Shoulder Impingement Syndrome

Shoulder Impingement Syndromes

By Dale Buchberger, DC, DACBSP, ART

Charles Neer first established the concept of impingement in 1972. He described this condition as subacromial outlet obstruction resulting in irritation of the supraspinatus tendon.¹

Shoulder Impingement Syndromes

1. primary impingement
2. secondary impingement
3. subcoracoid impingement
4. posterior-superior glenoid impingement                                                                                         

a."internal glenoid impingement"

Primary Impingement

Etiologies of primary impingement:

1. subacromial spurring
2. subacromial fibrosis
3. acromioclavicular (AC) joint spurring
4. type II or III acromion
5. os acromiale

Neer Classification of Impingement

Type I: < 25 years of age, reversible, swelling, tendonitis, no tears, conservative treatment.

Type II: 25-40 years of age, permanent scarring, tendonitis, no tears, subacromial decompression (SAD).

Type III: > 40 years of age, small RTC tear, SAD with debridement/repair.

Type IV: > 40 years of age, large RTC tear, SAD with repair.

Acromial Morphology

Type I Acromion: flat, minimal impingement.

Type II Acromion: curved, higher rate of impingement.

Type III Acromion: beaked, highest rate of impingement, may be degenerative or congenital.

Characteristics of Primary Impingement

1. patients > 50 years of age
2. consequence of aging
3. mechanical compromise of the subacromial space

1. degenerative joint diseases of the AC joint
2. subacromial spurring
3. cuff atrophy
4. cuff or scapular weakness (poor posture)

Terminology

1. Neer referred to primary impingement as "outlet" impingement.
2. Dr. James Andrews calls it primary or external/subacromial impingement.

a. The superior or bursal side of the cuff is involved.

Symptoms

1. pain with overhead activities
2. pain when sleeping on the affected shoulder
3. anterior or anterolateral pain

Characteristics of Secondary Impingement

1. Patients are under 50 years of age.
2. Pain is anterior or anterolateral in location.
3. It is usually associated with an overhead activity.
4. Rarely night pain, unless chronic.
5. Rursal side on the RTC is affected.
6. Attenuation of the static anterior stabilizers leads to fatigue of the dynamic anterior stabilizers and subsequent anterior subluxation.

1. Impingement is secondary to functional and/or static instability.

Internal Glenoid Impingement Characteristics

1. posterior-superior impingement
2. involvement of articular surface of the rotator cuff
3. primarily seen in athletes using extensive overhead activities
4. extension, abduction and external rotation
5. impingement of the under side surface of the rotator cuff against the post-superior glenoid²

Initial Presentation

1. 65-year-old female with anterior shoulder pain when brushing her hair

a. primary impingement

2. 18-year-old baseball pitcher with anterior shoulder pain

a. secondary impingement

3. History

4. Exacerbating activities: reaching overhead, behind back, throwing, etc.

5. How long have the symptoms been present?

6. Is there a history of past trauma (micro or macro)?

7. Any neurological complaints?

a. Weakness is a neurological complaint when presenting without pain.

Symptom Patterns

1. Pain exacerbated by overhead activities and or symptomatic at night is classic for primary impingement. (Patient cannot lie on the shoulder.)
2. Secondary and internal impingement may present in this manner; however, pain is more predictably associated with overhead throwing and is less symptomatic at night.
3. Pain associated w/internal impingement usually is localized to the posterior aspect of the shoulder.
4. Neurological symptoms usually are associated with instability and the "dead-arm syndrome."

a. Patients complain of heaviness, but lack true neurological deficit.

b. The "dead arm" results from the humeral head tractioning the brachial plexus during episodes of subluxation.³

References

1. Neer, JBJS (A), 1972.
2. Jobe, 1995; Arroyo, 1997; Buchberger, 2000
3. Rowe JBJS (A), 1981.

Dale Buchberger, DC, DACBSP, ART
Associate Professor New York Chiropractic College
Seneca Falls, New York 

Shoulder Impingement Syndrome

By Deborah Pate, DC, DACBR

The impingement syndrome is a frequently overlooked but important cause of chronic shoulder pain and disability. Impingement occurs when there is encroachment on the subacromial space with loss of the normal sliding mechanism between the superior periarticular soft tissues of the glenohumeral joint and the coracoacromial arch.

