The journal of pain : official journal of the American Pain Society
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Observational Study
Situational but not dispositional pain catastrophizing correlates with early postoperative pain in pain-free patients before surgery.
Pain catastrophizing may be assessed as a dispositional measure using a previous painful experience as a reference or as a situational measure using an actual ongoing pain as a reference. The latter has shown more robust correlations with pain-related outcomes; the relative influence of dispositional and situational pain catastrophizing remains unknown in relation to populations with no pain before surgery. Forty-two consecutive patients who underwent corrective surgery for funnel chest were asked to complete the Pain Catastrophizing Scale with reference to 1) a previous painful experience (dispositional pain catastrophizing), 2) experimental pain during a 2-minute cold pressor test (situational experimental pain catastrophizing), and 3) clinical pain 3 days after surgery (situational clinical pain catastrophizing) to investigate whether these measures predicted immediate pain intensity and unpleasantness in the early postoperative period. Thirty-four patients were available for analyses. Dispositional pain catastrophizing was unrelated to situational experimental and situational clinical pain catastrophizing and to postoperative pain and unpleasantness (P > .05). In contrast, the 2 situation-specific pain catastrophizing measures were strongly associated (ρ = .59, P = .0002). In analyses adjusted for preoperative anxiety, depression, and cold pressor pain sensitivity, situational experimental and situational clinical pain catastrophizing correlated with postoperative movement-evoked pain (β = 1.36, P = .01 and β = 1.24, P = .02, respectively) and unpleasantness (β = 1.32, P = .01 and β = 1.36, P = .01, respectively). ⋯ Pain catastrophizing should be captured in relation to specific painful events in otherwise healthy patients. Future studies might benefit from assessing situational pain catastrophizing to identify patients at risk for increased postoperative pain to optimize stratified pain treatment.
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Randomized Controlled Trial
High-Definition Transcranial Direct Current Stimulation Enhances Conditioned Pain Modulation in Healthy Volunteers: A Randomised Trial.
Transcranial direct current stimulation (tDCS) is a form of brain stimulation that allows for the selective increase or decrease in the cortical excitability of a targeted region. When applied over the motor cortex it has been shown to induce changes in cortical and subcortical brain regions involved in descending pain inhibition or conditioned pain modulation (CPM). The aim of the current study was to assess whether activation of pain inhibitory pathways via tDCS of the motor cortex facilitates the CPM response. Elevated CPM after active tDCS of the motor cortex was hypothesized. Thirty healthy male volunteers attended 2 experimental sessions separated by 7 days. Both sessions consisted of CPM assessment after 20 minutes of either active or sham (placebo) tDCS over the motor cortex. CPM capacity was assessed via the pain-inhibits-pain protocol; CPM responses were shown to be elevated after active compared with sham tDCS. This report concludes that tDCS of the motor cortex enhances the CPM response in healthy men. This finding supports the potential utility of tDCS interventions in clinical pain treatment. ⋯ The use of noninvasive brain stimulation over the motor cortex was shown to enhance the CPM effect. This finding supports the use of tDCS in the treatment of chronic pain, particularly in sufferers exhibiting maladaptive CPM.
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Central sensitization (CS), nociceptive hyperexcitability known to amplify and maintain clinical pain, has been identified as a leading culprit responsible for maintaining pain in several chronic pain conditions. Recent evidence suggests that it may explain differences in the symptom experience of individuals with sickle cell disease (SCD). Quantitative sensory testing (QST) can be used to examine CS and identify individuals who may have a heightened CS profile. The present study categorized patients with SCD on the basis of QST responses into a high or low CS phenotype and compared these groups according to measures of clinical pain, vaso-occlusive crises, psychosocial factors, and sleep continuity. Eighty-three adult patients with SCD completed QST, questionnaires, and daily sleep and pain diaries over a 3-month period, weekly phone calls for 3 months, and monthly phone calls for 12 months. Patients were divided into CS groups (ie, no/low CS [n = 17] vs high CS [n = 21]), on the basis of thermal and mechanical temporal summation and aftersensations, which were norm-referenced to 47 healthy control subjects. High CS subjects reported more clinical pain, vaso-occlusive crises, catastrophizing, and negative mood, and poorer sleep continuity (Ps < .05) over the 18-month follow-up period. Future analyses should investigate whether psychosocial disturbances and sleep mediate the relationship between CS and pain outcomes. ⋯ In general, SCD patients with greater CS had more clinical pain, more crises, worse sleep, and more psychosocial disturbances compared with the low CS group.
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By 2007, opioid-related mortality in Washington state (WA) was 50% higher than the national average, with Medicaid patients showing nearly 6 times the mortality of commercially-insured patients. In 2007, the WA Interagency Guideline on Opioid Dosing for Chronic Non-cancer Pain was released, which recommended caution in prescribing >120 mg morphine-equivalent dose per day for patients not showing clinically meaningful improvement in pain and function. We report on opioid dosing in the WA Medicaid fee-for-service population for 273,200 adults with a paid claim for an opioid prescription between April 1, 2006 and December 31, 2010. Linear regression was used to test for trends in dosing over that time period, with quarter-year as the independent variable and median daily dose as the dependent variable. Prescription opioid use among WA Medicaid adults peaked in 2009, as evidenced by the unique number of opioid users (105,232), the total number of prescriptions (556,712), and the total person-years of prescription opioid use (29,442). Median opioid dose was unchanged from 2006 to 2010 at 37.5 mg morphine-equivalent dose, but doses at the 75th, 90th, 95th, and 99th percentiles declined significantly (P < .001). These results suggest that opioid treatment guidelines with dosing guidance may be able to reduce high-dose opioid use without affecting the median dose used. ⋯ Some fear that opioid dosing guidelines might restrict access to opioid therapy for patients who could benefit. However, there is evidence that high-dose opioid therapy entails significant risks without demonstrated benefit. These findings indicate that high-dose opioid therapy can be reduced without altering median opioid dose in a Medicaid population.
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Patients with depression often report pain. Evidence regarding altered pain sensitivity in depressed patients remains, however, inconclusive. In a large cross-sectional study we investigated the association between depression and pain sensitivity with regard to 2 different dimensions of pain sensitivity, as well as the effect of somatic cofactors, symptom severity, and subtype of depression. In 735 patients with a current episode of major depression and 456 never-depressed control participants pain thresholds (pressure pain thresholds, PPTs) were measured at the index finger pad and self-rated suprathreshold pain intensity ratings were obtained using the Pain Sensitivity Questionnaire (PSQ)-minor subscore, an instrument that assesses pain intensity in daily life situations. Additionally, lifestyle factors, medical, and psychiatric conditions were assessed. Unadjusted, patients with depression had lower PPTs and higher PSQ-minor scores indicating increased pain sensitivity. After adjusting for potential mediators, such as poor sleep quality and physical inactivity, patients did not differ from control participants regarding PPTs, but still had significantly higher PSQ-minor ratings. Among patients with depression, severity of anxiety symptoms predicted higher PSQ-minor scores. In conclusion, we found a differential effect of depression on the 2 pain sensitivity dimensions: Decreased experimentally obtained pain thresholds were explained by depression-associated somatic factors whereas increased self-rated suprathreshold pain intensity ratings were associated with increased anxiety symptoms. ⋯ Because increased pain intensity perception is hypothesized to be a risk factor for the development of chronic pain, our findings may contribute to understanding the high incidence of chronic pain in depressed patients. They also encourage clinicians to consider the role of anxiety in treatment programs for pain in patients with depression.