Nerve Problems About the Shoulder

CHAPTER 27 Nerve Problems About the Shoulder

Scott P. Steinmann, MD, Robert J. Spinner, MD

Patients with shoulder pain or injuries not infrequently have concomitant neurologic conditions, and orthopaedic surgeons caring for such patients must be aware of them. In addition, the practice of reconstructive shoulder surgery carries an inherent risk of iatrogenic injury to neighboring neurologic structures. Knowledge of the common nerve lesions about the shoulder allows surgeons to recognize these entities when they see them, and familiarity with the relevant neural anatomy will help them avoid potential neural injuries when they operate. Surgeons must have a systematic approach to evaluating and treating these challenging patients with nerve-related disorders about the shoulder region.

CLINICAL EVALUATION

Patients with nerve injuries are often seen in situations involving significant trauma. Commonly, the patient is confused, incoherent, sedated, or even unconscious, and it can be difficult to perform a satisfactory neurologic examination before initiating surgical care. Nonetheless, a good neurologic examination should be attempted in the emergency department. If an adequate examination cannot be performed for any reason, this fact should be noted in the patient’s medical record. Specifically, if the function of a particular nerve cannot be assessed well preoperatively, the record should include such information. Too often in the emergency setting, the patient receives only a cursory evaluation and perhaps the most junior person on the orthopaedic surgical team writes in the clinical record that the extremity was “neurovascularly intact.” These two words, if inaccurate, are sometimes the origin of unnecessary litigation. Such general terms should not be used when recording a patient’s examination, but instead, individual muscle strength, sensory examination, and deep tendon reflexes should be carefully documented in the patient’s record.

A detailed neurologic evaluation of the upper extremity can be performed on a coherent patient in a relatively short time, even if the patient has a shoulder dislocation or proximal humeral fracture. It is often easiest to start at the hand and progress proximally during the examination. Radial, median, and ulnar nerve function can all be assessed by a thorough evaluation of the hand and wrist, which should take less than a minute. Elbow flexion and extension strength are relatively simple to determine. One should be aware, however, that it is possible to flex the elbow strongly with the action of the brachioradialis without having any function of the biceps. Loss of motor or sensory function in the distal end of the extremity can help direct examination of the more proximal musculature. For example, loss of radial nerve function should make the examiner look closely at axillary nerve function because they are both derived from the posterior cord. Likewise, loss of median nerve function might also affect the musculocutaneous nerve if the lesion is in the lateral cord.

Progressing up the arm, the condition of the medial and lateral pectoral nerves can be assessed by individually testing the strength of each of the major portions of the pectoralis major. The deltoid and rotator cuff muscles are then examined. The deltoid can be assessed even in the case of a painful proximal humeral fracture or glenohumeral dislocation. With the arm at the side, the patient is instructed to push out or “elbow” the examiner’s hand (one of which is placed at the lateral aspect of the elbow and the other over the deltoid region to feel for contracture). If the patient is in a great deal of pain and the examiner cannot adequately determine the condition of the axillary nerve, this information should be recorded in the clinical record. Do not assume that it “might be okay.”

Examining shoulder abduction is an important part of the examination both to record muscle strength and to visualize shoulder kinesis through the arc of motion. Two important points are relevant here. First, some patients can abduct the shoulder through a full arc of motion by using either just the supraspinatus or the deltoid in the face of complete paralysis of one or the other. Ensuring muscle contraction is a critical element in this part of the examination. Second, visualizing and palpating the scapula are a necessary part of the examination, especially when one is faced with dysfunction. For example, patients with winged scapulae from either serratus anterior or trapezius weakness might have difficulty abducting the arm fully without the scapula stabilized and might compensate with trick motions. Physicians should recognize the clinical appearances and know the techniques to examine winging of the scapula, particularly with respect to distinguishing serratus anterior, trapezius, or rhomboid muscle dysfunction. In addition, a useful test for serratus anterior function, in which the inferior pole of the scapula is stabilized and the patient pushes the arm forward, can be applied even in a patient with a complete brachial plexus lesion; patients unable to push their arms forward could not otherwise perform the more standard push-off test with the arms extended against the wall.

