Background and Purpose. Suprascapular neuropathy, resulting in shoulder pain and weakness, is frequently misdiagnosed. The consequences of misdiagnosis can include inappropriate physical rehabilitation or surgical procedures. The purpose of this case report is to describe the differential diagnosis of suprascapular neuropathy. Case Descriptions. Five patients were initially diagnosed with subacromial impingement syndrome and referred for physical therapy. Physical therapist examination findings were consistent with subacromial impingement syndrome and suprascapular neuropathy. Subsequent electrophysiologic testing confirmed the diagnosis of suprascapular neuropathy in all 5 patients. Discussion. The differential diagnosis of patients with suprascapular neuropathy includes subacromial impingement syndrome, rotator cuff pathology, C5–6 radiculopathy, and upper trunk brachial plexopathy. The diagnostic process and a table with key findings based on evidence and clinical experience is presented for differential diagnosis.
Suprascapular neuropathy (SSN) may be overlooked or mistaken for other conditions such as subacromial impingement syndrome (SAIS), rotator cuff injury, cervical radiculopathy, or brachial plexopathy.1–6 The signs and symptoms of SSN include shoulder weakness, atrophy, and diffuse aching or burning pain at the shoulder, which often includes the posterolateral aspect of the shoulder in the region of the scapula.1–5,7 However, painless cases, which involved denervation of the infraspinatus muscle only, also have been reported.8
Although SSN is uncommon, it should be considered in the differential diagnosis of patients with shoulder pain and weakness.1–5,7 Suprascapular neuropathy has been reported in 10 patients (0.4%) in a series of 2,520 patients with shoulder pain,6 but some authors7 have speculated that this condition is so frequently misdiagnosed that it is probably the cause in 1% to 2% of patients with shoulder pain. Of 10 patients with SSN reported by Post and Mayer,6 8 patients were initially misdiagnosed, leading to inappropriate intervention. Two patients were managed surgically for SAIS with acromioplasty, 1 patient was managed surgically with C4–5 diskectomy, 3 patients were managed with cervical traction, 1 patient was managed with a cervical soft collar, and 1 patient was managed for acromioclavicular joint sprain. Six of the 10 patients were managed with unspecified physical therapy interventions. In a later case series of 39 patients with SSN, 18 patients were managed with 30 inappropriate surgical procedures for SAIS, the cervical spine, and thoracic outlet syndrome.5 In another series of 27 patients, 6 patients underwent surgical procedures for thoracic outlet syndrome and 3 patients underwent cervical diskectomies without relief prior to their diagnosis of SSN.3
The suprascapular nerve is a mixed motor and sensory nerve arising from the upper trunk of the brachial plexus with contributions primarily from the anterior primary rami of the C5 and C6 nerve roots. It then courses posteroinferiorly beneath the superior transverse scapular ligament in the suprascapular notch to supply the supraspinatus muscle. It then passes inferolaterally around the lateral border of the scapular spine and beneath the inferior transverse scapular ligament in the spinoglenoid notch to innervate the infraspinatus muscle as depicted in Figure 1.4,9 Sensory fibers of this nerve supply the acromioclavicular and glenohumeral joint capsules as well as the scapula.4,10 Although the suprascapular nerve usually has no cutaneous sensory innervation, a cutaneous branch to the lateral shoulder has been reported in 3% to 15% of cadavers.11,12
Suprascapular neuropathy can be caused by compression or traction of the nerve at the suprascapular notch or spinoglenoid region. Injury to the nerve at the suprascapular notch causes weakness of both the supraspinatus and infraspinatus muscles, whereas injury at the spinoglenoid region affects only the infraspinatus muscle. Compression or traction of the suprascapular nerve in these regions can result from space-occupying lesions, traumatic injury, viral syndrome, repetitive use, or perioperative injury, or it can occur idiopathically.8,13–20 Repetitive scapular movements may cause traction or tethering of the nerve, because the suprascapular nerve is fixed proximally at the cervical spine and distally at the scapula as it passes through the suprascapular notch and around the spinoglenoid notch. For this reason, athletic or work activities involving forceful contractions of shoulder musculature or repetitive overhead movements such as those involved in weight lifting, tennis, throwing, swimming, and volleyball have been implicated in the development of this neuropathy.8,21–25
Signs and symptoms of other injuries of the upper extremity overlap with signs and symptoms of SSN. Patients with SAIS or another rotator cuff injury can have a history of repetitive overhead activities as well as distribution of pain and muscle weakness similar to patients with SSN.26–28 Cervical radiculopathy and upper trunk brachial plexopathy also can cause signs and symptoms similar to those of SSN, with weakness of the C5 and C6 innervated muscles, including the infraspinatus and supraspinatus muscles, as well as a similar pain distribution in the shoulder region. Differential diagnosis must rule out these other pathologies before diagnosing a patient with SSN.
