The presence of suprascapular neuropathy in rotator cuff tears Poberaj B, Kovacic L, – Int J Shoulder Surg

Year : 2007  |  Volume : 1  |  Issue : 2  |  Page : 58-63

The presence of suprascapular neuropathy in rotator cuff tears

Poberaj Boris1, Kovacic Ladislav2

1 Valdoltra Orthopedic Hospital, Jadranska cesta 31, 6280 Ankaran, Slovenia
2 Department of Traumatology, University Medical Centre, Zaloska Cesta 2, 1000 Ljubljana, Slovenia

Correspondence Address:Poberaj Boris Valdoltra Orthopedic Hospital, Jadranska cesta 31, 6280 Ankaran Slovenia

Source of Support: None, Conflict of Interest: None

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The suprascapular nerve has three distinctive anatomical locations where it is most vulnerable to injury: at the suprascapular and spinoglenoid notch and along the supraspinatus fossa, where it is relatively fixed to the periosteum. The supraspinatus muscle has closest relation to all three and is also the most studied muscle of rotator cuff in conjunction with the mechanism of nerve neuropathy. Several anatomical studies try to mimic rotator cuff rupture and surgical reconstruction and thus describe effect on nerve when medial retraction or lateral advancement of the supraspinatus is present. Clinical series do not correlate with anatomical studies concerning safe amount of lateral traction of supraspinatus tendon. It is recommended to do a neurological evaluation of the suprascapular nerve in patients who are being considered for surgical repair of the rotator cuff tears and have a significant degree of muscle atrophy, as the accompanying neuropathy may prolong post-surgical recovery or result in a poor outcome.
Recently new arthroscopic techniques have been described to release the suprascapular nerve at the suprascapular notch, and it is believed that this will have a beneficial effect on nerve recovery and resolution of pain in case of nerve entrapment.


Keywords: Arthroscopic release, rotator cuff tear, suprascapular nerve, suprascapular neuropathy


How to cite this article:
Poberaj B, Kovacic L. The presence of suprascapular neuropathy in rotator cuff tears. Int J Shoulder Surg 2007;1:58-63

Rotator cuff tears and shoulder neuropathies may have similar clinical presentations. Both conditions present with pain, shoulder muscle atrophy and limitation of motion. It seems that greater degrees of atrophy are significantly associated with the presence of neuropathy. When the diagnosis remains in doubt, magnetic resonance imaging (MRI) and electrodiagnostic (EMG) studies can help to confirm pathology. Retraction of the rotator cuff tear itself can cause mechanical stretching of the suprascapular nerve and subsequent neuropathy. However, it is important to think of other causes of nerve injury such as compression or traction by surrounding tissues. The purpose of this article is to review the anatomy and pathophysiology of suprascapular nerve involvement in rotator cuff tears, as well as clinical presentation, diagnostic examination and surgical treatment.

The suprascapular nerve receives fibers from fifth and sixth anterior cervical roots and has a variable contribution from the fourth anterior cervical nerve root. [1],[2],[3] Although the suprascapular nerve is predominantly a motor nerve, it also contains sensory components. It supplies motor innervation to the supraspinatus and infraspinatus muscles and sends sensory branches to the glenohumeral and acromioclavicular joints, coracohumeral and coracoacromial ligaments and subacromial bursa. [1] The variant cutaneous sensory branch is infrequently present. Few anatomical studies have identified a cutaneous branch which innervates a small, poorly defined area at the superior shoulder. [3],[4],[5]

The suprascapular nerve arises from the superior trunk of the brachial plexus at Erb’s point and runs an oblique course through the posterior cervical triangle toward the suprascapular notch. First, it passes laterally deep to the omohyoid and trapezius muscles, then turns posteriorly to run under cover of trapezius. Together with the suprascapular vein and artery it reaches the suprascapular notch. At the level of the suprascapular notch, the suprascapular nerve enters the suprascapular fossa beneath the suprascapular ligament, also known as superior transverse scapular ligament, while the artery and vein travel above the ligament. The blood vessels tend to travel laterally in relation to the nerve.