Entrapment of the soft tissue structures between the coracoacromial arch and greater tuberosity of the proximal humerus during abduction or elevation of the arm results in subacromial bursitis and rotator cuff tendinitis with eventual progression to fibrosis and rupture of the rotator cuff.

Clinically, the impingement syndrome is seen in two main groups of patients. In young athletic patients involved in sporting activities in which frequent and repetitive overhead throwing motions are used (i.e., baseball, football, tennis), the onset of symptomatic impingement frequently occurs before 25 years of age. A second group consists of older patients in whom symptoms may appear spontaneously or in association with sporting activities (golf, tennis) or occupational stresses.

The impingement syndrome is characterized by sharp pain associated with abduction 70-120 degrees, external rotation 20-30 degrees, and internal rotation greater than 30 degrees. Classically, a full range of shoulder motion is present. The severity of the discomfort varies from mildly irritating to totally debilitating. On physical examination, crepitance may be palpated over the superior aspect of the shoulder at the point of impingement. Radiographic evaluation will demonstrate the presence of bony excrescences arising from the anteroinferior aspect of the acromion (subacromial spur) and sclerosis of the greater tuberosity of the humerus. Magnetic resonance imaging (MRI) will demonstrate changes in the supraspinatus tendon and many times there will be evidence of swelling and fluid. If the clinical symptoms are present and a subacromial spur is demonstrable on the plain films, the only additional imaging modality that may be necessary is another plain film of the subacromial region in the anteroposterior projection, with an x-ray tube tilt of 15 degrees in the cephalad direction which would separate the posterior portion of the acromion allowing a better view of the spur. If a subacromial spur cannot be demonstrated and clinical symptoms still indicate an impingement syndrome, a MRI of the shoulder may be necessary to demonstrate the more subtle types of shoulder impingement syndrome.

The treatment of the impingement syndrome depends on the chronicity of the disorder and associated abnormalities. In many patients, especially young athletes, the syndrome is first recognized at the stage of rotator cuff tendinitis and will generally respond well with conservative care. In the more chronic cases in which large subacromial spurs have caused a rotator cuff tear, anterior acromioplasty may be required.

Diagram of the x-ray position for demonstrating the acromioclavicular joint and subacromial spur.

Deborah Pate, D.C., DACBR
San Diego, California

Shoulder Impingement Syndrome

By David R. Reich

The shoulder impingement syndrome (SIS) is one of the more frequently encountered conditions affecting the shoulder joint. The majority of the cases are chronic/recurrent.

Apley's scratch test will usually be normal with reference to the patient placing the involved extremity's hand in front of their upper chest on the opposite anterior shoulder.

The test is usually normal with the hand behind and over the head, touching the spine of the contralateral scapula. When the patient attempts to place their arm behind the low back, reaching to touch the inferior angle of the contralateral scapular (internal rotation, extension, and adduction), there is significant pain and restriction.

My favorite orthopedic test for SIS is what I feel comfortable calling the "Slap Me Five" test. If you're from a different part of the country other than Queens, New York, you may feel comfortable calling it "Give Me Five." Have the patient semi-flex their shoulder to 90 degrees, externally rotating the shoulder and pronating the hand (like doing the Macarena), so that the patient's thumb is facing lateral. The doctor places his/her hand along the anterior aspect of the forearm, and exerts muscle-testing pressure inferiorward. Recreation of pain and surrender of muscle resistance are good indications of SIS.

Plain film radiographs are usually negative, but they should still be evaluated to rule out calcific tendinitis, calcific bursitis, and degenerative changes of the glenohumeral and acromio-clavicular articulations. These conditions can be concurrent and asymptomatic. An MRI evaluation is best to evaluate possible soft tissue hypertrophy associated with SIS. Even though imaging findings may be positive for anatomical impingement, this does not mean that the patient will not respond to conservative care. The opposite seems to be true in most cases.

The procedure which I feel is most appropriate in treating SIS is the activator methods technique. The subluxations which I find relatively consistent are the superior scapular, the distal superior clavicle, and the posterior humerus. The external humeral subluxation can also be involved, so I suggest the entire shoulder girdle (including the upper rib cage) be evaluated. The ribs can be responsible for scapula subluxations and must be checked. Needless to say, subluxations in the lower cervical/upper thoracic region must be corrected.

