Disorders of the contractile structures

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Disorders of the contractile structures

Chapter contents

Introduction

Functionally, shoulder muscles are of two types: stabilizing muscles and effector muscles. Stabilizing muscles (A, Fig. 15.1) are relatively small, with insertion tendons that lie close to, or even in, the substance of the fibrous capsule. Therefore they are not capable of causing significant shoulder movement but rather maintain the humeral head in the glenoid fossa. These stabilizing muscles are called the rotator cuff and include supra- and infraspinatus, teres minor and subscapularis. They all originate from the scapula, run partly under the acromial roof and insert on the humeral tubercles.

Fig 15.1 A, Rotator cuff (stabilizing) muscles; B, large effector muscles.

Effector muscles (B, Fig. 15.1) are much larger, with tendon insertions at a greater distance from the joint. Consequently, they produce powerful movements and are not primarily involved in stabilization. They are the deltoid complex, the pectoralis major, the latissimus dorsi and the teres major.

Although the standard clinical examination tests both muscle groups, the great majority of the positive findings point towards lesions of the rotator cuff, because lesions of the large effector muscles are extremely rare.

Rotator cuff

Rotator cuff disorder is one of the commonest afflictions of the shoulder and is a major cause of impairment of health in the young as well as in older individuals.¹

Lesions of the rotator cuff should be recognized as different from those of other tendons in the body for a variety of reasons. The tendons of the rotator cuff blend intimately with each other and with the capsule. The insertion of the tendons, as a continuous cuff around the humeral head, permits the cuff muscles to provide an almost infinite variety of movements to rotate the head and to oppose unwanted movements generated by the larger effector muscles.² In addition, the long head of the biceps may be considered a functional part of the rotator cuff because tension in the tendon helps to compress the humeral head into the glenoid (Fig. 15.2).

Fig 15.2 Rotator cuff from above: 1, coracoacromial ligament; 2, subscapularis tendon; 3, biceps tendon; 4, supraspinatus tendon; 5, infraspinatus tendon.

Apart from their primary function (to rotate the humerus with respect to the scapula), the cuff muscles have two other actions: they compress the head of the humerus into the glenoid fossa and provide muscular balance (Box 15.1). The latter is mainly performed through eccentric contraction of the muscle. Both functions are extensively discussed in the online chapter Excessive range of movement: instability of the shoulder.

Box 15.1 Functions of the rotator cuff

1. Rotate the humerus

2. Compress the humeral head

3. Provide muscular balance

Pathology

Pathological changes associated with rotator cuff tendinopathy features are variable.

Inflammatory tendinitis is a reversible process, associated with an inflammatory infiltrate, increased vascularity and hyperaemic changes within the rotator cuff tendon.³

Partial rotator cuff tears may develop within the substance of the tendon on either the acromial (bursal) or articular surface of the tendon.⁴ Most of the lesions occur near to the tendon insertion side. Full thickness tears are often initiated by a partial tear. They can be associated with a traumatic event or can progress with normal daily use of the arm.

Changes in the rotator cuff may also involve calcifying tendinopathy and rotator cuff arthropathy (degenerative glenohumeral osteoarthrotic disease associated with chronic massive rotator cuff tears).

The pathogenesis of rotator cuff disease has been associated with three factors: age-related degeneration, impingement and microvascular blood supply.

The primary cause of tendon degeneration is age.⁵ Changes in the rotator cuff include diminution of fibrocartilage at the cuff insertion, diminution of vascularity, fragmentation of the tendon and disruptions of the attachment to the bone.^6,7

Changes in the coracoacromial arch have been described in association with cuff disease and it is quite clear from both cadaver and clinical data that individuals with full thickness rotator cuff tears have changes in the acromial shape, with spur formation on the undersurface of the acromion and/or hypertrophy of the acromioclavicular joint.8–11 Although these data indicate a strong association between the presence of cuff tears and alterations of acromial contour,^12–14 it is still unclear whether the change in acromial shape is the cause or the result of the cuff defect or if both are consequences of ageing.¹⁵ Recent studies suggest that acromial deformity is usually developmental. Most acromial ‘hooks’ develop within the acromial ligament as traction spurs (analogous to the traction spur in the plantar ligament at its attachment to the calcaneus – see Fig. 15.11). The traction results from loading of the ligament by the cuff, which is increased when superior instability and cuff degeneration are present.^16,17

Changes in the microvascular supply to the rotator cuff also have a possible role in the pathogenesis of rotator cuff lesions.¹⁸ A hypovascular region exists at the ‘critical zone’ of the supraspinatus (the deep surface of the anterior insertion).^19,20 Microangiographic studies demonstrate that inadequate vascular supply to this critical zone is present in the adducted position of the arm.²¹ Furthermore, microvascular supply changes within the thickness of the tendon: the acromial part has much better vascularity than the articular part.^22–24

It is likely that a combination of age, anatomical changes and vascular insufficiency is responsible for rotator cuff ‘failure’.²⁵ Throughout life the cuff is subjected to various adverse factors such as traction, compression, contusion, subacromial abrasion, inflammation and age-related degeneration. A lesion may start where the loads are the greatest and the vascular supply the lowest, i.e. at the deep surface of the anterior insertion of the supraspinatus.²⁶ Each fibre rupture then generates other adverse effects: it increases the load on the neighbouring fibres, it compromises the blood supply of the tendon fibres by distorting the microcirculation and it exposes increasing amounts of the tendon to joint fluid that contains lytic enzymes. The cuff is gradually weakened and at increased risk of further failure. With subsequent loading episodes the pattern repeats itself, rendering the cuff weaker and progressively more susceptible to additional failure (Fig. 15.3).²⁷

Fig 15.3 Tendon fibre failure.

Incidence

The incidence of rotator cuff tears has been studied both in cadaveric studies and in living subjects and found to range from 5 to 80%. All the studies show a strong relationship with age: rotator cuff tears are rare before age 40 and common after age 60.²⁸ However, almost all of the reported cadaver studies failed to correlate cuff disorder with a history of clinical symptoms (Table 15.1). Some of the most important studies in living subjects have concerned the prevalence of cuff lesions in asymptomatic patients (Table 15.2). They all demonstrated a high prevalence of tears of the rotator cuff in asymptomatic individuals, an increasing frequency with advancing age and compatibility with normal, painless functional activity.

Table 15.1

Incidence of rotator cuff tears in cadaver dissections

Table 15.2

Incidence of rotator cuff tears in asymptomatic patients

Authors	Incidence (%)	Remarks
Petterson (1942)⁴⁰	20 (partial and full)	50% in subjects 55–85 years of age
Milgrom et al (1995)⁴¹	50 (tears after age 50 years)	Rotator cuff lesions are a normal correlate of age; they often present without clinical symptoms
Sher et al (1995)⁴²	15 (full), 20 (partial)	Significant increase of tears with age; defects are compatible with normal, painless, functional activity
Yamaguchi (2006)⁴³	35.5% prevalence of a full thickness tear on the painless side	Sonography of 588 consecutive patients with unilateral shoulder pain
Tempelhof (1999)⁴⁴	Rotator cuff tears in 23% 13% age 50–59 years 20% age 60–69 years 31% age 70–79 years 51% age > 80 years	Ultrasonographic study of 411 asymptomatic volunteers
Shibany (2004)⁴⁵	Complete rupture of the supraspinatus tendon in 6%	Ultrasound examination of 212 asymptomatic shoulders at 56–83 years (mean: 67 years)
Kim (2009)⁴⁶	0% age 40–49 years 10% age 50–59 years 20% age 60–69 years 40.7% > 70 years	Ultrasound and MRI investigation of asymptomatic individuals
Moosmayer (2009)⁴⁷	Full thickness tears in 7.6% 15% age 70–79 years	420 asymptomatic volunteers aged 50–79 years
Yamamoto (2010)⁴⁸	16.9% asymptomatic 20.7% total group	Prevalence of tears among the 683 residents of a mountain village in Japan

It must be concluded from these studies that rotator cuff lesions are a natural correlate of ageing. They should be regarded as ‘normal’ degenerative attrition, not necessarily causing pain and functional impairment. This realization poses substantial questions about the anatomical diagnosis (magnetic resonance imaging (MRI) and sonography) of shoulder pain and of the indications for cuff surgery. Once again, it must be stressed that diagnosis and treatment should be based on clinical findings and not on the results of imaging.

