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ChiroCredit.com™ / OnlineCE.com presents

Soft Tissue Injuries 115a

Instructor: Linda Simon, DC

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Hour 1

Section I: Soft Tissue Injury – Scar tissue and Adhesions

In order to appreciate the importance and value of active myofascial rehabilitation, it is necessary

to understand the structural changes that occur to these tissues with injury. Once recognized,

these structural and functional changes can be evaluated and treated effectively. There are a large

variety of treatments available for the rehabilitation of soft tissue structures. Those include but

are not limited to stretching, massage, fascial release, proprioception rehabilitation, modalities

and mobilization and/or manipulation. In detail, this course will cover three techniques that have

been proven highly effective for the physical rehabilitation of injured soft tissue. Those

techniques are postfacilitation stretch, somatic technique and postisometric relaxation. There

will be mention of active release as it is an active method of soft tissue rehabilitation. However,

this technique was covered in detail in Soft Tissue Injury 114: Deep Tissue Muscle and Fascial

Release, Linda Simon, DC as it is a deep tissue release technique. There will also be mention of

therapeutic stretching and exercise rehabilitation. These methods along with proprioception

balance rehabilitation are covered in detail in Soft Tissue Injury 113, Linda Simon, DC.

In treatment of any condition, a variety of several treatment methods used in conjunction with

one another may be necessary to completely resolve the conditions mentioned in this course. The

presentation of this material focuses on protocols of the particular techniques as they apply to

one particular region. They can be used as adjuncts to current treatment or in combination to

achieve a desired result. There is no assertion that any one technique can completely resolve each

condition mentioned. The protocols for the techniques discussed in this course are described in

full. For a broader expanse of information presenting a large variety of treatment suggestions for

conditions mentioned in this course please refer to the following courses by Linda Simon, DC:

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Soft Tissue Injury 104, the shoulder; Soft Tissue Injury 105, elbow, wrist and hand; Soft Tissue

Injury 106, cervical spine; Soft Tissue Injury 107, TMJ; Soft Tissue Injury 108, thoracic spine

and ribs; Soft Tissue Injury 109, lumbopelvic spine; Soft Tissue Injury 110, hip and knee; Soft

Tissue Injury111, ankle and foot. For a more comprehensive understanding of soft tissue injury

and its examination with brief overviews of a great variety of techniques used for soft tissue

injury treatment please refer to Soft Tissue Injury 103.

There are several types of injuries that can be found with fascia, connective tissue, muscles,

tendons, ligaments and joint capsules.

Fascia:

The characteristic effects of injury on fascia alter the consistency and function of the tissue.

Fascia responds to stress and strain by becoming tough and resistant to flexibility. It also has the

tendency to become sticky when injured creating a glue-like effect to the tissues allowing

surrounding structures to adhere to it. This creates adhesions. Adhesions can be described as

fibrous connections that develop between tissues which should not have connections at the points

where adhesions develop. The tissues that can become adhered to the fascia are muscle tissue,

bones, joints and skin. When adhered, soft tissue structures are limited in flexibility and function.

It is important to understand the relationship that fascia has with its neighboring structures. One

of the functions of fascia is to surround nerves as a means of protection of these vulnerable

tissues. When the fascia becomes tough and resistant to flexibility, the sheath around the nerves

becomes taut and less flexible. This inhibits the normal movement of the nerve through the

structure of which it travels. When this movement is inhibited, compression from contracted

tissues can result creating a situation in which the nerve is being compressed. When the fascia

becomes sticky thus developing adhesions, the fascial sheath around the nerves become adhered

in place to the tissues in which it travels. When the body moves, the nerve is tugged as it tries to

function and move with the tissues that are now not functioning properly. This creates a chronic

irritation to that nerve and in time can lead to neurological consequences.

Connective tissue:

As fascia, the connective tissue throughout the body can become taut and less resilient upon

injury. Another result of injury to connective tissue besides tautness is dryness. The lack of

circulation and nutrition to the connective tissue from an injury allows the tissues to become

more brittle thus creating a situation in which the tissue cannot move properly with the body.

Adhesions also form in the connective tissue creating a situation in which the structures become

adhered to one another. The effect of this situation is that the lack of fluidity of motion creates

increased stress upon the tissues involved and tearing can occur. Within the connective tissue are

vital structures such as lymph flow and nerves. When there is a disconnect or compression within

the connective tissue due to tearing or adhesions, the normal lymph drainage cannot occur.

Swelling can result as the fluids have nowhere to go. Proper drainage of lymph is important for

normal functioning of not only organs but muscles as well. Severe adhesions create the same

effect as scar tissue. The most obvious result seen with connective tissue injury is with plastic

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surgery procedures. In some cases, the disruption of the fascia allows for the disruption of lymph

flow and lymphedema has been known to result from surgery which has disrupted the contents of

the connective tissue.