The purpose of this case report is to describe the process for the differential diagnosis of SSN. The primary differential diagnoses include SAIS, rotator cuff pathology, C5–6 radiculopathy, and upper trunk brachial plexopathy.
A summary of the patient history information is presented in Table 1. All patients were referred for physical therapy with a diagnosis of SAIS. The patients (1 female, 4 male) ranged in age from 19 to 36 years (X̄=29.6, SD=6.8). The duration of symptoms ranged from 1 week to 6 months. Four of the patients had symptoms in the nondominant shoulder. All patients had at least one suspected neural traction or compression mechanism of injury. All 5 patients had pain patterns that included, but were not all limited to, the posterior aspect of the shoulder.
Given the patients' histories, the examiners considered the primary potential diagnoses to be SAIS or other rotator cuff disorders such as tendinopathy or partial-thickness tear. Alternative diagnoses, such as cervical radiculopathy, brachial plexopathy, or proximal mononeuropathy (eg, SSN) could not be ruled out based on the histories.
The key physical examination data are summarized in Table 2. Shoulder flexion and abduction active range of motion (AROM) was limited in patient 1 only. The patient had full passive range of motion of the shoulder. Intraclass correlation coefficients (ICCs) for test-retest reliability of goniometric AROM measurements of the shoulder have been estimated to be .64 to .69.29 Despite the limitations of the measurement tool, we considered abduction AROM impairment of 40 degrees to be clinically meaningful.
Manual muscle testing (MMT) was performed and graded on a 5-point scale,30 with particular attention initially given to the rotator cuff muscles. Weakness was noted in the infraspinatus muscle in all patients and in the supraspinatus muscle in 4 of the patients. The infraspinatus muscle was tested by having the patients apply a shoulder lateral (external) rotation force with the arm at the side and the shoulder in 45 degrees of medial (internal) rotation.31 The supraspinatus muscle was tested using the “empty can” technique, resisting shoulder elevation in the scapular plane.30,31 A kinesiologic electromyographic (EMG) study31 has demonstrated the construct validity of data obtained with these techniques. Interrater kappa coefficients for identification of muscle weakness without using a muscle test grade have been estimated to be 0.62 to 0.69 for the muscles of the rotator cuff and C5–6 innervated muscles.32 When a formal muscle test grade was applied, these tests had ICCs that ranged from .79 to 1.00 for intrarater reliability and from .55 to .72 for interrater reliability.33 Although examiner agreement to detect weakness in the shoulder region and C5–6 myotomes is variable, we believed that the results of our tests of the supraspinatus and infraspinatus muscles were clinically meaningful.
We also observed atrophy of the supraspinatus muscle or the infraspinatus muscle in 4 of the 5 patients during the initial evaluation. Patient 3 developed atrophy 2 weeks after the initial examination. Atrophy of the supraspinatus and infraspinatus muscles of patient 1 is depicted in Figure 2. The reliability or diagnostic accuracy of observations of atrophy in these muscles has not been investigated.