Diagnosis and treatment

Given the high prevalence rate of asymptomatic macroscopic rotator cuff lesions, it is unwise to rely solely on imaging techniques (sonography, computed tomography (CT), MRI) for a diagnosis.⁴⁹ The examiner should be wary of the common belief that what is found on technical investigation is always relevant to the cause of the patient’s pain.⁵⁰ Diagnosis should first of all be made functionally; paraclinical and technical investigations have a secondary function only. During resisted movements, pain and weakness, separately or in combination with each other, are sought. If pain only is found, this points to an uncomplicated tendinitis or to a partial thickness lesion. A combination of pain and weakness brings a partial (full thickness) tendinous rupture to mind. Painless weakness is usually the outcome of a massive tear of a rotator cuff tendon or of a neurological problem. It is worth emphasizing once again that, when performing resisted movements at the shoulder, it is very important to use the correct technique, as has been explained earlier (see p. 214). If this is neglected, misdiagnosis can easily result.⁵¹

Treatment options are also determined only by the outcome of the clinical examination and not by the extensiveness of the (anatomical) lesion. Asymptomatic cuff lesions, for instance, in which the shoulder does not bother the patient but imaging studies document a partial or even full thickness lesion in the cuff tendon, should not receive treatment. However, if the rotator cuff lesion is symptomatic, it will usually not heal by itself because rotator cuff tendinitis is not self-limiting.⁵²

Initial treatment for a symptomatic cuff lesion should always be conservative, no matter what the result of imaging may be. Non-operative treatment consists of either deep friction transversely to the affected tendon fibres or local infiltration with small amounts of triamcinolone at the tenoperiosteal junction of the affected tendon. In recurrent cases it is wise to add functional exercises for strength and proprioception (see online chapter Excessive range of movement: instability of the shoulder).⁵³

The effectiveness and safety of steroids for the treatment rotator cuff disease remains the subject of much controversy. Repeated injections with steroids are believed to produce tendon atrophy or to reduce the ability of damaged tendon to repair itself. Animal studies suggest that corticosteroids damage the ultrastructure of collagen molecules ⁵⁴ and reduce collagen density, as well as inhibiting the reparative properties of tendon by inhibiting tendon cell migration and synovial fibroblast proliferation.⁵⁵ This has been shown experimentally to weaken collagen fibres and precipitate tendon ruptures.^56–58 In human subjects, repeated injections have been correlated with softening of the rotator cuff substance⁵⁹ and an inferior result of surgical repair.⁶⁰ Other studies, however, failed to find a deleterious long-term effect of corticosteroid injections in animal tendons,^61,62 and a recent case-controlled study suggests that corticosteroid use in patients with ‘subacromial impingement’ should not be considered a causative factor in rotator cuff tears.⁶³ Although rotator cuff disorders are generally believed to benefit from steroid injections, evidence for the efficacy of the injections is difficult to demonstrate. Most reviews have found conflicting results,⁶⁴ which can be explained mainly by the fact that very heterogenous populations with poorly designed subgroups were used.⁶⁵ In other studies that used a better anatomical classification, local triamcinolone infiltrations were shown to be superior to placebo^66–70 and to methylprednisolone⁷¹ in reducing pain, improving active abduction and reducing functional limitation. The success rate of the infiltrations is further increased if precise diagnostic and infiltration techniques are used.⁷² In a randomly allocated double-blind study, Hollingworth et al compared two different methods of corticosteroid injection. The method of anatomical injection after diagnosis by the technique of selective tissue tension gave a 60% success rate, compared with the method using tender or trigger point localization, which produced only 20% success.⁷³ Also, a recent meta-analysis concluded that injections of corticosteroids are effective for improvement for rotator cuff tendinitis for up to a 9-month period.⁷⁴

We strongly believe in the beneficial effect of small-dose (10 mg) and targeted infiltrations of triamcinolone in the treatment of rotator cuff disorder. Potential hazards are minimal if a few necessary precautions are taken:

• The infiltration is always on the tenoperiosteal junction, never in the body of the tendon.

• The arm should be rested for 2 weeks following the infiltration.

• No more than three consecutive infiltrations should be given.

The operative treatment of rotator cuff lesions without rupture is acromioplasty: a wedge-shaped piece of bone is resected from the anterior surface of the acromion, along with the entire attachment of the coracoacromial ligament. The operative treatment of rotator cuff tear is cuff repair.

Calcifying tendinitis

Calcium deposits may form in the tendons of the rotator cuff. The aetiology is still a matter of speculation but it is generally accepted that degeneration precedes calcification. The incidence of calcification ranges from 3 to 20%75,76 and in most instances the lesion is completely asymptomatic.⁷⁷ The highest incidence occurs in those aged between 31 and 50,^78,79 and calcification is absent in elderly patients. The disease is usually self-limiting with a variable natural course: 80% of calcific lesions show spontaneous resorption over a period of 3 years.⁷⁹ If the lesion causes symptoms, these are treated in the same way as uncomplicated tendinitis of the rotator cuff. The treatment of choice is infiltration with triamcinolone. If the pain reappears after initially successful treatment, the calcium deposits can be dissolved with weekly infiltrations of procaine 0.5%.⁸⁰ Surgical intervention is seldom necessary but if it is indicated, most calcifications can easily be removed by arthroscopic procedures.⁸¹ In recent years extracorporeal shock wave therapy has been proposed as an alternative to operative treatment.^82,83

Resisted abduction

Pain

Pain on resisted abduction is the consequence of a lesion of either the deltoid or the supraspinatus muscle.

Deltoid muscle

The deltoid is very seldom at fault, although a lesion can sometimes occur as a result of direct injury. The lesion usually lies in the muscle belly.

Disorders of the deltoid cannot provoke a painful arc, because no part of it can be trapped between two osseous structures. Therefore the presence of a painful arc excludes a deltoid lesion. If any doubt exists, two accessory tests are used:

• Resisted horizontal adduction (Fig. 15.4): the examiner stands at the painful side and stabilizes this shoulder with one hand. With the other hand, he grasps the patient’s arm just above the elbow and brings it into horizontal abduction. The patient is now asked to push the arm forwards against the examiner’s hand. This tests the anterior portion of the deltoid.

Fig 15.4 Resisted horizontal adduction.

• Resisted horizontal extension (Fig. 15.5): this is the exact opposite of the previous test. The patient is asked to push backwards, the examiner applying counterpressure in an anterior direction. The posterior fibres of the deltoid are tested in this movement.

Fig 15.5 Resisted horizontal extension.

Treatment

A lesion in the muscle belly of the deltoid responds equally well to deep transverse friction or to infiltration with 20–30 mL of procaine 0.5% once a week, for about 3 weeks. Friction is given on alternate days until full cure is achieved.

