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πŸ”₯+ osteoarthritis lower back icd 10 02 Jun 2020 Read about the common causes of joint pain, including injury and arthritis.

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Arthritis Res for 1 last update 2020/06/02 TherArthritis Res Ther. 2007; 9(3): 214.
Published online 2007 Jun 11. doi:Β 10.1186/ar2147
PMCID: PMC2206347
PMID: 17572915

Bruce L Kidd

1William Harvey Research Institute, Barts and The London, Queen Mary School of Medicine and Dentistry, Charterhouse Square, London EC1M 6BQ, UK

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Richard M Langford

1William Harvey Research Institute, Barts and The London, Queen Mary School of Medicine and Dentistry, Charterhouse Square, London EC1M 6BQ, UK

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osteoarthritis lower back icd 10how to osteoarthritis lower back icd 10 for Theresa Wodehouse

osteoarthritis lower back icd 10how to osteoarthritis lower back icd 10 for 1William for 1 last update 2020/06/02 Harvey Research Institute, Barts and The London, Queen Mary School of Medicine and Dentistry, Charterhouse Square, London EC1M 6BQ, UK1William Harvey Research Institute, Barts and The London, Queen Mary School of Medicine and Dentistry, Charterhouse Square, London EC1M 6BQ, UK

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1William Harvey Research Institute, Barts and The London, Queen Mary School of Medicine and Dentistry, Charterhouse Square, London EC1M 6BQ, UK
Corresponding author.
Bruce L Kidd: [email protected]
Copyright © 2007 BioMed Central Ltd
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Abstract

Current evidence suggests that although persistent arthritic pain is initiated and maintained by articular pathology, it is also heavily influenced by a range of other factors. Strategies for treating arthritic pain are therefore different from those adopted for acute pain. Although published guidelines offer general assistance, the complexity of underlying mechanisms requires that measures designed to relieve pain must take into account individual biological, psychological and societal factors. It follows that a combination of both pharmacological and non-pharmacological approaches offers the best opportunity for therapeutic success, although determining the effectiveness of such complex interventions remains difficult. Pharmacological therapy is often prolonged, and safety and tolerability issues become as important as efficacy over time.

Introduction

Arthritic pain is common and is associated with worse functional outcomes and poorer quality of life when compared with a range of other chronic conditions [1]. A bewildering array of guidelines and other evidence-based resources are available, but the variability of therapeutic responses can lead to frustration and disappointment for both patients and health professionals.

This review categorizes different pain states associated with arthritis and discusses the extent to which an understanding of underlying mechanisms can be used to inform the choice of analgesic therapy. Although a detailed and systematic evaluation of specific interventions is beyond the scope of the review, evidence for the utility of general approaches is presented. The limitations of current approaches to assessment and management are discussed along with the rationale for use of integrated care in patients with persistent pain.

Mechanisms of pain

Pain classification

Traditionally, pain has been regarded as being either nociceptive (arising in response to tissue injury) or neuropathic (arising in response to nerve injury). Although this distinction has had some therapeutic utility, it has served to maintain the Cartesian concept of a fixed immutable pain system that faithfully transmits information from a site of injury to pain centres within the brain. Although this is largely true after acute injury, it is clear from epidemiological studies that in the presence of persistent disease a range of additional factors, often unrelated to the musculoskeletal system, serve to modify activity within pain (nociceptive) pathways.

Implicit in recent classification schemes is the notion that acute and chronic pain states are different and that functional changes within the nociceptive system are important in determining the signs and symptoms experienced by individuals with somatic disease [2]. Currently, four different pain states are recognized (Figure (Figure1).1). The first of these, nociceptive pain, refers to those transient symptoms and signs that arise in response to acute injury and reflects the activation of specialized pain receptors (nociceptors) and corresponding activity in more central pathways. Under these conditions, symptoms broadly reflect the initiating stimulus or injury; treatment at a peripheral level is likely to be successful.

Classification of pain. Nociceptive pain is triggered by tissue injury and activates unmodified nociceptive neurons (light arrow) inducing acute pain. In contrast, normally innocuous stimuli produce pain in neuropathic and neuroplastic conditions in consequence of sensitized nociceptive pathways (dark arrows). Note: Idiopathic pain omitted from figure. (Adapted from [3].)

