Lumbo Pelvic Hip Complex Dysfunction (LPHCD):
Predictive Model of Lumbo Pelvic Hip Complex Dysfunction
By Brent Brookbush MS, PES, CES, CSCS, ACSM H/FS
In this article we will discuss a predictive model of Lumbo Pelvic Hip Complex Dysfunction (LPHCD) as it relates to movement impairment, injury prevention, movement preparation, performance enhancement and rehabilitation. Specifically, this article will relate these concepts to the selection of exercise and corrective techniques.
For an introduction to Postural Dysfunction and Movement Impairment please refer to this article:
Introduction to Postural Dysfunction and Movement Impairment
What’s in a name?:
“Lumbo Pelvic Hip Complex Dysfunction” (LPHCD) is a purposely chosen title for the impairment discussed in this article. Although I would prefer to use the term “Core Dysfunction,” the term core has been defined in a variety of ways by various, well-respected practitioners. Although the core is commonly defined, as “the hip, SI joint, pelvis, lumbar spine, and all the structures that cross those joints,” the term core is also used to describe the muscles of the trunk alone and/or the muscles of the abdomen. To mitigate any potential confusion this body segment will be referred to by its constituent parts, as above.
By using a title that refers to a body segment, rather than the specific muscle activity or joint position, the title itself will not imply a certain set of joint actions, muscle activity, or length/tension relationships. I do not wish for the title itself to bias/limit the future evolution of this model, nor bias the debate and discussion of this model as more research becomes available. Common compensation patterns leading to LPHCD have been previously described as an “anterior pelvic tilt,” “lower cross syndrome,” and “excessive lordosis”2-4. However, these terms may limit the model to a particular set of joints, one variation of the dysfunction, and/or may be misleading. For example, “lower cross syndrome” implies a set of underactive and overactive muscles, but does not consider all of the structures involved in this movement impairment.
The corrective exercise strategies discussed later in this article are used by the Brookbush Institute (http://www.brookbushinstitute.com/) and have their foundation in the corrective exercise model (CEx) developed by the National Academy of Sports Medicine (NASM), and described in the text “NASM Essentials of Corrective Exercise Training” by Dr. Mike Clark & Scott Lucette (7).
Why do we need a better model?
The Search for Congruence – my revision of this model is nothing more than a search for congruence – an explanation that can find congruence between theory, research, observation, practice, and outcomes. That is, a better model would be evidence-based, accurately describe what we see during assessment, predict exercise and techniques that will enhance performance, and contribute to our understanding of the etiology of common lower-body pathologies. For more on my views of evidence and the development of this model click here – Search for Congruence
Note: The movement impairment model discussed and developed in this article may not describe the compensation pattern adopted immediately post acute orthopedic injury (ex. impact injuries) or accurately describe neurologic dysfunction (ex. stroke); however, they may be useful in describing some of the compensation patterns adopted weeks, months and years post injury.
Somewhat ironically, the common conditions that may be explained by LPHCD, may also help to refine our model of movement impairment. We could view some of these syndromes as the “extremes of LPHCD,” or the outcome of a lifetime with LLD. It’s as if the conditions are the “answer” to an “equation” we are trying to solve for. This is analogous to how the brain may be studied by examining the effects of brain injury on cognition, sensation, and motion.
Signs of Lumbo Pelvic Hip Complex Dysfunction:
Overhead Squat Assessment:
- Knees Bow in
- Knees Bow Out
- Excessive Forward Lean
- Low Back Arches
- Abdominal Distension
- Asymmetrical Weight Shift
- Arms Fall Forward
- Hip Internal Rotation: < 45°
- Hip External Rotation < 45°
- Hip Abduction < 35°
- Hip Extension < 15º
- Knee Extension (90/90) >v20°
- Anterior translation of femoral head in acetabulum
- Superior translation of femoral head in acetabulum
- Anterior rotation of innominate on sacroiliac joint
- Rotation of sacrum (for more info see Sacroiliac Joint Motion and Predictive Model of Dysfunction)
- Posterior translation of proximal tibiofibular joint
- Posterior translation of the tibia on the femur (inability to glide anteriorly, may be limited to the lateral compartment).
