CAPA ROLF LINES 2000-04-Fall

Refrying Freyette

Pages: 29-34
Year: 2000
Dr. Ida Rolf Institute


Volume: 28

Before continuing the discussion of Dr. Harrison Freyette’s laws of spinal Motion, I want to express toy appreciation to Robert Schleip and Jeff Mainland for devoting time In tackling the thorns subject of spinal biomechanics and sharing their knowledge with how Rolf Lines readers. Any undertaking to apply mechanical laws to human structures particularly the locomotion system of the human body is almost guaranteed to result in either controversy or confusion. Sadly, both non quantifiable data and non-conformity inherent in spinal design are highly visible parties in this age-old debate.

Phillip Greenman fondly speaks of many heated exchanges between him and James Cyriax concerning joint mechanics and spinal pathologies, published over the years in Manual ‘therapy Journal. This public discourse proved not only thought provoking for readers, but also formed t lit long bond between these two great thinkers.

In the Winter issue of Roll Lines. Jeff expressed concern over Robert’s footnote about the validity of Freyetle’s Laws of Spinal Motion. While both gentlemen did agree that these laws might be imperfect when explaining certain aspect, of vertebral motion, the nature of the implied imperfections was not examined. With Frevette’s laws now being taught in some Rolling’ classes, perhaps further exploration into the controversy may be beneficial.

The great debate is embedded in Freyette’s Second Law of Spinal Motion: “When the spine is either forward or backward bent and It to bending is introduced. the vertebrae will rotate toward the concavity” (rotation and side bending coupling to the same side).1 Frevette’s conclusion,, concerning joint coupling during spinal It hyperextension and hyper flexion were developed by studying movements of cadaver spines. Unfortunately, cadaver spines are significantly relaxed and therefore not subject to the stresses of living spines.

Today, most Modern researchers agree that in the presence of free and ease articular and soft tissue motion in the lumbarpine, coupled movements of rotation and side bending do occur to the same side in full forward bending. This is consider non neutral type 2 mechanics. However, in backward bending or hyperextension, contrary to Freyette’s observations, rotation and side bending of the lumbar spine usually couple to opposite sides (neutral type I coupling). As Robert mentioned, this highly important distinction is critical when assessing and correcting facet dysfunctions

One simple technique commonly used for testing non neutral FRS(flexed, rotated & side bent) dysfunctions in the low back begins with the client sealed and the spine in neutral. The therapist introduces extension and side bending right, while palpating for fullness in the erectors overlying the lumbar transverse processes. In the absence of vertebral dysfunction or pathologies such as irregularly shaped facets this maneuver should cause lumbar TP’ s to rotate left into the palpating hand. Try this on your own body. The findings of this simple exercise are in direct opposition to Freyette’s cadaver observations for joint coupling in the hyper extended position.

The relevance of this shortcoming in Freyette’s Second Law scents insignificant until the therapist begins assessing and correcting more complex vertebral dysfunctions. Example: With the client in a prone hyper extended “sphinx” position, if L5 and L4 TP´s test level but L3 appears posterior on the left, the therapist , an assure that the right facet at 3 is not closing forcing the vertebra to rotate left and side bend left (FRSI ). Armed with this piece of information a therapeutic technique can be developed to close the facet (it)the right using the appropriate vector of force lot side bending and rotation right.

Moving up one segment, if L2 appears level compared to 13, it is also dysfunctional. Spinal mechanics rule #6 states: “motion is described by the movement of the superior facet on the inferior.” Therefore L2 should follow L3 even though L3 is dysfunctional. But what if L2 does follow L3 by rotating left and side bending right? The therapist may begin to suspect formation of a type 1 group curve where three or more vertebrae rotate and side bending to the same side.

Group dysfunctions display a restricted coupled movement of side bending to one side and rotation to the opposite. Type 1 group curves are exclusive to the lumbar and thoracic spines (exception O-A joint), and are commonly recognized by Rolfers as compensatory scoliosis strain patterns, and not true structural scoliosis.2 Proper understanding of how these functional scoliotic type 1 curves should behave during forward and backward bending allows the therapist to develop a therapeutic approach that addresses the cause of the group dysfunction: either a non neutral lesion above or below the curve, or possibly on leveling of the sacral base.

Freyette’s Second Law of Spinal Motion is also problematic when applied to the thoracic spine. According to Dr. Vladimir Janda and Dr. Phillip Greenmail, “‘the thoracic spine can couple in bulk neutral or non neutral mechanics depending on whether the therapist is working; above or below the apex of the kyphotic curve and whether side bending or rotation is introduced first.”‘ In most cases, introduction of extension and side bending causes coupling of rotation to the opposite side and vice-versa.

