Clinical Questions

I’m curious what the reasoning is around maximizing hemi-90-90 position for pelvis patients. I’m certainly doing my best to engage in more hemi 90-90 positions for my pelvis patients but would love to wrap my head around the ways it particularly helps focus on the right pelvic mechanics.

The hemi 90-90 position maximizes the frontal plane of the pelvis in the inlet and outlet.

For example, in the Right Sidelying Supported Hemi 90-90 with FA IR, when the left knee is pressing into the towel roll you’re getting left femoral adduction which places the left obturator internus/iliococcygeus in a position to allow the left pelvic outlet to abduct. Then as the you get the left femur to IR, the left posterior inlet goes into IS ER allowing the anterior left pelvic INLET TO ADDUCT via the left iliacus. So, the left femur adducts, left outlet abducts, and left inlet ADDUCTS = desired frontal plane activity of the pelvis on the left.

And now let’s discuss an example of right pelvis frontal plane desired activity, with the Left Sidelying Supported Right Glute Max with Hip Extension and FA Abduction technique. The right femur abducts therefore the right outlet adducts (via inferior fibers of the right glute max) and the right inlet ABDUCTS (via superior fibers of the right glute max).   – Lori Thomsen, MPT, PRC

Is there a list of considerations regarding test findings, observations and treatment guidelines for those with left hand preference?

A couple of things that helped generate the question include:

  • I think I heard Ron say in a PRIVY episode that the Standing Lateral Shift Occlusal Test might remain positive in “left-handed” folks.
  • In the recent Human Evolution course, Ron made comments about case study subject “John” (page 120) to the effect that he wondered if he was left-handed. I think the observations included the proximity of the left hand and left hip when centering himself to initiate gait and the fact that he didn’t fall to the right during static left single leg balance despite a significant list.

Lateralization is an ongoing interest of mine and has been for years. There is so much I could comment and reflect on regarding handedness, (which is not a single phenomenon); there are degrees of handedness in different individuals for different activities and there are different footedness, earedness and eyedness as McGilchrist points out in his book ‘The Master and his Emissary’. As I said, I have probably not researched, nor read material on any other subject, more than material on limb dominance and lateralization, as related to functional or structural asymmetries of the primary cortex and descending pathways. So, I say this in earnest…handedness and other neural control patterning is usually traced to asymmetric neurodevelopment influences that occurred in the prenatal environment. Researchers like Previc, Bagesteiro, and McManus, and so many recent articles in Nature, have helped me understand the relationships of handedness to psychology and embryology.

11% of humans are considered broadly left-handed. And many are ambidextrous or do some activities with one hand and other activity with the other hand. The majority, or about 75% (of this 11 %) still have their speech centers in the left hemisphere and would appear to follow the standard definition of “left-handed”. 5% of the population overall who are known not to lateralize for speech in the left hemisphere, have a simple inversion of the hemispheres. They would have to read ‘right’ to ‘left and ‘left’ to ‘right’. What normally happens in the right hemisphere is happening in the left and vice versa. Small number of people.

A subset of left handers, as well as some people with other conditions, irrespective of handedness, such as probably schizophrenia and dyslexia individuals, those with some forms of autism, Aspergers, savant conditions, etc. may have a partial inversion, leading to brain functions being lateralized in unconventional combinations. For them, the normal partitioning of motor and sensory function breaks down, and making sense of conscious and non-conscious thought and delivery can be challenging. This may confer special benefits, or lead to disadvantages and confusion, in carrying out of different activities, as McGilchrist points out.

I believe, after much thought and understanding of multi-theorists, that left handers (as well as other people with non-standard lateralization) are living with the abilities to pattern activities like painting, running, talking, planning, etc. etc. with bilateral parts of each cortical hemisphere that either make their world of decision making and behavior, less or more challenging when asked to use one arm, one leg, one eye, etc. They are all less alike than those who are “standardized” and fall into the 89% norm of being left cortically dominant and consistently operating with the left cerebral hemisphere integrating right-sidedness, right handedess/footedness, speech production and language processing into successful expression and confidence. This is theoretically, why for me, that ‘normal’ PRI testing results will reflect this 89%, but not necessarily the 11% of unconventional cerebral processing. Left-handed people are not necessarily right hemispheric dominant nor left hemispheric dominant. They have neuro tendencies for both, or either one, depending on the processes used for consistency or creativity.

Therefore, in the Standing Lateral Shift Occlusal Test, a ‘left handed person’ might not follow conventional cerebral hemispheric organization, and the management of mass and environmental forces are possibly patterned in organization that requires dissociation from other vestibular processes that are typically witnessed in the 89% of those who depend on the left cerebral hemisphere for postural organization and conventional sensory combinations to empower the right thoracic diaphragm. Some of the most creative, broad thinking, artistic, organized leaders also may have challenging moments with expression, dyslexic behavior, and concepts that are confusing to the listener, but not to the deliverer. The accuracy of the discussion usually is higher in the deliverer. These same people usually will not fall, even when they have a significant list. Their asymmetrical behavior is so engrained by gravity, that they appear, look and demonstrate more of an unstable method to offset gravity or force demands, but their tensegrity is more stable overall than someone who was just repositioned with a 90-90 left hemibridge activity.     – Ron Hruska, MPA, PT

What are some PRI considerations for a practitioner treating a patient with situs inversus? I have a patient who is a mirror twin diagnosed with situs inversus, confirmed by MRI.  He presented with hip impingement type symptoms – difficulty bending forward in a sitting position to put his socks on in the morning due to radiating pain from the right groin down the front of the right thigh to the knee.