SI Joint Dysfunction
Common Symptoms of LPHCD:
- Low Back Pain
- Disk Injury
- Stiffness of Lumbar Facets
- Sacroiliac Joint Dysfunction
- Hip Impingement Syndrome
- Labral Tears
- Groin Pull (Adductor Strain)
- Iliopsoas Tendonitis
- Lesser Trochanteric Bursitis
- Hamstring Strains
- Abdominal Strains (Hernia?)
- Lateral knee pain (Runners Knee)
- Patellar Tendonitis (Jumpers Knee)
- Degenerative Joint Disease (DJD)
- Degenerative Disk Disease (DDD)
Lumbo Pelvic Hip Complex Dysfunction and Performance:
Postural dysfunction effects length/tension relationships, resting tone, afferentation, alters proprioception, joint dyskinesis, and maladaptive changes in connective tissue length (2,7,8). These neuromuscular and articular changes have an impact on force output, coordination, and endurance, leading to a decrease in performance. A model of LPHCD that implies a set of corrective exercises will be instrumental in refining movement prep/corrective exercise warm-ups for use in performance enhancement programs. In my opinion, the corrective warm-up renders the “general warm-up” obsolete. You have 2 choices before you start training – “improve the quality of human movement and optimize mechanics, or spend 10 minutes on a treadmill reinforcing your compensation patterns.”
Traditional Model of Lumbo Pelvic Hip Complex Dysfunction
- Unlike the traditional models of Lower Leg Dysfunction and Upper Body Dysfunction, the traditional model of Lumbo Pelvic Hip Complex Dysfunction (a.k.a. lower cross syndrome, or an anterior pelvic tilt) is congruent with the alterations in muscle length and activity presented in this model. (If the sacroiliac joint is considered separately, this is presented in a separate article)
As the pelvis is not a joint, but a bone controlled by the lumbosacral joints and hip joints – the graph below divides pelvic motion into lumbar and hip joint motion.
- Anterior Pelvic Tilt = Lumbar Extension + Hip Flexion
|Observed Joint Action||Short/Overactive Muscle||Opposing Joint Action||Long/Underactive Muscles|
|Lumbar Extension||Latissimus Dorsi, Erector Spinae||Lumbar Flexion||Rectus Abdominis, External Obliques, Internal ObliquesIntrinsic Stabilization Subsystem|
|Hip Flexion||Psoas, Iliacus, Tensor Fascia Latae (TFL)Rectus FemorisAnterior Adductor Complex||Hip Extension||Gluteus Maximus, Biceps Femoris, Semitendinosus and SemimembranosusAdductor Magnus|
If we stay true to the graph above, we would release and lengthen the short/overactive structures, and activate and integrate the long/under-active muscles.
The first issue with this model is the exclusion of several muscles that cross the hip and lumbar spine.
Rule #2 of Human Movement Science:
“Every structure that crosses a joint influences motion”
- Corollary to Rule #2: Every structure that crosses a joint is affected by- or contributes to- postural dysfunction.”
Practice Contributes to Theory (Positive Trendelenburg Sign):
LPHCD often results in an inability to maintain neutral frontal plane alignment of the pelvis during single leg stance – this is known as a “Positive Trendelenburg Sign.” It indicates that the gluteus medius is weak, deconditioned, and/or inhibited. Note, you may not see this sign in relatively healthy individuals until they perform an activity that approximates the intensity of their most demanding daily activity – example: you may need to do a “frontal plane hop to single leg balance” with a basketball player to note a positive finding. The frequency with which gluteus medius inhibition is noted in individuals with LPHCD suggests there is a frontal or transverse plane component to this compensatory pattern.
We have actually solved for the dyskinesis at the hip joint in the (Lower Leg Dysfunction) model. By “borrowing” the “math” that solved for the hip contribution to lower leg dysfunction we can solve for the remaining muscles in the LPHCD model. (We will assume that common dysfunction at each joint is generally the same regardless of which dysfunctional segment initiated the compensatory pattern.) Recent research has implied that hip dysfunction will often result in an inability to eccentrically decelerate femoral internal rotation3. If we consider “Hip Internal Rotation” as a compensatory joint motion (over-activity of internal rotators) and add it to the short/overactive side of the graph, and add “Hip External Rotation” (under-activity of external rotators) to the long/under-active side of the graph – all hip musculature is accounted for. Further, we find a solution that is congruent with our findings in practice: gluteus medius = long/under-active.
