CHAPTER 2 Shoulder Disorder: From Dysfunction to the Lesion
“From dysfunction to lesion” is a very complex concept that involves knowledge and interpretation of different parameters that could alter a function and bring about a short-term and more often a long-term anatomic lesion. Initially, an ultrastructural lesion may evolve with distinctive peculiarities, and can be clinical or subclinical. It can show up with subjective and objective symptoms only under certain circumstances and according to intrinsic and extrinsic factors combined.1
Subacromial impingement syndrome is the most common shoulder disorder. It is present in 44% to 65% of all patients with a painful shoulder. This disorder can present in many forms, ranging from inflammation to degeneration of the bursa and rotator cuff tendons. It may lead to a full-thickness tear of the rotator cuff tendons and degenerative disease of the joints of the shoulder girdle. Impingement arises from mechanical compression of the rotator cuff, centered primarily on the supraspinatus tendinous insertion onto the greater tuberosity against the undersurface of the anterior third of the acromion.
Over the past few decades, this syndrome has been increasingly diagnosed. It was first described in the early 20th century. In 1931, Meyer2 proposed that rotator cuff tears occurred secondary to friction against the undersurface of the acromion and described corresponding lesions on the undersurface of the acromion and greater tuberosity. However, he did not implicate the acromion directly. Codman,3 in 1934, defined the critical zone where most degenerative changes occur as the portion of the rotator cuff located 1 cm medial to the insertion of the supraspinatus on the greater tuberosity. Armstrong4 introduced the term supraspinatus syndrome.
Neer and Welsh5 have described subacromial impingement syndrome as a distinct clinical entity and hypothesized that the rotator cuff is impinged on by the anterior third of the acromion, coracoacromial ligament, and acromioclavicular joint, rather than merely by the lateral aspect of the acromion. The clinical diagnosis of impingement syndrome is commonly based on findings defined by the impingement sign and test. The patient’s history typically includes pain at night and positional discomfort referred as a painful arc. The clinical presentation may be confusing, and it is important to differentiate subacromial impingement syndrome from other conditions that may cause symptoms in the shoulder. Especially in young patients and in overhead athletes, the diagnosis of impingement should be made carefully.
Partial or complete resection of the acromion has been reported to be a promising method in the treatment of rotator cuff syndrome. On the other hand, the disappointing results of complete and lateral acromionectomy prompted Neer6 to focus on the undersurface of the acromion as the offending area. He developed the technique of anterior acromioplasty, which includes acromioclavicular resection arthroplasty, when indicated, to correct impingement by decompressing the subacromial space. This procedure has been the gold standard for the treatment of impingement and still represents the main procedure for many surgeons.
The fact that acromioplasty relieves the impingement pain suggests the importance of the acromion in the cause of this disease. The shape of the acromion and angles of the spine of the scapula are associated with the pathogenesis of impingement syndrome. On the other hand, the mechanical cause of impingement might be related to several other factors. These numerous aspects are attributed to the extrinsic theory of the cause of impingement, according to which the lesion appears purely mechanical. The alternative to this mechanical theory is called the intrinsic theory. Its central idea is that the impingement syndrome occurs because of inherent degeneration of the rotator cuff tendons and associated shoulder muscle dysfunction.
Many causes have been proposed for subacromial impingement syndrome. These factors can be broadly classified as intrinsic or intratendinous factors, which are related to the intrinsic theory on the origin of impingement, and extrinsic or extratendinous factors, which are related to the mechanical theory. They can be further characterized as primary or secondary. A primary cause, either intrinsic or extrinsic, results in the impingement process by decreasing the subacromial space or by causing a degenerative process of the rotator cuff tendons. A secondary cause is the result of another process, such as instability, neurologic injury, tight posterior capsule of the glenohumeral joint, or muscle dysfunction.
Ozaki and colleagues7 have studied the pathologic changes on the undersurface of the acromion as associated with tears of the rotator cuff in 200 cadaveric shoulder. They suggested that rotator cuff tears or injuries are the result of intrinsic rather than extrinsic causes associated with impingement, as advocated by Neer.8 They found that although a lesion in the anterior third of the undersurface of the acromion was always associated with a rotator cuff tear, the reverse was not true, and they concluded that the pathogenesis of most cuff tears was probably an intrinsic process.
