Pain
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Randomized Controlled Trial
Pain assessment in advanced dementia.Validity of the German Painad -a prospective double-blind randomised placebo-controlled trial.
Pain in combination with dementia is a common condition that makes pain recognition significantly more difficult. This results in undertreatment of pain in those suffering from dementia. The Pain Assessment in Advanced Dementia (PAINAD) scale currently represents one of the best approaches to pain detection in dementia. ⋯ Equally, none of the other 3 observational tools were able to demonstrate a significant difference between the study groups. However, correlations among the 4 observational tools were mostly moderate to high. A number of possible reasons for this observation, such as difficulties regarding sensitivity to change/responsiveness, consistence of the fundamental construct, influence of the early onset study, and efficacy of the analgesic in advanced dementia are discussed.
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We aimed to investigate the pattern and utilization of neuropathic pain medications in peripheral neuropathy patients. Using a privately insured, health care claims database from 2001 to 2014, we identified a retrospective cohort of incident peripheral neuropathy patients (validated ICD-9 definition) after excluding other chronic pain conditions. Outcome measures included opioid prescriptions, chronic opioid therapy (greater than or equal to 90 days of continuous supply), guideline-recommended medications for painful peripheral neuropathy (serotonin reuptake inhibitors, tricyclic antidepressants, and gabapentinoids), and pain specialists (neurologists, physiatrists, and anesthesiologists). ⋯ Pain specialists were associated with high opioid utilization and high guideline-recommended medication utilization. In conclusion, opioid initiation and transition to chronic opioid therapy are frequent in a peripheral neuropathy population despite few patients receiving more than one guideline-recommended medication. Efforts to decrease opioid utilization and increase guideline-recommended medication use are needed to improve current neuropathic pain treatment.
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Multicenter Study
Obesity increases the risk of chronic pain development following motor vehicle collision.
Obesity has been found to increase the risk of musculoskeletal pain (MSP) in other settings, but to our knowledge, the influence of increased body mass index on pain outcomes after common trauma exposures such as motor vehicle collision (MVC) has not been assessed. In addition, obesity results in biomechanical changes, as well as physiologic changes including reduced hypothalamic pituitary adrenal axis negative feedback inhibition, but mechanisms by which obesity may result in worse post-traumatic outcomes remain poorly understood. ⋯ After adjusting for an array of sociodemographic factors, obesity (particularly morbid obesity) was an independent risk factor for worse MSP after MVC (eg, RR 1.41 [95% CI 1.11, 1.80] for moderate or severe MSP 6 months after MVC among morbidly obese vs normal weight MVC survivors). Interestingly, substantial effect modification was observed between obesity risk and a genetic variant known to reduce hypothalamic pituitary adrenal axis negative feedback inhibition (FKBP5 rs9380526). (eg, 41% vs 16% increased risk of moderate or severe MSP at 6 months among obese individuals with and without the risk allele.) Further studies are needed to elucidate mechanisms underlying chronic pain development in obese trauma survivors and to develop interventions that will reduce chronic pain severity among this common, at-risk group.
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Randomized Controlled Trial
The association between endogenous opioid function and morphine responsiveness: a moderating role for endocannabinoids.
We sought to replicate previous findings that low endogenous opioid (EO) function predicts greater morphine analgesia and extended these findings by examining whether circulating endocannabinoids and related lipids moderate EO-related predictive effects. Individuals with chronic low-back pain (n = 46) provided blood samples for endocannabinoid analyses, then underwent separate identical laboratory sessions under 3 drug conditions: saline placebo, intravenous (i.v.) naloxone (opioid antagonist; 12-mg total), and i.v. morphine (0.09-mg/kg total). During each session, participants rated low-back pain intensity, evoked heat pain intensity, and nonpain subjective effects 4 times in sequence after incremental drug dosing. ⋯ In the absence of significant interactions, lower EO function predicted significantly greater morphine analgesia (as in past work) and euphoria. Results indicate that EO effects on analgesic and subjective responses to opioid medications are greatest when endocannabinoid levels are low. These findings may help guide development of mechanism-based predictors for personalized pain medicine algorithms.
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Painful and disabling musculoskeletal disorders remain prevalent. In rats trained to perform repetitive tasks leading to signs and dysfunction similar to those in humans, we tested whether manual therapy would prevent the development of the pathologies and symptoms. We collected behavioral, electrophysiological, and histological data from control rats, rats that trained for 5 weeks before performing a high-repetition high-force (HRHF) task for 3 weeks untreated, and trained rats that performed the task for 3 weeks while being treated 3x/week using modeled manual therapy (MMT) to the forearm (HRHF + MMT). ⋯ Neurons from HRHF rats had a heightened proportion of ongoing activity and altered conduction velocities compared with control and MMT-treated rats. Median nerve branches in HRHF rats contained increased numbers of CD68 macrophages and degraded myelin basic protein, and showed increased extraneural collagen deposition, compared with the other groups. We conclude that the performance of the task for 3 weeks leads to increased ongoing activity in nociceptors, in parallel with behavioral and histological signs of neuritis and nerve injury, and that these pathophysiologies are largely prevented by MMT.