Pain
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To evaluate in patients with different types of facial pain the association between muscle tenderness and a set of characteristics, 649 consecutive outpatients with facial myogenous pain (MP), TMJ disorder, neuropathic pain (NP) and facial pain disorder (FPD) (DSM-IV) were enrolled. For each patient a psychological assessment on the Axis 1 of the DSM-IV and standardized palpation of pericranial and cervical muscles were carried out. A pericranial muscle tenderness score (PTS), a cervical muscle tenderness score (CTS) and a cumulative tenderness score (CUM, range 0-6) were calculated. ⋯ To assess associations between CUM score and patients' demographic and clinical characteristics an ordered logit model was fit and interactions between psychiatric disorders and diagnostic groups were tested. The analysis showed that, regardless of the diagnostic group, anxiety and depression independently increase the likelihood of having one point higher muscle tenderness score (OR=1.55, 95% CI: 1.13-2.12 and OR=1.56, 95% CI: 1.10-2.21, respectively). A careful screening for the presence of an underlying psychiatric disorder, either anxiety or depression, should be part of the clinical evaluation in patients suffering from facial pain.
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The majority of research on pain catastrophizing has focused on its negative consequences for adjustment to chronic pain, with few investigations of factors that influence catastrophizing or its detrimental effects. Using a daily process methodology, the current study examined, first, the extent to which a supportive social environment plays a role in reduced catastrophizing, and second, the extent to which support might protect against the detrimental effects of catastrophizing on well-being. Sixty-nine married individuals with rheumatoid arthritis took part in an initial background interview, followed by twice daily telephone interviews (regarding pain intensity, negative affect, catastrophizing and satisfaction with spouse responses) for 1 week. ⋯ The relationship between pain and catastrophizing was attenuated in the context of increases in satisfaction with spouse responses. Negative affect was associated with increases in catastrophizing, but only when individuals reported decreases in satisfaction with spouse responses. Overall, findings were consistent with a model in which satisfaction with spouse responses serves as a coping resource, and suggests the importance of involving close others in treatments to reduce pain and catastrophizing.
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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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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.