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IMPINGEMENT RELIEF TEST: AN ADJUNCTIVE PROCEDURE TO TRADITIONAL ASSESSMENT OF SHOULDER IMPINGEMENT SYNDROME Gary Corso, MS, PT, ATC Assistant Professor, Department of Physical Therapy, Touro College,
Barry Z. Levine School of Health Sciences, Dix Hills, NY 11746. ABSTRACT Shoulder impingement syndrome is a common disorder that is directly related to the unique anatomy, mobility and biomechanics of the shoulder girdle complex. Shoulder impingement syndrome is usually a condition that results from repetitive microtrauma to the structures within the subacromial space such as the supraspinatus, infraspinatus, long head of the biceps and the subacromial bursa (19). Kamkar states that impingement syndrome has been classified as primary or secondary impingement.(12) The purpose of this article is to briefly review the biomechanics of the shoulder girdle and the pathology of impingement syndrome. The author also introduces an adjunctive assessment procedure that will help isolate and confirm the etiology of the shoulder impingement, as primary or secondary, so that treatment management can be directed toward the appropriate contractile or noncontractile tissue. KEY WORDS: impingement syndrome, impingement relief test, biomechanics. BIOMECHANICS A thorough knowledge of the anatomy, biomechanics, and movements of the shoulder girdle complex enhances the understanding of shoulder function. Inman's studies show that to maintain the shoulder in equilibrium, a minimum of three forces are required. The first is gravity acting through the center of the mass; secondly, the abducting muscles, primarily the deltoid; and lastly, the humeral head depressors. The rotator cuff and the long head of the biceps, acting in opposition to the forces of gravity, along with the abductors, are the main humeral head depressors (8). To elevate the humerus, either in flexion or abduction, the muscles must accommodate the spin, roll and glide of the head of the humerus. During forward flexion of the humerus, the humeral head glides inferiorly, rolls posteriorly and spins into internal rotation (12). The primary humeral flexors are the anterior deltoid, the clavicular portion of the pectoralis major and the coracobrachialis. During humeral abduction, the humeral head glides inferiorly, rolls superiorly and spins into external rotation (12). The primary abductors are the middle deltoid and supraspinatus. However if the flexors and/or abductors acted alone, they would result in GH compression of the subacromial space with little elevation. Therefore the humeral head depressors, the infraspinatus, subscapularis, teres minor and the long head of the biceps must contribute their combined actions to allow elevation of the humerus so that subacromial compression and impingement is reduced. Neer has stated that the primary cause of the impingement syndrome is the compression of the suprahumeral structures against the anteroinferior aspect of the acromion and coracoacromial ligament (8). Since the functional range of motion of the shoulder is primarily in the sagittal plane, the anterior structures, specifically the subacromial bursa, supraspinatus and biceps tendon are usually impinged (4,7,8). Full elevation of the arm requires scapular upward rotation and clavicular elevation to be effectively executed without impingement. Scapular positioning is essential to provide maximum stability, muscular advantage and full range of motion (ROM). For every fifteen degrees of humeral elevation, there are five degrees of scapular upward rotation and ten degrees of GH joint motion. Clavicular elevation is consistent in the first ninety degrees of humeral elevation. For every ten degrees of humeral elevation there is four degrees of clavicular elevation (8). Muscular force couples combine to move the clavicle, scapula and the humerus for proper stability and mobility of the arm. The muscles responsible for glenoid positioning are the trapezeii, levator scapulae, serratus anterior and the rhomboids. The force couples responsible for scapular upward rotation are the upper and lower trapezeii and the serratus anterior. Stability in rotation is accounted for by the rhomboids, trapezeii, and the pectoralis minor (8). PATHOLOGY The primary mechanism for impingement in the subacromial space is the approximation of the greater tubercle under the coracoacromial arch. The result is compression of the structures in the subacromial space, primarily the subacromial bursa, the supraspinatus and the long head of the biceps tendon. Kamkar cites Harner, (12) in defining a primary impingement is usually the result of subacromial crowding and posterior capsule tightness and humeral head depressor weakness. Kamkar also cites Harner, (12) in defining secondary impingement is a relative decrease of the subacromial space due to instability of the glenohumeral joint or functional scapulothoracic instability. Anatomically, the rotator cuff functions beneath the coracoacromial arch under the posterior two-thirds of the acromion and the anterior one-third of the thick coracoacromial ligament (4,5). As the arm is elevated past 80 ° of abduction held in neutral or internal rotation (IR), the supraspinatus tendon is impinged against the anterior one-third of the acromion. The biceps tendon, although not part of the cuff , also courses through this arch adjacent to the supraspinatus and is therefore impinged in the same manner. Pappas