Adjunctive therapy should be performed taking into account the condition of the soft tissue. In most cases, there is little, if any, significant muscle spasm; however, true trigger points are usually evident, especially if the condition is chronic/recurrent. True trigger points may be tender to thumb pressure, but refer or radiate pain to a remote location. A good example may be a trigger point along the anterior shoulder radiating down the arm, or a trigger point along the posterior scapular referring pain into the superior distal clavicle. I like using combination therapy due to the fact that it is both diagnostic and treatment oriented. Between 6-8 treatments are usually necessary to resolve the majority of trigger points when proper adjustive procedures are being used.

With SIS, I recommend the Theraciser Rehabilitation System by Foot Levelers to the patient to exercise the shoulder joint. It is low-cost, low-tech, and very effective. Pendulum and wall-crawling exercises are also helpful.

Nutritional support is vital when treating SIS. Most chiropractors have developed their own protocols with regards to support of the musculo-skeletal system.

Most cases show significant improvement within the first 2 weeks of care with care rendered on a 3x/week basis, or daily if very acute. Treatment should be continued at a lesser frequency until maximum improvement is reached.

The criteria I use to determine MMI is after thorough evaluation of the shoulder, including basic, major and minor activator methods testing, the patient remains subluxation-free in the shoulder for 3 consecutive visits. This typically occurs after the symptoms have resolved, usually within 2-3 months of initiating active care.

Changes in activities of daily living may be in order for the patient, dependant on the patient's occupation, lifestyle, etc. In many cases, due to pre-existing degenerative changes, joint instability, or occupational predisposition, maintenance or symptomatic care may be necessary after MMI is reached.

David Reich, DC
Richmond Hill, New York

Impingement Syndrome

By Mark A. King, DC

Shoulder impingement syndromes are seen routinely in the chiropractic office and with the proper treatment, often can be resolved conservatively. You will tend to see this condition more commonly as your patients age, but it also is seen in younger patients who perform overhead movements repetitively (for example, swimmers) or overhead movements at high intensity (volleyball players, baseball pitchers, tennis players).

This condition also can come on from postural stress over a prolonged period of time; for example, sitting at a computer year after year.

The acromion type of shoulder impingement has a significant impact on prognosis; it is seen easily on MRI and typically commented on in the report. With a type I acromion, the prognosis is better because the acromion is relatively flat. The end of the acromion tends to arc downward with type II, and downward more significantly with type III.¹ So, for example, a 20-year-old competitive freestyle swimmer who has a type II or type III acromion would be more difficult to manage successfully with a conservative approach. The arced or curved acromion, seen with a type II or type III acromion, creates a structural irritation to the subacromion space, irritating the supraspinatus tendon. Initially, the tendon is irritated somewhat like a blister that progresses with hypertrophy of the ligamentous structures in the area. This leads to progressive stenosis in the area and a more challenging case.

There are several tests to check for impingement, including Hawkins test, in which the patient's arm is brought forward to the sagittal plane and then internally rotated. A positive test would cause pain specifically in the area of the A/C joint. This is also called the coracoacromial - clavicular impingement test.^2,3 Neer's test brings the arm up into full abduction to 180 degrees with passive forward elevation, and this impinges on the suprahumeral tissues.^2,3 The impingement syndrome is sometimes divided into an internal and external impingement, whereby external impingement is related primarily to the bursal side of the tendon and the closeness of this side with the coracoacromial arch. The internal impingement is related more to the articular side of the tendon near the glenoid labrum. Either way, the tests described to evaluate this are clinically relevant.

With regard to treatment, I use a comprehensive approach, in that I utilize adjustments, stretching of shortened tissues, elimination of any trigger points, soft-tissue work for musculature adhesions and fibrotic tissue, and low-tech rehab. I typically also add some anti-inflammatory nutritional recommendations.⁴ When adjusting this patient, it is particularly important to evaluate the sternoclavicular joint, C/T junction, and upper thoracic area. Be very careful with the A/C joint and glenohumeral joint, as vigorous adjusting in this area can aggravate the tissues, and these areas are sometimes irritating if you bring the arm too high up for the pectoralis minor. So, you will need to be cautious, talk to your patient about discomfort, and perhaps start with the pectoralis major in a more horizontal fashion.