Aside from Freyette’s early misperceptions, I still agree whole heartedly with Jeff’s comment to the effect that Dr. Frevette’s formulations have considerable practical utility for our Rolfing community. As Freyette´s noted, facet joints are “in control in any area of the spine” and “govern rotation …and side bending. “‘Therefore, it is obvious that a systems approach to postural alignment which includes myofascial as well as skeletal methods world help us to better achieve Our goals of creating body balance and symmetry, while establishing pain free movement during the walking cycle.

Dr. Freyette’s many contributions to the understanding of joint mechanics are truly remarkable given the absence of radiographic technology in 1918, and credit must be given to Robert Schleip for alerting RoIf lines readers to possible Claws in Freyette’s formulations. In the complex world of spinal biomechanics, it is imperative that practitioners not base their work on faulty concepts.

Dr. Freyette commonly receives credit for a Third Law of Spinal Motion, although it was actually developed later by Beckwith, Hoover and Nelson.4 This law has special significance for Rolfing practitioners in an indirect way. The Third Law states: “Initiating notion of a vertebral segment in any plane of motion w ill modify the movement of that segment in other planes of motion”.

Another way to express this is that “when vertebral motion is Introduced in any one direction, million in all other directions is reduced.” Labeled type 3 mechanics, muscle energy and high velocity thrusting techniques utilize this law by introducing motion above and below a dysfunctional segment in order to localize down to the non neutral lesion to be manipulated.

Normally, Rolling sessions do not incorporate techniques that twist the torso and lock down a dysfunctional vertebral segment to be mobilized. However, this law does become relevant to our particular type of therapy when it is reversed to read: “increase in range of motion in any one plane will increase the available motion in all other planes”.

Example: Rolfers with a keen eye often observe elderly “feet shufflers” strolling the aisles of the local market. We assume hypertonic hip flexors are creating loss of hip extension, but commonly the culprit is anterior hip capsule adhesion. In chronic cases, the adhesive capsule will limit trunk extension causing the person to present with a slight forward bending from the hips. Pressure sensitive type 3 mechanoreceptors located in the joint capsules increase their frequency of afferent discharge as the hip joints roach their end range of motion in extension. At the same time, a local neurological phenomenon labeled arthrogenic muscular weakness5 is activated, that inhibits the prime mover (gluteus maximus) and facilitates the antagonist Iiliopsoas) ass the joint reaches its extension barrier.

Apparently, this protective device is designed to prevent damage to the joint cartilage from excessive or sudden hip hyperextension. This is ordinarily not a big deal except in the case of a tight, fibrous capsule, which lends to foot the mechanoreceptors into believing that the hip has prematurely reached its end range of motion immediately, this built-in, local reflex mechanism begins to neurologically facilitate the flexors and inhibit the extensors that cross the hip joint.6

Because the hip flexors are already too tight, increased psoas facilitation initiates a “Catch 22” cycle that reciprocally inhibits the already weak glute max, further compresses the fibrous joint capsule, creates excessive lumbar extension during gait, and introduces excessive strain on the inter vertebral lumbar discs and ligaments.

Anterior hip capsule adhesions are often tough to mobilize using traditional myofascial approaches. By applying the Third Law of Spinal Motion, however, a very therapeutic routine can he performed to help address the problem. The therapist first begins by lengthening the hip flexors and applying muscles spindle techniques a, tone the weak, inhibited glute max. Next, the hip is mobilized in various planes of motion such as abduction, adduction, flexion or circumduction before finally attempting to treat the anterior portion of the capsule. Muscle energy (contract-relax) techniques are especially effective in “freeing-up” the ornery anterior capsule at this lime.

After the hip flexors and capsule have been reasonably mobilized, it is appropriate to offer the client a movement cue to help maintain his new found hip extension. Sun ply request that during the client’s daily walk, he focus on keeping his back heel down a second longer with each step. This movement cue is only beneficial it the lip fluxurs and capsule have been thoroughly treated rod are moving freely, bilaterally. Introduction of this movement cue too early can have disastrous long term effects. Serious disc and ligament pathology can develop from increased lumbar hyper extension during the walking cycle.

In Robert’s response In Jeff’s article, he included a drawing of a typical idiopathic S-draped scoliosis (Fig.1). The subject in this drawing appears to have a superior ilium on the right which usually indicates right side bending of the lumbar spine. This insignificant looking high right ilium is a common finding in S-shaped rotoscoliotic cases, and is an extremely important assessment too for understanding the muscle imbalance patterns that have perpetuated the dysfunction.

