Pain
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To assess whether pseudoradicular low-back pain may be associated with subclinical sensory deficits in the distal extremity, we applied the quantitative sensory testing protocol of the German Research Network on Neuropathic Pain (DFNS) in 15 patients with pseudoradicular pain distribution. Sixteen age- and gender-matched healthy control subjects as well as 12 patients with radicular pain syndromes (L4-S1) were studied with the same protocol. Radicular pain was diagnosed using clinical criteria (pain radiation beyond the knee, motor-, sensory-, or reflex deficits, positive Laségue's test). ⋯ In contrast to some central pain syndromes this sensory loss involved predominantly large fiber functions. The subclinical sensory loss in pseudoradicular cases suggests that these patients may also have a neuropathic component of their chronic pain. The spatial incongruence of pain and sensory loss in pseudoradicular pain, however, may also indicate that the two are not causally related.
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Increased blood pressure and sweet taste are often associated with decreased pain sensitivity. Animal research suggests that endogenous opioids are involved in both these relationships. Fifty-eight healthy young adults (36 male, 22 female) participated in two sessions receiving a placebo tablet or 50mg of naltrexone on counterbalanced days. ⋯ However, the GLM of tolerance also produced a significant drug by DBP interaction suggesting that blood pressure-related analgesia is at least partially opioid-mediated. Also participants with higher DBP showed dampened mood reactivity to the experiment, which was partially reversible by naltrexone. These results are consistent with findings suggesting that endogenous opioid activity may contribute to generally reduced pain sensitivity, and perhaps mood reactivity, in those with higher BP.
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Psychological and social factors have been shown, separately, to predict outcome in individuals with chronic low back pain. Few previous studies, however, have integrated both psychological and social factors, using prospective study of clinic populations of low back pain patients, to identify which are the most important targets for treatment. One hundred and eight patients with chronic low back pain, newly referred to an orthopaedic outpatient clinic, completed assessments of demographic characteristics, details of back pain, measures of anxiety and depression (Hospital Anxiety and Depression Scale, HADS), fearful beliefs about pain (Fear Avoidance Beliefs Questionnaire), social stresses (Life Events and Difficulties Schedule) and physical aspects of health-related quality of life [SF-36 Physical Component summary Score scale (PCS)]. ⋯ Number of healthcare contacts over the 6 months ranged from 1 to 29, and was independently predicted by perceived cause of pain [Incident Rate Ratio (IRR)=1.46, p=0.03], Fear Avoidance Beliefs about work (IRR=1.02, p=0.009) and back pain related social difficulties (IRR=1.16, p=0.03). To conclude, anxiety, depression, fear avoidance beliefs relating to work and back pain related stresses predict impairment in subsequent physical health-related quality of life and number of healthcare contacts. Interventions targeting these psychosocial variables in clinic patients may lead to improved quality of life and healthcare costs.
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Glial activation is a typical response of the central nervous system to nerve injury. In the current investigation, we characterized the temporal and spatial pattern of glial proliferation, one of the most conspicuous features of glial activation, in relation to nerve injury-induced neuropathic pain. Using bromodeoxyuridine (BrdU) as a mitotic marker, we analyzed cell proliferation in the spinal cord, identified the phenotype of dividing cells, traced their fate, and correlated these phenomena with behavioural assays of the neuropathic pain syndrome. ⋯ These newly generated cells continued to divide over time with the response peaking at day 14 post-injury. Microglia were always the predominant phenotype which made up over 60% of activated microglia derived from this newly generated cell population. There was a close temporal correlation between microglial proliferation in the spinal cord dorsal horn and the abnormal pain responses, suggesting a contribution of the new microglia to the genesis of the neuropathic pain symptoms.
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Thermal burns induce pain at the site of injury, mechanical hyperalgesia, associated with a complex time-dependent inflammatory response. To determine the contribution of inflammatory mediators to burn injury-induced mechanical hyperalgesia, we measured dynamic changes in the levels of three potent hyperalgesic cytokines, interleukin IL-1 beta, IL-6, and tumor necrosis factor-alpha (TNFalpha), in skin of the rat, following a partial-thickness burn injury. ⋯ Spinal intrathecal injection of oligodeoxynucleotides antisense for gp130, a receptor subunit shared by members of the IL-6 family of cytokines, attenuated both burn- and intradermal IL-6-induced hyperalgesia, as did intradermal injection of anti-IL-6 function blocking antibodies. These studies suggest that IL-6 is an important mediator of burn-injury pain.