I do postisometric relaxation stretches, but there are other ways to stretch out those shortened pectoralis muscles and scalenes; this is really up to the doctor and his or her preference. The soft-tissue treatments are varied and several are quite effective if you are proficient, including transverse friction at the musculotendinous junction and Graston Technique or Active Release Technique, etc., to the rotator cuff muscle adhesions and/or trigger points.

With regard to low-tech rehab, I start with the core because the first muscle that contracts with shoulder movement (in the non-low-back-pain population) is the transverse abdominis.⁵ I want the patient to have a stable foundation, because the scapulas and scapular stabilizers, including the rhomboids, middle and lower trap and serratus anterior are linked to the lumbar inner unit muscles via the thoracodorsal fascia. Scapular stabilization is very important in this condition because the rotator cuff muscles need something to anchor to, and an unstable scapula does not supply that. Regaining control of the scapula with modified push-ups to retrain the serratus anterior and middle and lower trap rehab, such as wall angels, will help stabilize the scapula and allow the rotator cuff muscles to start the process of returning to normal function.⁶ Once the scapulas are stabilized, rotator cuff rehab can be implemented. We have all seen patients who have done lots of rotator cuff rehab, to no avail. With some core stabilization and scapular rehab established first, your clinical success should improve significantly.

Learn to evaluate and treat these impingement syndromes, and you will expand your practice base. We are uniquely qualified as chiropractors to evaluate and treat these conditions successfully. Your patients will be most appreciative of you allowing them to avoid surgical intervention and returning them to their normal activities.

References

1. Souza T. Sports Injuries of the Shoulder. Churchill Livingstone, New York, 1994: p.5-6; see figures 1-6.2.
2. Porterfield J. DeRosa C. Mechanical Shoulder Disorders. Saunders, St. Louis, 2004: p.153-154; see figures 5-17.
3. Hammer W. Functional Soft Tissue Examination & Treatment by Manual Methods. Aspen Publishing, St. Louis, 1999: p.75; see figures 3-58 & 3-59.
4. Seaman D. Clinical Nutrition for Pain, Inflammation, and Tissue Healing. Nutranalysis, Hendersonville, NC, 1998: p.167.
5. Richardson C, Jul, G, Hodges P, Hides J. Therapeutic Exercise for Spinal Segmental Stabilization in Low Back Pain. Churchill Livingstone, New York, 199: p.44-48.
6. Murphy D. Cervical Spine Syndromes. McGraw-Hill, New York, 2000: p.505-508.

Mark King, DC
Cincinnat, Ohio

Avoiding Shoulder Impingement

Impingement syndrome is a common problem, often involving the supraspinatus muscle. Athletes and recreational weightlifters may unknowingly create shoulder problems through improper weight-training techniques that promote muscular imbalances and decrease the stability of scapulohumeral movement.

This article examines the role of the dynamic stabilizers in scapulohumeral motion and the potential contribution of poor weight-training techniques to shoulder impingement syndrome.

Specifically discussed are the role of the serratus anterior and the lower trapezius in generating shoulder impingement. Also included is a discussion of:

* scapular function and impingement;
* weight-training mistakes and alternative methods; and
* traditional rehabilitation techniques.

Suggestions are made to alter weight-training techniques to avoid impingement and promote facilitation of the lower trapezius and other dynamic scapula stabilizers. The author concludes that "by seeking balance within the musculature and avoiding impingement positions during exercise, the weightlifter reduces the likelihood of impingement."

Weinert D. Scapular stabilization exercises for weightlifters. Journal of Sports Chiropractic & Rehabilitation 1999:13(4), pp139-44.

Shoulder: Primary or Secondary Impingement?

By Warren Hammer, MS, DC, DABCO

In 1972 a surgeon by the name of Neer developed the theory of shoulder impingement caused by hereditary anterior acromial enlargement resulting in a stenosis of the coracoacromial arch.¹This theory greatly influenced the surgical community and acromioplasty became the operation of choice for shoulder impingement problems. 

