Pain
-
Randomized Controlled Trial
The hidden effects of blinded, placebo-controlled randomized trials: an experimental investigation.
The knowledge of having only a 50% chance of receiving an active drug can result in reduced efficacy in blinded randomized clinical trials (RCTs) compared to clinical practice (reduced external validity). Moreover, minor onset sensations associated with the drug (but not with an inert placebo) can further challenge the attribution of group differences to drug-specific efficacy (internal validity). We used a randomized experimental study with inert placebos (inert substance) vs active placebos (inducing minor sensations), and different instructions about group allocation (probability of receiving drug: 0%, 50%, 100%). ⋯ Moreover, minor drug onset sensations can challenge internal validity. Effect sizes for these mechanisms are medium, and can substantially compete with specific drug effects. For clinical trials, new study designs are needed that better control for these effects.
-
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.
-
Slow-release strong opioids (SRSO) are indicated in patients with severe chronic pain. Side effects, lack of efficacy and risk of dependency limit their use in clinical practice. The aim of this study was to explore prescription patterns of SRSO in Swedish real-world data on patients with a diagnosis related to chronic pain (DRCP). ⋯ In conclusion, fewer patients remain on SRSO in the long-term in clinical practice than reported in previous clinical trials. Oxycodone is the most common first SRSO prescription and one-third of patients get a prescription indicating psychiatric comorbidity. Our interpretation of these findings are that there is need for better treatment options for these patients, and that more effort is needed to improve treatment guidelines and to ascertain that these guidelines are followed.
-
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.