I have only worked with 2 individuals with situs inversus that had issues that made them seek attention from me. Honestly, I cannot remember the reason or reasons why they sought treatment from me. But, I do remember that I treated them by balancing their chest wall expansion, using PRI techniques that may have to be reversed for the establishment of air flow into the lungs. Cortically, they still have the same brain that a non situs individual has, which is why you still have to go after AFIR on the left,  ground them on the left at the floor, hip, and scapula thoracic region.    
Specific advice would depend on the individual. But, the bottom line is, the more the practitioner can do to expand and open up the posterior chest wall and lower back, through wall reaches, 90-90 hip lifts with a balloon, the better chances of reducing their symptoms and restoring trunk and hip rotation. I would start some overhead pulley work and lat hangs, if tolerated. Lateral intercostal wall opening with a Swiss ball next to a wall that could be repeated on both sides as a balloon is blown up would also be recommended. 

Remember that their left brain will still want the body it owns, to go to the right, stand more on the right, sit more on the right and adapt with sensory processes that bias the left Wernicke and Broca regions.
– Ron Hruska, MPA, PT

Why is the right hip (femur) in the non-compensatory skeleton sheet in ER, and on the compensatory skeleton sheet it is in IR?

That’s a good question, and honestly we get it quite a bit.  I’ll do my best to explain it, and it may be helpful to have your PRI Myokinematic Restoration manual handy during this explanation.  

As we discuss early in the Myokinematic Restoration course, the Left AIC pattern has a direct influence on the pelvis and its orientation.  If you look at page 2, you’ll see two pictures of a pelvis in the L AIC pattern.  Page 2 is a picture of the L AIC pattern in a vacuum, without the influence of the leg muscles or ground reaction form (GRF).  These pictures depict what happens to the pelvis and femurs because of the unavoidable influence of human asymmetry before the body attempts to walk or perform any other upright, WB task.  As a result, page 2 is a picture of the non-compensatory L AIC pattern.  When I am teaching the Myokinematics course, I’ll ask the attendees to write at the top of page 2 "Page 6" and "Non-Compensatory Skeleton Sheet".  Similarly, I ask the attendees to follow suit for page 6 and the non-compensatory skeleton sheet.

The reason the R femur orients into ER and the L femur into IR in this non-compensated version of the L AIC pattern is the result of osteokinematic roll and glide.  In a vacuum, without the influence of leg muscles or GRF, when the L pelvis is moved into an position of AF ER, the roll and glide mechanics of the acetabulum on the femur direct the femur into a position of IR.  Similarly, when the R pelvis is moved into a position of AF IR, the acetabulum directs the R femur into a position of ER.  These femur positions are due to the position of the L and R acetabulums, which are being influenced by the components of the L AIC pattern.  It’s purely a joint mechanic concept.   

This concept helps explain why PRI assesses passive hip rotation in a seated position.  Yes, seated hip rotation allows for better iliofemoral and ischiofemoral assessment (page 14).  But seated hip rotation is also a position where these same non-compensatory roll and glide rules apply.  When someone is sitting on a table without their feet touching the floor to remove GRF, and they are sitting in the L AIC pattern determined by other PRI tests, the R femur should be restricted in ER and the L femur should be restricted in IR (page 38).  Due to the sitting position resulting in a passive test without GRF, the R femur is sitting on the table already in a position of ER and the L femur is sitting on the table in a position of IR because of the position of the acetabulum and their influence on the femoral head.  As a result, when testing PROM ER of a R femur that is already positioned in ER, the amount of passive FA ER will appear to be restricted. Similarly, the L femur will appear to be restricted in FA IR in the L AIC pattern because its position on the table prior to PROM testing is one of IR.  This limitation in PROM is influenced by the position of the acetabulums due to roll and glide mechanics.  As a result, stretching someone who has a restriction in PROM will be generally unsuccessful and potentially harmful if the clinician has not helped the patient or client achieve pelvis and acetabulum neutrality first.  

Compensation is a product of upright and WB activity due to GRF, proprioception, VOR, and a perceived sense of compression or decompression in the body, among other things.  The main concept to remember is that compensation occurs when upright and WB.  When the L AIC or B PEC patterned human is upright and WB against gravity, the previously mentioned factors have the potential to influence body movement strategies.  Compensation is the likely result.  Compensation isn’t necessarily bad, unless the body is unable to get out of the compensatory patterned behavior.  One of the more common compensatory strategies as a result of the L AIC pattern is femoral rotation.  

During swing phase, the pelvis moves into AF ER, and roll and glide mechanics dictate that the femur should move into IR.  However, due to GRF, forward locomotor movement, respiration, compression sence, etc…the femur appropriately chooses to compensate into FA ER.  This is a quality decision as FA ER during swing phase allows for proper feedforward neuromechanics and gives the body an opportunity to perform heel strike correctly.  At the same time, the femur on the other side is in stance phase, and is being rotated upon by the pelvis above it.  During stance phase, the pelvis is moving into AF IR as the body’s COM is laterally shifting on top of that femoral head because the other leg is in swing phase.  These factors result in an obligated position of FA IR of the stance femur because the pelvis and acetabulum are moving into IR while the femur is fixed and stationary due to stance phase.

