Pain
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Comparative Study
Phantom limb pain after amputation in diabetic patients does not differ from that after amputation in nondiabetic patients.
There is a commonly held belief that diabetic amputees experience less phantom limb pain than nondiabetic amputees because of the effects of diabetic peripheral neuropathy; however, evidence to verify this claim is scarce. In this study, a customised postal questionnaire was used to examine the effects of diabetes on the prevalence, characteristics, and intensity of phantom limb pain (PLP) and phantom sensations (PS) in a representative group of lower-limb amputees. Participants were divided into those who had self-reported diabetes (DM group) and those who did not (ND group). ⋯ Using a 0-10 visual analogue scale, the average intensity of PLP was 3.89 (±0.40) for the DM group and 4.38 (±0.41) for the ND group, which was not a statistically significant difference (P=0.402). Length of time since diagnosis of diabetes showed no correlation with average PLP intensity. Our findings suggest that there is no large difference in the prevalence, characteristics, or intensity of PLP when comparing diabetic and nondiabetic amputees, though a larger adjusted comparison would be valuable.
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Given the inherent variability in pain responding, using an "average" pain score may pose serious threats to internal and external validity. Using growth mixture modeling (GMM), this article first examines whether infants can be differentiated into stable groups based on their pain response patterns over a 2-minute post-needle period. Secondary analyses, to specifically address the issue of averaging pain scores to represent a sample, qualitatively described clinically meaningful differences between pain scores of the discerned groups and the overall mean (irrespective of groups). ⋯ Our secondary suggested that the overall mean pain score immediately post-needle reflected most groups well at every age. However, for older infants (6 and 12months, especially), the overall mean pain responses at 1 and 2minutes post-needle significantly over or underestimated groups that contained 48% to 100% of the sample. These results combined highlight the significant variability of infant pain responding patterns between groups of infants and furthermore, calls into question the validity of using an overall mean in research with older infants during the regulatory phase post-needle.
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Comparative Study
Noxious stimulation excites serotonergic neurons: a comparison between the lateral paragigantocellular reticular and the raphe magnus nuclei.
The present study was designed to record electrophysiological responses to graded noxious thermal stimuli of serotonergic and nonserotonergic neurons in the lateral paragigantocellular reticular (LPGi) and the raphe magnus (RMg) nuclei in rats. All of the neurons recorded were juxtacellularly filled with neurobiotin and identified with double immunofluorescent labeling for both neurobiotin and serotonin. Under halothane anesthesia (0.75%), noxious thermal stimuli ⩾48°C activated almost all (88%) of the serotonergic neurons located within the LPGi (n=16). ⋯ Recording of serotonergic neurons in the RMg (n=21) demonstrated that the proportion of strongly activated (>2spike/s) neurons (19% vs 59% for the LPGi) as well as the magnitude of the activation (2.1±0.4spike/s: mean of responses above the population median) to thermal noxious stimuli were significantly lower than in the LPGi (P<.05). Within the boundaries of both the LPGi and the RMg (B3 group), nonserotonergic neurons were also predominantly excited (75%) by noxious stimuli, and the resulting activation (7.9±1.2spike/s) was even greater than that of serotonergic neurons. Thermal noxious stimuli-induced activation of LPGi serotonergic cells probably plays a key role in serotonin-mediated modulations of cardiac baroreflex and transmission of nociceptive messages occurring under such intense noxious conditions.
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Factors underlying individual differences in pain responding are incompletely understood, but are likely to include genetic influences on basal pain sensitivity in addition to demographic characteristics such as age, sex, and ethnicity, and psychological factors including personality. This study sought to explore the relationship between personality traits and experimental pain sensitivity, and to determine to what extent the covariances between these phenotypes are mediated by common genetic and environmental factors. A sample composed of 188 twins, aged 23 to 35years, was included in the study. ⋯ In contrast, associations between HPI and personality seemed weak and unstable, but a significant effect of Angry Hostility (a facet of Neuroticism) emerged in generalized estimating equations analysis. Although the genetic correlation between these phenotypes was essentially zero, a weak but significant individual-specific environmental correlation emerged (re=.21, P<.05). Taken together, these findings suggest that CPI is more consistently related to personality dispositions than HPI, both phenotypically and genetically.
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Calcitonin gene-related peptide (CGRP) is known to play a major role in the pathogenesis of pain syndromes, in particular migraine pain. Here we focus on its implication in a rat pain model of inflammation, induced by injection of complete Freund adjuvant (CFA). The nonpeptide CGRP receptor antagonist BIBN4096BS reduces migraine pain and trigeminal neuronal activity. ⋯ The same amount of reduction occurred after topical administration onto the paw, with resulting systemic plasma concentrations in the low nanomolar range. However, spinal administration of BIBN4096BS did not modify the neuronal activity in the CFA model. Peripheral blockade of CGRP receptors by BIBN4096BS significantly alleviates inflammatory pain.