Archives for posts with tag: fascia

Many clinicians are still focused on “stretching fascia”. Research shows that fascia requires up to 1997 N/cm2 of force (448.9 pounds of force) to stretch and deform it.(1) Not that clinicians would be able to deform it with manual techniques but the questions becomes if it should be deformed. When a structure or tissue is deformed, it loses its structural integrity. With connective tissues, muscle loses its ability to lengthen or contract due to tearing of the fibers where fascia loses its ability to dissipate electrical discharge to coordinate movement patterns.(2, 3) Our manual techniques do produce mechanical changes, it is on the abnormal collagen crosslinks that form during the inflammatory process that, hopefully, are still immature and malleable. However, there is also an effect via the nervous system provided by sensory input and muscle spindle stretch that can also be utilized to create functional changes and decreasing symptoms.

A review of myofascial grading system finds the range from I-V and encompasses both passive (grades I-III) and active (grades IV-V) techniques. With increases grades, many assume this corresponds with increasing pressure but that is an incorrect assumption; it corresponds with increased tissue tension. If there is significant pressure applied, the brain interprets it as a painful stimuli and will contract the tissues to protect the underlying structures. Even though the techniques are designed to be inhibitory, the patient may present as tighter after the techniques if the self-protection mechanisms have been activated via the nociceptor stimulation.

Here is a review of myofascial release techniques, their purpose and their mechanism of action:

Grade I

Rationale: to decrease pain after acute trauma or in instance of central sensitization (fibromyalgia, complex regional pain syndrome, reflex sympathetic disorder, thoracic outlet syndrome)

Technique: pressure is applied to tissue is passively placed in the position it assumes as it contracts

Mechanism: neurological: autogenic inhibition via decreased tension of the muscle spindle

Basis for: Jones Strain-Counterstrain (SCS), Positional Release Techniques (PRT)

Grade II

Rationale: to decrease pain after acute trauma or in instance of central sensitization (fibromyalgia, complex regional pain syndrome, reflex sympathetic disorder, thoracic outlet syndrome)

Technique: pressure is applied to tissue in a shortened positioned then moved to neutral

Mechanism: neurological: autogenic inhibition via decreased tension of the muscle spindle

Basis for: pin-and-stretch technique

Grade III

Rationale: to improve mobility in areas of myofascial adhesions and mechanical restrictions

Technique: pressure is applied to tissue in a shortened positioned then passively moved to a stretch

Mechanism: mechanical: stretching and shearing of abnormal collagen crosslinks

Basis for: pin-and-stretch technique, Active Release Techniques (ART)

Grade IV

Rationale: to improve mobility in areas of myofascial adhesions, mechanical restrictions or trigger points

Technique: pressure is applied to tissue in a shortened positioned then actively moved to a stretch

Mechanism:   mechanical: stretching and shearing of abnormal collagen crosslinks

Neurological: relaxation of the tissue via reciprocal inhibition

Basis for: pin-and-stretch technique, Active Release Techniques (ART)

Grade V

Rationale: to improve mobility in areas of myofascial adhesions and mechanical restrictions

Technique: pressure is applied to tissue in a lengthened positioned then concentrically contracted

Mechanism: mechanical: stretching and shearing of abnormal collagen crosslinks

Basis for: pin-and-stretch technique, Active Release Techniques (ART)


  1. Chaudhry H, Schleip R, et al. Three-dimensional model for deformation of human fasciae in manual therapy. 2008. Journal of the American Osteopathic Association. 108:379-390.
  2. Langevin HM. Connective tissue: a body-wide signaling network? 2006. Medical Hypothesis. 66(6):1074-77.
  3. Ingber DE. Tensegrity and mechanotransduction. 2008. Journal of Bodywork and Movement Therapies. 12(3):198-200.

We are the society that thinks more is better and “no pain, no gain”. However, pain is a warning system in the body. Deep pressure can be applied without being painful but oo much pressure too soon can lead to guarding by the patient which, even though relaxation or inhibitory techniques are being applied, can make the person tighter as a means of self protection.

Fascia, the primary tissue for most manual techniques responds to “gentle, sustained pressure”, according the John F. Barnes’ Myofascial Release Approach. This allows for the patient to adapt and respond to the pressure for adaptive changes to occur rather than forcing changes on the person which equates to trauma.