Muscles:

There is an abundance of information on the effects of injury to muscle tissue due to the focus

and extent of research on this tissue. When muscle is injured, tears will occur. They can be gross

tears or microtears. In either case, the muscle fibers contract to maintain the cohesiveness of the

muscle. This contraction will allow the tissues to fold upon one another adhering to one another

creating palpable lumps. These folds can compress nerves creating trigger points. Trigger points

can compress nerve tissue as well as lymph and vascular tissue.

There are four types of injury to muscle classified as contusion, strain, laceration and ischemia

induced muscle damage.

A contusion is described as a trauma occurring from a direct blow or a sudden heavy

compressive force. The injury site is local and deeper injuries toward the bone will occur to more

relaxed muscle tissue than contracted muscle tissue.

A strain is the result of an excessive tensile force upon the myofiber and can lead to a rupture

near the myotendinous junction. The most common muscle types that strain are those that cross

two joints known for eccentric contraction such as the gastrocnemius and hamstrings.

A laceration is a tear in the muscle fibers creating a complete disconnect in the integrity of the

muscle tissue. A tear of this type will cause the muscle to swell, become imbibed with blood and

possibly contract. Depending upon the degree of injury, surgical intervention may be warranted.

Ischemia induced muscle damage results from damage to blood vessels supplying a muscle. It

can be secondary to a compartment syndrome and atrophy can result. Here there may be

disruption to the sarcolemma, contractile apparatus, mitochondria and the sarcotubular system.

The degree of muscle injury has been classified as mild, moderate and severe:

Mild or first degree muscle injury is described as a tear of only a few muscle fibers with minor

swelling and discomfort. There is usually no or a minor loss of strength and movement.

Moderate or second degree muscle injury is considered to have a greater damage of the muscle

with a loss of the ability of the muscle tissue to contract.

Severe or third degree muscle injury is defined as a tear extending across the entire muscle

resulting in complete loss of muscle function.

A complication of muscle injury can be myositis ossificans. This is a condition in which a severe

muscle injury develops calcification amongst the fibrous collagen deposits. The result is an

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ossified region of the muscle in which little muscular contraction can occur. Effective treatment

early on is vital to avoid this condition.

Section II: Soft Tissue Injury – Scar tissue and Adhesions

Scar tissue and Adhesions (continued):

Tendons:

There is very limited information regarding the mechanism of injury to tendons but research is

ongoing. What is currently understood is that upon injury to a tendon, there is an immediate but

brief and limited inflammatory response. The term tendonitis is used but cannot be applied to the

results of injury to a tendon. Tendinosis, a degenerative process has been discovered to be the

main causative factor of tendon injury sequela. Degeneration and disordered arrangement of

collagen fibers and increased vascularity contribute to the state of the tendon upon injury and its

aftereffects. When injured, the collagen fibers tear and degenerate. Around the resulting torn

fibers is the accumulation of fibrin and an increase in ground substance. There is a definite

absence of inflammation leading to a poor healing response, thusly collagen degeneration. Due

to this degenerative process, the collagen fibers become thinner than normal and lose their

spindle shape. In this case, the remaining healthy collagen fibers must bear an increased load to

compensate for the degenerated collagen fibers. These healthy tissues themselves become more

vulnerable to tear. What was originally considered the cause of pain in tendon injuries was

inflammation. Since research has found that the inflammatory process is limited in tendon

injuries, the theory of pain from the production of chemical irritants from anoxia and the lack of

phagocytes to remove the noxious byproducts of chemical activity has been investigated.

Chemicals theorized are chondroitin sulfate as well as glutamate and substance P.

Ligaments:

Found around joint capsules and between bones, these cordlike structures are made primarily of

dense collagenous connective tissue. Seventy percent of the ligament is water. The matrix

material within the ligament may be organized into functionally distinct subunits allowing for

different parts of the ligament to tighten at different joint positions.

Upon injury, the fibers tear as they would in a tendon injury. Collagen fibers are also known to

misalign after injury creating a haphazard pattern of support, protection and movement limiting

elasticity and flexibility. Degeneration of collagen fibers as well as scar tissue can result.

Provided with a higher degree of flexibility than tendons, crimping is also demonstrated in

ligaments. Ligament injuries are characterized as sprains from a shearing force.

There are three classifications of ligament injury; mild, moderate and severe:

Mild or grade I injury is characterized with no associated joint laxicity. There is little tearing.