According to the extrinsic theory of the pathogenesis of impingement, the lesion in the rotator cuff tendon is caused by mechanical compression by the coracoacromial arch. Consequently, the disease process should come to a halt after decompressive acromioplasty, and the surgical outcome should be permanent. On the other hand, if the symptoms recur and the disease progresses to the tear stage despite acromioplasty, intrinsic factors, a degenerative process in the rotator cuff tendons, might be significant.
They concluded that the pathogenesis of most tears is probably a degenerative process. Ogata and Uhthoff9 have suggested that tendon degeneration is the primary cause of partial tears of the rotator cuff, and that they might allow proximal migration of the humeral head, which could result in impingement and lead to complete tears of the rotator cuff.
It has been observed that an intrinsic contractile tension overload on the muscle rather than primary impingement is the major factor in the cause of rotator cuff tendinitis. When the arm is in the overhead position, eccentric contraction of the supraspinatus decelerates internal rotation and adduction of the arm, causing an overload. This phenomenon is most dramatic in those involved in overhead sports, and it may also occur in manual workers who use overhead motions in their work. The proximal migration of the humeral head has also been associated with muscle fatigue, injury, and degenerative changes in the rotator cuff tendons. Bigliani and Levine10 have noted that resection of the coracoacromial ligament should be avoided in this situation because it may not relieve the impingement, but could allow for additional proximal migration of the humeral head. Decrease in proprioceptive sense with muscle fatigue might play a role in decreasing athletic performance and in fatigue-related shoulder dysfunction.
Imbalance of the rotator cuff muscles in athletes, who have developed this as a result of training or sport activities, has generally been found to be a predisposing factor or a consequence of the impingement syndrome. Brox and coworkers11 have reported that surgery and supervised exercise improve rotator cuff disease equally and significantly compared with placebo, suggesting the importance of considering this factor.
Acromial morphology and differences in the shape and slope of the acromion as a potential source of symptoms in the shoulder have often been observed. Neer6 focused on the cause and effect relationship between acromial morphology and subacromial impingement. He proposed that variations in the shape and slope of the anterior aspect of the acromion were responsible for subacromial impingement and associated tears of the rotator cuff. A spur protruding into the subacromial space10 apparently was thought to be caused by tensile forces on the coracoacromial ligament. In another study, Morrison and Bigliani12 evaluated supraspinatus outlet radiographs and found that 80% of 82 patients who had a tear of the rotator cuff visible on an arthrogram had a type III acromion (hook acromion).
The classification system described by Bigliani and colleagues13 has been cited widely in the literature, but investigators have questioned its reliability. Zuckerman and associates14 reported low interobserver reliability during the evaluation of 110 anatomic specimens to determine acromial shape according to this classification.13 Jacobson and coworkers15 also reported low interobserver reliability when the system was used to evaluate acromial morphology as seen on a supraspinatus outlet view. They also questioned the correlation between acromial morphology and tears of the rotator cuff. The classification of acromial morphology on the basis of a subacromial outlet projection has reportedly been difficult because of individual differences in the supraspinatus outlet angle. Some investigators have stated that fluoroscopic control is necessary for a proper supraspinatus outlet view.
Wuh and Snyder16 have modified their classification system13 by addressing the thickness as well as the shape of the acromion. Three types of acromion were identified: type A (<8 mm), type B (8 to 12 mm) and type C (>12 mm).
Toivonen and colleagues17 measured the acromial angle, which is in accordance with the hypothesis proposed by Morrison and Bigliani12 of an association between acromion type III and rotator cuff tears. Aoki and associates18 studied 130 cadaveric shoulders and found that acromions with spur formation had a flatter slope and were associated with increased pitting on the surface of the greater tuberosity. They also showed that the prevalence of spurs in the subacromial space increased with age and noted a decreased alpha angle (also called acromial tilt) in the patients with impingement.
