Suprascapular Nerve Injury

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Continuing Education Activity

There is increasing interest in the literature regarding the clinical delineation of suprascapular nerve (SSN) injuries. While the underlying etiology of SSN neuropathy remains elusive, multiple compression, traction, and inflammatory pathophysiologic cascades have been previously considered. The latter are often readily grouped with other clinical manifestations of SSN dysfunction and inevitably become labeled as idiopathic. The anatomically tortuous course of the SSN predisposes it to direct mechanical compression at the suprascapular and spinoglenoid notches. Moreover, anatomic variations along the nerve's course, as well as occupational or athletic overuse conditions, can predispose the SSN to varying degrees of dysfunction. This activity highlights the role of the interprofessional team in the diagnosis and management of SSN injuries.


  • Identify the etiology of suprascapular nerve injuries.
  • Review the diagnosis of suprascapular nerve injury.
  • Outline the treatment for suprascapular nerve injury.
  • Discuss interprofessional team strategies for improving outcomes for patients with scapular nerve injury.


There is increasing interest in the literature regarding the clinical delineation of suprascapular nerve (SSN) injuries. While the underlying etiology of SSN neuropathy remains elusive, multiple compression, traction, and inflammatory pathophysiologic cascades have been previously considered.[1][2][3][4] The latter are often readily grouped together with other clinical manifestations of SSN dysfunction and inevitably become labeled as idiopathic. The anatomically tortuous course of the SSN predisposes it to direct mechanical compression at the suprascapular and spinoglenoid notches. Moreover, anatomic variations along the nerve's course as well as occupational or athletic overuse conditions, especially in overhead athletes, can predispose the SSN varying degrees of dysfunction.[5][6]


First described in the French literature in 1936, and the English literature in 1959, SSN dysfunction is implicated in approximately 1-2% of cases of shoulder pain, and up to 33% of cases of shoulder pain in overhead athletes.[7] Causes of SSN injury include primary etiologies that can be attributed to anatomical entrapment of the SSN along the nerve's course or functional impingement of the SSN with repetitive use, as in overhead athletes. Some of the most common anatomic sites of SSN entrapment include:[8][9]

  • Suprascapular notch
  • Spinoglenoid notch
  • Superior transverse scapular ligament

Other secondary etiologies of SSN dysfunction include, but are not limited to:

  • Scapulothoracic dyskinesia, shoulder girdle dysfunction
  • Traumatic injuries with SSN injury occurring secondary to the nerve's proximity to the primary injury and associated mechanism of action[10][11]
    • Fractures of the scapula, clavicle, proximal humerus
    • Glenohumeral dislocations
    • Acromioclavicular (AC) joint injuries
  • Iatrogenic injuries during arthroscopic or open shoulder surgeries[12]
  • Space-occupying lesions[13]
    • Ganglion cysts
    • Paralabral cysts
    • Bone cysts
    • Osteosarcoma, soft tissue sarcoma, metastatic lesions
  • Systemic conditions[14][15][15]
    • The systemic lupus erythematosus (SLE)
    • Rheumatoid arthritis (RA) 

Historically a diagnosis of exclusion, SSN dysfunction has become an increasingly recognized clinical condition with an often discrete underlying pathologic process. Moreover, while isolated SSN injuries remain relatively uncommon, it is the most frequently injured peripheral branch of the brachial plexus in athletes[6].

Primary etiologies of SSN compression and injury include the at-risk anatomic sites along the course of the SSN in addition to repetitive overhead activities that are often seen during various sports and manual labor with excessive overhead occupational demands. The former includes throwing athletes and those athletes exposed to repetitive overhead trauma and repetitive motions, such as baseball players, tennis players, weight lifters, swimmers, and volleyball players.[16][17][18][19][20]


SSN dysfunction epidemiological data are lacking and often debated given the heterogeneous reports in the literature in general, combined with the relatively recent increases and advancements in diagnostic imaging modalities. Moreover, the clinical significance of SSN dysfunction varies from complete irrelevance in asymptomatic patients who can be diagnosed with possible SSN dysfunction incidentally to increasing degrees of shoulder pain and dysfunction related to the supraspinatus and/or infraspinatus atrophy and degeneration. Thus, incidence and prevalence rates remain elusive.[5]

