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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When painful stimuli are evaluated at the time they are experienced, judgments are made not in isolation but with reference to other experienced stimuli. We tested a specific quantitative model of how such context effects occur. Participants experienced 3 blocks of 11 different pressure pain stimuli, and rated each stimulus on a 0-10 scale of intensity. ⋯ Study 2 found that pain ratings were higher in a context where most stimuli were relatively intense, even when the mean stimulus was constant. It is suggested that pain judgments are relative, involve the same cognitive processes as are used in other psychophysical and socioemotional judgments, and are well described by range frequency theory. This approach can further inform the existing body of research on context-dependent pain evaluation.
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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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Toll-like receptors (TLRs) play a pivotal role in inflammatory processes, and individual TLRs have been investigated in nociception. We examined overlapping and diverging roles of spinal TLRs and their associated adaptor proteins in nociceptive processing. Intrathecal (IT) TLR2, TLR3, or TLR4 ligands (-L) evoked persistent (7-day) tactile allodynia (TA) that was abolished in respective TLR-deficient mice. ⋯ Hence, spinal TIR domain-containing adaptor protein (TIRAP) and TRIF cascades differentially lead to robust TA by TNF-dependent and independent pathways, whereas activation of TRIF modulated processing through type I IFN receptors. Based on these results, we believe that processes leading to the activation of these spinal TLRs initiate TNF-dependent and -independent cascades, which contribute to the associated persistent pain state. In addition, TRIF pathways are able to modulate the TNF-dependent pain state through IFNβ.