PREOPERATIVE CONSIDERATIONS

Suprascapular nerve (SSN) dysfunction is an uncommon cause of shoulder symptoms and is therefore often overlooked as a potential source of pathology. Compression of the nerve occurring at the suprascapular notch was originally described by Thomas¹ in 1936 and later by Kopell and Thompson² in 1959. However, compression at the spinoglenoid notch was not described until 1982 by Aiello and colleagues.³ Of all causes of shoulder pain, isolated SSN pathology represents just 1% to 2% of cases presenting to shoulder surgeons.⁴

SSN dysfunction can result from a variety of mechanisms, including direct trauma, indirect trauma (traction), space-occupying lesions (e.g., ganglion cysts, lipomas), repetitive overuse (e.g., overhead sports such as volleyball,^5,6 baseball⁷), rotator cuff tears,^8,9 and anatomic variants such as suprascapular artery passage through the suprascapular notch¹⁰ and an anomalous transverse ligament.¹¹

Until recently, open decompression has been the mainstay of surgical treatment for this disorder, using an anterior, superior, or posterior approach.¹² These approaches inevitably required some degree of muscle splitting or detachment to gain adequate exposure.¹³ Despite this wide dissection, the supraspinous notch is often difficult to visualize because of its close proximity to the clavicle and its deep position.

Arthroscopy offers a minimally invasive approach to this area, with reduced morbidity and improved visualization of the anatomy of this region. It was the natural progression of improved arthroscopic anatomic knowledge and awareness, particularly through rotator cuff surgery, that led to the evolution of the arthroscopic SSN release.

ANATOMY AND PATHOANATOMY

Anatomy

The SSN arises from the upper trunk of the brachial plexus, usually from the ventral fibers of the C5 and C6 nerve roots. The nerve then takes a course through the posterior triangle accompanied by the suprascapular artery and vein, passing inferior and parallel to the posterior belly of the omohyoid and deep to the trapezius. It enters the supraspinous fossa deep to the supraspinatus. As these neurovascular structures approach the suprascapular notch, their courses become briefly divergent so that the nerve takes a path deep to the transverse scapular ligament (TSL), whereas the artery remains superficial to this (Fig. 24-1). Variations have been reported in this arrangement, with the artery passing beneath the ligament in up to 2.5% of shoulders.¹⁰

FIGURE 24-1 Three-dimensional representation of SSN and suprascapular artery and their relationship with the TSL.

The transverse scapular ligament spans the suprascapular notch, extending from the base of the coracoid and creating the suprascapular foramen. Because it is a ligament that connects two parts of the same bone, it is considered by some to represent a continuation of the coracoclavicular ligaments.¹⁰ Variable degrees of ossification have been reported in the ligament, with complete ossification in 3.7% in one series¹⁴ and partial ossification seen in 18%.¹⁵ It has also been seen to be bifid or trifid in 3% of cases in the same cadaveric series. It is important to remember, therefore, that in up to 25% of cases, the TSL is represented by an ossified variant or one with multiple bands.

As the nerve passes beneath the TSL, it gives two motor branches to supraspinatus, with the first branch generally being the larger of the two. It has been reported that one of these motor branches can pass superficial to the TSL.¹⁶ According to Hilton’s law, the SSN gives articular branches to the acromioclavicular and glenohumeral joints.¹⁰ On a microscopic level, it can be seen that the superficial part of the nerve carries afferent fibers (i.e., proprioception, pain), whereas the deeper fibers are responsible for motor innervation.¹⁷

The nerve then descends around the lateral margin of the scapular spine (Fig. 24-2) to split into three or four terminal motor branches supplying the infraspinatus. In doing so, it passes beneath the spinoglenoid ligament, forming the soft tissue boundary of the spinoglenoid notch. This quadrangular ligament extends from the posterior glenoid neck and capsule to insert onto the scapular spine.¹⁸

FIGURE 24-2 Three-dimensional view of distal SSN passing around the spine of the scapula.

A cutaneous branch has been found in 14.7% of cadaveric specimens examined, which supplies the skin overlying the proximal lateral third of the arm.^17,19 These cutaneous and articular branches may in part explain the nature and location of pain in some patients with SSN dysfunction.

HISTORY AND PHYSICAL EXAMINATION

Diagnosis is not always straightforward in SSN neuropathies and important information is gleaned from a detailed history and clinical examination. Epidemiologically, patients tend to be men younger than 40 years.

