McKenzie Course Review: Part II
This is Part II of a two-part blog series on McKenzie; Part I can be read here.
On the third and final day of the McKenzie Part B course that I attended recently, the course instructors showed the following video of a sample evaluation during a McKenzie Part D course (Advanced Cervical Spine, Thoracic Spine & Extremities).
The person being evaluated (Christine) is an active PT who runs, works out, participates in CrossFit and bodybuilds. Around the 0:19 mark Christine describes how about two years ago during a team competition, she experienced a right shoulder subluxation (and what sounds like a spontaneous reduction) during a power snatch into an overhead squat. This led to discomfort and movement issues in her right shoulder that impaired her athletic performance, particularly her ability to perform overhead strength movements in the past year.
The whole video is only 7:13 long so it won’t take long to watch the whole thing, but I’ve also summarized the main points here along with timestamps (each link will open into a new window):
3:14 - ROM assessment reveals loss of shoulder flexion and abduction in right shoulder. Right shoulder external rotation strength easily breaks with MMT.
4:51 - Instructor performs repeated passive extensions to Christine’s right shoulder
5:40 - Shoulder flexion reassessment (spoiler alert, right shoulder AROM significantly increases from baseline)
6:04 - Christine performs banded shoulder external rotation x15
6:36 - Shoulder flexion AROM reassessment (spoiler alert again, right shoulder AROM returns to it’s limited impaired baseline)
6:45 - Instructor repeats passive extensions for right shoulder
7:07 - Shoulder flexion AROM reassessment (Right shoulder flexion AROM fully restored once again)
After displaying the video, it was explained that Christine’s shoulder derangement (in which she had a significant flexion AROM limitation) was resolved by the repeated shoulder extensions, but that the fifteen repetitions of resisted shoulder external rotations had “re-deranged” her shoulder, once again returning her to her impaired flexion baseline. Successful management of Christine’s shoulder mobility issues therefore would include a temporary stop on external rotation strengthening (at least in this manner displayed) as that could potentially be a mechanical trigger for her shoulder flexion impairment.
There was a lot to unpack and process here for me. After we saw this video I raised my hand to ask what were the possible reasons or mechanisms behind these rapid back-and-forth changes. The instructors replied that we cannot know the precise reason as to why this occurs, and that the McKenzie approach is focused on clinical decision-making based on the patient’s mechanical response as opposed to speculating on pathological theory.
This is a fair statement and consistent with McKenzie’s official position on what’s going on with the intervertebral disc when someone has low back pain with a possible discogenic source. At multiple times throughout both McKenzie courses that I’ve taken, there is no mention of “pushing a disc back into place” as a reason for pain resolution when someone has a disc herniation, with many references provided that challenge the pathoanatomical model of pain and injury. I also appreciate that they say “we don’t know” about a question for for which there is truly no definitive, unequivocal answer. At least for now.
But then I began to press. Not because I wanted a precise, definitive answer behind the reason for this almost instantaneous resolution of chronic symptoms, but because I wanted at least to inquire about what other plausible physiological mechanisms could be at play here. I’m always curious about the possible reasons WHY an approach might work because I want to know the NARRATIVE or governing principles behind the approach.
There are so many different “camps” of PT styles out there—McKenzie, Maitland, SFMA, NAIOMT, IPA, PRI, the Functional Anatomy Seminars, Mulligan, etc. Physical therapists may lean towards one or another for many reasons—perhaps they had a mentor who was well-versed in one approach, or their school had faculty whose majority were trained in one particular style, or their student clinical affiliations influenced them towards one approach. When I was younger I had colleagues, instructors and professors who said no one approach is necessarily better the other and encouraged me to seek out whichever approach resonated with me the most and allowed me to practice in a manner in which I could achieve the most success with my patients. I’ve heard a million times about the proverbial toolbox of skills to have, and the more tools one had the more versatile one could be.
I’ve since moved away from that mindset because after a while I found myself being more curious about the similarities between all the different schools of thought out there instead of their differences. Some questions I ask myself:
What are the underlying scientific principles, narratives and explanations that govern these approaches?
Are some approaches actually extremely similar but just use different terminology?
Are there any approaches that are diametrically opposed? What’s the reason?
How does each approach respond to the emerging research and evidence that comes out over the years?
Do the approaches ever update their position statements or pillars? Why or why not?
I’ve digressed. Back to the McKenzie example—the purpose of my question was to see how McKenzie could explain the phenomenon that occurred in the video in a manner that reflected it’s core and underlying narrative. The answer I first received was unsatisfying—that it was simply a derangement as McKenzie defines it. A matter of seeking a patient’s directional preference that results in improvement of pain or resolution of symptoms. I wasn’t satisfied with this, which was basically just resorting to an explanation of what was observed.
