Continuum of Injury for Disorders of the Rotator Cuff
Impingement Syndrome<--------------------------------------------------->Full-Thickness Rotator Cuff Tears
Classification of Rotator Cuff Disease
(modified from Wilk KE)
- Primary compressive
- Primary tensile overload
- Secondary compressive
- Secondary tensile overload
- Internal Impingement
- Posterior internal
- Anterior internal
- Rotator cuff failure/tear
- Calcific tendonitis
- PASTA lesions: Partial Articular-sided Supraspinatus Tendon Avulsion
Wilk KE. Recent Advances in the Evaluation and Treatment of the Shoulder. Advanced Continuing Education Institute Course, 2006 (www.advancedceu.com)
Biomechanics of Impingement Syndrome
Translation of the humeral head in the magnitude of 1-3 mm occurs in the superior direction in the first 30 to 60 degrees of active GH scapular plane elevation (Poppen and Walker, 1976; Chen et al, 1999; Ludewig and Cook, 2002) or during simulated elevation in the scapular plane (Kelkar et al, 1992; Thompson et al, 1996).
After the initial phase of elevation in the scapular plane or frontal plane abduction, the humeral head remains somewhat centered on the glenoid cavity, with fluxuations between inferior and superior translations typically less than 1 mm (Poppen and Walker, 1976; Ludewig and Cook, 2002; Kelkar et al, 1992; Thompson et al, 1996; Eisenhart-Rothe et al, 2002; Sharkey and Marder, 1995; Deutsch et al, 1996; McMahon et al, 1995; Wuelker et al, 1994b; Paletta et al, 1997; Yamaguchi et al, 2000; Graichen et al, 2000). The glenohumeral joint demonstrates essentially ball and socket kinematics above approximately 60 degrees of glenohumeral elevation.
Anterior humeral head translations in the magnitude of 2.5 mm have been demonstrated during simulated active glenohumeral flexion (Wuelker et al, 1994b). During active glenohumeral flexion, anterior humeral head translation or less than 1 mm occurs over the course of motion (Wuelker et al, 1994b; Harryman et al, 1990a, b, 1992).
Other studies have revealed 0.7-2.7 mm of anterior translation in the first 30- to 60-degree phase of scapular plane abduction, 0-1.5 mm of posterior translation in the 60- to 90-degree phase, and 4.5 mm of posterior translation in the 90- to 120-degree phase (Ludewig and Cook, 2002, Eisenhart-Rothe et al, 2002; Graichen et al, 2000). Conversely, one study demonstrated anterior translation of approximatey 1 mm in the final phase of 90 to 120 degrees of elevation (Graichen et al, 2000).
During active glenohumeral elevation, increased superior humeral head translation of 1-1.5 mm (Poppen and Walker, 1976; Deutsch et al, 1996) and increased anterior translations of approximately 3 mm (Ludewig and Cook, 2002) has been demonstrated in patients with impingement syndrome. Increased superior humeral head translations have also been demonstrated, with RTC tendon degeneration during active or simulated active glenohumeral elevation of 1.5-5 mm (Poppen and Walker, 1976; Thompson et al, 1996; Deutsch et al, 1996; Paletta et al, 1997; Yamaguchi et al, 2000).
Excessive superior translations were also demonstrated (Chen et al, 1999; Sharkey and Marder, 1995), with weakness or induced fatigue of the deltoid and RTC in healthy subjects during abduction in the coronal plane or scapular plane. The amounts of excessive anterior anterior and superior translations range from 1-5 mm, which would appear to be potentially insignificant due to their small magnitude. However, because the subacromial space is small in volume and contains the subacromial structures, there is little room for "error."
Three-dimentional scapular kinematics in asymptomatic shoulders have utilized a variety of techniques including radiographs, magnetic tracking devices, and electric digitizers (Ludewig and Cook, 2000; Lukasiewicz et al, 1999, van der Helm and Pronk, 1995; Kondo et al, 1984; Hogfors et al, 1991, Johnson et al 1993, McQuade et al 1995, Ludewig et al, 1996; Meskers et al 1998b; de Groot 1999; Price et al 2000; Karduna et al 2001). The scapula demonstrates a pattern of upward rotation, external rotation, and posterior tilting during glenohumeral elevation, with the predominate motions being upward rotation. For translations during glenohumeral elevation, the clavical retracts posteriorly and elevates, putting the scapula in essentially a more superior and posterior position (van der Helm and Pronk, 1995; McClure et al, 2001; Meskers et al, 1998a).