Estimations have cited SSN neuropathy, mechanical irritation during repetitive traction and overhead motions, and focal entrapment to represent anywhere from 0.4 to 2% of cases of shoulder girdle pain. Consensus does exist that SSN dysfunction is often seen in association with various sport-specific positions and elite levels of performance. Isolated infraspinatus muscle atrophy is often utilized as it is readily detectable on physical exam or other diagnostic modalities such as ultrasound, electromyographic (EMG) studies, or magnetic resonance imaging (MRI). While the clinical relevance of isolated infraspinatus atrophy remains unclear, with most patients reporting normal shoulder function and no pain, the associated incidence rates seen in the dominant shoulder of overhead athletes ranges from 4% to 52%, with the highest rates recently reported in a 2015 study that investigated the incidence seen in elite professional female tennis players.[21] Interestingly enough, the authors noted that clinically relevant infraspinatus atrophy as detected on physical examination alone was associated with a higher performance ranking, and no functional deficits or associations with concurrent shoulder disorders were appreciated.[22][23][24] Even studies from the early 1990s cited a 34 to 45% incidence rate of infraspinatus muscle impairment in both baseball pitchers elite volleyball players.[25][26][27]


Muscle wasting, atrophy, and degeneration are thought to occur secondary to either direct mechanical compression from an underlying anatomic variation, space-occupying lesion, or secondary to repetitive traction and irritation of the nerve at one of the anatomically predisposed sites of SSN focal entrapment as described below. 

Anatomic sites of entrapment

The SSN is derived from the upper trunk of the brachial plexus, consisting of fibers from the C5 and C6 nerve roots.[28] A mixed motor and sensory nerve, the SSN supplies motor innervation to the supraspinatus and infraspinatus muscles in addition to sensory innervation to the coracohumeral and coracoacromial ligaments (CHL, CAL), subacromial bursa, and the acromioclavicular and glenohumeral joint capsules.[29]

The SSN traverses through the supraclavicular fossa, passing through the posterior triangle of the neck before coursing deep to the trapezius muscle and the clavicle. Continuing laterally toward the suprascapular notch, the SSN is accompanied by its artery and vein. Aiello et al.[30] first identified the suprascapular and spinoglenoid notches as two potential sites of SSN entrapment secondary to direct mechanical compression. The SSN passes inferior to the superior transverse scapular ligament (STSL), a fibrous, banded structure that traverses the superior aspect of the scapula, serving as the superior boundary of the suprascapular notch (image 1). Direct compression at the suprascapular notch remains the most common site for SSN entrapment. After traversing the suprascapular notch, the SSN enters the suprascapular fossa before dividing it into the supraspinatus and infraspinatus nerve branches.[31] The nerve has greater mobility at the level of the suprascapular fossa, but it remains limited given its adherence to the periosteum in addition to the motor branches given off to the supraspinatus muscle.[32] Furthermore, the aforementioned space-occupying lesions (e.g., ganglion or paralabral cysts) and fracture sequelae (i.e., malunion/nonunion) can also cause compression and resultant nerve injury. Distally, the SSN turns medially at the spinoglenoid notch and can is at risk of localized compression secondary to paralabral cysts, prominent hardware, and enlarged veins.[33][34] Although overall less common in comparison to its suprascapular notch counterpart in reference to a focal site of SSN entrapment, the spinoglenoid notch is becoming an increasingly appreciated site of mechanical compression.[35][36][35][37]

Anatomic variants

Multiple anatomic variations have been gaining increasing attention in the literature as additional elements predisposing to SSN dysfunction. Much of the attention has focused on variations in the morphology of the suprascapular notch itself, given that it remains the most common site of SSN focal entrapment. SSN neuropathy has been reported in the setting of an ossified STSL, with varying degrees including the presence of a double suprascapular foramen created by multiple, discrete osseous bridges.[38] The morphological risk factors of the suprascapular notch also include osseous prominences at the margins of the bony incisura, a bifid STSL, and a narrowed "V" shape configuration of the notch itself.[39] The anterior coracoscapular ligament (ACSL)[40], spinoglenoid ligament (inferior transverse scapular ligament, ITSL), and a hypertrophied subscapularis muscle are other less common anatomic variations that have been reported in the literature.[41][42][43][44][45][42]

The ITSL has continued to gain literature support and documented evidence of its physiologic existence in the majority of the population. While historical studies reported the presence of the ITSL in about half of the population, more recent cadaveric specimen dissections identify a discrete, complex ITSL structure in 100% of the dissected specimen. In 2005, Plancher et al. identified the spinoglenoid ligament in all cadaveric specimens, with the ligament reproducibly demonstrating an irregular quadrangular shape, thinnest in its midportion and fanning out to its insertions superomedially and inferolaterally. The inferolateral portion of the ligament demonstrates distinct superficial and deep layers inserting into the posterior aspect of the shoulder capsule and the posterior aspect of the glenoid neck, respectively.[45]

History and Physical

Patients typically present with dull, aching pain in the superior and/or posterolateral shoulder that can radiate down the arm or into the neck. If the injury is distal to the spinoglenoid notch, patients may not complain of pain at all. Additional symptoms include a sense of instability if there is associated shoulder pathology, such as a labral or rotator cuff tear.[32] Symptoms most commonly develop gradually and may worsen over time to the point of being constant. However, some studies have reported a traumatic injury as the initial cause in 40% of patients.[46] SSN injury is typically related to repetitive overhead activities in athletes (baseball players, tennis players, weight lifters, swimmers, and volleyball players) or laborers.