One needs to evaluate patients for other conditions causing lack of movement besides a neurologic etiology. Certainly, one needs to consider that the inability of a patient to externally rotate the arm or perform the lift-off test might represent a neurologic lesion affecting the infraspinatus or subscapularis, a rotator cuff tear, or both. A patient who is feigning paralysis in the upper limb for secondary gain issues cannot voluntarily stop the latissimus dorsi from contracting while coughing.

Examination of the shoulder must include examination well above the shoulder and even above the neck, as well as the distal portion of the limb. Proximal and distal lesions must always be considered when one is examining a patient with shoulder pain or weakness and establishing a differential diagnosis. Cervical radiculopathy is a common cause of pain in the shoulder accompanied by motor weakness and sensory loss in the upper extremity. In this situation, flexion and extension of the cervical spine or Spurling’s maneuver might reproduce or exacerbate the patient’s symptoms. Upper motor neuron lesions can also result in shoulder weakness. In these cases, the deep tendon reflexes may be hyperreflexic, pathologic reflexes may be present, and tone may be increased. Referred pain should be excluded as a possibility during the clinical examination because cardiac and other intrathoracic as well as intra-abdominal complaints may be manifested as shoulder pain.

Finally, examination of the shoulder can be performed only with both shoulders exposed. Visualization is the first component of a physical examination, but this step is often neglected because of either time constraints or modesty issues. It is easy to miss atrophy of the spinatus muscles if one does not look at the bare scapula. Bilateral atrophy or weakness would certainly change the differential diagnosis and force the examiner to consider an underlying neurogenic or myopathic condition.

MUSCULOCUTANEOUS NERVE INJURY

Etiology

Musculocutaneous nerve injury is most commonly associated with severe brachial plexus trauma. Although the nerve can be injured in glenohumeral dislocation, it is unusual to diagnose such injury as an isolated neuropathy.¹ If it is seen as an isolated nerve injury, it is most often associated with a form of penetrating trauma, open surgical reconstruction, or a direct blow to the chest (near the coracoid). Occasionally, musculocutaneous neuropathy can occur after strenuous physical activity such as rowing.²

The musculocutaneous nerve travels obliquely below the coracoid process and enters the coracobrachialis. The anatomy of this juncture has been investigated in several studies. Small branches of the nerve can be found inserting into the coracobrachialis as close as 17 mm below the coracoid.³ The main trunk of the musculocutaneous nerve enters the coracobrachialis approximately 5 cm from the coracoid and exits at 7 cm.^3,⁴ The nerve then enters the biceps, typically more than 10 cm from the coracoid.⁴ The nerve is at risk during anterior shoulder procedures that result in significant retraction medially or during medial surgical dissection. The Bristow procedure has been thought to be associated with injury to the nerve,⁵ but such injury is probably related less to transfer and more to manipulation of the nerve.⁶

The operating surgeon must recognize the protective value of maintaining the origins of the coracobrachialis and biceps. When these muscles are allowed to remain on the coracoid during surgery, they act as a tether to overzealous medial retraction. In fact, exposure of the posterior cord or the axillary nerve can lead to musculocutaneous nerve palsy as a result of retraction. Care must be taken to avoid excessive traction on the musculocutaneous nerve during dissection. Alternatively, detachment of the conjoined tendon allows excellent exposure and potentially decreased pressure in the entire brachial plexus. Actual detachment of these muscles from the coracoid and reattachment to the anterior glenoid (the Bristow procedure) will relax the musculocutaneous nerve. Nonetheless, the surgical manipulation required can result in damage to the nerve.