One common misconception is that the fascia needs to be stretched. Research by Dr. Robert Schliep states we cannot stretch fascia as it would take almost 1400 pounds of pressure to do so. What we are trying to do is to stretch and break down the small collagen cross-links between the skin and the superficial/deep fascias and the muscle. As the tissues are decompressed, they regain the sliding movements which restore mobility. The decompression also elevates pressure of the peripheral nerves so the brain no longer has sensations it interprets as pain.

For those “deep tissue” therapists that doubt the affects of gentle sustained pressure:

Patient Instructions:

Place the tips of your thumbs together and raise your hands above your head

Typical Dysfunctions:
Tight latissimus dorsi = decreased shoulder flexion / lumbar lordosis
Tight pectorals = decreased shoulder abduction (Y’ing)
Weak rectus abdominis = cervical flexion to tension anterior line

Atypical Dysfunction (from seminar in Houston TX):
Picture 1 demonstrates limited right shoulder abduction with hyperabduction on the left. Her torso also laterally flexed to the right.

Patient had “bone scrapping” performed on her right femur when she was 5 years old. A total of 4 vertical scars averaging 3 inches each were placed around her right patellofemoral joint. As she continued age and grow, the scar tissue did not resulting in her movement patterns being pulled to the scar due to the limitation.

Treatment initiated consisted of r 3-4 minutes of scar tissue mobilization via gua sha followed by scar tissue mobilization taping with Rocktape kinesiology tape resulted in substantial changes to her bilateral shoulder mobility.

Scar tissue creates binding of the superficial skin to the superficial layer of fascia to the deep fascia to the muscle. When these adhesions form, it prevents the gliding ability necessary between these tissue for movement to occur. The adhesion can also encapsulate the nociceptors creating chronic pain.
Her right shoulder and trunk were limited due to her right lateral and anterior spiral lines (Anatomy Trains) whereas her left shoulder was affected by both her anterior spiral and anterior functional lines.

POSE DESCRIPTION – see picture


standing with hips adducted and neutrally rotated

ankle is neutral

knees extended but soft

spine erect


rotation occurs about the femoro-acetabular joint to produce hip flexion

ankle should remain neutral and not fall into plantarflexion

spine rounds slightly into flexion, curve should be evenly distributed


relevant for bending and lifting, may replicate dressing (pulling on pants/shoes)



mobilization of sciatic and tibial nerves

appropriate tone of all muscles involved


concentric contraction of anterior chain

anterior tibialis – prevents ankle plantarflexion

rectus femoris – maintains knee extension, creates anterior pelvic rotation

rectus abdominis – provides trunk stability

eccentric contraction of posterior chain

plantar fascia/toe flexors – maintains neutral arch

triceps surae – maintains neutral ankle

hamstrings – control of knee extension and hip flexion

erector spinae – maintain spinal stability


appropriate length of posterior chain

allows for neutral ankle, extended knee and flexed hip


Patients can be instructed on more traditional stretches initially that breaks the movement into its individual parts: ankle/hip mobility and knee/trunk stability. Once appropriate mobility/stability of the impaired joint(s) has been achieved, the full hip hinge may be instituted back into the patient’s routine.

CLINICIAN EDUCATION:  dissociative movements

One of the primary causes of musculoskeletal pain outside of trauma is compensatory movement patterns. Individuals often lose the ability to perform a movement due to muscular tightness, joint/capsule restriction or muscular weakness. The brain automatically creates compensation to try to maintain movement homeostasis. This single segment hypomobility often creates dysfunction (hypermobility) and pain in the compensating structures. Often, the patients feel they have full range of motion due to the compensation but present clinically with abhorrent movement patterns. Appropriate treatment should emphasize not only stabilizing the hypermobility but finding and mobilizing the hypomobility.

Common movement compensations:
Trunk flexion for limited cervical flexion
Trunk rotation for limited cervical rotation.
Scapular elevation for limited shoulder flexion/abduction
Scapular protraction for limited shoulder IR
Scapular retraction for limited shoulder ER
Shoulder IR for limited radio-ulnar (elbow) pronation
Shoulder ER for limited radio-ulnar (elbow) supination
Trunk extension for limited shoulder flexion
Trunk extension for limited hip extension
Posterior pelvic tilt for limited hip flexion
Anterior pelvic tilt for limited hip extension
Increased knee flexion for limited hip flexion
Increased knee extension for limited hip extension
Increased knee flexion for limited ankle dorsiflexion
Increased tibial (knee) rotation for limited ankle inversion/eversion
Increased midtarsal supination for limited ankle inversion
Increased midtarsal pronation for limited ankle eversion

Look for upcoming posts on evaluation and treatment options for each dissociative pattern!