The only muscle left is the quadratus lumborum (QL). Practice would suggest that this muscle is over-active, but bilateral activation of the QL would only contribute to stabilization and/or compression of the lumbar vertebrae (depression of the 12th rib), not compensatory motion. This may be a contributing factor to lumbar disk injury/low back pain; however, you may find a more satisfying answer when reading the article – Sacroiliac Joint Motion and Predictive Model of Dysfunction.
- Lumbar Extension
- Hip Flexion
- Hip Internal Rotation
- Lumbar Flexion
- Hip Extension
- Hip External Rotation
4 Muscles That Keeps Us Guessing
The sartorius seems to play both sides. Although it is a hip flexor and should act as a short/overactive structure, it is also an external rotator making it long/under-active. Further, it is a tibial internal rotator/abductor (contributes to varum force) of the knee acting as a long/under-active muscle in lower leg dysfunction, unless the knees bow out, in which case the sartorius may contribute to femoral external rotation and abduction. The muscle does have a propensity toward trigger point development in both LLD and LPHCD, but my gut (for whatever that’s worth) says long and under-active due to its role in knee internal rotation. Long story, short, I have not found an effective, self-administered exercise for the activation of this muscle without increasing the activity of several over-active structures. However, trigger point release of the superior portion of this muscle, using a foam roll, does seem to be effective for improving hip mechanics and relieving anterior thigh discomfort.
The biceps femoris, adductor magnus and piriformis are listed on the long/underactive side of our graph but behaves as over-active structures. They are often trigger point laden, the biceps femoris may be the limiting structure of knee extension ROM both passive and active, the adductor magnus and piriformis may limit hip internal rotation, and all may be felt in hip extension activities despite the gluteus maximus being the prime mover. A common occurrence in those who use loaded squats during their exercise routine is soreness in the back of the leg, inner thigh or horizontally accross the top of the gluteal region with little or no soreness felt in the broader gluteus maximus.
This is likely due to a phenomenon referred to as “synergistic dominance.” Due to the inhibition of the glute complex (gluteus maximus and gluteus medius) as a result of altered reciprocal inhibition via the short/overactive iliacus – your biceps femoris, adductor magnus and piriformis must act as the prime mover and stabilizers of the hip during extension. This leads to the biceps femoris, adductor magnus and piriformis becoming over-active and adopting the rather peculiar combination of attributes of “long and overactive” in LPHCD.
Due to the propensity toward over-activity and adaptive lengthening (in most cases), the long head of the biceps femoris, adductor magnus and piriformis are generally released and not stretched. If stretching techniques are utilized, active and dynamic stretching is preferred, as static stretching has the largest likelihood of increasing muscle length and may exacerbate this postural dysfunction.
In the most common presentation of LPHC dysfunction the Anterior Oblique Subsystem (AOS) is under-active. The AOS is not capable of tilting the pelvis posteriorly or maintaining enough lumbar flexion to attain a neutral spine. This is likely due to synergistically dominant lumbar extensors reciprocally inhibiting spinal flexors. Cuing a posterior pelvic tilt to reinforce optimal pelvic alignment and Integrating the AOS (legs w/ push exercise) is an effective means of improving this dysfunction.
Note: The use of an AOS integration exercise with an individual who has an APT will usually correct lumbo-pelvic hip alignment, but in some cases results in an excessive forward lean. In this case it is appropriate to follow an AOS integration exercise with a Posterior Oblique Subsystem (POS) integration exercise.
In LPHCD the AOS under-activity is paired with Posterior Oblique Subsystem (POS) under-activity. The glute complex is grossly inhibited by over-active of the hip flexors, resulting in synergistic dominance of the biceps femoris and lumbar extensors, i.e. the Deep Longitudinal Subsystem (DLS). POS integration exercise should be done post release, stretch, mobilization, activation of the DLS and integration of the AOS.
