Today's Q&A comes from Chris Fox, from the we graduated, but are still students and always learning thestudentphysicaltherapist.com
Hi Dr. E,
First off, I love the videos on the premium channel. I have learned quite a bit and had some success with the stuff I've added in the clinic already. I have some questions about the McKenzie approach. My residency has a background in Sahrrman training that discusses hypermobility over time leads to hypomobility via repetitive microtrauma. With the repeated motions emphasized by McKenzie, do you have concern in this area? Also with the cervical retraction and sidebend, do restricted uncinate joints of the cervical spine that occur with aging limit the effectiveness of the repeated motions? Thanks!
Chris Fox, DPT - thestudentphysicaltherapist.com
Thanks for the great question! My fellowship had an emphasis on Sahrmann's work too, and I still keep a copy of her previous edition of Dx and Tx of Movement Impairment Syndromes around. I appreciate her attempt to standardize PT and help with patient classification, which leads to improved clinical decision making and direct your treatment, thus improving patient outcomes.
However, like most old school PTs (and indeed, most PT programs, fellowships, and manual therapy curriculums), the approach is stuck in pathoanatomy. Hypermobility does not lead to hypomobility over time. True hypomobility (what I would classify as a slow responder) is only caused by immobilization, or the still a mystery adhesive capsulitis.
Remember, whether you're doing IASTM, joint mobilizations/manipulations, repeated end range loading, or corrective exercises for a muscle imbalance, any time we make a rapid change, that change is neurophysiologic, not mechanical.
Whether these changes arise from
- changes in the homuncular representation of the body in the CNS
- tone changes around the area peripherally
- improvement of skin mobility on the superficial fascial layers
- decrease in perceived threat, thus an increase in movement tolerance
- or any/all of the above
This leads me to my next point, which hopefully should answer the second part of your question.
Typically, aging seems to bring on features that I would associate more of a slow responder, i.e. multiple planes of at least moderate motion loss. However, the good news about a slow responder in pain, we can still modulate their pain rapidly with education and repeated end range loading. The even better news is that due to some of these kisses of time, or wrinkles on the inside, they actually get to end range sooner. Getting to end range sooner means you can fire those mechanoreceptors in the capsules, thus bombarding the CNS with properioceptive information that eventually resets the CNS alarm that is lowering pain/movement thresholds. It potentially may be easier to modulate pain in someone with restricted motion!
Take away points:
- repeated end range loading has the same effects as mobilization
- typical gradual and progressive loss of multiplanar ROM over time cannot be rapidly improved range wise, but pain can still be rapidly changed
- if scans show no fracture/tumor or anything else we have no business treating, don't worry about "facet degeneration," "disc dessication," "moderate to severe degenerative changes," or any other of the thought viruses patients are exposed to by misinformed but well meaning medical professionals.
Keeping it Eclectic...