Page 4 in the Myokinematic manual is an artist’s rendering of what the pelvis and femurs are doing during WB activities with the addition of GRF and muscle activity.  As you’ll note, the femurs on page 4 are different compared to the femurs on page 2.  I ask the attendees to write "Compensatory Skeleton Sheet" and "Bottom Figure on Page 7" on page 4, and follow suit on page 7 and the compensatory skeleton sheet.  All three of those pages represent femoral activity while the pelvis is in the L AIC pattern once upright and WB activity is taken into consideration due to the addition of GRF, muscle activity, VOR, compression, etc…

The main difference between page 2/page 6/non-compensatory skeleton sheet and page 4/bottom of page 7/compensatory skeleton sheet is the influence of gravity when undertaking WB tasks, and the orientation the body is going, straight ahead (not to the right) for Forward Locomotor Movement.  Once the body is upright and must contend with gravity, normal roll and glide rules are temporarily "bent" to achieve accurate, non-patterned, and therefore non-destructive movement strategies, provided the body knows how to move through neutral from one pattern to another.  A great example of that is when the body can alternate between L AIC/R BC and R AIC/L BC patterns during walking and breathing.  The body’s "bending" of normal roll and glide rules is called compensation, and is not a problem because the body is efficient and is not locked into a single movement strategy.  However, if the body is locked into a single pattern of movement, such as the L AIC/R BC pattern, during all activities including walking, standing, stairs, squatting, running, athletic events, etc…pathological compensation is the likely result.  Soft tissue is required to pay a steep price in the absence of correct alternating movement strategies.  In the Myokinematic course, we discuss the instability commonly found in the L iliofemoral and pubofemoral ligaments, which is an example of pathological compensation.  
The overwhelming majority of the time, your patients or clients will present as a "page 4/page 7/compensatory skeleton sheet human" because of the influence of gravity.  Once gravity is removed, such as during seated passive hip ROM, normal roll and glide rules apply, which is when page 2/page 6/non-compensatory skeleton sheet mechanics will apply.  It’s rare to see someone walk into your facility with a presentation similar to the non-compensatory skeleton sheet.  I believe that those humans probably do exist, but I have not had the pleasure of working with one in my PRI career to this point. 

Dan Houglum, MSPT, ATC/L, PRC

One of the great questions that I have been asked is the reasoning for some of the differences between the PRI L AIC, R BC, and R TMCC patterns from the Common Compensatory Pattern (CCP). In this article, there seems to be a slightly different attitude with respect to the right side of the hemipelvis and the convexity of the right lumbar spine. I’ll share a quote below outlining this difference.
"Other findings associated with the anatomical short right leg include a pronated left foot with a supinated right, an anteriorly rotated right innominate, and a posteriorly rotated left innominate. Functional rotoscoliosis is also observed with a lumbar convexity to the right, thoracic convexity to the left and cervical convexity to the right."

It seems as though the way Pope has describes this CCP phenomenon is with a left ASIS and hemipelvis that is higher than the right with a shortened and concave left lumbar spine. I would be so curious to hear the stance of the institute on this subject.

I appreciate your question regarding Zink’s and Pope’s thoughts and findings about leg length and innominate positions. There are so many juxtapositional discussions in this article. Although I believe the majority of it I can personally make sense of, I cannot follow their explanation of the lumbosacral junction discussion. Without getting into details regarding Denslow and Chace, and Mitchell findings, I want to remind every reader of this article, that when the left innominate anteriorly rotates and the right innominate posteriorly rotates, the sacrum (right rotation of sacrum on a right oblique axis) directs the entire column to the right through the sacral promontory base the spine sits on. Both femurs are also directed to the right, and the right leg needs to rotate inwardly (adduct) as the tibia also compensates into supination as weight of the body is dispersed over to the right side. Often the left internally positioned femur will be rotated out or externally to compensate for both top down and bottom up neurologic patterning of this lateralized displacement of body weight and function. This compensatory activity on the left often lends to a longer leg on the left because of femoral head outward and forward translation on an innominate or acetabulum that is anteriorly positioned when you lay someone with this orientation in supine.    

There are so many possibilities on what “they” see or perceive from an osteopath perspective, that may or may not correspond to what is actually true or not to neurological function from the top down. Although I agree with figure 22 regarding the feet, I do not believe there is a majority of people with this compensatory (left on left OA axis) pattern that is “commonly seen” with “an associated supinated foot on the right” because of a “left on left” patterned sacrum; when in actuality if you look at the soft tissue ligaments, and the frontal plane, like we objectively do in the Myokinematic Restoration course you will find there is no short leg issue on the right as much as there is a long left LE. The left LE more than likely is externally rotated forward, in the inwardly or medially directed oriented acetabulum that could contribute to the left femur appearing longer as it translates out of an acetabulum that is pulling the femur slightly up because of right on right axis positioned sacrum; with an innominate on the left that is anterior to the one on the other side. But because of a number of factors associated with supine or standing testing, subjective measurements (palpation) do not reflect the ligamentous muscle that is limiting or providing the appearance of a longer leg on the right, and thus comparatively a shorter leg on the left. The same would be true regarding convexity and concavity of the spine… Supine? Or standing?    