The principal complaint is usually one of deep diffuse pain or aching, often localized posteriorly or laterally in the proximal arm. Some have described this pain as burning in nature, which can radiate down the arm or into the neck. The onset of symptoms is usually insidious in nature, however, if trauma has been a precipitating feature; the cause is commonly compression at the level of the TSL.⁴ Patients also complain of weakness, particularly in movements involving external rotation and abduction and their symptoms are typically exacerbated with overhead activities. However, all these symptoms can be difficult to differentiate from those of rotator cuff tears or impingement, which may be coexistent. As such, pathology related to the SSN continues to be underdiagnosed. Symptoms from nerve compression at the suprascapular notch tend to be more severe than those compressive causes occurring distally.²⁶ Because of the poorly defined nature of the symptoms, patients frequently present many months after symptoms have begun and, in many cases, after having had previous surgery. These patients remain troubled by persistent symptoms; by this stage, their pain has become chronic and muscle atrophy has become apparent. One of the most important aspects in the management of SSN neuropathy is to detect it early to prevent it reaching this late stage.

Clinical examination reveals only a subtle loss of external rotation and abduction strength in the early stages of compression. Atrophy is seen later in the course of the disorder; it affects the supraspinatus and infraspinatus in cases of proximal nerve entrapment at the suprascapular notch, although in some cases isolated infraspinatus wasting is seen with proximal compression.⁴ Nerve compression at the level of the spinoglenoid notch causes only infraspinatus atrophy. Tenderness may found in the suprascapular notch, but this is a relatively nonspecific sign. Long-standing compression can cause profound weakness in external rotation and abduction, with marked muscle atrophy, although deltoid mass should be reasonably maintained (Fig. 24-3).

FIGURE 24-3 Marked atrophy of supraspinatus and infraspinatus.

Provocative tests may be used to increase tension in the nerves and reproduce symptoms. Cross-arm adduction can re-create the posterior shoulder pain found in SSN compression but it may also be positive with acromioclavicular joint degeneration.

DIAGNOSTIC IMAGING

Even after clinical history and examination, making the diagnosis of an SSN neuropathy can still be difficult. It is often discovered as a diagnosis of exclusion, made after multiple imaging investigations and unsuccessful surgery.

Plain x-rays are usually unremarkable, although they may reveal signs of trauma to the clavicle, scapula, or glenoid neck. Tilting the x ray beam 15 to 30 degrees on an anteroposterior (AP) scapular film may give a better view of the suprascapular notch and any calcification of the ligament, but we do not routinely perform this. Computed tomography (CT) scanning is useful for defining osseous abnormalities or fractures and fatty infiltration; nevertheless, it only poorly defines the pathology in what is often a soft tissue problem.

Magnetic resonance imaging (MRI) remains the best imaging tool in suspected SSN pathology because of its soft tissue resolution. It can be used to visualize the course of the nerve and integrity of the rotator cuff, demonstrate the presence of fatty infiltration, and is very helpful for identifying space-occupying lesions. The presence of muscle edema on MRI scanning has been suggested as a more sensitive and specific early sign of SSN entrapment than that of muscle atrophy and fatty infiltration.²⁷ Caution should be exercised in interpreting the clinical significance of a cyst because the presence of a cyst does not always indicate whether there is SSN compression (Fig. 24-4). If CT and MRI fail to show a ganglion cyst or other space-occupying lesion and there remains a clinical suspicion of SSN pathology, it is our practice to request a nerve conduction study (NCS) and electromyography (EMG). This not only provides a diagnosis but also locates the level of the lesion. It is important to state the suspected pathology and need for SSN testing on the request card because this nerve is not always routinely sought with NCS and EMG. Positive findings include denervation potentials, fibrillations, reduced amplitude of evoked potentials, and prolonged motor latencies. However, as an added complication, SSN dysfunction can present with a normal NCS.

FIGURE 24-4 Spinoglenoid notch cyst.

A further diagnostic aid is the use of a local anesthetic injection placed ideally under radiologic guidance. This can help confirm the diagnosis if it successfully relieves the patients symptoms but, given the difficulty of locating this notch, a negative test does not exclude SSN pathology.²⁸

INDICATIONS AND CONTRAINDICATIONS

Indications for surgical release of SSN include the following:

Repetitive overhead activity–related neuropathy and traction injuries tend to respond equally well to operative and nonoperative management. Thus, we prefer to recommend 6 months of nonoperative management prior to any surgical intervention.