For differential diagnosis of cervical radiculopathy and brachial plexopathy, we performed myotomal strength, dermatomal sensation, and muscle stretch reflex testing. We found MMT grades of 5/5 for other C5–T1 innervated muscles. These tests have variable agreement (kappa=0.23–0.69) and variable sensitivity (0.03–0.73), but fair to good specificity (0.61–0.94) using the reference standard of the results from electrophysiologic testing for confirmation of cervical radiculopathy.32,34 Results of reflex testing of the biceps brachii, brachioradalis, and triceps brachii muscles were normal and bilaterally symmetrical in all patients. Interrater reliability (kappa) for muscle stretch reflexes has been estimated to be 0.73, and specificity values ranged from 0.95 to 0.98.32,34 Stretch reflex testing, however, has low sensitivity (0.03–0.24) for patients with cervical radiculopathy.32,34 Cutaneous sensory testing was performed of the C5–T1 dermatomes, and the results were determined to be normal and bilaterally symmetrical in all patients. Interrater reliability (kappa) for dermatomal sensory testing of the C5 distribution has been estimated to be 0.67, but examination of other dermatomes has not been as reproducible (kappa=0.16–0.46). These tests also have demonstrated low sensitivity (0.12–0.38) and moderate to high specificity (0.46–0.86) in patients with cervical radiculopathy.32,34 Although dermatome, myotome, and reflex tests have low sensitivity when considered individually, the sensitivity for diagnosing cervical radiculopathy, if any of the 3 tests is abnormal, is 0.84. The specificity for diagnosing cervical radiculopathy in the presence of 2 or 3 abnormalities with these tests ranges from 0.74 to 0.98.34
We also used the Spurling test to test for cervical radiculopathy.32 The test was negative in all patients. This test has estimated interrater reliability (kappa) of 0.60 and specificity of 0.86, but sensitivity for diagnosing cervical radiculopathy is only 0.50.32 Thus, this test also may have little utility as a screening tool.
Special tests for SAIS were performed as described by Hawkins and Kennedy27 and Neer and Welsh28 and in Magee's Orthopedic Physical Assessment.35 These 2 tests are referred to as impingement “signs.” All patients had at least one positive SAIS sign, and 3 patients had positive results for both signs. Although no estimates of reliability for these signs exist, both signs have sensitivity of 0.75 to 0.92 and specificity of 0.25 to 0.51 for diagnosing SAIS.36 Thus, positive findings for these signs do not confidently rule in SAIS. Four of the 5 patients also had a painful arc during shoulder elevation. This examination finding had specificity of 0.80, but sensitivity of only 0.32. Thus, it is useful for ruling in SAIS when a painful arc is present.37 Evidence of the reliability of data obtained with the painful arc test is lacking.
All patients underwent radiographic examination of the cervical spine, shoulder, and scapula in an attempt to screen for relevant bone or other dense tissue abnormalities. These findings were normal. Patient 5 also had a magnetic resonance imaging (MRI) study of his shoulder, which demonstrated a posterior glenoid cyst, acromioclavicular joint degeneration, and supraspinatus tendonosis.
The clinical examination findings suggested diagnoses of both SSN and SAIS in all patients. The diagnosis of SSN was based on the presence of posterior shoulder pain in conjunction with weakness and atrophy isolated to the suprascapular nerve field. Negative cervical provocation tests, no other myotomal weakness, normal reflexes, and normal sensation suggested that C5–6 radiculopathy and upper trunk brachial plexopathy were less likely diagnoses. Patients with full thickness rotator cuff tears often have weakness and atrophy similar to that of patients with SSN; thus, differentiating a full-thickness tear from SSN can be difficult.38 Incidence of full-thickness tear increases after the age of 50 years and is most common in patients over 60 years of age,39,40 whereas SSN is most common in patients under 40 years of age.41 Therefore, SSN was considered a more likely diagnosis than full-thickness rotator cuff tear in these patients.
The patients also demonstrated many clinical signs and symptoms of the referral diagnosis of SAIS. All of the patients described worsening pain with shoulder elevation, which is a common finding in both SSN and SAIS. All patients had at least one positive impingement sign (Hawkins or Neer test), and all patients had a painful arc except patient 5. Because the Neer and Hawkins tests have low specificity for the diagnosis of SAIS, but the painful arc test has high specificity, we thought the evidence for a diagnosis of SAIS was strong for patients 1 to 4 and was weaker for patient 5. Patient 5, however, did have an MRI demonstrating supraspinatus tendon degeneration and acromioclavicular joint degeneration, which are suggestive of SAIS. Magnetic resonance imaging has demonstrated high sensitivity (0.93) and specificity (0.87) for imaging signs of SAIS.42 Thus, we thought that evidence for diagnosing SAIS in all 5 patients was compelling.
Suprascapular neuropathy is rare; thus, a definitive diagnosis of SSN requires the exclusion of alternative diagnoses. Many of the clinical examination techniques used to diagnosis SSN and many of those used to rule out alternative diagnoses have imperfect reproducibility and diagnostic accuracy. In particular, the tests performed for cervical radiculopathy and brachial plexopathy are generally not sensitive; thus, false negative findings are possible. In addition, pain with muscle testing interfered with identifying any true weakness in patients 1 and 2.
