Disorders Of The Rotator Cuff

Continuum of Injury

Impingement Syndrome<-------——>Full Thickness Rotator Cuff Tears
All tears are not symptomatic

Classification of Rotator Cuff Disease

  • Primary
    • Primary Compressive
    • Primary tensile overload
  • Secondary
    • 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

Rehabilitation of disorders of the rotator cuff will be different based on the type of underlying pathology or type of rotator cuff disorder. Therapeutic interventions performed will not only be based on impairments found during the examination but will also be chosen based on the underlying pathology. In other words, treatment for primary compressive disorders will differ from interventions chosen to treat secondary compressive disorders.

Citiations

Wilk K.E. Recent Advances in the Evaluation and Treatment of the Shoulder. Advanced Continuuing Education Institute Course, 2006. www.advancedceu.com

Primary Impingment Syndrome

Primary impingment can either be compressive, where the rotator cuff becomes physically damaged by the the coracoacromial arch structures, or can be the result of tensile overload, whereby 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 to 13 mm (.7-1.3 cm) in patients with shoulder pain (Golding, 1962) and 6 to 14 mm in normal shoulders ( Cotton & Rideout, 1964; Flatow et al., 1994). This is a relatively small space for the the subacromial tissues to occupy. The subacromial space and it's occupying tissues from superior to inferior is as follows: the acromion, subacromial and subdeltoid bursa, supraspinatus tendon, joint capsule, biceps tendon, and the humeral head. Any alteration in the space occupying these tissues has the potential to create pathology. 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, and Type III or hooked. Bigliani and Morrison (1986) reported on a morphological study in 140 cadaver shoulders where shape of the acromion was correlated with tears of the RTC. In other words, those with hooked typed acromions have less room for the subacromial tissues to function. An acute event or repetitive trauma to the tendon in the presence of a hooked acromion can result in damage to the tendon. Type or size of the acromion can not be modified by physical therapy intervention. Also, an inflamed, hypertrophic bursa can decrease the subacriomial space.

The goals of physical therapy for those with primary compressive impingement is to restore normal function of the shoulder by addressing causes or impairments that may be affecting the subacromial space. Causes of primary compressive impingement include acromial morphology, coracoacromial ligament hypertrophy, subacromial bursa thickening and fibrosis, trauma (acute traumatic or repetitive microtrauma), overhead activity, and coracoid impingement. Initially, intervention is directed at decreaseing 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 body, behind 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 ultrsound (Philadelphia Panel Evidence-Based Clinical Practice Guidelines on Selected Rehabilitation Interventions for Shoulder Pain. Phys Ther. 2001;81:1719 —1730; Robertson & Baker, 2001). After the initial acute inflammatory phase, interventions are aimed at restoring normal range of motion and strength of the glenohumeral joint and scapula.

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 causes by strength, fatigue, and/or motor control impairments of the glenohumeral or scapulothoracic joint, capsular instability, posture, capsular tightness, nerve injury (long thoracic, spinal accessory) and lesions of the biceps tendon or labrum.

Alterations in strength and motor control of the glenohumeral and scapulothoracic joints

Translation of the humeral head in the magnitude 1-3 mm occurs in the superior direction in the first 30-60 degrees of active GH scaplar plane elevation (Poppen and Walker, 1976, Chen etal 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 somewheat 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; Haryyman et al. 1990a, b, 1992). Other studies revealed that in the first 30-60 degrees phase of scapular plane abduction 0.7-2.7 mm of anterior translation, 0-1.5 mm of posterior translation in the 60-90 phase, and 4.5 mm of posterior translation in the 90-120 phase of scapular plane elevation (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 90-120 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 patiens 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. Howere, beause the subacromial space is small in volume and contains the subacromial structures, ther 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). Using two 3/16 mm steel bone pins drilled directly into the scapula (McClure et al 2001) of eight healthy subjects. The results revealed a mean of 50 degrees of UR, 30 degrees of PT, and 24 degrees of ER during scapular plane glenohumeral elevation. For glenohumeral flexion in the coronal plane the results revealed a mean of 46 degrees 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 elecation was 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, which both appear to be important during glenohumeral 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 as compared to shoulder protraction (Bertoft et al., 1993). Scapular kinematics can be altered by various 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).