Many therapists mistakenly assess this lumbar scoliotic curve as side bent left, because that is how it appears in the drawing. However, if this scoliosis, is truly functional and not structural, when loaded in gravity, expect it to follow the rules of a typical type one group curve by side bending right and rotating left.

In Robert’s original article “Lecture Notes on p’soas and Adductors,” he states: “if a short iliopsoas would indeed function a, a significant factor for the side bending of a lumbar scoliosis, this should be testable in the following way: with the pelvis kept immobile a hip, joint flexion on the side of the short psoas would result in immediate decrease of the scoliosis, whereas bringing the femur back to line would increase the scoliosis again. Definitely not what one sees in scoliotic people.7”

Indeed it would be wonderful it wee only had to release the myofascial restrictors for the hones to magically tall into plate. Regrettably, that does not always happen. For example, in Robert’s illustration (fig.1) it seems doubtful that the non neutral dysfunctions at L5 (bottom of the curve) and T-12 (top of the curve) would allow this lumbar scoliosis to straighten simply by relieving unilateral psoas contracture.

Over approximation of joint surfaces caused by sustained isometric muscle contraction inevitably leads to irritation tit the sensitive mechanoreceptors and nociceptors located in the joint capsule. Therefore, it is unlikely that the facet and sacroiliac joints, haying been locked in a state of chronic compression great enough to cause this degree of scoliosis, will he relieved simply by releasing pull front a hyper contracted psoas. Remember, true type I group curves, by definition, should not improve greatly during forward or back ward bending because of the non neutral (locked) facets above and below the curve, or sacral base unleveling.

In Robert’s response to Jeff’s article, lie again refers to the drawing of an idiopathic S-shaped scoliosis, and makes this comment: “It fits the description of side bending and rotation of scoliosis in my article and shows how the explanatory theory of an unilateral psoas shortness (e.g. on the left here) would be partly in conflict with the direction of rotation shown.” ‘this statement is true – it would definitely he in conflict with the direction of lumbar rotation in the drawing, particularly when specifying the psoas as the primary contributor to this curve. Unfortunate, the explanatory theory doesn’t really make sense, simply because a unilateral short psoas can not fit- perpetuating this scoliotic pattern any way. So why label it short just to explain the theory?

No doubt, Robert clearly understands scoliosis dysfunctions, so perhaps the contusion lies in interpretation. It is somewhat unclear, but it seems that the gist of what Robert is asking Roll Limy, readers to consider, is the idea that the psoas muscle is not really a major contributing factor in torsions of the pelvis leading to common functional scoliotic stain patterns. However, the missing piece to the psoas puzzle may be this.

Although it is possible for the left psoas to be tighter than the right as shown in Robert’s illustration, it is unlikely that it is, shorter. Let’s not underestimate the power of a tight, hyper tonic ipsilateral QL that Likes to battle the psoas over anterior or posterior rotation of that left drum. Sometimes even to the point of creating a painful hyper extended lumbosacral joint. Occasionally when the QL combines with other strong myofascial forces they possess the ability to overpower the psoas and other hip flexors, causing unilateral flattening of the lumbars, posterior rotation of the ipsilateral ilium and compensatory lumbar scoliosis. During assessment of this condition, confusion usually develops when the therapist palpates an extremely tight unilateral psoas and jumps to the conclusion that it is also short.

It is well documented how light and wiry eccentrically contracted hamstrings can feel to the touch in those presenting with increased anterior rotation of the ipsilateral ilium. The hamstrings are tight and hypertonic on that side, but they are not short. The hip flexors overstretch the hams by increasing the distance between origin and insertion and create anterior/inferior rotation of the ilium that side.

Likewise, by increasing the distance between the origin and insertion of the psoas, the overstretched psoas finds itself holding on for dear life, fiercely fighting the posterior pull from other typically hypertonic muscles such as the multifidus, quadratus and hamstrings. The hip flexors usually win, but sometimes the hip extensors win. The point here is simply that a unilateral psoas can feel tight and fibrous when manually palpated, but still have decent range of motion when being passively stretched by the thetapist. The psoas is tight but it is definitely not short.

If a short left psoas is not primarily responsible lot- the idiopathic scoliosis in Fig. 1, then what structures are contributing to this strain pattern? A more plausible explanation might be facet dysfunction at T12-L1 (non neutral compensation) inhibiting the left psoas, facilitating the right psoas, and causing the right quadratus and short head of the iliocostalis to hip-hike and side bend the lumbars.

