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Shoulder Pain and Dis Function

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Shoulder pain and dysfunction

Manual medicine
History of manual medicine:
• Manual medicine is as old as the science and art of medicine itself.
• Strong evidence shown in thailand 4000 years.
• Hipocrates,father of modern medicine.use traction for spinal deformity.
• In 19 th century found a renaiissance of interest,was a popular period of bone
setting in England and in the United States.
• 2 individuals who profoundlyinfluence the field of manual medicine:
• 1.Andrew Taylor Still MD(1828-1917) was a medical physician trained in the
preceptor fashion of the day. Proposed his phylosophy and practice Osteopathy.
• 2Daniel David Palmer(1845-1913).he was known as magnetic healer and became
self educated manipulative therapist.He is given credit for the origin of
chiropractic.
• In the first part of 20 th century,James Menell and Edgar Cyriax brought joint
manipulation recognition within the london medical community.
• John Bourdillon MD,a british- trained ortopedic- surgeon,he learned to perform
manipulation under general anesthesia and used the same techniques without
anesthesia.
• In the first part of 20 th century,James Menell
and Edgar Cyriax brought joint manipulation
recognition within the london medical
community.
• John Bourdillon MD,a British- trained
ortopedic- surgeon,he learned to perform
manipulation under general anesthesia and
used the same techniques without anesthesia.
• The practice of manual medicine should not be viewed in
isolation nor separate from regular medicine, and clearly is
not the panacea for all ills of humans.
• Manual medicine focuses on the musculoskeletal
system,which comprises more than 60% of human
organism and through of which evaluation of other organ
systems must be made.
• Manipulative medicine can be clinically effective in reducing
pain within the musculoskeletal system,in increasing the
level of wellness of patient and in helping patients with
myriads of disease processes.
• The goal of manipulation is to restore maximal pain free
movement of musculoskeletal system in postural balance
(Philip Greenman)
• Shoulder pain and dysfunction refer to pain
and decreased mobility localised to shoulder
region;base of neck,and the elbow but more
specifically to the region of deltoid
m,acromioclavicular joint,the sup part of
trapezius m,and the scapula
• Shoulder pain and dysfuction is characterised
by pain and decreased quality or quantity of
motion on active or passive movement of the
shoulder,is directly related to the shoulder
joints,articulations and muskuloskeletal origin.
• Preferred term that responds to manual
medicine is Shoulder somatic dysfunction.
Somatic Dysfunction
• Somatic dysfunction is the diagnostic criterion for which
manipulative/manual medicine is indicated.
• Definition of somatic dysfunction is as follows: Impaired or
altered function of related components of the somatic
(body framework) system: skeletal, arthrodial, and
myofascial structures, and related vascular, lymphatic,
and neural elements.
• Somatic dysfunction is treatable using manipulative
treatment.
• Criteria for diagnosis of somatic dysfunction;
• T .Tissue texture abnormalities.
• A. Asymmetry of bony landmark
• R. Range of quality of motion abnormalities.
• T. T enderness of temperature variations.
Epidemiology:shoulder pain and dysfunction
• Age:all,peak incidence:40-60years
• Gender:female
• Prevalence:most common msk disorder;UK;msk
complaints;Back
(23%),Knee(19%),shoulder(16%).
• Natural clinical course ;about 50% of all
episodes of shoulder dys.presenting in primary
care persist at least 1 year,regardless treatment
Common causes of shoulder pain and
decreased mobility
• Risk factor:
• Reduced mobility of the cervicothoracic junction has
an 84%predictive value for shoulder dys, and
increases the risk of developing disorder 3 fold.
• Depression;impaired conciousness
,elderly,spur,surgical intervention,th kyfosis,trauma.
• Work related risk factor;high level of
distress,repetitive shoulder motion,high job
demand,force and vibration.
• Associated conditions with pain and disability;
Ankylosing spondilitis,DM,fibromyalgia,
Multiple sklerosis,Neck dys,OA,polymyalgia,
Polineuropathy,RA,stroke.
Psychosomatic in adolescence.
Women living alone,smoking ,with social
support ,increase risk.
• Perpetuating Factors.

