Pain
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Persistent postsurgical pain is a prevalent but underacknowledged condition. The aim of this study was to assess the prevalence, sensory qualities, and postoperative determinants of persistent pain at 3 to 4years after total knee replacement (TKR) and total hip replacement (THR). Patients completed a questionnaire with included the Western Ontario and McMaster Universities Index of Osteoarthritis (WOMAC) Pain Scale, PainDetect Questionnaire, Short-Form McGill Pain Questionnaire, and questions about general health and socioeconomic status. ⋯ In conclusion, this study found that persistent postsurgical pain is common after joint replacement, although much of the pain is mild, infrequent, or an improvement on preoperative pain. The association between the number of pain problems elsewhere and the severity of persistent postsurgical pain suggests that patients with persistent postsurgical pain may have an underlying vulnerability to pain. A small percentage of patients have severe persistent pain after joint replacement, and this is associated with depression and the number of pain problems elsewhere.
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Review Meta Analysis
Relationship between physical activity and disability in low back pain: a systematic review and meta-analysis.
It is often assumed that patients with pain-related disability due to low back pain (LBP) will have reduced physical activity levels, but recent studies have provided results that challenge this assumption. The aim of our systematic review was to examine the relationship between physical activity and disability in LBP. The literature search included 6 electronic databases and the reference list of relevant systematic reviews and studies to May 2010. ⋯ Persons with chronic LBP with high levels of disability are also likely to have low levels of physical activity. Persons with acute or subacute back pain appear to vary in the levels of physical activity independent of disability. Persons with chronic back pain with high levels of disability will likely have low levels of physical activity.
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Randomized Controlled Trial Clinical Trial
Effect of ketamine on endogenous pain modulation in healthy volunteers.
Inhibitory and facilitatory descending pathways, originating at higher central nervous system sites, modulate activity of dorsal horn nociceptive neurons, and thereby influence pain perception. Dysfunction of inhibitory pain pathways or a shift in the balance between pain facilitation and pain inhibition has been associated with the development of chronic pain. The N-methyl-d-aspartate receptor antagonist ketamine has a prolonged analgesic effect in chronic pain patients. ⋯ These findings suggest that the balance between pain inhibition and pain facilitation was shifted by ketamine towards pain facilitation. The absence of an effect of ketamine on OA indicates differences in the mechanisms and neurotransmitter influences between OA and DNIC. Diffuse noxious inhibitory control responses following a 1-hour low-dose ketamine treatment displayed facilitation of pain in response to experimental noxious thermal stimulation.
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Nociceptor inputs can trigger a prolonged but reversible increase in the excitability and synaptic efficacy of neurons in central nociceptive pathways, the phenomenon of central sensitization. Central sensitization manifests as pain hypersensitivity, particularly dynamic tactile allodynia, secondary punctate or pressure hyperalgesia, aftersensations, and enhanced temporal summation. It can be readily and rapidly elicited in human volunteers by diverse experimental noxious conditioning stimuli to skin, muscles or viscera, and in addition to producing pain hypersensitivity, results in secondary changes in brain activity that can be detected by electrophysiological or imaging techniques. ⋯ Diagnostic criteria to establish the presence of central sensitization in patients will greatly assist the phenotyping of patients for choosing treatments that produce analgesia by normalizing hyperexcitable central neural activity. We have certainly come a long way since the first discovery of activity-dependent synaptic plasticity in the spinal cord and the revelation that it occurs and produces pain hypersensitivity in patients. Nevertheless, discovering the genetic and environmental contributors to and objective biomarkers of central sensitization will be highly beneficial, as will additional treatment options to prevent or reduce this prevalent and promiscuous form of pain plasticity.