CLINICIAN EDUCATION:  Thoracolumbar Fascia

There is much discussion as of late regarding the importance of the thoracolumbar fascia. Yet, few realize the importance of its role in both pain and movement dysfunctions.

The thoracolumbar fascia (TLF) is a dense area of connective tissue and is the largest aponeurosis in the body. It spans from the sacrum, coccys and posterior spine of the ilium inferiorly to the iliac crest laterally. Its expanse has connections to each spinous process before ending superiorly as the nuchal fascia of the cervical spine.

It is comprised of 3 layers: anterior (thinnest), middle and posterior (thickest). The quadratus lumborum (QL) is located between the anterior and middle portions while the erector spinae are encapsulated between the middle and posterior sheets. The TLF continues to cover the paraspinal muscles in the thoracic region where it serves to separate them from the muscles that attach to and move the shoulder girdle complex.

The TLF is highly innervated with free nerve endings (nociceptors for pain transmission). These fibers are known to give sensory input and are highly responsive to both mechanical and noxious chemical stimulation. The TLF fibers also appear to be an extension of the dorsal horn neurons for innervation of the posterior trunk.

The TLF serves as an aponeurosis to protect the abdominal organs. While the bony thorax protects the organs of the thoracic cavity, the abdominal aponeurosis combines with the TLF to protect the small and large intestines. The TLF specifically serves to protect the lower portions of the kidney as well as the ureters in the retroperotineal space.

The primary role of the TLF is to transmit forces between the upper and lower extremities. The transverse abdominis (TrA) is under somatic control and is designed to create trunk stability by tensioning the TLF. The tension of the TLF creates stable proximal attachments for the latissimus dorsi to create forceful shoulder extension and the gluteus maximus for hip extension. During ambulation, the TLF transfers force from the gluteus maximus to the contralateral latissimus dorsi (superficial posterior fascial line of Anatomy Trains) while the opposite limbs move into flexion (cross-crawl patterning).

As the TLF tensions, it pulls on the spinous process at each level and stiffens the spine. Once the lumbar spine is stable, the psoas has a firm proximal attachment to contract against to create a forceful hip flexion. Tensioning of the thoracic spine and rib cage creates stable proximal attachments for the rectus abominis and pectoralis major to contract against.

Samples taken from individuals undergoing back surgery demonstrate numerous encapsulations of the free nerve endings that may be responsible for some of their pain. These encapsulations can occur from healing micro- or macro-traumas to the fascia that heals improperly.

Areas of adhesions in the TLF can create abnormal shearing forces on the spine itself. This can create a variety of tilts and rotations of the spinal vertebrae as they are pulled towards the areas of adhesion in the fascia. The TLF can create so much shearing force that it can actually fracture the spinous processes of the lumbar spine.

Other sources of lumbar pain are related to dysfunction of the TrA. If the TrA is not contracting or undergoes delayed contraction, the spine loses its stability. Furthermore, the extensors lose their proximal stability and are unable to appropriately contract leading to abnormal hip extension and arm swing during ambulation.

Appropriate medical care is needed to appropriate diagnose the source of low back pain. While low back pain can be an indicator a disease state (cancer, kidney stones, etc), it is primarily a musculoskeletal condition. Treatment should consist of manual therapy techniques to restore normal mobility to the TLF and the overlying skin to decrease shear on the spine and compression of nociceptors. Neuromuscular re-education techniques should be utilized to restore appropriate timing of TrA contraction.

Barker PJ, Briggs CA, Bogeski G. Tensile transmission across the lumbar fasciae in unembalmed cadavers: effects of tension to various muscular attachments. Spine. 2004. 29:129-38.
Gracovetsky S. Is the lumbodorsal fascia necessary? J Bodywork Mvmnt Therap. 2008. 12:194-197.
Gray H. Gray’s Anatomy.
Langevin HM, et al. Reduced thoracolumbar fascia shear in human chronic low back pain. BMC Musculoskeletal Disorders. 2011. 12:203-15.
Tesarz J, Hoheisel U, Wiedenhofer B, Mense S. Sensory innervation of the thoracolumbar fascia in rats and humans. Neuroscience. 2011. 194:302-308.
Zorn A, et al. The spring-like function of the lumbar fascia in human walking. Journal of Bodywork and Movement Therapies. 2008. 4(23):261-3.
Schelip R, Klinger W. Chronic low back pain may originate from subfailure injuries in lumbar fasciae. Journal of Bodywork and Movement Therapies. 2008. 4(23):263.
Vleeming A, et al. The posterior layer of the thoracolumbar fascia: Its function in load transfer from spine to legs. Spine. 1995. 20:753-8.