I continued to inquire. What was it specifically about glenohumeral shoulder external rotation at zero degrees of abduction that prevented Christine from achieving full flexion ROM? I was puzzled by another explanation that was offered: That there could have been a torn piece of labrum that was blocking the patient from achieving shoulder flexion that was moved after the patient performed multiple repetitions of extension, thereby allowing flexion. And that it was possible that the repeated shoulder external rotations caused the piece of torn labrum to obstruct the shoulder flexion, thereby re-deranging the patient and inhibiting shoulder flexion.
Wait, what?
I couldn’t believe that this was being offered as a possible explanation. After all the effort that McKenzie had made to move away from a pathoanatomical model of pain with herniated intervertebral discs, I was now hearing an explanation that essentially uses that same kind of reasoning for the upper extremity.
When I questioned the validity of such a phenomenon occurring the response was basically, “It could be happening, it could not be happening, we can debate about the mechanism behind pathology theoretically but we’ll never know.” These kinds of responses don’t really sit well with me because it’s kind of a dead-end zone for critical thinking. There was no discussion about any evidence on the matter and any continuation of the conversation just led us back to the definition of what a derangement was, which is circular reasoning.
Another point that was made pivoted the conversation into a direction I’ve ventured into many times in the past. Does the underlying reason behind WHY something works matter, as long as the patient is getting better? Why should we care as long as the patient is satisfied and is achieving outcomes? Shouldn’t we just care about the patient in front of us and helping her achieve her goals?
To me, the reasons WHY something might work will always be important.
If we know how something works, we can figure out ways to make it better.
We don’t want to make the mistake of perpetuating false beliefs that may be masked by the red herring of treatment efficacy (i.e. inducing a nocebo effect based on rationale used to support inert or harmless treatments).
Understanding the true phenomena behind something may allow you to apply that knowledge to other aspects of your practice. And you can improve and learn more about those things too.
When I encounter situations that are slightly different than the original way that the intervention worked, I want to be able to navigate those nuances with critical thinking—which leads me back to the possible question of why the original thing may have worked.
Going back to the example of Christine and her shoulder derangement: 1 set of 15 repetitions of basic shoulder ER with a theraband was enough to re-impair her shoulder flexion, and she was discouraged from doing shoulder external rotation exercises in case it makes her shoulder worse. To me that’s potentially a really big fear-mongering piece of patient education, and I would need at least some sort of sensible reason that has a little physiological bearing for me to instruct. The fact that the assessment and repeated shoulder extensions satisfies the heuristics and McKenzie evaluation algorithm is insufficient in and of itself—it’s basically just justifying the intervention using definitions and rules that it has created. This isn’t too far away from using “This is just how McKenzie always does it” as a reason.
I’m happy to use interventions that helps the patient in front of me, and I would happily have this patient do repeated shoulder extensions as long as I have a justification for why it works. My goal as a PT is to not only treat the patient I’m seeing in front of me, but to have a bigger vision of how I can consistently treat the hundreds or thousands of patients that I’m going to see in the future. I want to make sure the message I’m delivering to those patients is rooted in a principle that can be as applicable as possible regardless of what particular technique or approach I’m using. And I don’t want to unnecessarily perpetuate nocebic ideas surrounding the danger in doing certain exercises.
One of the glaring holes in the way McKenzie discusses these matters both in the live courses and in the course manuals is that it misses the boat when it comes to pain neuroscience and the nervous system. Here’s an excerpt from Part I of my McKenzie course review regarding what I think is happening with rapidly observed changes and improved outcomes:
When seldom-performed movements are gradually re-introduced into a a region where pain is perceived, the novel afferent input to the nervous system decreases the perception of threat and thus mitigates the pain response.
In the clinic, we can’t verify which tissue or anatomical structure is the main source of nociception. Besides, what if there’s more than one? Either way, it doesn’t matter because our goal isn’t to direct an intervention at a structure.
So, when we resolve a derangement we’re affecting the way the central nervous system perceives a threatening, pain-eliciting movement. We do this by performing graded exposure in the form of repeated movements at end range, and determining the specific direction and dosage based on patient response.
I’ll continue to use the McKenzie principles that I learned in Parts A & B but I don’t see myself taking any more courses in the future for some of the reasons I’ve outlined here. Rules and heuristics are great but teach me the underpinnings of why those rules and heuristics work. And if you don’t have a definitive answer, we should be able to consider mechanisms in a way that influences the way we practice and not just for the sake of debate and speculation.