Two 3/16-mm steel bone pins were drilled directly into the scapula of eight healthy subjects by McClure et al (2001). A mean of 50 degrees of UR, 30 degrees of PT, and 24 degrees of ER were seen during scapular plane glenohumeral elevation. For glenohumeral flexion in the coronal plane, the results revealed a mean of 46 degrees of UR, 31 degrees of PT, and 26 degrees of ER. A mean of 21 and 20 degrees of clavicular retraction and a mean of 10 and 9 degrees of clavicular elevation were revealed during glenohumeral scapular plane elevation and flexion respectively.
Altered scapular kinematics have been demonstrated in patients with SAIS (Ludewig and Cook, 2000; Lukasiewicz et al, 1999; Warner et al, 1992; Endo et al, 2001). Warner et al (1992) demonstrated a pattern of increased scapular winging with GH elevation, using a Moire topography technique. This winging pattern appears to represent scapular internal rotation and anterior tilting.
Three-dimentional kinematic analysis during GH elevation revealed decreased posterior tilt (Ludewwig and Cook, 2000; Lukasiewicz et al, 1999), upward rotation (Ludewig and Cook, 2000), and external rotation (Ludewig and Cook, 2000). Radiographic assessment at multiple joint angles revealed a decrease in scapular posterior tilt and upward rotation at 90 degrees of glenohumeral elevation, and a decrease in posterior tilt at 45 degrees of GH elevation (Endo et al, 2001). Scapular upward rotation results in elevation of the acromion, while posterior tilting elevates the anterior acromion, both of which appear to be important during GHE to prevent impingement (Flatow et al, 1994).
Shoulder retraction, of which scapular posterior tilting seems to be a component, has been demonstrated to increase the area of the subacromial space compared with shoulder protraction (Bertoft et al, 1993). Scapular kinematics can be altered by surrounding soft tissues and bone, such as weak or dysfunctional scapular musculature (Ludewig and Cook, 2000; McQuade et al, 1998; Pascoal et al, 2000), fatigue of the infraspinatus and teres minor (Tsai, 1998), and changes in thoracic and cervical spine posture (Kebaetse et al, 1999; Ludewig and Cook, 1996; Wang et al, 1999).
Rehabilitation of Subacromial Impingement Syndrome
Therapeutic interventions will be based on underlying pathology, impairments, functional limitations (activity restrictions), and disability (participation restrictions). Treatment for the various types will be discussed below.
Primary Impingement Syndrome
Primary impingement can be either compressive, where the rotator cuff becomes physically damaged by the the coracoacromial arch structures, or can be the result of tensile overload, where the tendon becomes inflamed from an acute event or repetitive microtrauma.
The subacromial space, or the space between the inferior acromion and superior surface of the rotator cuff tendons, has been measured on anteroposterior radiographs as 7-13 mm (0.7-1.3 cm) in patients with shoulder pain (Golding, 1962) and 6-14 mm in normal shoulders (Cotton and Rideout, 1964; Flatow et al, 1994). This is a relatively small space for the the subacromial tissues to occupy. Any alteration in the space occupying these tissues has the potential to create pathology. The subacromial space and its occupying tissues, from superior to inferior, are follows:
- Subacromial and subdeltoid bursa
- Supraspinatus tendon
- Joint capsule
- Biceps tendon
- Humeral head
The type of acromion has an effect on the subacromial space. There are three types of acromions:
- Type I, or flat
- Type II, or curved
- Type III, or hooked.
Reporting on a morphological study in 140 cadaver shoulders, Bigliani and Morrison (1986) found that the shape of the acromion was correlated with tears of the RTC. Candavers with hooked (Type III) acromions had less room for the subacromial tissues to function and were more susceptable to tears.
An inflamed, hypertrophic bursa can also decrease the subacriomial space.
Physical Therapy for Primary Impingement Syndrome
The goals of physical therapy for patients with primary compressive impingement are to restore normal function of the shoulder by addressing the cause of the dysfunction or addressing the impairments that may be affecting the subacromial space. The type or size of the acromion cannot be modified by physical therapy intervention.