The nerve can also be damaged during arthroscopic surgery, although such injury is quite rare. Anterior portals straying medial to the coracoid put the musculocutaneous nerve and other branches of the brachial plexus at potential risk for injury. Low anterior portals such as the 5-o’clock portal can bring instruments to within 10 mm of the nerve.⁷ A patient with a musculocutaneous nerve lesion typically has a mixed sensory and motor lesion. Less commonly, a pure sensory lesion of the lateral antebrachial cutaneous nerve, the distal sensory termination of the musculocutaneous nerve, can occur. Lesions of the lateral antebrachial cutaneous nerve at the level of the elbow often have an atraumatic etiology and must be distinguished from more proximally occurring (incomplete) musculocutaneous lesions manifesting with sensory loss. These patients might have numbness or paresthesia along the lateral elbow crease that extends distally along the anterolateral aspect of the forearm. Treatment involves splinting or corticosteroid injection and, possibly, surgical exploration.⁸ Surgical exploration on occasion reveals a thickened aponeurosis compressing the lateral antebrachial cutaneous nerve as it transits between the biceps and brachioradialis muscles. Patients might respond to surgical decompression of the nerve in this area.⁹

Nonoperative Treatment

If a patient is seen after trauma or surgery with an injury to the musculocutaneous nerve, the patient should be observed for 3 to 4 weeks. If at that time no improvement in function is noted, electromyography and nerve conduction studies (EMG/NCS) may be performed to assess the extent of nerve damage. Most postoperative musculocutaneous neuropathies are traction injuries that resolve over a period of weeks to months, depending on the extent of the injury.

Operative Treatment

If biceps and brachialis function are not seen to improve either by clinical examination or by electrophysiologic studies, surgical exploration should be undertaken, ideally before 6 months has transpired from the injury. Surgical treatment options vary for persistent musculocutaneous neuropathy. If at surgical exploration the nerve appears intact but compressed by scar and demonstrates electrical conduction across the lesion, neurolysis may be indicated. If a neuroma in continuity (that does not conduct a nerve action potential [NAP])¹⁰ or a rupture or transection of the nerve is discovered, additional treatment options should be considered.

In patients who have an isolated musculocutaneous nerve injury, a standard approach is to perform interpositional nerve grafting across the lesion. However, nerve transfers could also be used to shorten the distance (and time) for reinnervation or to bypass a scarred or avascular segment. A new nerve transfer is the Oberlin transfer, a technique in which one or two fascicles of the ulnar nerve are transferred directly to the motor branch to the biceps.^11,¹² The distance to achieve reinnervation is extremely short because the site of repair is in the proximal part of the arm (several centimeters from the biceps end-organ) rather than a more lengthy repair from the neck or shoulder region. This technique can be used in patients with upper plexus lesions. Grade 3 or 4 Medical Research Council (MRC) function was achieved in more than 90% of patients treated with this technique in two large series (each with more than 30 patients).^12,¹³ Reinnervation in the biceps was noted approximately 3 months after the procedure. Importantly, no patient suffered loss of distal ulnar nerve function or sensation. Recent modifications of this procedure have been reported with double reinnervation of elbow flexion: An ulnar nerve fascicle may be transferred to the biceps motor branch, and a median nerve fascicle may be transferred to the brachialis branch.^14,¹⁵

If patients are seen longer than 1 year after musculocutaneous nerve injury, nerve repair or reconstruction is significantly less likely to be effective.¹⁶^–²² Still, in select cases, nerve transfer techniques can be considered.

Some patients with little or no biceps or brachialis strength still function extremely well solely by using their brachioradialis for elbow flexion. The majority of patients, however, need augmentation. A number of tendon or muscle transfer procedures that achieve good results can be used. Popular options include Steindler’s flexorplasty (proximal advancement of the flexor–pronator muscle group) and triceps, pectoralis major, pectoralis minor, and latissimus dorsi transfer. Free muscle transfer is also a possibility in patients without these other available potential donor muscles.