In light of the examination findings and the associated diagnostic accuracy and reliability of the examination procedures used, the diagnoses of SSN and SAIS were considered to be likely in all 5 patients. The alternative diagnoses of cervical radiculopathy, other rotator cuff pathology, and upper brachial plexopathy were considered less likely, but still possible. Thus, electrophysiologic evaluation was necessary to rule out these alternative diagnoses, confirm the diagnosis of SSN, and determine the severity of the neuropathy.
Electrophysiologic Evaluation: Electromyography and Nerve Conduction Studies
Abnormal spontaneous potentials (fibrillation potentials and positive sharp waves), indicating axonal injury, were observed in the involved muscle(s) of the suprascapular nerve field in all patients.43 Electromyographic interference patterns were estimated based on the percentage of a normal, full interference pattern of motor unit action potentials present.43 Particular attention was given to EMG examination of other C5–6 and upper trunk innervated muscles, which demonstrated normal electrophysiologic function. Nerve conduction studies (NCS) were performed with electrical stimulation at the supraclavicular fossa while using needle recording electrodes in the supraspinatus or infraspinatus muscle. These NCS techniques have been demonstrated to be reproducible and to have established accepted normal value ranges.44,45 Although EMG and NCS are often considered the criterion validity standard for correlating clinical findings in diagnosing nerve injuries,5,7,32,34,43 the interrater agreement of detecting abnormal EMG potentials has not been investigated. Electromyography and NCS have demonstrated a high level of accuracy (91%), however, in clarifying the diagnosis of patients with weakness.46 Table 3 gives a summary of the suprascapular nerve field EMG and NCS findings.
In all patients, the examination findings were consistent with both SSN and SAIS. Electrophysiologic findings confirmed the presence of SSN at the area of the suprascapular notch in patients 1 to 4 and in the region of the spinoglenoid notch in patient 5.
Intervention and Outcomes
The interventions and outcomes are summarized in Table 4. All patients were instructed to protect the suprascapular nerve and minimize their risk of aggravating SAIS symptoms by avoiding carrying backpacks or bags with straps over their shoulders, repeated overhead actions, nerve traction maneuvers such as horizontal adduction, and any other aggravating activities. All 5 patients were referred to orthopedic surgeons. The surgeon for patient 4 chose to operate because her symptoms had been present for 9 months and she had not improved with 3 months of nonsurgical intervention.
Compression or traction of the suprascapular nerve can result in signs and symptoms that are similar to those of other upper-extremity disorders. Several key clinical findings may indicate the possibility of SSN. These findings include pain in the posterior shoulder, a history of direct trauma or repetitive traction to the suprascapular nerve, and weakness and atrophy of the muscles innervated by the suprascapular nerve.
Posterior shoulder pain is common with SSN; however, this pain is often diffuse and not limited to that region.1–5,7,47,48 Four of our 5 patients noted posterior shoulder pain, which is consistent with a previously reported case series in which 34 of 35 patients with SSN described posterior shoulder pain.48
Injury to the suprascapular nerve may occur in a variety of ways. The mechanism of injury may include a single traumatic event, such as a glenohumeral dislocation or scapular fracture, or a repetitive microtrauma, such as athletes performing repetitive overhead activity.4,8,12,19–23,25,38,49 A history of repetitive overhead activity may suggest the possibility of SAIS or rotator cuff pathology as well as SSN. A history of surgery, recent viral illness, glenoid cyst, or metastatic disease also may be the cause of SSN; however, in many cases, the cause remains undetermined.1–5,7,47,48,50
In 4 of our 5 patients, we could not determine the cause of SSN with certainty. All patients were military service members and engaged in regular physical exercise. Patient 1 first noted symptoms after awakening from sleep with his shoulder fully abducted. Patient 2 first noted his symptoms the day after abdominal surgery; however, he was also a serious weight lifter and routinely carried an equipment bag over the involved shoulder. Patient 3 first noted symptoms after repetitive digging and lifting, but he also routinely wore a military backpack over his shoulders for several hours per day. Patient 4 first noted her symptoms after carrying luggage; however, she was also 3 days postpartum. Patient 5 was active in martial arts. Therefore, it is possible that compression or traction of the suprascapular nerve could have occurred from any of these potential mechanisms of injury.