Causes of primary compressive impingement include:
- Acromial morphology
- Coracoacromial ligament hypertrophy
- Subacromial bursa thickening and fibrosis
- Trauma (acute traumatic or repetitive microtrauma)
- Overhead activity,
- Coracoid impingement
Initially, intervention is directed at decreasing pain and calming inflammation of the subacromial tissues. This can be achieved through rest; avoidance of aggravating factors (lifting, activities that involve movements overhead, across the body, behind the back, and into horizontal abduction beyond neutral); ice; gentle passive, active assist and active range of motion; and submaximal isometrics. There is currently little evidence for use of therapeutic ultrasound (Philadelphia Panel Evidence-Based Clinical Practice Guidelines on Selected Rehabilitation Interventions for Shoulder Pain. Phys Ther. 2001;81:1719 -30; Robertson and Baker, 2001).
After the initial acute inflammatory phase, interventions are aimed at restoring normal range of motion and strength of the glenohumeral joint and scapulothoracic joints.
Secondary Impingement Syndrome
Secondary impingement syndrome is a problem with keeping the humeral head centered in the glenoid fossa during movement of the arm. It can be caused by deficits in strength; fatigue; and/or motor control impairments of the glenohumeral or scapulothoracic joint, capsular instability, poor posture, capsular tightness, nerve injury (long thoracic, spinal accessory), and lesions of the biceps tendon or labrum.
Posterior capsule tightness
The posterior capsule is the main restraint against posterior translation of the humerus of the glenoid fossa with the arm below 90 degrees abduction (O'Brian, 1988). At 90 degrees abduction, the IGHL and the posterior inferior capsule become the main restraint (the ligament also resists inferior translation at 90 degrees abduction and shows significant strain with the arm elevated and internally rotated in the sagittal plane [Urayama, 2001]). Posterior capsule tightness had been suggested as a contributing factor to secondary impingement in the thrower (Wilk, 1993). Harryman et al (1990) demonstrated in vitro that posterior capsule tightness causes increased anterior and superior migration of the humeral head during forward flexion, terming the concept capsular constraint mechanism. They state that GH translation during active and passive movement is primarily controlled by by capsular tension, rather than the posterior contractile structures. This has been confirmed by Howell et al (1988).
Wilk et al (1993) introduced the term asymmetrical capsular tightness, where one portion of the capsule is tighter than others, inhibiting translation in the direction of the tightness. Tightness of the inerior and posteroinferior capsule may inhibit the humeral head from gliding inferiorly during overhead movements (Conroy, 1998). Tyler et al (1999) have also suggested that a tight posterior capsule may cause antero-superior migration of the humeral head during forward elevation, contributing to impingement.
The surgical procedure of choice in patients with tight posterior shoulder structure is selective release of the posterior capsule and not of the posterior contractile structures (Branch, 1999; Bennett, 2000). Surgical studies have demonstrated a relationship between the posterior shoulder capsule and shoulder ROM, showing an increase in IR when posterior portions of the capsule are released (Branch, 1999). Bennet (2000) and Warner et al (1997) showed a significant increase in IR after posterior capsule release.
Long Head of the Biceps
Andrews et al (1985) theorized a role for the long head of the biceps in controlling humeral head subluxation, especially superiorly. EMG studies have shown that the biceps is an important muscle in the cockin phase of throwing and studies on the biomechanical role of the biceps tendon have shown a significant increase in glenohumeral stability with firing of this tendon (Fu et al, 1991).
The forward head posture (FHP) and rounded shoulder posture (FSP) have been theoretically implicated as a potential causes or factors related to the inability to improve in subacromial impingement syndrome (SAIS). Postural correction has been used as part of rehabilitation programs to address the musculoskeletal imbalances in shoulder disorders (Chaitow,1996; Host, 1995; Kendall, 1992; Morrissey, 2000; Sarhrmann, 2002; Thein and Greenfield, 1997). Lewis et al (2005) showed that static postural variables (kyphosis, scapular position, forward head and shoulders) can be changed in those with and without SIS through the use of corrective taping compared to placebo. The taping was applied in a way to reduce thoracic kyphosis and to retract, depress, and posterior tilt the scapula. In addition, the corrective taping allowed the SIS subjects to increase their maximal flexion and scapular plane ROM by 16.2 and 14.7 degrees, respectively, compared to placebo. ROM in those with SIS was stopped at the first onset of pain.
