Mechanistic pain profiling as a tool to predict the efficacy of 3-week nonsteroidal anti-inflammatory drugs plus paracetamol in patients with painful knee osteoarthritis

Petersen, Kristian Kjær; Olesen, Anne Estrup; Simonsen, Ole; Arendt-Nielsen, Lars

doi:10.1097/j.pain.0000000000001427

Cited by 61 publications

(90 citation statements)

References 59 publications

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“…The potential benefits of such an approach include the identification of key prognostic factors that predict treatment response and, ultimately, the development of more targeted treatments that are personalized to the individual and their dominant pain mechanism(s). For example, individuals with OA who have more pronounced central sensitization, as evidenced by increased temporal summation [259,260,261,262,263,264] and, in some cases, widespread pain sensitivity [265] and reduced conditioned pain modulation [261,266] may experience less pain relief and are at higher risk of persistent pain after peripherally targeted treatments, such as NSAIDs or total joint replacement surgery.…”

Section: Promising Directions For Researchmentioning

confidence: 99%

Best Evidence Rehabilitation for Chronic Pain Part 5: Osteoarthritis

Rice

McNair

Huysmans

et al. 2019

JCM

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Osteoarthritis (OA) is a leading cause of chronic pain and disability in older adults, which most commonly affects the joints of the knee, hip, and hand. To date, there are no established disease modifying interventions that can halt or reverse OA progression. Therefore, treatment is focused on alleviating pain and maintaining or improving physical and psychological function. Rehabilitation is widely recommended as first-line treatment for OA as, in many cases, it is safer and more effective than the best-established pharmacological interventions. In this article, we describe the presentation of OA pain and give an overview of its peripheral and central mechanisms. We then provide a state-of-the-art review of rehabilitation for OA pain—including self-management programs, exercise, weight loss, cognitive behavioral therapy, adjunct therapies, and the use of aids and devices. Next, we explore several promising directions for clinical practice, including novel education strategies to target unhelpful illness and treatment beliefs, methods to enhance the efficacy of exercise interventions, and innovative, brain-directed treatments. Finally, we discuss potential future research in areas, such as treatment adherence and personalized rehabilitation for OA pain.

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Section: Promising Directions For Researchmentioning

confidence: 99%

Best Evidence Rehabilitation for Chronic Pain Part 5: Osteoarthritis

Rice

McNair

Huysmans

et al. 2019

JCM

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“…It is important to differentiate between patients with purely nociceptive pain and those with neuropathic or nociplastic pain, because the usual pain treatments (analgesics, anti-inflammatory drugs) are less effective for neuropathic or nociplastic pain, 9 while specific treatments such as tricyclic antidepressants can be effective. NP component is also an independent prognostic factor for knee prosthetic replacement failure.…”

Section: Introductionmentioning

confidence: 99%

Part of pain labelled neuropathic in rheumatic disease might be rather nociplastic

et al. 2020

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Pain in rheumatic diseases is primarily due to mechanical or inflammatory mechanism, but neuropathic pain (NP) component is also occurring in many conditions and is probably underdiagnosed. The purpose of this article is to provide an overview of prevalence, pathophysiological and currently available treatment of NP in rheumatic diseases. When associated with clinical evaluation assessing neurological clinical signs and neuroanatomical distribution, Douleur Neuropathique 4 Questions, painDETECT, Leeds assessment of neuropathic symptoms and signs and Neuropathic Pain Questionnaire can detect NP component. Inflammatory or connective diseases, osteoarthritis, back pain or persistent pain after surgery are aetiologies that all may have a neuropathic component. Unlike nociceptive pain, NP does not respond to usual analgesics such as paracetamol and non-steroidal anti-inflammatory drugs. Entrapment neuropathy, peripheral neuropathy or small-fibre neuropathy are different aetiologies that can lead to NP. A part of the pain labelled neuropathic is rather nociplastic, secondary to a central sensitisation mechanism. Identifying the right component of pain (nociceptive vs neuropathic or nociplastic) could help to better manage pain in rheumatic diseases with pharmacological and non-pharmacological treatments.

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“…Mechanistic pain profiling assesses the underlying pain mechanisms in the peripheral and central nervous system and includes pain thresholds, temporal summation of pain (TSP), and conditioned pain modulation (CPM) [16]. TSP and CPM are the human surrogate models for wind-up and descending pain inhibitory control, respectively [17,18].…”

Section: Introductionmentioning

confidence: 99%

“…Facilitated TSP is reflected by an intensified gradual response to pain stimuli. TSP is facilitated in multiple chronic pain conditions [22] and emerging evidences suggests that facilitated TSP might be a more reliable predictor for poor response to standard pain therapy [16,26–28]. TSP is facilitated in many chronic pain conditions [29–31].…”

Section: Introductionmentioning

confidence: 99%

Total sleep deprivation increases pain sensitivity, impairs conditioned pain modulation and facilitates temporal summation of pain in healthy participants

et al. 2019

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Chronic pain patients often suffer from insomnia or impaired sleep which has been associated with increased pain sensitivity, but a limited amount of studies have investigated the effects of total sleep deprivation on central pain mechanisms. Therefore, the aim of this study was to determine the effects of total sleep deprivation on temporal summation, conditioned pain modulation, thermal and pressure pain sensitivity in healthy participants. Twenty-four healthy participants took part in this two-session trial. The measurements were conducted after a night of habitual sleep (baseline) and following 24 hours of total sleep deprivation. Detection thresholds for cold and warmth and pain thresholds for cold and heat were assessed. Cuff induced pressure pain detection and tolerance thresholds, temporal summation and conditioned pain modulation were assessed with user-independent, computer-controlled cuff algometry. Conditioned pain modulation was significantly impaired, temporal summation was significantly facilitated and pain sensitivity to pressure and cold pain were significantly increased at follow-up compared with baseline. In conclusion, this study found that one night of total sleep deprivation impaired descending pain pathways, facilitated spinal excitability and sensitized peripheral pathways to cold and pressure pain. Future studies are encouraged to investigate if sleep therapy might normalize pain sensitivity in sleep-deprived chronic pain patients.

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Mechanistic pain profiling as a tool to predict the efficacy of 3-week nonsteroidal anti-inflammatory drugs plus paracetamol in patients with painful knee osteoarthritis

Abstract: , L. (2019). Mechanistic pain profiling as a tool to predict the efficacy of 3-week nonsteroidal anti-inflammatory drugs plus paracetamol in patients with painful knee osteoarthritis. Pain, 160(2), 486-492.

Cited by 61 publications

References 59 publications

Best Evidence Rehabilitation for Chronic Pain Part 5: Osteoarthritis

Best Evidence Rehabilitation for Chronic Pain Part 5: Osteoarthritis

Part of pain labelled neuropathic in rheumatic disease might be rather nociplastic

Total sleep deprivation increases pain sensitivity, impairs conditioned pain modulation and facilitates temporal summation of pain in healthy participants

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