• Cervicothoracic spine and upper rib somatic


dysfunction that maintain shoulder
dysfunction.
• Fear –avoidance behavior.
• Psychosocial,cognitive and behaviour traits
Capsuloligamentous structures.
Schematic drawing
illustrating the glenoid fossa surrounded
by the labrum. Note
the infoldings of the capsule
representing the glenohumeral
ligaments. Outside of the capsule note
the rotator cuff muscles
and their corresponding tendons: SS:
Supraspinatus; IS: Infraspinatus;
TM: Teres minor; SSC: Subscapularis. The
coracoid
ligaments are also depicted: cc:
Coracoclavicular; ca: Coracoacromial;
ch: Coracohumeral
Shoulder region (Philip Greenman)
• sternoclavicular,acromioclavicular and glenohumeral
articulations,scapulocostal junction is not true articulation.
• direct restriction of this joint are the muscles and fasciae
that hold the scapula to the trunk.
• these myofascial elements best approached by soft tissue
and myofascial release techniques.
• particular att.must be given to trap,scm,lev
scap,rhomboids,seratus ant and lat dorsi muscles and their
fasciae
• Evaluation and treatment of the muscles should precede the
articulation in the shoulder region
Historical characteristic of shoulder somatic dysfunction;
• 1.Intensity; pain is sharp,and severe when from acute
muscle spasm,and its dull ,achy when chronic,as occurs
after inflammatory processes subside.
• 2.Precipitating factors;
• overuse or trauma,entails inflammation of soft tissue
structures ,leads to muscle imbalance and Shoulder
dysfunction,movement make pain worse.
• Cervic,thoracic or costal somatic dysfunction or pain
can precipitate or accompany shoulder pain and
dysfunction
• 3.location.pain and motion abnormal,can
include lower cervical,upper thoracic
spine.upper ribs.
• 4.Radiation;to upper arm or back from
shoulder somatic dysfunction.
• 5. Characteristics:Motion loss,weakness,muscle
imbalance,pain worse with movement.and
tenderness to palpation are more common.
• 6.Associated symptoms:cervicothoracic and
upper rib pain and dysfunction
Pathophysiology;
• Intrinsic shoulder pain can be caused by dys or
inflammation within structures,
• most commonly pain is generated from
articulations,muscles,tendons or lig of the shoulder
complex and shoulder girdle.
• Pain on movement is associated with entrapment of
subacromial soft tissue under the coracoacromial
complex.
• Reduced range of motion is associated with fibrosis
and adhesion of glenohumeral joint capsule and
surrounding soft tissue strucrures
• Loss of muscle strength occurs most often
with tears of the rotator cuff muscles or biceps
tendon.
• Whether these shoulder disorder are a
continum s part of the evolution of an initial
strain or sprain is unclear
• The impingement syndrome entails a series of pathologic
changes in supraspinatus tendons;
1. 1 stage 1:hemorrhage and edema
2. 2 stage2:tendonitis and fibrosis
3. 3 stage3: tendon degeneration of the rotator cuff and
biceps,bony changes,and tendon rupture
Special tests
Test Procedure Positive Sign Interpretation

Adson’s Practicioner passively slightly abducts and Diminished pulse Compression or occlusion of
slightly extends patient’s arm on affected the subclavian artery as it
side and palapates patient’s radial pulse traverses between the
while patient turns head toward or away anterior and the middle
from the affected arm and inhales deeply scalene muscles( thoracis
outlet syndrome)

Apley’s scratch Patient touches superior and inferior Decreased range Rotator cuff dysfunction
aspects of opposite scapula

Apprehension Practicioner abducts affected arm to 90⁰, Pain or apprehension about Anterior glenohumeral
externally rotates and applies anterior impeding subluxation instability
pressure on the humerus.

“Clunk” With patient supine, practicioner A “clunk” sound or clicking Glenoid labrum disorder
passively rotates and flexes the affected sensation is heard or felt (tear)
shoulder through its range

Cross-arm Patient actively flexes the affected arm to Acromioclavicular joint


90⁰ and actively adducts across his or her inflammation
trunk
Drop arm Passively abduct patient’s Arm drops without Rotator cuff tear;
affected arm to at least to control to the side supraspinatus
90⁰ and ask patient to lower weakness
it slowly down to the side

Empty can Patient attempts to elevate Weakness Rotator cuff tear;


arms against resistance with suprascapular nerve
shoulder flexed to 90⁰ and entrapment or
internally rotated , elbow neuropathy
extended, and forearm
pronated (thumb pointing
inferiorly)
Special test-cont’d
Test Procedure Positive Sign Interpretation