states that rotator cuff contraction provides joint stabilization, approximation and centralization of the humeral head within the glenoid fossa. Weakness of the rotator cuff results in insufficient stabilization allowing excessive movement of the humeral head in the glenoid fossa. This excessive movement will alter normal mechanics and irritate adjacent soft tissues (16,19). A thickening or separation at the AC joint may cause a secondary impingement syndrome. Neer states that the variations in shape and slope of the acromion may predispose some people to the impingement syndrome. Additionally, Kennedy asserts that chronic irritation of the avascular region of the supraspinatus, which is the anterior portion proximal to the insertion, may initiate inflammation resulting in a tendinitis (19). The irritation leading to inflammation will result in an encroachment of all the structures within the subacromial space (4,5).Neer and Welsh (15) classify impingement among three groups of people: (1) young athletes; (2) weekend athletes; and (3) middle-aged workers. Repetitive overhead stress to the shoulder results from many sports activities (19). Neer has characterized the impingement syndrome into three stages: Stage I: Typically the patient is 25 years of age or younger and predominantly engages in repetitive overhead work in ADL or athletics. The patient will often complain of a dull ache and occasionally biceps tendon tenderness. According to Hawkin's and Kennedy who comment on Neer's findings, evaluation of the patient will reveal a positive Speed's Test, positive impingement tests and a painful arc between 70 °-120° of abduction. Hallmark signs of this stage include edema and hemorrhage in the subacromial space accounting for the dull ache (9,19).Stage II: Typically 25-40 year old athletes. Stage I symptoms are still present with an increase in pain that limits activities and includes night pain. Limitations in both passive and active ROM are evident. Soft tissue crepitus may also be palpated and is usually caused by scarring in the subacromial space (9,19). Stage III: Forty year old and older athletes with a history of chronic tendinitis, significant tendon degeneration and an increased severity of pain and tenderness for prolonged periods. Infraspinatus atrophy is present on palpation and observation,. Manual muscle testing will usually reveal weak shoulder abduction and/or flexion. Limitation in shoulder motion is present more in active ROM than in passive ROM (9,19). DIAGNOSIS The most significant symptom of impingement is pain, specifically at night and with overhead activities. Progression of the impingement leads to impairment of function, fibrosing of the tendons and bursae and eventual tearing or rupturing of the involved tendons. Occasionally the chronic inflammation and pain can lead to stiffness (9). Most patients will complain of pain over the anterior shoulder or slightly lateral to the acromion. Pain is typically localized to the C5 dermatome. A positive impingement sign consists of a reproduction of pain by the examiner with an impingement test. Pain occurs with forceful flexion as the rotator cuff abuts against the anterior portion of the acromion with the arm in neutral (9). The patient may present with positive findings in any or all of the following special tests: 1. Supraspinatus Test: The patient's shoulder is passively abducted to 90°, angled forward 30° on the horizontal and maximally internally rotated so that the thumbs point toward the floor. A positive finding is confirmed if pain is elicited or a compensatory shoulder shrug occurs when resistance is applied (2,11,14,17). 2. Neer Impingement Test: The patient's arm is forcefully elevated in forward flexion by the examiner causing a "jamming" of the greater tuberosity against the anteroinferior acromion. Pain with this motion is an indication of a positive test. The shoulder is injected with 10ml of 1% Lidocaine into the subacromial space. A positive finding is confirmed if relief of pain is established on retesting (2,11,14,17,19). 3. Hawkin's-Kennedy Impingement Test: The test is administered in the standing position. The shoulder and elbow are passively flexed 90° and the shoulder is internally rotated. A positive test is if pain is elicited as the greater tuberosity and the supraspinatus tendon impinge under the anterior surface of the coracoacromial ligament and coracoacromial arch. (2,11,14,17). 4. Clancy Impingement Test: The arm is passively abducted to 90°, horizontally adducted and internally rotated across the chest. The test will be considered positive if pain is elicited as the greater tubercle hits under the coracoacromial arch (2,11,14,17). The long head of the biceps tendon, although not part of the rotator cuff, is adjacent to the supraspinatus and is often affected by impingement resulting in pain and tenderness. When the biceps tendon is inflamed, the patient may present with positive findings on the following tests: 1. Yergason's Test: The patient's elbow is flexed to 90° and stabilized against the thorax with the forearm pronated. The examiner resists forearm supination while the patient externally rotates the arm. A positive test elicits pain in the bicipital groove (2,11,14,17). 