Supraspinatus

Clinical experience shows that the most frequent reason for pain on resisted abduction is tendinitis of the supraspinatus muscle, which is by far the most common tendinous lesion at the shoulder. The tendon may be affected at four different sites; these each give rise to a slightly different clinical picture but are all characterized by a common major finding, which is pain on resisted abduction.

Most of the lesions occur at the tenoperiosteal insertion into the greater tuberosity. Inflammation and partial tears may develop within the substance of the tendon on the acromial surface (bursal side) or the deep surface (articular side of the tendon).⁸⁴ If situated on the deep part, pain on full passive elevation is also present. This is believed to be caused by the abutment of the deep surface of cuff insertion against the glenoid rim at the extremes of motion (Fig. 15.6).⁸⁵ If situated on the bursal part of the tendon, a painful arc is found. Cyriax regarded this as the most common cause of a painful arc on shoulder elevation.⁸⁶ A third possibility is a lesion that involves both superficial and deep aspects tenoperiosteally. In this case, pain on full passive elevation is present, together with a painful arc (Fig. 15.7).

Fig 15.6 On full passive elevation the undersurface of the supraspinatus tendon may become squeezed against the upper labral rim.

Fig 15.7 Accessory signs indicate the exact localization of the supraspinatus lesion: 1, pain at the end of passive elevation; 2, painful arc; 3, painful arc and pain on full passive elevation; 4, no localizing sign.

The lesion sometimes lies at the musculotendinous junction, just beneath the acromion. In this case, the only sign is pain on resisted abduction. Because this type of lesion is rare, its presence should always be confirmed by a diagnostic infiltration with local anaesthetic.

Figure 15.8 summarizes the differential diagnosis of painful resisted abduction.

Fig 15.8 Differential diagnosis of painful resisted abduction.

Treatment of tenoperiosteal lesions

The lesions situated at the tenoperiosteal insertion can be treated either by deep friction or by infiltration with steroid. Friction takes longer but has a more definite effect; steroids work quicker but there may be a tendency to recurrence.

Localization by palpation

The main problem in treatment is finding the structure involved. Although the tendon lies quite superficially, many have difficulty in localizing it. It cannot be easily localized with the arm in the neutral position at the side. Although the greater tuberosity points laterally in this position, part of the insertion can be covered by the outer rim of the acromion. Moreover, all structures here feel the same on palpation. Therefore, it is better to bring the upper arm into full medial rotation by asking the patient to put the lower arm behind the back, with the elbow bent to 90° (Fig. 15.9). In this position the tenoperiosteal insertion lies anterior to the acromion.^87,88 The fibres at the insertion are now situated in a sagittal plane because the tendon curves around the base of the coracoid process as a result of the medial rotation.

Fig 15.9 Position for localization of a tenoperiosteal lesion of the supraspinatus.

First, bony landmarks are defined. Starting at the posterior acromial angle, the lateral rim of the acromion is localized. The finger then moves over to the anterior acromial border, until the acromioclavicular joint is met. The supraspinatus insertion lies lateral to this joint line, just anteriorly to the acromion.

Next, the infraclavicular fossa is palpated. This is best started medially, at the level of the coracoid process. The finger is moved laterally, retaining close contact with the anterior border of the clavicle and acromion. Initially, the finger digs smoothly into the deltoid muscle, and continues to do so until the tenoperiosteal insertion of the supraspinatus is reached. Then a much tougher resistance is felt under the finger, which does not sink in deeply. The supraspinatus insertion has a width of about 1.0–1.5 cm. It is important to define the medial edge of this insertion accurately, since it permits the localization of the rest of it. The lateral edge is more difficult to palpate because the fibres merge with the anterior of the infraspinatus tendon.

Technique: infiltration of the supraspinatus

A tuberculin syringe, filled with 1 mL of triamcinolone, is fitted to a 2.5 cm needle. The patient sits in the same position as for palpation, the arm behind the back. After the insertion has been precisely located, the needle is thrust in vertically downwards at its centre (Fig. 15.10). The needle glides in smoothly initially, until it encounters the tenoperiosteal junction, at which point the typical tendinous resistance is felt. When the needle is thrust in a little further, it is arrested against the bone. Then 1 mL of triamcinolone is infiltrated at 5–10 different places over an area of 1 cm², in close bony contact. During the whole infiltration, a typical counter-pressure is felt.

Fig 15.10 Infiltration of a tenoperiosteal lesion of the supraspinatus.

After-pain is seldom severe and wears off spontaneously. The arm should be rested for about 2 weeks, and reassessment follows after 2 weeks. If the clinical examination is still positive, a second infiltration is given. One to three infiltrations are usually curative.

Treatment that leads to good but temporary results is a common experience in supraspinatus tendinitis. After one or two infiltrations the pain has disappeared but recurs a few months later. The patient should then be sent for standard radiography of the shoulder. If some intratendinous calcification is confirmed, 4–5 weekly infiltrations with 5 mL of procaine 2% are administered. In most cases this is sufficient to dissolve the calcium deposits and to alleviate the pain. If no calcification is visible, the patient must be referred to the therapist for deep transverse friction because it is unwise to infiltrate the tendon repeatedly, even with small doses such as 10 mg of triamcinolone. In cases of recurrent tendinitis it is also good practice to look for an underlying cause. This may be a small multidirectional or superior instability or an anatomical divergence in the acromial roof that causes recurrent impingement. The diagnosis and treatment of the former have been discussed earlier (see online chapter Excessive range of movement: instability of the shoulder). The diagnosis of the latter is through a lateral X-ray that visualizes the so-called ‘supraspinatus outlet’ – the space between the coracoacromial roof and head of the humerus (Fig. 15.11). If there is an anatomical divergence in the supraspinatus outlet, and the tendinitis tends to recur despite proper treatment, surgical decompression (deletion of anterior and inferior parts of the roof) is highly recommended.⁸⁹

Fig 15.11 Supraspinatus outlet: (a) normal acromion; (b) hooked acromion.

The treatment of supraspinatus tendinitis is summarized in Figure 15.12.

Fig 15.12 Treatment of supraspinatus tendinitis.

Treatment

Conservative treatment is reasonable for most partial ruptures of the supraspinatus tendon.⁹³ Treatment is relief of pain, achieved by infiltration of 1 mL of triamcinolone at the tenoperiosteal insertion and into the most distal part of the tendon. The same position and technique are used as for an uncomplicated tendinitis.

Infiltration of a partially ruptured tendon is not without danger. Disappearance of inflammation and pain usually removes the natural reserve towards movement and load. A weakened tendon in combination with increased load must inevitably lead to further ruptures and disaster. Before any decision to infiltrate is made, the patient must be warned about the dangers. Furthermore, if complete rest cannot be fully guaranteed, the therapist must stop infiltrations and refer the patient for deep transverse friction.

If the treatment leads to good but only temporary results, the same measures should be taken as in uncomplicated but recurrent supraspinatus tendinitis.

Painless weakness

A painless inability to abduct the shoulder actively can be caused by either a complete rupture of the supraspinatus tendon or a neurological lesion.

Total rupture of the supraspinatus tendon

The supraspinatus muscle initiates active elevation of the arm and is active during the entire arc of abduction. It is responsible for about 50% of the torque and can abduct the joint without action of the deltoid.⁹⁴ Therefore a total rupture of the supraspinatus tendon presents as painless weakness on resisted abduction.

In massive tears of the supraspinatus, the patient is unable to abduct the arm actively. This is caused not only by loss of muscular power but also by loss of the passive stabilizing effect of the tendon.