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Moderate or grade II injury presents with mild but clinically insignificant laxicity. There is some

tearing but not enough to compromise the integrity of the ligament. Ligament function is

compromised.

Severe or grade III injury presents with significant laxicity resulting from a complete tear of the

ligament. This is usually a surgical condition.

Joint Capsules:

Ligaments comprise the main component of joint capsules. However, due to their location and

function of the stability of the joint, the results of a joint capsule injury can have devastating

effects. If the ligaments of a joint capsule are subjected to tension beyond what the ligament can

sustain, they undergo plastic deformation. They become longer and less capable of holding the

bones in their place. The result is aberrant and unwanted movement. There are two degrees of

joint capsule damage; subluxation and dislocation. Subluxation is defined as joint laxicity with

contact remaining between the bones. Dislocation occurs when the bones of a joint are no longer

in contact with one another. Other structures within the joint capsule that may be damaged are

nerves and blood vessels. Proprioception is an important part of the healing of a joint capsule.

This is where load, stretching and mobilization are vital.

Types of Soft Tissue Pain:

Muscle pain:

The neurological contribution to muscular tissue pain occurs in the nerve endings with the

production of what is known as Factor P. This chemical is produced upon stress and

inflammation and will create the sensation of pain. Chronic production of Factor P has been seen

in the condition of fibromyalgia. Also within muscle is the decrease of blood flow due to spasm.

This ischemia or anoxia will further contribute to the spasm of the muscle and create a sensation

of discomfort. The ischemia has also been hypothesized to encourage the production of Factor P.

Periosteal pain:

The periosteum is highly sensitive tissue around the bone and is intimately associated with the

attachment of muscle and tendons to bone. In an avulsion stress of the myotendon, the

periosteum will be lifted from the bone which will stimulate the nerve response on the periosteal

tissue causing pain. This is common in tennis elbow.

Joint pain:

Muscular stress patterns can place undue stress upon the joint itself which can become restricted

or over-approximated. Over time, these microtraumas can lead to damage to the ligamentous

aspects of the joint capsules. A lack of blood supply can result in a joint that is restricted due to

chronic soft tissue spasm. This can lead to osteoarthritis. Overuse can lead to tears and laxicity in

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the ligament of a joint capsule. One can see this as the tear of the ligaments of a disc leading to

protrusion of the annulus or herniation.

Nerve irritation:

This can occur due to the result of chronic muscle spasm as well as the entrapment of nerve

tissue within injured soft tissue such as connective tissue and fascia. As a patient ages, the

attachments of the fascia have a tendency to shorten after periods of marked activity. The

ligaments become tighter and thicker. The tendons become more deteriorated and the muscles

become shorter due to microtraumatic tears. It is important to consider these factors when

evaluating a patient.

Trigger Points:

Trigger points can occur not just within the belly of muscular tissue but within myofascia, skin,

ligaments, bone lining and other susceptible tissues. It has been noted that as a reaction to stress,

trigger points can form from overuse, repetitive motion trauma, bruises, strains, joint dysfunction

and surgery. A trigger point can be defined as a site of injured tissue from which scar tissue has

developed, oxygen levels are diminished (either from poor vascularization or innervation overall

resulting in lactic acid accumulation) and the functionality of the tissue has been altered in some

way. Active trigger points or injured tissues that cause pain at or distant from the site of injury

has within them some aspect of nerve entrapment.

When a trigger point occurs in a muscle, the resultant mass of scar tissue and adhesions causes

the muscle to remain contracted and therefore shorter. This overall shortening of the muscle

creates biomechanical mayhem to the particular musculoskeletal system that is involved.

Secondary trigger points develop when a muscle is subject to stress because another muscle with

a trigger point is not functioning properly. This secondary injury is the result of a biomechanical

instability causing the second site to be exposed to repetitive stress. Reactive trigger points occur

as stimulus from primary, secondary, tertiary, etc. sites respond to proprioceptive information in

the functioning of particular muscles involved in a specific motion. At times of mechanical

stress, one or more of these trigger points can become active. Due to the aberrant muscle

function pattern, they become proprioceptively and neurologically linked and stress to one

trigger point can cause pain to any others in the chain.

Satellite trigger points develop to a muscle in the referred or dermatome pain pattern. This differs

from reactive trigger points in that those develop along the muscular functional pattern.

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Section III: Diagnostic Evaluation of Soft Tissue

Several methods have been developed for the evaluation and palpation of soft tissue. The

methods described here have been identified by Dr. James Cyriax.

Palpation:

Static and motion palpation assess the functionality and condition of soft tissue. Pain is not a

reliable factor. Very often with soft tissue injury, pain is distant from the injury source. This is

also common with neurological radicular pain. The difference must be established if the source

of injury (lesion) is to be found. This may not be initially clear. For example, a soft tissue

shoulder injury may have a radicular pain pattern similar to that of a C5 nerve root inflammation.

