Pain
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Low back pain is a widespread debilitating problem with a lifetime prevalence of 80%, with the underlying pain mechanism unknown in approximately 90% of cases. We used the painDETECT neuropathic pain screening questionnaire to identify likely pain mechanisms in 343 patients with low back pain with or without leg pain in southeastern England referred for physiotherapy. We related the identified possible pain mechanisms nociceptive, unclear, and neuropathic to standardised measures of pain severity (Numeric Rating Scale), disability (Roland Morris Low Back Pain Disability Questionnaire), anxiety and depression (Hospital Anxiety and Depression Scale), and quality of life (Short Form 36 Health Survey Questionnaire Version 2). ⋯ A total of 96% of participants with possible neuropathic pain reported pain radiating to the leg (76% below the knee); however, leg pain was still more common in patients with nociceptive pain, suggesting that leg pain is sensitive to, but not specific to, possible neuropathic pain. No relationship was demonstrated between possible neuropathic pain and evidence for or absence of nerve root compression on magnetic resonance imaging scans. These findings suggest possible neuropathic pain is less common in low back pain patients referred through primary care and clarifies the usefulness of clinical tests for identifying possible neuropathic pain.
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This study examined processes that contribute to the changing painfulness of a repeatedly presented thermal (heat) stimulus. The 3-second pulses were presented to the side of the hand at a rate of 4/min, too slow to engage wind-up. Over the course of 32 trials, pain intensity (measured by verbal report on a 0-100 scale) first declined and then (in most cases) rose again, indicating adaptation and sensitization, respectively. ⋯ Adaptation and sensitization were comparable in participants with fibromyalgia, temporomandibular disorders, and in healthy controls, indicating that these processes occur before the perceptual amplification that characterizes fibromyalgia and temporomandibular disorders. The ability of vibration to reduce pain has previously been shown to involve segmental inhibition; the finding in the present study that vibratory gating of pain is significantly (inversely) related to the rate of sensitization suggests that the latter also reflects segmental processes. Several lines of evidence thus point to the conclusion that adaptation and sensitization occur at early stages of sensory information processing.
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The present study examined existing communal and operant accounts of children's pain behavior by looking at the impact of parental presence and parental attention upon children's pain expression as a function of child pain catastrophizing. Participants were 38 school children and 1 of their parents. Children completed a cold pressor pain task (CPT) twice, first when told that no one was observing (alone condition) and subsequently when told that they were being observed by their parent (parent-present condition). ⋯ Specifically, low-catastrophizing children expressed more pain in the presence of their parent, whereas high-catastrophizing children showed equally pronounced pain expression when alone or in the presence of a parent. Furthermore, children's catastrophizing moderated the impact of parental attention upon facial displays and self-reports of pain; higher levels of parental nonpain talk were associated with increased facial expression and self-reports of pain among high-catastrophizing children; for low-catastrophizing children, facial and self-report of pain was independent of parental attention to pain. The findings are discussed in terms of possible mechanisms that may drive and maintain pain expression in high-catastrophizing children, as well as potential limitations of traditional theories in explaining pediatric pain expression.
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Neuropathic pain is often "spontaneous" or "stimulus-independent." Such pain may result from spontaneous discharge in primary afferent nociceptors in injured peripheral nerves. However, whether axotomized primary afferent nociceptors give rise to pain is unclear. The rostral anterior cingulate cortex (rACC) mediates the negative affective component of inflammatory pain. ⋯ Lesion of the rACC did not block cocaine-induced reward, indicating that rACC blockade did not impair memory encoding or retrieval but did impair spontaneous aversiveness. These data indicate that spontaneous pain arising from injured nerve fibers produces a tonic aversive state that is mediated by the rACC. Identification of the circuits mediating aversiveness of chronic pain should facilitate the development of improved therapies.