Compressive lesions such as spinoglenoid cysts and lipomas respond better to operative than nonoperative intervention.²⁹ We prefer to operate on these early rather than subject the patient to a protracted period of physiotherapy. This is particularly true for space-occupying lesions found by MRI, with an accompanying abnormal NCS EMG result. This also allows us to treat the commonly associated intra-articular pathologies at the same time (e.g., posterosuperior labral lesions in the case of spinoglenoid cysts).

In the case of large and massive rotator cuff tears, there remain unanswered questions in terms of suprascapular nerve release. The first question relates to whether the cuff tear itself and subsequent retraction lead to SSN dysfunction through a traction or kinking mechanism. Mallon and colleagues⁸ have demonstrated the presence of SSN neuropathy as proven on NCS and EMG in a series of eight patients with massive rotator cuff tears. These patients also had MRI changes of fatty infiltration; of the eight patients, four underwent débridement and partial repair of their cuff tear. Subsequent EMG testing in two patients demonstrated good signs of nerve recovery.

It has been proposed by some authors that the improvement experienced by some patients with massive rotator cuff tears is partly the result of the partial or complete decompression of the tethered SSN, which occurs by reducing the retraction of the supraspinatus tear.^8,30 Vad and associates³¹ have also demonstrated that peripheral neuropathy can be found in 28% of full-thickness rotator cuff tears presenting with shoulder muscle atrophy; of these neuropathies, the SSN is involved in 29%. Costouros and coworkers³² have found that 27% of patients (7 of 26) with massive rotator cuff tears accompanied by muscular atrophy and fatty degeneration on MRI were also found to have SSN neuropathy on EMG testing. Of their patients, 6 underwent arthroscopic rotator cuff repair and all went on to demonstrate clinical and EMG improvements in SSN and shoulder function. They now recommend routine EMG testing in cases of massive rotator cuff tears, given the high prevalence of associated SSN neuropathy and the likely improvement with surgical repair. Along with Albritton and colleagues,³⁰ they have postulated that the cuff retraction results in tethering of the nerve at the suprascapular notch, and this gives rise to a subsequent neuropathy. By reducing the cuff, the nerve is moved more laterally, thereby releasing its tension.

The second question relates to whether the reduction of a large to massive cuff tear can itself cause SSN dysfunction through advancement of the cuff. Warner and associates¹⁶ have demonstrated in their anatomic study that neither the supraspinatus nor infraspinatus could be advanced more than 3 cm before being restricted by tension in the motor branches of the SSN, even after a modified deinsertion-advancement technique. Furthermore, when no release was performed, only 1 cm of lateral advancement was possible before the nerve came under tension. This study found that in the process of lateral advancement, the motor branches to the supraspinatus pivoted 180 degrees around the SSN pedicle, which remained fixed in the fossa. In the same study, they noted that releasing the TSL affords further cuff advancement before tension again becomes a limiting factor.

By releasing the TSL, particularly in large, chronically retracted tears, SSN mobility is improved in the retracted state and for reduction of the cuff, therefore enhancing the chances of neuromuscular recovery.

TREATMENT OPTIONS

Arthroscopic Release

The goal of surgery is to improve pain and symptoms, prevent irreversible muscle atrophy, and improve strength. Despite open surgery being an accepted method of treatment,^13,36,37 we think that arthroscopy has several advantages:

1. The excellent magnification afforded allows the small nerve (less than 2 mm) to be seen more easily and the TSL to be divided with more accuracy

2. It is significantly less invasive than an open approach which requires some detachment or splitting of trapezius

3. It can be performed as day case surgery with an operative time now approximately 5 to 10 minutes.

The location and type of release we perform are determined by the preoperative history and examination, anatomy, and pathology, as revealed by imaging and NCS EMG findings.

