Pain
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Randomized Controlled Trial Clinical Trial
Preinjury treatment with morphine or ketamine inhibits the development of experimentally induced secondary hyperalgesia in man.
We examine the effect of morphine or ketamine (N-methyl-D-aspartate receptor antagonist; NMDA) treatment on secondary hyperalgesia. Drug treatment started preinjury and continued into the early postinjury period. Hyperalgesia was induced by a local 1 degrees burn injury covering 12.5 cm(2) on the medial side of the calf. ⋯ In a previous study, we found that postinjury treatment alone with morphine did not affect secondary hyperalgesia, whereas ketamine did so significantly. The differential response to morphine administered pre- or postinjury may be relevant to the recently shown NMDA receptor mediated interaction of central hyperexcitability and morphine antinociception. The effect of ketamine supports the hypothesis of the role of NMDA receptor mediation in central hyperexcitability.
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Comparative Study
Neuropsychological performance in cancer patients: the role of oral opioids, pain and performance status.
The aim of the present study was to evaluate the possible influence of oral opioids, pain and performance status on some aspects of psychomotor function and cognition in cancer patients. One hundred and thirty cancer patients between 40 and 76 years of age were consecutively included in the study. In order to separate the impact of performance status, pain and oral opioids on neuropsychological functioning the patients were allocated in a cross-sectional design to five different groups. ⋯ Concerning PASAT, groups 1 and 4b performed statistically significantly better than group 4a. Furthermore, the pain-relieved groups 2 and 4b performed statistically significantly better in PASAT than the pain-suffering groups 3 and 4a. We conclude that in cancer patients the impact of stigmatizing factors (oral opioids, pain and reduced performance status) seems to impair some important aspects of neuropsychological performance, but more specifically our results indicate that (1) the use of long-term oral opioid treatment in cancer patients per se did not affect any of the neuropsychological tests used in the present study, (2) cancer patients being in KPS B had statistically significantly slower CRT than patients being in KPS A and (3) pain itself may deteriorate the performance of PASAT more than oral opioid treatment.
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Patient readiness to adopt new beliefs and coping responses to pain may predict response to multidisciplinary or cognitive-behavioral pain treatments that emphasize changes in beliefs and coping behaviors. According to the transtheoretical model of change, individuals go through specific stages in the process of changing maladaptive behaviors. Based on this model, Kerns et al. (1997) (Kerns RD, Rosenberg R, Jamison RN, Caudill MA, Haythornthwaite J. ⋯ The internal consistency and concurrent validity of the PSOCQ subscales were largely replicated, supporting the validity of the subscales as measures of readiness to self-manage pain. However, the PSOCQ demonstrated less utility as a tool for classifying individuals into one of four specific stages of readiness to adopt a self-management approach. This result may be due to the classification procedure used in the current study, the characteristics of the samples in the study, specific limitations of the measure, and/or limitations in the applicability of the transtheoretical model of change to patients with chronic pain.
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Although intrathecal administration of baclofen, a selective GABA(B)-receptor agonist, is known to have an antinociceptive effect on various pain models, the role of presynaptic GABA(B) receptors in antinociception is not well characterized. In the present study, the action of baclofen on primary afferent-evoked glutamatergic excitatory transmission was examined in substantia gelatinosa (SG) neurons of an adult rat spinal cord slice with an attached dorsal root, prepared from the lumbar segment, by use of the blind whole-cell patch-clamp technique. Under the condition where a postsynaptic action of baclofen was inhibited, baclofen (1 microM) reduced the amplitudes of excitatory postsynaptic currents (EPSCs; V(H)=-70 mV) which were monosynaptically evoked by stimulating primary-afferent C- and/or Adelta-fibers and which were remarkably depressed by CNQX (10 microM). ⋯ Baclofen (1 microM) did not affect a response of SG neurons to bath-applied AMPA (10 microM). These results indicate that baclofen inhibits the release of L-glutamate from Adelta and C primary-afferent terminals in the SG through the activation of GABA(B) receptor; this action is more effective to C-fiber than Adelta-fiber transmission. Considering that the SG is the main part of termination of Adelta- and C-fibers transmitting nociceptive information, the present finding would account for at least a part of the inhibitory action of baclofen on pain transmission.
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This study tested the hypothesis that fibromyalgia patients display hypervigilance for somatosensory signals. Hypervigilance was operationalized as the detection of weak electrocutaneous stimuli. Innocuous electrical stimuli gradually increasing in strength were administered to one of four different body locations. ⋯ No evidence for hypervigilance for innocuous signals was found: patients did not show superior detection of electrical stimuli either under single or dual task conditions. Also, no differences were found between patients and controls on the body vigilance questionnaire. Detection of electrical stimuli was, however, predicted by pain-related fear and pain vigilance.