Långvarig förskrivning av opioidläkemedel är en komplex klinisk situation där indikationen långvarig icke-malign smärta är mindre önskvärd men ändå förekommer.

Problematisk användning av opioider eller utvecklande av opioidbrukssyndrom förekommer i populationen. 

Nedtrappning med planerat stöd och uppföljning är en medicinsk intervention som bör övervägas.

Potentiella fördelar inkluderar ökad patientsäkerhet, reversering av biverkningar och en förbättrad helhetssituation.

Risker inkluderar akuta och långvariga abstinenssymtom samt försämrad psykisk hälsa.

There is a lack of evidence for long-term opioid treatment of chronic non-cancer pain. According to European guidelines, opioids should not be used for primary chronic pains.  It is important to continuously assess the benefits and harms of each opioid treatment and, if indicated, discontinue it as early as possible to prevent an adverse trajectory. Long-term opioid treatment is a clinically complex situation in which the issue of tapering (deprescribing) should be considered. Tapering is a medical intervention that entails planned support and close follow-up. Potential benefits include increased safety, reversal of side effects, and an improved overall situation. Risks include acute and protracted withdrawal symptoms (including worsening pain) and impaired mental health. Problematic use of opioids (including opioid use disorder) occurs in this population, but prescribers should avoid a stereotypical and stigmatizing attitude.

Objective: Essential tremor (ET) is the most common movement disorder, with a prevalence of approximately 5 % in individuals over 65 years old. The pathophysiology behind ET is still largely unknown but emerging evidence indicates that ET can be a neurodegenerative disorder. Our aim in this pilot study was to evaluate alterations in inflammatory cytokines in ET patients undergoing deep brain stimulation (DBS) compared to healthy controls. Methods: Ten patients with severe ET were included in this study. Cerebrospinal fluid was analyzed in healthy controls and in ET patients before and after deep brain stimulation. The samples were analyzed with a U-PLEX assay, based on an electrochemiluminescent detection method. Results: Several cytokines were downregulated or upregulated in patients with ET compared to the healthy control group. Interestingly, macrophage migration inhibitory factor (MIF) was one of the significantly upregulated inflammatory mediators. There was no difference in the analyzed cytokines before and after DBS. Conclusion: Inflammatory proteins are altered in patients with ET compared to healthy individuals. The finding of an upregulation of MIF, an interesting cytokine that plays a role in other neurodegenerative disorders, suggests evidence for a neurodegenerative pathophysiology in ET. Inflammatory biomarkers might be promising to be future biomarkers and targets of therapeutics against several neurodegenerative disorders.

Introduction: Opioid treatment may affect endocrine measures in humans either through centrally or peripherally mediated mechanisms. There is a general lack of longitudinal studies examining endocrine measures in opioid-treated patients. Objectives: To longitudinally follow the levels of select endocrine measures in men and women with head and neck cancer for 1 year, who after having completed radiotherapy began tapering opioids. Methods: This was a prospective, longitudinal, observational study. Testosterone and estradiol were measured in men and women, respectively. Follicle-stimulating hormone (FSH), luteinizing hormone (LH), dehydroepiandrosterone sulfate (DHEAS), and prolactin were measured in both sexes. Women were grouped based on if premenopausal or postmenopausal. Samples were collected when opioid tapering started and at 1, 3, 6, and 12 months after tapering start. Daily opioid doses at the same time points were registered. Results: Twenty-five men and 12 women were followed for 12 months. In men, testosterone levels increased significantly during the first month after opioid tapering started (P < 0.001). Levels of testosterone, FSH, DHEAS, and prolactin changed significantly in men during the study period. A moderate correlation between opioid dose reduction and testosterone level increase in men aged <= 60 years was found (r(s) = -0.577, 95% CI -0.854 to -0.044, P = 0.039). In postmenopausal women (n = 10), levels of FSH and LH changed significantly during the study period. Conclusion: Previously known effects of opioids on endocrine measures in humans seem to be reversible as select endocrine measures changed significantly in men and postmenopausal women after opioid tapering was initiated.

