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Shoulder pain and dysfunction Manual medicine

Shoulder Pain and Dis Function

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Shoulder pain and dysfunctionManual 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 testsTest Procedure Positive Sign Interpretation

Adson s

Practicioner passively slightly abducts and slightly extends patient s arm on affected side and palapates patient s radial pulse while patient turns head toward or away from the affected arm and inhales deeply

Diminished pulse

Compression or occlusion of the subclavian artery as it traverses between the anterior and the middle scalene muscles( thoracis outlet syndrome) Rotator cuff dysfunction

Apley s scratch

Patient touches superior and inferior aspects of opposite scapula

Decreased range

Apprehension

Practicioner abducts affected arm to 90 , externally rotates and applies anterior pressure on the humerus.

Pain or apprehension about impeding subluxation

Anterior glenohumeral instability

Clunk

With patient supine, practicioner passively rotates and flexes the affected shoulder through its range

A clunk sound or clicking sensation is heard or felt

Glenoid labrum disorder (tear)

Cross-arm

Patient actively flexes the affected arm to 90 and actively adducts across his or her trunk

Acromioclavicular joint inflammation

Drop arm

Passively abduct patient s affected arm to at least to 90 and ask patient to lower it slowly down to the side

Arm drops without control to the side

Rotator cuff tear; supraspinatus weakness

Empty can

Patient attempts to elevate arms against resistance with shoulder flexed to 90 and internally rotated , elbow extended, and forearm pronated (thumb pointing inferiorly)

Weakness

Rotator cuff tear; suprascapular nerve entrapment or neuropathy

Special test-cont dTest Procedure Positive Sign Interpretation

Hawkin s

Pracitioner passively toward flexes patient s shoulder to 90 and internally rotates it

Subacromial pain

Supraspinatus tendon impingement or rotator cuff tendonitis

Neer s

Patient s arm is passively flexed and forearm pronated.

Subacromial pain

Subacromial impingement

Relocation

Pracitioner performs this after a positive apprehension test result with patient supine. Pracitioner applies a posterior force on patient s humerus while externally rotating the arm. Patient pushes against the wall with pracitioner behind patient observing scapulae for symmetry and degree of winged apperance of medial border.

Decrease in pain or apprehension

Anterior glenohumeral joint instability

Scapula winging

Medial scapula border displays posterior displacement

Serratus anterior weakness or injury

Speed s

Patient s elbow is passively flexed to 20-30 and forearm is supinated with the shoulder flexed to 60 . The pracitioner resists patient s active attemps to further flex the affected shoulder while palpating with the other hand the proximal biceps tendon at the shoulder. With patient seated, patient actively extends his or her spine, and pracitioner passively rotates patient s head to the side of the affected shoulder while pressing down on the top of patient s head. With patient s elbow flexed to 90 ,pracitioner pulls downward on patient s elbow or wrist and and observes the shoulder for a sulcus or depression lateral or inferior to the acromion Patient s elbow flexed to 90 with the forearm pronated. Pracitioner holds patient s wrist and resists patient s attempt to actively supinate and flex the elbow fully.

Pain or lateral or medial movement of the biceps tendon

Biceps tendon instability or tendonitis

Spurling s

Radicular pain or paresthesias in a dermatomal pattern

Cervical nerve root impingement or inflammation

Sulcus sign

Shoulder depression or sulcus upon provoaction

Inferior glenohumeral joint instability

Yergason s

Pain in the biceps tendon ( long head)

Biceps tendon instability or tendonitis

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 Flexed1. 2. 3. 4. 5. 6. 7. 8. 9. The physician stands facing the patient. 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. The physician's caudad hand grasps the patient's elbow. The patient's shoulder is moved into extension in the horizontal plane to the edge of the restrictive barrier. A slow, gentle springing (articulatory, make and break) motion (arrows, Fig. 1) is applied at the end range of motion. 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. After a second of relaxation, the shoulder is extended to the new restrictive barrier (Fig.3). Steps 6 and 7 are repeated three to five times and extension is reassessed. Resistance against attempted extension (white arrow, Fig. 4) (reciprocal inhibition) has been found to be helpful in augmenting the effect.

