Pain
-
The Child Activity Limitations Interview (CALI) is a measure designed to assess functional impairment due to chronic pain in school-age children. In this study, we present a self-report questionnaire version of the CALI (the CALI-21) that extends the original interview measure. The purpose of this study was to provide internal consistency, cross-informant reliability and construct validity of the CALI-21 on a clinical sample of children and adolescents with chronic pain conditions. ⋯ The CALI-21 showed good internal consistency, high cross-informant reliability, and demonstrated construct validity. The CALI-21 provides increased flexibility via the questionnaire format in the assessment of pain-related activity limitations in children. Factor analysis extends information about specific types of activity limitations experienced by children.
-
Chronic pain is a public health problem with high impact on various population segments. There are few population studies with the aim of delineating the profile of the chronic pain patient, and generating data for actions to prevent, control and minimize the problem. The aim of this study was to estimate the prevalence of chronic pain in the population of Salvador, Bahia, Brazil and identify independent predictors associated with this morbidity. ⋯ Among the studied factors, in the gross analysis, the following were shown to be associated with chronic pain: conjugal situation, smoking, excessive alcohol consumption, presence of central obesity and age, all with p<0.05. In the multivariate analysis, female sex, smoking, excessive alcohol consumption, and age were sustained as independent predictors. The presence of chronic pain was predominant in women, the elderly, smokers or ex-smokers and excessive alcohol consumers.
-
The standard rodent model of itch uses scratching with the hind limb as a behavioral response to pruritic stimuli applied to the nape of the neck. The assumption is that scratching is an indicator of the sensation of itch. But because only one type of site-directed behavior is available, one cannot be certain that scratching is not a response to nociceptive or other qualities of sensations in addition to, or instead of, itch. ⋯ In contrast, when the same chemicals were injected into the cheek of the mouse, there were two site-directed behaviors: histamine again elicited scratching with the hind limb, but capsaicin evoked wiping with the forelimb. We conclude that the "cheek model of itch" in the mouse provides a behavioral differentiation of chemicals that elicit predominantly itch in humans from those that evoke nociceptive sensations. That is, the model provides a behavioral differentiation between itch and pain in the mouse.
-
The glial cytokine, interleukin-1beta (IL-1beta), potentiates the excitability of nociceptive trigeminal ganglion (TRG) neurons via membrane depolarization following peripheral inflammation. Perforated patch-clamp technique was used this study to show that the mechanism underlying the excitability of small-diameter TRG neurons following inflammation is due to IL-1beta. Inflammation was induced by injection of complete Freund's adjuvant (CFA) into the whisker pad. ⋯ IL-1beta inhibited I(A) to a significantly greater extent than I(K). These results suggest that the inhibitory effect of I(A) and I(K) currents by IL-1beta in small-diameter TRG neurons potentiates neuronal excitability thereby contributing to trigeminal inflammatory hyperalgesia. These findings provide evidence for the development of voltage-gated K(+) channel openers and IL-1beta antagonists as therapeutic agents for the treatment of trigeminal inflammatory hyperalgesia.
-
EphBs receptors and ephrinBs ligands are present in the adult brain and peripheral tissue and play a critical role in modulating multiple aspects of physiology and pathophysiology. Ours and other studies have demonstrated that spinal ephrinBs/EphBs signaling was involved in the modulation of nociceptive information and central sensitization. However, the role of ephrinBs/EphBs signaling in peripheral sensitization is poorly understood. ⋯ EphrinB1-Fc-induced hyperalgesia is accompanied with the NMDA receptor-mediated increase of expression in peripheral and spinal phosphorylated mitogen-activated protein kinases (phospho-MAPKs) including p-p38, pERK and pJNK, and also is prevented or reversed by the inhibition of peripheral and spinal MAPKs. Furthermore, in formalin inflammation pain model, pre-inhibition of EphBs receptors by the injection of EphB1-Fc reduces pain behavior, which is accompanied by the decreased expression of peripheral p-p38, pERK and pJNK. These data provide evidence that ephrinBs may act as a prominent contributor to peripheral sensitization, and demonstrate that activation of peripheral ephrinBs/EphBs system induces hyperalgesia through a MAPKs-mediated mechanism.