Within one cm after crossing the suprascapular notch, the suprascapular nerve sends off one to two motor branches to innervate the supraspinatus muscle. Just proximal or at the suprascapular ligament the suprascapular nerve receives sensory fibers from the acromioclavicular joint, coracoclavicular and coracohumeral ligaments and the subacromial bursa. After traversing the notch, the suprascapular nerve travels obliquely along the floor of the supraspinatus fossa under the supraspinatus muscle toward the spinoglenoid notch. There, it receives sensory fibres from the posterior part of the glenohumeral joint capsule. The suprascapular nerve then travels around the lateral margin of the base of the scapular spine, passing the spinoglenoid notch and enters the infraspinatus fossa. At the spinoglenoid notch, the nerve may be covered with the spinoglenoid ligament, also known as the inferior transverse scapular ligament. Thereafter, it divides into two, three or four motor branches. All motor branches to infraspinatus muscle are of the same length and diameter. The motor branches to the infraspinatus are significantly longer and slightly larger than those to the supraspinatus. [6]

Several anatomical studies have been done to consider important anatomical locations where the suprascapular nerve may be endangered during surgical procedures or where neuropathy may evolve.

Variations in morphology around the suprascapular notch have been identified. Rengachary et al., classified the suprascapular notch and reported on six types depending on their configuration and enclosure. The most common type was U-shaped notch identified in 48% of the cadavers. A small V-shaped notch was identified in only 3%. [7],[8] Several variations in the suprascapular ligament morphology have been reported. These include partial or complete ossification, anomalous bands of the ligament including bifid and trifid ligaments, hypertrophy of the ligament or no discernible transverse scapular ligament. [6],[7],[9],[10],[11] At the suprascapular notch and in the supraspinatus fossa no significant movement of the suprascapular nerve is possible because the neurovascular pedicle is fixed to the periosteum. This results in the vulnerability of the motor branches of suprascapular nerve. [12] Rengechary et al. , in their study, evaluated motion of the suprascapular nerve relative to the suprascapular notch with various movements of the arm and shoulder and noted that the nerve was often apposed to the sharp inferior margin of the superior transverse scapular ligament. They termed this mechanism of injury as “sling effect”. [1],[13] Anatomical variants of the suprascapular vessels passage through the suprascapular notch have been described. An anomalous suprascapular artery (2.5%) or its prominent branch (32%) may pass underneath the suprascapular ligament along with the nerve. [6],[14] The vessel always coursed lateral to the nerve and was thus closer to the glenoid rim. [6]

Several papers have described the neurovascular anatomy of the rotator cuff. Typically, there are two motor branches to the supraspinatus muscle and the first motor branch is the larger of the two. The first motor branch originates either under the suprascapular ligament or within one mm distal or proximal to it. [6],[15] Warner et al. , in their study, found that in one of the 31 shoulders (3%) the first motor branch originated proximal to the suprascapular notch and passed above the ligament. [6] Albritton et al., theorized that the bifurcation of the first motor branch distal to the notch increases the risk of injury to the suprascapular nerve and its subsequent innervation of the infraspinatus. This is thought to result from tethering of the suprascapular nerve by tension on the first motor branch from medial retraction of the supraspinatus. [15] The study suggests that suprascapular nerve injury may result from retraction of a torn rotator cuff.

The spinoglenoid ligament has a variable presence in 14% to 80% of cadavers. It can be a thin fibrous band (13-60%) or a thick, well-defined ligament (3-20%). [11],[16] Recently, a spinoglenoid septum has been described; this is formed by the thickening of the fascial cover of the supraspinatus and infraspinatus muscles. It originates from the spinoglenoid notch and extends into posterior capsule. [17] A “safe zone” for avoiding suprascapular nerve injury during surgical procedures has been described by several authors. On the lateral side, motor branches to the supraspinatus muscle lie on average three centimeters from the origin of the long tendon of the biceps and the average distance from the posterior rim of the glenoid to the motor branches of the infraspinatus muscle is two centimeters. The minimum distance from the superior rim of the glenoid to the suprascapular nerve at the suprascapular notch is 2.3 cm and from the posterior rim of the glenoid to the suprascapular nerve at the level of the base of the scapular spine is 1.4 cm. The medial safe zone is situated medial to the layer of fat tissue surrounding the neurovascular pedicle in the supraspinatus fossa. [6],[18],[19]