A summary of the Subsystem involvement in Lumbo Pelvic Hip Comples Dysfunction:
|LPHC Dysfunction||ISS||AOS –> POS||DLS|
Overactive (Release and Stretch):
Underactive (Activate and Integrate):
Before we go any further:
The model for LPHCD created above (that includes Hip Internal Rotation and Hip External Rotation) provides a high quality list of overactive and under-active structures. Utilizing release and lengthening techniques on the short/overactive structures, and activation and integration techniques on the long under-active structures will result in effective corrective exercise strategies. If you are new to corrective exercise, postural assessment, kinesiology; specifically SI joint arthrokinematics, it may be wise to start with the list of muscles above before progressing to the more complicated article detailing SI Joint motion.
Arthokinematic Dyskinesis (Joint Dysfunction)
Vertebral Facets and Disks:
- Over-activity of the erector spinae and the increased lordosis disrupt normal arthrokinematics of the lumbar spine, resulting in inferior glide of the superior facets on the inferior vertebrae – often referred to as “closing” of the facets. This increases compressive forces on the joint surfaces, and compressive force on the posterior portion of the intervertebral disks, forcing the nucleus populous anteriorly. Further the increased lordosis increases anterior shear forces on the lumbar spine placing considerable strain on the passive and active structures that mitigate these forces. The resulting change in vertebral position and force vectors results in multifidus, intertransversarii, interspinalis and rotatores length and activity and decreases the capacity to produce force (altered length/tension relationships and force couple relationships). Long term compensation may result in adaptive lengthening of supporting ligaments, hypermobility, and lumbar instability.
- Anterior and superior migration of the femoral head in the acetabulum is the common dysfunctional pattern seen at the hip, and is likely best explained by this model of LPHCD. Below is an analysis of the force vectors created by muscles crossing the hip (posterior left, anterior right). Although all muscles will contribute to a superior glide (not to mention gravity), if you imagine the vectors of the hip flexors (anterior vectors) increasing due to over-activity, and the vectors of the hip extensors decreasing due to under-activity (posterior vectors) you can imagine how the sum of these forces would pull the femoral head anteriorly. In essence this propensity toward anterior and superior migration may be explained quite eloquently by the adaptive shortening and over-activity noted in the hip flexor musculature in those who present with this dysfunction.
- The broad attachment of the erector spinae via the deep layer of the thoracolumbar fascia (common erector tendon) attaches to both the sacrum and posterior ilium. Although the erector spinae has a line of pull that would lead to flexion (nutation) of the sacrum, this cannot occur without an anterior rotation of the pelvis as well. Because the erector spinae cause both the sacrum and the ilium to rotate in the same direction, bilateral activation would result in little if any motion at the SI joint. Joint motion at the SI joint can only occur it the erector spinae contract unilaterally. That is, the erector spinae would nutate the sacrum and anteriorly tilt the pelvis ipsilaterally, causing a relative posterior rotation of the contralateral ilium and SI joint motion on the contralateral side (flexion/nutation). These forces may also result in a relative superior and anterior glide, and rotation of the sacrum around a central axis compressing joint surfaces on the contralateral side. Actual arthrokinematics are not easily studied and have been the topic of much debate and discussion. More refined research methods are desperately needed. Although the sacrum is undoubtadly affected by lumbo pelvic hip dysfunction the resulting compensation pattern is generally asymmetrical and is more easily viewed as a “compensation within a compensation”. The common compensation pattern seen at the sacrum is discussed further in this article – Sacroiliac Joint Motion and Predictive Model of Dysfunction.
The fascial system needs more consideration in our corrective exercise strategies. The work of Tom Myers has brought this system to the forefront of human movement4, however, self-administered techniques for addressing fascial restriction are still fairly crude. There are many brilliant practitioners developing exercise strategies specific to fascia, and we can expect to see rapid development in this area in the years to come. This model does reinforce some of Tom Myers work, and illustrate some important fascial connections.
