It is generally agreed upon that the very first modern positional release technique was discovered by Lawrence Jones, DO, in 1981. He called this technique ‘strain/counterstrain’ (SCS).

Arthur Pauls (1992) accurately termed this counterstrain inspired orthobionomy technique ‘the homeopathy of bodywork’ because positional release techniques subtly allow the body to correct and heal itself.  These indirect techniques are often superior to the direct techniques of bodywork which use force in the attempt to impose solutions upon dysfunctional structures.

Chaitow’s genius was synthesis, integrating ideas of different thinkers and clinicians, including DOs, DCs, PTs, MDs, and Bodyworkers.

Chaitow has described and demonstrated precise diagnostic and potent treatment techniques.  In fact, counterstrain diagnostics have been found to be more accurate than standard osteopathic and chiropractic assessments of patients with neck pain (McPartland, Goodridge & Brodeur, 1996).  In this study, the strain/counterstrain method of diagnosis known as ‘provocative palpation’ was found to be superior to three traditional palpation methods:  assessment of segmental motion (ROM range of motion), local tissue texture changes, and elicitation of pain of joint capsule tenderness.

Patients prefer positional release treatments: there are fewer side effects and the methods are easier to learn.  As John Goodridge, DO has suggested, ‘positional release techniques are the future’.

Several different methods exist that involve the positioning of an area of the body, or the whole body, in such a way as to evoke a therapeutically significant physiological response which helps to resolve musculoskeletal dysfunction.  The means whereby these beneficial changes occur seem to involve a combination of the circulatory and neurological changes that take place when a distressed area is placed in its most comfortable, its most ‘easy’, most pain free position.  The developer of the positional release technique known as ‘functional technique’, Harold V. Hoover (1969), termed this position ‘dynamic neutral’.  Charles Bowles (1969) has further discussed dynamic neutral:

“Dynamic neutral is the state in which tissues find themselves when the motion of the structure they serve is free, unrestricted and within the range of normal physiological limits… Dynamic neutral is not a static condition… it is a continuing state of normal, living motion, during living activity… it is the state and condition to be restored to a dysfunctional area.”

The terms ‘ease’ and ‘bind’ are frequently used to describe the extremes of restriction and freedom of movement.  The term ‘dynamic neutral’ is considered interchangeable with ‘ease’.

The position of ‘ease’ that Jones discovered was an exaggeration of the position in which spasm was holding his patient.  Since this discovery, that a position which exaggerated a patient’s distortion could provide an opportunity for a release of spasm and hypertonicity, several variations on this basic theme have emerged.  These include:

• Exageration of Distortion
• Replication of Position of Pain
• Using Jones Tenderpoints as Monitors
• Goodheart’s Approach
• Functional Technique
• Any Painful Point as a Starting Point for SCS
• Facilitated Positional Release
• Induration Technique
• Integrated Neuromuscular Inhibition Technique (INIT)

The commonality of all these approaches is that they move the patient or the affected tissues away from any resistance barriers and toward positions of comfort… the position of ‘ease’.  Some approaches require verbal feedback from the patient regarding the degree of tenderness in a ‘tender point’ which is being used as a monitor, and which the operator is palpating while attempting to find a position of ease.  Other ‘functional’ methods or ‘positional release’ approaches involve the operator finding the position of maximum ease by means of palpation alone.

It is important to note that if positional release methods are being applied to chronically fibrosed tissue the result would produce a reduction in hypertonicity but would not result in any reduction of fibrosis.  Pain relief or improved mobility may be only temporary or partial in such cases.

Excerpted from:  (Chaitow, Leon.  Positional Release Techniques. 1996, Churchill/Livingstone.)

Myoskeletal Alignment Therapy (MAT)

The founder of the Myoskeletal Method is Erik Dalton, Ph.D.  The foundation of the Myoskeletal Method is recognizing and treating imbalanced myofascial and skeletal strain patterns.  By learning to recognize and treat muscle imbalances and strain patterns in the body, the Myoskeletal therapist can bring order and balance to the body even before the onset of pain.  Prevention of pain is the primary goal of the Myoskeletal Alignment System.

The second goal of MAT is to re-establish ‘whole-body, pain-free movement’, especially during the walking (gait) cycle.  To accomplish this task, the Myoskeletal Therapist must test for muscle imbalance, recognize strain patterns as they present themselves, and always attempt to restore function in the alignment process.

Myofascial and skeletal alignment therapy begins with a well-developed therapeutic strategy.  The development of the strategy is based on the therapist’s ability to recognize common strain patterns in the human body.  The most common alignment problems therapists encounter today are centered in the lumbopelvic and cervicothoracic spine.  This is precisely where Dalton’s Myoskeletal Method is most effective!

The two most prevalent strain patterns seen in today’s culture are known as the ‘upper and lower crossed syndromes’.  These syndromes were originally described by Dr. Vladimir Janda who named these observations the ‘proximal and distal crossed syndromes’.