I do know this, there are many researchers, especially of the sacral iliac joint that would whole heartedly disagree with both Zink, Pope, me and others. “Compensation” and “Orientation” are two very different words and worlds. I try to do everything I can to clarify what is doing what for compensation of a directed and positioned pattern because of cortical, visuo-spatial, binaural echolocation and dental occlusion. There is no “common compensatory pattern” that multidisciplinary researchers will ever agree with in total. Although there are many things I agree with in this article, there are MANY that I don’t agree with. I hope you can respect me for who I am and not who I agree or disagree with.  

I would like to cover more, in detail, “Other findings associated with the anatomical short right leg …" but quite honestly it really will not help the student who is interested in compensation as a result of the “Common Orientation Pattern” as it relates to the human asymmetrical respiratory AND hemi-cortical asymmetrical pattern. Compensation will always follow orientation, and trying to make sense out of someone else’s lexicon and perspective is difficult at best. I have been asked about this article more than any other article on the internet, and although will often refer to it for Janda, Greenman, Zink, references, the fetal growth, fascial bias, etc. I don’t believe there is a predominance of asymmetric leg growth as depicted, nor do I believe figure 28 (short right leg structural findings) is accurate. The most common finding of the thoracic curve in those with “common scoliosis” is convexity, not concavity on the right, and concavity not convexity at the thoracic lumbar curve, reflecting the L AIC and R BC pattern I reference in this Institute. Supported by many multidisciplinary evidence based studies. The osteopathic field is wonderful, but it is not universal.

Ron Hruska, MPA, PT

Could you explain to me why quad function could be lost on either side as a result of a left AIC or PEC and how re-establishing a neutral zone of transition can allow us to regain quad girth and function? I recognize it has to do with general length-tension dynamics, but could you specifically explain why positionally the quad is at a disadvantage in the above patterns?

In the L AIC pattern, the L pelvis is in a position of flexion, abduction, and external rotation. The sagittal position of flexion (anteriorly tipped pelvis) is the problem for the quad. This position places the L quad in a passively shortened state. As a result, the rectus femoris becomes hyperactive during inappropriate times, such as heel strike and mid stance.

The L vastus intermedius is asked to contract all the time because the position of the pelvis inhibits the hamstring (because it’s now too long) and gluteus maximus (because it’s now too short). In the interest of not falling over, the vastus intermedius is asked to work with the rectus femoris to pull the COM forward as the hip extensor group is lost.  

The L vastus lateralis becomes leveraged as the "accidental gluteus complex" to attempt to generate some frontal plane activity, but it is a poor femoral rotator and abductor. Since the body has no choice, the vastus lateralis is overworked to perform the incorrect jobs of FA IR and FA ABD.

Essentially, the entire quad group is in a shortened state and is overworked. The hamstring, gluteus max, anterior gluteus medius, piriformis, adductors, and deep rotators of the hip are effectively inactive due to either being habitually too long or too short. Unless the pelvis is able to move from the position of AF ER into AF IR to alter these length-tension relationships, the quads are the only muscles of the thigh that can work, so they become overworked. The result of this forced hyperactivity of the quads can result in what appears to be weak quads; the quads aren’t weak, they are overworked and get fatigued and need a break.

If the pelvis is able to be moved into AF IR (extension, adduction, and internal rotation) the quad muscles are now in a lengthened state, and they will need to be re-trained to learn how to work in conjunction with a fully functional hamstring, gluteus complex, and adductor group from a lengthened state. That’s why many people appear to have weak quads after they have been repositioned. The quads literally have not been asked to work from a lengthened state with other leg muscles contributing properly in a long time.

Personally, I don’t really pay attention to quad girth because you can get a lot of girth that is phony. Just because someone has a large thigh circumference doesn’t mean they know how to use it, or are using is properly. I’m much more interested in function than muscle girth because of how easy it is for a muscle to become hypertrophied while either performing the wrong job, or the correct job at the wrong time with the wrong co-workers.  

I want to make sure I have this right for the right quad. In a L AIC, it appears weak because it is in a positionally lengthened state at the rectus femoris and sartorius and does not know how to contract and coordinate from a shortened position. Or would you expect to see more of a hypertrophied quad on the left with an actually normal right quad? Could you please clarify this for me?

Yes, the right quad is in a lengthened state and is perpetually asked to contract from a lengthened state. Any muscle that is consistently asked to contract without the muscle actually getting shorter at the proximal attachment site can appear to be weak just because of its position. In the L AIC pattern, the muscles on the R side that are accessible are early to mid stance muscles, and the muscles for late stance and push off are less accessible because of the lack of pelvic movement.  

Once again, I don’t really look at quad hypertrophy because from my experience, it’s not an accurate reflection of function. However, due to the L AIC/R BC and their influence on our COM, we are likely to spend more time on the R leg as a general statement. That alone can cause any muscle to become hypertrophied on the R side. It doesn’t mean the muscle is functionally superior or better at its job; it’s merely because our COM is positioned on top of our R calcaneus. If I do happen to note that the R thigh is bigger, my goal is not to make the L thigh as big as the R one. My goal is to improve the functional performance of the entire R and L side so they work together as teammates for walking and breathing.  