Neer6,8 proposed that degeneration of the acromioclavicular joint may contribute to subacromial impingement. This hypothesis is supported by several other authors. Osteophytes protruding inferiorly from the undersurface of a degenerative acromioclavicular joint can contribute to impingement narrowing the supraspinatus outlet. Kessel and Watson19 found that one third of the patients in their study had lesions of the supraspinatus tendon, usually associated with degeneration of the acromioclavicular joint. Penny and Welsh20 subsequently found that osteoarthritis of the acromioclavicular joint may lead to failure of operative treatment of subacromial impingement. However, resection of the acromioclavicular joint should be performed only if the patient has symptoms in the joint region and if osteophytes contribute to the impingement.10
Coracoid impingement along the more medial aspect of the coracoacromial arch is less common, but has been reported.21 In patients with coracoid impingement, the pain is usually located on the anteromedial aspect of the shoulder and is felt in the arm and forearm. Forward elevation and internal rotation may elicit pain.10 In a recent study, cine magnetic resonance imaging was used to measure the interval between the coracoid process and the lesser tuberosity. In the asymptomatic control group, the average interval between the coracoid process and the lesser tuberosity was 11 mm, whereas in symptomatic patients the interval was found to be 6 mm. Gerber and coworkers22 have reported that coracoid impingement can be idiopathic, iatrogenic, or traumatic. As a choice for operative treatment, Dines and colleagues23 have recommended coracohumeral decompression.
A number of investigators6,8,24 have also implied the coracoacromial ligament as a source of impingement. McLaughlin25 observed the condition termed snapping shoulder and concluded that the coracoacromial ligament is an offending structure in painful shoulders.
Soslowsky and colleagues26 found statistically significant changes in the geometric dimensions of the lateral band of the coracoacromial ligament, which is the region most likely to impinge on the rotator cuff. In another study, they found significant changes in the material properties of the ligament. Sarkar and associates27 and Uhthoff and coworkers24 reported that histologic studies of specimens of the coracoacromial ligament from patients who had impingement syndrome revealed only degenerative changes without thickening.
Os acromiale is an unfused distal acromial epiphysis first described in 1863 by Gruber.28 Folliasson29 classified the lesion into four distinct types according to the anatomic location, with mesoacromion being the most common type. The prevalence of os acromiale, as reported in both radiographic and anatomic studies, has varied a great deal, with a range from 1% to 15%. It is difficult to detect an os acromiale on routine anteroposterior plain x-rays and an axillary view may thus be needed.10 An association between os acromiale, impingement syndrome, and rotator cuff tears has been reported. Impingement may occur because the unfused epiphysis on the anterior aspect of the acromion may be hypermobile and may tilt anteriorly as a result of its attachment to the coracoacromial ligament. Hertel and colleagues30 have recommended stable fusion of a sizeable and hypermobile os acromiale.
There is a subset of patients who may have an initial diagnosis of impingement syndrome, but remain refractory to nonoperative and traditional operative treatment. Posterior capsule tightness may be forcing the humeral head forward, causing mechanical impingement and a loss of range of motion as a result of the avoidance of painful movements. Although the factors contributing to secondary shoulder impingement are multiple, the posterior capsule tightness is thought to alter arthrokinematics, with superior translation of the humeral head during flexion such that the rotator cuff is compromised by the overlying coracoacromial arch.
Harryman and associates31 have stated that oblique glenohumeral translations are not the result of ligament insufficiency or laxity. Instead, translation results when the capsule is asymmetrically tight. Asymmetrical tightness is thought to cause anterior and superior migration of the humeral head during forward elevation of the shoulder, possibly contributing to impingement.
Glenohumeral joint inflexibility can also create abnormal biomechanics of the scapula. Posterior shoulder inflexibility caused by capsular or muscular tightness affects the smooth motion of the glenohumeral joint31 and creates a wind-up effect so that the glenoid and scapula actually get pulled in a forward and inferior direction by the moving and rotating arm. This can create an excessive amount of protraction of the scapula on the thorax as the arm continues into the horizontally adducted position in follow-through. Because of the geometry of the upper aspect of the thorax, the more the scapula is protracted in follow-through, the farther it and its acromion move anteriorly and inferiorly around the thorax.