This is because the pain pattern follows the dermatome corresponding to the embryological

derivation of C5 for the shoulder structures. The practitioner must evaluate the entire shoulder

joint capsule as well as the rotator cuff, scapula, elbow and forearm to discern. If other areas

demonstrate pain upon static or motion palpation, a greater problem triggered by an underlying

lesion must be considered.

According to Dr. Cyriax, the least reliable way to diagnose soft tissue lesions is to palpate or

prod the area of pain. It is the larger picture formed by a well trained physician that will provide

insight into the determination of the primary lesion. Each tissue that produces pain upon

movement must be challenged to determine the cause of the patient’s condition. Tension is

applied to all aspects of the region and its associated structures to identify which tissue produces

pain.

Inert structures lack the ability to contract and relax. They encompass the joint capsule,

ligaments, fascia, bursa, dura mater and dural sheaths to the nerve roots. Testing of these

structures is passive.

Contractile structures are muscles and tendons. Testing of these structures is active.

Passive Testing:

Passive testing involves stretching or placing manual tension to the inert structures. The patient

is supported and there is no active muscular contraction. The practitioner must place particular

care not to force movement into a joint with restricted range of motion. Be cognizant of the

patient’s level of pain and possible tears to the underlying tissues. Differential diagnoses will be

most effective when the passive structures are evaluated first as active testing will involve some

inert structures.

*Note: Regarding the cervical spine, passive and active evaluation should be postponed until

diagnostic tests rule out disc lesions or moderate to severe ligament or muscle tears found with

acceleration/deceleration injuries.

Passive testing is through the evaluation of what Dr Cyriax describes as “end feel”.

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1. Bone to bone – This is a hard end feel. An example of normal would be in elbow

extension.

2. Soft Tissue – What is evaluated is tissue approximation. Abnormal would show

restrictions from scar tissue, contracture or arthrosis.

3. Spasm or twang - The abnormal results when passive movement stresses a fracture,

inflamed joint or metastasis.

4. Capsular – The firm end feel shows a hard stoppage of motion with give.

5. Springy block – Abnormal is a hard rebound feeling indicative of an intra-articular

pathology such as a torn meniscus or loose body in the knee.

6. Empty feeling – The examiner feels more movement is possible but the patient insists the

examiner stop because of severe pain. This is common in acute bursitis.

Capsular lesions encompass a joint capsule. A lesion of the entire capsule will give rise to

limitation in a particular “capsular pattern”. This is characteristic of arthritis and varies from

joint to joint. It is also denoted by limitation not in a fixed degree but in a fixed proportion.

Noncapsular lesions are determined after capsular lesions are ruled out. If a pain pattern does not

conform to a capsular pattern and arthritis has been ruled out, the possibilities are ligamentous

strain (pain on one movement) and internal derangement (pain in varying movements and

degrees) such as a carpal bone subluxation.

Active testing:

This involves assessment of contractile tissue; muscle belly, musculotendinous junction, tendon

body and tenoperiosteal junction. The muscle is tested to elicit maximum strength while the inert

structures are most relaxed. This eliminates the pain of impingement and instability. Isometric

contraction is used; the muscle is contracted without shortening and strain is put upon the muscle

without movement.

The contractile tissue is placed through several ranges of motion giving the practitioner

information as to the position of pain. More than one muscle is involved with each range of

motion, therefore, the practitioner needs to understand the muscles involved and isolate the

offending muscle. The offending muscle(s) will be the one that is affected in all ranges of

motion. With more than one lesion, practice will assist the practitioner to narrow the focus to the

one or two lesions that are most offending.

Muscle testing can be interpreted as follows:

1. Normal - muscle testing without pain and has normal strength.

2. Tendinosis - pain with normal strength.

3. Tear - pain and weakness. Be wary of placing too much tension on a possibly torn muscle

during testing. Weakness without pain can also indicate a complete tear.

4. Neurological deficit - weakness without pain.

5. Intermittent claudication - pain upon repetition.

6. Atrophy - Pain upon repetition.

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The technique for testing contractile tissue:

1. Hold the joint at mid range so no inert structures are stretched.

2. No movement should take place at the joint.

3. Isolate the muscles being tested. This may be difficult, so minimize muscles that are

recruited. Observe and discuss the issue of muscle recruitment with the patient.

4. The patient must put full effort into demonstrating the full strength of the muscle.

The grading of muscle strength:

Grade 5 is normal - full ROM against gravity and full resistance.

Grade 4 is good - full ROM against gravity and some resistance.

