The journal of pain : official journal of the American Pain Society
-
Persistent postsurgical pain (PPSP) is a major clinical problem with significant individual, social, and healthcare costs. The aim of this study was to examine the role of demographic, clinical, and psychological risk factors in the development of PPSP after hysterectomy due to benign disorders. In a prospective study, a consecutive sample of 186 women was assessed 24 hours before surgery (T1), 48 hours after surgery (T2), and 4 months after surgery (T3). Regression analyses were performed to identify predictors of PPSP. Four months after hysterectomy, 93 (50%) participants reported experiencing pain (numerical rating scale >0). Age, pain due to other causes, and type of hysterectomy emerged as significant predictive factors. Baseline presurgical psychological predictors identified were anxiety, emotional illness representation of the condition leading to surgery, and pain catastrophizing. Among the identified psychological predictors, emotional illness representation emerged as the strongest. Acute postsurgical pain frequency and postsurgical anxiety also revealed a predictive role in PPSP development. These results increase the knowledge on PPSP predictors and point healthcare professionals toward specific intervention targets such as anxiety (presurgical and postsurgical), pain catastrophizing, emotional illness representations, and acute pain control after surgery. ⋯ This study found that presurgical anxiety, emotional illness representations, and pain catastrophizing are risk factors for PPSP 4 months after hysterectomy, over and above age and clinical variables. These findings improve knowledge on PPSP and highlight potential intervention targets for healthcare professionals.
-
Although many cancer patients who have pain are smokers, the extent of their symptom burden and risk for opioid misuse are not well understood. In this study we analyzed records of patients being treated for cancer pain, 94 of whom were smokers and 392 of whom were nonsmokers, to determine smoking status group differences. Smokers had significantly higher pain intensity, fatigue, depression, and anxiety than nonsmokers (independent samples t-tests P < .002). Smokers were at higher risk for opioid misuse based on the short form of the Screener and Opioid Assessment for Patients with Pain (SOAPP). Specifically, smokers had more frequent problems with mood swings, taking medications other than how they are prescribed, a history of illegal drug use, and a history of legal problems (chi-square tests P ≤ .002). Changes in pain and opioid use were examined in a subset of patients (146 nonsmokers and 46 smokers) who were receiving opioid therapy on at least 2 of the 3 data time points (consult, follow-up 1 month after consult, follow-up 6 to 9 months after consult). Results based on multilevel linear modeling showed that over a period of approximately 6 months, smokers continued to report significantly higher pain than nonsmokers. Both smokers and nonsmokers reported a significant decline in pain across the 6-month period; the rate of decline did not differ across smokers and nonsmokers. No significant difference over time was found in opioid use between smokers and nonsmokers. These findings will guide subsequent studies and inform clinical practice, particularly the relevancy of smoking cessation. ⋯ This article describes pain, symptom burden, and risk for opioid misuse among cancer patients with pain across smoking status. Smoking appears to be a potential mechanism for having an increased pain and symptom burden and risk for opioid misuse. This improved understanding of cancer pain will inform clinical practice.
-
Factors associated with high-dose opioid therapy for noncancer pain are poorly understood. We documented the prevalence of high-dose opioid use as well as associated demographic, clinical, and health service utilization correlates among low back pain patients. Patients prescribed higher doses of opioids (≥100 mg/day morphine equivalent at last dispensing; n = 453) and receiving opioids for 90+ consecutive days were compared to 2 groups: lower-dose opioid group (1-99 mg/day; n = 4,815) or no-opioid group (n = 10,184). Higher-dose opioid use occurred in 2.9% of patients who received any opioids and in 8.6% of patients who received opioids long-term. The median dose in the higher-dose group was 180.0 mg/day. Compared to the no-opioid group, higher-dose users reported poorer health. Compared to either comparison group, patients in the higher-dose group had higher rates of mental health and substance use disorders, concurrent sedative-hypnotic use (60.5%; n = 274), and health service utilization. After adjusting for select covariates, male gender (odds ratio [OR] = 1.68, 95% confidence interval [CI] = 1.37-2.06), higher comorbidity, Medicare coverage (OR = 1.65, 95% CI = 1.22-2.23), any mental health or substance use diagnosis (OR = 1.58, 95% CI = 1.28-1.95), co-prescriptions of sedative-hypnotics (OR = 1.75, 95% CI = 1.42-2.16), and more emergency department and specialty pain clinic visits were associated with higher likelihood of high-dose prescriptions. ⋯ Higher-dose opioid therapy is being prescribed to 8.6% of back pain patients who receive long-term opioids. These patients had higher mental health and medical comorbidities and co-prescriptions of sedative-hypnotics, raising potential safety concerns.