PATIENT EDUCATION:  Sitting Posture #2

The vast majority of our patients sit at desks for their 8-10 hour workday. They tend to present with neck and upper back pain due their jobs. But why is this happening?

Sitting posture can have a significant impact on the body as a whole. Often, it is a hip restriction that prevents proper sitting posture. In the image below, the postural compensations (kyphosis, forward head posturing) are a result of the hip being unable to reach 90 degrees of flexion. This is required in order to keep the spine in neutral.

However, many people develop poor sitting posture during their teen years by slumping or lounging in chairs where their hips never reach 90 degrees or above. Others develop hip hypo mobility due to poor furniture design: most chairs and couches are too deep where the back is not supported in an upright position so the person ends up leaning backwards (hip < 90 degrees flexion) in order to have their spine supported.

Physiologically, several pathologies may be contributing to this long term dysfunction. The person may develop posterior soft tissue shortening: gluteus maximus and hamstrings primarily. S/he may also develop contractors of the joint capsule that will prevent the hip from moving to 90+ degrees. Skilled therapy services are required to identify which, if not both, of the conditions are affecting overall posture and the symptoms associated with it.

PATIENT EDUCATION:  Sitting Posture #1

Rarely do we think of how we are sitting. Often, we are given a chair at work or purchase a chair for home without ever trying it out by seeing how it fits our body type.

Most people are unaware that chairs are designed for a certain height range. Do you know what it is? (see image below)

People outside of this height range have to make compensations to be able to sit somewhat comfortably. Individuals below this height, typically females, tend to tuck their feet back so they can tip-toe balance on the chair. Males above this height range also tend to tuck their feet in order to get their knees out of their chests.

As the feet tuck back, this leads to shortening of the calf muslces (gastrocnemius and soleus). The increased knee flexion also leads to shortening of the hamstrings and the popliteus. With the feet unsupported, the pelvis tilts anteriorly which leads to compensatory arching of the low back (lumbar hyperextension) which shortens the lumbar paraspinals, thoracolumbar fascia and latissimus dorsi. The majority of these are components of the Posterior Fascial Line from Anatomy Trains. This can lead to pain in the primarily in the ankles but may also affect the knees, hips, low back and even the neck and shoulders with tightness initially but progressing to pain with prolonged abnormal use.

A better option would be to make the chair compensate to you. If you are shorter than the range, use a small box or phone book under your feet to bring the floor closer to you. If you are taller than the chair range, placing a pillow or cushion in the seat to make it taller would be beneficial.

CLINICIAN EDUCATION:  Therapeutic Exercise

Does a muscle that tests weak automatically need strengthening?

The functional unit of a muscle, a myofibril, is comprised of 2 primary fibers: actin and myosin. Muscles have optimum lengths determined by the amount of actin and myosin overlap. At optimal length, the actin and myosin are able to couple and create a ratcheting force to pull the fibers closer together and create a concentric contraction (shortening) to move the corresponding joint.

It is well accepted that a muscle that is too long (>4 mm of striation spacing), the muscle well test weak during manual muscle testing (MMT) with a grade of 4/5 or less. Strengthening exercises are required to provide appropriate neural input and muscular strengthening. However, the muscle may be inhibited by a hypertonic (short/tight) antagonist that needs to be appropriately lengthened to allow the agonist to contract properly.

However, a muscle that is too short (2.0 mm or less of striation spacing) will also test weak. In this case, there exists excessive overlap where the actin and myosin are already so contracted that the fibers cannot slide further to create a concentric contraction. In this instance, strengthening the weak muscle will actually make it more hypertonic and, subsequently, weaker if the person is even able to perform the exercise. These shortenings are most likely due to a myofascial adhesion where a more appropriate treatment option would be myofascial release, instrument assisted soft tissue mobilization and/or stretching to restore appropriate muscle length which should restore strength by allowing appropriate sliding of the actin and myosin filaments.


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