I was reading the article mentioned in the title of this post.
Tendinopathy means microscopic changes in the tissue structure of a tendon.
In some cases significant tendon changes are observed in imaging findings in individuals that have no symptoms. And pain does not reflect ongoing tissue damage or harm.
I.e., some have pain but no tendinopathy, while others have tendinopathy yet no pain.
My question is what the following quote then actually means: “Full functional recovery from tendinopathy typically takes several months”
Recovery from what, exactly? 1) Recovery from pain in the case of no tissue damage; 2) recovery from tissue (tendon) damage in the case of no pain; or 3) recovery from tissue (tendon) damage AND its symptoms?
My guess would be that the sentence refers to the third scenario; in the first one there’s no tendinopathy to recover from, and in the second one there’s no reason to engage in a recovery process because there are no symptoms to precipitate such an undertaking.
I don’t quite get it. So are there cases where damaged tendons á la tendinopathy cause symptoms (such that a professional can be confident in that the symptoms that are described by the client are indeed caused (or at least heavily contributed to) by tendinopathy, even though pain doesn’t reflect damage, and damage doesn’t necessarily cause pain)?
Tendinopathy means microscopic changes in the tissue structure of a tendon.
This definition is incomplete. Quoting from the article: “The word “tendinopathy” is a general term used to describe changes in a tendon typically relating to pain, reduced tolerance for loading, and microscopic changes in the tissue structure.” The aspects of pain and reduced tolerance for loading are essential to the clinical diagnosis of tendinopathy.
My question is what the following quote then actually means: “Full functional recovery from tendinopathy typically takes several months”
This refers to the recovery of full function (i.e., restored tolerance for loading without pain symptoms), hence “full functional recovery”.
RWulys - I agree with what Austin stated above. Additionally, the likelihood of having/developing symptoms does appear to increase when tendionpathic (morphological) findings are observed. However, this isn’t sufficient reason to engage in screening given the murkiness of correlation of observed findings and symptomatic development, as well as the ability for case outcome improvements (pain experienced and function) without tendon changes. We see similar discussions in the context of low back pain and imaging findings. Ultimately, this begs the question, how much do such findings matter and generally speaking in regards to management they do not matter sufficiently to alter broad recommendations/interventions.
fbc91 - That line of inquiry has been proposed by folks like Ebonie Rio et al (see: The pain of tendinopathy: physiological or pathophysiological? - PubMed & Adaptation of the pathological tendon: you cannot trade in for a new one, but perhaps you don’t need to? | British Journal of Sports Medicine). I can say at the clinical level, I would not recommend such labels or narratives as CNS sensitization given this tends to drive the false premise “pain is the output of the brain” leading to “retrain your brain”. Rehab and exposure therapy - yes, that is a major aspect of treatment in this context (e.g. guided behavioral experiments - individualized progressive rehab plan driven by patient activity goals). However, we do still advocate (as discussed in the guide) for isolation to the area because IF morphological and mechanical alteration at the tendon level matter, then we are covering our basis.
Could this then mean that a client is diagnosed with tendinopathy even when there are no tissue changes? I mean, being that imaging usually isn’t done, perhaps the question of whether or not there are any tissue changes remains unanswered (in those cases), but the diagnosis is given anyway because of the particular set of symptoms? On that note, if those certain symptoms, and the long recovery time that tendinopathy has, are present, how confident would you be that there are tissue-level tendon changes? Is it a total coin flip?
I get that peripheral inputs from tissues to the brain are A factor among many in the final product of the pain experience generated by the brain. I realize that it’s impossible to say exactly how significant of a factor it is in general, but maybe in the case of a specific condition, like tendinopathy, we have more of an idea than 50-50.
Noted. I guess that simply having screening done being an independent risk factor in a pain experience confounds how much the tendon changes in themselves are actually hurting.
This is the essence of my inquiry. The biopsychosocial model is very interesting. As I said to Dr. Baraki, I get that it’s impossible to say how much (like percentage-wise) tissue damage contributes to the final Pain Picture painted by the brain, but I’m trying to get a grasp on when, with which type of conditions, can we say that the tissue damage is probably contributing “significantly” to the pain that is felt… it hurt when I broke my arm, but acute, traumatic injuries are more obvious than atraumatic ones, obviously.
RWulys -
I encourage you to read more on healthcare models (not just BPS) as well as disease classificatory systems (nosology). This will not likely provide the black and white answer you are looking for but will make it easier to accept uncertainty. I think it’s great you are asking such questions as this curiosity will lead to further inquiry and reading, but rarely does it lead to certainty but rather the opposite - we just tend to accept the uncertainty more.
