The journal of pain : official journal of the American Pain Society
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Comparative Study
Neonatal hind paw injury alters processing of visceral and somatic nociceptive stimuli in the adult rat.
Tissue damage during the first few weeks after birth can have profound effects on sensory processing in the adult. We have recently reported that a short-lasting inflammation of the neonatal rat hind paw produces baseline hypoalgesia and exacerbated hyperalgesia after reinflammation of that hind paw in the adult. Because the contralateral hind paw and forepaws also displayed hypoalgesia, we speculated that effects of the initial injury were not somatotopically restricted and would alter visceral sensory processing as well. In the present study we tested this hypothesis by examining the effects of neonatal hind paw injury at P3 or P14 on visceral and somatic sensitivity in the adult rat. In P3 rats, the visceromotor response evoked by colorectal distention in the absence of colonic inflammation was attenuated in carrageenan-treated neonatal rats compared to naive rats. Colonic inflammation in the adult reversed this hypoalgesia and evoked a level of visceral hyperalgesia similar to naive rats. There were no consequences of the P14 injury observed in the adult. In a second experiment, colonic inflammation in naive rats induced viscerosomatic inhibition to thermal stimulation of the forepaw and hind paw. This inhibition was reversed, and the paw withdrawal latency was slightly decreased in neonatal (P3) carrageenan-treated rats. Rats treated on P14 appeared similar to naive rats. These data support the hypothesis that neonatal hind paw injury during a critical period permanently alters sensory processing of multiple sensory modalities in the adult. Animals develop with greater inhibitory processing of somatic and visceral stimuli throughout the neuraxis. However, inflammation in the adult in previously uninjured tissue reverses the hypoalgesia and evokes development of normal hyperexcitability associated with tissue injury. ⋯ Trauma experienced by premature infants can lead to alterations in sensory processing throughout life. This study shows that short-term somatic tissue injury to neonatal rats during a well-defined critical period alters several aspects of viscerosensory processing in the adult, demonstrating that injury to one tissue affects sensory processing throughout the body.
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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
Development of a measure of the burden of pain due to herpes zoster and postherpetic neuralgia for prevention trials: adaptation of the brief pain inventory.
In preparation for clinical trials of a vaccine against herpes zoster (HZ), we conducted a prospective, observational study to evaluate (1) the Zoster Brief Pain Inventory (ZBPI), an HZ-specific questionnaire to quantify HZ pain and discomfort, (2) an operational definition of postherpetic neuralgia (PHN), and (3) a severity-duration measure of the burden of illness caused by HZ. HZ patients aged 60 years or older (n = 121) were enrolled within 14 days of rash onset and completed ZBPI, McGill Pain Questionnaire Present Pain Intensity (PPI), quality of life (QoL), and activities of daily living (ADL) questionnaires on a predetermined schedule. Reliability, measured by intraclass correlation coefficients within 14 days of rash onset, ranged between 0.63 and 0.78. ZBPI pain scores were strongly correlated with other pain measures, interference with ADL, and worsening QoL. The operational definition of PHN, a ZBPI pain score of 3 or greater occurring 90 or more days after rash onset, had high agreement with pain worse than mild on the PPI (kappa = 0.72). The ZBPI pain severity-duration measure had high correlations with severity-duration measures of ADL interference, worsening QoL, and other pain scales. These findings support the validity and utility of the ZBPI, the definition of PHN, and the severity-duration measure of the burden of HZ illness. ⋯ Herpes zoster pain, as measured by the ZBPI severity-duration measure, is associated with impairment in daily living activities and quality of life. The ZBPI measure appears useful for quantifying herpes zoster pain, postherpetic neuralgia, and impairment in daily living activities for clinical trials of herpes zoster prevention.