Previously it was believed that the arm could not be abducted actively by the deltoid muscle alone if some contraction of the supraspinatus did not initiate the movement.⁹⁵ However, studies in which the suprascapular nerve and the axillary nerve were blocked have shown that both the supraspinatus and the deltoid muscles are capable of initiating elevation of the arm, in both sagittal and coronal planes.^96–98 This is not in accord with what is found clinically. When the supraspinatus tendon is massively ruptured, the patient is unable to initiate active scapulohumeral abduction. Starting from a position of 0° (the arm hanging by the side), the deltoid muscle only pulls the humerus upwards. Elevation is then only produced by rotation of the scapula in relation to the thorax and not by any movement between scapula and humerus. This is explained by the superior displacement of the humerus that occurs during active contraction of the deltoid in the absence of an intact supraspinatus tendon.^99,100 In a normal situation the rotator cuff muscles form a supplementary musculotendinous glenoid which, in conjunction with the osseous glenoid, holds the humeral head stable. Experimental sections of the supraspinatus tendon also show the humeral head to move in a cranial direction until the superior humeral load is applied directly to the acromion (Fig. 15.15).¹⁰¹ This phenomenon has been referred to as ‘the spacer effect’¹⁰² and is one of the most significant plain radiographic signs of massive cuff deficiency.¹⁰³

Fig 15.15 (a) The glenoid: 1, tendinous; 2, osseous. (b) Spacer effect: massive rupture of the supraspinatus leads to a cranial subluxation of the humeral head during deltoid contraction.

Symptoms and signs

The lesion usually affects middle-aged and elderly people. In patients under 40 years of age a rupture is usually acute and results from indirect trauma, such as a fall on the outstretched hand.104,105 In most cases the rupture is due to a chronic failure of the tendon: repeated failure of small groups of fibres leads to progressive weakness of the supraspinatus, making it increasingly susceptible to damage from lesser loads.^106,107 The observation that major cuff defects may occur without recognized injury has led to the concept of ‘creeping tendon failure’.¹⁰⁸

An acute trauma is usually accompanied by a sharp pain and followed by complete inability to raise the arm actively. The pain remains severe for the first few days and diminishes progressively, later becoming bearable without drugs but still sufficient to interfere with normal activities.

On clinical examination active elevation is limited to about 30°, which is fully accounted for by scapular rotation: no active humeroscapular movement is noted. A very pronounced painful arc is present when the elevation is performed passively. On muscular testing there is a complete but painless weakness of resisted abduction. After a few weeks the supraspinatus becomes atrophic; the deltoid maintains its normal size and strength. Although the patient cannot actively elevate the arm from 0°, active elevation becomes possible if the arm is passively moved through the first 30°.

Frequently, because the patient is unable to move the arm actively, an immobilizational arthritis will set in after a few months and a capsular pattern emerges (see p. 228).

Treatment

Because most total ruptures occur insidiously in the elderly, surgical correction to restore normal function will not be the first option.¹⁰⁹ Some defects cannot be repaired simply because they only offer ‘rotten cloth to sew’ (McLaughlin).¹¹⁰ Many defects do not need to be repaired because they exist without causing much in the way of clinical symptoms.¹¹¹ However, surgery should always be considered in a younger patient with a significant acute tear in a previously normal shoulder,^112,113 and in the patient with a chronic tear associated with significant symptoms and not responding to conservative treatment. Fair functional results have been observed using open^114,115 and arthroscopic techniques,¹¹⁶ but it is important to bear in mind the fact that repair does not restore the quality of the tendinous tissue. Reported recurrence rates after rotator cuff repair range between 15% and 90%.^117,118 Because rotator cuff integrity is important to its function,¹¹⁹ long-term results of repair are better in younger patients with acute tears.^120,121

For most supraspinatus ruptures the treatment of choice is conservative. The primary aim is to get rid of the pain. To that end, an infiltration with 10 mg of triamcinolone should be given at the remnants of the insertion into the humeral tuberosity to abolish the painful arc, following the same procedure as for uncomplicated supraspinatus tendinitis. The therapist should try to reach the inflamed tissue because infiltrating the gap is useless. Therefore the typical counterpressure on syringe and needle should be felt during the entire procedure. Once the painful arc has gone, patients should be encouraged to use the arm normally. To lift the arm up, they should initiate elevation via a swinging movement of the trunk so that the arm is thrown laterally until it reaches the point where the deltoid muscle becomes effective. It is also wise to prescribe functional exercises for the antagonists of the deltoid and the remaining rotator cuff muscles. In spite of the slight disability, the function of the joint is usually good and the patient should be capable of doing light work.122–124 Outcome studies report good to fair results in 60–90% of conservatively treated supraspinatus ruptures.^125–127

Neurological lesions

Several neurological disorders may provoke painless weakness on resisted abduction.

Axillary nerve palsy

This may follow a subluxation of the humeral head. The axillary nerve innervates the deltoid muscle. Differential diagnosis is based on testing the strength of both the deltoid and infraspinatus muscles. Isolated painless weakness of abduction is found. A painful arc is not present, which differentiates this disorder from a supraspinatus rupture. Active elevation is difficult but possible (see online chapter Nerve lesions and entrapment neuropathies of the upper limb).

Suprascapular nerve palsy

This is most often the result of idiopathic neuritis, and seldom of an injury. The suprascapular nerve innervates both supra- and infraspinatus muscles. Weakness of abduction and lateral rotation is present. This disorder can be differentiated from a combined supra- and infraspinatus rupture by the absence of a painful arc (see online chapter Nerve lesions and entrapment neuropathies of the upper limb).

Fifth cervical root palsy

The C5 root innervates both spinatus muscles, the deltoid and the biceps brachii. Weakness on abduction and lateral rotation of the arm and on flexion of the elbow is present (see p. 155).

See (Fig. 15.16) for a summary of resisted abduction.

Fig 15.16 Resisted abduction positive.

Resisted adduction

Pain

A painful but strong resisted adduction movement of the arm may be caused by a lesion of one of the adductor muscles, a sprain of the acromioclavicular joint or tendinitis of the long head of the biceps.

It may happen that isometric movements indirectly provoke pain in structures other than the ones that are supposed to be tested. Cyriax called this phenomenon ‘transmitted stress’. During strong resisted adduction with the arm hanging alongside the body, the strong actions of the latissimus dorsi and pectoralis major pull indirectly on the acromioclavicular joint. Resisted adduction may therefore also provoke local shoulder pain in a chronic strain of the acromioclavicular joint. The pain will then be localized within the C4 dermatome and other passive tests will point to the acromioclavicular joint (see p. 241).

Pain on resisted adduction of the arm may rarely be caused by a tendinitis of the long head of the biceps at the glenoid origin. Cyriax arrived at this conclusion after finding that resisted adduction proved to be painful with the elbow in extension but not if it was kept in flexion. As a consequence, the structure at fault must overlie both shoulder and elbow (see p. 269). The pain is mainly felt under the acromioclavicular joint.

More often, however, a positive test will indicate a lesion of one of the adductors: pectoralis major, latissimus dorsi, teres major and teres minor.¹²⁸ An important element in distinguishing between them is the localization of the pain. Pain in the thorax anteriorly suggests the pectoralis major and posterolaterally the other three muscles. Axillary pain may be the result of a problem in the pectoralis major, teres major or latissimus dorsi.

The four adductors can be more accurately differentiated by additional tests. Because the pectoralis major, latissimus dorsi and teres major are medial rotators and the teres minor a lateral rotator, resisted medial and lateral rotation of the arm is the next test to perform in order to arrive at an exact diagnosis.