Position and Portals

The patient is placed in the beach chair position with the arm held in 60 degrees of flexion and with 3 kg of longitudinal traction. This traction increases the size of the subacromial space, permitting improved instrument access to the suprascapular notch. The portals we use to perform our releases include the standard posterior soft spot portal, required to visualize the glenohumeral joint and subacromial space. A posterolateral portal can be used to gain access to the posterosuperior labrum and can be used subacromially or intra-articularly as a transcuff portal. A lateral subacromial portal and anterolateral portal are also used. Lafosse and associates have described³⁸ a new superior portal, which is now required, known as the G or SSN portal. It is positioned between the clavicle and scapular spine, approximately 7 cm medial to the lateral border of the acromion (Fig. 24-5). This portal is approximately 2 cm medial to the classic Neviaser portal. These portals are created using an outside-in technique.

FIGURE 24-5 External view demonstrating the A (posterior, soft spot), B (posterolateral), C (lateral), D (anterolateral), and G (SSN) portals.

To ensure optimum viewing conditions, we prefer the systolic blood pressure to be safely kept at less than 120 mm Hg, maintaining a pump pressure of at least 50 (5 feet of gravity pressure equivalent to 112.5 mm Hg).

Transverse Scapular Ligament Release

The procedure commences with a glenohumeral joint inspection through the posterior A portal (see Fig. 24-5). Once completed, the arthroscope is introduced into the subacromial space and a lateral C portal is created. Using a radiofrequency probe or shaver, the soft tissue of the anteromedial bursa is cleared. The arthroscope is then moved to the lateral C portal and an anterolateral D portal is created 1 cm lateral to the anterolateral corner of the acromion. This portal is ideal for continuing the medial dissection with the shaver and radiofrequency probe toward the suprascapular notch.

Next, it is important to identify landmarks. This is done by following the coracoacromial ligament down to the coracoid anterior to the anterior border of supraspinatus. Then, the coracoclavicular ligaments are identified (trapezoid followed more medially the conoid) by continuing the dissection posteriorly and medially (Fig. 24-6). The medial border of the conoid ligament coincides with the lateral attachment of the TSL; the two are considered continuous. It is of great assistance during this dissection to remain anterior to the muscle belly of supraspinatus and to use this border of the muscle as a landmark as it appears to disappear medially.

FIGURE 24-6 View of the ligaments leading to the TSL. 1, Conoid. 2, Trapezoid. 3, Coracoacromial. 4, TSL.

To aid in the exposure and definition of the TSL, a SSN (G) portal is created using a spinal needle with an outside-in technique (see earlier). A knife is used to incise the skin, after which a blunt trocar is inserted to determine the path for a specialized TSL-cutting scissor (Fig. 24-7). This instrument is blunt at its tip to allow gentle dissection and has a side cutting arm. The tip is used to displace the tissues around the notch carefully. It is usually necessary to retract the supraspinatus muscle and fat around the TSL posteriorly to get a good view of the TSL, suprascapular artery, and SSN (Fig. 24-8). The suprascapular artery should now be seen passing superiorly to the TSL, with the nerve passing underneath. The instrument is then introduced directly into the suprascapular notch and the nerve is displaced medially by the blunt tip, thereby protecting it (Fig. 24-9). The TSL is divided and the mobility of the nerve assessed with the blunt tip to ensure that an adequate release has been accomplished (Figs. 24-10 and 24-11). A normal blunt-tipped trocar followed by a meniscectomy punch can be used as alternatives, although this combination does not provide the same protection to the nerve as it is being cut. If there is any bony narrowing of the foramen or ligament ossification, it can be dealt with now by performing a notchplasty with a burr. Others have reported using a Kerrison punch rongeur or osteotome as alternatives for the notchplasty.^39,40

FIGURE 24-7 External view of a blunt-tipped trocar used to create the G (SSN) portal.

FIGURE 24-8 TSL passing over SSN (suprascapular artery not shown on this image).

FIGURE 24-9 Standard arthroscopic scissors being used to approach the ligament. Note that the neurovascular structures remain under direct vision.

FIGURE 24-10 Ligament now divided, liberating the nerve. The SSN has moved superiorly from its previous site of entrapment.

FIGURE 24-11 SSN and scapular spine revealed after cyst decompression.

Our early experiences with this technique involved 10 patients (8 men and 2 women) with EMG-proven SSN compression, a mean age of 50.4 years (range, 36 to 73 years), and an average 15-month follow-up.³⁸ All patients had posterior shoulder pain and weakness, with symptoms on overhead activity, and had failed 6 months of conservative management. They had supraspinatus and infraspinatus atrophy and weakness in abduction and external rotation. All patients underwent SSN release and were reviewed 6 months postoperatively with repeat EMG examination in 8 of 10 patients; 7 had normalization of nerve conduction velocity, latency, and amplitude and an increase in their Constant score from 60.3 to 83.4.

