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Inside-Out Paradigm

By Dale G. Alexander, LMT, MA, PhD

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The Aspiration to Prevent Hip, Knee and Shoulder Replacements, Part 2

The extrinsic variables that contribute to hip, knee and shoulder degeneration were outlined in my last column in the November 2014 issue. That article proposed that the hip and shoulder joints have a genetic propensity for subluxations. In the shoulder, this involves its anterior capsule, while for the hip joint this relates to its posterior capsule.

My theory suggests that this propensity comes to us from our primate evolution when our ancestors needed to develop ways to fall (as from trees) and somehow survive. For any who may have experienced a significant fall, our human tendency is to tuck and roll involving a sudden movement forward of one shoulder and a corresponding posterior movement of the opposite sided hip. Another way to appreciate this large body reflex is to reflect on the Olympian springboard and platform divers with their truly awesome ability to harness this capacity for combinations of flips, spins, tucks and rolls.

The second article of this series describes our internal anatomical structures whose cringing, shortening or twisting are proposed to be primary contributors for progressing toward hip subluxations.1,2,3 I theorize that hip subluxation and its accompanying typical soft tissue compensations are principal variables leading to many knee and hip replacement surgeries which are often attributed to the nebulous cause of aging.

To my perception, the primary factor in this all too common degenerative progression is how the femoral head interfaces with its socket, the acetabulum. Specifically, how shifts in each hip bone or, between both and the sacrum, may participate in pre-disposing hip subluxation(s) of the femoral head. Internal influences related to shoulder subluxations and further relationships influencing the knee joint will be addressed in separate articles.

My clinical experiences suggest that the cringing of the peritoneal sac, the shortening of the mesenteric root of the small intestine and the shortening of the tubes that comprise the ascending and the descending colons, are commonly associated with the local influences within the abdominopelvic cavity which can act on the lower spine and pelvis thus pre-disposing the posterior slide of the femoral head.4,5

Specifically, the ascending and descending colons have firm visceral ligamental attachments to the ilia and are incredibly powerful muscles very capable of distorting the acetabulum/femoral relationship. Additionally, the mesenteric root of the small intestine has the capacity to rotate the pelvis by virtue of its attachments to the left side of L2 and to the right sacro-iliac joint.6 Both of these structures are invested within folds of the peritoneal sac whose cringing response to stress or trauma initiates and exaggerates the responses of those previously described.1 Other organ attachments certainly co-participate as variables; yet, working with these three viscera have produced the most favorable outcomes for clients.

Consider the following: should the peritoneal sac, small intestine or large intestine structures contract significantly in response to a virulent digestive flu, food poisoning, extended constipation, infection or amebic dysentery then... "Katie bar the door, "... the relationship between the acetabulum and the proximal femur is rather likely to be affected. Little considered is the possible displacement of the acetabulum/femoral head relationship associated with these small and large bowel episodes. Sometimes everything settles back into dynamic balance yet, many times I propose, it does not.

Additionally, consider the mesenteric root of the small intestine experiencing a similar sequence of events: such a oblique/diagonal contraction between its left side lumbar attachments and its attachment to the right sacro-iliac joint may well induce a torque to the pelvis thus creating the pre-disposition of the femoral head to displace posteriorly, at least on one side.

Let's now consider the typical soft tissue compensations I have clinically experienced. When the femoral head slips posterior, I propose it begins to ride the edge of the acetabulum, thus creating a hip joint instability. The most common compensation pattern involves the gluteus medius and minimus muscles, the tensor fascia lata and its iliotibial band all contracting around the femoral head to prevent its possible dislocation. Ironically, this still allows relatively normal function and range of motion; yet, I propose that this fixes the femoral head against the lip of the acetabulum which over many years grooves a flat spot on the naturally spherical shape of the bone.

Further, I propose that any posterior glide is also accompanied by rotation of the femoral head which translates itself all the way down to its distal condyles creating rotation in the knee joint and contributing to the distortion of how the knee tracks in its normal flexion and extension movement during the walking cycle. Over time, this distortion of knee joint mechanics translates into compression, thus accelerating the wear and tear of its cartilages. It is no accident that roughly twice as many knee replacements occur than hip replacements during each calendar year.7 This is my proposed answer to how hip distortions influences knee degeneration.

