Pain
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Pain is known to interrupt attention. This interruption is highly sensitive to the extent of involvement of both attentional control and the level of threat associated with the sensation. However, few studies have examined these factors together. ⋯ However, independent of pain, threat did moderate performance on the divided attention task. These findings support the robustness of the effect of pain on performance on higher-order attention tasks. Future research is needed to examine what factors alter the cognitive interruption caused by pain.
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Injury or disease affecting the spinal cord is often accompanied by abnormal, chronic pain. Recent estimates suggest that approximately 60% of patients with multiple sclerosis are affected by significant changes in pain sensitivity or experience ongoing neuropathic pain of unknown etiology. Chronic pain is also a significant concern after direct spinal cord trauma. ⋯ A number of similar changes at the behavioural and cellular level occur in this model that mimic the responses seen in animal models of multiple sclerosis or spinal cord injury (SCI). However, these changes are short lived and resolve over the course of a 2-week observation period. Our findings suggest that the chronicity of pain after injury or disease in the nervous system is dependent on the integrity of the BBB/BSCB.
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Hydrogen sulfide (H(2)S), an endogenous gas molecule synthesized by cystathionine-β-synthetase (CBS), is involved in inflammation and nociceptive signaling. However, the molecular and epigenetic mechanisms of CBS-H(2)S signaling in peripheral nociceptive processing remain unknown. We demonstrated that peripheral inflammation induced by intraplantar injection of complete Freund adjuvant significantly up-regulated expression of CBS at both protein and mRNA levels in rat dorsal root ganglia (DRG). ⋯ Peripheral inflammation did not alter expression of DNA methyltransferase 3a and 3b, the 2 major enzymes for DNA methylation, but led to a significant up-regulation of methyl-binding domain protein 4 and growth arrest and DNA damage inducible protein 45α, the enzymes involved in active DNA demethylation. Our findings suggest that epigenetic regulation of CBS expression may contribute to inflammatory hyperalgesia. H(2)S seems to increase TTX-resistant sodium channel current, which may be mediated by protein kinase A pathway, thus identifying a potential therapeutic target for the treatment of chronic pain.
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The objectives of this study were to examine whether (1) daily pain-related changes in physical functioning differed between happily partnered, unhappily partnered, and unpartnered female chronic pain patients, and (2) affect and pain cognitions mediated the partner status effect on pain-related changes in physical functioning. Two hundred fifty-one women with chronic pain due to osteoarthritis and/or fibromyalgia completed 30 daily electronic diaries assessing pain, affect, pain-related cognitions, and physical functioning. Patients living with a romantic partner also completed a modified version of the Locke-Wallace Marital Adjustment Scale to assess relationship satisfaction. ⋯ The impact of relationship status on pain-related changes in physical functioning was partly mediated by the pain cognitions catastrophizing and coping difficulty. These results indicate that happily partnered pain patients show less pain-related physical disability and more adaptive affective and cognitive responses to daily pain changes than do unhappily partnered and unpartnered patients. Living in a happy union may bolster the capacity of patients to sustain a sense of pain coping efficacy during pain episodes, which in turn, minimizes pain-related physical activity limitations.
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Randomized Controlled Trial
Optimism lowers pain: evidence of the causal status and underlying mechanisms.
Previous studies have demonstrated a relation between dispositional optimism and lower pain sensitivity, but the causal status of this link remains unclear. This study sought to test the causal status by experimentally inducing a temporary optimistic state by means of writing about and visualizing a future best possible self. In addition, we explored pain expectations and (situational) pain catastrophizing as possible underlying mechanisms of the link between optimism and pain. ⋯ Situational pain catastrophizing, however, did seem to mediate the relation between optimism and pain. This study is novel in that it confirms the causal status of optimism towards pain. Additionally, the results reveal that positive interventions might provide a useful alternative in reducing pain catastrophizing as an extremely relevant target in pain treatment.