The suprascapular nerve is susceptible to compression and stretch because of its relatively fixed position under the ligaments and rotator cuff. It is very rarely affected by mononeuropathy as an idiopathic cause. [20] The nerve may be compressed by intraneural or extraneural ganglion cysts; both have been explained by synovial theory which has the origin in superior labral tears. [21],[22],[23],[24] Besides these, the nerve may be compressed by lipomas, [25],[26] suprascapular ligament, or spinoglenoid ligament. In addition, the nerve may be compressed as it courses between the fascial encasements of the anterior and middle scalene muscles, within the fascia of the subclavius and omohyoid muscles or under the hypertrophic supraspinatus muscle and coracoid. [8] The more frequent sites of compression are the suprascapular notch and the spinoglenoid notch. The spinoglenoid septum formed by the thickening of the fascial cover of the supraspinatus and infraspinatus muscles may be a cause of dynamic compression of the suprascapular nerve. [17] Another mechanism of injury is traction or mechanical stretching of the nerve combined with kinking of the nerve at the suprascapular and spinoglenoid notches. Because of circuitous pathway with acute angles and multiple areas of fixation, the nerve is susceptible to friction or rubbing against the ligament or notch edge, reported as a “sling effect”. [1],[13] Cross-body adduction, forward flexion and external rotation have been reported to place the nerve at risk for this mechanism of injury. It is the extreme scapular motions, such as scapular depression, retraction or abduction that may exacerbate the traction forces. Studies have shown that altered conduction within the nerve is identified when the nerve is stretched 6% beyond resting length. Stretching the nerve more than 15% leads to irreversible nerve damage. [8] An alternate hypothesized cause of suprascapular nerve damage is traction injury to the blood vessels supplying the nerve which can result in intimal damage and microemboli of the vasa nervorum. [8] The suprascapular nerve is most prone to traumatic injury during falls on an out-stretched hand, as well as blunt trauma to the top of the shoulder, due to its high position on the brachial plexus. Most studies favor a traction neuropraxia or axonotmesis as the major mechanism of injury. [27] Shoulder trauma resulting in a simultaneous rotator cuff tear and brachial plexus injury is a very rare entity. [27] However, Vad et al found the prevalence of peripheral neuropathy in full-thickness rotator cuff tears with atrophy to be 28%. [4] Electromyographic examinations were done before any operative procedure. Suprascapular nerve was affected in two of the seven cases.

Anatomic study by Albritton et al., was done to assess the risk to suprascapular nerve with medial supraspinatus tendon retraction. [15] With the supraspinatus muscle in its anatomic position, the suprascapular nerve and its first motor branch angle measured 124.6º at the scapular notch. After retraction of the supraspinatus, the angle markedly decreased to 98.7º and 34.6º with one cm and five cm of medial retraction, respectively. This increased tension on the nerve could cause nerve injury and lead to fatty infiltration of the cuff muscles. [15] In one study was shown that infraspinatus fatty degeneration can occur in the presence of large anterosuperior tears even when the infraspinatus tendon is intact [Figure – 1]. [28] Nerve injury before rotator cuff repair has been demonstrated by another study with electromyographic evidence of denervation of the suprascapular nerve in eight patients before surgical intervention. [15] Studies by Paleta have shown that, in the absence of a rotator cuff, there is excessive scapular motion that may put traction on the nerve. [29]

The risk of iatrogenic damage to the suprascapular nerve and its branches during muscle advancement in rotator cuff reconstruction is demonstrated by anatomic studies. [6],[12] Two steps of the operation are considered to be responsible: first, sharp detachment of the supraspinatus muscle from its fossa and second, forced traction to the muscle to gain sufficient lateral shifting of the tendon. Greiner et al., showed that muscle can be shifted laterally over a distance of 10 millimeters without damage to its medial branches. [12] This is twice the length of the mobile part of the branch (i.e., distance between the point where the branch exits from the neurovascular pedicle and the point where the branch is fixed to the muscle). Warner et al., showed that with the open advancement technique of Debeyre et al. , or its modification, the maximum lateral advancement of supraspinatus and infraspinatus that is allowed by the neurovascular structures is 3 cm. [6] In some cases release of suprascapular ligament is needed to get additional 5 mm of lateral advancement. [6] This study represents mobilization of the muscle / tendon from its original anatomical position and not the extent of mobilization of retracted tissue. When a tendon has retracted in a chronic tear of rotator cuff, the neurovascular bundle may be tethered by scar tissue and may not be safely mobilized that far.