By recognizing and understanding the mechanisms of these dysfunctional patterns, the Myoskeletal Therapist can quickly locate and treat the muscle imbalances responsible for creating the asymmetries and functional lesions, which if not treated, can result in muscle and movement impairment, and chronic pain.  Even if the client does not present with either of these two common patterns, the Myoskeletal Method muscle testing system will still differentiate and correct the dysfunctional pattern successfully.

For best results, the idea of muscle/movement impairment must be taken one step further to include skeletal alignment techniques.  When shortened tight muscles overpower weaker structures, the uneven pulling distorts our skeletal framework.  Whole body alignment requires both myofascial (muscle) and osseous (bone) structures be systematically treated to prevent strain patterns from becoming, or continuing as chronic pain patterns.

Excerpted from:  (Dalton, Erik.  Myoskeletal Alignment Techniques. 2014, Freedom From Pain Institute.)

This type of bodywork is not relaxation massage, or what is known as ‘passive treatment’.  This is a paradigm shift from ‘relaxation’ to ‘realignment’.  We will be engaged in a combination of ‘active assessment and treatment’ (hands-on bodywork and functional movement modalities) for approximately 90 minutes.

Orthopedic Massage (Waslaski) is a multimodal and multidisciplinary approach for evaluating and treating clients presenting with a wide variety of musculoskeletal disorders, chronic pain, sports injuries, and structural imbalances.  It can be utilized by a variety of healthcare professionals including physical and occupational therapists, athletic trainers, personal trainers, strength and conditioning coaches, chiropractors, osteopaths, nurses, manipulative therapists, and physicians.  Waslaski’s technique seeks to bridge all manual therapy disciplines through a unique 12-step approach based on soft tissue and structural balancing, which can be integrated as a model in most manual therapy training programs.

Waslaski’s 12-step approach is not considered a cookbook approach to manual therapy, but is a unique system that allows the therapist to quickly identify the key areas of pain and dysfunction so that appropriate treatment techniques can be matched to the underlying pathology.  Consistent attention is given to restoring myoskeletal imbalance by correcting structural asymmetries prior to treating each individual clinical symptom.  This process is also referred to in manual therapy literature as ‘normalizing the periphery’…  As Ida Rolf would say, “First, put the tissue back where it belongs.”

The causes and contributing factors involved in myoskeletal pain are always addressed prior to treating and eliminating the client’s pain symptoms.  In Waslaski’s model, the recommended treatment sequence is to first restore balance to opposing muscle groups throughout the body.  This is accomplished by lengthening short, tight muscle groups and then tonifying the opposing weak, inhibited tissues.  The most effective treatment protocol begins by addressing myofascial tension, tight muscle bands, muscle belly trigger points, scar tissue, joint capsule adhesions, and finally the resulting joint pain.  Tight muscle bands can be teased apart by gentle cross-fiber gliding strokes, while trigger points are addressed by direct, moderate pressure, with all the work performed pain-free.

Waslaski’s approach to scar tissue also sets him apart from typical, conventional treatment methods, which recommend ‘deep cross-fiber friction’, in one direction only, to realign the scar tissue’s injured or disorganized fibers.  An examination of the collagen fiber formation following injury reveals the potential problem with the conventional approach.  Scar tissue being formed at the site of an injury consists of a fiberglass-like matrix of collagen fibers oriented in multiple directions and multiple layers, which result in pain and limited range of motion for the client.  Simple cross-fiber friction does not mobilize multilayered/multidirectional fibers, effectively.

James recommends and teaches the much more effective technique of ‘multidirectional friction’, which works to mobilize the scar tissue by focusing on the softening of the thickest fibers in the collagen matrix, superficial to deep.  This process is then followed by pain-free mobilization, pain-free eccentric muscle contractions, and pain-free stretching/strengthening to better facilitate functional and more aligned scar tissue.  This unique strategy makes it possible for the area of scar tissue to remain smooth to palpation after treatment, enabling the client to remain pain-free following treatment.

Waslaski suggests that no single modality is the answer for treating all conditions.  Rather it is the synergy of many modalities and disciplines integrated together that allows the therapist to treat each client in a truly individualized manner.

Excerpted from:  (Waslaski.  Cinical Massage Therapy, A Structural Approach to Pain Management.  2010, Pearson Education)

In musculoskeletal medicine, there are two main schools of thought:

One, is the traditional ‘western’ structural approach.  This structural approach is rooted in anatomy and biomechanics.  Orthopedic medicine is greatly influenced by a structural approach to pathology, relying heavily on visualization of structures through imaging (X-Ray, MRI, CT Scan, etc.). Structural lesions are damage to physical structures such as ligaments, bones, cartilage, etc., that can be diagnosed by imaging and/or special clinical tests. These types of lesion are repaired through immobilization, surgery, or rehabilitation.  The diagnosis and treatment of structural lesions is well supported in the scientific literature.  The structural approach is a foundational aspect of medical education and practice, in the U.S.