Personally, I’m not sure you can assign hypertrophied muscles as a clinical assessment of the AIC or BC patterns. Which muscle the brain decides to use as its best option to move the body through space incorrectly and with compensation varies person to person. I can’t tell you in the L AIC pattern you will see a larger L quad or a larger R quad because it varies person to person.  

If there is one thing I have learned over the course of nearly 20 years in PRI is to never trust your eyes. The tests don’t lie; your eyes do. If anyone is attempting to assess patterned behavior based on what they see or palpate, their assessment will be incorrect the overwhelming majority of the time. The most common question I get is some version of "how do I get better at PRI?" My answer is to get better at performing and interpreting the tests. They tell you everything you need to know and how to proceed with any client or patient.  

The people who struggle with the application of PRI concepts often rely on what their eyes and fingers tell them. I’m sorry, but our eyes and palpation skills are not accurate enough to determine the neuromechanical influence that patterned respiration has on our musculoskeletal system. Thanks for the great questions!

Dan Houglum

On the Postural Respiration post-test regarding right lower trap function, I can see retaction of the scapula and rotation of the lower spine to the left, but I can’t see how it assists upper trunk rotation to the right. Can you clarify action of the right lower trap for me?

This is a question that comes up fairly often, and this discussion and response turned into a little white paper by Dr. Robert "Skip" George. CLICK HERE to read more about this!

Question: If a patient is looking like a Superior T4 syndrome having more restricted left apical expansion after a Superior T4 manual technique, I would attempt to clear this with right subclavius manual technique and then have them do a left low trap and left serratus anterior program. My question is if anyone can explain why the non-manual techniques for this program in the course manual, namely Supine Weighted Punch with Right Apical Expansion and Seated Resisted Serratus Punch with Left Hamstrings both show the subject doing a RIGHT serratus punch??
(*This question came up on the PRI Google group, and we loved the dialogue and response, so we have posted it here for others to learn from as well.)

This is a common question, and to be fair, it does seem counter-intuitive. Louise Kelley and I, along with Skip George, have had several conversations with Ron about this question, and we hope our explanation is helpful. My apologies that it has taken us a couple of days to get this to you, but we wanted to make sure we answered your questions.
Just so we are all on the same page, a Superior T4 syndrome shows up as a compensatory respiration strategy because the body realizes that there isn’t enough air getting into the body by inflating the L lung alone. The respiratory demand exceeds what can be drawn into the already expanded L lung. As a result, the body attempts to open the R apical region in the interest of seeing if air will find its way into that region, thus assisting with air flow. The problem is that the center of mass remains lateralized to the R, so the elevated R upper rib cage can’t accept air. As long as the COM remains lateralized R, and we don’t have a L ZOA, that open R apical chamber is a non-usable region of respiration. Over time, the overactive accessory muscles become shortened, causing a loss of reciprocal rotation of the upper ribs and alternating apical expansion and compression.
We want the upper four ribs on the R to ER with respiration and a L ZOA. But at this point, they don’t know how to do any of that because the R clavicle and R 1st rib are glued together. The right subclavius becomes very tonic because of the elevated position of the 1st rib to the clavicle. The subclavius inhibition technique is designed to get the clavicle and first rib to separate and allow the top four ribs to move in unison into IR with the lower ribs. Subsequently, we can institute proper breathing mechanics via proper group function rib mechanics on the R and L side.
After the R subclavius release, it’s time to get all the ribs on the R side to ER correctly, and all the ribs on the L side to IR correctly, with the COM shifted to the L. This is why most of the initial non-manual activities in the L low trap/serratus section involve a R arm reach. We need the serratus to ER the rib cage, but the overwhelming big deal is we need the R serratus to push the center of mass to the L.  
Following the R subclavius technique, we begin with a R arm reach because:
We want to promote universal R rib cage ER. Think of the R serratus as like a sideways diaphragm on the lateral rib cage. When it contracts and flattens, it pushes the center of mass to the L side with some R rib cage ER. This is assisted by the R low trap as it rotates the spine below T8 to the L.  
As an aside, just a piece of clinical advice: when you have them reach with their R arm, make sure their hand is above their head. This brings in some R upper trap to help elevate the scapula and clavicle correctly, allowing the upper 4 ribs to properly and freely elevate. Also, if the R scapulae isn’t higher than the L, you aren’t really on your L side.  
This activity of the R serratus puts them into the L side of their body, properly positioning the frontal plane L lower trap and the sagittal plane L serratus to perform L thoracic abduction and L rib retraction to assist in the maintenance of the L ZOA, while the COM is lateralized to the L. The action of the L low tap, L serratus, and R serratus are all concentric in nature.
Upon inhalation, the right ribs will now ER, in unison, to assist with filling of right lung regions – apical and lateral – with air.
In that R arm reach/L ZOA position, every inhale is R upper trunk rotation and L low trap/L serratus activation, which is driven by respiration. The reason that the R arm reach/L ZOA position is R upper trunk rotation during inhalation: in that position, the L ZOA will promote air flow into the R lung. When air arrives into the R lung, the R rib cage must ER. This L rib cage IR and R rib cage ER is R upper trunk rotation from a neuromechanical/respiratory point of view.
As you’ll note, the later exercises in the L low trap/L serratus section will have L arm reaching. This is to engrain the concept of "delay" so the COM stays lateralized to the L a bit longer, and the L arm understands how to reach up and forward without L rib cage ER. We then reverse and reach with the left arm to rotate the spine and rib cage to the right while maintaining a left ZOA and COM to the left.  We cue our patients to expand the left posterior ribs, or move the left ribs back, with each inhale. This is left serratus anterior activity. The left lower trap stabilizes the spine in right trunk rotation and assists with maintaining a left ZOA with L thoracic abduction. Now, the L diaphragm is able to move air into the left posterior lung and right apical lung region during right trunk rotation, without losing left rib IR.
This is what cements the references of the L heel, L anterior hip, L ischial tuberosity, L PME, L ab wall, R scapula/lateral rib cage, and R suboccipital region.  As a result, this is compression of the L side of the body, and decompression of the R side of the body.  
We hope this helps to better understand why the Right arm reach is included in the Left low trap/Left serratus program, and why the Right arm reach precedes the Left.