In contrast to the anatomic studies, clinical studies showed that mobilization of retracted cuff tendons toward their normal attachment on the humerus does not put as much tension on the nerve as anatomic studies would suggest. [28],[30],[31] Hoellrich et al., performed an electromyographic (EMG) analysis, after primary open repair of massive tears, in nine patients at a mean of 17 months postoperatively. Rotator cuff mobilization and lateral advancement of up to 3.5 cm were performed safely with no indication of suprascapular nerve damage on EMG testing. [31] Zanotti et al., evaluated the suprascapular nerve in 10 patients after primary open repair of massive rotator cuff tears (measurement of 15 cm² was selected as criteria for a “massive” tear). [30] The amount of lateral mobilization ranged from 2.5 to 4.0 cm. Denervation of the infraspinatus muscle was found in one of 10 patients and was localized to the distal portion of the suprascapular nerve at its insertion into the infraspinatus. A preoperative EMG study had been obtained in this patient for evaluation of another injury and showed no evidence of muscle denervation, indicating that the nerve injury was likely the consequence of surgical mobilization. [30] Goutallier et al., reported on six EMG anomalies among 24 patients probably related to surgery, although the extent of the tear of the cuff in coronal plane was nearly always more than three cm. Four of these six shoulders had been explored preoperatively by EMG and were recorded as normal. [28] A recent study done by Mallon et al., [32] showed significant renervation potentials on EMG of the suprascapular nerve in 4 patients after even partial cuff reconstruction via mini-open approach without nerve decompression.

The etiology of the suprascapular nerve injury may vary, but usually patients present with a similar clinical presentation. Typically, there is involvement of the dominant upper extremity in the patient aged between twenty and fifty years. Sometimes, there may be an acute event that triggered the symptoms, but more often the onset is insidious.

The most common presenting symptom is pain. It is localized over the lateral and posterior shoulder, often described as a dull ache or burning; rarely it is deep and diffuse. The pain is exacerbated by overhead activities. Over time, the pain may become constant, awakening the patient at night. Proximal lesions of the suprascapular nerve are more likely to be associated with pain, in comparision with more distal injuries. This finding is related to the anatomical origin of the nerve’s sensory fibers. Patient may complain of weakness in shoulder. External rotation and abduction is affected. Some patients may present with weakness as the chief complaint, with little or no pain. [33],[34],[35],[36] Some overhead throwing athletes, in whom suprascapular nerve neuropathy is recognized with increasing frequency, may be completely asymptomatic and the atrophy may be detected as an incidental finding. [37] In addition, symptoms similar to glenohumeral instability due to infraspinatus weakness have been reported. [8] Physical examination consists of shoulder, cervical spine and neurological evaluation to exclude other causes of the symptoms. In suprascapular nerve injury, a common finding is wasting or atrophy of the scapular muscles. The atrophy is seen more easily with the arms brought in forward flexion and by evaluating the patient from above. Atrophy of the supraspinatus muscle may be difficult to recognize because of the overlying trapezius muscle. There is often tenderness on palpation at the location of the injury, typically at the suprascapular notch or the spinoglenoid notch. Weakness of involved muscles may be demonstrated. Abduction and external rotation are affected depending on the location of the nerve injury. Loss of function of the infraspinatus muscle may be difficult to identify because of contribution of posterior deltoid and teres minor muscles to external rotation strength. The cross-body adduction test with the arm extended or internally rotated may exacerbate the posterior shoulder pain. This maneuver tenses the nerve on the suprascapular ligament. [38] The diagnosis of suprascapular nerve entrapment is based on history and physical examination, but variety of diagnostic tests help us to rule out other causes of shoulder pain and dysfunction. Relief of shoulder pain after diagnostic nerve block into the suprascapular notch is in accordance with suprascapular nerve injury at this site. [39],[40] Electrodiagnostic studies confirm and localize the lesion and include both electromyography and nerve conduction studies. X-rays may be useful to assess the suprascapular notch and to demonstrate if the suprascapular ligament is calcified. Ultrasonography is an excellent method to identify an anatomical etiology of shoulder disability, but the sensitivity and specifity is highly dependent on the individual performing the study. Ultrasonography may reveal a ganglion cyst and also show a coexisting rotator cuff rupture. Computed tomography reveals osseous abnormalities affecting the suprascapular nerve, it may also be used to evaluate soft-tissue masses about the shoulder. The best imaging modality for depicting soft tissue lesions is magnetic resonance imaging. It is useful in identifying the course of the suprascapular nerve, the presence of soft tissue lesions such as ganglion cyst, changes in the supraspinatus and infraspinatus muscles secondary to denervation, intraarticular lesions, and rotator cuff tears.