The pectoralis major muscle can be tested on its own by resisted horizontal adduction with the arm forwards (Fig. 15.17a). The examiner stands on the painful side. One hand is placed on the patient’s shoulder. With the other hand, the patient’s arm is grasped just above the elbow and brought anteriorly to the horizontal. The patient is now asked to exert further medial force against the examiner’s hand. The same can be achieved, but with loss of assessment of muscle strength, when the patient pushes both hands against each other holding both arms horizontally in front of the body.

Fig 15.17 Resisted horizontal adduction with the arm forward (a) and resisted extension (b).

Further differentiation is done by a resisted extension movement (Fig. 15.17b), which involves the latissimus dorsi, teres major and teres minor muscles. The patient tries to move the arm backwards with the arm hanging down and the examiner applying anteriorly directed counterpressure.

The only further differentiation required is between a lesion of the latissimus dorsi and the teres major. Because the latissimus dorsi also causes side flexion of the trunk and depression of the scapula, while the teres major does not, testing resisted side flexion towards the painful side and resisted scapular depression may be helpful.

Because lesions of the teres minor and teres major are extremely rare, these structures are not discussed in detail.

Pectoralis major

Lesions of the pectoralis major may be the result of overuse or of direct injury.

The lesion usually lies in the muscle belly, either in its lateral lower portion or in the fibres just below the outer portion of the clavicle (Cyriax:⁸⁶ p. 145). In rare instances, the pain is felt at the shoulder and radiates down the inner aspect of the arm. The problem must then be sought at the insertion at the crest of the greater tubercle.

It should be noted that in severe lesions of the pectoralis major, full passive elevation of the arm and resisted adduction and medial rotation are positive. In minor lesions, resisted medial rotation is sometimes negative.

The functional tests are followed by palpation, best performed with the patient’s arm slightly abducted and the hand resting on the iliac crest.

Differential diagnosis is a rib fracture. In fracture in the anterior thorax, the same tests as in pectoralis major strain are painful. Additionally, all movements of the thoracic spine influencing the site of fracture are painful as well, as is deep inspiration.

Treatment

Infiltration of the muscle belly with procaine usually has a good therapeutic effect. Two or three infiltrations suffice. If not, or if the lesion lies at the insertion, infiltration can be replaced by deep transverse friction.

Technique: infiltration of the pectoralis major

The patient adopts the half-lying position and puts the hand on the affected side on the iliac crest. A 4 cm needle is fitted to a syringe filled with 10–20 mL of procaine 0.5%. After accurate palpation, the lesion is held between thumb and index finger and the needle is introduced between them obliquely and to its full length. The finger and thumb are kept in this position during the infiltration, to feel whether the product is deposited at exactly the right place (Fig. 15.18). The injection is given while withdrawing the needle. The syringe is emptied gradually, over about five withdrawals and reinsertions.

Fig 15.18 Infiltration of the pectoralis major belly.

Technique: deep transverse friction to the pectoralis major

Palpation will demonstrate whether the lesion lies in the belly or the insertion of the muscle and so determine the friction method.

• To the muscle belly: massage is best given with the patient in the half-lying position and the hand resting on the iliac crest, so that the upper arm is somewhat abducted. This brings the pectoralis major more into prominence. The therapist sits facing the patient at the painful side. With the ipsilateral hand, the painful spot is taken between fingers and thumb and pulled laterally while pressure is applied (Fig. 15.19). This is the active moment of the friction. Massage is given for 20 minutes. Cure is normally obtained after 10 sessions.

Fig 15.19 Deep transverse friction to the pectoralis major belly.

• To the insertion: if palpation shows the lesion to lie at the insertion, deep friction is the only treatment. First the bicipital groove is localized, which is best done by putting the finger proximally between the minor and major humeral tubercles and in the long axis of the arm. By rotating the arm alternately medially and laterally, the groove can be identified. The therapist sits facing the patient at the painful side and places the contralateral thumb between the fibres of the deltoid muscle at the outer aspect of the bicipital groove. Counterpressure is applied over the dorsal aspect of the arm by the other fingers. Friction is given by pronation–supination movements.

Latissimus dorsi

Lesions of the latissimus dorsi are sometimes met with in gymnasts and water-skiers but are rare. They are usually found laterally at the uppermost part of the muscle belly. On clinical examination, full passive elevation of the arm and resisted adduction and medial rotation are painful.

Treatment

The responses to infiltrations with procaine and deep friction are equally good. The infiltration technique is the same as for the pectoralis.

Technique: deep transverse friction to the latissimus dorsi

The patient lies prone, the hand on the iliac crest. The therapist faces the patient’s painful side. The tender area is taken between thumb and fingers of the ipsilateral hand, and friction is performed by pulling the hand laterally (Fig. 15.20).

Fig 15.20 Deep transverse friction to the latissimus dorsi.

Painful weakness

Ruptures of the pectoralis major follow extreme muscle tension or direct trauma, or a combination of both. They have been reported in gymnastics or after a fall.129,130 The lesion is more common in weightlifting and is caused in particular by a bench press.¹³¹ The rupture usually occurs at the lateral fibres when the bar is at its lowest (loading of the fibres that are maximally stretched).^132,133

In an acute injury there is sharp and burning pain, sometimes accompanied by significant swelling and ecchymosis. Passive elevation of the arm is very painful and somewhat limited. Resisted adduction and medial rotation of the arm are painful ¹³⁴ and weak.

The functional tests are followed by palpation for tenderness and for a gap, and are best performed with the patient’s arm slightly abducted and the hand resting on the iliac crest (see Fig. 15.19).

Treatment consists of surgical repair. Results are usually good to excellent.¹³⁵

Painless weakness

A severe C7 root palsy can provoke painless weakness of adduction (see p. 156). Resisted extension of the elbow is also remarkably weak. The triceps reflex is sluggish or absent, together with some weakness on flexion of the wrist, more rarely on extension or on both. Numbness of the second and third fingers is usually present.

See Fig. 15.21 for a summary of resisted adduction.

Fig 15.21 Resisted adduction positive.

Resisted lateral rotation

The main lateral rotators of the shoulder are the infraspinatus and teres minor. The former is by far the stronger of the two. The teres minor also adducts, so that resisted adduction offers the key to differential diagnosis.

Pain

If both resisted lateral rotation and resisted adduction are painful, the teres minor is at fault, although this is extremely uncommon. In contrast, when resisted lateral rotation is painful but other resisted movements are normal, the lesion lies in the infraspinatus.

Infraspinatus

There are some localizing signs of lesions of the infraspinatus. A painful arc indicates that the lesion lies at the superficial part of the tenoperiosteal insertion. If full passive elevation causes pain, the deep part of the tenoperiosteal insertion is affected (Fig. 15.22). If, apart from resisted lateral rotation, no other tests are painful, the lesion is in the body of the tendon or at the musculotendinous junction.^136,137 Palpation will disclose the exact location of the lesion.

Fig 15.22 Lesions of the infraspinatus; 1, superficial aspect tenoperiosteal insertion; 2, deep aspect tenoperiosteal insertion; 3, body of tendon.

Treatment

A lesion at the tenoperiosteal insertion of the infraspinatus can be treated either by deep friction or by infiltration with steroid. The general remarks made for the supraspinatus also apply here. The superficial part responds better to friction than does the deep aspect. It takes longer to achieve a cure by friction than by steroid infiltration but recurrence is less frequent. The body of the tendon is only treatable by deep friction.

