosis was scrapped, but the second patient had a clear history of depression. These cases substantiate the suspicion of a causal relationship between ziconotide and suicidality even in symptom-free patients with a history of depression. Therefore, a comprehensive psychiatric evaluation is unavoidable before and during ziconotide treatment.
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Peripheral mechanisms are known to play a role in phantom pain following limb amputation, and more recently it has been suggested that central mechanisms may also be of importance. Some patients seem to have a psychological sensitivity that predisposes them to react with pain catastrophizing after amputation of a limb, and this coping style may contribute to increased facilitation, impaired modulation of nociceptive signals, or both. To investigate how pain catastrophizing, independently of anxiety and depression, may contribute to phantom limb pain and to alterations in pain processing twenty-four upper-limb amputees with various levels of phantom limb pain were included in the study. ⋯ Catastrophizing was also positively associated with wind-up-like pain in non-medicated patients (p=0.015), but not to pain thresholds. These findings suggest that cognitive-emotional sensitization contributes to the altered nociceptive processing seen in phantom limb pain patients. The possible interactions between pain catastrophizing, wind-up-like pain, and peripheral input in generating and maintaining phantom limb pain are discussed.
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To elucidate the mechanisms of antinociception mediated by the dopaminergic descending pathway in the spinal cord, we investigated the actions of dopamine (DA) on substantia gelatinosa (SG) neurons by in vivo whole-cell patch-clamp methods. In the voltage-clamp mode (V(H)=-70mV), the application of DA induced outward currents in about 70% of SG neurons tested. DA-induced outward current was observed in the presence of either Na(+) channel blocker, tetrodotoxin (TTX) or a non-NMDA receptor antagonist, CNQX, and was inhibited by either GDP-β-S in the pipette solution or by perfusion of a non-selective K(+) channel blocker, Ba(2+). ⋯ We showed that DA produced direct inhibitory effects in SG neurons to both noxious and innocuous stimuli to the skin. Furthermore, electrical stimulation of dopaminergic diencephalic spinal neurons (A11), which project to the spinal cord, induced outward current and suppressed the frequency and amplitude of EPSCs. We conclude that the dopaminergic descending pathway has an antinociceptive effect via D2-like receptors on SG neurons in the spinal cord.
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The intensity of experimental pain is known to be dependent on stimulation duration. However, it remains unknown whether this effect arises largely from the actual stimulus duration or is substantially influenced by the subject's perception of the stimulus duration. In the present study, we questioned this issue by misleading the perception of the duration of pain in a population of 36 healthy volunteers stimulated with a thermode. ⋯ Although the intensity and the real duration of stimulation were identical in both conditions, the intensity of pain was significantly reduced when the perception of time was misleadingly shortened by the manipulated clock. This study suggests that the perceived duration of a noxious stimulation may influence the perceived intensity of pain. The perceived duration of the length of a noxious stimulation influences (decreases) the intensity of perceived pain.