Hawkin’s Pracitioner passively toward flexes Subacromial pain Supraspinatus tendon


patient’s shoulder to 90⁰ and internally impingement or rotator
rotates it cuff tendonitis

Neer’s Patient’s arm is passively flexed and Subacromial pain Subacromial


forearm pronated. impingement

Relocation Pracitioner performs this after a positive Decrease in pain or Anterior glenohumeral
apprehension test result with patient apprehension joint instability
supine.
Pracitioner applies a posterior force on
patient’s humerus while externally
rotating the arm.

Scapula winging Patient pushes against the wall with Medial scapula border Serratus anterior
pracitioner behind patient observing displays posterior weakness or injury
scapulae for symmetry and degree of displacement
“winged” apperance of medial border.
Speed’s Patient’s elbow is passively flexed to Pain or lateral or Biceps tendon
20-30 ⁰ and forearm is supinated medial movement instability or
with the shoulder flexed to 60⁰. The of the biceps tendonitis
pracitioner resists patient’s active tendon
attemps to further flex the affected
shoulder while palpating with the
other hand the proximal biceps
tendon at the shoulder.
Spurling’s With patient seated, patient actively Radicular pain or Cervical nerve root
extends his or her spine, and paresthesias in a impingement or
pracitioner passively rotates patient’s dermatomal inflammation
head to the side of the affected pattern
shoulder while pressing down on the
top of patient’s head.
Sulcus sign With patient’s elbow flexed to Shoulder Inferior glenohumeral
90⁰,pracitioner pulls downward on depression or joint instability
patient’s elbow or wrist and and sulcus upon
observes the shoulder for a sulcus or provoaction
depression lateral or inferior to the
acromion
Yergason’s Patient’s elbow flexed to 90⁰ with the Pain in the biceps Biceps tendon
forearm pronated. Pracitioner holds tendon ( long head) instability or
patient’s wrist and resists patient’s tendonitis
attempt to actively supinate and flex
the elbow fully.
Muscle energy techniques (MET)

• Muscle energy techniques are a class of soft


tissue osteopathic (originally) manipulation
methods that incorporate precisely directed
and controlled, patient initiated, isometric
and/or isotonic contractions, designed to
improve musculoskeletal function and reduce
pain.
• Professor of biomechanics Philip Greenman (1996)
accurately and succinctly summarises most of the
potential benefits of correctly applied MET:
• The function of any articulation of the body, which
can be moved by voluntary muscle action, either
directly or indirectly, can be influenced by muscle
energy procedures … . Muscle energy techniques can
be used to lengthen a shortened, contractured or
spastic muscle; to strengthen a physiologically
weakened muscle or group of muscles; to reduce
localized edema, to relieve passive congestion, and
to mobilize an articulation with restricted mobility.
• Upper Extremity Region,
• Shoulder Girdle: Spencer Technique
• Indications;
• Adhesive capsulitis
• Bursitis
• Tenosynovitis
• Arthritis
Stage 1 Shoulder Extension with Elbow Flexed

1. The physician stands facing the patient.


2. The physician's cephalad hand bridges the shoulder to lock out any acromioclavicular and
scapulothoracic motion. The fingers are on the spine of the scapula, the thumb on the
anterior surface of the clavicle.
3. The physician's caudad hand grasps the patient's elbow.
4. The patient's shoulder is moved into extension in the horizontal plane to the edge of the
restrictive barrier.
5. A slow, gentle springing (articulatory, make and break) motion (arrows, Fig. 1) is applied at
the end range of motion.
6. Muscle energy activation: The patient is instructed to attempt to flex the shoulder (black
arrow, Fig. 2) against the physician's resistance (white arrow). This contraction is held for 3
to 5 seconds.
7. After a second of relaxation, the shoulder is extended to the new restrictive barrier (Fig.3).
8. Steps 6 and 7 are repeated three to five times and extension is reassessed.
9. Resistance against attempted extension (white arrow, Fig. 4) (reciprocal inhibition) has been
found to be helpful in augmenting the effect.
Figure 2. Stage 1, step 6.
Figure 1. Stage 1, steps 1 to 5.