Palpation

The patient lies prone, resting on the elbows, the shoulders vertically above them. The elbows are flexed to 90°. The upper arm of the affected side is brought into slight lateral rotation by asking the patient to hold the edge of the couch. In this position the whole infraspinatus structure is within the reach of the finger. In order to tighten the tendon and to bring it further laterally from underneath the acromion, the patient moves the shoulder slightly over towards the painful side.

First the spine of the scapula is palpated, then the posterior angle of the acromion and the lateral acromial edge. In the infraspinal fossa, the muscle belly of the infraspinatus is located and, when the fingers are moved further towards the greater tuberosity, the musculotendinous junction, the tendon and finally the tenoperiosteal insertion are located. The latter is about 2 cm wide and lies partly lateral to the outer rim of the acromion and partly lateral behind the acromial angle.

Technique: infiltration of the infraspinatus tenoperiosteally

A 1 mL syringe is filled with 10 mg of triamcinolone and fitted to a 3 cm long needle. After the landmarks have been located, the needle is introduced in an anterocaudal direction, aiming at the tenoperiosteal insertion, which is reached after passing through soft tissue for about 2 cm (Fig. 15.23). Just before bone is reached, the tough tendinous resistance of the insertion is felt. The total amount is now injected in 5–10 slightly different sites. At each partial injection, strong counterpressure is felt.

Fig 15.23 Infiltration of the infraspinatus.

The patient should rest the arm for about 2 weeks and is then re-examined. If pain remains, a second infiltration is given. Two infiltrations normally suffice.

Technique: deep friction to the infraspinatus

Deep friction is indicated in athletes, if infiltration has been unsuccessful or when the body of the tendon is affected.

The patient lies in the same position as for infiltration. The therapist stands at the painful side. The thumb of the ipsilateral hand is placed on the lesion, while counterpressure is applied with the other fingers at the front of the shoulder (Fig. 15.24). The body of the tendon feels like a cord, whereas the tenoperiosteal insertion feels more like a flat resistance just covering the underlying bone.

Fig 15.24 Deep friction to the infraspinatus.

Friction is undertaken in a caudocranial direction by pronation–supination movements of the arm. The active moment is on supination. To avoid blisters, a piece of cotton wool between thumb and skin can be used: indeed, it may be necessary because in this position the skin is stretched, which allows the finger to glide over it too easily. Firm skin contact must be maintained.

Friction is given for 20 minutes, three times a week, and is usually curative after 10–15 sessions.

It may be difficult for the patient to hold this position for 20 minutes, so a break in treatment and sitting up for a few minutes should be allowed.

A specific case: abduction and lateral rotation against resistance are both painful

Both resisted abduction and lateral rotation are frequently painful on clinical examination and often there is a painful arc. This clinical pattern usually causes differential diagnostic difficulties that are not always easy to solve (Fig. 15.25).

Fig 15.25 Differentiation between subdeltoid bursitis and infra- and supraspinatus tendinitis.

No painful arc

If a painful arc is not present and both resisted abduction and lateral rotation are equally painful, the question is whether a supraspinatus or an infraspinatus tendinitis is present or whether both structures are inflamed. The test of resisted lateral rotation is first repeated, asking the patient to pay special attention to holding the elbow against the body when pushing the forearm sideways. Abducting the arm at the same time as resisted lateral rotation is performed could render the latter falsely painful when supraspinatus tendinitis is present. If the patient has difficulty in performing the test correctly, a sheet of paper should be placed between the elbow and the body during the test.

If both tests are still painful when correctly performed, they should be repeated in a supine position, which fully relaxes all the shoulder structures not intended to be tested. If one test becomes painless, the other one remaining painful, full value is given to the latter. For example, if resisted lateral rotation remains painful and resisted abduction becomes negative, the infraspinatus is at fault. If, on testing in the supine position, both tests remain painful, it is more likely that the supraspinatus is at fault because this structure is more frequently affected. To obtain diagnostic certainty an infiltration with local anaesthetic is necessary and is the only way to determine whether the supraspinatus, infraspinatus or both together are affected.

Painful arc

If a painful arc is also found, then the following lesions may be present:

• Chronic subdeltoid bursitis

• Supraspinatus tendinitis

• Infraspinatus tendinitis

• Tendinitis of both supraspinatus and infraspinatus.

If a painful arc is present, the tests should be repeated standing and lying.

Signs in favour of chronic bursitis

Presence of these signs makes it more likely that chronic bursitis is present:

• Very pronounced painful arc

• All passive movements painful at full range

• Tests are less painful in a supine position

• Resisted movements become less painful with axial traction, which prevents the humeral head approaching the coracoacromial roof

• Tenderness of the superficial part of the subdeltoid bursa on palpation

• Infiltration of the deep part of the bursa with local anaesthetic abolishes the pain.

Signs in favour of supraspinatus and infraspinatus lesions

Presence of these signs means it is more likely that tendinitis is the problem:

• Less pronounced painful arc

• Testing standing and lying are similarly painful

• Testing resisted abduction under axial traction is equally painful

• Tender spot in the tendon or tenoperiosteally

• Infiltration of the suspected tendon with a local anaesthetic diminishes the pain.

Painful weakness

Painful weakness on resisted lateral rotation is caused by a partial rupture of the infraspinatus tendon. The treatment is the same as for uncomplicated tendinitis at the insertion. The same remarks as for the treatment of a partial rupture of the supraspinatus also apply here: infiltrations are not given in athletes but rather only if the patient can guarantee complete rest.

Painless weakness

If resisted lateral rotation is painlessly weak, differential diagnosis between the following lesions must be made.

Muscular disorder: total rupture of the infraspinatus tendon

This usually happens in patients over 50 years old who have suffered from overstrain or trauma, very often a fall.

Infraspinatus tears may present in isolation or in combination with a partial or total rupture of the supraspinatus tendon. The infraspinatus defect then propagates in a posterior direction from an established full thickness tear in the supraspinatus.¹³⁸

As in supraspinatus tears, the lesion usually develops in patients over 50 years of age and is often asymptomatic (see p. 145). The lesion results from a combination of wear and tear and repetitive minitrauma. Sometimes the tear occurs suddenly during an acute overload or a fall.

Acute symptoms will be a painful arc on active and passive elevation and pain on full lateral rotation. Resisted lateral rotation is extremely weak but painless. The painful arc is caused by impingement of the tendon remnants between the greater tuberosity and the coracoacromial roof; the pain at the end of lateral rotation is caused by squeezing against the bulging posterior labrum. After some time (often many months), the inflammation decreases and the pain disappears. Resisted lateral rotation remains weak.

Chronic tears are characterized by marked and visible atrophy in the infraspinatus fossa. Secondary to the permanent loss of the infraspinatus, the patient can no longer bring the arm into full lateral rotation. This reduces the elasticity of the anterior capsule of the shoulder and results in a permanent isolated limitation of external rotation. The impaired external rotation leads to the typical ‘hornblower’s sign’: bringing the hand to the mouth is only possible in internal rotation of the arm with accompanying excessive elevation of the elbow. Hornblower’s sign has a 100% sensitivity and 93% specificity for irreparable degeneration of the infraspinatus.139,140

Treatment

When a painful arc is present, an infiltration is given in the tendinous remnants. For this, 1 mL of triamcinolone is infiltrated at the tenoperiosteal insertion, using the same technique as for uncomplicated tendinitis. It is repeated after about 2 weeks if the painful arc has not fully disappeared.

Abolishing the pain is only half the treatment. To prevent later limitation of lateral rotation, older patients are instructed to move the arm regularly into full lateral rotation with the help of the other arm or by twisting the trunk to the contralateral side while the forearm is stabilized against a fixed object.