Given the symptoms can overlap with other shoulder pathologies and sometimes present without pain, it is often difficult to diagnose an SSN injury on history alone. A comprehensive exam includes a detailed shoulder and cervical spine exam to rule out alternative or co-morbid etiologies. One of the most common findings on physical exam is atrophy of the infraspinatus and/or supraspinatus muscles, with one meta-analysis finding atrophy in one or both muscle groups in nearly 80% of patients with confirmed suprascapular neuropathy. Patients may endorse tenderness to palpation posterior to the AC joint and/or the posterosuperior joint line.

The patient's pain may be exacerbated by cross-body adduction and internal rotation.[47] weakness may be noted with shoulder external rotation and/or shoulder abduction. However, if the nerve injury is at or distal to the spinoglenoid notch and as a result, only the infraspinatus is affected, weakness may not be as pronounced given the patient's deltoid, supraspinatus, and teres minor can aid in functional and strength compensation. A specific physical exam maneuver that has been described to help with the diagnosis is the SSN stretch test. This test consists of laterally rotating the patient's head away from the painful shoulder and retracting the neck and shoulder. A positive test is when the pain at the posterior shoulder is exacerbated.[48]


Suprascapular neuropathy is very difficult to diagnose from history and physical examination alone. As such, further evaluation with imaging and diagnostic testing, including electrodiagnostic testing and nerve blocks, is warranted.

Initially, plain radiographs should be obtained to evaluate for possible osseous abnormalities that are impinging on the nerve or other comorbid shoulder conditions, such as arthritis or evidence of dislocation or subluxation.[32] Radiographs are particularly important in patients with an acute injury causing pain and weakness as the clinician will need to rule out a scapular fracture, first rib fractures, AC joint disruption, or shoulder dislocation.[17] Including the Stryker notch view when ordering shoulder radiographs helps visualize the suprascapular notch and any associated osseous abnormalities at the foramen.[1] If osseous abnormalities are thought to be the primary cause of injury, a CT scan may help further localize the area of nerve compression.[49]

MRI can be helpful in the evaluation of suprascapular neuropathy given its ability to assess for indirect signs of SSN injury such as areas of soft tissue compression as well as the quality of the rotator cuff musculature looking for areas of muscle atrophy and fatty infiltration.[50] MRI can also help rule out other causes of shoulder pain on the differential, such as labral or rotator cuff tears.

Musculoskeletal ultrasound can be particularly useful in diagnosis for not only visualizing the nerve course and performing a dynamic muscle and nerve exam, but also for guidance for an SSN block.

With ultrasound, the SSN is best visualized during in its supraclavicular course as this is when the nerve is most superficial. It has been suggested that the most useful visualization of the nerve is in the coronal plane over the suprascapular fossa between the spinoglenoid and scapular notch. However, using the anatomic landmarks of the nerve’s origin at the interscalene triangle, the first rib, the lateral supraclavicular fossa below the omohyoid muscle, the supraspinatus fossa, and the spinoglenoid notch, it has been shown that the nerve can be accurately followed through its entire course until its termination in the infraspinatus fossa.[51] Furthermore, one area that ultrasound is chiefly superior to MRI is for dynamic visualization of the SSN. A dynamic exam allows the practitioner to visualize the nerve as it travels through or near the sites of impingement, as mentioned above. This portion of the exam can show how overhead movements can impact the course of the nerve or how potential pathologic sites can cause nerve compression (e.g., paralabral cyst compressing the SSN (Image 5)). And like MRI, ultrasound is able to evaluate the quality of the rotator cuff musculature again, looking for indirect signs of SSN injury such as muscle atrophy and fatty infiltration (Image 2)(Image 3). Increased intramuscular fat causes an increase in muscular echogenicity on ultrasound, with further increases depending on muscle diameter and amount of subcutaneous fat.[52]

Injection of an anesthetic to the suprascapular or spinoglenoid notch with resultant pain relief helps support the diagnosis of suprascapular neuropathy. Using ultrasound to guide the procedure allows for accurate localization and delivery of medication, with one study showing correct placement, 95% of the time using cadavers (Video 1). Gorthi et al. found that compared to a blind SSN block, ultrasound guidance improved localization and provided significantly longer-lasting relief for patients in one month.[53] Visualization of the needle during the procedure helps to avoid possible complications such as pneumothorax or injury to neighboring vascular structures. In patients in which symptoms are only present during overhead sport or occupational specific activities, the authors recommend an ultrasound-guided nerve block with a trial of light sport or occupational specific activities in a controlled practice environment while in the therapeutic window of the local anesthetic used.