Certainly, the iliopsoas is also a significant variable; yet, I suggest not in the manner you might imagine. More commonly, I believe that the psoas is often in spasm because of the posterior and inferior slide of the femoral head rather than the other way around. Its attachment to the lessor trochanter is being stretched by the posterior position of the femoral head. Also, the typical soft tissue compensations (the fixation of the gluteus medius and minimus, tensor fascial lata and the iliotibial band to prevent further displacement) create more inertia for the psoas contraction to overcome while initiating flexion of the femur in relationship to the trunk.

These protective contractions also disrupt the psoas' external rotation function that is essential to coordinating with the distal femoral condyles that participate in unlocking the knee and allowing it to functionally participate in a normal gait pattern.8 This extra effort to overcome the soft tissue protection of the hip joint over time influences the adductors to shorten in order to counterbalance the power of the femur's external rotation by the iliopsoas. This triangular protective shortening of the soft tissues involved in hip motion is part of the reason that clients with hip degeneration so often present with groin pain. With such a wide-ranging compensation pattern the femoral triangle is bound to be affected and vascular congestion will eventually ensue.

Further, it is my interpretation of anatomy that when the psoas tendon is constantly on stretch, its tension contributes to occluding the medial circumflex artery which effectively starves the femoral head. Avascular necrosis is a common diagnosis leading to hip replacements.9,10

The big picture of life is that our bodies consistently trade off "mobility for stability" during the aging process, as well in response to physical traumas of all varieties and intensities. In my view, this construct leads us back to the invisibility of flexor/extensor reflex systems that are a part of the evolutionary momentum which produced more distensibility in the anterior shoulder joint and the same in the posterior hip joint. These were all designed to prevent falling, surviving a significant accident and to prevent one's pre-mature death.

Sadly, the echo of these survival mechanisms has left us a Gordian Knot to unravel in our efforts to assist our clients in maintaining their quality of life.

In truth, my successes with undoing the progression of hip and knee degeneration is much less than I would prefer to report. However, what I have learned from my clients, I do believe can contribute to a foundation for us as a profession to build a commonly accepted model of how this progression occurs and what we might do to stabilize its downward spiral. And, if identified in its early stages, the progression may even be reversed. This understanding also points us as dedicated professionals toward building additional skill sets to address these human difficulties.

References:

  1. The Sacs & Tubes Theory of Stress, Dale G. Alexander PhD, LMT, Massage Today, January, 2014 (Vol. 14, Issue 01).
  2. Freeing the Heart: Protection of the Hip and Shoulder Joints, Massage Today, June, 2013 (Vol. 13, Issue 06).
  3. A New Model for Low Back Pain & Dysfunction, Massage Today, August, 2013, (Vol. 13, Issue 08).
  4. Dr. Jean Pierre Barral D.O., all books published by him and my class notes & experiences with him from 1986 -1993. Encourage all massage therapists to study his ideas and to gain training from his skilled instructors, www.barralinstitute.com.
  5. Lansing Barrett Gresham's construct that our viscera are fully functioning long before we have gross motor capacity and that their developmental tensions have pre-disposing influences on our eventual movement patterns. Founder of Integrated Awareness®, www.inawareness.com.
  6. Gray's Anatomy, 37th Edition, Williams, Warwick, Dyson, Bannister, Churchill Livingstone, 1989, pg. 1358.
  7. FastStats - Inpatient Surgery, www.cdc.gov/nchs/fastats/inpatient-surgery.htm, 719.000 Knee Replacements and 332,000 hip replacements, 2010.
  8. Unpublished manuscript on The Biomechanics of the Walking Cycle, Dale G. Alexander PhD, LMT, 1990. (The popliteus muscle is theorized to be the first contraction that unlocks the knee allowing the external rotation of the distal femoral condyles produced by contraction of the iliopsoas muscle.)
  9. bonesmart.org › BoneSmart › Hip Replacement Articles
  10. Atlas of Human Anatomy, Frank Netter M.D., Plate 474, Ciba-Geigy, 1989.
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