Surgical treatment should be considered in younger patients with acute traumatic ruptures.

Neurological disorders

C5 root palsy

Resisted abduction of the arm and flexion of the elbow are also weak (see p. 155).

Suprascapular nerve palsy (see online chapter Nerve lesions and entrapment neuropathies of the upper limb)

Suprascapular nerve entrapment is usually an acquired neuropathy secondary to compression of the nerve in the bony suprascapular notch. Chronic mechanical irritation may be caused by overhead activities such as raquet sports, lifting and volleyball. Direct trauma, compression (e.g. backpacking) or a fracture of the scapula may also cause the lesion.¹⁴¹ Sometimes it is idiopathic.

Symptoms are constant pain in the trapezius and scapular area for about 3 weeks, followed by functional disturbances in the arm (difficulties in performing overhead activities of the arm). Clinical examination reveals normal movement of neck, scapula and shoulder. Resisted movements show some painless weakness of abduction (although the supraspinatus is paralysed, the deltoid remains fully active) and gross but painless weakness of lateral rotation (the infraspinatus is completely paralysed).

Spontaneous cure is the rule in an idiopathic ‘neuritis’. The pain disappears within 3 weeks, weakness within 6–12 months.¹⁴²

During the last few decades, there have been several reports of isolated infraspinatus muscle paralysis in volleyball players. The reported incidence in high-level volleyball players is between 25 and 45%.143,144. Usually the finding is accidental and the disorder without any complaint: no pain, no loss of function, and even no reduced efficiency in playing volleyball.¹⁴⁵ The most plausible pathomechanism for this suprascapular neuropathy is traction or stretching of the nerve.¹⁴⁶ This traction injury may occur when repetitive overhead activities result in local nerve strain that exceeds the passive tolerance of the nerve.^147,148 In one study the players with suprascapular nerve entrapment displayed significantly greater shoulder mobility than those without.¹⁴⁹

Neuralgic amyotrophy

This usually affects young males and starts with central neck pain, later spreading towards both shoulders and arms. Finally it leaves one arm and remains only in the other one. The pain is very severe and may last for about 6 months. Right from the onset, muscular involvement is visible. Often wasting is present together with a total palsy, not just weakness. It affects muscles of both sides, irrespective of segmental origin. Paralysis of the infraspinatus and the triceps, extensors of the fingers or extensors of the thumb is a common pattern (Cyriax:⁸⁶ p. 90) (see p. online chapter Nerve lesions and entrapment neuropathies of the upper limb).

Myopathy

Bilateral painless weakness of the upper limbs can be the result of myopathy affecting serratus anterior, deltoid and both spinatus muscles. If this is the case, then pronounced weakness and wasting of both spinatus muscles and of the serratus anterior muscle are present. Because of the muscular weakness there is sometimes some degree of immobilizational arthritis.

See Figure 15.26 for a summary of resisted lateral rotation.

Fig 15.26 Resisted lateral rotation.

Resisted medial rotation

Pain

Four different structures are tested on resisted medial rotation: subscapularis, pectoralis major, latissimus dorsi and teres major. The latter three are adductors as well and have been discussed previously (see above). If resisted adduction is painless, the lesion must lie in the subscapularis, the insertion of which is large and flat.

Subscapularis

The upper portion of the subscapularis inserts through a collagen-rich tendon into the lesser tuberosity. The rest (about 40%) of the tendon inserts into the humerus below the lesser tubercle and medial to the bicipital groove. Here the insertion is directly from muscle to bone.¹⁵⁰

Tendinitis of the subscapularis can be localized tenoperiosteally in the cranial or caudal part of the tendon. Lesions in the muscle belly or in the tendon itself do not seem to occur. A lesion in the cranial part causes a painful arc because of impingement under the coracoacromial arch.¹⁵¹ If the caudal portion is affected, the accessory test of passive horizontal adduction is painful as a result of pinching of the lesion between the lesser tuberosity and the coracoid process. Full active and passive elevation and full lateral rotation may be painful as well, because they stretch the subscapularis. Passive lateral rotation can even be so painful that it seems limited. To exclude arthritis, the examiner must gently try to bring the arm to full range, so as to confirm that limitation does not exist.

Treatment

Tendinitis of the subscapularis can be treated by friction or infiltration. Friction is a rather painful and difficult technique and so preference is often given to infiltration.

Technique: anatomical localization by palpation

The patient sits on the couch, the hand of the affected side resting on the thigh and the arm rotated slightly laterally. The bicipital groove is now located at the anterolateral aspect of the arm. This is best done at the proximal part, between the two tuberosities. In this position the lesser tuberosity points anteriorly, the greater tuberosity laterally. The examiner places one thumb longitudinally between the tuberosities. Using the other hand, the patient’s arm is moved into lateral and medial rotation. On lateral rotation the lesser tuberosity contacts the thumb in the groove, while on medial rotation it is the greater tuberosity which comes in contact with it.

Once the lesser tuberosity has been identified, the finger is placed at the anteromedial aspect of it and, further distally, at the lesser tubercular crest. This is where the insertion of the subscapularis is found: partly on the lesser tuberosity, partly on its crest. The total width is about 3 cm.

The insertion does not offer any particular sensation to the palpating finger: it feels as hard as bone. Depending on the localizing sign (painful arc or passive horizontal adduction positive), the proximal or the distal half of the structure must be dealt with. Before any treatment is started, the affected part is carefully palpated to localize the most painful region. Palpation vaguely around the insertion must be avoided because this area is always tender.

Technique: infiltration of the subscapularis

A 3 cm needle fitted to a syringe filled with 1 mL of triamcinolone is inserted at the subscapularis insertion in the middle of the most painful part, and directed towards the bone (Fig. 15.27). Just before the humerus is reached, tendinous resistance is felt. As always, the infiltration is given in droplets. This time the needle is moved along a line in a craniocaudal direction over about 1.5 cm so as to include the whole lesion. Counterpressure is experienced during the infiltration. Care must be taken not to move the needle too far laterally, so as to avoid infiltrating the tendon of the long head of biceps, which could lead to its early degeneration.

Fig 15.27 Infiltration of the subscapularis.

The patient is told to avoid using the arm for about 2 weeks and then reassessed. If full cure is not attained, infiltration is repeated. Results are usually very good, as long as the correct point has been dealt with. Recurrences are less frequent than in supra- or infraspinatus tendinitis.

Technique: deep friction to the subscapularis

This form of treatment is mainly used in recurrences or in patients who refuse steroids.

The patient is brought into the half-lying position, the arm in slight lateral rotation. Palpation is done in the same way as for infiltration.

The therapist stands on the affected side and faces the patient. The contralateral hand is used. Beginning at the coracoid process, the thumb is brought just underneath it and the other fingers curved laterally around the arm, on to the back of the shoulder. The thumb is now pulled laterally while pressure is applied in a posterior direction. During this movement two tendinous structures are momentarily felt slipping under the thumb; these are the coracobrachialis muscle and the short head of the biceps. By moving the thumb yet further laterally, while maintaining some dorsal pressure, the anteromedial edge of the deltoid is reached and is pulled to the side. Finally the lesser tuberosity is contacted (Fig. 15.28a). The hand is now turned into a vertical position (Fig. 15.28b), still keeping the deltoid to the side.

Fig 15.28 Deep friction to the subscapularis. (a) Preparative position of the hand. (b) Position of the hand for friction.

