Pain
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The communication of pain has received a great deal of attention in the pain literature; however, one form of pain communication--emotional disclosure of pain-related distress (e.g., sadness, worry, anger about pain)--has not been studied extensively. This study examined the extent to which this form of pain communication occurred during an observed conversation with one's spouse and also investigated the correlates and consequences of disclosure. Individuals with chronic pain (ICP) and their spouses (N=95 couples) completed several questionnaires regarding pain, psychological distress, and relationship distress as well as video recorded interactions about the impact of pain on their lives. ⋯ Furthermore, spouses were more likely to engage in invalidation after attempting more neutral or validating responses, suggesting an erosion of support when ICPs engaged in high rates of disclosure. Correlates of spousal invalidation included both spouses' helplessness catastrophizing, ICPs' affective distress about pain, and spouses' anxiety, suggesting that both partners' distress are implicated in maladaptive disclosure-response patterns. Findings are discussed in light of pain communication and empathy models of pain.
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A connection between pain and depression has long been recognized in the clinical setting; however, its mechanism remains unclear. This study showed that mechanical hyperalgesia induced by unilateral temporomandibular joint (TMJ) inflammation was exacerbated in Wistar-Kyoto (WKY) rats with genetically predisposed depressive behavior. Reciprocally, TMJ inflammation enhanced depressive behavior such that a lower nociceptive threshold correlated with a higher score of depressive behavior in the same WKY rats. ⋯ Intracisternal administration of 6-chloromelatonin (250 μg, twice daily for 7 days) concurrently attenuated mechanical hyperalgesia and depressive behavior in WKY rats as well as downregulated the NR1 expression in the ipsilateral Sp5C. In patch-clamp recordings, melatonin dose-dependently decreased NMDA-induced currents in spinal cord dorsal horn substantia gelatinosa neurons. These results demonstrate a reciprocal relationship between TMJ inflammation-induced mechanical hyperalgesia and depressive behavior and suggest that the central melatoninergic system, through modulation of the NMDA receptor expression and activity, may play a role in the mechanisms of the comorbidity between pain and depression.