Figure 3. Stage 1, step 7. Figure .4. Reciprocal inhibition.


Stage 2 Shoulder Flexion with Elbow
Extended
1. The physician's hands reverse shoulder and arm contact positions. The caudad hand
reaches over and behind the patient and bridges the shoulder to lock out
acromioclavicular and scapulothoracic motion. The fingers are on the anterior surface of
the clavicle, the heel of the hand on the spine of the scapula.
2. Using the other hand, the physician takes the patient's shoulder into its flexion motion
in the horizontal plane to the edge of its restrictive barrier.
3. A slow, springing (articulatory, make and break) motion (arrows, Fig.5) is applied at the
end range of motion.
4. Muscle energy activation: The patient is instructed to extend the shoulder (black arrow,
Fig. 6) against the physician's resistance (white arrow). This contraction is maintained for
3 to 5 seconds.
5. After a second of relaxation, the shoulder is flexed further until a new restrictive barrier
is engaged (Fig.7).
6. Steps 4 and 5 are repeated three to five times and flexion is reassessed.
7. Resistance against attempted flexion (reciprocal inhibition) has been found to be helpful
in augmenting the effect (Fig. 8).
Figure 5. Stage 2, steps 1 to 3 Figure 6. Stage 2, step 4.

Figure 8. Reciprocal inhibition.


Figure 7. Stage 2, step 5.
Stage 3 Circumduction with Slight Compression
and Elbow Flexed
1. The original starting position is resumed with the cephalad hand.
2. The patient's shoulder is abducted to the edge of the restrictive barrier
(Fig.9).
3. The patient's arm is moved through full clockwise circumduction (small
diameter) with slight compression. Larger and larger concentric circles
are made, increasing the range of motion (Fig. 10).
4. Circumduction may be tuned to a particular barrier. The same
maneuver is repeated counterclockwise (Fig.11).
5. There is no specific muscle energy activation for this step; however,
during fine-tuning of the circumduction, it may be feasible to
implement it in a portion of the restricted arc.
6. This is repeated for approximately 15 to 30 seconds in each direction,
and circumduction is reassessed.
Figure 9. Stage 3, steps 1 to 2. Figure 11. Stage 3, step 4.

Figure 10. Stage 3, step 3.


Stage 4 Circumduction and Traction with Elbow
Extended
1. The patient's shoulder is abducted to the edge of the restrictive barrier
with the elbow extended.
2. The physician's caudad hand grasps the patient's wrist and exerts vertical
traction. The physician's cephalad hand braces the shoulder as in stage 1
(Fig. 12).
3. The patient's arm is moved through full clockwise circumduction with
synchronous traction. Larger and larger concentric circles are made,
increasing the range of motion (Fig.13).
4. The same maneuver is repeated counterclockwise (Fig.14).
5. There is no specific muscle energy activation for this step; however, during
fine-tuning of the circumduction, it may be feasible to implement it in a
portion of the restricted arc.
6. This is repeated for approximately 15 to 30 seconds in each direction, and
circumduction is reassessed.
Figure 1 2. Stage 4, steps 1 to 2.

Figure 14. Stage 4, step 4.

Figure 13. Stage 4, step 3


Stage 5 A—Abduction with Elbow Flexed
1. The patient's shoulder is abducted to the edge of the restrictive barrier.
2. The physician's cephalad arm is positioned parallel to the surface of the table.
3. The patient is instructed to grasp the physician's forearm with the hand of the arm being
treated (Fig. 15).
4. The patient's elbow is moved toward the head, abducting the shoulder, until a motion
barrier is engaged. Slight internal rotation may be added.
5. A slow, gentle (articulatory, make and break) motion (arrows, Fig.16) is applied at the end
range of motion.
6. Muscle energy activation: The patient is instructed to adduct the shoulder (black arrow,
Fig. 17) against the physician's resistance (white arrow). This contraction is held for 3 to 5
seconds.
7. After a second of relaxation, the shoulder is further abducted to a new restrictive barrier
(Fig. 18).
8. Steps 6 and 7 are repeated three to five times, and abduction is reassessed.
9. Resistance (white arrow, Fig. 19) against attempted abduction (black arrow) (reciprocal
inhibition) has been found to be helpful in augmenting the effect.
Figure 15. Stage 5A, steps 1 to 3. Figure 16. Stage 5A, steps 4 to 5.

