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Chronic opioid use is unfortunately perceived among these postoperative patients, specifically within orthopedic surgery. Patients having orthopedic surgeries are at risk for becoming addicted to opioids, and one benefit of peripheral nerves blocks could be to provide an alternative mode of pain control. This study takes a retrospective look at the use of peripheral nerve blocks for pain control following surgery for isolated traumatic ankle injuries. We hypothesize that when peripheral nerve blocks are administered preoperatively to patients with closed ankle fractures, they will have overall better control of postoperative pain compared to patients who did not receive a peripheral nerve block.
Learn More >We previously reported promising results for a 4-month patient-centered voluntary opioid tapering study. Key questions remain about the durability of effects and possible risks after opioid reduction. We provide the longest follow-up data to date for prospective opioid tapering: 2- to 3-year follow-up for pain intensity and daily opioid use in a subset of patients from our original 4-month opioid tapering study.
Learn More >The use of analgesics for the treatment of post-operative pain is common, however, such medications are known to have potential side effects. These undesirable secondary effects can have an important impact on patients and impede their recovery.
Learn More >Cancer pain is often treated with opioids, a therapeutic regimen that can become a challenge in patients with an opioid use disorder (OUD). While use of the buprenorphine-naloxone combination is an effective medication-assisted treatment (MAT) for OUD, its use in pain patients with OUD has been controversial due to concerns that co-administration of buprenorphine can reduce or block analge-sia and precipitate opioid withdrawal in those patients requiring full opioid agonists. Data on its use in cancer pain patients are lack-ing. In this case series, the authors explore the frequency of buprenorphine-naloxone use and its outcomes in patients in a Compre-hensive Care Center (CCC) Pain Registry. OUD was deduced from an International Classification of Diseases (ICD-10) diagnostic code for opioid-related disorders recorded in the electronic medical records. Of 2,320 chronic cancer pain patients, 125 patients had ICD-10 code for opioid-related disorders, and 43 had a diagnosis of opioid abuse of whom 11 received buprenorphine-naloxone combina-tions. Eight patients on 18 (6-24) mg per day of buprenorphine-naloxone remained in therapy for 4 (2-7) years without opioid abuse relapse. This assessment was based on clinician's notes, the Prescription Monitoring Program, random urine drug screening, and the absence of Urgent Care Center visits for opioid withdrawal or overdose. When short-term opioids were administered for acute pain, these patients were able to taper down and stop them quickly without an opioid abuse relapse. Buprenorphine-naloxone was effec-tive as the sole analgesic in selected patients. Given its success at the CCC, buprenorphine-naloxone should be made available and strongly considered as a treatment for patients suffering from OUD during and following cancer treatment and when cancer pain re-duces or resolves.
Learn More >The voltage-gated sodium channel Na1.2 is responsible for the initiation and propagation of action potentials in the central nervous system. We report the cryo-electron microscopy structure of human Na1.2 bound to a peptidic pore blocker, the μ-conotoxin KIIIA, in the presence of an auxiliary subunit β2 to an overall resolution of 3.0 Å. The immunoglobulin (Ig) domain of β2 interacts with the shoulder of the pore domain through a disulfide bond. The 16-residue KIIIA interacts with the extracellular segments in repeats I to III, placing Lys7 at the entrance to the selectivity filter. Many interacting residues are specific to Na1.2, revealing a molecular basis for KIIIA specificity. The structure establishes a framework for rational design of subtype-specific blockers for Na channels.
Learn More >Medication-overuse headache (MOH) is a common chronic headache caused by overuse of headache analgesics. It has similarities with substance dependence disorders. The treatment of choice for MOH is withdrawal of the offending analgesics. Behavioral brief intervention treatment using methods adapted from substance misuse settings is effective. Here we investigate the severity of analgesics dependence in MOH using the Severity of Dependence Scale (SDS), validate the SDS score against formal substance dependence diagnosis based on the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV) and examine whether the SDS predicts successful withdrawal.
Learn More >Features suggestive of neuropathic pain (NP) have been described in RA in addition to nociceptive pain. We aimed to determine the clinical predictors of NP in RA patients and study its association with radiographic structural damage.
Learn More >When investigating the role of facilitatory and inhibitory pain mechanisms such as conditioned pain modulation (CPM) and temporal summation of pain (TSP), it is important to take both into consideration in a single experimental model to provide the most information on subgroups of patients. Therefore, the objective of this study was to identify subgroups in a large population of pediatric patients with chronic pain based on their facilitatory and inhibitory pain mechanisms and compare them with control subjects.
Learn More >Altered pain facilitatory and inhibitory mechanisms have been recognized as an important manifestation in patients with chronic pain, and quantitative sensory testing (QST) can act as a proxy for this process. We have recently developed a simple bedside QST tool kit () for more clinical use. The purpose of this study was to investigate its test-retest reliability and to evaluate its validity compared with the laboratory-based QST protocols in patients with knee osteoarthritis (OA).
Learn More >Oxytocin has been shown to increase trust, decrease anxiety and affect learning as has been observed in conditioning paradigms. Trust, anxiety and learning are important factors that influence placebo effects. In this study we investigated whether oxytocin can increase placebo analgesia, decrease nocebo hyperalgesia, and influence extinction processes of both. Eighty male volunteers were assigned to a 40 IU of oxytocin nasal spray group, or to a placebo control group. Placebo analgesia and nocebo hyperalgesia were induced by a conditioning procedure in combination with verbal suggestions. The results demonstrate that the conditioning procedure successfully elicited significant placebo analgesia and nocebo hyperalgesia responses (p < .001). Furthermore, extinction was observed (p < .001), although placebo and nocebo responses did not return to baseline and remained significant. Oxytocin did not influence placebo analgesia or nocebo hyperalgesia and had no effect on extinction. This study provides support against the placebo-boosting effects of oxytocin and was the first one to demonstrate that it also did not influence nocebo effects or extinction processes, however, these results pertain to only a male sample. As managing placebo and nocebo effects has widespread clinical implications, further research should investigate other neurobiological or behavioral pathways to boost placebo and decrease nocebo effects. Trial registration: The study protocol was preregistered on the website www.trialregister.nl under the number NTR6506. Perspective: The present study demonstrated that placebo analgesia and nocebo hyperalgesia can be successfully induced by conditioning and verbal suggestions. We could not confirm the hypothesis that oxytocin affects either of these phenomena. Other pharmacological agents and behavioral manipulations for increasing placebo and decreasing nocebo effects should be investigated.
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