The gold standard for diagnosis and confirmation of suprascapular neuropathy is electrodiagnostic evaluation, including nerve conduction studies (NCS) and EMG. This test can specifically focus on the SSN and its innervations. Findings on electrodiagnostic evaluation that suggest compression and denervation of the SSN include prolonged latency, decreased amplitude, fibrillation potentials, and positive sharp waves.[32] Electrodiagnostic evaluation can also be key to ensure the clinician rules out additional etiologies that may mimic suprascapular neuropathy, e.g., a cervical (C5-6) radiculopathy or Parsonage-Turner syndrome.

Treatment / Management

Given the difficulty with diagnosis, patients may present after months of dealing with persistent pain and weakness without an identified cause or after failing to improve with treatment of co-morbid findings on exam or imaging, e.g., rotator cuff strains, osteoarthritis, and labral pathology. However, once a diagnosis of SSN injury is confirmed, treatment can start. 

Non-operative management can be effective for patients who have isolated suprascapular neuropathy without co-morbid pathology, e.g., of the intra-articular shoulder or rotator cuff pathology.[46] Most studies have shown that patients see benefit with conservative management in 6 to 12 months.[54] The conservative treatment approach entails non-steroidal anti-inflammatory medications, activity modification, physical therapy, and ultrasound-guided injections. Specifically for overhead athletes, given the suspected cause being repetitive microtrauma, sport-specific activity modification is key to the initial management of the nerve injury. Physical therapy exercises should focus on maintaining a full range of motion to avoid the development of adhesive capsulitis. Exercises should focus on stretching the posterior shoulder capsule and strengthening the rotator cuff and surrounding shoulder musculature as well. Stretching the posterior capsule is especially important in athletes, as it is hypothesized to reduce tension on the spinoglenoid ligament, which can reduce repetitive microtrauma during sports activities. Although physical therapy is beneficial for these patients with SSN injury, there is no definitive protocol for treatment. An ultrasound-guided injection at the suspected place of entrapment, e.g., at the superior boundary of the suprascapular notch where the SSN passes inferior to the STSL (Video 1), can help with diagnostic confirmation and therapeutic relief. 

If there is an identified pathology causing compression of the nerve or have not improved with 6-12 months of the above conservative management, surgical intervention is warranted. Some surgeons contend that surgical intervention should be performed immediately upon diagnosis because patients have likely had the symptoms for at least six months leading up to the presentation.[55][56] Surgical management options depend on the cause and suspected location of the nerve injury. However, the exact surgical option varies with some authors reporting improvement with the isolated repair of the shoulder pathology without decompression while others state decompression of the nerve should occur simultaneously.[57][58][59] If the nerve injury is due to a paralabral cyst, a percutaneous cyst decompression under imaging guidance can also be an effective treatment. However, failure rates have been reported up to 50%, given the inability to correct the contributing intra-articular lesions.[60][61] Postoperatively, most patients had resolution of pain and improved muscle strength.[62]

Differential Diagnosis

The diagnosis of SSN injury can be challenging, given the overlap in presentation with other pathologies of the shoulder and cervical spine region. The differential diagnosis includes, but is not limited to, the following:[32]

  • Cervical radiculopathy (C5-6)
  • Parsonage-Turner syndrome
  • Brachial plexopathy (upper trunk)
  • Rotator cuff pathology (e.g., tendinitis, bursitis, partial or complete strain/tear)
  • Subacromial impingement syndrome
  • Scapular dyskinesia
  • Labral pathology (e.g., superior labral tear from anterior to posterior (SLAP tear))
  • Adhesive capsulitis
  • Glenohumeral arthritis
  • Facet mediated pain


The prognosis for isolated suprascapular neuropathy is generally favorable, with one study reporting 80% of patients having good or excellent improvement in pain and function.

