931 resultados para Oneness of pain
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There is growing clinical evidence that even young children experience pain and accompanying anxiety. Few instruments have been validated to assess pain characteristics in children. The study of related demographic, illness, psychologic and parental factors in children has also been limited. This study examines the reliability and validity of pain assessment tools in an outpatient pediatric cancer population. A total of 78 children from three to fifteen years of age were observed and interviewed about the pain of invasive procedures. The effect of cultural factors and the stress of acculturation were examined by comparing data from two cultural groups, Anglo and Hispanic.^ Spielberger State-Trait Anxiety Scales were administered to children and parents prior to an invasive procedure. The Procedure Behavioral Checklist (PBCL) was used for observation of the child's response during the procedure. The Children's Procedural Interview (CPI) which contains items on the PBCL and visual analogues (scales of faces indicating varying degrees of pain and anxiety) was administered following the procedure.^ Reliability coefficients for Anglos were.78 on the PBCL,.79 on the CPI and.85 on the visual analogue scales. For Hispanics, the reliability for the PBCL was.54, while the CPI had a reliability of.72 and the visual analogue scales,.87. Construct validity was demonstrated by high correlations between the PBCL and CPI scores for both ethnic groups (.66 for Anglos and.64 for Hispanics) and by the significant correlation of State anxiety scores with both PBCL and CPI scores. Age was inversely correlated with PBCL and CPI scores for both ethnic groups. Hispanic parents' anxiety scores were higher than Anglo parents, but were not highly correlated with their child's PBCL, CPI or State-Trait anxiety scores. Caregivers' ratings were correlated with the PBCL scores for Anglos but not for Hispanics.^ The findings of this study indicate that pain responses may be reliably assessed using both observational and self-report methods in children, though differences in Anglo and Hispanic cultures exist. Differences in pain symptomatology and assessment in the two cultural groups warrant further study. ^
The spinal biology in humans and animals of pain states generated by persistent small afferent input
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Behavioral models indicate that persistent small afferent input, as generated by tissue injury, results in a hyperalgesia at the site of injury and a tactile allodynia in areas adjacent to the injury site. Hyperalgesia reflects a sensitization of the peripheral terminal and a central facilitation evoked by the persistent small afferent input. The allodynia reflects a central sensitization. The spinal pharmacology of these pain states has been defined in the unanesthetized rat prepared with spinal catheters for injection and dialysis. After tissue injury, excitatory transmitters (e.g., glutamate and substance P) acting though N-methyl-d-aspartate (NMDA) and neurokinin 1 receptors initiate a cascade that evokes release of (i) NO, (ii) cyclooxygenase products, and (iii) activation of several kinases. Spinal dialysis show amino acid and prostanoid release after cutaneous injury. Spinal neurokinin 1, NMDA, and non-NMDA receptors enhance spinal prostaglandin E2 release. Spinal prostaglandins facilitate release of spinal amino acids and peptides. Activation by intrathecal injection of receptors on spinal C fiber terminals (μ,/∂ opiate, α2 adrenergic, neuropeptide Y) prevents release of primary afferent peptides and spinal amino acids and blocks acute and facilitated pain states. Conversely, consistent with their role in facilitated processing, NMDA, cyclooxygenase 2, and NO synthase inhibitors act to diminish only hyperalgesia. Importantly, spinal delivery of several of these agents diminishes human injury pain states. This efficacy emphasizes (i) the role of facilitated states in humans, (ii) shows the importance of spinal systems in human pain processing, and (iii) indicates that these preclinical mechanisms reflect processes that regulate the human pain experience.
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Numerous human and animal studies indirectly implicate neurons in the anterior cingulate cortex (ACC) in the encoding of the affective consequences of nociceptor stimulation. No causal evidence, however, has been put forth linking the ACC specifically to this function. Using a rodent pain assay that combines the hind-paw formalin model with the place-conditioning paradigm, we measured a learned behavior that directly reflects the affective component of pain in the rat (formalin-induced conditioned place avoidance) concomitantly with “acute” formalin-induced nociceptive behaviors (paw lifting, licking, and flinching) that reflect the intensity and localization of the nociceptive stimulus. Destruction of neurons originating from the rostral, but not caudal, ACC reduced formalin-induced conditioned place avoidance without reducing acute pain-related behaviors. These results provide evidence indicating that neurons in the ACC are necessary for the “aversiveness” of nociceptor stimulation.