In contrast, neuroplastic pain (also called inflammatory pain) occurs in response to more persistent tissue injury and is the most common pain state associated with musculoskeletal disease [3]. It arises as a result of mediators released from damaged tissues acting to increase the excitability of the nociceptive pathway and has the effect of making everyday activities such as standing or walking painful. Effective therapy requires that attention be directed to both the originating injury and those additional factors (see below) that influence nociceptive activity.

Third, neuropathic pain occurs in the presence of nerve injury, as might occur in association with carpal tunnel syndrome or after lumbar disc prolapse. Ectopic expression of ion channels, receptors and related phenomena occur in both injured and neighbouring non-injured neurons, with resultant regional pain hypersensitivity and sensory disturbance.

There is currently debate as to the origins of a fourth pain category, idiopathic pain, which covers such medically unexplained disorders as fibromyalgia syndrome, irritable bowel syndrome and tension headache. In all of these disorders, evidence for peripheral pathology is minimal and symptoms are considered to reflect disordered pain processing at more central levels.

Arthritic pain

At a local level, mediators released from synovium, bone or other tissues will induce the sensitization of articular pain receptors. The clinical correlate of sensitization at this peripheral level is that musculoskeletal symptoms will be localized, with a relatively close relationship to mechanical stimuli such as walking or standing (Figure (Figure2).2). Treatment with systemic or topical therapies designed to reduce inflammatory mediators might be expected to have a beneficial effect, which is in accord with clinical experience [4].

Causes and consequences of neural plasticity. Although tissue injury or inflammation can trigger nociceptor sensitization in peripheral neurons (1), other somatic, psychological and environmental influences are likely to determine the magnitude of any subsequent change as a result of modulation of activity at spinal (2) or cortical (3) levels. (Adapted from [3].)

In chronic conditions such as osteoarthritis (OA) or rheumatoid arthritis (RA), neural sensitization will not be confined to the periphery. The finding of increased areas of punctate hyperalgesia in patients with RA after topical application of capsaicin is in accord with increased excitability of spinal neurons in this condition [5]. Clinically, this leads to enhanced pain perception at the site of injury, as well as to the development of pain and tenderness in normal tissues both adjacent to and removed from the primary site.

Spinal nociceptive processing in arthritic patients is under the influence of descending inhibitory controls and inputs from other somatic structures [6]. Both previous pain episodes and genetic factors are also likely to influence activity. The multiplicity of mediators involved provides an opportunity for therapeutic intervention, and many of the commonly used therapeutic strategies including acupuncture, transcutaneous electrical nerve stimulation (TENS) and pharmacological agents such as non-steroidal anti-inflammatory drugs (NSAIDs) and the weaker opioid drugs are likely to be exerting an effect at this level.

Psychological and social factors have been shown to be the most important predictors of both the presence and severity of pain the 1 last update 2020/06/02 in a range of disorders including RA, OA and persistent low back pain. It seems logical to assume, but remains unproven, that these external factors modulate nociceptive processing at a supraspinal or cortical level [7]. The overall effect is to enhance pain perception and to increase pain reporting and behavioural change, including disability.Psychological and social factors have been shown to be the most important predictors of both the presence and severity of pain in a range of disorders including RA, OA and persistent low back pain. It seems logical to assume, but remains unproven, that these external factors modulate nociceptive processing at a supraspinal or cortical level [7]. The overall effect is to enhance pain perception and to increase pain reporting and behavioural change, including disability.

Reliance on peripherally or spinally active therapies alone is unlikely to prove successful in those patients with more general symptoms arising from central sensitization. Prostanoid and opioid receptors are constitutively expressed in cortical tissues, and the relevant therapeutic agents are undoubtedly exerting an effect at this level. Nevertheless, additional measures often using non-pharmaceutical approaches, including education and cognitive behavioural therapy, may be required.

Despite the progress that has been made over the past several decades to define key pain processes, the need remains to translate this knowledge into better assessment techniques and more effective pain therapy. Attempts to devise mechanism-based approaches to therapy have met with mixed success, in part as a result of lack of clinical techniques by which to define specific nociceptive processes. Quantitative sensory tests and cortical imaging can be used to quantify central changes associated with articular pathology but are not suitable for more general clinical use. In practical terms, the duration of symptoms is important: the likelihood of a significant central component increases with time. Referred pain and tenderness away from the site of joint pathology are suggestive of a neuroplastic pain state, whereas radicular pain is inevitably associated with neuropathic syndromes.

General approaches to pain management

Clinical guidelines

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