In many patients, however, the diagnostic tests for structural lesions may be inconclusive, or altogether negative.  Or, immobilization, surgery, and/or rehabilitation do not cure the lesion, leaving the patient and clinician at a loss.  More than likely, a functional lesion is the cause of the problem.

In the functional approach, Janda defines functional pathology as impairment in the ability of a structure or physiological system to perform its job; muscle and movement impairment often manifest in the body through reflexive changes.  Typically, this type termed functional lesion, is more difficult to understand, assess, and treat, requiring an alternative way of thinking and seeing.

Functional lesions cannot be observed directly with structural tools such as MRI.  Clinicians must envision the dysfunction by understanding the complex interactions of the ‘sensorimotor’ system. This is a paradigm shift from thinking only in terms of structure, and not understanding the functional aspect.  The functional approach allows us to discover and treat the cause of the pathology rather than focus only on the pathology itself.

The traditional structural approach relies on visualizing static structures, where clinicians typically look at function from an origin/insertion point of view, suggesting that a muscle functions only to move the insertion closer to the origin.  The functional approach recognizes the true function of the muscle, which is based on coordinated movement in relation to other structures, and takes into account the stabilizing role of muscle.  For example, the primary function of the rotator cuff is not to rotate anything; (you knew that, right?), rather it is to adduct the humeral head and stabilize the glenohumeral joint.

Structure and function have been described as the ‘two sides of the same coin’.  They are not independent of each other, but deeply connected to and dependent on each other.  However, when our attention becomes imbalanced toward ‘structure’ our approach to evaluating, treating, and preventing ‘functional lesions’, becomes ineffective.

While understanding both the structural and functional approach is necessary for clinical practice, the fuctional approach is the key to rehabilitating dysfunctional muscle and movement syndromes.

Excerpted from:  (Page, Frank, Lardner.  Assessment and Treatment of Muscle Imbalance, The Janda Approach.  2010, Human Kinetics, Champagne IL.)

I am passionate about promoting pain-free living and an active lifestyle, optimum sports performance and the prevention of injuries through integrating the science and art of Manual Therapy (Structural Bodywork, Myoskeletal Alignment), and Functional Movement (Exercise/Neuromuscular Re-education). I strongly believe there is a holistic connection between these fields which can be accessed through a cross-disciplinary approach that has previously been missed, misunderstood, or ignored by most practitioners.

My intention is to both expand and integrate the fields mentioned above into what can appropriately be termed a “Next Generation” configuration for physical wellness that is based on myoskeletal alignment, functional movement, and the pain-free movement experience that leads to sleeping, eating, and feeling better, exercising more, training more effectively and performing at a higher level!

My approach is called ‘The Castle Method’.

I believe the following statements reveal the key to the successful treatment of chronic pain arising from functional lesions.  My approach is based on these statements:

Dr. Ida P. Rolf   “First, put everything back where it belongs. Get ‘em balanced and realigned. Then introduce movement.  If the pain goes away, that’s their tough luck.”                          

Waslaski, 2014   “The manual therapy industry has evolved to a place where specializing in just one discipline is no longer   sufficient to treat complicated pain conditions and sports injuries.  Integrated Manual Therapy connotes the synergy of many modalities and disciplines integrated together, that allows the therapist to treat each client in a truly individualized manner.”                                                                            

 Meyers, 2016    “Our understanding of the body is about to go through a radical shift.  Everything we ‘know’ about how our (bio)mechanics work—that we have 600 muscles that work via tendons over separate ligaments that limit our joint movement—has been to date the best model we have had, but it has become inadequate.  These are all elements of one integrated system—the BARS (biomechanical auto-regulatory system), otherwise known as the ‘fascial system’.  Our old vectors-and-levers understanding of how that system works is about to go out the window.  We can now see how our fascia reaches into and affects all our cellular physiology and even our genetic expression.  Our children will understand the mechanics of movement in a totally different way from how we learned it.”                                                                                                         

 Dalton, 2016    “Despite the variety of pain-management approaches available in today’s ever-expanding bodywork field, the therapeutic goal should remain the same: restoration of maximal pain-free movement within postural balance.”                                     

Dr. Vladimir  Janda     “Functional lesions, which are the result of muscle/movement impairment, often the cause of chronic pain, cannot be observed directly with structural tools such as MRI.  Clinicians must be able to envision the dysfunction by understanding the complex interactions of the ‘sensorimotor’ system.”                                      

First, put everything back where it belongs,

Bodywork

• Integrated Manual Therapy
  • Orthopedic Massage (Waslaski)
  • MAT… Myoskeletal Alignment Therapy (Dalton)
  • PR… Positional Release (Chaitow)
  • MET… Muscle Energy Technique (Chaitow)

then, introduce movement.