This operation "often failed to return the athletically active patient to a prior level of athletic activity."² Neer also developed an hypothesis describing three progressive stages of impingement³which has appeared in many articles over the years. Like much information available to us these stages have been accepted as gospel: 

• Stage I referred to patients under 25 years old with a reversible condition due to edema, inflammation and hemorrhage.
  
  
• Stage II involved patients between 25 and 40 years of age with a thickened bursa, fibrosis and scarring of cuff tendons and biceps which was considered irreversible.
  
  
• Stage III referred to patients over 40 years of age with partial or full thickness rupture and bony changes.

Radiographic signs appeared which were not present in the first two stages. According to Uhthoff and Sarkar⁴ "there has been no adequate pathologic studies to establish the characteristic features of the first two stages." They feel that at present science is unable to classify impingement syndrome on the basis of pathologic changes. It is better to think of the syndrome as either uncomplicated (early and late stages usually responding to conservative treatment) or complicated (cuff ruptures and bony spurring which may require surgery). Ruptures can be due to chronic degeneration and be associated with impingement, but not necessarily a consequence of impingement.⁴

Tendon overuse that would be found aggravating younger patients under 25 rarely shows evidence of inflammatory cells. Nirschl² has coined the term angiofibroblastic tendinosis (disorganized collagen, fibroblasts and vascular elements without inflammation) to describe the pathology in Stage I and into the succeeding stages.

Neer was describing a primary impingement due to pressure of the anterior acromion. Therefore, according to his theory most of the pathology leading to eventual rupture should occur on the bursal or superior portion of the tendon. Based on the experience of Uhthoff and Sarkar⁴ most of the tears begin at the articular side (i.e., below the tendon) close to the insertion of the tendon. Nirschl² states that "The theory of primary impingement therefore comes under major challenge in that no clinical series reports clear, observable evidence of subacromial changes in over 25 percent of the cases." The supraspinatus first, then the infraspinatus and rarely the teres minor bare the brunt of most of the rotator cuff pathology.

Especially in the younger age group below 40 the etiology of most shoulder impingement problems are due to secondary factors rather than hereditary anomalies (anterior acromial beaking). Some secondary causes are: 

• eccentric muscular overload causing cuff fatigue and tendon swelling;
  
  
• muscle imbalances (such as tight posterior shoulder muscles and overdeveloped internal over external rotators) causing excessive anterior-superior humeral translation, stressing the cuff and capsuloligamentous tissue, or glenohumeral instability (anterior subluxation) resulting in: upward humeral migration and stress of the articular portion of the cuff tendons; fibrosis of the subacromial bursa; hypertrophy of the cuff (weightlifters); lagging of scapular motion, a result of weakened scapular rotators (especially the serratus anterior) failing to provide a stable base for the humerus and allowing excessive anterior superior humeral head translation.

Rehabilitation should be directed to strengthening all of the glenohumeral and scapular muscles that are weak. Soft tissue methods such as friction massage and Leahy's active release technique are excellent methods of eliminating adhesions and restoring normal mechanical motion. While except for gout, rheumatoid arthritis, pyogenic infections or tuberculosis, most bursitis conditions are secondary pre-tendinitis problems.⁵ The chronic fibrous bursa responds extremely well to deep friction over the involved bursa,⁶ although the patient should be warned that the first three visits may temporarily aggravate the condition.

References 

1. Neer C. Anterior acromioplasty for the chronic impingement syndrome in the shoulder: A preliminary report. J Bone Joint Surg (Am). 1972;54A:41.
   
   
2. Nirschl RP. Rotator cuff disease: etiology, pathology, treatment: In: Pettrone FA. Athletic Injuries of the Shoulder. New York: McGraw-Hill;1995:155-165.
   
   
3. Neer CS. Impingement lesions. Clin Orthop 1973;173:70-77.
   
   
4. Uhthoff JK, Sarkar K. Classification and definition of tendinopathies. Clin in Sports Med 1991;10,4:707-720.
   
   
5. Neviaser TJ. The role of the biceps tendon in the impingement syndrome. Orthopo Clin North Am 1987;18:383-6.
   
   
6. Hammer WI. The use of transverse friction massage in the management of chronic bursitis of the hip or shoulder. JMPT 1993;16,2:107-111.

Warren Hammer, MS, DC, DABCO
Norwalk, Connecticut