Pain Medicine最新文献

Objective: We evaluated whether more severe back pain phenotypes-persistent, frequent, or disabling back pain-are associated with higher mortality rate among older men.

Methods: In this secondary analysis of a prospective cohort, the Osteoporotic Fractures in Men (MrOS) study, we evaluated mortality rates by back pain phenotype among 5215 older community-dwelling men (mean age, 73 years, SD = 5.6) from 6 sites in the United States. The primary back pain measure used baseline and Year 5 back pain questionnaire data to characterize participants as having no back pain, nonpersistent back pain, infrequent persistent back pain, or frequent persistent back pain. Secondary measures of back pain from the Year 5 questionnaire included disabling back pain phenotypes. The main outcomes measured were all-cause and cause-specific death.

Results: After the Year 5 exam, during up to 18 years of follow-up (mean follow-up = 10.3 years), there were 3513 deaths (1218 cardiovascular, 764 cancer, 1531 other). A higher proportion of men with frequent persistent back pain versus no back pain died (78% versus 69%; sociodemographic-adjusted HR = 1.27, 95% CI = 1.11-1.45). No association was evident after further adjustment for health-related factors, such as self-reported general health and comorbid chronic health conditions (fully adjusted HR = 1.00; 95% CI = 0.86-1.15). Results were similar for cardiovascular deaths and other deaths, but we observed no association of back pain with cancer deaths. Secondary back pain measures, including back-related disability, were associated with increased mortality risk that remained statistically significant in fully adjusted models.

Conclusion: Although frequent persistent back pain was not independently associated with risk of death in older men, additional secondary disabling back pain phenotypes were independently associated with increased mortality rate. Future investigations should evaluate whether improvements in disabling back pain affect general health and well-being or risk of death.

Objective: To determine if patients with chronic migraine continue onabotulinumtoxinA (onabotA) long-term.

Methods: We performed a retrospective cohort analysis using aggregated, de-identified patient data from the Stanford Headache Center. We included patients in California who received at least one prescription for onabotA during the years of 2011-2021. The primary outcome was the number of onabotA treatments each patient received. Secondary outcomes included sex, age, race, ethnicity, body mass index (BMI), distance to the treatment facility, and zip code income quartile.

Results: A total of 1551 patients received a mean of 7.60 ± 7.26 treatments and a median of 5 treatments, with 16.2% of patients receiving only one treatment and 10.6% receiving at least 19. Time-to-event survival analysis suggested 26.0% of patients would complete at least 29 treatments if able. Younger age and female sex were associated with statistically significant differences between quartile groups of number of onabotA treatments (P = .007, P = .015). BMI, distance to treatment facility, and zip code income quartile were not statistically significantly different between quartile groups (P > .500 for all). Prescriptions of both triptans and non-onabotA preventive medications showed a statistically significant increase with each higher quartile of number of onabotA treatments (P < .001; P < .001).

Discussion: We show long-term persistence to onabotA is high and that distance to treatment facility and income are not factors in continuation. Our work also demonstrates that as patients continue onabotA over time, there may be an increased need for adjunctive or alternative treatments.

Background: PTSD is associated with greater incidence of chronic pain. Pain catastrophizing often accounts for this association. Less is known about these relationships during the acute phase (1-2 months) following orthopedic traumatic injuries. We sought to understand which orthopedic traumatic injury-related PTSD symptoms were associated with acute pain and physical dysfunction and whether pain catastrophizing accounted for these associations.

Methods: This secondary analysis uses baseline data from a multisite randomized controlled trial of an intervention for individuals with heightened pain catastrophizing or pain anxiety following acute orthopedic injury. We used partial correlations to examine associations between PTSD symptom clusters (re-experiencing, avoidance, negative alterations in cognitions and mood, and hyperarousal) and pain outcomes (pain intensity and physical dysfunction) controlling for pain catastrophizing. We used hierarchical regressions to evaluate unique associations between PTSD clusters and pain outcomes. In exploratory analysis, we examined the indirect effects of PTSD symptoms on pain outcomes through catastrophizing.

Results: Hierarchical linear regressions indicated that hyperarousal was uniquely associated with greater pain intensity with activity (β = 0.39, p < 0.001, ΔR2 =0.06) and physical dysfunction (β = 0.22, p = 0.04 ΔR2 =0.02). PTSD symptoms were still associated with pain with activity even with pain catastrophizing included in the models, and catastrophizing did not have a significant indirect effect on the relationship between PTSD and physical dysfunction (b=0.06, SEBoot=0.04, 95% CIBoot = [-0.003, 0.14]). Pain catastrophizing did largely account for the association between re-experiencing, avoidance, and negative alterations in cognitions and mood symptoms and pain at rest.

Conclusions: Pain catastrophizing interventions may be best suited for limiting the impact of PTSD symptoms on pain at rest, but catastrophizing alone may not fully explain the relationship between PTSD symptoms and physical dysfunction after acute orthopedic injury. To prevent the negative association of PTSD symptoms, especially hyperarousal, on physical outcomes in acute pain populations, interventions may require more than solely targeting pain catastrophizing.

Background: Buprenorphine, a partial opioid agonist, has emerging evidence as an alternative to full agonist opioids for treatment of acute pain. This systematic review aimed to evaluate the safety and efficacy of buprenorphine for acute pain in older adults.

Methods: PubMed Medline, Embase, Cochrane Central Register of Controlled Trials, CINHAL, Web of Science database, and Google Scholar were searched. We included articles that reported buprenorphine as an intervention to treat acute pain among patients 60 years or older. Primary outcome was difference in pain scores for patients treated with buprenorphine compared to other analgesia. Secondary outcomes included adverse events, opioid consumption, and patient satisfaction. Meta-analysis was conducted on difference in pain scores and differences in nausea and vomiting.

Results: Twenty-two studies were included (n = 2610). Buprenorphine was administered as nerve blocks in six studies, transdermal in eight, intravenous or intramuscular in five, sublingual in two studies, and both intravenous and sublingual in one study. 10 out of 20 (50%) studies found improved pain control in buprenorphine groups. Meta-analysis found no significant difference in pain scores between buprenorphine and control analgesia at 24 hours (Cohen's d = -0.29 [95% CI -0.85 to 0.27]) and 7 days (Cohen's d = -0.89 [95% CI -2.66-0.88]). Six studies (54.5%) found reduced opioid consumption in patients receiving buprenorphine. There was no difference in adverse effects in most studies.

Conclusions: This review did not find buprenorphine to be superior to alternative analgesia; however the mixed results provide scientific rationale for future studies testing buprenorphine in older populations.