Movement  (The Self-Care Tool Box)

• Basic Stretching Routine (my own work based on Janda’s ‘Classification of Muscle Imbalance’)
  • Reinforcing ‘corrected’ muscle length/strength balance
• Basic Fascial Fitness Training
  • Rejuvenating deteriorated connective tissue (my own work based on Schleip & Muller ‘Training Principles for Fascial Connective Tissue’)
    • ‘Slow’ dynamic and ‘fast’ dynamic stretching patterns for:
      1. Abdominal fascia
      2. Thoracolumbar fascia
      3. Lateral line, including latissimus, gluteals, TFL, ITT, abductors, peroneals
      4. Superficial back line, including plantar fascia, soleus, gastrocnemeius, achilles tendon
• Gait Pattern Analysis and Training (based on my own work and practice developing movement components for rehabilitating ankle, knee, hip, back, and shoulder pain)
  • Evaluating for required kinematics of functional gait
  • Neuromuscular Re-education;
  • Correcting dysfunctional muscle firing sequences and compensated movement patterns
  • Re-establishing and reinforcing primary movement patterns that compose the complex Gait ‘Walking’ Pattern
  • Gait Pattern Training (mat work)  (supine and prone positions); increasing proprioceptive awareness
    • Bilateral bridging w/bilateral shoulder flexion/extension
    • Single-leg bridge w/contralateral hip flexion, including appropriate contralateral shoulder flexion/extension
    • Bilateral supine straight-leg bridge w/bilateral shoulder flexion/extension
    • Single-leg, straight-leg bridge w/contralateral straight-leg hip flexion, w/appropriate alternating shoulder flexion/extension
    • Prone, quadruped, oscillating, tail-wag
    • Supine, quadruped, oscillating hip-shoulder counter-rotation
  • ‘Form’ walking (track); exaggerated movement pattern training
    • Exaggerated hipshift,
    • Hipshift crossover,
    • Exaggerated arm swing,
    • Wide-track walking,
    • Exaggerated hip-shoulder counter-rotation
  • Walking ‘with a purpose’ (track); putting it all together

Kelly is an age-group triathlete who has been training for Lake Placid Ironman for the past 12-months.  She came to my office complaining of a ‘tightness’ or what felt like a ‘restriction’ on her whole right side.  Her health history indicated no specific injuries that could be contributing to these symptoms.

I started the session with a standing postural assessment.  I could see right away that her R shoulder was low, and her upper traps were facilitated on the L side.  Kelly’s R iliac crest and R ASIS appeared high, in comparison to her left.  Further observation of her shoulder and hand positions indicated symmetry of her shoulders in the transverse plane.  At this point I started to think about R lateral line compression (coronal plane).

Next, I performed the standing/forward bending test to determine if there was a possible iliosacral fixation on either the left or right side.  There was neither.  So, I put her in the supine position on the table, and utilized the sitting/lying test to check for any anterior/posterior (sagittal plane) rotation of the ilia. There was none.   So, I rolled her over into the prone position and checked her iliac crests and PSISs.  Her R PSIS appeared high in comparison to her left.  To double check for R upslip of the ilium, I kept her in the prone position and rechecked her iliac crests for symmetry.  The R side still appeared high, so I tractioned both hips at the ankles.  Upon releasing the traction, her R hip rebounded into a superior position, in comparison to her left.  This confirmed the R upslip (coronal plane) within the R lateral line compression (coronal plane).

Finally, I rolled her back into the supine position and observed her ASISs in relation to her belly button.  An asymmetry here could indicate an inflare/outflare relationship of the ilia (rotation of the hips in the transverse plane).  I was relieved to see there was no inflare or outflare.  It’s less complicated to work in one plane of motion, especially if it’s associated with a ‘cardinal’ line.

From the supine position, I moved Kelly into the side-lying position, with her right side up.  Since I already knew her R QL was short and her L QL was overstretched, I wanted to test RROM to see if her R QL was harboring any strain or scar tissue. Kelly tested positive for a strain near the midline, just inferior to the 12^th rib.  I decided to work on this last.

I had a pretty good idea about where I was heading with this session, but I also wanted to check some hip range of motion.  So I did.

Results:                arom     L              R             prom end-feel    L            R             rrom pain    L          R

Extension                            45˚          30˚                                      S            H                                   NO      NO

Flexion                                 90˚          90˚                                      S            S                                    NO      NO

Int. Rotation                       40˚          30˚                                      S            H                                   NO      NO

Ext. Rotation                      60˚          60˚                                      S             S                                    NO      NO

Abduction                           45˚          35˚                                       S             S                                    NO      YES

Adduction                           30˚          30˚                                       S             S                                    NO      NO

I began the Tx portion of the session with Kelly in the prone position so that I could work on the R anterior joint capsule release.  Then, I flipped her over (supine), and proceeded with the R iliopsoas release.  Between the two protocols, Kelly’s R hip extension returned to an AROM of 45˚ and a PROM soft end-feel.