Despite these findings, the intervention did not produce a decrease in pain with upper extremity elevation compared to baseline or placebo. The results also showed that although many of the variables changed positively, there were other subjects who were adversely affected by the corrective taping, producing worsening of ROM and pain measurements. Limitations included the lack of published validity of the measurement tools, no dynamic assessment, no subsequent treatment, outcomes, or function measurement.
Studies by Lewis et al (2005) and others (Grimmer, 1997; Lewis, in press; Raine and Twomey, 1997; Raine and Twomey, 1994) have suggested that upper body posture does not follow the set patterns described in the literature and have challenged the belief that clinicians may assume the presence of a specific changes in posture based on the presence of a FHP. It may be more useful clinically to assess the individual components of posture and their effect on ROM and pain than to examine sagittal plane posture (Lewis et al, 2005).
Wang et al (1999) assessed the effect of a 6-week exercise program aimed at correcting posture on 20 asymptomatic subjects who exercised three times per week, performing pectoral muscle stretching and strengthening for the scapular retractors, glenohumeral external rotators, and abductors. The results showed a mean increase of 6.6 degrees of shoulder abduction after the intervention, including a more downwardly rotated scapula and reduced thoracic kyphosis. Roddey et al (2002) investigated the short-time effect of a daily pectoralis major stretching program in asymptomatic individuals. Treatment groups included control, mild FHP, and moderate FHP groups. A significant decrease in the scapular protraction distance (from the spine) was reported in the moderate FHP group only. Effects on ROM were not assessed.
- Progressive resistive exericse vs. no intervention
- Lombardi et al (2008) showed statistically significant difference in improvement in pain on VAS and function on DASH between patients in the experimental group (PRE) and those in the control group (no intervention) (p < 0.05).
- Physical therapy and non-steroidals
- Morrison et al (1997) performed a retrospective study on 636 shoulders treated with therapy and non-steroidal anti-inflammatories. Successful resolution of symptoms occured in 67% of patients. Further, Type I acromions had a 91% success rate, Type II acromions had a 68% success rate, and Type III acromions had a 78% success rate when the symptoms were present for less than 4 weeks, versus 63% success rate for those whose symptoms had lasted longer than 4 weeks.
- Physical therapy vs. guided home intervention vs. control
- Walther et al (2004) looked at 60 patients, 20 for each group. Controls wore a brace; the intervention groups focused on strengthening humeral head depressors and scapular stabilizers. All groups improved. There were no statistically significant differences among the groups.
- Manual joint and soft tissue mobilization techniques vs. other
- Senbursa et al, 2007: The self-training group's routine consisted of self-stretching and strengthening exercises. The other group received manual therapy, which included joint mobilizations. Subjects in both groups experienced a significant decreases in pain and increases in shoulder function, but there was significantly more improvement in the manual therapy group compared to the exercise group. For example, pain in the manual therapy group was reduced from a pre-treatment mean of 6.7 to a post-treatment mean of 2.0. In contrast, pain in the exercise group was reduced from a pre-treatment mean of 6.6 to a post-treatment mean of 3.0. ROM at flexion, abduction, and external rotation in the manual therapy group improved significantly, while ROM in the exercise group did not. There were statistically differences among the groups in function (P > 0.05), whereby the manual therapy group showed significantly greater improvements in the Neer Questionnaire score and shoulder satisfaction score than the exercise group.
- Bang and Deyle (2000) compared an exercise group that performed supervised flexibility and strengthening exercises and a manual therapy group that performed the same program and received manual physical therapy treatment. Subjects in both groups experienced significant decreases in pain and increases in function, but there was significantly more improvement in the manual therapy group compared to the exercise group
- Physical therapy vs. subacromial decompression
- Haahr et al (2005) randomised 90 patients to either arthroscopic subacromial decompression or physiotherapy with exercises aimed at strengthening the stabilisers and decompressors of the shoulder. The mean Constant score at baseline was 34.8 in the training group and 33.7 in the surgery group. After 12 months, the mean scores improved to 57.0 and 52.7, respectively, the difference being non-significant. No group differences in mean pain and dysfunction score improvement were found.