Grade 3 is fair - full ROM against gravity and no resistance.

Grade 2 is poor - full ROM with gravity eliminated and no resistance.

Grade 1 is trace - slight contractility with no resistance.

Grade 0 is zero - no evidence of contractility.

It is important to differentially diagnose a neurological involvement versus a soft tissue pattern

of pain. Within the soft tissue components lay neurological structures. The lesion, as is often

found with trigger points, may be near a neurological component such as a peripheral nerve.

Inflammation can produce compression of the neurological structure causing a neurological

symptom. The differentiation is vital for proper diagnosis and treatment.

Referred pain can be characterized as follows:

1. Pain is referred segmentally and follows a dermatome pattern. The course may follow the

entire dermatome, be in portions, or one region.

2. The exception to the segmental referral of pain is from the dura mater. This refers pain

extrasegmentally and is most often noted during dura mater injury, possibly from PLL

compression in the cervical spine. The pain pattern can follow the entire region from the

head to the top of the shoulders.

3. Pain is referred distally. Exception is knee and elbow pain which can be referred in either

direction.

4. Referred pain never crosses the midline. If pain is shifting from side to side, the examiner

must look at the spine and pelvis for a displacement and instability.

5. The extent of pain is controlled by the size and position of the dermatome of the involved

lesion. A more proximal lesion will refer pain over a larger area of a dermatome than if it

were more distal.

6. The deeper the lesion, the more pronounced will be the pain. An exception to this is bone

pain which rarely radiates.

Referred pain from the nervous system can be characterized as follows:

1. Compression of the spinal cord – no pain. Paresthesia may occur and is usually bilateral.

This is a dangerous situation and the patient must be referred accordingly.

2. Compression of the dural sleeve to a nerve root – pressure on the dural sleeve of a nerve

root exiting the dura mater will produce dermatome pain and paresthesia in the digits.

Paresthesia can be produced with mild to moderate pressure on the nerve root. Numbness

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displaces the sensation of paresthesia. Pressure on a dural sleeve will cause analgesia.

Muscle weakness is caused by pressure on the nerve root.

3. Compression of the nerve trunk – no pain, however, direct pressure on the surrounding

dural tissues will produce pain. There will be weakness and paresthesia (as opposed to

numbness).

4. Compression of a small nerve – no pain or weakness. No paresthesia but there will be

numbness.

Section IV: Postfacilitation Stretch

Postfacilitation Stretch:

Postfacilitation stretch is a proprioceptive neuromuscular facilitation (PNF) technique used to

treat chronically tight muscles. It is a specifically timed active isometric contraction

immediately followed by a passive stretch. PNF allows for a depression of a post contraction

reflex which normally perpetuates the stretch. What occurs with this combination of isometric

contraction and relaxation is an inhibition of the reflex excitability of the motor neuron pool.

This has been termed the H-reflex. The H-reflex response has been theorized to be based on a

primary afferent depolarization. This is produced by Ia afferent terminals synapsing on other Ia

afferents reducing the muscle spindle responsiveness to reflex stimuli.

Although thought to be a presynaptic inhibition, the mechanism is not completely understood.

What is understood is that a muscle contraction immediately followed by a stretch will decrease

neurological excitability within the muscle as confirmed by EMG. This allows for a greater

stretch. Greater range of motion at the joint associated with the muscle will be an effect of a now

more permanent stretch of the muscle.

The propensity of a muscle to become chronically short, tight, overactive or weak and

neurologically compromised is termed muscle imbalance. This seems to occur to particular

muscles in combination with other particular muscles throughout the body. There are two types

of muscles, fast twitch and slow twitch. Fast twitch are for rapid responses and upon stress tend

to fatigue easily becoming weak. The weakness is not necessarily from lack of exercise but

neurological. Slow twitch are antigravity postural muscles that tend to tighten/shorten upon

stress instead of fatiguing. It is common that the fast twitch muscles and slow twitch muscles are

antagonists to one another. This sets up the situation where a muscle will be in spasm and its

antagonist is weak.

It is important to treat the spastic muscle before attempting to strengthen the weak muscles with

exercise rehabilitation. It has been found that the weak muscle can regain strength once its

antagonist has been relaxed and lengthened.