Objectives: Physical inactivity is a global health concern and a significant problem among chronic pain patients. They often experience pain flare-ups when they try to increase their physical activity level. Most research on the relationship between pain sensitivity and physical activity has been on healthy participants. Data on chronic pain patients are lacking. Using cuff pressure algometry, this study investigated tonic cuff pressure pain sensitivity and its associations to self-reported physical activity and other patient-reported outcomes in chronic pain patients.Methods: Chronic pain patients (n=78) were compared to healthy controls (n=98). Multivariate data analysis was used to investigate the associations between tonic cuff pressure pain sensitivity, physical activity, and other patient-reported outcome measures.Results: The three most important variables for group discrimination were perceived health status (EQVAS: p(corr)=-0.85, i.e., lower in patients), depression (HADS-D: p(corr)=0.81, i.e., higher in patients), and the tonic cuff pressure pain sensitivity variable maximum pain intensity (VAS-peak-arm: p(corr)=0.75, i.e., higher in patients). In patients, the most important predictors for high VAS-peak-arm were female sex (p(corr)=-0.75), higher number of painful regions (p(corr)=0.72), higher pain intensity (p(corr)=0.55), followed by lower level of self-reported physical activity (p(corr)=-0.39). VAS-peak-arm in patients correlated negatively with self-reported physical activity (rho=-0.28, p=0.018).Conclusions: Physical activity may be the most important patient-changeable variable correlating to pain sensitivity. This study highlights the importance of more research to further understand how increased physical activity may decrease pain sensitivity in chronic pain patients.

Det är ofta fruktbart att betrakta långvarig smärta mer som en grupp sjukdomar än som ett symtom. Om man till exempel ser på smärtsam diabetesneuropati som en sjukdom, infinner sig frågan: vad är dess patofysiologi? Vad är det för mekanismer som gör att vissa neuropatipatienter får ont och andra inte? I två biomarkörstudier inom ramen för ett internationellt samarbete publicerade i smärttidskriften Pain [1, 2] har vi analyserat blodprov från patienter med smärtsam respektive icke-smärtsam diabetesneuropati.

Läkarrollen är inte huggen i sten. Den har förändrats över tid, och den kommer att fortsätta förändras. Men mitt i denna föränderlighet finns ändå en kontinuitet som gör att vi fortfarande kan känna igen oss i den hippokratiska läkareden. Emmanuel Bäckryd resonerar kring läkarrollen i går, i dag och i morgon.

Depression and anxiety are highly prevalent in chronic pain. Clinicians often interpret depression/anxiety as consequences of chronic pain, but some psychiatrists contend that the consequence hypothesis is overrated and that psychiatric symptoms in pain patients should be understood as part of the psychiatric disease. In this overview, the potential bidirectional nature of the relationship between chronic pain and depression/anxiety is discussed on a conceptual level. Two additional possible ways of understanding the relationship are presented: psychological vulnerability can be a risk factor for the chronification of pain, and an underlying mild chronic pain can be exacerbated when the patient encounters a new psychosocial stressor. In clinical practice, it is important not to get stuck in a fruitless chase for a causal understanding. However, it is of great value for clinicians to reflect upon the complexity and dynamic nature of the relationship between pain and depression/anxiety.

Enligt den nyantagna elfte versionen av International Classification of Diseases (ICD-11), som ännu inte översatts till svenska, definieras långvarig smärta som ihållande eller återkommande smärta med mer än 3 månaders varaktighet [1]. Denna tidsgräns är numera väl etablerad inom smärtforskarkollektivet, även om 6 månader ibland också anges [2]. Någon absolut tidsgräns föreligger förstås inte, utan poängen är att termen »långvarig smärta« begripliggör att smärta inte enbart är ett kortvarigt fenomen som beror på en akut vävnadsskada utan att smärta också kan bestå under lång tid – även när en initial skada har läkt ut som den ska. Ett annat sätt att uttrycka det är att smärta inte enbart är ett symtom, utan tämligen ofta i stället kan vara en sjukdom i sig. Enkelt uttryckt: även smärtsinnet kan bli sjukt [3]. Detta sätt att tänka går på tvärs mot allmänhetens intuitiva sätt att tänka om smärta, och det är ett stort problem att tanken på smärta som liktydig med vävnadsskada fortfarande verkar dominera även bland sjukvårdspersonal. Smärta är ett mångfasetterat fenomen, och det är viktigt att sjukvårdspersonal inte har ett stereotypt förhållningssätt utan förmår utföra en smärtanalys som tar hänsyn till smärtans många skepnader [4-11]. Dikotomin akut/långvarig må vara simpel, men för klinisk praxis har den ändå påtagliga praktiska implikationer, till exempel gällande indikationen för att förskriva opioider [4]. Ungefär var femte vuxen är drabbad av påtaglig långvarig smärta [2, 12, 13].