Granted, the QL usually extends and flattens lumbar lordosis when unilaterally hypertonic. However, when combined with torsional forces from tight ipsilateral iliocostalis, psoas, and piriformis muscles, the four have the ability to bind down the lower ribs, TPs, and sacrun, forcing the vertebrae to ipsilaterally side bend and contra laterally rotate, as illustrated in Fig. 1, p. 24.

Two other important muscle imbalance patterns should be mentioned when discussing this type of S-shaped scoliosis. One typical substitution pattern arises when a short and tight right quadratus lumborum and a short and tight right tensor fasciae combine forces to initiate hip abduction by overpowering the weak gluteus medius/ minimus during the walking cycle. the inhibited gluteus medius allows the right hip to sway on a transverse axis with each step, resulting in a gait similar to the classic Marilyn Monroe walk.

But by far the most common and usually the most painful finding in clients presenting with lumbar scoliotic cases of this nature, is unilateral multifidus fibrosis On the concave side and atrophy on the convex side. In chronic cases, the concave side will be exquisitely tender to the touch because of multifidus hypertrophy or erector spinae compartmental syndrome. Therapists often attribute these painful muscular conditions to myofascial trigger points, adhesions, or overuse syndromes. However, the protective muscle spasm will keep returning until the underlying facet joint in stability is corrected.

Unfortunately, many other structures are often responsible for the dysfunctions commonly found in clients presenting with idiopathic scoliosis. Due to apparent sacral base unleveling in Fig.1. p. 24, it is possible that either a right unilateral extended sacrum or a left unilateral Flexed sacrum may be the culprit. A right unilateral extended sacrum would manifest as left convex lumbar scoliosis, reduced lumbar lordosis, posterior right sacral base, short right lug, positive spring test as well as a positive seated flexion and stork test on the right.

However, if the owner of this spine presents with increased lumbar lordosis (negative spring test), positive left seated flexion test, deep left sacral base, and a long left leg then this dysfunctional scoliotic pattern may be the result of a left unilateral flexed sacrum. Ninety-five Percent of flexed sacrums are on the left and occasionally produce a scoliotic pattern that closely resembles the drawing in Fig. 1.

As Jeff mentioned, unilateral psoas contraction usually causes contra lateral vertebral rotation and ipsilateral side bending. Commonly seen in clients presenting with functional scoliosis is a counterbalancing dance between the iliopsoas and the quadrates. A familiar pattern has the right iliopsoas flexing the right ilium and the QL fighting back by extending and hip-hiking the left ilium. Left untreated, this condition can worsen.

Occasionally, when one psoas is shorter than the other, the result is pelvic “side-shift”. This occurs when the base of support (pelvis) is shifted laterally from the mid line. In an attempt to compensate for the flexed position of the upper lumbar spine, the QL and erectors contract, resulting in extension of the lumbosacral joint. A unilaterally extended lumbosacral joint is an extremely painful condition for those who have experienced it.

The client with this dysfunction commonly presents with flattened lumbar lordosis, with hyper extension of L5 on the sacrum. If the condition persists, the iIiolumbar Iigament will soon become a pain general or, because the pelvic side shift stretches the ligament on the side to which the pelvis has shifted. The looseness created in the iliolumbar ligament eventually loads to instability of the fifth Iumbar vertebra irritation of the sinovertebral nerve, and chronic hip/ back pain.

Rolfers should always he alert to this condition when a client presents with a unilaterally tight psoas with flattened lumbar lordosis. To correct the alignment problem, the therapist should first address the facet dysfunction in the upper lumbar area. This will relieve tension on the psoas and take pressure off the L5-S1 junction. Typically when most manual therapists observe clients presenting with painful, flattened lumbars, they immediately begin work in the lower lumbar area because that is where the client hurts. Unfortunately, Ibis airs is already unstable, and treatment here at this time only compounds the problem.

As Robert implies in his excellent article “Lecture Notes on P’soas and Adductors” , and in several other articles located on his equally sophisticated website (www.somatics.de) actions of the iliopsoas arc often unpredictable and bit -mechanically debatable. For example during standing, the iliopsoa, Muscles are always active, while the erectors should be silent.

We often observe a pattern in low back pain client, where they present with a slightly stooped posture. This stance renders the iliopsoas virtually inactive. An absence of iliopsoas activity means less load on the SI joint and therefore les pain in many clients presenting with lumbopelvic dysfunction. This forward trunk posture fires the erectors and, with the help of gravity. tends to move the sacrum into mutation. Tension release in the iliopsoas by way of a forward trunk posture correlates with lumbar lordosis reduction, which lessens the compressive forces through the pelvis and relieves low back pain in the client.

