We try to separate whether an abnormal pain processing is more of a problem than the physical impairment. if that seems likely, then we direct treatment towards the processing. This is primarily education for the patient, but also some sensory reducation/desensitisation, paced loading (see 'pain neuromatrix' - melzack-moseley) and sometimes tens/acupuncture (which seem to have some benefit in about 1 in 5or 6 patients only for us). We also liase with their medic regarding analgesia review.

is that what you were asking or have I missed the point and patronised everyone?

That is exactly what I was getting at! How do you evaluate if one or the other is the problem (or both!)?

I deal with Generalised OA as both a clinician and an academic.

Centralisation of pain is important in the treatment plan and is something we see in clinic, particularly if there is concurrent anxiety/depression, high levels of impairment and long term disability. I also I think understanding sleep quality and the number of painful OA joints can provide important insights into the management of such complex patients.

Where centralisation of pain is suspected patients are managed differently using medications such as amitriptyline and psychological input can be helpful.

OA trial guidelines recommend inclusion of the HADS and full body joint pain manikins. I believe this may be an important tool for clinicians to plan further interventions.

Further research is needed to understand the role of chronic pain in OA. The work undertaken by Anne-maree Keenan on the psychological and functional impact of OA suggests psychological component of OA is compounded by poor clinical management.

For cervical and lumbar back pain, in the absence of documented nerve root compression, by far the most common source of pain is pain arising in muscle, a clinical diagnosis based on the palpation of myofascial trigger points. So-called “central pain” remains controversial and can be separated into three categories: 1) thalamic syndromes such as post-stroke, 2) psychosomatic, typically an obsession with missed diagnoses and 3) tolerance to narcotic pain medications. True osteoarthritis is typically associated with only mild pain and is over-diagnosed in the presence of degenerative spine changes found in almost all patients over the age of 30. Thus the diagnostic evaluation should always focus on identifying peripheral sources of pain, especially muscle, and recognizing the role of secondary gain in patients seeking narcotics and/or disability.

Many investigators agree that pain in OA has a central component. The underlying mechanisms are similar to those elucidated in fibromyalgia and chronic back pain. They consist essentially in a pain amplification syndrome often accompanyng the usual mechanic and inflammatory pain sources of OA.

Recent research data from our group has shown that about 30% of those with knee OA show signs of centrally augmented pain independent of psychological / social factors (yet to be published). This includes both generalised neuropathic-type symptoms and widespread hyperalgesia to quantitative sensory tests (especially cold). I think the challenge is to find a valid clinical test to reliably identify this group and also of course to decide on the optimal treatment. We are working on it!

If central sensitization is present, I do not think that you could assess if peripheral sensitization is also present because the central system will mask the peripheral input. However, it is believed that in non-neuropathic pain of inflammatory nature that peripheral sensitization happens as a result of the "inflammatory soup" and that continued peripheral C-fiber input will eventually lead to central sensitization. I can't recall if long-term animal studies have shown that peripheral sensitivity dies down and central sensitivity remains. There is evidence that neo-innervation is present in the periphery in chronic pain states (tendinopathies, not sure about OA).

As for assessing it clinically, pressure pain threshold tests of affected and unaffected areas could be performed, but you would have to have a database of what is "normal" for people of the same age group without pathology for comparison (and include psych influences and gender as covariates).

By the way, strong sensory-level TENS and noxious TENS may affect both peripheral and central pain mechanisms.

My experience is from the viewpoint of a clinician in musculoskeletal medicine working in a multidisciplinary practice for over 25 years. The assessment is very much a clinical one. As a simplification the more localised and consistent the pain the more lilkely there is a persistent local peripheral nociceptive focus. The clinical examination is much underestimated by most clinicians working in pain medicine. Of course the longer that pain is present the greater the central sensitisation over time. Sleep disturbance contributes to this and should be always adressed as early as possible. In my experience it is unwise to ignore peripheral nociceptive drivers of pain, even years down the track, but a multidisciplinary approach is needed. The pain diagram is one of the best screening tools to quickly identify what is likely to be largely nociceptive, but it isnt foolproof. Hope that helps.

The therapeutic approach is based on the patient's response over time to a number of different interventions, as above-mentioned in other comments. You start off first with simple agents such as acetaminophen, then perhaps NSAIDS, if the patient's co-morbidities allow it, and later perhaps additional agents such as gabapentin, tramadol, or other analgesics that would work better to control "central" pain, etc. The pain in OA is mutifactorial.

NGF plays a strong role in peripheral and central mechanism of OA PAIN

Dear all,

Thank you very much for the very interesting discussion about the basic question 'Do you consider pain from peripheral tissue sources vs. alterations in pain processing in the CNS (central nervous system) when you treat patients with osteoarthritis?'

We have developed clinical guidelines for the recognotion and assessment of peripheral (PS) and central sensitization (CS) in patients with musculoskeletal pain Nijs et al, 2010).

Currently, an international consensus definition or clinical criteria for CS is essentially lacking. A body of scientific literature reporting original data of signs and symptoms in relation to established measures of CS in patients with musculoskeletal pain is available (see article) and is used to develop these clinical guidelines.

Listening to the story of the patient will provide a number of clues that potentially point towards the presence of CS. CS is characterized by an increased responsiveness to a variety of stimuli including mehanical pressure, cold and heat temperature, electrical stimuli. All stimuli are used in physiotherapy. An overview of history takling and clinical examination of patients with suspected CS are emphasized in the clinical practical guidelines.

Based on evidence literature combined with our clinical experience, we have developed a clinical reasoning process ro recognize patients with CS.

CS is not only a theoretical frame work but also a practical reality. Recognition of CS is one of the most important clinical skills of the physiotherapist. The outcome of the diagnostic process (CS present or absent) is used to determine the appropriate treatment parameters.

I wish you all good succes.

With best greetings,

Rob Oostendorp.

Reference.

1. Nijs J, VanHoudenhove B, Oostendorp RAB. Recognotion of central sensitization in patients with musculoskeletal pain. Appliation of pain neurophysiology in manula therapy practice. Manual Therapy 2010;15:135-141.

Yet the scientific literature offers few information addressing the treatment of aberrant pain processing in the CNS, specifically in OA patients.

Interventions which have proved successful in other chronic pain situations (phantom limb pain, CRPS), like cognitivebehavioral therapy and neuroscience education potentially target cognitive-emotional sensitization (and descending facilitation), while centrally acting drugs and exercise therapy can improve endogenous analgesia (descending inhibition) in patients with OA.

I think this approach in patients with OA may be useful, and in daily clinical practice I always have it in mind.

https://www.researchgate.net/publication/235422182_Pain_Treatment_for_Patients_With_Osteoarthritis_and_Central_Sensitization?ev=prf_pub

Article Pain Treatment for Patients With Osteoarthritis and Central ...