Pain
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Lidocaine is clinically widely used as a local anesthetic inhibiting propagation of action potentials in peripheral nerve fibers. Correspondingly, the functional magnetic resonance imaging (fMRI) response in mouse brain to peripheral noxious input is largely suppressed by local lidocaine administered at doses used in a clinical setting. We observed, however, that local administration of lidocaine at doses 100 × lower than that used clinically led to a significantly increased sensitivity of mice to noxious forepaw stimulation as revealed by fMRI. ⋯ Additional experiments with nociceptor-specific CB(1) receptor knockout mice indicated an involvement of the CB(1) receptors located on the nociceptors. We conclude that low concentrations of lidocaine leads to a sensitization of the nociceptors through a CB(1) receptor-dependent process. This lidocaine-induced sensitization might contribute to postoperative hyperalgesia.
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Methods for classifying chronic pain in population studies are highly variable, and prevalence estimates ranges from 11% to 64%. Limited knowledge about the persistence of pain and the validity of recall questions defining chronic pain make findings difficult to interpret and compare. The primary aim of the current study was to characterize the persistence of pain in the general population and to validate recall measures against longitudinal reporting of pain. ⋯ When defined as moderate pain or more on at least 3 of 4 consecutive measurements, the prevalence was 26%. Compared with the longitudinal classification, a cross-sectional measure of moderate pain or more during the last week on the SF-8 scale presented a sensitivity of 82% and a specificity of 84%, and a sensitivity of 80% and a specificity of 90% when combined with a 6-month recall question. Thus pain reporting in the general population is stable and cross-sectional measures may give valid prevalence estimates of chronic pain.
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Randomized Controlled Trial
Cognitive Behavioral Therapy increases pain-evoked activation of the prefrontal cortex in patients with fibromyalgia.
Interventions based on Cognitive Behavioral Therapy (CBT) are widely used to treat chronic pain, but the brain mechanisms responsible for these treatment effects are poorly understood. The aim of this study was to validate the relevance of the cortical control theory in response to an exposure-based form of CBT, Acceptance and Commitment Therapy, in patients with chronic pain. Forty-three female patients diagnosed with fibromyalgia syndrome were enrolled in a randomized, 12-week, waiting-list controlled clinical trial (CBT n=25; controls n=18). ⋯ An analysis of fMRI scans revealed that CBT led to increased activations in the ventrolateral prefrontal/lateral orbitofrontal cortex; regions associated with executive cognitive control. We suggest that CBT changes the brain's processing of pain through an altered cerebral loop between pain signals, emotions, and cognitions; leading to increased access to executive regions for reappraisal of pain. Our data thereby support our hypothesis about the activation of a cortical control mechanism in response to CBT treatment in chronic pain.