Figure 17. Stage 5A, step 6. Figure 18. Stage 5A, step 7.
Figure 19. Reciprocal inhibition.
Stage 5B Adduction and External Rotation with
Elbow Flexed
1. The patient's arm is flexed sufficiently to allow the elbow to pass in front of the
chest wall.
2. The physician's forearm is still parallel to the table with the patient's wrist resting
against the forearm.
3. The patient's shoulder is adducted to the edge of the restrictive barrier (Fig. 20).
4. A slow, gentle (articulatory, make and break) motion (arrow, Fig.21) is applied at the
end range of motion.
5. Muscle energy activation: The patient lifts the elbow (black arrow, Fig.22) against
the physician's resistance (white arrow). This contraction is held for 3 to 5 seconds.
6. After a second of relaxation, the patient's shoulder is further adducted until a new
restrictive barrier is engaged (Fig.23).
7. Steps 5 and 6 are repeated three to five times, and adduction is reassessed.
8. Resistance against attempted adduction using the physician's thumb under the
olecranon process (reciprocal inhibition) has been found to be helpful in augmenting
the effect (Fig.24).
Figure 20. Stage 5B, steps 1 to 3. Figure 21. Stage 5B, step 4.

Figure .22. Stage 5B, step 5. Figure .23. Stage 5B, step 6.
Figure 24. Reciprocal inhibition.to control joint movement,
when a group of muscle is activated
The opposing group is inhibited
Stage 6—Internal Rotation with Arm Abducted,
Hand Behind Back
1. The patient's shoulder is abducted 45 degrees and internally rotated approximately 90
degrees. The dorsum of the patient's hand is placed in the small of the back.
2. The physician's cephalad hand reinforces the anterior portion of the patient's shoulder.
3. The patient's elbow is very gently pulled forward (internal rotation) to the edge of the
restrictive barrier (Fig..25). Do not push the elbow backward, as this can dislocate an
unstable shoulder.
4. A slow, gentle (articulatory, make and break) motion (arrows, Fig. 26) is applied at the
end range of motion.
5. Muscle energy activation: The patient is instructed to pull the elbow backward (black
arrow, Fig. 27) against the physician's resistance (white arrow). This contraction is held
for 3 to 5 seconds.
6. After a second of relaxation, the elbow is carried further forward (arrow, Fig. 28) to the
new restrictive barrier.
7. Steps 5 and 6 are repeated three to five times, and internal rotation is reassessed.
8. Resistance against attempted internal rotation (arrows) (reciprocal inhibition) has been
found to be helpful in augmenting the effect (Fig. 29).
Figure 25. Stage 6, steps 1 to 3. Figure 26. Stage 6, step 4.

Figure 27. Stage 6, step 5. Figure 28. Stage 6, step 6.


Figure 29. Reciprocal inhibition.
Stage 7 Distraction, Stretching Tissues, and
Enhancing Fluid Drainage with Arm Extended
1. The physician turns and faces the head of the table.
2. The patient's shoulder is abducted, and the patient's hand and forearm are placed on the
physician's shoulder closest to the patient.
3. With fingers interlaced, the physician's hands are positioned just distal to the acromion
process (Fig. 30).
4. The patient's shoulder is scooped inferiorly (arrow, Fig. 31) creating a translatory motion
across the inferior edge of the glenoid fossa. This is done repeatedly in an articulatory
fashion.
5. Alternatively, the arm may be pushed straight down into the glenoid fossa and pulled
straight out again (arrows, Fig 32) with a pumping motion.
6. Muscle energy activation: Scooping traction is placed on the shoulder and maintained.
While the traction is maintained (curved arrow), the patient is instructed to push the hand
straight down on the physician's resisting shoulder (straight arrows). This contraction is
held for 3 to 5 seconds. After a second of relaxation, further caudad traction is placed on
the shoulder until a new restrictive barrier is engaged (Fig. 33).
7. Step 6 is repeated three to five times.
Figure 30. Stage 7, steps 1 to 3 Figure 31. Stage 7, step 4.

Figure 32. Stage 7, step 5. Figure 33. Stage 7, step 6.


