Potential impact of abrupt opioid therapy discontinuation in the management of chronic pain: a pilot study on patient perspective.

OBJECTIVES: This survey highlights the perspective of patients with chronic pain when confronted with the possibility of abrupt opioid discontinuation. DESIGN: Anonymous and self-administered survey. SETTING: Pain Clinic in an urban academic hospital setting. PARTICIPANTS: Patients with chronic pain of at least 6 months, and age 18 years or older. MAIN OUTCOME MEASURES: The perceived impact of abrupt opioid discontinuation on mood, daily functioning, and potential for opioid misuse. RESULTS: When patients were asked how they would feel if told their opioids would be discontinued, the responses were neglected (scale mean, 7.1), angry (6.3), helpless (6.7), and upset (7.0) on a scale of 0-10. The majority predicted loss of independence in activities of daily living (scale mean, 7.5), inability to enjoy their lives (7.4), and inability to work (7.8). A group of 19 patients (11.6 percent) reported that they would obtain opioids from friends or family, and 7 (4.4 percent) would obtain them illegally. These patients reported higher scores of neglect, anger, suspicion, helplessness, and upset (p = 0.000-0.019) and were more likely to have previously obtained opioids illegally (p = 0.008-0.023). The most common nonopioid strategies tried by patients were lumbar epidural (71.5 percent), physical therapy (78.9 percent), and exercise (83.5 percent). The strategies considered to be effective as opioid replacement therapy were lumbar epidural (42.3 percent), exercise (43.2 percent), and massage (42.0 percent). CONCLUSIONS: These data suggest that opioid therapy discontinuation is an emotionally distressing experience for most patients, and the transition to nonopioid treatments is a complex process that will require patient participation to achieve optimal care.

False sense of safety by daily QTc interval monitoring during methadone IVPCA titration in a patient with chronic pain.

It has been proposed that some deaths attributed to methadone are related to prolongation of the QTc interval; however, there are no clear recommendations on electrocardiogram (ECG) monitoring in patients undergoing intravenous methadone infusion. This is a report on a patient receiving methadone intravenous patient-controlled analgesia titration for the treatment of chronic pain. Initially, her daily ECGs showed QTc intervals within normal limits; however, she experienced a rapid increase in QTc interval from 317 ms to 784 ms within a 24-hour period after methadone had been discontinued for excessive sedation. QTc interval greater than 500 ms is considered to be high risk for the fatal arrhythmia Torsades de Pointes. Daily ECGs did not detect a gradual increase in the QTc interval that would have alerted the medical staff of the need to decrease or stop the methadone before reaching a prolonged QTc interval associated with cardiotoxicity. In selected cases where aggressive methadone titration is required, more intensive monitoring, such as telemetry or ECG determinations every 12 hours, might help detect changes in QTc interval duration that might otherwise be missed by daily ECG determinations.

Effects of central leptin infusion on the reward-potentiating effect of D-amphetamine.

It was previously reported that chronic food restriction and maintenance of rats at 75-80% of initial body weight enhanced the reward-potentiating effect of D-amphetamine in the lateral hypothalamic self-stimulation (LHSS) paradigm. Moreover, the enhancement reversed in parallel with body weight recovery when ad libitum access to food was reinstated. The present study tested the hypothesis that hypoleptinemia during food restriction is necessary for expression of enhanced drug reward. In Experiment 1, intracerebroventricular (i.c.v.) infusion of leptin (0.5 microg/0.5 microl/hr for 8 days) in food-restricted rats did not alter the rewarding effect of D-amphetamine (0.5 mg/kg, i.p.). Considering that i.c.v. leptin may not diffuse into deep brain regions where direct effects on drug reward sensitivity may be exerted, effects of acute bilateral microinjection of leptin (0.5 microg) in ventral tegmental area and nucleus accumbens were tested in Experiment 2 and found to have no effect. In Experiment 3, chronic i.c.v. leptin infusion in ad libitum fed rats decreased food intake and body weight and enhanced the rewarding effect of D-amphetamine. Sensitivity to D-amphetamine returned to normal as body weight recovered following cessation of leptin infusion. This result suggests that weight loss, whether from hormone-induced appetite suppression or experimenter-imposed food restriction, is sufficient to enhance drug reward sensitivity. Experiment 4 tested whether food restriction in the absence of body weight loss alters drug reward sensitivity. Rats received chronic i.c.v. infusion of the orexigenic melanocortin receptor antagonist, SHU9119 (0.02 microg/0.5 microl/hr for 12 days), and a subset were pair-fed to vehicle-infused controls. Although these subjects ingested approximately 50% of the amount of food ingested by free-feeding SHU9119-infused rats, they displayed no weight loss and no change in sensitivity to D-amphetamine. Together, results of this study support the importance of weight loss, but not leptin, in the enhancement of drug reward sensitivity.