AXILLARY NERVE

Anatomy

The axillary nerve is one of the more commonly injured nerves about the shoulder. It is a terminal branch of the posterior cord and is derived from the fifth and sixth cranial nerves. The axillary nerve lies lateral to the radial nerve, posterior to the axillary artery, and anterior to the subscapularis muscle. It enters the quadrilateral space accompanied by the posterior humeral circumflex artery and is in close contact with the inferior shoulder capsule.

It is easy to locate at surgery during an anterior exposure by sweeping an index finger inferiorly over the anterior subscapularis and gently hooking the axillary nerve while simultaneously palpating the nerve on the underside of the deltoid with the other index finger.²³ As it exits the space, the nerve continues to the posterior aspect of the humeral neck and divides into anterior and posterior branches. The position of the anterior branch is commonly reported as lying 4 to 7 cm inferior to the anterolateral corner of the acromion.²⁴ The posterior branch innervates both the teres minor and the posterior portion of the deltoid. The branch to the teres minor usually arises within or just distal to the quadrilateral space and enters the posteroinferior aspect of the teres minor muscle.

The internal topography of the axillary nerve has been studied by Aszmann and Dellon.²⁵ As the nerve leaves the posterior cord, it is monofascicular, but as it enters the quadrilateral space, it has three distinct groups of fascicles: motor groups to the deltoid and teres minor and the sensory group of the superior lateral cutaneous nerve. The deltoid motor fascicles are found in a superolateral position; those of the teres minor and superior lateral cutaneous nerve are located inferomedially.

Etiology and Clinical Manifestation

Most axillary nerve injuries occur as part of a combined brachial plexus injury; isolated axillary nerve injury occurs in only 0.3% to 6% of brachial plexus injuries.²⁶ Injury to the axillary nerve most often follows closed trauma involving traction on the shoulder. Axillary nerve paralysis is the most common neurologic complication of shoulder dislocations. Some patients with a proximal humeral fracture or shoulder dislocation have a subclinical axillary nerve lesion that is evident by EMG/NCS but that is not apparent clinically because of the associated discomfort.²⁷^–³¹ The vast majority of these patients recover from the nerve injury as they rehabilitate from the dislocation or fracture. Blunt trauma to the anterolateral aspect of the shoulder has also been noted to cause axillary nerve injury as it travels on the deep surface of the deltoid muscle.³²

Open reconstructive surgery (Fig. 27-1) or newer arthroscopic techniques can put the axillary nerve at risk. For example, capsular shrinkage procedures can create a local increase in temperature in the inferior capsule that can lead to nerve injury.^33,³⁴ The nerve has been reported to be injured in 1% to 2% of thermal capsular shrinkage procedures, but fortunately, the vast majority of these injuries seem to be only temporary.³⁵ The axillary nerve is also at risk during capsular resection for adhesive capsulitis.³⁶ Because the nerve is in close proximity to the anteroinferior capsule, great care should be taken when resecting in this area. A safer method of inferior capsular resection in this area is to visualize the axillary nerve with the arthroscope during the procedure.

FIGURE 27-1 Axillary nerve palsy. This 21-year-old man underwent arthroscopic repair for recurrent left anterior shoulder dislocation. Postoperatively, new shoulder weakness and deltoid atrophy developed, and the patient was referred to our institution 6 months after the operation. He had 120 degrees of abduction and 160 degrees of forward flexion. Electromyography demonstrated dense fibrillations in the deltoid without voluntary activation. A severe axillary nerve lesion was diagnosed. A, At surgery, the conjoined tendon was taken down. The axillary nerve was encased in scar (arrow) and was decompressed. B, At the inferior portion of the glenoid, a suture anchor splitting the axillary nerve in half was noted. C, Stimulation across the lesion resulted in a deltoid response. The indentation within the nerve from which the suture anchor was removed can be seen (arrow).

