Pain
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Patients with temporomandibular disorder (TMD) perform poorly in neuropsychological tests of cognitive function. These deficits might be related to dysfunction in brain networks that support pain and cognition, due to the impact of chronic pain and its related emotional processes on cognitive ability. We therefore tested whether patients with TMD perform poorly in cognitive and emotion tasks and whether they had abnormal task-evoked brain activity. ⋯ These findings suggest that the slow behavioral responses in idiopathic TMD may be due to attenuated, slower, and/or unsynchronized recruitment of attention/cognition processing areas. These abnormalities may be due to the salience of chronic pain, which inherently requires attention. Sluggish performance in cognitive and emotional interference tasks in patients with nontraumatic temporomandibular disorder is associated with pronounced and unsynchronized task-evoked fMRI brain responses.
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Proteinase-activated receptor-4 (PAR(4)) is a G-protein-coupled receptor activated by serine proteinases released during tissue repair and inflammation. We have previously shown that PAR(4) activation sensitises articular primary afferents leading to joint pain. This study examined whether mast cells contribute to this PAR(4)-induced sensitisation and consequent heightened pain behaviour. ⋯ These effects were blocked by pretreatment with cromolyn. These data reveal that PAR(4) is expressed on synovial mast cells and the activation of PAR(4) has a pronociceptive effect that is dependent on mast cell activation. Proteinase-activated receptor-4 is expressed on synovial mast cells, and the activation of Proteinase-activated receptor-4 has a pronociceptive effect that is dependent on mast cell activation.
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Attention is acknowledged as an important factor in the modulation of pain. A recent model proposed that an effective control of pain by attention should not only involve the disengagement of selective attention away from nociceptive stimuli, but should also guarantee that attention is maintained on the processing of pain-unrelated information without being recaptured by the nociceptive stimuli. This model predicts that executive functions are involved in the control of selective attention by preserving goal priorities throughout the achievement of cognitive activities. ⋯ Results showed that, while novel nociceptive stimuli induced greater distraction than regular tactile stimuli in the control condition, the distractive effect was suppressed in the working memory condition. This suggests that actively rehearsing the feature of pain-unrelated and task-relevant targets successfully prevents attention from being captured by novel nociceptive distracters, independently of general task demands. Working memory can help to inhibit the involuntary capture of attention by pain by preserving cognitive goal priorities.