Pain
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One frequently described feature of depression is an increased vulnerability to pain complaints, and chronic pain is frequently accompanied by symptoms of depression. In contrast to this, a decreased sensitivity to experimental pain has been described in major depression. The physiological basis of this phenomenon is yet elusive. ⋯ Furthermore, thermal pain tolerance and electrical pain tolerance were significantly increased on the right hand side confirming previous results of a lateralized perception of pain in depression. Our main finding suggests that painful stimuli are processed differentially depending on the localization of pain induction in depression. This knowledge may enable us to understand and ultimately treat pain complaints more appropriately in depressed patients.
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Comparative Study Clinical Trial
The impact of ethnic differences in response to capsaicin-induced trigeminal sensitization.
Ethnic differences in the experience of pain, pain-related health care utilization and pain-reducing activities have been reported. Thus, evaluating of such variations is important in clinical and experimental pain. Since clinical pain is greatly influenced by disease-specific factors (severity, duration, type and treatment), evaluating ethnic differences in experimental pain models may not only provide some information about underlying mechanisms but also may predict or explain group differences in clinical pain. ⋯ Pain sensitivity, secondary hyperalgesic area, and pressure pain threshold were assessed. Overall, the model showed significant greater pain responses in South Indians (8.75+/-1.25 cm pain intensity and 9.33+/-2.32 cm2 hyperalgesic area) compared to Caucasians (6.25+/-1.95 cm pain intensity and 6.25+/-1.41 cm2 hyperalgesic area). The model may provide important information for further clinical research, e.g. migraine or differences in mechanisms underlying trigeminal sensitization.
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Comparative Study
Mechanisms involved in the nociception produced by peripheral protein kinase c activation in mice.
Protein kinase C (PKC) is able to phosphorylate several cellular components that serve as key regulatory components in signal transduction pathways of nociceptor excitation and sensitisation. Therefore, the present study attempted to assess some of the mechanisms involved in the overt nociception elicited by peripheral administration of the PKC activator, phorbol 12-myristate 13-acetate (PMA), in mice. The intraplantar (i.pl.) injection of PMA (16-1600 pmol/paw), but not its inactive analogue alpha-PMA, produced a long-lasting overt nociception (up to 45 min), as well as the activation of PKCalpha and PKCepsilon isoforms in treated paws. ⋯ Finally, mast cells as well as capsaicin-sensitive and sympathetic fibres, but not neutrophil influx, mediated the nociceptive effect produced by PMA. Collectively, the results of the present study have shown that PMA injection into the mouse paw results in PKC activation as well as a relatively delayed, but long-lasting, overt nociceptive behaviour in mice. Moreover, these results demonstrate that PKC activation exerts a critical role in modulating the excitability of sensory neurons.
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Comparative Study
Anatomy of the cervical intervertebral foramina: vulnerable arteries and ischemic neurologic injuries after transforaminal epidural injections.
Cervical transforaminal epidural steroid injections are performed for the treatment of radicular pain. Multiple recent case reports have raised safety concerns regarding neurologic deficits such as anterior spinal artery syndrome and cerebellar injury after these injections. To investigate the potential causes of these injuries, an anatomic study was conducted. ⋯ Variable anastomoses between the vertebral and cervical arteries were found. Therefore, it is possible to introduce steroid particles into the vertebral circulation via the cervical arteries. Critical arteries are located in the posterior aspect of the intervertebral foramen and may be vulnerable to injection or injury during transforaminal epidural steroid injection.
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Questions have been raised about the potential neurotoxicity of the neuraxial use of ketamine although ketamine and its active enantiomer S(+)-ketamine have been used intrathecally and epidurally (caudally) for the management of perioperative pain and in a variety of chronic pain syndromes. Clinical experience following neuraxial administration of S(+)-ketamine has been documented without reference to local central nervous system toxicity following this approach. ⋯ However, postmortem observation of the spinal cord and nerve roots revealed severe histological abnormalities including central chromatolysis, nerve cell shrinkage, neuronophagia, microglial upregulation, and gliosis. Based on our results, neuraxial administration of S (+)-ketamine cannot be recommended for clinical practise before a systematic study of toxicology of neuraxial S(+)-ketamine in animals or humans has been performed.