Nonoperative Treatment

Young patients may be able to compensate for complete deltoid paralysis and can often perform activities of daily living with only partial disability. The shoulder can easily maintain a full range of motion with an intact rotator cuff. However, most patients have early fatigue in the involved side if asked to perform repetitive activities. Although deltoid atrophy is quite evident in a fit person, in a less-fit patient, the examiner occasionally finds it difficult to detect deltoid atrophy. Injury to the superior lateral cutaneous nerve of the arm can lead to sensory loss over the lateral aspect of the shoulder. It is possible for patients with a complete deltoid motor deficit to have only mild loss of sensation over the lateral part of the shoulder. The diagnosis of axillary neuropathy should not be determined by the presence or absence of lateral shoulder sensation. It is unclear whether the sensory branch is spared from injury or whether the sensory zone is supplied by overlapping innervation from other cutaneous branches.

The quadrilateral space syndrome has been described as another potential cause of posterior shoulder pain, and it presumably results from compression of the axillary nerve within the quadrilateral space. This syndrome is a controversial clinical entity; it might simply be a manifestation of Parsonage–Turner syndrome (brachial neuritis). Tenderness may be noted posteriorly along the shoulder joint; otherwise, the clinical examination is often normal. Deltoid atrophy or lateral sensory changes are uncommon, and EMG examination is usually normal. Magnetic resonance imaging (MRI) might demonstrate signal change indicating denervation in the deltoid and teres minor muscles.³⁷ Observation is the usual treatment for quadrilateral space syndrome, and the vast majority of patients improve with time.³⁸ Surgical exploration of the quadrilateral space and release of scar or fibrous bands to achieve decompression of the axillary nerve are rarely needed.³⁹

Patients with a history of blunt trauma to the axillary nerve should be observed over at least a 3-month period before operative treatment is considered. At 3 to 4 weeks, a baseline EMG/NCS examination should be obtained. Physical therapy, including active and passive exercises, should be initiated to preserve maximal range of motion and prevent joint contracture while awaiting return of function. Electrical stimulation of the deltoid has been used in an attempt to preserve muscle viability, although it is unclear whether this approach has any genuine effect.

The results of nonoperative treatment of a blunt traumatic lesion have generally been good. Leffert stated that axillary nerve injury after fracture or dislocation is more common than usually appreciated, yet the majority of patients progress to full recovery.⁴⁰ In a study of 73 patients with proximal humeral fracture or dislocation, 33% were noted on EMG to have an axillary nerve injury, with 9 complete and 15 partial lesions.⁴¹ All patients recovered with no objective loss of function, including those with complete nerve lesions. In a series of 108 elderly patients with anterior shoulder dislocation, 9.3% were found to have an axillary nerve injury, but all patients went on to full recovery by 12 months.²⁷ Nonetheless, some patients do not make the expected recovery. In these patients, surgical exploration with neurolysis or possibly nerve grafting can be undertaken if no clinical or EMG recovery is evident by 3 to 4 months.⁴²^–⁴⁵ If the patient has a history of a sharp penetrating wound or if a surgical injury has occurred, surgical exploration should be performed at an earlier date.

Operative Treatment

The proximal monofascicular structure of the axillary nerve with primarily motor fibers and its relatively short length from the posterior cord to the deltoid motor end plate are characteristics that lend themselves to surgical intervention. Alnot and Valenti reported on 37 axillary nerve surgeries, including 33 cases of sural nerve grafting, 3 neurolysis procedures, and 1 direct repair.⁴² In 23 of the 25 isolated axillary nerve lesions, M4 or M5 strength was achieved. The fact that 33 of the 37 patients required sural nerve grafting illustrates the difficulty in adequately mobilizing the nerve for direct repair. The small number of patients undergoing neurolysis (3 of 37) is an indication that mild nerve compression by scar or fibrous bands is not common. Repair of the nerve with a short interposed cabled sural nerve graft has been the most common method and has demonstrated the most consistent results.^43,⁴⁶^–⁵⁰

We have found the use of intraoperative NAPs and EMG techniques to be invaluable in evaluating neuromas and helping us decide whether to perform neurolysis alone or to resect the neuroma and perform a graft. In all cases, we are also prepared to expose the axillary nerve posteriorly. In selected cases, such exposure is necessary to identify normal nerve more distally for grafting.

