Pain
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Review Meta Analysis
Evidence for working memory deficits in chronic pain: a systematic review and meta-analysis.
People with chronic pain commonly report impaired cognitive function. However, to date, there has been no systematic evaluation of the body of literature concerning cognitive impairment and pain. Nor have modern meta-analytical methods been used to verify and clarify the extent to which cognition may be impaired. ⋯ High heterogeneity within the field was found with the inclusion of 24 papers using 21 different working memory tests encompassing 9 different working memory constructs and 9 different chronic pain populations. Notwithstanding high heterogeneity, pooled results from behavioural outcomes reflected a consistent, significant moderate effect in favour of better performance by healthy controls and, with the exception of one study, pooled results from physiological outcomes reflected no evidence for an effect. Future research would benefit from the use of clearly defined constructs of working memory, as well as standardised methods of testing.
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A link between fibromyalgia syndrome (FMS) and posttraumatic stress disorder (PTSD) has been suggested because both conditions share some similar symptoms. The temporal relationships between traumatic experiences and the onset of PTSD and FMS symptoms have not been studied until now. All consecutive FMS patients in 8 study centres of different specialties were assessed from February 1 to July 31, 2012. ⋯ In 4.0% of patients' most burdensome traumatic experience, PTSD and FMS symptoms occurred in the same year. FMS and PTSD are linked in several ways: PTSD is a potential risk factor of FMS and vice versa. FMS and PTSD are comorbid conditions because they are associated with common antecedent traumatic experiences.
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Research shows that placebo analgesia can be induced through social observational learning. Our aim was to replicate and extend this result by studying the effect of the sex of both the model and the subject on the magnitude of placebo analgesia induced by social observational learning. Four experimental (1 through 4) and 2 control (5 and 6) groups were observed: groups 1, 3, and 5 were female; groups 2, 4, and 6 were male. ⋯ Regardless of the sex of the subject, nocebo hyperalgesia was greater after the male model was observed. The results show that social observational learning is a mechanism that produces placebo effects. They also indicate that the sex of the model plays an important role in this process.
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Migraine is a highly prevalent, disabling and complex episodic brain disorder whose pathogenesis is poorly understood, due in part to the lack of valid animal models. Here we report behavioral evidence of hallmark migraine features, photophobia and unilateral head pain, in transgenic knock-in mice bearing human familial hemiplegic migraine, type 1 (FHM-1) gain-of-function missense mutations (R192Q or S218L) in the Cacna1a gene encoding the CaV2.1 calcium channel α1 subunit. Photophobia was demonstrated using a modified elevated plus maze in which the safe closed arms were brightly illuminated; mutant mice avoided the light despite showing no differences in the standard (anxiety) version of the test. ⋯ These behaviors were: (1) more frequent in mutant versus wildtype mice; (2) lateralized in mutant but not in wildtype mice; (3) more frequent in females versus males; and (4) dose-dependently normalized by systemic administration of 2 different acute analgesics, rizatriptan and morphine. Furthermore, some of these behaviors were found to be more frequent and severe in 218L compared to 192Q mutants, consistent with the clinical presentation in humans. We suggest that Cacna1a transgenic mice can experience migraine-related head pain and can thus serve as unique tools to study the pathogenesis of migraine and test novel antimigraine agents.
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Recent functional brain connectivity studies have contributed to our understanding of the neurocircuitry supporting pain perception. However, evoked-pain connectivity studies have employed cutaneous and/or brief stimuli, which induce sensations that differ appreciably from the clinical pain experience. Sustained myofascial pain evoked by pressure cuff affords an excellent opportunity to evaluate functional connectivity change to more clinically relevant sustained deep-tissue pain. ⋯ Moreover, greater connectivity during pain between contralateral S1/M1 and posterior insula, thalamus, putamen, and amygdala was associated with lower cuff pressures needed to reach the targeted pain sensation. These results demonstrate that sustained pain disrupts resting S1/M1 connectivity by shifting it to a network known to process stimulus salience. Furthermore, increased connectivity between S1/M1 and both sensory and affective processing areas may be an important contribution to interindividual differences in pain sensitivity.