-
Sigma-1 (σ(1)) receptors play a role in different types of pain and in central sensitization mechanisms; however, it is unknown whether they are involved in chemotherapy-induced neuropathic pain. We compared the ability of paclitaxel to induce cold (acetone test) and mechanical (electronic Von Frey test) allodynia in wild-type (WT) and σ(1) receptor knockout (σ(1)-KO) mice. We also tested the effect on paclitaxel-induced painful neuropathy of BD-1063 (16-64 mg/kg, subcutaneously) and S1RA (32-128 mg/kg, subcutaneously), 2 selective σ(1) receptor antagonists that bind to the σ(1) receptor with high affinity and competitively. The responses to cold and mechanical stimuli were similar in WT and σ(1)-KO mice not treated with paclitaxel; however, treatment with paclitaxel (2 mg/kg, intraperitoneally, once per day during 5 consecutive days) produced cold and mechanical allodynia and an increase in spinal cord diphosphorylated extracellular signal-regulated kinase (pERK) in WT but not in σ(1)-KO mice. The administration of BD-1063 or S1RA 30 minutes before each paclitaxel dose prevented the development of cold and mechanical allodynia in WT mice. Moreover, the acute administration of both σ(1) receptor antagonists dose dependently reversed both types of paclitaxel-induced allodynia after they had fully developed. These results suggest that σ(1) receptors play a key role in paclitaxel-induced painful neuropathy. ⋯ Antagonists of the σ(1) receptor may have therapeutic value for the treatment and/or prevention of paclitaxel-induced neuropathic pain. This possibility is especially interesting in the context of chemotherapy-induced neuropathy, where the onset of nerve damage is predictable and preventive treatment could be administered.
-
Our aim was to assess the relationship of the Val158Met polymorphism to pain, anxiety, depression, functional ability, and pressure pain sensitivity in women with fibromyalgia (FMS). One hundred (n = 100) women with FMS diagnosed according to the American College of Rheumatology criteria participated. A numerical pain rate scale (0-10) was used to assess the intensity of pain; the Hospital Anxiety and Depression Scale was calculated to determine anxiety and depression; and functional ability was determined with the Fibromyalgia Impact Questionnaire. Further, pressure pain thresholds (PPTs) were bilaterally assessed over C5-C6 zygapophyseal joints, second metacarpal, and tibialis anterior muscles. Finally, after amplifying Val158Met polymorphisms by polymerase chain reaction, catechol-O-methyltransferase (COMT) genotype was divided into Val/Val, Val/Met, or Met/Met genotypes. Women with FMS with the Met/Met genotype exhibited higher disability (F = 11.836; P < .001), anxiety (F = 13.385; P < .001), and depression (F = 6.931; P = .002) than those with Val/Val and Val/Met genotypes. No differences for the intensity of widespread pain (F = .154; P = .857) and PPT levels over C5-C6 joints (F = 1.014; P = .336), second metacarpal (F = .216; P = .806), and tibialis anterior muscle (F = 1.179; P = .311) were found. Our results suggest that the Val158Met COMT polymorphism modulated some psychological variables but not pressure pain sensitivity in FMS, because women carrying the Met/Met genotype show higher disability, depression, and anxiety but similar PPTs than those with Val/Met or Val/Val genotypes. This study is important because it strives to understand potential genetic factors that predispose some women with FMS to exhibit a more severe phenotypic expression of the disease. Future studies are needed to elucidate potential relevance of the differences. ⋯ This study suggests that the Val158Met COMT polymorphism modulated some psychological variables but not pressure pain sensitivity in FMS because women with FMS carrying the Met/Met genotype exhibit higher disability, depression, and anxiety than but similar PPTs to those with Val/Met and Val/Val genotypes. This study provides further evidence of potential genetic factors that predispose women with FMS to exhibit the disease more severely.