Next, I concentrated on Kelly’s abduction issue.  Her AROM was a bit restricted, but it didn’t seem to be coming from a tight adductor, so I decided to focus on her R quadratus lumborum.  I proceeded with the QL/erector spinae protocol.  I was wondering if, or how much of the abduction restriction was being caused by the strain/scar tissue.  I went through the protocol as described in Clinical Massage Therapy (Waslaski, 2012).  The multi-directional friction and eccentric scar tissue alignment worked well, and the strain/scar tissue cleared after a few sequences.  The hip-hiking portion of the QL PNF stretch must have gotten the QL firing, because after the stretching (during therapy) Kelly’s R hip abduction was into the 40-45˚ range.

I then moved on and addressed Kelly’s internal rotation restriction.  I kept her in the prone position and started with internal rotation joint capsule work on her R hip.  As usual, this proved to be exceptionally effective in yielding a soft end-feel and increased ROM.  I also utilized the lateral hip rotator protocol, especially on the piriformis and quadratus femoris.  I finished this portion of the Tx with the deep six stretch.

Because I thought the whole R lateral line could be involved, I wanted to include some work on her R ITB and R lower leg (tibialis anterior and peroneals).  I utilized the ITB Syndrome protocol  to release the TFL and gluteus maximus, hoping to reduce the tension on the ITB.  Then I worked to release the ITB from the vastus lateralis.

Finally, I addressed Kelly’s lower leg.  She described a sensation of feeling tight on the lateral portion of her lower leg.  In the neutral position, I could see that her R foot was significantly more everted than what would be considered neutral.  This observation suggested the possibility that the peroneals were short and tight, leaving the tibialis anterior overstretched and weak.  I did a quick AROM test and found her eversion was WNL, but her R inversion was restricted at about 25˚.  Both end-feels seemed about right, with eversion feeling a bit more ligamentous.  RROM did not yield any painful points so I just released the peroneals  ( origin to insertion) and worked the tibialis anterior (distal to proximal), trying to put everything back where it belonged.

To end the session, I reviewed home stretching techniques for the iliopsoas, quadratus lumborum, lateral hip rotators, gluteus maximus andTFL.

Kelly completed her first iron man triathlon in 13:16.

Chris is a half-marathon runner for Stotan Racing, a Nike sponsored running team in Central New York.

Chris arrived at my office complaining of L lateral knee pain.  Based on the initial palpation I performed, I thought it might be ITB Friction Syndrome, but the first thing I did was test for hyper-mobility/instability.

Anterior/Posterior Drawer Tests were negative, as was the Lachman’s.  The Valgus Stress (MCL Sprain Test) was also negative.  I then proceeded with the Varus stress test (LCL Sprain Test) to determine if there was any damage to the fibular collateral ligament (also known as the lateral collateral ligament, or LCL).  The LCL Sprain Test was negative.

Next, I tested Apley’s Compression for any meniscus problem.  L Lateral and medial meniscii were both negative…  Apley’s Decompression with lateral medial/tibial rotation was also negative.

Next, I tried the ITB friction test, and this was a positive (4/10) on the pain scale.

AROM testing revealed both knee flexion and extension to be WNL, 135˚ and 0˚, respectively.  Slightly abnormal external tibial rotation was observed at 10-15˚.

Since I wasn’t picking up much in terms of ‘causality’, I decided to run through the hip ROM tests.

AROM L hip flexion was somewhat restricted at approx. 75˚, with PROM exhibiting a soft end-feel, and RROM performed with no pain.

AROM L hip extension was WNL at 35-40˚, with a soft PROM end-feel.  RROM did however, create some lateral knee pain.

AROM, PROM, and RROM for L internal hip rotation were all WNL.

AROM L hip external rotation was restricted to 45˚.  PROM was soft, and no pain was observed with RROM.

Hip abduction and adduction were WNL for all tests.

The limited external rotation made me think ‘short/tight, TFL/Gmax’, which fed into the possibility of ITB Friction Syndrome.  The restricted hip flexion and abnormal external tibial rotation left me thinking ‘short/tight biceps femoris (lateral hamstring)’, not so much ITB Friction Syndrome, but maybe some lateral patellar tracking leading to Chondromalacia.  (I immediately performed the patella femoral compression test, but discovered neither grating nor pain).

To begin treatment, I first performed the ITB Friction Syndrome protocol for Knee and Thigh Conditions.  This included Gmax compression broadening and TFL myofascial release, the Gmax lateral fiber stretch and TFL stretch. I then performed ITB mobilization.

I ended the session by instructing Chris in the ‘home’ stretching techniques for the TFL/Vastus Lateralis, Gmax, and Biceps Femoris.  I also instructed him in strengthening exercises for the lateral hip rotators, VMO, and medial hamstrings.