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The following is a list of slow twitch postural muscles:

Gastrocnemius/soleus

Tibialis posterior

Adductors

Hamstrings

Rectus femoris

Iliopsoas

Tensor fascia lata

Piriformis

Long back extensors

Quadratus lumborum

Pectoralis major

Upper trapezius

Levator scapulae

SCM

Biceps/brachioradialis

Forearm and wrist flexors

The following is a list of fast twitch muscles:

Peroneii

Tibialis anterior

Vastus medialis and lateralis

Gluteal group

Rectus abdominus

Serratus anterior

Rhomboids

Lower trapezius

Scalenes

Triceps

Forearm and wrist extensors

There are many reasons muscle and connective tissue structures shorten. Chronic overuse or

injury alters the elasticity of the muscle fibers. Poor posture and lack of exercise also alter the

elasticity of muscle and allow for atrophy and the replacement of healthy muscle tissue with

noncontractile scar tissue. This decreases strength. Connective tissue also shortens when it

remains chronically shortened as in poor postural components or lack of movement. The

neurological feedback from these poorly adapted tissues alters the CNS neurological firing

patterns. These in turn perpetuate the poor posture and contribute to further deterioration of the

mechanics of movement.

Tight muscles are not the same phenomenon as muscle spasm but they do occur together. The

tightness is due to the development of noncontractile scar tissue and the tight muscles are shorter

at rest whereas muscle spasm is a result of contraction. Tight muscles also become more easily

excited to contract than normal muscle. This causes the muscles to contract during movements in

which they should be relaxed further perpetuating the tightness. This can be found with the

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relationship between the abdominal muscles and the erector spinae. With tight erector spinae

muscles, when a patient attempts an abdominal crunch, the erector spinae will contract and

become stronger altering the antagonist relationship and making it almost impossible to

strengthen weak abdominals. This can be considered substitution.

Throughout the body there are muscle imbalance syndromes that involve combinations of

muscles and their antagonists. Alteration in normal mechanics of these relationships tends to

create specific patterns of dysfunction with these syndromes. These patterns have specific joint

dysfunction manifestations due to the inappropriate contractions and lengths and strengths of its

associated muscles.

Muscle Imbalance Syndromes:

The images in this section, the weak muscles are indicated with dotted lines and the tight

muscles have striated lines to define them. The crossed arrows indicate weak muscle patterns

with dotted arrows and tight muscle patterns with the solid black arrow.

Pelvic Crossed Syndrome (PCS):

4-1

In Pelvic Crossed Syndrome, short tight muscles are the iliopsoas, rectus femoris, erector spinae

and hamstrings. Weak and neurologically compromised muscles are gluteal group and abdominal

group. When the iliopsoas is short, there is a flexion of the hip causing an anterior pelvic tilt.

There is also an increase in lumbar lordosis approximating the lumbar facets. This increases

pressure on the posterior disc and decreases pressure on the anterior disc. The lumbosacral

region will receive excess stress causing the reaction of joint hypermobility, soft tissue irritation

and pain.

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Consider the act of walking:

The body requires a fixed point above to allow for movement below. The pelvis must remain

fixed for the hip to extend. The lumbar spine must remain fixed for the pelvis to tilt. A tight

psoas will anteriorly tilt the pelvis. This position creates difficulty in extending the hip. In order

to do so, the pelvis must pivot further anteriorly to accomplish this goal. This prevents the pelvis

from acting as a fixed point for hip extension decreasing the movement. The anterior pelvis tilt

will also cause excessive movement at the lower lumbar spine preventing this region from acting

as a fixed point for pelvic movement. A fixed point at the lower thoracic/upper lumbar region

will develop in compensation for the excessive movement in the lumbopelvic spine and limited

movement at the hip.

It will be common to find an anteriorly tipped pelvis and fixations of the upper lumbar/lower

thoracic region as well as hypermobilities, facet syndrome, posterior disc degeneration at the

lower lumbars with this condition. Contractures at the erector spinae muscles nearer to the

thoracolumbar region are common and can be assessed upon testing of hip extension in the prone

patient, these muscles will contract instead of those in the lower lumbar region.

Spastic quadratus lumborum and/or tensor fascia lata is usually found with a weak contralateral

gluteus medius antagonist. This alters the lateral lumbopelvic mechanics shifting weight and

structures accordingly. Gait, stance and hip abduction will all be affected. With a weak gluteus

medius there will be a lateral shift to the opposite tensor fascia lata which will continue to strain

this already tight muscle.

A tight quadratus lumborum can lead to an increased elevation of the pelvis during gait

increasing the movement of the pelvis laterally and obliquely tilting the pelvis.

Consider a sit-up:

Tight iliopsoas muscles will contract upon the act of sitting up from a supine position. The weak

abdominal muscles will not contract due to the substitution of the iliopsoas group. This will alter

the normal mechanics of this act creating stress on the lumbar spine.