– Pathophysiology of musculoskeletal Pain
Characteristics of Somatic-Neural Reflexes
Somatic Motor and Sensory Systems
• Neural control of the somatic motor system involves complex feedback
mechanisms between the brain, spinal cord, peripheral nerves, and
musculoskeletal structures.
• Each component is functionally and structurally capable of adaptation and
modulation to maintain as much as efficiency as possible
• The motor system continually adapts to injuries and somatic dysfunctions,
but each adaptation is less efficient than its predecessor. Manual treatments
are designed to alleviate somatic dysfunction to help the motor system
improve is efficiency.
• Afferent nerve impulses travel from the peripheral muscle or join structures
to the spinal cord, conveying information about pain, temperature, and
position.
• The afferent information from the muscles and joints is
transmitted to the dorsal root ganglion (DRG) and then to the
dorsal horn of the spinal cord
• Vibratory sensation or proprioception is transmitted superiorly
to the ipsilateral side of the brain, and other information, such
as pain and temperature, is transmitted across the cordto the
spinothalamic tract before being transmitted to the
contralateral side of the brain (Fig.2.1A)
• Somatic afferent impulses may also be transmitted to somatic
efferent cell bodies in the ventral horn, which send axons back
to the muscles to regulate muscle length and tone,completing
the somatosomatic reflex (see Fig.2.1B)
• Afferent impulses may travel to one or several levels of the spinal cord before the information
is sent out of the cord to the brain or to the periphery
• At every level, there is modulation and processing of the information with other afferent
stimuli.
• After the central nervous system processes and integrates the information it receives from the
peripheral structures, it sends out commands for action or inhibition of action to achieve a
desired result.

The Myotatic Reflex


• Muscle tension is regulated by the golgi tendon apparatus, which responds to the forces of
muscle strech and contraction (Fig 2.2).

1. Alpha motor eurons are efferent nerves from the ventral horn of the spinal cord that stimulate
the extrafursal muscle fibers to contract in response to central nervous system(i.e., brain and
spinal cord) demands
1. The Golgi tendon apparatus reports to the central nervous system the effect of the

eferent stimulus from the alpha motor neuron and enables refinement and further

modulation for controlled and appropriate activity.

• Muscle length is regulated by spinal nerves that innervate the muscle spindle in

the belly of the muscle ( see Fig 2.2)

• The spindle is innervated by gamma afferents and efferents and regulates

intrafusal muscle fiber length

• There are annulospiral and flower spray-type nerve endings within th emuscle

spindle that work in tandem

• The muscle spindle reports the changes of muscle length and the rate of change in

response to alpha ad gamma motor neuron activity and enables appropriate

adjusment by the central nervous system to regulate musle length


Neuroimmune Pathophysiology

Strain injury or trauma causes peripheral stimultion of prionflammatory


compounds ( e.g., bradykinin, histamine, cytokines, prostaglandins),
which extravasate fluids and irritate primary afferent nerves ( Fig. 2.3)
• Primary afferent nociceptors are small nerve fibres that transmit
impulses to the spinal cord from peripheral structures such as muscles
and joints in response to noxious stimulli
• They have little or no myelin and are classified as C- fibers.

• Their excitation often causes the perception of pain, but they can be
stimulated without eliciting a pain sensations.
• They are capable of promoting pain and of inhibiting pain
• The peripheral nerves become sensitized, lowering their treshold of
activation and increasing their rate of firing.

• Although sensory nerve fibers used to be considered only capable of


sending impulses and transmitting action potentials from the periphery
to the spinal cord and releasing neurotransmitter peptides at their
spinal cord synapses, it is now understood that they can be stimulated
from reflex activity by interneurons within the spinal cord ‘s dorsal horn
and through the dorsal root ganglia (i.e., dorsal foot reflexes).
Transmittion of neuropeptides to peripheral tissues through afferent
nerves from spinal cord stimulation is called antidromic transmission.
• At low levels of intensity,nociceptors can inhibit pain sensation, but at the
higher intensity, they can generate a series of spinal cord reflexes that
increase the sensitivity of the peripheral tissues, increasing pain sensation
to lesser stimuli and facilitating further inflammatory response
• The nociceptors that are stimulated also relese subtance P, calcitonin
gene-related peptide(CGRP) and somatostatin antidromically, which also
mediate vasodilation, spread the inflammatory response and contribute to
hyperalgesia of the inflamed area.
• Increased peripheral nervous system C- fibers afferent activity leads to
increased release of glutamates from the dorsal horn. The process, called
windup, occurs when the DRGs become sensitized to afferent input, which in
effect amplifies the nociceptive message. This hyperexcitability also affects
spinal cord neurons and results in central sensitization or facilitation (see Fig
2.3).
• This neurogenic inflammation is mediated from spinal neurotransmitter such