I asked him to text me about his progress, or lack thereof, over the next few days.  Chris did so, but he was not experiencing any improvement of his L lateral knee pain.  Unfortunately, I was unable to resolve the problem, based on Chris’ description of his pain and my assessment/treatment choices.  I rescheduled him immediately, but felt that I was missing something.

I had tried to follow the logic of Occam’s Razor, and look for the simplest or most obvious answer to the problem, first.  This being ITB Friction Syndrome or Lateral Patellar Tracking, but neither appeared to be the correct solution.  I had to dig deeper.  So, before Chris next session I reviewed movement system impairment syndromes of the knee and the foot /ankle, especially during running.

Review of the knee was great stuff, but didn’t clarify much regarding Chris’ L lateral knee pain.  I was starting to think that Chris’ problem might not be lateral knee, but something else (close by) that could be mistaken for lateral knee pain.

I found some ideas that made sense in ‘Movement Impairment Syndromes of the Foot and Ankle’, (Sahrmann, Elsevier, 2011).  I also reviewed the Knee/Thigh material and Lower Leg, Ankle, and Foot Conditions in Clinical Massage Therapy (Waslaski, 2012), to see if there was something I was missing, but I couldn’t get anything to add up, so I moved on to reviewing the respective DVDs.

The DVD for Complicated Knee Conditions had a section that addressed a fixated fibular head, so I reviewed that material and decided to test Chris’ L proximal fibular head to determine whether or not it was stuck.  I also reviewed ‘Movement Impairment Syndromes of the Foot and Ankle’, (Sahrmann, Elsevier, 2011).  Sahrmann did not address a fixated fibular head, but did go into depth concerning what she termed ‘Proximal Tibiofibular Glide Syndrome’ (PTGS).

The principal movement impairment (pain) associated with PTGS is posterior and or superior motion of the fibula on the tibia during active hamstring contraction (especially during running).  The principal positional impairment is the fibula located anteriorly, posteriorly, superiorly, or inferiorly to the normal position on the tibia after trauma, particularly an ankle sprain.  Pain in the posterolateral or lateral aspect of the tibiofibular joint is often associated with running, or general tibiofibular pain is associated with a history of lateral ankle sprains.  Hamstring length and talocrural dorsiflexion impairment (Insufficient Dorsiflexion Syndrome, IDS) are common with this diagnosis.  PTGS is either a positional fault generally occurring after ankle and foot trauma (ankle sprain) or movement impairment (pain) as a result of hamstring contraction pulling the fibula posteriorly.

From my previous work with Chris, I knew that there was some L hamstring tightness as well as L external tibial rotation.  The external tibial rotation was leading me toward thinking ‘a possible fixated fibular head’, but I also wanted to test for PTGS and insufficient talocrural dorsiflexion.

At the beginning of this session, I asked Chris about any previous ankle sprains, particularly left ankle sprains, and he reported that he had had several over the years.

Next, I assessed the four single-plane movements of the ankle joint:

AROM for plantar flexion was WNL (30-50˚).  PROM was soft/ligamentous.  RROM was negative.

AROM for dorsiflexion was restricted (<20˚).  PROM was bone-on-bone.  RROM was negative.

AROM for inversion was WNL, but all the way out to 50˚, maybe 50˚+.  PROM was soft/ligamentous.  RROM was negative.

AROM for eversion was restricted (<15˚).  PROM was bone-on-bone (normal).  RROM was negative.

I put Chris in the prone position and began treatment by releasing the plantar flexors—gastrocnemius, soleus, tibialis posterior, flexor digitorum longus, flexor hallicus longus, peroneus brevis, peroneus longus and plantaris—trying to restore normal muscle resting lengths. I then retested dorsiflexion ROMs.  There was no change in AROM and PROM was still bone-on-bone.  I concluded possible Insufficient Dorsiflexion Syndrome (fixated talus).

I then moved Chris into the supine position with his left hip and knee both flexed at 45˚. I grasped Chris’ fibular head between my thumb and first two fingers (being careful not to irritate the common fibular (peroneal) nerve.  I then tested the mobility of the fibular head by trying to create both anterior and posterior motion.  I was looking for either a fixation (hypomobility), or hypermobility in the form of excessive posterior glide.  There was no fixation, but significant posterior hypermobility.  As I pushed the fibular head posteriorly, Chris reported lateral knee discomfort similar to what he was experiencing when running.

I then tested Chris’ R fibular head in an identical manner, to compare sides.  There was neither a fixation, nor hypermobility, as compared to the left leg.

My conclusion was that Chris had a combination of a fixated L talus and short/tight L lateral hamstring.  Every time his hammy contracted, the fibular head was getting pulled posteriorly, irritating the common fibular nerve and causing lateral knee pain (at the proximal tibiofibular joint).  The fixated talus may have contributed to a fixated (hypomobile) distal fibular head, which in turn contributed to the hypermobile proximal fibular head.