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Shoulder Crossed Syndrome (SCS):

4-2

Short and tight muscles in this syndrome are the pectoralis major and minor, upper trapezius,

levator scapulae and the SCM. Also tight can be the masseter, temporalis, digastric, and upper

cervical and occipital muscles. Weak and neurologically compromised muscles are the serratus

anterior, rhomboids, middle and lower trapezius, scalenes, suprahyoid and mylohyoid. These are

the lower stabilizers of the scapula. The result of this combination of tight and weak muscles will

lead to elevation and protraction of the shoulders and forward head tilt. There will also be a

hyperextension of the upper cervical spine and stress upon the mid cervical region down to T4.

Two types of anomalous curves can develop from this condition. The patient can develop an

increase in cervical lordosis in the upper cervical spine with C4 being a transition vertebra in a

situation where C5 inferiorly forms a kyphosis, thus a lateral S curve in the cervical spine.

Another anomalous cervical curve that can result from this syndrome is a situation where the

entire cervical spine becomes hyperlordotic with the apex at C5. Shoulder function is altered

from these presentations because the angle of the scapula is altered putting undue stress on the

anterior of the glenoid fossa creating increased tautness of the shoulder capsule, supraspinatus

and posterior fibers of the deltoid. The excess stress on the supraspinatus and deltoid muscles

will cause the levator scapulae and upper trapezius to activate to reestablish a more normal

scapula movement. This will lead to spasm in the upper trapezius and levator scapulae.

Regarding movement of the cervical spine and shoulder; the elevation of the arm requires a fixed

point in the scapula but due to the increased muscle activity of the trapezius and levator scapulae

the fixed point is moved to the head and neck creating increased stress on the cervical spine.

There will be contralateral cervical rotation due to increased tightness in the upper trapezius. The

opposite trapezius will have to contract more to right the head. This can eventually involve the

opposite shoulder as well.

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Section V: Postfacilitation Stretch (continued)

Postfacilitation Stretch (continued):

Muscle Imbalance Syndromes (continued):

Combination of PCS and SCS:

5-1

The combination of Pelvic Crossed Syndrome and Shoulder Crossed Syndrome is an expression

of the most involved general muscle imbalance. As we go down the back, the upper back and

neck are tight, the mid back is weak, the thoracolumbar region is tight, the lumbopelvic spine is

weak and the hamstrings are tight.

The characteristic tight muscles are as follows:

hamstrings

back extensors from T9-L2

cervical extensors

upper trapezius

levator scapulae

The characteristic weak muscles are as follows:

gluteal group

back extensors from L3-L5

rhomboids

middle trapezius

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abdominal group

The postural and functional alterations are as described for both pelvic crossed syndrome and

shoulder crossed syndrome.

Movement patterns:

Muscles work in groups to coordinate movement. This is programmed neurologically. Abnormal

movement can reprogram the brain to perpetuate the abnormal movement. Abnormal movement

can produce pain and perpetuate dysfunction in a related region. When evaluating muscle

movement patterns it is important to note which muscle groups are functioning in which order to

accomplish a particular goal. This is muscle sequencing. It is also important to note the degree to

which the muscle is contracting to create a particular movement.

The following movement patterns will be described: hip extension, hip abduction, sit-up, neck

flexion, push-up and shoulder abduction.

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Hip extension:

5-2

Normal gait requires 10-15 degrees of hip extension. The sequence of movement begins with the

hamstrings and gluteus maximus, then contralateral lumbar extensors, ipsilateral lumbar

extensors, contralateral thoracolumbar extensors and ipsilateral thoracolumbar extensors. Based

on the premise that for normal movement, there must be a fixed point above the motion; the

pelvis must be stable for normal hip movement, the lumbar spine must be fixed for normal pelvic

movement.

With normal hip extension, the contralateral lumbar extensors fire before the ipsilateral lumbar

extensors to allow for a long axis lever. This is necessary for cross pelvic stabilization and to

protect the low back. Without this sequencing, the lumbar spine would hyperextend to allow for

hip extension. This would create an unstable low back. Also, an internally rotated hip which is

commonly found in an arthritic capsular pattern will prevent the gluteus maximus from firing.

Without the gluteus maximus, hip extension cannot occur normally and the lumbar spine is

forced to hyperextend. Therefore, degeneration of the hip can cause low back pain.

There are three patterns of abnormal sequencing with hip extension.

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Sequence 1:

5-3

Delay in activation of the gluteus maximus will cause the ipsilateral lumbar extensors to fire

before the contralateral extensors. This prevents the necessary cross pelvic stabilization

mentioned in the previous paragraph. Decompensation in the lower back will occur leading to

possible lumbar injury.

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Sequence 2:

5-4

Less gluteus maximus firing than mentioned above results in excessive activity of the hamstrings

and thoracolumbar extensors. This also results in an unstable low back. The thoracolumbar

region becomes the fixed point for stabilization allowing for excessive movement of the lumbar

spine and subsequent injury.