Friction is given by a flexion–extension movement at the wrist, the active moment being when the thumb moves upwards. During the whole procedure the deltoid is kept to the side. This is a painful, difficult and, for the therapist, tiring technique. Progress towards cure tends to be slow and it may take about 1 month’s friction before the patient starts to get better. Only two-thirds of patients can be fully cured in this way and, if no improvement has occurred after 1 month of friction, it is useless to continue and an infiltration should be given.

Painless weakness

Rupture of the subscapularis tendon

Tears of the subscapularis tendon occur either in isolation or as a propagation of a supraspinatus tear.¹⁵² The former usually is the result of a hyperextension–external rotation trauma or follows an anterior dislocation of the shoulder.¹⁵³ The lower part of the muscle is mostly affected, where the insertion is more or less directly from muscle to bone. In the latter, the lesion is more proximal at the lesser tubercle, the distal part of the tendon remaining unaffected.^154,155 In traumatic rupture there may also be an excessive range of passive lateral rotation. Weakness of internal rotation can also be demonstrated by the ‘lift-off’ signs described by Gerber and Krushell: the patient places the arm in internal rotation with the dorsum of the hand on the sacroiliac joint. If the patient is unable to rotate the arm internally any further and lift the hand off the pelvis, incompetence of the subscapularis is suspected.¹⁵⁶

Treatment

Isolated traumatic tears of the subscapularis are best treated with surgery.¹⁵⁷ The surgical outcomes are less favorable when other tendons are involved.¹⁵⁸ If the condition remains painful, an infiltration with corticosteroid into the remnants at the tenoperiosteal insertion can be helpful.

Neurological lesion

Internal rotation is controlled by C5 and C6

In painless weakness of internal rotation, a lesion of these nerve roots should be ruled out.

See Figure 15.29 for a summary of resisted internal rotation.

Fig 15.29 Resisted internal rotation positive.

Resisted elbow flexion

An examination of the shoulder is incomplete until the biceps has been tested. The muscle mainly moves the elbow but, as it crosses the shoulder joint, it can be the cause of pain around the shoulder as well. For this reason, resisted flexion of the elbow must always be included when the shoulder is assessed.

Pain

A positive test implicates the biceps. If pain is felt in the shoulder area, it is unlikely that the brachialis muscle is at fault, because a lesion in this muscle is more likely to cause pain around the elbow. The diagnosis can be confirmed by testing resisted supination of the forearm with the elbow flexed. If this is positive, the brachialis muscle is excluded.

The classification of biceps lesions can be divided into tendinosis of the biceps and biceps instability. The former may be an impingement lesion or occurs in isolation as a primary lesion of the biceps tendon.¹⁵⁹

Lesions of the biceps can lie at different levels. Only those that can provoke pain at the shoulder are discussed here. These are tendinitis of the long tendon at the glenoid insertion, in its intra-articular course and at the bicipital sulcus (Fig. 15.30). Lesions of the muscle belly and further down are discussed in Chapter 19.

Fig 15.30 Lesions of the biceps at the shoulder: 1, at the glenoid insertion; 2, at the intra-articular course of the tendon; 3, at the tendon in the sulcus; 4, subscapularis muscle.

Lesion of the long bicipital tendon at the glenoid origin

Strain on the glenoid from the working biceps is greatest when the arm is in overhead abduction and lesions are usually caused in throwing athletes by traction injuries.160,161 The pain is usually felt underneath the acromioclavicular joint but may radiate in the C5 dermatome. Besides pain on resisted flexion and supination of the elbow, resisted adduction of the arm will also show positive. When the resisted adduction is tested again, this time with the elbow flexed, it becomes painless. This phenomenon is explained by the constant-length phenomenon on a structure spanning two joints (see Ch. 4): the degree of stress on the painful tissue in one joint depends on the position in which the adjacent joint is held.

Treatment

The condition can usually be treated successfully with one or two infiltrations of 20 mg of triamcinolone.

Technique: infiltration of the long bicipital tendon

The condition can be treated by infiltration only. The patient lies supine, the arm in 90° elevation, and the elbow flexed at a right angle. An assistant now turns the arm into 45° lateral rotation. In this position, the bicipital groove lies on a line extended from the anterior margin of the acromion.

A 2 mL syringe is filled with 20 mg of triamcinolone and a 4 cm needle fitted to it. One thumb is placed just beyond the acromion at the groove. The needle is inserted just distally to the thumb parallel to the bicipital sulcus and aiming at the glenoid (Fig. 15.31). It is then moved further in between the humeral tuberosities until it strikes the glenoid. A tough resistance is felt just before touching the bone. The steroid is infiltrated here in drops so that the whole insertion is treated. During the infiltration some counterpressure is felt.

Fig 15.31 Infiltration of the long bicipital tendon at the glenoid.

The patient is re-examined after 2 weeks and, if necessary, the infiltration is repeated.

Intra-articular lesion of the long head of biceps

Pain on resisted flexion and supination of the elbow is found, together with a painful arc, which shows that the lesion lies at the intra-articular part of the tendon. As this part of the tendon lies intra-articularly, an intra-articular injection with 2 mL of steroid is required.

Lesion in the sulcus of the long head of biceps

The only positive sign is pain on resisted flexion and supination felt at the upper part of the arm. There is a full range of movement and a painful arc is absent. Palpation localizes the lesion in the sulcus.

Technique: deep friction to the long head

This lesion responds well to deep friction. The patient adopts the half-lying position, the palm of the hand on the thigh and the elbow at the side. The greater tuberosity then points laterally, the lesser tuberosity anteriorly. The sulcus lies in between the tubercles. In order to locate the groove precisely, the first part of the procedure for palpation for subscapularis tendinitis is performed (see above).

The therapist sits at the side, facing the patient. The patient’s arm is put into a degree of lateral rotation. The thumb of the contralateral hand is put flat in the sulcus, the tip pointing cranially and the radial side in contact with the medial aspect of the sulcus. In this position the thumb lies on the medial aspect of the tendon. The other fingers apply counterpressure at the back of the arm. Pressure towards the bone is applied with the thumb.

With the other hand the therapist grasps the patient’s lower arm, the elbow bent to 90°, and brings the arm into medial rotation until the radial side of the frictioning thumb comes in contact with the outer edge of the sulcus (Fig. 15.32). During this movement the tendon glides under the thumb and friction is achieved. The arm is now brought back into lateral rotation while releasing the pressure on the tendon (passive moment).

Fig 15.32 Deep friction to the long head of the biceps.

Treatment is carried out for 20 minutes, three times a week. Two to four sessions should be sufficient.

Alternative technique

Instead of the patient’s arm being rotated, pronation–supination movements of the therapist’s contralateral arm have the same effect. The active movement is on supination.

Snapping the long head of biceps

Biceps instability is seen most commonly in throwing athletes. Motion is often accompanied by a palpable snap or pop at a certain position in the arc of rotation.¹⁶²

According to Slätis and Aalto, a rupture of the intertubercular transverse ligament allows for no appreciable medial or lateral movement of the tendon.¹⁵⁹ The key structure which guides the tendon in its groove is the medial portion of the coracohumeral ligament, which inserts at the lesser tubercle. It fills the space between the upper margin of the subscapularis and the anterior border of the supraspinatus. If it is transected, the long tendon of the biceps can easily be displaced medially.

Instability test

Dislocation of the biceps is tested with the biceps instability test of Abbott and Saunders.¹⁶³ The arm, abducted to 90° and fully rotated externally, is slowly brought to the side and rotated slightly internally. A palpable and even audible and sometimes painful click is noted as the biceps tendon, now forced against the lesser tuberosity, becomes subluxated or dislocated from the groove.