Hamstring length and talocrural dorsiflexion impairment are common with this diagnosis.  Positions when the lateral hamstring is stretched or when the talocrural joint is at the end-range of motion can reproduce the symptoms.  Correction of a suspected positional impairment or stabilization of the proximal fibular head during the stretch (contracting biceps femoris) decreases symptoms.

The positional or movement impairments are difficult to see and palpate, but when correction of a suspected positional impairment or stabilization against a suspected motion decreases the symptoms, the diagnosis is supported.

I proceeded to:

• Release the L biceps femoris (and teach Chris how to stretch the biceps femoris and strengthen the L medial hamstrings).
• Release the L ankle inverters—extensor hallicus longus, flexor digitorum longus, flexor hallicus longus, tibialis anterior, and tibialis posterior—to restore normal muscle resting lengths, and return the L ankle everters—extensor digitorum longus, peroneus brevis, peroneus longus, and peroneus tertius—to normal muscle resting lengths, so they could be strengthened.
• Teach Chris how to stretch the ankle inverters and strengthen the ankle everters.
• Mobilize the L talus with ankle joint play (arthrokinetics).
• K-tape the head of the L proximal fibula to resist posterior glide.

Chris ran with no pain immediately following the session (on a treadmill), and continues to train and race pain-free.

Dave is an age-group national competitor in tennis.  Two years ago, he was 2^nd in his age-group (70-75) in Houston, Texas, and this past year he was 3^rd at the national championship held in Cleveland, Ohio.

Dave arrived at my office complaining of L lateral elbow pain.  He was experiencing pain while playing, especially when hitting backhand, and also after playing.  He indicated that he was using ice after playing to reduce both discomfort and inflammation, but wasn’t having much success relieving the condition.

At first, I thought he might have gotten the injury bull fighting in Mexico (you know, waving that cape, wrist extension/supination, and all) but after agonizing for 30 seconds, I decided to go with the possibility of Lateral Epicondylitis (tennis elbow).

Lateral Epicondylitis is an overuse condition involving the extensor muscles that originate on the lateral epicodylar region of the distal humerus.  It is more properly termed tendinosis that specifically involves the origin of the extensor carpi radialis brevis muscle.  Any activity involving wrist extension or supination can be associated with overuse of the muscles originating at the lateral epicondyle.  Tennis has been one of the activities most commonly associated with the disorder, (Waslaski, 2012).

I was playing a hunch, so I started by assessing range of motion.  In my opinion, this condition usually occurs because the wrist and hand flexors are short, strong, and tight…resulting in weak and inhibited wrist extensors.  If this is the case, I also think it’s vital to first release the wrist flexors and forearm pronators, in order to bring the weak, inhibited or overstretched wrist extensors and supinator back to normal resting muscle lengths.

I began by assessing both the elbow and wrist single-plane movements.

AROM for both elbow single-plane movements, elbow flexion and extension, were WNL at 145˚ and 0˚, respectively.

PROM for both elbow single-plane movements, elbow flexion and extension, was normal tissue-on-tissue approximation and bone-on-bone, respectively.

No pain was elicited during RROM testing of elbow flexion and extension.

AROM for wrist flexion was WNL at 80-85˚.  PROM was soft tissue stretch.  RROM elicited no pain.

*AROM for wrist extension was a bit restricted at about 55-60˚.  PROM was soft tissue stretch.  RROM produced 5/10 pain in the extensor carpi radialis brevis-longus/supinator area.

AROM for wrist pronation was WNL at 80-85˚.  PROM was soft tissue stretch.  RROM elicited no pain.

*AROM for wrist supination was WNL at 90˚.  PROM was soft tissue stretch.  RROM produced 4/10 pain in the extensor carpi radialis brevis-longus/supinator area.

AROM for wrist radial deviation was WNL at 20˚.  PROM was a normal abrupt, ligamentous end-feel.  RROM produced some 4/10 pain, again in the extensor carpi radialis brevis-longus/supinator area.

AROM for ulnar deviation was WNL at 35˚.  PROM was a normal abrupt, ligamentous end-feel.   RROM elicited no pain.

I decided to begin the treatment by releasing the wrist flexors, flexor carpi radialis, flexor carpi ulnaris, and palmaris longus.  I started with myofascial release, working from elbow toward the wrist.  This included myofascial spreading and compression broadening of the forearm and wrist flexors.

I didn’t come across any trigger/tender points so I continued by releasing the flexor retinaculum, sometimes known as the transverse carpal ligament.  I followed this with wrist joint play (arthrokinetics).  To complete the flexor release, I tested RROM for scar tissue/muscle strain, but found pain-free movement only.

At this point, I felt I had released the wrist flexors/forearm pronators, thereby taking the tension off the weak, inhibited, or overstretched wrist extensors and forearm supinator, and creating the opportunity to put these muscles back where they belonged (in terms of being overstretched).

