I was getting sick. Ugh. I was able to hold off long enough to finish my caseload, but once I was home, I let my resistance to the bug go. My clinical crew knew I wasn’t feeling well, but I thought I’d be back by the next day.
Next morning: nope. I needed to stay home. I tell my wife I’ll be staying home as she leaves for work, “s’all good, honey.”
So I call in to the clinic to let them know. When they answer the phone my voice changes a bit ( I notice retrospectively). I explain I’m worse *cough*, and thank them for arranging the schedule to cover me *cough*. Then hang up.
What was that about? I ask myself. I was not sure that I sounded sick, or did I? Did I just throw in an extra throat-clear for emphasis? I realized that I felt a strong urge to sound sick, to “sell” that I wasn’t feeling well. My sickness was the truth. Yet, I was pulled very strongly to embellish it in my short 30 second interaction… hmmm.
The purpose of communication is often to get a point across to some audience outside of yourself. You express yourself so others will know what you mean, how you feel, why you think, etc. Continue reading
There is no more credible a thing than an image. Seeing is believing. I’ll have to see it to believe it. A picture is worth a thousand words. Vision trumps other senses (McGurk Effect).
How are the words you choose to use, in the healing context of your presence, going to combat the fact that it has been visually shown that things are “messed up in there” ?
It is not our fault, us humans. Wilhelm Conrad Roentgen developed this lovely technology. About a month later, humans were using it clinically. It is amazing. And I mean X-ray, CT-scans, MRI, fMRI, UltraSound… it’s all incredible. It was developed so we used it. We used it on people in pain, people with broken limbs, people with ailments of this nature or another, and that is the vantage point from which our opinions were based. We saw people with pain have strange looking images. We therefore conclude, that the changes we saw were the cause of the pain, and here we are today.
Post Hoc, Ergo Proctor Hoc. After this, therefore because of this. It is all in the development of the tool. We pointed our delicate and precise imaging tools at the sick, and we found sickness. Continue reading
“But I have in my spine.”
“Oh I can’t, my is really bad.”
“I guess I’ll just have to live with this .”
Fill in the blank with your own patient comments, but they are all essentially the same. Some gigantic, devastating, destruction is occurring inside of their body…and there’s no hope.
I don’t know if it’s funny or just sad, but the fact that such a large amount of patients respond to such “terminal” (i.e. chronic) conditions with statements like Continue reading
After a few weeks back in the out patient physical therapy setting I am re-confronted with the pathoanatomical-ness of diagnosis.
The battle for language and context of explanation rages on: full strength, full power, full speed. Whew, just trying to hang on. Daily I must combat the destructive thoughts of a fragile body, or a decaying joint, a shredded tendon, or a tear from here to there.
Sometimes it is very true. Others not. But trying to de-fixate an individual’s thoughts off of the negativity of their structures is unaided by visual proof that they are internally “disfigured.” Continue reading
How do I help my patient get better? It may depend on many things, the disease, injury, co-morbidities, etc. And in many cases it can be hard to ignore big factors that “stand in the way” of recovery. Some patient’s are just tough. Complex. Hopeless.
Of course, we make sure to keep a mask on. We attempt to prevent our patients from seeing Continue reading
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… Continue reading
Nocebo Confession: this image makes my knee hurt!
The recently published prospective (March 2014) Future directions in painful knee osteoarthritis: Harnessing complexity in a heterogeneous population really breaks-down some wonderful concepts about pathoanatomy and pain perception.
The article reports that 50% of individuals with osteoarthritis-like knee pain have positive radiographs for osteoarthritis (OA). Interestingly enough, 50% of those with positive radiographs for OA have knee pain. Citing the NIH they quote “it is important to separate conceptually the disease process of OA and the syndrome of musculoskeletal pain and disability.” They also refer to N. Hadler’s paper Knee Pain is the Malady, Not Osteoarthritis, which is a wonderful title indeed!
The authors propose a new conceptual model which is outstanding in breadth and scope. They delineate the disease process into three contributing categories: 1) Knee pathology 2) Psychological distress 3) Pain neurophysiology.
Knee pathology involves the regular and commonly held positions about OA. They include the radiographic (X-Ray) evidence, the chondral changes, osteophytes, the joint narrowing, the “bone-on-bone”, the “you have the knees of a 90 year old.” This part of the puzzle obviously contributes, but the relationship is NOT 1-to-1 for pain and dysfunction. – Try explaining that to someone who has knee pain, has been told they have OA and been told they have the knees of a 90 yr old. It will be a long discussion. Of course there are the biomechanical stresses on the knee including increased body mass and joint positioning that are implicated in the knee pathology puzzle piece.
The psychological distress part has to do with fear of movement (moving could cause pain!!) and catastrophizing (ruminating over the situation and winding it up into a hypersensitive syndrome) and other factors (don’t want to give it all away, read the article!) similar to other chronic pains. It is shown that the better the coping mechanisms and the better the positive belief strategies that the patient can employ the better the outcomes.
The pain neurophysiology aspect is… well, please allow me to quote: Continue reading