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Sequence 3:

5-5

Complete inactivity of the gluteus maximus forces the hamstrings and thoracolumbar region to

perform most of the extension. The upper trapezius and latissimus dorsi is the first muscle to

activate. This is followed by the hamstrings and thoracolumbar extensors.

All of the abnormal firing sequences can lead to excessive activity in the shoulders and neck

muscles. This leads to cervical spine dysfunction. During walking, with a decrease in firing of

the gluteus maximus with each step, there is an increase in firing of the upper trapezius. This

leads to an anterior tilt and rotation of the lower cervical spine to the same side as the hip

extension and subsequent anterior pelvic tilting. The dysfunction in the cervical spine can lead to

shoulder dysfunction on the same side and eventually, in compensation, the opposite side as

well.

Hip abduction:

Normal hip abduction begins with the gluteus medius and minimus, then the TFL, quadratus

lumborum, abdominals, iliopsoas and rectus femoris.

There are two patterns of abnormal sequencing with hip abduction.

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Sequence 1:

5-6

Decreased activity of the gluteus medius will lead to the TFL acting as the primary mover. This

causes the external rotation of the pelvis upon abduction with the addition of external rotation

and flexion. This will be seen when the leg is raised into adduction as shown above. Sequence 1

is common in women and is found to begin in young adolescent girls. The gluteus medius

responds to hormonal changes as it is part of the muscles of the pelvic wall and is sensitive to the

hormones. The TFL does not belong to the pelvic wall muscle group and does not weaken with

hormonal changes. Therefore, the TFL becomes the muscle that supports the frame upon weight

shift during gait. This leads to tightness and contractures in the TFL and iliotibial band.

Sequence 2:

Excessive firing of the quadratus lumborum will raise the ilia cephalid during abduction altering

normal hip abduction. This firing may also be related to overactive back extensors.

Sit-up:

Overactive iliopsoas group can inhibit abdominal muscle function. An overactive psoas is tight

and can be recognized by anterior pelvic tilt, hip flexor contraction and/or loss of lumbar

lordosis. Antagonists that will inhibit a tight iliopsoas are the gastrocnemius/soleus, hamstrings

and gluteus maximus. As mentioned previously, tight lumbar extensors can inhibit abdominal

muscles.

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Neck flexion:

The primary muscle for neck flexion is the SCM. This is assisted by the accessory muscles

longus capitis, scalenes, rectus capitus and the infrahyoid. The accessory muscles flex the head

and stabilize the cervical spine as the SCM flexes the neck. With weak accessory muscles, the

contraction of the SCM will increase the cervical lordosis. The head will raise but the cervical

spine will rotate posteriorly on that side. The occipital muscles may also be overactive.

It is common in the neck that the SCMs are tight and the deeper neck flexors such as the scalenes

are weak. With this abnormal sequencing, when flexing from supine, the patient will

hyperextend their upper cervical spine then thrust the head and chin forward followed by the

neck flexion. This altered pattern is common after acceleration/deceleration impact.

Push-up:

During a push-up, it is important to view the firing of the scapula stabilizers which affect the

functionality of the upper extremity. During a push-up, if the scapula moves superiorly, it

indicates a tight upper trapezius and possible cervical spine issue. If the scapula shifts laterally,

there may be weak rhomboids and middle trapezius or possible tight pectoralis major or minor.

Scapula winging may indicate weak or inhibited serratus anterior. If the patient hyperextends

their lumbar spine, there may be weak abdominal muscles. Medial rotation of the scapula may be

due to tight upper trapezius and levator scapulae or weak mid and/or lower trapezius.

Shoulder abduction:

The normal sequencing during shoulder and arm abduction is from the supraspinatus and deltoid.

This is followed by a bilateral contraction of the upper trapezius in order to stabilize the neck.

The quadratus lumborum will then fire along with the contralateral peroneii. If the tip of the

acromion elevates prior to 60 degrees of abduction, this indicates issues in the shoulder or neck.

It could be an overactive upper trapezius. This can be seen with a weak deltoid. A rotation of the

scapula supero-medially may be caused by overactive levator scapulae.

There are two patterns of abnormal sequencing with shoulder abduction.

Sequence 1:

The upper trapezius is tight elevating the shoulder before 60 degrees abduction. This is noticed

when the patient will shrug their shoulders initially when attempting to abduct.

Sequence 2:

The quadratus lumborum becomes the initial prime mover so when the patient lifts an object,

they will first bend laterally to the opposite side. The peroneii and upper trapezius will contract

as well. This will all occur before the contraction of the supraspinatus and deltoid.