Pain
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Concepts originating from ancient Eastern texts are now being explored scientifically, leading to new insights into mind/brain function. Meditative practice, often viewed as an emotion regulation strategy, has been associated with pain reduction, low pain sensitivity, chronic pain improvement, and thickness of pain-related cortices. Zen meditation is unlike previously studied emotion regulation techniques; more akin to 'no appraisal' than 'reappraisal'. ⋯ The activation pattern is remarkably consistent with the mindset described in Zen and the notion of mindfulness. Our findings contrast and challenge current concepts of pain and emotion regulation and cognitive control; commonly thought to manifest through increased activation of frontal executive areas. We suggest it is possible to self-regulate in a more 'passive' manner, by reducing higher-order evaluative processes, as demonstrated here by the disengagement of anterior brain systems in meditators.
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Chronic pain is more common in the elderly and impairs functioning and quality of life. Though obesity, defined by body mass index (BMI), has been associated with pain prevalence among older adults, the mechanism of this association remains unclear. We examined components of the metabolic syndrome, insulin resistance, a marker of inflammation, and the presence of painful comorbidities as possible mediators of this association. ⋯ Of the clinical components of metabolic syndrome, central obesity was significantly associated with pain (OR 2.03, 95% CI 1.36-3.01). After adjustment for insulin resistance, inflammation, and pain-related comorbidities, central obesity predicted higher TPI scores (OR 1.55, 95% CI 1.04-2.33) and nearly doubled the risk of chronic pain (OR 1.70, 95% CI 1.05-2.75). Central obesity is the metabolic syndrome component showing the strongest independent association with pain, and the relationship is not explained by markers of insulin resistance or inflammation, nor by the presence of osteoarthritis or neuropathy.
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Multiple pathological mechanisms at multiple sensory sites may underlie the pain that follows nerve injury. This provides a basis for recommending more than one agent, either sequentially or in combination, for its treatment. According to this premise, new drugs that combine different mechanisms of analgesic action in a single molecule are gaining momentum, such as tapentadol which stimulates mu-opioid receptors (MOR) and acts as a noradrenaline reuptake inhibitor (NRI) in the CNS. ⋯ In particular, we performed a series of in vivo electrophysiological tests in spinal nerve ligated and sham-operated rats to show that systemic tapentadol (1 and 5mg/kg) dose-dependently reduced evoked responses of spinal dorsal horn neurones to a range of peripheral stimuli, including brush, punctate mechanical and thermal stimuli. Furthermore, we showed that spinal application of the selective α(2)-adrenoceptor antagonist atipamezole, or alternatively the mu-opioid receptor antagonist naloxone, produced near complete reversal of tapentadol's inhibitory effects, which suggests not only that the spinal cord is the key site of tapentadol's actions, but also that no pharmacology other than MOR-NRI is involved in its analgesia. Moreover, according to the extent that the antagonists reversed tapentadol's inhibitions in sham and SNL rats, we suggest that there may be a shift from predominant opioid inhibitory mechanisms in control animals, to predominant noradrenergic inhibition in neuropathic animals.
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The prefrontal cortex may be a promising target for transcranial magnetic stimulation (TMS) in the management of pain. It is not clear how prefrontal TMS affects pain perception, but previous findings suggest that ventral lateral and medial prefrontal circuits may comprise an important part of a circuit of perceived controllability regarding pain, stress, and learned helplessness. Although the left dorsolateral prefrontal cortex is a common TMS target for treating clinical depression as well as modulating pain, little is known about whether TMS over this area may affect perceived controllability. ⋯ Although it is not clear whether this cortical area is directly involved with modulating perceived controllability or whether downstream effects are responsible for the present findings, it appears possible that left dorsolateral prefrontal TMS may produce analgesic effects by acting through a cortical perceived-control circuit regulating limbic and brainstem areas of the pain circuit. Despite evidence that prefrontal TMS can have analgesic effects, fast left prefrontal TMS appears to acutely suppress analgesia associated with perceived-control. This effect may be limited to the emotional dimension of pain experience.
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This study evaluated prospectively the incidence of neuropathic pain after thoracotomy, described its clinical characteristics, and delineated landmarks for its diagnosis in daily practice. We evaluated clinically painful symptoms and sensory deficits in 54 patients after lateral/posterolateral thoracotomy for broncho-pulmonary carcinoma with standardized surgical and analgesic procedures. At 2months, 49 patients suffered from non malignant thoracic pain, and at 6months 38 patients (loss to follow-up for 7) reported persisting pain. ⋯ Morphine consumption during the early post-operative period (mean 111.3±30.8mg/day) and pain intensity (VAS: mean 5.71±2.1) were significantly higher in patients suffering from neuropathic pain than in other patients with pain (mean 80±21.4mg/day; VAS: mean 3.9±2.4). The clinical picture in most patients with neuropathic pain included electric shocks and severe multimodal hypoesthesia in the sensory area of 5th/6th intercostal nerves. Thus, our results indicate a minimal incidence of chronic post-thoracotomy pain at 70% and that of neuropathic pain at 29%, this latter being clinically suggested by a combination of certain symptoms and reinforced by the DN4 questionnaire when sensory deficit at scar is present.