Even though most patients with suprascapular neuropathy will experience an improvement in pain and function, whether treated surgically or conservatively, once significant atrophy has occurred, it is unlikely that muscle bulk or strength will return to post-injury levels.[55] However, even with persistent atrophy, a majority of patients will see improvement in supraspinatus and infraspinatus strength, with supraspinatus strength showing greater improvement.[62] Furthermore, as mentioned previously, the deltoid, supraspinatus, and teres minor can compensate for the loss of infraspinatus strength.[63]


Pain and weakness have been shown to improve with both conservative management as well as surgical decompression of the nerve as clinically indicated. However, depending on the chronicity of symptoms, the patient may have persistent atrophy and weakness of the affected rotator cuff muscles.


Given the usual delay in diagnosis, if suprascapular neuropathy is in the differential for the patient’s symptoms, a referral to a Physical Medicine & Rehabilitation physician, sports medicine physician, and/or an orthopedic surgeon is warranted for continued workup and management.

Deterrence and Patient Education

The most important aspect of this condition is initial recognition or diagnosis, so it is imperative to educate patients that early presentation for clinical evaluation is key. When discussing treatment options, clinicians should address the patient’s understanding and expectations and be prepared to answer questions regarding prognosis. Patients should also be educated on the expected timeline for improvement of muscle strength and function.

Pearls and Other Issues

  • The two main sites of SSN compression are the suprascapular notch and the spinoglenoid notch.
  • The compression of the SSN at the spinoglenoid notch likely will result in isolated infraspinatus atrophy and is painless.
  • Diagnosis of suprascapular neuropathy may be delayed due to co-morbid but asymptomatic findings of the rotator cuff and labral pathology on examination and/or imaging.
  • The authors recommend electrodiagnostic testing to confirm suprascapular neuropathy and avoid the pitfall of misdiagnosis of Parsonage-Turner Syndrome or cervical radiculopathy.
  • In patients in which symptoms are only present during overhead sport or occupational specific activities, the authors recommend an ultrasound-guided nerve block with a trial of light sport or occupational specific activities in a controlled practice environment while in the therapeutic window of the local anesthetic used.
  • Prompt diagnosis and treatment are keys to symptom improvement and the potential return to a prior level of function because once significant atrophy has occurred, it is less likely for the patient to return to pre-morbid muscle bulk and strength in the affected muscles.

Enhancing Healthcare Team Outcomes

SSN injury is a diagnosis that requires a keen diagnostic acumen and an effective multidisciplinary team to effectively manage. Early identification and initiation of treatment are key to symptom improvement and return to the prior level of function. Efficient consultation to specialty providers, such as physical medicine & rehabilitation, sports medicine, and/or orthopedic surgery provides the best prognosis and outcome for the patient. Once diagnosed prompt referral to physical therapy to begin rehabilitation is also beneficial for patients to increase range of motion and strengthen the rotator cuff and surrounding musculature whether it is the definitive treatment or ends up ultimately being part of a pre- and post-operative rehabilitation protocol. Referrals should include a summary of the history of present illness, physical exam, a detailed social history (with close attention to occupations, hobbies, and sports with repetitive overhead motions), patient’s goals of treatment, and treatments already trialed. This information sharing allows for a more complete view of the patient's problem and allows all team members access to important information necessary to effectively treat the patient and meet their goals.

(Click Image to Enlarge)
Arthroscopic image of demonstrating the Suprascapular nerve (SSN) coursing inferiorly to the Superior transverse scapular ligament (STSL).  The image demonstrates the SSN's course at the suprascapular notch
Arthroscopic image of demonstrating the Suprascapular nerve (SSN) coursing inferiorly to the Superior transverse scapular ligament (STSL). The image demonstrates the SSN's course at the suprascapular notch
Contributed by Matthew Varacallo, MD.

(Click Image to Enlarge)
Ultrasound of infraspinatus (IS) and teres minor (TM) in short axis with infraspinatus showing
evidence of atrophy and fatty infiltrate versus the normal teres minor.
Ultrasound of infraspinatus (IS) and teres minor (TM) in short axis with infraspinatus showing evidence of atrophy and fatty infiltrate versus the normal teres minor.
Credit: Nelson Hager, MD, Department of Physical Medicine & Rehabilitation, USUHS

Credit: Eric Helm MD, Department of Physical Medicine & Rehabilitation, University of Pittsburgh Medical Center

(Click Image to Enlarge)
Ultrasound imaging of the supraspinatus muscle in short axis with evidence of atrophy on left and normal comparison on right.
Ultrasound imaging of the supraspinatus muscle in short axis with evidence of atrophy on left and normal comparison on right.
Contributed by Peck E, Strakowski JA. Ultrasound evaluation of focal neuropathies in athletes: a clinically focused review. Br J Sports Med. 2015;49:166-175.
Article Details

Article Author

Christopher Reece

Article Author

Matthew Varacallo

Article Editor:

Adam Susmarski


4/30/2022 6:33:56 PM



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