Pain
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The perception of pain results from an interaction between nociceptive and antinociceptive mechanisms. A better understanding of the neural circuitry underlying these physiological interactions provides an important opportunity to develop better treatment strategies for and ultimately even prevent pain. Here, we investigated how repeated painful stimulation over several days is processed, perceived and finally modulated in the healthy human brain. ⋯ The decreased perception of pain over time is reflected in decreased BOLD responses to nociceptive stimuli in classical pain areas, including thalamus, insula, SII and the putamen. In contrast to this finding, we found that pain-related responses in the rACC, specifically the subgenual anterior cingulate cortex (sgACC), significantly increased over time. Given this area's predominant role in endogenous pain control, this response pattern suggests that habituation to pain is at least in part mediated by increased antinociceptive activity.
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Pain is an experience including physiological and psychological factors. We assume that emotions may be elicited and increased through self-perceived role identity and that change of role identity alters quality and intensity of pain perception. We used role-play strategies to assess whether pain can be better tolerated whenever, in an unavoidable and unpleasant context, role identity confers pain a meaningful and thus suitable character. ⋯ Women showed higher pain ratings. Hence, self-perception influences pain perception. Role-play strategies may be of value for new pain management strategies.
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The effects of differential aversive Pavlovian conditioning on the functional organization of primary somatosensory cortex (SI) were examined in 17 healthy participants. Neuroelectric source imaging from 60 electrodes was employed while nine subjects received an innocuous electric stimulus (conditioned stimulus, CS) to one finger (left or right) that was followed by painful electric shock to the lower back (unconditioned stimulus, US) and an innocuous stimulus to the other finger that was never followed by pain. Eight subjects received a presentation of the innocuous and painful stimuli with equal probability to both fingers (control group). ⋯ Intensity and unpleasantness ratings were altered in a more unspecific manner and did not differ between groups and stimulus conditions. The data suggest that SI contributes to memory processes in associative learning. Pavlovian conditioning of tactile responses might be important in the altered processing of painful stimuli in chronic pain patients where enhanced conditioning has been demonstrated.
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Many children and adolescents experience recurrent pain, but only a few become disabled by it. Research has established that higher pain intensity and worse depression seem to predict poorer functioning in this population. Parent and family variables have been minimally researched. ⋯ Pain intensity and depression predicted functional disability. However, social/adaptive functioning was associated with different variables, including parent factors, and school attendance showed no association with pain intensity or anxiety. The results emphasise the need to measure multiple domains of functioning, and show that the connections between pain, physical disability and adaptive functioning are looser than might be predicted.
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In humans, the acute inflammatory reaction caused by ultraviolet (UV) radiation is well studied and the sensory changes that are found have been used as a model of cutaneous hyperalgesia. Similar paradigms are now emerging as rodent models of inflammatory pain. Using a narrowband UVB source, we irradiated the plantar surface of rat hind paws. ⋯ Sequestration of NGF, starting at the time of UVB irradiation, significantly reduced sensory changes. We conclude that UVB inflammation produces a dose-dependent hyperalgesic state sensitive to established analgesics. This suggests that UVB inflammation in the rat may represent a useful translational tool in the study of pain and the testing of analgesic agents.