- TFL/VL/ITB Complex (Tensor fascia latae, vastus lateralis, iliotibial band) – The tensor fascia latae (TFL) uses the iliotibial band (ITB) as a tendon. The ITB is invested by fascial slips from the vastus lateralis (VL). In essence, these fascial slips implicate the vastus lateralis in this lateral thigh synergy that may contribute to an increased moment arm for hip flexion. In postural dysfunction, pattern overload of the ITB may lead to vastus lateralis trigger points, and the superficial fascia of the vastus lateralis becoming bound to an iliotibial band that has been pulled tight and shifted anteriorly by a TFL that is short and overactive. Because of these factors it may be necessary to add self-administered static release techniques for the vastus lateralis, and myofascial shear techniques for the ITB to a routine aimed at returning optimal TFL neuromuscular efficiency and improving LPHCD. Another potential relationship may exist between the TFL’s nasty cousin – the gluteus minimus - and the vastus lateralis, whose attachments border one another.
- The sacrotuberous ligament – may infer a relationship between the piriformis, adductor magnus and biceps femoris. I find this to be an interesting coincidence, as these are the same muscles that are likely to become long/overactive in LPHCD. The sacrotuberous ligament may act to transmit force and proprioceptive information, stimulating a reflexive increase in tone and integrated function when any one of these muscles is stimulated. As mentioned above this may explain the over-activity seen in all of these muscles when inhibition of the gluteus maximus results in excessive external rotation during extension (“Knees Bow Out) during functional movement patterns or sacral counternutation due to reduced sacral compression via gluteus medius contraction and sacroiliac instability.
- The Thoracolumbar Fascia: This fascial structure may be one of the most complex structures in the human movement system. Studies have verified a rich presence of pacini corpuscles(quick adapting receptors that respond to pressure and vibration), paciniform corpuscles (like pacini corpuscles but smaller), golgi tendon organ (slower adapting receptors that respond to muscular contraction), and interstitial receptors (free nerve ending they may respond to tension, pressure, or noxious stimulation). Check out this article on receptors and fascia, great read – “Innervation Excerpt”. Increased lumbar extension and anterior pelvic tilt will alter length and tension in this structure resulting in altered receptor activity. Often this position includes an increase in activity of the erector spinae, latissimus dorsi, quadratus lumborum, and iliopsoas. Mechanically, the presence of an increased lordosis in the lumbar spine increases compression and extension forces and due to the lordotic curve in the lumbar spine an anterior translatory force (anterior shear force). Despite the erector spinae, latissimus dorsi, quadratus lumborum, and iliopsoas having important roles as movers and stabilizers of the core, these muscles will also contribute to an increase in these forces. To mitigate these forces the Intrinsic Stabilzation Subsystem (ISS) increases pressure in the peritoneum (similar to squeezing a balloon) creating a posterior force against the anterior surface of the lumbar spine. In addition to this increased intra-abdominal pressure, the transverse abdominis (TVA) contributes to rigidity of the thoracolumbar fascia providing lateral stability to the lumbar spine, and increases the compressive forces between sacrum and ilium resulting in greater stability of the sacroiliac joint (10). Although, this subsystem is intimately invested in the thoracolumbar fascia, alterations to length and tension seem to be inhibitory of these muscles. If the ISS is not functioning optimally to mitigate the anterior shear force, than the forces created during movement may result in anterior subluxation, excessive force to passive structures, pain, dysfunction, and injury (sprains, strains, bulging disks, herniated disks, capsular damage, nerve impingement, arthritic changes, etc.). Further, intersegmental muscles of the spine (rotatores, interspinales and intertransversarii) relay proprioceptive information back to the CNS and maintain micro-alignment of the lumbar vertebrae with the aid of co-contraction of the multifidus. These muscles also contribute to increased lumbar stiffness which may also play a role in receptor activity of the thoracolumbar fascia. Last, the gluteus maximus and medius increases the tension of the thoracolumbar fascia during functional tasks, and both are long and under-active in this dysfunction.
A Common Variation – “Knees Bow Out:”
Although most variations in postural dysfunction are relatively rare (let’s say less than 15%), and most involve the same musculature; both Lumbo Pelvic Hip Complex Dysfunction and Lower Leg Dysfunction present with the fairly common variation of “Knees Bowing Out” during eccentric control of hip flexion – squatting, siting, descending from stairs, etc.
