The journal of pain : official journal of the American Pain Society
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The purpose of this article is to explore the multidimensionality of the pain experience for patients with chronic pain by using a within-person, longitudinal approach. An Ecological Momentary Assessment design with a patient electronic diary was used to collect random momentary pain assessments several times a day for 2 weeks. We examined the within-person relationships between pain intensity, sensory characteristics, affective qualities, and activities limited by pain. All 3 dimensions (sensory, affective, and activities) were significantly related to pain intensity in a monotonic, but nonlinear, manner. These results expand our understanding of the pain experience by showing that changes of pain over time are associated with changes in sensory symptoms, affective distress, and activity limitations. ⋯ Although the relationships between pain dimensions have been examined between people, the results have been interpreted as within-persons. This article confirms that pain intensity is significantly related to sensory characteristics of pain, affective qualities of pain, and activity limitations due to pain within a person.
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Several investigators have reported weak or no associations between self-report and facial expression of pain, concluding that both parameters appear to be unrelated. However, studies so far have only focused on an overall association, not considering psychophysical relationships between stimulus intensities and pain responses while computing correlations. In the present study these psychophysical relationships, between stimulus intensity on the one hand and response magnitudes (of self-report and facial expression) on the other hand, were described in terms of intercept and slope. Correlation analyses were conducted between intercept and slope parameters of self-report and facial expression of pain. Forty young, pain-free individuals were investigated for their responses to mechanically and electrically induced pain. Self-report was assessed by Visual Analog Scales. Facial expression was examined by using the Facial Action Coding System. There were significant correlations between the linear slopes of the psychophysical functions of self-report and facial expression in pressure pain. Neither the intercepts nor overall mean responses in the 2 pain-signaling systems were significantly correlated. These findings suggest that the facial expression of pain appears to mirror self-report ratings, when their increases over a range of increasing stimulus intensities are considered in parallel. ⋯ In future studies, our psycho-physically derived observation that incremental changes in facial expression during developing pain are more characteristic for individuals than static levels needs further corroboration.
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Glia are now recognized as important contributors in pathological pain creation and maintenance. Spinal cord glia exhibit extensive gap junctional connectivity, raising the possibility that glia are involved in the contralateral spread of excitation resulting in mirror image pain. In the present experiments, the gap junction decoupler carbenoxolone was administered intrathecally after induction of neuropathic pain in response to sciatic nerve inflammation (sciatic inflammatory neuropathy) or partial nerve injury (chronic constriction injury). In both neuropathic pain models, a low dose of carbenoxolone reversed mirror image mechanical allodynia, while leaving ipsilateral mechanical allodynia unaffected. Ipsilateral thermal hyperalgesia was briefly attenuated. Critically, blockade of mechanical allodynia and thermal hyperalgesia was not observed in response to intrathecal glycyrrhizic acid, a compound similar to carbenoxolone in all respects but it does not decouple gap junctions. Thus, blockade of mechanical allodynia and thermal hyperalgesia by carbenoxolone does appear to reflect an effect on gap junctions. Examination of carbenoxolone's effects on intrathecal human immunodeficiency virus type 1 gp120 showed that blockade of pain facilitation might result, at least in part, via suppression of interleukin-1 and, in turn, interleukin-6. These data provide the first suggestion that spread of excitation via gap junctions might contribute importantly to inflammatory and traumatic neuropathic pain. ⋯ The current studies provide evidence for involvement of gap junctions in spinal cord pain facilitation. Intrathecal carbenoxolone, a gap junction decoupler, reversed neuropathy-induced mirror image pain and intrathecal gp120-induced allodynia. In addition, it decreased gp120-induced proinflammatory cytokines. This suggests gap junction activation might lead to proinflammatory cytokine release by distantly activated glia.
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The purpose of this study was to examine sex differences in the stability of experimental pain responding across time. Stability was assessed by using 2 forehead cold pressor applications separated by 9 months. Twenty-eight men and 20 women completed both Session 1 and Session 2. Repeated measures analysis of variance showed a main effect for Session on maximum pain level. Women reported significantly more pain at Session 2, whereas men showed no difference between sessions. There were no differences on pain report between men and women at Session 1. A significant Session by Sex interaction was associated with perceived chronic stress and trait anxiety levels. At Session 2 but not Session 1, women endorsed a significantly greater expectation than men to experience unpleasant aftereffects from the cold pressor task. Additional analysis showed that chronic stress and trait anxiety were significantly associated with sex-specific pain responding. We propose that the influence of a prior painful incident on an identical repeated painful experience differs between men and women. We speculate that this influence is related to sex differences in psychological mechanisms used to interpret painful stimuli within the context of remembered experiences. To our knowledge, this is the first report of sex differences in the long-term stability of an experimental laboratory pain stimulus, controlling for follicular phase of the female menstrual cycle. ⋯ This study examines sex differences in the stability of experimental pain responding across a 9-month period. We speculate that psychological mechanisms influence one's interpretation of a prior painful incident and that this interpretation facilitates increased pain reporting in response to an identical repeated exposure, as was observed for women.
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Comparative Study
Body pain area and pain-related negative affect predict clinical pain intensity in patients with fibromyalgia.
Patients with fibromyalgia (FM) report widespread chronic musculoskeletal pain. Palpation of 9 paired tender points (TPs) is commonly used for the diagnosis of FM according to criteria specified by the American College of Rheumatology. Although TP palpation can be used to assess deep tissue hypersensitivity, it has failed as a reliable indicator of clinical pain intensity in FM. The sum of local areas of pain (SLAP) obtained from a body pain diagram represents a relevant measure of the spatial extent of clinical pain, a feature most likely important for FM pain. Because spatial summation of pain can be an important determinant of clinical pain intensity, we hypothesized that this measure would predict clinical pain intensity in FM patients. Because pain is strongly associated with negative emotions, we evaluated the relationship of pain-related negative affect (PRNA) with clinical pain intensity in FM. The independent contributions of SLAP, PRNA, and TP count to the variance of clinical pain intensity were assessed in 280 FM patients. Clinical pain intensity of 280 FM patients was measured by using a visual analogue scale. FM patients shaded all painful body areas on body pain diagrams. Dolorimetry was used for TP evaluations. PRNA was assessed with the Medical College of Virginia Pain Questionnaire. Hierarchical linear regression was used to test the association of SLAP, TPs, and PRNA with clinical pain intensity. FM patients' mean visual analogue scale rating (0 to 100) of usual clinical pain was 50.1. Mean SLAP, TP count, and PRNA were 11.4, 16.0, and 44.3, respectively. Hierarchical linear regression analysis identified SLAP, TP count, and PRNA as independent predictors of clinical pain that accounted for 45% of the variance in clinical pain intensity ratings in FM patients. Consistent with the literature, TP count predicted only a small part (4%) of this variance. Our statistical model of body pain areas and negative affect predicts a large portion of the variance of pain intensity in FM. This result suggests that the extent of pain areas and negative emotions are uniquely associated with clinical pain intensity in FM. ⋯ The number of painful body areas obtained by body pain diagrams is a better predictor of clinical pain intensity than TPs in FM patients. The combination of painful body areas, TP counts, and PRNA predicts 45% of the clinical pain intensity of FM patients. This finding might be useful for clinical evaluations of FM patients.