as - aminobutyric acid (GABA)
• Sympathetic efferents from the spinal cord can modulate this neurogenic
inflammation
• Enchanced sympathetic output from hypersensitive spinal cord segments
induces palpable alterations in local temperature and hydration of soft tissues.
• Increased blood flow,heat and moisture in
acute stage of injury and inflammation under
influence of local vasoactive peptides and
nitric oxide can be modulate modulated by
sympathetic tone and decreased blood flow
,coolness and dryness in chronic stage.
• This leads to palpable abnormal tissue texture
(edema) and hyperalgesia(sensitivity to
touch)characteristics of somatic dysfunction.
Central peripheral nevous system
sensitization
• Beta afferent nerve stimulaton(i.e., nociception)
alters patterns of neural activityin the dorsal and
ventral horns of the spinal cord

• Persistent spinal cord stimulation leads to


hypersensity and adaption of the spinal cord
at the segment affected.
• Spinal facilitation (i.e., central sensitization) also
causes sensitizationin related sensory receptive
regions of the brain
• Dorsal root reflexes can be generated by
descending activity from the brain
1. Stimulation of the midbrain periaquadetal
gray(PAG) increases serotonin release from
descending fibers originating in the raphe
magnus nucleus in the brain stem and GABA
release from spinal interneurons.
2. PAG stimulation is influenced by higher center,
such as the prefrontal cortex and amygdala,
which are associated with emotions.
3. Emotional processes likely modulate spinal cord
and peripheral nerve activity and influence
muscle and joint responses to strains, damage,
or trauma.
• The result of this sensitization is a sustained
hypertonicity of muscles innervated by the
facilitated spinal cord segment and
hypotonicity of antagonistic muscles( fig.2.5)
1. It is hypothesized that muscle spindles are
influenced by neurogenic antidromic stimulation
as well as the familiar effect of ventral horn
alpha motor neuron and gamma efferent
modulation as part of the myotatic reflex
2. Sustained muscle hypertonicity as found in
muscle spasm and somatic dysfunction is
thought to be the result of a combination of
peripheral and and central neuronal reflex
activity that involves prodromic and antidromic
neurotransmission.
• This reaction produces visible anatomic asymmetry of
easily identified bony landmarks and measurable
abnormal quality and quantity of related joint motion.

Myofascial Adaptions
• Myofascial connetcive tissue matrix adaptions
accompany the articular and periarticular motion
restrictions and muscle imbalance
• Joint immobilization or prolonged periods of
decreased motion enable the formation of an
increased amount o collagen crosslinks that cause
myofascial connective tissue stiffness
• The fluid content and contractile elements
within these connective tissues adapt to
modify tensions and maintain biomechanical
integrity and efficiency of the region.
1. Glycosaminoglycans (GAGs) are generated
from fibrocytes in response to motion
Table 2.2 palpable skin changes from altered
blood flow due to somatic dysfunction
Acute Phase Chronic Phase
(hours to days) (weeks to months)

Hyperemic Ischemic

Boggy or edematous Firm or flat

Warm Cool

Moist Dry

Sticky Slippery
2. GAGs are the linear polymers of repeating
disaccharide units that make up the ground
substance in the connective tissues
throughout the body
3. GAGs form the milieu in which the fibrous
collagenous fibers provide the form and
stiffness of the connective tissue.
4. GAGs are hydrophilic, and the amount of
GAGs present determines the relative fluid
content of the connective tissue
5. The more GAGs there are, the more water
binds to them, forcing the collagen fibers to
be farther apart and less able to form
crosslinks.
6. The fewer GAGs there are in the ground
substance, the stiffer and more noncompliant
in the connective tissue.
• Myofascial structures respond to sustained
stress forces (e.g., muscle spasms) by
undergoing deformation to accommodate the
load (i.e., creep). After the load is released,
the myofascial structures return toward their
initial state, but they never regain their exact
preload structure(i.e., hysteresis)

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