Posterior Capsule

The Posterior capsule is the main restraint against posterior translation of the humerus of the glenoid fossa with the arm below 90 abduction (O'Brian, 1988). At 90 abduction, the IGHL and the posterior inferior capsule become the main restraint (the ligament also resists inferior translation at 90 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). Posterior capsule tightness had been suggested as a contributing factor to secondary impingement in the thrower (Wilk, 1993). Harryman and colleagues 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 (Harryman, 1990). 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 and associates have also suggested that a tight posterior capsule may cause antero-supeior migration of the humeral head during forward elevation, contributing to impingement (Tyler, 1999). 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 an shoulder ROM, showing an increase in IR when posterior portions of the capsule are released (Branch, 1999). Bennet (2000) and Warner and colleagues (1997) showed a significant increase in IR after posterior capsule release.

Long Head of the Biceps

Andrews et al (1985) theorize a role for the long head of the biceps in controling humeral head subluxation, especially superiorly. EMG studies have shown that the biceps is an improtant 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 firiing if this tendon (Fu et al, 1991).

Posture
The forward head (FHP) and rounded shoulder (FSP) has been theoretically implicated as a potential cause or factor 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 & 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 where adversely affected by the corrective taping, producing worsening of ROM and pain measurements. Limitations include the lack of published validity of the measurement tools, no dynamic assessment, no subsequent treatment, outcomes, or function measurement. The study by Lewis et al (2005) and by others (Grimmer 1997, Lewis in press, Raine & Twomey 1997, Raine & 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 range of movement and pain that 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 3 time 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.

Scapular Elevation
Wang et al (1999) reported that the scapula was less elevated following their exercise program. Other studies have reported that the scapula is more elevated in slouched postures (Kebaetse et al, 1999) and in subjects with SIS (Cole et al 1996, Lukasiewicz et al 1999). Warner et al (1992) also reported increased scapular elevation in 4 subjects out of a group of 7 with shoulder pathology. Lewis et al (2005) showed a mean decrease of resting scapular elevation following a postural correction taping technique of 1.7 cm for both symptomatic and asymptomatic individuals. *
Lateral Linear Displacement of the Scapula (Protraction)
Lewis et al (2005) showed a mean decrease (retraction) in linear displacement of 1.4 cm for the asymptomatic subjects and 1.7 cm for those with SIS. Previous research (DiVeta 1990) has suggested that there is no statistical difference between function and the amount of medial/lateral displacement of the scapula from the thoracic spine. *
Sagittal plane acromion position and scapular tilt
Studies have reported the scapula is more anteriorly tilted in slouched postures (Kebaetsse et al 1999) and in subjects with SIS (Ludewig & Cook 2000, Lukasiewicz et al 1999). Lewis et al (2005) showed a taping technique significantly reduced the sagittal plane position of the acromion by 1.7 and 2.5 cm in the asymptomatic and symptomatic subjects respectively. *
Thoracic Kyphosis
Lewis et al (2005) were able to decrease the kyphosis angle by 6.4 and 5.8 degrees in the asymptomatic and symptomatic subjects using a corrective taping technique.

Outcomes

Progressive Resistive Exericse vs. no intervention

  • Lombardi I Jr. 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. This was further divided among acromial types. Type I acromions had a 91% success rate, 68% for Type II, and 64% for Type III. 78% success rate when the symptoms were present for less than 4 weeks versus 63% success rate for those symptoms longer than one month.

Physical Therapy vs. guided home intervention vs. control

  • Walther et al (2004) looked at 60 patients, 20 for each group. Controls wore a brace, intervention groups focuses 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): Self-training consisted of self-stretching and strengthening exercises. Subjects in both groups experienced 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 (/-SD) of 6.7 (/-0.3) to a post-treatment mean of 2.0 (/-2.0). In contrast, pain in the exercise group was reduced from a pre-treatment mean of 6.6 (/-1.4) to a post-treatment mean of 3.0 (+/-1.8). 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). Group 2 showed significantly greater improvements in the Neer Questionnaire score and shoulder satisfaction score than Group 1.
  • Bang and Deyle (2000) compared 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 a (2005) randomised 90 patients to either to arthroscopic subacromial decompression, or to physiotherapy with exercises aiming 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.
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