Figure 1. Stage 1, steps 1 to 5.

Figure 2. Stage 1, step 6.

Figure 3. Stage 1, step 7.

Figure .4. Reciprocal inhibition.

Stage 2 Shoulder Flexion with Elbow Extended1. 2. 3. 4. 5. 6. 7. 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. 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. A slow, springing (articulatory, make and break) motion (arrows, Fig.5) is applied at the end range of motion. 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. After a second of relaxation, the shoulder is flexed further until a new restrictive barrier is engaged (Fig.7). Steps 4 and 5 are repeated three to five times and flexion is reassessed. 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 7. Stage 2, step 5.

Figure 8. Reciprocal inhibition.

Stage 3 Circumduction with Slight Compression and Elbow Flexed1. 2. 3. The original starting position is resumed with the cephalad hand. The patient's shoulder is abducted to the edge of the restrictive barrier (Fig.9). 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). Circumduction may be tuned to a particular barrier. The same maneuver is repeated counterclockwise (Fig.11). 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. This is repeated for approximately 15 to 30 seconds in each direction, and circumduction is reassessed.

4. 5. 6.

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 Extended1. 2. 3. 4. 5. 6. The patient's shoulder is abducted to the edge of the restrictive barrier with the elbow extended. 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). 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). The same maneuver is repeated counterclockwise (Fig.14). 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. 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 Flexed1. 2. 3. 4. 5. 6. 7. 8. 9. The patient's shoulder is abducted to the edge of the restrictive barrier. The physician's cephalad arm is positioned parallel to the surface of the table. The patient is instructed to grasp the physician's forearm with the hand of the arm being treated (Fig. 15). The patient's elbow is moved toward the head, abducting the shoulder, until a motion barrier is engaged. Slight internal rotation may be added. A slow, gentle (articulatory, make and break) motion (arrows, Fig.16) is applied at the end range of motion. 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. After a second of relaxation, the shoulder is further abducted to a new restrictive barrier (Fig. 18). Steps 6 and 7 are repeated three to five times, and abduction is reassessed. 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 Flexed1. 2. 3. 4. 5. 6. 7. 8. The patient's arm is flexed sufficiently to allow the elbow to pass in front of the chest wall. The physician's forearm is still parallel to the table with the patient's wrist resting against the forearm. The patient's shoulder is adducted to the edge of the restrictive barrier (Fig. 20). A slow, gentle (articulatory, make and break) motion (arrow, Fig.21) is applied at the end range of motion. 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. After a second of relaxation, the patient's shoulder is further adducted until a new restrictive barrier is engaged (Fig.23). Steps 5 and 6 are repeated three to five times, and adduction is reassessed. 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 Back1. 2. 3. 4. 5. 6. 7. 8. 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. The physician's cephalad hand reinforces the anterior portion of the patient's shoulder. 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. A slow, gentle (articulatory, make and break) motion (arrows, Fig. 26) is applied at the end range of motion. 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. After a second of relaxation, the elbow is carried further forward (arrow, Fig. 28) to the new restrictive barrier. Steps 5 and 6 are repeated three to five times, and internal rotation is reassessed. 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 Extended1. 2. 3. 4. 5. 6. The physician turns and faces the head of the table. The patient's shoulder is abducted, and the patient's hand and forearm are placed on the physician's shoulder closest to the patient. With fingers interlaced, the physician's hands are positioned just distal to the acromion process (Fig. 30). 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. Alternatively, the arm may be pushed straight down into the glenoid fossa and pulled straight out again (arrows, Fig 32) with a pumping motion. 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). Step 6 is repeated three to five times.

7.

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 ReflexesSomatic 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. 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, predecessor. 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. efficiency. Afferent nerve impulses travel from the peripheral muscle or join structures to the spinal cord, conveying information about pain, temperature, and position. 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) (Fig. 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. 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. 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. 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. 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 e.g.,

stimultion

of

prionflammatory

compounds

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) K

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 dysfunctionAcute Phase (hours to days) Hyperemic Chronic Phase (weeks to months) 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)