Patients with SSN may have weakness of both the supraspinatus and infraspinatus muscles or of the infraspinatus alone because the suprascapular nerve innervates these muscles. In distal lesions of the suprascapular nerve in the spinoglenoid region, shoulder lateral rotation may be the only detectable weakness due to loss of infraspinatus muscle function. However, this weakness may be difficult to discern because shoulder lateral rotation force is produced by the infraspinatus, teres minor, and posterior deltoid muscles. In more proximal lesions, such as at the suprascapular notch, shoulder elevation in the scapular plane ("empty-can” test) also may be weak due to supraspinatus muscle involvement.1–5,7 All of our patients demonstrated weakness of the infraspinatus muscle, and 4 patients demonstrated supraspinatus muscle weakness. Patient 5, who did not have weakness of the supraspinatus muscle, had evidence of spinoglenoid cyst visible on MRI. Observation of atrophy in the involved muscle(s) can frequently be associated with findings of weakness within 2 to 3 weeks of the onset of symptoms (Fig. 2).1–5,7
Differential diagnosis of SSN can be difficult due to overlap in the clinical presentation with other pathologies of the shoulder and cervical spine region. To aid in differential diagnosis, key diagnostic findings of SSN, SAIS, rotator cuff pathology, cervical radiculopathy, and upper trunk brachial plexopathy are presented in Table 5. This table is based on an integration of the evidence and our clinical experience.
Radiculopathy at the C5 and C6 levels can cause shoulder pain and weakness of the supraspinatus and infraspinatus muscles; however, several clinical features may distinguish SSN from cervical radiculopathy. Symptom reproduction with cervical spine maneuvers, a dermatomal pattern of impaired sensation, impaired muscle stretch reflexes, and myotomal weakness that is more extensive than the suprascapular nerve field may be present in patients with cervical radiculopathy.32,34,43 Symptom reproduction that occurs with the Spurling test is indicative of cervical spine dysfunction, rather than SSN. Dermatomal testing should typically reveal no sensory deficits with SSN. A close overlap exists, however, between the C5 dermatome and the suprascapular nerve's cutaneous sensory field in the small percentage of people with a cutaneous branch of the suprascapular nerve. Thus, sensory impairment alone should be used with caution for differential diagnosis. Reflex testing for the C5–6 innervation pathways of the biceps brachii and brachioradialis muscles may be abnormal with radiculopathy, but not with SSN. Weakness of the infraspinatus and supraspinatus muscles should be the only strength impairment present in patients with SSN. Testing of other C5–6 innervated muscles may aid in the differential diagnosis of a cervical radiculopathy. As discussed previously, the Spurling test, MMT, reflex testing, and cutaneous sensory tests are highly specific, but generally are not sensitive for diagnosing cervical radiculopathy. Therefore, although positive findings are strongly suggestive of radiculopathy, negative tests do not rule out cervical radiculopathy with a high level of confidence.32
The upper-limb tension test (ULTT) is a sensitive (0.97) clinical screening tool for cervical radiculopathy.32 The ULTT is not specific, however, so a positive ULTT still requires further clinical correlation before diagnosing cervical radiculopathy. Additional positive findings with 2 tests of provocation of symptoms with the Spurling test and limited cervical rotation increased the positive likelihood of cervical radiculopathy to 65%.32 When a third positive finding was added, relief of symptoms with cervical traction, the positive likelihood increased to 90%.32 Because this evidence was not published at the time we saw our patients, we did not use the ULTT.