Dan Houglum, MSPT, ATC/L, PRC and Louise Kelley, DPT, PRC

Further contribution to this discussion by Michael Mullin, PTA, ATC, PRC:

Dan Houglum and Louise Kelley, you are fantastic. This is an incredibly helpful explanation for everyone….

While being hesitant to try and supplement in any way, I might also offer that the manual Sibson’s fascia technique is very helpful and I use it after I perform the subclavius technique. I teach a self manual technique as well. It helps keep that pesky tissue from trying to continue to yank things from both attachments.

From an anatomical perspective, it’s important to remember that the apex of the lungs extend up above the level of the clavicle. It is trying so hard to expand on that right side that it will find any "space" it can find to try and open things up.  And when a system is right anchored, it will stretch out wherever possible to try and breathe.  

The Institute’s algorithm is excellent and Dan and Louise’s explanation should be carefully reviewed–a couple times–so you can fully appreciate what they are saying.

Response by Dan Houglum: 

I appreciate your kind words. We debated about talking about Sibson’s fascia in our email. But since you brought it up…..

While I don’t disagree that the fascia can be a problem, I would be cautious about doing a Sibson’s release on every patient on whom you perform a subclavius release, mainly because not everyone’s Sibson’s fascia requires releasing. I don’t want to put words in your mouth, but I don’t believe you’re saying to automatically do a Sibson’s release on everyone every time. But I just wanted to clarify so there is no misinterpretation.    

If the fascia doesn’t require releasing, and that manual release is performed, you run the risk of inducing neural tension and scalene over-stretching. Remember, we need the scalenes to elevate the ribs properly. We don’t want to over-inhibit them unnecessarily. The Sibson’s release is great after you’ve done some R UE reaching (which quiets the anterolateral neck muscles anyway) and you’re transitioning to L UE reaching, but they just don’t seem to be able to perform R scapular retraction. Or, they perform R shoulder extension instead of R scapular retraction. Or, they just don’t seem to be getting off their R leg because their head is still centered over the R leg. Or, their R HG IR just isn’t cleaning up, but everything else is. I’d also suggest performing Sibson’s release in conjunction with L pec inhibition because tightness in both of those structures will inhibit the rhomboids on the R, causing difficulty in performing R scapular retraction and R upper trunk rotation while staying lateralized to the Left.   

I couldn’t agree more with your email, and particularly your statement that it’s hard to inhale into the R apical lung cupula if there is no room. I only wanted to chime in purely in the interest of clarification. Observing the vascular and neural anatomy related to Sibson’s fascia and the neurological reasons for that fascia becoming tight in the first place are important things to consider before performing a Sibson’s release.   

Question: What is the difference between the posterior mediastinum and the posterior left lung & rib cage and why do we strive to expand it?

We define the posterior mediastinum as the area in the thorax that provides positional support for organs, vessels, and nerves from T4 to T12. Its boundaries are: the pericardium anteriorly; the diaphragm inferiorly; the transverse thoracic plane “T4” superiorly; the vertebral column posteriorly; and the pleura laterally. The posterior mediastinum, therefore, is an area between the right and left lungs. This area is more closed and anteriorly positioned on the left vs. right in a right BC pattern and closed bilaterally in a B PEC pattern. The challenge is this: because it can’t be sensed or felt, how does one accomplish expansion of the posterior mediastinum, especially on the left? The short answer is through expansion of the left posterior lung and rib cage, which we assign as a reference, or sensorium, in many of our non-manual techniques.

Posterior mediastinum expansion first requires activation of L IOs/TAs to establish a left ZOA to: IR the left ribs in front and ER the left ribs in the back and to improve the respiratory role of the left diaphragm. This emphasis better biases air flow into the left posterior lung and better expands the left posterior rib cage. Furthermore, through costo-vertebral coupling, the thoracic vertebrae will be directed more to the right (transverse plane) and posterior (sagittal plane), therefore re-establishing a normal thoracic kyphosis and creating more posterior mediastinum expandability and, thus, allowance for the posterior lung to move and migrate into. This expandability of the posterior mediastinum’s ribcage, and increase in potential room for lung inflation, allows the left posterior lung to alternately inflate and deflate into the more expansive posterior mediastinum area. The alternating compression-decompression provided by the left posterior lung into and out of this expanded space keeps the vessels of the “main highway” (sympathetic trunk, esophagus, circulatory and lymph vessels) more viable. These vessels thrive on this oscillatory compression-decompression for their health and function.