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The present review summarizes the current state of knowledge about the genetics of pain-related phenomena and illustrates the scope and power of genetic approaches to the study of pain. We focus on work performed in our laboratories in Jastrzebiec, Poland; Portland, OR; and Los Angeles, which we feel demonstrates the continuing usefulness of classical genetic approaches, especially when used in combination with newly available molecular genetic techniques.
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Mode of access: Internet.
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Mode of access: Internet.
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Mode of access: Internet.
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Second ed. of G/M 2, no. 4791.
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Pain self-efficacy and anxiety have each been shown to contribute substantially to pain intensity and pain-related disability. Although adult attachment theory has been related separately to chronic pain, anxiety, and self-efficacy, it has not before been investigated with either pain self-efficacy or anxiety in the context of chronic pain. This study investigated the interrelations between these aspects of the chronic pain experience and their relative contributions towards pain intensity and disability. A clinical sample of 152 chronic pain patients participated in this study, completing self-report measures of attachment, self-efficacy, pain intensity, and disability, prior to attending a multidisciplinary pain clinic. Results revealed that fearful and preoccupied (anxious) attachment categories were associated with low pain self-efficacy, while high scores on the attachment dimension of comfort with closeness were linked with high pain self-efficacy, particularly for males. Insecure attachment (whether defined in terms of categories or dimensions) was related to higher levels of anxiety. Pain self-efficacy proved a stronger predictor of pain intensity than did anxiety and was a stronger predictor of disability than pain intensity or anxiety. In addition, comfort with closeness moderated the associations between pain self-efficacy and disability, pain self-efficacy and pain intensity, and anxiety and disability. Together, these findings support the value of adopting an attachment theoretical approach in the context of chronic pain. Treatment considerations and future research directions are considered. (c) 2006 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
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Highly selective Cav2.2 voltage-gated calcium channel (VGCC) inhibitors have emerged as a new class of therapeutics for the treatment of chronic and neuropathic pain. Cone snail venoms provided the first drug in class with FDA approval granted in 2005 to Prialt (ω-conotoxin MVIIA, Elan) for the treatment of neuropathic pain. Since this pioneering work, major efforts underway to develop alternative small molecule inhibitors of Cav2.2 calcium channel have met with varied success. This review focuses on the properties of the Cav2.2 calcium channel in different pain states, the action of ω-conotoxins GVIA, MVIIA and CVID, describing their structure-activity relationships and potential as leads for the design of improved Cav2.2 calcium channel therapeutics, and finally the development of small molecules for the treatment of chronic pain.
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This thesis investigates changes in the oscillatory dynamics in key areas of the pain matrix during different modalities of pain. Gamma oscillations were seen in the primary somatosensory cortex in response to somatic electrical stimulation at painful and non-painful intensities. The strength of the gamma oscillations was found to relate to the intensity of the stimulus. Gamma oscillations were not seen during distal oesophageal electrical stimulation or the cold pressor test. Gamma oscillations were not seen in all participants during somatic electrical stimulation, however clear evoked responses from SI were seen in everyone. During a train of electrical pulses to the median nerve and the digit, a decrease in the frequency of the gamma oscillations was seen across the duration of the train. During a train of electrical stimuli to the median nerve and the digit, gamma oscillations were seen at ~20-100ms following stimulus onset and at frequencies between 30-100Hz. This gamma response was found to have a strong evoked component. Following a single electrical pulse to the digit, gamma oscillations were seen at 100-250ms and between 60-95Hz and were not temporally coincident with the main components of the evoked response. These results suggest that gamma oscillations may have an important role in encoding different aspects of sensory stimuli within their characteristics such as strength and frequency. These findings help to elucidate how somatic stimuli are processed within the cortex which in turn may be used to understand abnormal cases of somatosensory processing.