European journal of pain : EJP
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Functional magnetic resonance imaging (fMRI) studies are increasingly employed in different conscious states. Autogenic training (AT) is a common clinically used relaxation method. The purpose of this study was to investigate the cerebral modulation of pain activity patterns due to AT and to correlate the effects to the degree of experience with AT and strength of stimuli. ⋯ This study revealed an effect on cerebral pain processing while performing AT. This might represent the cerebral correlate of different painful stimulus processing by subjects who are trained in performing relaxation techniques. However, due to the absence of a control group, further studies are needed to confirm this theory.
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Growing pains (GP) is a prevalent familial childhood disorder of unknown aetiology. Familial occurrence of GP, and individual and familial association of GP with restless legs syndrome (RLS) has been reported. ⋯ This first twin family study of GP provides evidence for a genetic aetiology and for a genetic relationship to RLS.
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Temporomandibular joint (TMJ) receives rich sympathetic innervations that may contribute to TMJ pain through the local release of sympathomimetic amines. The aim of this study was to determine whether blockade of β-adrenoceptors in the TMJ of male and female rats reduces formalin-induced TMJ nociceptive behaviour. ⋯ We conclude that blockade of β-adrenoceptors in the temporomandibular joint suppresses formalin-induced TMJ nociceptive behaviour in both males and females but females are more responsive. These findings suggest that the use of β-blockers in the treatment of TMJ pain might be of benefit, especially in females.
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Neuropathic pain is caused by neural damage or dysfunction and neuropathic pain-related symptoms are resistant to conventional analgesics. Neuroinflammation due to the cytokine-chemokine network may play a pivotal role in neuropathic pain. We demonstrate that macrophage inflammatory protein-1β (MIP-1β) participates in neuropathic pain. ⋯ These results suggest that MIP-1β is a novel key mediator, and the peripheral MIP-1β-CCR5 axis contributes to neuropathic pain. Therefore, investigation of this cascade might be a validated approach for the elucidation of neuropathic pain mechanisms.