Pain
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This study projected the indirect costs of back problems through lost productive life years (PLYs) from the individual's perspective (lost disposable income), the governmental perspective (reduced taxation revenue, greater welfare spending), and the societal perspective (lost gross domestic product, GDP) from 2015 to 2030, using Health&WealthMOD2030-Australia's first microsimulation model on the long-term impacts of ill-health. Quantile regression analysis was used to examine differences in median weekly income, welfare payments, and taxes of people unable to work due to back problems with working full-time without back problems as comparator. National costs and lost GDP resulting from missing workers due to back problems were also projected. ⋯ National costs consisted of a loss of AU$2931 million in annual income in 2015, increasing to AU$4660 million in 2030 (60% increase). For government, extra annual welfare payments are projected to increase from AU$1462 million in 2015 to AU$1709 million in 2030 (16.9% increase), and lost annual taxation revenue to increase from AU$671 million in 2015 to $961 million in 2030 (43.2% increase). We projected losses in GDP of AU$10,543 million in 2015, increasing to AU$14,522 million in 2030 due to back problems.
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Migraine attacks are often preceded by premonitory symptoms (PS) that may be triggered pharmacologically. We investigated the incidence of PS after administration of calcitonin gene-related peptide (CGRP) or pituitary adenylate cyclase-activating peptide-38 (PACAP38) in patients with migraine without aura (MO) who reported and did not report migraine-like attacks induced by these pharmacological triggers. In addition, we investigated the association between PS and familial predisposition for migraine. ⋯ Additionally, we found no difference in PS between patients with familial predisposition of migraine (75%) and patients with no family predisposition (56%) (P = 0.101). In conclusion, CGRP did not induce PS, whereas PACAP38 induced PS in 48% of patients. However, CGRP and PACAP38 did not induce more PS in patients who developed an attack compared with those who did not develop an attack.
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Pain is one of the most challenging and stressful conditions to patients with sickle cell disease (SCD) and their clinicians. Patients with SCD start experiencing pain as early as 3 months old and continue having it throughout their lives. Although many aspects of the disease are well understood, little progress has been made in understanding and treating pain in SCD. ⋯ We further targeted CaMKIIα by siRNA knockdown. Both evoked pain and ongoing spontaneous pain were effectively attenuated in BERK mice. These findings elucidated, for the first time, an essential role of CaMKIIα as a cellular mechanism in the development and maintenance of spontaneous and evoked pain in SCD, which can potentially offer new targets for pharmacological intervention of pain in SCD.