I proceeded with myofascial release techniques and compression broadening of the wrist extensors, working from distal to proximal.  My intention was to try to get this group back to their normal resting length.  As I worked through this group, I did not come across any muscle belly trigger points, so I checked for pain-free movement, and found it so.  I then tested RROM for wrist extension and found that it was not pain-free.  Dave indicated some pain in the extensor carpi radialis brevis-longus/supinator area.

I utilized a multi-directional friction technique on the area for 20-30 seconds to soften the collagen, and then checked for pain-free movement.  Dave indicated that the pain had diminished, but was not completely gone, so I went back to the multi-directional friction technique but work deeper and slower to soften the deeper layers of collagen.

I tested RROM again, and got a pain-free response, so I proceeded with an eccentric scar tissue alignment technique beginning with two finger resistance and increasing the resistance each time the movement was pain-free.

Before Dave left the office, I instructed him in stretching the wrist flexors/forearm pronator and strengthening the wrist extensors and supinator.

Dave continues to compete 2-3 times a week, pain-free.

Rob is an active businessman in his late 50s who travels by car and plane a great deal of the time.  When he is home, in Syracuse, he works out regularly at one of the local gyms with a personal trainer.  Unfortunately, Rob is twice as old as his trainer, so there is not much empathy between them regarding what it’s like to work out at 60 years of age.  I can tell you one thing for sure (because I’m 62, and still work out regularly), it’s not the same as when you are in your 30s.

Rob came to see me complaining of L lateral knee pain.  He reported the onset of the pain occurring during, and/or as the result of his training.  He had informed his trainer of his condition, but it was not getting any better, in fact it was becoming more of a problem as time went on.

The first thing I did was perform a standing postural assessment with Rob.  Rob is a pretty tall guy, about 6’2”, and lean.  Right off, I could notice some ankle pronation that was a bit more prominent on the left side, and valgus knees again more prominent on the left side.  Neither the ankle pronation nor the valgus knees were extreme, just there, and slightly more noticeable on the left side.  (Tight ITB, short/tight TFL, dominant adductor complex)

Next, I had Rob move into a single-leg stance with his right leg as the stance leg and his left leg flexed to 90˚ at both the hip and knee.  I observed the L femur pull across the midline and the left foot abduct to about 20˚.  (dominant adductors, short/tight biceps femoris, short/tight TFL)

Following the standing postural assessment, I had Rob move to the table where I could test for hypermobility situations.  I began by testing single-plane anterior, posterior, and lateral instability.  The anterior drawer, Lachman’s and posterior drawer tests were all negative, as were the valgus and varus stress tests.  Apley’s Compression and Distraction were also negative.  This pretty much ruled out ligament and meniscus injury, so I continued by testing for Patellar Tendinosis and Chondromalacia.  The Patellar Tendinosis test was definitely negative, but the Test for Chondromalacia was minimally positive.  There may have been some minor lateral patellar tracking, but I didn’t think it was the major cause of Rob’s discomfort.

Finally, I used a resisted test for a possible Plantaris/Popliteus strain.  It was a long shot, but since the Plantaris and Popliteus both originate at the lateral epicondyle of the femur, I wanted to be sure.  Both tests were negative, so my last option was to check for Iliotibial Band Friction Syndrome.

I placed Rob in a sitting position, with his legs hanging off the side of the table.  I then C-clamped the distal end of the L ITB with my right hand and had Rob slowly extend his knee.  This reproduced his pain exactly, and was most painful at about 30˚ of extension.

ITB Friction Syndrome would probably be anyone’s first guess, but you have to rule out the other possibilities, to be sure.

I moved Rob into the prone position to test PROM and RROM and began treatment by performing the anterior quadriceps release (from the pelvic stabilization protocol).  ROM was a bit restricted at about 120˚ with a tissue-on-tissue (leathery) end-feel.

Next, I checked for a possible anterior rotation of the L ilium (sagittal plane) by assessing the relative positions of Rob’s ASISs.  His L ASIS was slightly inferior.  I utilized a muscle energy technique to correct this rotation (resisting anterior rotation).  I followed this with myofascial release up the quadriceps and rectus femoris.  These techniques returned Rob’s ROM to about 135˚, which was appropriate.

Since RROM of Rob’s L Quad revealed no trigger/tender points, I moved on to releasing the Gmax/med and TFL utilizing myofascial release and compression broadening techniques, respectively.  I followed with a Gmax Lateral Fibers Stretch and a TFL Stretch.

To finish the session, I performed an ITB Mobilization Technique, working from the hip to the knee.  To follow up on the possibility of some minor patellar tracking, I also performed a compression broadening technique working proximal to distal through the Vastus Lateralis.

I then had Rob actively perform knee flexion and extension, testing for pain-free movement.  Rob was able to perform this test pain-free.

I completed the work by instructing Rob in an at home program for stretching the Gmax and TFL, and strengthening the VMO.