Ok, so we discussed some of the contributing mechanisms of knee pain in Part 1/2 and we have yet to look at diagnosis, prognosis and treatment. Let’s see what this prospective article, my main reference for this post series, suggests!
We have postulated that knee pain from osteoarthritis (OA) has three contributing factors: knee pathology, psychological distress, and neurophysiology. So when diagnosing individuals with knee OA who have pain we must see if these criterion are met. The authors in the article propose a phenotypical diagnostic thought process since the OA population is heterogeneous and broad.
The patient could present with varying levels of each of the three domains noted above along with a reported pain rating. Example: a patient may have minimal radiographic changes, high psychological distress and moderate pain neurophysiology (central sensitization, etc) and report a 7/10 on the pain scale. Another phenotype could present with high radiographic damage, and low distress and neurophysiology and report a 3/10. This form of diagnosing a patient may help lead to the next two important steps; prognosis and treatment.
The authors do not state how to determine some of the levels in the different domains. My question: how do you differentiate a person with high radiographic OA evidence with appropriate nociceptive input vs a person with high radiographic OA evidence with central sensitization as well? I am sure there are diagnostic methods that are appropriate for PTs to administer in this arena. (post to comments if you have some good guidelines!). Ok, we continue…
A recent study (April 2014) by Riddle DL, and Stratford PW titled Knee pain during daily tasks, knee osteoarthritis severity, and widespread pain showed that certain pain/pathology presentations were more/less likely to have widespread pain. (In this case those with minimal knee OA with high pain rating were more likely to report widespread pain as well) So a presentation of diagnostic factors can be shown to be prognostic, even in a complicated pain disease.
Prognosis, currently, is extremely variable in this population. Well, that certainly makes sense since pain is the outcome the patient and clinician are trying to address. The authors propose that phenotype diagnosis can help in prognoses because you can boil down the elements. Having limited experience (student status at this time!) I will defer to the authors, but from what I have read and understand about pain presentations … well, I certainly don’t see them fitting nicely into any package. They state that this diagnostic set-up could further our understanding of the disease process and allow for future prognostic research in the area. Sure it would be nice to have a Risk Ratio/Odds Ratio to reference, but it is unlikely that a researcher could isolate the contributing variables in a meaningful way. The authors admit this, but we will use all the information we can gather and forge on. (More research is needed!)
So, we have defined the presentation of our patient and we have made thoughtful and educated prognostic predictions. Now on to the treatment! The most effective treatment at this time is Total Knee Arthroplasty (TKA), and yet 34% of patients who have this procedure still endure pain. As we all know; the ratio of pain to tissue damage is not 1-to-1. Research has shown, however, that addressing the individual aspects of this disease will yield results. This is how treatment should be guided. Here’s a nice quote:
Such knowledge may lead the physical therapists to select treatment strategies that harness the patient’s innate ability to modulate nociception. A patient who possesses the capacity to modulate nociceptive information might benefit from interventions that involve a short term increase in pain- through manual therapy techniques or aggressive strengthening interventions- to achieve long term benefits. Conversely, patients who lack the ability to endogenously modulate nociception might warrant strategies that seek to diminish sensitivity of the nervous system, through modalities such as transcutaneous electrical nerve stimulation or other emerging techniques. (pg. 430)
(Here is more research from Riddle et al. on treating pain catastrophizing in TKA patients; which is a distress factor seen in the knee OA population.)
OK Sure, address the patient’s tissue damage, use the descending control theory and help them drop some endogenous opioids. Boom. Find out what is going on with your patient, use your brain and treat each patient as an individual, even if they do fit a phenotype. (The phenotype? Yeah, I like the idea of it in guiding treatment, especially as a new practitioner.)
In conclusion, as always, more research is needed! I do like the new conceptual framework that the authors propose. It seems to try to address and encompass the breadth of the disease. These complex biological dysfunctions are tricky enough without being confounded by pain reports. Each one prong is just that, a prong, not the whole. These patients need to be understood first, before being treated like any simple abnormal joint surface. This prospective article was well timed in it’s publication. What do you think?
Please drop your thoughts in the comments if you desire.