Louise Kelley, DPT, PRC and Dan Houglum, MSPT, ATC/L, PRC

Question: For a few years I have questioned bilateral hip external rotation limitation and restricted left hip external rotation. I have seen the limitation primarily in a PEC pattern and L AIC, which can be contributed to pelvic alignment, however, my question remains how to improve left hip external rotation after bilateral negative ADT. I have sent patient’s for MRIs with negative results for pathologies.

Lack of L FA ER, particularly after repositioning, can be tricky. It doesn’t happen often, and there are a few different reasons for it. So I thought I’d add my two cents, and hopefully I can shed some light on the topic. 

How the body attains a reduction in L FA ER and R FA ER are can occur similarly, but often they don’t occur for the same reason. However, it’s not usually due to anterior hip capsule pathology. The iliofemoral ligament is designed to limit FA ER. So if FA ER is limited, it’s probably not due to a hyper-lengthening of the ligament designed to limit that motion. And in a PEC patterned individual, you may see a decrease in FA ER, but not normally. In a PEC patterned individual, you’d normally see a reduction of FA IR, and normal range of FA ER.  

Often you’ll see an abundance of FA IR in an individual with a pathologically unstable anterior hip ( + ADT and – EDT) usually in the patho PEC pelvis individual, or an exceptionally unstable hip capsule in the L AIC presentation. In that instance, the femoral head has essentially moved so far anteriorly because the iliofemoral ligament isn’t available to stop it. The result is a hyper-lengthened iliofemoral ligament that presents with an excessive amount of FA IR, as well as FA ER. In order for the ischiofemoral ligament to become pathologically long and unstable, the femoral head would have to be properly seated (intact anterior hip ligaments) and weight bearing tasks would have to be in a position of AF ER and excessive FA IR for an extended period of time. That would be someone who is walking in a non-compensatory gait pattern. Their femur has not compensated into FA ER during swing phase. It happens, but is very rare. 

Mechanically speaking, a reduction in seated R FA ER is usually seen in a pelvic position of AF IR, specifically, pelvic inlet adduction and ipsilateral thoracic abduction. If it is seen in a patient after repositioning, it’s usually indicative of a posterior pelvic inlet issue that requires inhibition, or the inferior gluteus maximus requires inhibition, but probably both. And in both instances, improved contralateral posterior mediastinum expansion is a must.  

However, in this particular scenario, we have a reduction of L FA ER. Even if this particular patient presented as a L AIC with an unstable anterior L hip ( + ADT and – EDT), or as a non-patho PEC pelvis with an unstable anterior L hip, the laxity of the anterior hip capsule is not going to limit FA ER. Similarly, pathological tightness of the L ischiofemoral ligament, or really anything in the posterior pelvic outlet, is not going to cause a lack of L FA ER because all of those structures either promote or permit FA ER. Posterior capsule tightness will cause a limitation in FA IR, not FA ER. There are absolutely instances in which an excessively unstable anterior hip requires posterior capsule inhibition in order to properly seat the femoral head into the posterior hip socket to ensure proper transverse plane mechanics. And in those instances, you will need to perform AF IR while in FA IR. And that is where the Pelvis Ascension Drop Test becomes valuable. But even then, FA ER is probably not going to be limited.   

James, Jesse, and I have talked about this event on numerous occasions, and 90+% of the time when L FA ER is limited after repositioning it’s because the L anterior pelvic inlet needs to be inhibited. One good cue is most of the time, they can’t shut off their L quad, or their L quad is much more active than it ought to be when performing L hamstring, L IC adductor, L thoracic adduction, L ZOA, or L serratus activities. All of which causes a problem with the L pelvic anterior inlet.  

Couple of testing items I would consider. My hunch is currently this individual has less than a 3/5 on their L Hruska ADDuction Lift test. Their L Hruska ABDuction Lift test is probably less than a 3/5 as well, but it might be a 3/5 or 4/5. My hunch is this patient probably had Superior T4 Syndrome upon initial evaluation, and very well still might. And it wouldn’t surprise me if they had a B TMCC presentation upon initial evaluation as well. Regardless if this patient’s initial presentation was PEC, patho pelvis PEC, or very unstable L anterior hip L AIC, they are not going to know how to perform L swing phase properly because their L quad will prohibit it. Other phases of gait will clearly be limited as well. But specific to this particular question, L FA ER is a push off/swing phase issue. Just because the dominant neuromechanical pattern is L AIC/R BC/R TMCC doesn’t mean they actually know how to appropriately get into and perform the L AIC/R BC/R TMCC pattern correctly, particularly after getting them neutral, and particularly after a R AIC/L BC/L TMCC pattern activity.  