It is unclear why the posterior capsule becomes scarred and contracted, although some would postulate that in case of injury associated with a traction mechanism, trauma to the posterior capsule results in localized and excessive scarring. In patients who underwent a posterior capsular shift procedure, the repair might too tight or there might be an excessive scarring in this region following the repair.
Reeves32 has proposed that the stiff shoulder be classified as a frozen shoulder or post-traumatic stiff shoulder. The term frozen shoulder, introduced by Codman33 in 1934, refers to no traumatic stiffness of the glenohumeral joint capsule.
Idiopathic adhesive capsulitis is a condition of uncertain cause characterized by limited active and passive shoulder motion. Primary adhesive capsulitis develops insidiously, following minimal or no trauma, with a gradual loss of function caused by pain and restriction of motion. Adhesive capsulitis may also occur secondary to intrinsic shoulder pathology, such as subacromial impingement syndrome, extrinsic disorders such as pulmonary disease, or systemic conditions such as diabetes. Despite these associations, the underlying cause and pathophysiology of this disorder remain unknown.
Although many different causes have been proposed for frozen shoulder, the common thread in most causal theories is the presence of inflammation. On the other hand, a post-traumatic stiff shoulder may originate from a traumatic extracapsular process; however, subsequent capsular contracture may soon develop. Each of these diagnoses may exhibit a different underlying pathology, history, and treatment.
Clinically, much attention has been paid to how a tight posterior capsule might affect normal glenohumeral arthrokinematics. In all cases of suspected impingement, a careful examination of passive and active motion in all planes is needed. In patients with limited internal rotation and flexion, a therapy program should be directed at improving these motion planes.
Scapulothoracic dyskinesia is abnormal scapular motion characterized by medial border prominence or inferior angle prominence, early scapular elevation or shrugging, rapid downward rotation during lowering, or a combination of these. It is noteworthy that in the causative pathogenetic classification of the most common shoulder disorder (impingement syndrome), an anatomostructural alteration (e.g., acromion III, os acromiale, posterior capsule tightening) is often seen as the trigger element, without considering the shoulder as part of a kinetic chain.
Our research, based on a number of studies, leads us to consider more comprehensively the causative pathogenetic mechanisms of this joint’s pathologies. Always bearing in mind possible local anatomic lesions, we try to interpret those distant musculoskeletal dysfunctions as trigger points that through neurophysiologic and biomechanical mechanisms, can lead to ligament and shoulder tendon lesions. In this case, the shoulder joint becomes the victim and not the culprit of a dysfunction, eventually resulting in an anatomic injury, with clinical findings affecting the shoulder girdle.
This type of approach might explain the failure of some surgical ligament and tendon repair techniques, often attributed to failed materials (e.g., anchors, suture, biologic and not reabsorbable) or local biologic factors (e.g., vascularization, fatty infiltration), forgetting that these anatomic lesions are often the end point of a failure in the kinetic chain, which if not corrected could inevitably reproduce the lesion over time, even after surgery.
The dynamic scapulothoracic stability and importance of the core stability strongly indicate that those mechanisms, when altered, can lead to shoulder dysfunction. The shoulder is a complex mechanical structure containing several joints connecting the humerus, scapula, clavicle, and sternum. The scapula slides over the dorsal part of the thorax; it can glide over the so-called scapulothoracic gliding plane. It is a closed-chain mechanism. The relationship between the rotations of the humerus and scapula is commonly referred to as the scapulohumeral rhythm. The scapular motion strongly affects the mechanical energy delivered by muscles and the metabolic cost required to obtain the desired force. At the same time, the scapula has different roles; it is a functional part of the glenohumeral joint, retracting and protracting along the thoracic wall and elevating the acromion. It is a site for muscle attachment and a link in the proximal to distal sequencing of velocity, energy, and force that allows the most appropriate shoulder function.34