2. Speed's Test: The examiner resists forward flexion of the shoulder distally at the wrist, while the patient's forearm is supinated and the elbow is completely extended. Pain is elicited in the bicipital groove or cubital fossa for a positive test (2,11,14,17). Manual resisted muscle testing is necessary for differential diagnosis and to help isolate the etiology of the impingement. Loading the rotator cuff will give a relative idea of strength and discomfort (4). IMPINGEMENT RELIEF TEST The impingement relief test is used to confirm whether the cause of the impingement is due to muscle weakness secondary to a force couple imbalance, poor arthrokinematics in the joint and/or capsular restrictions that do not allow the head of the humerus to glide inferiorly or posteriorly. The author evaluated numerous shoulders with a diagnosis of impingement syndrome, rotator cuff tears and/or shoulder tendinitis over a three year period. Positive impingement tests were found in all cases utilizing a Hawkins-Kennedy and Clancy procedure. On evaluation all presented with painful arcs as well as varied muscle weakness especially with resisted external rotation and abduction. Altered scapulohumeral rhythm with pain in either flexion and/or abduction of the shoulder was also evident. Assessment of joint mobility will determine if restrictions are secondary to the inert structures that may impair GH mobility (12). Joint play mobility was utilized to assess the arthrokinematics for all shoulder motions with emphasis on inferior and posteroinferior glides for abduction and flexion respectively. When impingement tests proved positive, a relief test was immediately performed. The impingement relief test is performed with the patient standing. The patient actively abducts the shoulder to the point of pain. At the point of pain, the therapist applies a gentle inferior glide to the proximal humerus as the patient continues abducting the shoulder. The force should not hinder the abduction movement. The inferior glide is similar arthrokinematically to humeral head depression usually performed by the rotator cuff muscles and long head of the biceps. The patient should report a relief or a decrease in pain if the inferior capsule is not tight, restricted or impaired, therefore allowing the humeral head to "clear" under the coracoacromial arch without impingement. If relief can not be attained, the posteroinferior or inferior capsule may be restricting the humeral head from fully depressing, thus causing pain and dysfunction as the structures impinge under the coracoacromial arch. Joint mobilization is then performed to stretch the inferior and posteroinferior capsule. The test is repeated to determine whether joint mobilization was successful in decreasing or completely relieving pain. Treatment management will be directed to emphasize inert soft tissue mobilization, joint mobilization and stretching of the GH ligaments and capsule to allow the head of the humerus to depress and thus "clear" under the acromion and coracoacromial arch. If the patient has no inert structure limitations, complete relief will be achieved with the inferior glide on shoulder abduction. The cause may be related to contractile tissue weakness or imbalances, specifically between the rotator cuff muscles and the scapular upward rotators and the deltoid muscle. Strengthening of these muscles will be essential to provide proximal stability and will be the primary mode of treatment management. The impingement relief test gives a clear picture of the etiology of the impingement. Relief of pain is indicative of muscle weakness or muscle imbalance with no inert tissue restrictions. The inability to relieve the pain may possibly indicate a non-contractile or capsular lesion that does not permit humeral head depression. The relief test used in conjunction with other objective testing procedures, will help to direct the therapist to the best and most appropriate course of treatment. Treatment will address the primary tissue or structures involved. All conservative treatment revolves around three main principles: (1) diminish the inflammatory response; (2) maximize shoulder function including ROM and muscle balance; and (3) correct, modify and/or remove the cause of irritation. Joint mobilization, ROM and soft tissue mobilization are incorporated to restore GH ligament and capsular restrictions. Therapeutic strengthening exercises for the rotator cuff and the biceps are used to enhance muscular balance, strength and arthrokinematic function (4,12,19). SUMMARY Shoulder impingement syndrome is a common disorder addressed in orthopedic and sports physical therapy. The condition is a result of repetitive microtrauma to the structures in the subacromial space. A thorough knowledge of anatomy and biomechanics of the shoulder enhances the understanding of shoulder function. Traditional impingement tests, when positive, do very little except cause pain. In terms of confirming the structures involved the introduction of this adjunctive assessment procedure, used in conjunction with the traditional diagnostic techniques described in this article, will help to isolate the etiology of the impingement. The adjunctive assessment procedure will help to determine whether the cause of the impingement is contractile or non-contractile tissue therefore helping to direct the proper course of physical therapy treatment and provide for optimal recovery of patients with impingement signs.
1. Altchek D, Warren R, Wickiewicz T, Skyhar M, Ortiz G, Schwartz E:
Arthroscopic Acromioplasty. The Journal of Bone and Joint Surgery Vol 72-8,8:1198-1207,
Sept 1990
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