Brachial plexopathies of the upper trunk can be affected by idiopathic lesions, viral illness, or compression or traction injuries such as “burners,” “stingers,” and “rucksack palsies.” This region also can be affected perioperatively after scalene anesthetic block or due to surgical positioning.43 In idiopathic lesions or cases of viral illness, the onset of symptoms is usually marked by severe shoulder and brachial pain. Patients with upper trunk brachial plexopathies may have clinical examination findings of sensory impairments following the C5–6 dermatomes, biceps brachii and brachioradialis muscle stretch reflex abnormalities, and weakness of C5–6 innervated muscles with sparing of the serratus anterior, rhomboid, and paraspinal muscles. We are unaware of any highly sensitive screening tests for upper trunk brachial plexopathy. Muscle and reflex testing, therefore, are most likely the best clinical tools for ruling out this condition. Due to the low sensitivity of muscle and reflex testing, electrophysiologic examination may be particularly useful in differentiating brachial plexopathies from SSN or cervical radiculopathy.43,51
Patients with full-thickness tearing of the rotator cuff typically have weakness of shoulder elevation and lateral rotation, secondary to trauma or insidious onset. The patient's age may be particularly useful in determining whether SSN or a full-thickness rotator cuff tear is more probable, as the incidence of full-thickness rotator cuff tear increases after the age of 50 years.39,40 A cluster of 3 positive findings of supraspinatus muscle weakness, infraspinatus muscle weakness, and a positive impingement sign have demonstrated high probability (98%) for predicting whether a patient will develop a rotator cuff tear.37 This cluster, however, would have yielded false positive diagnoses in 4 of our 5 patients. Evidence also suggests that the drop arm test may be helpful in discriminating between full-thickness rotator cuff tear and SSN, because this test is highly specific (0.98) for full-thickness rotator cuff tear.37 The drop arm test, however, is not sensitive (0.10).2,52 We did not perform this test with our patients. Magnetic resonance imaging42,50,53–55 and electrophysiologic testing5,6,43 also may be helpful in differentiating full-thickness rotator cuff tears and SSN.
Inflammation, degeneration, and partial-thickness tearing of the rotator cuff may occur in isolation, but they are commonly associated with SAIS. Subacromial impingement syndrome involves abnormal contact between the coracoacromial arch and subacromial soft tissues (rotator cuff tendons, long biceps tendon, and bursae). Symptoms of this disorder often include anterior, superior, or deep shoulder pain that is worsened with shoulder elevation.26,27,56,57 As with SSN, patients with SAIS may have weak shoulder abduction and lateral rotation,26,58,59 Moreover, SAIS often occurs in patients who perform repetitive overhead activity, but it also can occur insidiously or can result from trauma.26,27,56,57 The Hawkins and Neer impingement signs may not be helpful in differentiating SSN from SAIS because these tests have been demonstrated to have low specificity. Thus, false positive results are likely.37,57 The painful arc test, which has higher specificity, may be more useful in ruling in SAIS.37 Lateral rotation weakness and atrophy may be useful in differentiating SSN from SAIS because, in our experience, these symptoms are typically more severe in patients with SSN. However, interrater reliability for grading weakness with MMT is not high.33 Posterior shoulder pain also may be a discriminator because patients with SAIS do not typically have pain in this region.26,27,56,57
Subacromial impingement syndrome and SSN may occur simultaneously in patients. Evidence suggests that SAIS may be caused by altered neuromuscular control of the shoulder girdle.60–62 Suprascapular neuropathy can diminish neuromuscular control through weakness of rotator cuff muscles, thus disrupting normal shoulder mechanics and increasing the likelihood of the occurrence of SAIS. The supraspinatus and infraspinatus muscles stabilize the glenohumeral joint, while the infraspinatus muscle also depresses the humeral head and laterally rotates the shoulder. With a reduction of muscle performance of one or both of these suprascapular innervated muscles, impingement of subacromial structures against the coracoacromial arch during shoulder elevation could result.61–67 Simulated SSN in cadaver models has demonstrated excessive humeral head translation during shoulder elevation, indicating theoretical support for the increased risk of development of SAIS in patients with SSN.65 Thus, patient education to avoid repetitive overhead activities in order to minimize the risk for developing SAIS is appropriate for patients with SSN. We hypothesize that our patients developed SAIS as a result of weakness caused by the SSN. However, it also was possible that both the suprascapular nerve and the subacromial soft tissue structures were injured concomitantly due to repetitive shoulder activities or positioning during sleep or surgery.