Here’s a few suggestions that have worked for me. First, consult the L pelvic anterior inlet inhibition section of your Pelvis Restoration manual, or the PRI Non-Manual CD, if you have it. I would consider taking some of the standard PRI right gluteus max activities and flipping them around to do them on for the left gluteus max (as this is more of an orthopedic issue). For example, from the Myokinematic Restoration CD, Supine R Gluteus Max 1, Sidelying R Gluteus Max 10, 14 (with or without the band), or 15. I would consider flipping all of those over and work on L AF ER/FA ER so they can perceive L gluteus max activity, but don’t spend a lot of time on those activities. The other thing I would consider is an Infraclavicular Pump PRI Manual Technique. Make sure you’ve done some kind of L AIC Manual Technique first and make sure they have attained a quality L ZOA before doing the IC Pump. Consider Seated Integration 36 and/or 39. They need to learn how to alternate their rib cage and pelvis frontal plane mechanics, particularly their pelvic inlet. I would also consider Sidelying L Gluteus Medius 32 because they have to use R and L obliques (in a different manner) to stay on the wall, L gluteus max for AF ER, L hamstring for hip extension during knee extension without L quad dominance, and L posterior gluteus medius for FA ER because the femur is in FA IR. And I would consider Standing Integration 55 to ensure they understand how to perform L AIC/R BC properly. Obviously, you’ll probably want to follow that up with Standing Integration 53 or 56. 

I think the L pelvic anterior inlet inhibition section is tricky. The real trick with L pelvic anterior inlet inhibition is the make sure the left quad/rectus femoris/vastus lateralis doesn’t take over. As you’ll notice in the inhibition section, all the activities are regular, normal stuff. The key is to make sure the individual can do any of those tasks without use of their left quad. Some of them are harder than others, but I’d focus on the standing ones. Pick one or two standing ones, and make sure they are using their L IC adductor, anterior gluteus medius, hamstring, and obliques. If they are using their quad in a dominant fashion, they have an anterior inlet problem.  

Yes, the PRI left standing tasks instructions say something like "feel the anterior thigh." While they should feel the L quad, it should be the 4th most dominant muscle they feel working. If it is a strong #1, they have an inlet issue. And here’s a little secret about decreased FA ER, particularly after repositioning: it’s an inlet problem; R posterior inlet or L anterior inlet.  

Once they have figured out how to not use their left quad during L stance tasks (which is anterior inlet inhibition), you can then go through the process of getting into L AF ER/FA ER. But if their L quad is on during mid stance, it will be on too much during late stance, push off, and swing, thus preventing FA ER. Gotta start with L AF IR/FA IR, but this issue has literally nothing to do with the hip capsule. Need to inhibit the L quad during AF IR/FA IR, so you can perform AF ER/FA ER well.  

After you can perform L AF IR/FA IR without the quad dominating, then make sure you can perform L AF ER/FA ER with the gluteus max, and not the quad. That’s where you I would suggest flipping some of the regular R gluteus max activities. Then work on some rib cage and pelvis alternation, L FA ABD (sidelying L gluteus medius #32 is a gold mine), L AIC/R BC activities and R AIC/L BC for alternating reciprocal tasks. But the initial process of making sure you can have them do WB tasks without use of the L quad is the important first step to get them to learn how to go from L mid stance to L swing without quad dominance.  

Hopefully, I was able to clear things up a bit. Additionally, the lack of L FA ER is a topic that we don’t usually have the opportunity to talk about or explain very often, mainly because it doesn’t happen as often as other FA or AF issues. But, the L pelvic anterior inlet inhibition section is in the manual and discussed during the Pelvis Restoration course, so it should give you a pretty good head start.  

Dan Houglum

I know this is a broad question but was wondering what you all feel contributes most to tight left scalenes and upper trap. Would this be from poor ZOA and left abs, or would you maybe see this more with pathological patients?

Whenever I hear patients complain of left upper trapezius tightness, I think of their possible limitation of right hip abduction, either passively or actively. They are attempting to pull more into right thoracic abduction with their right lateral abdominal and lateral intercostals, and in the process of doing so compensate and integrate with their left upper traps to help “pull” the head over to the left, in addition to their entire upper thorax. So these patients lack frontal plane alternation with appropriate abdominals. Whenever I hear patients complain of or feel left scalene tightness, I think of a Superior T4 Syndrome pattern of respiration, where they are having difficulty getting air into their left apex because of left upper three ribs being in a state of internal rotation and their inability to expand the left upper apical lung region requires the left scalenes to help “pull” air into this region. The failed attempt to externally rotate the upper three ribs on the left because of the over active subclavius on the right, reinforces these left scalenes to become over used for both respiration and cervical stabilization during Superior T4 respiration. It is very common to find scalenes and upper trap tightness on the left with patients who are chronically engaged in respiratory challenge at the pelvis and thorax, as you mentioned, that results in compensation patterns that are not always necessarily associated with pathology, but could be.  
–Ron Hruska

I am confused of the pelvic position when  a person has a kypholordosis or sway back. Is the pelvis in anterior pelvic tilt or posterior pelvic tilt or it can be either. Sahrmann looks at this pelvis  as  posterior pelvic tilt position. I looked at the PRI pelvic manual and PEC/Patho PEC are both anterior inlets in flexed position which I think is anterior pelvic tilt. Is the PEC/Patho PEC equivalent to the same pelvis in a swayback posture/kypholordosis posture?

You are correct that both the PEC and Patho PEC are in the same position in the anterior inlet of flexion/abduction/ER.  The Patho PEC, however maximizes more of an end-range in this position.  These individuals will stabilize themselves with ligaments and/or joints in addition to musculature because of this end-range position.  They hang out on their Y ligaments and to counteract this they can stabilize themselves through their thoracic spine and develop kyphosis overtime.  They look "sway" back, however they are still in an anterior pelvic tilt with + Bilateral Adduction Drop Tests to verify this position.

-Lori Thomsen, MPT, PRC

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