However, the opposite may also occur when the forward bent posture actually perpetuates SI pain, due to the relationship between the lumbar erectors and the long dorsal sacroiliac ligament. Because fibers of the erectors attach to this ligament, trunk flexion can slightly compress nr completely close-pack the sacroiliac joint unilaterally or bilaterally. If the SI joint is dysfunctional, local or referred pain patterns Seam appear.

Discussion of biomechanical laws of spinal motion specifically related to the scoliosis population is always debatable, and ultimately who really knows who is right? What we do know is that facilitated muscles create and inhibited muscles permit asymmetry in the skeletal system. But muscle imbalances alone do not create the alignment and pain problems we encounter in our daily practice’s joint fixations commonly found in facet, hip, and SI capsules possess the ability to facilitate specific muscles and inhibit others, often rendering myofascial techniques alone inadequate. In fact, any alternation in joint function caused by loss of joint play or capsular restriction will affect the muscles that cross the dysfunctional joint in either an inhibitory or facilitatory way.

Functional and degenerative lesions of joints are in principle the result not only of a pathological process in a joint, but also of altered function at the motor system as a whole. Due to their physiological properties the muscles, which represent the most labile link of the motor system, respond very early and distinctly in most clinical pictures of functional and degenerative joint disease. The muscular reaction, however, is not of the same quality in all muscles: muscles with predominantly postural function tighten whereas muscles with predominantly postural function tighten whereas muscles with predominantly phasic function weaken. In this way, not only a typical imbalance between these two muscular systems is produced” forming typical syndromes of muscular imbalance, but also even the alteration of the position and function of a particular joint Vice versa, altered joint function influences muscular function, thus producing a self-sustaining chain reaction. In this respect, the erect stance on two Iegs should not be considered as the typical human posture. Since the proper function of the motor system, is notion, posture” i.e., statics, should be derived front the most typical human movement, which is walking.

In order to understand the fine control of motion the separate activity of individual muscles is not of such importance as their coordinated activity within different movement patterns. This statement follows Dr. Rolf’s teachings and should be obvious to most Rolfing practitioners and movement teachers.

Therefore. proper understanding of this concept seems to be the best basis for rational treatment and good long term therapeutic results in the general population, as well as in those presenting with functional joint dysfunctions such as scoliosis.

Fortunately, we are blessed with dedicated teachers and practitioners working hard to incorporate this magnificent osteopathic model of spinal biomechanics and adapting it to the outstanding vision passed on by Dr. Rolf. Dialogue is what makes us grow and I applaud The Rolf Institute and its instructors for guiding us in this important path of continual evolution.

1. Freyette, H.H.: Principles of Osteopathic Technique. Indianapolis, Ind. (1918).

2. Structural scoliotic curves are fixed curves that do not reduce with side bending or rotation. This is usually due to remodeling of the spinal bones and discs (facet and disc tropism).

3. Class notes from American Low Back Conference, with Drs. Phillip Greenman & Vladimir Janda, 1992.

4. Beckworth, C.G.: “Vertebral mechanics”[,] in American Academy of Osteopathy Yearbook. Indianapolis, Ind. 1944.

5. Warmerdam, A.: International Federation of Orthopaedic Manipulative Therapists, 5th Conference, Vail, Co., 1992; pg. 204.

6. Hilton’s Law states: “Any nerve trunk that supplies the joint also innervates the muscles that cross the joint.”

7. Robert’s psoas test is valid but will probably produce more reliable results when applied to torsions of the cervical spine. Because of their tendinous attachments to the top three cervical TP’s, the levator scapulae and splenius cervicis commonly tug on the upper neck, creating what looks like a Type 1 group curve. Because rotation and side bending occur to the same side in the typical cervical complex (C2-7), this curve will usually straighten simply by releasing tension in these muscles by hyper extending the neck on the shoulders (provided the ipsilateral anterior scalenes are not also hypertonic).

Rotation in a spine is just what it says. It’s like a cork in a bottle that has been twisted around. Now imagine that the cork is stuck in a bottle with very thin elastic around both. That thin elastic is going to show a lot of strain. The only way you could turn that cork in that bottle without causing strain is if the cork is independent with no outer elastic. This cork (the spine) isn’t independent; it’s very much dependent. It’s in that outer skin called the superficial fascia. When the cork turns inside that superficial fascia, the superficial fascia shows strain.
Ida Rolf Talks about Rolfing and Physical Reality, p.185.

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