Electrophysiologic abnormalities are generally considered necessary to confirm a diagnosis of SSN.5,6,43 Electrophysiologic studies are particularly useful in differentiating SSN from brachial plexopathy, cervical radiculopathy, or nonneurologic disorders. Findings from EMG and NCS also may be useful in directing imaging studies to the appropriate anatomic location by localizing a neurologic lesion. Electromyographic abnormalities that occur in resting muscle, such as fibrillation potentials and positive sharp waves, suggest axonal injury to motoneuron fibers. Absent or decreased motor unit action potential interference patterns with attempts to contract the muscle suggest that the number of functioning motor units is decreased.43 Nerve conduction studies for the suprascapular nerve typically measure latency to the infraspinatus or supraspinatus muscle. Conduction abnormalities can include delayed latency or an absent response.44
Electrophysiologic studies also may yield some prognostic value. In a series of 53 patients with SSN with 1-year follow-up,2 EMG findings were useful in predicting functional outcome. More severe EMG findings were more predictive than mild EMG findings of greater improvement with either surgical or nonsurgical intervention.
Imaging studies may be helpful in defining the source of SSN because they may provide evidence of an anatomic source of compression.2,47 Plain radiographs of the cervical spine, scapula, and shoulder are considered an inexpensive screening tool. Their results, however, are typically negative. Ultrasonography, MRI, and computed tomography all have some utility in identifying ganglion cysts, other masses, bone abnormalities, muscle atrophy, and fatty infiltration. However, MRI is considered the best imaging modality for most lesions in the shoulder region and is useful in detecting sources of nerve compression such as glenoid cysts or malignancy.4,12,47,50,53,68 The reported accuracy for using MRI to detect changes suggestive of denervation in the infraspinatus or supraspinatus muscle in patients with SSN ranges from poor to excellent and is generally not considered as good as that of EMG and NCS.50,53 Thus, electrophysiologic examination is a particularly useful diagnostic tool for augmenting the clinical examination when a diagnosis of SSN is being considered, whereas MRI is most useful in determining the presence of space-occupying lesions as the source of SSN. In this manner, electrophysiologic studies and MRI are complementary procedures in the examination of patients with SSN. Only one of the patients discussed in this case report received an MRI. Retrospectively, we would have ordered MRI for the other 4 patients in an effort to rule out the presence of space-occupying lesions.
Evidence for the optimal management of SSN is conflicting and primarily is in the form of case series and “expert” opinions. Although glenoid cysts may resolve spontaneously,12,68 these cysts and other sources of nerve compression generally respond best to surgical management.2 Patients with other sources of SSN seem to respond equally well to both surgical and nonsurgical intervention.2 Thus, imaging studies to determine the location and source of the lesion, if possible, may be useful in guiding intervention.2,47 Several authors16,38 have reported good or excellent results in a majority of patients managed with a conservative (nonsurgical) approach. Other authors1,3,5,7,48 have reported good or excellent results in a majority of patients managed surgically. Of patients who receive surgery, those operated on within 6 months after developing symptoms tended to have better results.48 In the absence of an identifiable anatomic source of nerve compression, a trial of nonoperative intervention as outlined in Table 4 is probably most appropriate.16,38,47,48
Three of the patients presented in this case report were managed nonsurgically and had complete or nearly complete return of strength and resolution of pain in the time that they were followed. The patient who was managed surgically had only minimal improvement in symptoms and function. We speculate that the poor outcome was due to severe nerve entrapment for a prolonged period. One patient was lost to follow-up soon after the initial evaluation, so his outcome is unknown.
Patients who have a mechanism of possible injury to the suprascapular nerve, posterior shoulder pain, or weakness or atrophy of the infraspinatus muscle with or without involvement of the supraspinatus muscles should be considered for a diagnosis of SSN. Before diagnosing SSN, other disorders such as C5–6 radiculopathy, upper trunk brachial plexopathy, rotator cuff pathology, and SAIS should be ruled out. Further research is needed to determine the diagnostic accuracy of various tests and measures for SSN, the optimal management of patients with SSN, and whether a relationship exists between SSN and SAIS.
All content of this article represents the shared work and responsibility of the authors. Mr Walsworth and Mr Mills provided concept/idea/project design, data collection, subjects, and facilities/equipment. Mr Walsworth provided project management and institutional liaisons. All authors provided writing, data analysis, and consultation (including review of manuscript before submission). The authors thank Venetia Valiga for providing the illustration of the suprascapular nerve.
The material in this manuscript was presented in part as the Expert Clinical Benchmarks Annual Robert M Kellogg Honorary Lecture for Excellence in Clinical Electrophysiology, 2003.
The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense.
- Received October 18, 2002.
- Accepted October 12, 2003.
- Physical Therapy