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

Shoulder instability can result from several factors including: altered glenoid position (hypoplasia), humeral retroversion (the normal humeral head has 30º of retroversion to the frontal axis of the elbow joint), and rotator cuff weakness.  Glenohumeral instability is classified by the direction of instability.  The most common directions are anterior and inferior.  Instability in these directions is often due to capsular deficiency in the inferior glenohumeral ligament.  Multidirectional instability describes a more global instability of the glenohumeralcapsule, one that involves multiple planes.

Instability is classified as traumatic or atraumatic in origin.  Traumatic instability involves unilateral dislocation in one direction (usually anterior and inferior) and usually requires reconstructive surgery.  Atraumatic instability is often multidirectional, evident in both shoulders and treated with rehabilitation.

Impingement is related to instability.  The term functional instability, which is defined as activity–related symptoms with or without clinically detectable laxity, is often used to describe the phenomenon of instability leading to impingement.  Mild instability increases the demands on the rotator cuff for stabilization, causing fatigue, anterior subluxation, and functional impingement.  Functional instability is related to sensorimotor dysfunction and often exhibits altered muscle activation patterns and muscle imbalances in strength and flexibility.

The glenohumeral joint provides important proprioceptive information to the surrounding muscles that provide dynamic stability.  Damage to the glenohumeral ligaments disrupts the capsular mechanoreceptors, thus reducing feedback to the dynamic stabilizing muscles.

The rotator cuff provides primary dynamic stabilization, while the biceps and deltoid provide secondary stabilization.  Any imbalance in strength or activation of the dynamic stabilizers can contribute to functional instability.  For instance, weakness of the infraspinatus decreases the compressive forces of the rotator cuff, while tightness of the pectoralis major increases anterior shear forces, promoting anterior instability.

Patients with shoulder instability often demonstrate altered muscle activation patterns.  Typically, activation of the serratus anterior, deltoid, and supraspinatus is decreased, while biceps activation is sometimes increased.  Scapular kinematics may also be altered (similar to impingement) by decreased posterior tilt and decreased upward rotation of the scapula.  The important role dynamic scapular stabilization plays in instability is supported by the high correlation between scapular position and centering of the humeral head on the glenoid.

Athletes who perform overhead movement patterns are particularly vulnerable to functional instability.  Swimmers with instability often have impingement, a condition otherwise known as ‘swimmers shoulder’.  Throwing athletes with shoulder instability demonstrate altered EMG patterns during throwing , including increased activity in the biceps and supraspinatus and decreased activity in the internal rotators and serratus anterior in order to avoid anterior instability.

Glenohumeral instability has been associatedwith imbalances in ROM, most notably an increase in external rotation and a decrease in internal rotation.  Excessive external rotation or a tight posterior capsule , commonly seen in athletes performing overhead movement patterns, is thought to increase inferior and anterior translation of the humerus, thus leading to instability.  Recently, some experts have suggested that capsular length is not associated with the characteristic imbalance of increased external rotation and decreased internal rotation.  They discovered significantly more posterior translation of the glenohumeral joint in both shoulders of baseball pitchers when compared to internal rotation.  This finding suggests laxity rather than tightness of the posterior capsule.  So, it is possible that the lack of internal rotation is related to muscular tightness rather than capsular tightness.

Shoulder and neck pain (described as ‘cervicobrachial pain syndrome’ or ‘trapezius myalgia’) is characterized by muscular pain in the upper trapezius and levator scapulae.  It is often related to overhead work activities or prolonged postures and is most often observed in females.

The ratio of UT:LT EMG activation is often elevated due to an overactive upper trapezius.  The symptom is described as pain over the upper medial angle of the scapula that radiates into the neck and shoulder.

Shoulder and neck pain are often seen in conjunction with UCS, impingement, and TOS.

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

Thoracic outlet syndrome (TOS) is characterized by compression of the neurovascular structures between the neck and the shoulder— specifically, between the scalenes and the first rib or between the pectoralis minor and the coricoid process.  Symptoms include parethesia, numbness, and pain in the upper extremity.  Obviously, muscle tightness and imbalance play a role in TOS.

Poor posture or repetitive overhead work can contribute to TOS.  Abnormal posture and compensated movement patterns cause an imbalance in muscle tightness and weakness in the upper back, neck, and shoulder contributing to increased mechanical pressure around the nerves.

The postural deviations that result from muscle imbalance in TOS include: tightness of the SCM leading to a forward head position, tightness of the upper trapezius and levator scapula causing elevation and protraction of the shoulder girdle.  Janda recommends releasing the short/tight ‘tonic’ structures (upper trapezius, levator scapula, scalenes, SCM, and suboccipitals).  The ‘phasic’ muscles (middle and lower trapezius and serratus anterior) will easily recover their strength, on their own.

Some schools of therapy (?), who shy away from hands-on bodywork, mistakenly attempt to strengthen (with exercise) the weak phasic muscles first.  From a neuromuscular perspective, this is ‘putting the cart before the horse’.  A basic understanding of Sherrington’s Law of Reciprocal Inhibition will clarify why the short/tight ‘tonic’ structures must be released first. 

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

Impingement is caused by narrowing of the SAS (subacromial space) either due to boney growth (primary impingement) or superior migration of the humeral head caused by weakness or muscle imbalance (secondary impingement).  The result is inflammation or damage to the rotator cuff tendons; therefore, chronic impingement can lead to rotator cuff tendinosis.  As secondary impingement is related to glenohumeral instability, it is sometimes described as functional instability; it occurs mostly in athletes less than 35 years of age who use overhead throwing motions.

Pathomechanics of Impingement

The pathomechanics of secondary impingement may involve one or both of the shoulder force couples:  the deltoid and rotator cuff or the scapular rotators.  Weakness or damage of the rotator cuff leads to an inability to control the upward shear of the humeral head into the SAS after activation of the deltoid during shoulder abduction.

Imbalance in the scapular rotator force couple leads to weakness and altered activation of the middle and lower trapezius and serratus anterior in impingement.  These alterations are often seen bilaterally, a finding that suggests a central mechanism of chronic tendinosis pain, consistent with Janda’s theories.

Patients with impingement demonstrate altered kinematics, including less upward rotation and external rotation as well as increased anterior tilt.  The change in scapular kinematics changes the orientation of the glenoid and is thought to reduce the SAS, thus compressing the rotator cuff and biceps tendon.  These changes also progress with age.

Scapular dyskinesis can be describes as a loss in scapular retraction and external rotation with altered timing and magnitude of upward scapular rotation.  This leads to an anterior tilt of the glenoid and subsequent reduction of rotator cuff force.

Athletes with impingement have significantly more EMG activity in the upper trapezius and significantly less EMG activity in the lower trapezius.In addition to weakness and muscle imbalance, muscle fatigue alters both glenohumeral and scapulothoracic kinematics.  Rotator cuff fatigue allows the humerus to migrate superiorly, while scapular fatigue leads to less posterior tilt and external rotation of the scapula.

Muscle tightness has also been implicated in secondary impingement.  A tight pectoralis minor limits upward rotation, external rotation and posterior tilt, and reduces SAS.