Chronic pain is the most prevalent disease worldwide, leading to substantial disability and socioeconomic burden. Therefore, it can be regarded as a public health disease and major challenge to scientists, clinicians and affected individuals. Behavioral lifestyle factors, such as, physical (in)activity, stress, poor sleep and an unhealthy diet are increasingly recognized as perpetuating factors for chronic pain. Yet, current management options for patients with chronic pain often do not address lifestyle factors in a personalized multimodal fashion. This state-of-the-art clinical perspective aims to address this gap by discussing how clinicians can simultaneously incorporate various lifestyle factors into a personalized multimodal lifestyle intervention for individuals with chronic pain. To do so the available evidence on (multimodal) lifestyle interventions targeting physical (in)activity, stress, sleep and nutritional factors, specifically, was reviewed and synthetized from a clinical point of view. First, advise is provided on how to design a personalized multimodal lifestyle approach for a specific patient. Subsequently, best-evidence recommendations on how to integrate physical (in)activity, stress, sleep and nutritional factors as treatment targets into a personalized multimodal lifestyle approach are outlined. Evidence supporting such a personalized multimodal lifestyle approach is growing, but further studies are needed.

Chronic pain is a source of substantial physical and psychological suffering, yet a clear understanding of the pathogenesis of chronic pain is lacking. Repeated studies have reported an altered behaviour of the salience network (SN) and default mode network (DMN) in people with chronic pain, and a majority of these studies report an altered behaviour of the dorsal ventromedial prefrontal cortex (vmPFC) within the anterior DMN. In this topical review, we therefore focus specifically on the role of the dorsal vmPFC in chronic pain to provide an updated perspective on the cortical mechanisms of chronic pain. We suggest that increased activity in the dorsal vmPFC may reflect maladaptive overthinking about the meaning of pain for oneself and one’s actions. We also suggest that such overthinking, if negative, may increase the personal “threat” of a given context, as possibly reflected by increased activity in, and functional connectivity to, the anterior insular cortex within the SN.

Age-related decline in voluntary force production represents one of the main contributors to the onset of physical disability in older adults and is argued to stem from adverse musculoskeletal alterations and changes along the descending neuroaxis. The neural contribution of the above is possibly indicated by disproportionate losses in voluntary activation (VA) compared to muscle mass. For young adults, resistance training (RT) induces muscular and neural adaptations over several levels of the central nervous system, contributing to increased physical performance. However, less is known about the relative neuroadaptive contribution of RT in older adults. The aim of this review was to outline the current state of the literature regarding where and to what extent neural adaptations occur along the descending neuroaxis in response to RT in older adults. We performed a literature search in PubMed, Google Scholar and Scopus. A total of 63 articles met the primary inclusion criteria and following quality analysis (PEDro) 23 articles were included. Overall, neuroadaptations in older adults seemingly favor top-down adaptations, where the preceding changes of neural drive from superior levels affect the neural output of lower levels, following RT. Moreover, older adults appear more predisposed to neural rather than morphological adaptations compared to young adults, a potentially important implication for the improved maintenance of neuromuscular function during aging.

Recent scientific advances point towards an important role for oral and gastrointestinal health in people with chronic pain. Poor oral health (e.g., periodontitis, tooth loss) is observed in subgroups of the chronic pain population, including abdominal pain, low back pain, fibromyalgia, and rheumatoid arthritis. In addition to poor oral health, studies have also revealed altered intestinal microbiota compositions in various types of chronic pain, including people with chronic low back pain, knee osteoarthritis, visceral pain, fibromyalgia, tinnitus, and migraine. While overweight/obesity contributes to the likelihood of gut dysbiosis, normal-weight individuals with chronic pain also more often present with poor gut health. Both gastrointestinal and oral health problems (e.g., periodontitis, tooth loss) are increasingly recognized across multiple chronic pain conditions, including abdominal pain, low back pain, fibromyalgia, and rheumatoid arthritis. This perspective paper provides an overview of the requirements for integrating oral and gastrointestinal health in chronic pain management. First and foremost, oral and gastrointestinal health issues need to be recognized as common chronic pain comorbidities that require tailored treatment. Next to recognition of the issue, individuals seeking care for chronic pain need to be screened routinely for these oral and gastrointestinal comorbidities. In terms of management, the following options are suggested: (1) providing oral and gastrointestinal health science education; (2) considering the possible interplay between the gut microbiome and drug treatment (including polypharmacy); (3) expanding the importance of dietary interventions; and (4) considering the potential interplay with other lifestyle factors (e.g., chronic insomnia, overweight/obesity, depression and anxiety). To inform the implementation of these suggestions, longitudinal cohort studies investigating the role of oral and gastrointestinal health in people with chronic pain, as well as studies exploring possible (modifiable) factors that affect the oral and/or gut microbiome, are needed. This includes the bidirectional interplay between the gut microbiome and drugs commonly prescribed to patients with chronic pain. Likewise, adequately powered and controlled clinical trials evaluating the effectiveness of possible treatments for oral and/or gastrointestinal comorbidities in people with chronic pain represent another research priority. Such randomized clinical trials can not only examine the possible causal link between poor oral/gut health and treatment outcomes, but also inform the development of new, innovative ways to improve care for people with chronic pain.

Objectives: To investigate the relationship between offset analgesia magnitude and the responsiveness to conditioned pain modulation (CPM), temporal summation of (second) pain (TSP), and clinical pain severity in people with knee osteoarthritis (KOA). Methods: Electrical stimuli were applied to 88 participants with KOA to measure offset analgesia at the volar forearm of the dominant hand, and CPM and TSP at the most symptomatic knee and ipsilateral volar wrist. Clinical pain severity was assessed using the pain subscale of the Knee injury and Osteoarthritis Outcome Score (KOOS_PAIN). Linear mixed-effects models evaluated pain modulatory effects across all tests, and Spearman partial correlations assessed associations between offset analgesia, CPM, TSP, and KOOS_PAIN while accounting for covariates of interest. Participants unable to validly finish all psychophysical tests were excluded from effect and correlation analyses but were evaluated for predictors of nonvalid completion using bivariate Stochastic Search Variable Selection. Results: Significant pain modulation was observed across all psychophysical tests (P<0.05), and no meaningful predictors of nonvalid test completion were found. Offset analgesia magnitude did not significantly correlate with CPM, TSP, or KOOS_PAIN (P≥0.05), with a maximum partial correlation coefficient of ρ=0.21. Discussion: Offset analgesia was not associated with CPM, TSP, or KOOS_PAIN in people with KOA. Despite the lack of case-control studies comparing offset analgesia between people with KOA and healthy controls, these findings suggest that offset analgesia may provide information about endogenous pain modulation beyond CPM and TSP, though its clinical translation remains uncertain.