Spinoglenoid Notch Decompression

Extra-Articular Subacromial Technique at the Posterior Interval.

Because of the high incidence of capsulolabral pathology associated with spinoglenoid cysts, a detailed glenohumeral joint arthroscopy is performed assessing these structures. In the absence of any intra-articular pathology, the arthroscope is moved subacromially to the C portal. Using the posterolateral B portal as a working portal, the connective tissue surrounding the posterosuperior cuff and lateral aspect of the scapula spine is removed using a shaver and radiofrequency device. A probe is then used from the A portal to retract the infraspinatus, allowing better access to the spinoglenoid notch deep to the scapula spine. By careful soft tissue dissection, the cyst can be visualized, opened, and excised. Once this is completed, the decompressed suprascapular nerve can be demonstrated.⁴¹

Intra-Articular Technique

If intra-articular pathology is identified, a transarticular arthroscopic release of the spinoglenoid notch or cyst decompression is performed. The main viewing portal is the transrotator cuff B portal at the posterior interval, this time passing through the cuff between the infraspinatus and supraspinatus. In addition, an anterolateral D portal and standard posterior A portal are used for instrumentation.

We perform a selective capsulotomy of the posterosuperior capsule in the area of pathology until the muscle fibers or the fat pad surrounding the neurovascular structures can be seen. The rotator cuff is elevated from the labrum using a blunt trocar. This provides access to the spinoglenoid notch as well as the supraspinatus or infraspinatus fossa, allowing good visualization of the suprascapular nerve. Depending on its location, a complete evacuation of a cyst and decompression of the nerve can be performed with this approach.

Compressive lesions were demonstrated in one series to have an improved outcome when decompressed surgically, especially in the cases of spinoglenoid cysts and compressive lesions of the suprascapular notch.²⁹

Cadaveric studies have demonstrated that the distance of the SSN in the suprascapular notch from the supraglenoid tubercle is 3.0 cm and the distance from the glenoid rim to the nerve at the base of the spine of the scapula is 1.8 cm.⁴² These distances are important, especially if an intra-articular approach is taken to decompress the SSN, releasing retracted rotator cuff tears.

PEARLS& PITFALLS

PEARLS

• Use your landmarks—follow the anterior border of supraspinatus and identify the coracoclavicular (CC) ligaments.

• Be prepared to use electrocautery and increase the pump pressure to control bleeding.

• Perform a diagnostic glenohumeral joint arthroscopy to exclude associated pathologies.

• Retract the nerve after blunt dissection with the trocar to define the boundaries of the notch.

• Visualize the nerve clearly passing under the ligament before cutting the TSL.

PITFALLS

• Avoid dissecting too medially to prevent inadvertent nerve damage.

• Incomplete nerve release—check nerve mobility with a blunt-tipped instrument.

POSTOPERATIVE REHABILITATION PROTOCOL

Postoperatively, we allow our patients to mobilize immediately as comfortable, without restriction. This is modified if any concomitant pathology is found that requires treatment (e.g., superior labrum anteroposterior [SLAP] tear).

In our early study, two patients did not show complete normalization of their electromyograms until 1 year after SSN decompression. Hence, 6 months may not be enough time to analyze the physiologic outcome of this procedure by electromyography.

SUMMARY AND CONCLUSIONS

Suprascapular nerve pathology is an uncommon cause of shoulder pain and weakness but should be suspected particularly in younger patients who fail to respond to conventional therapies. Careful history and examination can yield vital clues to the diagnosis, which can be confirmed by MRI imaging and NCS EMG. Half of patients who have had surgical decompression of the SSN in one meta-analysis had persistent muscle atrophy,⁴ suggesting that early surgical intervention may be advisable to prevent irreversible nerve damage and muscle changes.

We believe that arthroscopic release of the suprascapular nerve provides a controlled reproducible technique that is minimally invasive and takes minimal time. It can be performed as day case surgery and our early results have been encouraging. We are currently undertaking a study in over 100 patients to determine whether SSN release should form part of routine rotator cuff surgery for retracted tears.