The differential diagnosis of suprascapular nerve palsy includes cervical spine disease, brachial plexopathy, rotator cuff and intra-articular glenohumeral pathology, biceps tendon pathology and degenerative arthritis of the acromioclavicular joint. Rotator cuff tears and suprascapular neuropathy may have similar clinical presentation. [4] Pain, scapular muscle weakness and atrophy, limitation of motion are main complaints in both. When the diagnosis remains in doubt, magnetic resonance imaging and electrodiagnostic studies will document rotator cuff tears and neuropathy, respectively. However, both conditions may be present in the same patient. Clinical distinction can be difficult and rotator cuff tears can mask a neuropathy. This is especially the case with full-thickness cuff tears, where MRI provides a ready explanation for muscle weakness and atrophy while obscuring the clinical features of a coexistent neuropathy. [4] When a patient with rotator cuff tear has severe degree of atrophy, a potentially associated peripheral neurological injury (suprascapular neuropathy) must be ruled out. Furthermore, a possibility of suprascapular nerve entrapment must be considered if pain and weakness persist after surgical repair of the rotator cuff tear.

EMG study for each retracted supraspinatus tear is necessary to reveal nerve injury. Reduction of the rotator cuff tear alone may have beneficial effect on renervation potential of suprascapular nerve probably in cases without any adhesions under the transverse ligament. Recently new arthroscopic techniques for nerve decompression at the notch have been described with distinct advantages over the traditional open approach. [41],[42],[43],[44],[45] They provide superior visualization of neurovascular and ligamentous structures and thus permit safer nerve release. Arthroscopic release is also significantly less invasive approach. The technique of arthroscopic release is based on standard and reproducible anatomic landmarks and utilization of these as reference points for arthroscopic orientation. The acromioclavicular joint is first identified. The distal clavicle is then followed medially until trapezoid and conoid ligaments are identified. The conoid ligament is followed inferiorly and medially to the base of the coracoid. At the base of coracoid, the confluence of the trapezoid and conoid ligaments and suprascapular ligament is identified. The suprascapular ligament courses horizontally across the field of view. The suprascapular ligament, suprascapular artery and suprascapular nerve should be clearly visualized before sectioning of the suprascapular ligament through the suprascapular portal [Figure – 2],[Figure – 3]. [41],[42],[43],[44],[45] Preliminary clinical results done by Lafosse et al . [41],[44] have shown improvement of 31 points, assessed by Constant score in eight patients after concomitant arthroscopic rotator cuff reconstruction and nerve release. In a new prospective study by the same authors, the beneficial effect of nerve release is pointed out in patients with persistent pain after they underwent successful RC repair.

The suprascapular neuropathy may evolve at different anatomical locations and has a variety of causes. Suprascapular notch is one of the most studied anatomic location of the suprascapular nerve injury in conjunction with rotator cuff pathology.

Anatomical studies explained the mechanism of medial traction injury to the nerve while retraction after supraspinatus rupture. [15] Natural history of muscle retraction in a chronic tear may cause additional tethering of neurovascular bundle by scar tissue. This may explain the fatty degeneration of infraspinatus in the presence of large anterosuperior cuff tears even when the infraspinatus tendon is intact. [15] Furthermore infraspinatus muscle shows no recovery after surgical reconstruction of supraspinatus tendon. It seems that infraspinatus muscle is less resistant (more prone) to nerve insult.

The safe amount of lateral mobilisation of supraspinatus tendon is one cm [6],[12] according to anatomical studies and up to 3.5 cm during primary repair of massive rotator cuff tears in most clinical cases. [28],[30],[31] The discrepancy between anatomic dissection and clinical results may be due to the fact that the clinical cuff deficiency is caused not only by loss of tendon substance but also by muscular retraction. In these cases a certain degree of lateral mobilization of retracted muscle may actually be beneficial to nerve function. [32]

New arthroscopic techniques for nerve decompression have been described with the use of a suprascapular portal, and even use of a nerve stimulator for identification and confirmation of the nerve during arthroscopic procedure. [41],[42],[43],[44],[45] A recent clinical study [44] has shown the potential benefit of arthroscopic repair of rotator cuff tears and concomitant release of suprascapular ligament on nerve recovery and possible pain relief.

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[Figure – 1], [Figure – 2], [Figure – 3]

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