However, we have already solved for this variation. The synergistic dominance seen in the piriformis, biceps femoris, and adductor magnus (possibly via communicating synergy at the sacrotuberous ligament) results in excessive external rotation as way to compensate for an inability to eccentrically decelerate femoral adduction and internal rotation in the presence of prime mover inhibition. This results in one small but meaningful change in our programming. Rather then these muscles being “long/over-active” they are now “short/over-active” implying they should be released and stretched.
A Variation on Variation – Or is It?
Occasionally it is noted that an individual,s “Knees Bows Out,” or “Turns-Out” during end range hip extension. Generally this dysfunction is noted as excessive abduction of the knee during during the eccentric phase of exercises or movement patterns similar to static lunge in which the knee “flares out” during decent.” This is likely due to a synergy at the ASIS between the TFL, Sartorius and Rectus Femoris. However, this is not the variation described above as as these individuals usually present with “Knees Bow In” during an overhead squat assessment. Further, you may note that these muscles are already labeled as short and over-active in our refined model of LPHCD and would be treated the same – release and stretch.
Variations Between Individuals – Time Course of Dysfunction Hypothesis:
I hypothesize that much of the variations between individuals with LPHCD can be explained by a time-course of dysfunction. That is, LPHCD is a progressive syndrome that slowly modifies structures over time. This may be due to the rate of adaptability in various tissues, mechanical restriction having a larger impact on movement than soft tissue, muscle fiber type and resistance to fatigue, or motor patterns that are “hard-wired” alternatives to optimal human movement.
At this point, I seem to note the following trend (generally, it would appear that dysfunction moves proximal to distal).
- Adaptive Shortening of Hip Flexors
- Intrinsic Stabilization Subsystem Inhibition
- Synergistic Dominance of Lumbar Erectors
- Glute Complex Inhibition
- Synergistic Dominance of Biceps Femoris
- SI joint Dyskinesis
Note: This dysfunction may progress in either direction
For a complete repertoire of Corrective Exercise and a Sample Corrective Strategy check out this article – Lumbo Pelvic Hip Complex Corrective Exercise and Sample Routine
For a case study and sample resistance training program - Lumbo Pelvic Hip Complex Dysfunction and Weight Loss
And if you really want to twist your mind and take your understanding and programming to a whole new level check out the dysfunction within this dysfunction – Sacroiliac Joint Motion and Predictive Model of Dysfunction
- Phillip Page, Clare Frank, Robert Lardner, Assessment and Treatment of Muscle Imbalance: The Janda Approach © 2010 Benchmark Physical Therapy, Inc., Clare C. Frank, and Robert Lardner
- Dr. Mike Clark & Scott Lucette, “NASM Essentials of Corrective Exercise Training” © 2011 Lippincott Williams & Wilkins
- Donald A. Neumann, “Kinesiology of the Musculoskeletal System: Foundations of Rehabilitation – 2nd Edition” © 2012 Mosby, Inc.
- Michael A. Clark, Scott C. Lucett, NASM Essentials of Personal Training: 4th Edition, © 2011 Lippincott Williams and Wilkins
- Leon Chaitow, Muscle Energy Techniques: Third Edition, © Pearson Professional Limited 2007
- Tom Myers, Anatomy Trains. © Elsevier Limited 2001
- Shirley A Sahrmann, Diagnoses and Treatment of Movement Impairment Syndromes, © 2002 Mosby Inc.
- David G. Simons, Janet Travell, Lois S. Simons, Travell & Simmons’ Myofascial Pain and Dysfunction, The Trigger Point Manual, Volume 1. Upper Half of Body: Second Edition,© 1999 Williams and Wilkens
- Cynthia C. Norkin, D. Joyce White, Measurement of Joint Motion: A Guide to Goniometry – Third Edition. © 2003 by F.A. Davis Company
- Carolyn Richardson, Paul Hodges, Julie Hides. Therapeutic Exercise for Lumbo Pelvic Stabilization – A Motor Control Approach for the Treatment and Prevention of Low Back Pain: 2nd Edition (c) Elsevier Limited, 2004
(C) 2014 Brent Brookbush
Comments, questions, and critiques are welcome and encouraged.