Other techniques for repair of the axillary nerve include nerve transfer. Direct neurotization with a donor nerve such as the medial pectoral, thoracodorsal, or radial has yielded satisfactory results in cases in which direct repair or short cable grafting of the axillary nerve itself is not possible or not preferable.⁵¹^–⁵³ Nerve transfers using the spinal accessory nerve or upper intercostal nerves have been described but require an interpositional sural nerve graft^53,⁵⁴ and have demonstrated less-optimal results.^53,⁵⁵ A recent nerve transfer using a triceps branch to the anterior division of the axillary nerve has been described in cases of upper trunk brachial plexopathy,⁵⁶ and because of promising results it is now being used by some surgeons instead of nerve-grafting techniques in cases of isolated axillary paralysis.

Patients seen longer than 15 to 18 months after trauma usually do not benefit from surgical repair of the nerve because of the poor condition of the deltoid muscle and its motor end plates. In patients who have poor shoulder function limiting their activities of daily living but a normal rotator cuff, muscle transfer procedures can be considered. Potentially, if the posterior deltoid and middle deltoid are innervated and the anterior deltoid is not functioning, the posterior-middle deltoid can be rotated anteriorly on the clavicle. This procedure, however, has the potential to harm the remaining deltoid and is not strongly recommended.

Alternatively, the pectoralis major can be transposed laterally on the clavicle and acromion. Mobilization of the pectoralis major is limited somewhat by the relatively tight anatomic dimensions of the pectoral nerves. If the deltoid is completely paralyzed, the trapezius can be mobilized off the clavicle and spine of the acromion, and the lateral acromion with attached trapezius can be inserted into the proximal end of the humerus. This procedure can restore some shoulder abduction to a patient who has none; however, it does create a change in the normal slope of the shoulder and therefore has a less than desirable cosmetic result. More-advanced techniques such as free muscle transfer have been attempted, but the results have been less than uniform.

SPINAL ACCESSORY NERVE

Etiology

Injury to the spinal accessory nerve can occur after penetrating trauma to the shoulder. Blunt trauma can also cause loss of trapezius function. Most commonly, surgical dissection in the posterior triangle of the neck, such as for lymph node biopsy, can expose the nerve to possible damage (Figs. 27-2 and 27-3).⁵⁷^–⁶¹

FIGURE 27-2 Spinal accessory nerve paralysis. This 53-year-old man underwent a cervical lymph node biopsy that was performed to exclude tuberculous lymphadenitis. The specimen was nondiagnostic. Severe pain and deformity developed in the affected shoulder after surgery. A postoperative pain syndrome was thought to have developed. The diagnosis of spinal accessory nerve paralysis was not made until several months later. A, An asymmetric shoulder shrug and trapezius atrophy are evident. B, A small transverse incision from the lymph node biopsy is seen directly posterior to the sternocleidomastoid muscle. This incision is directly over the oblique course of the accessory nerve. C, The patient had significant difficulty with shoulder abduction. D, Resultant shoulder droop can be seen from loss of the trapezius.

FIGURE 27-3 A 60-year-old woman with spinal accessory paralysis after lymph node biopsy undergoing an Eden–Lange procedure of the rhomboid and a levator scapulae transfer. A, Rhomboid major and minor of right shoulder elevated. B, Levator scapulae elevated for transfer. C, Sutures passed through drill holes in the scapula for rhomboid fixation. D, Rhomboid muscle sutured to scapula.

Anatomy

The spinal accessory nerve passes through the upper portion of the sternocleidomastoid muscle, which it innervates, and then crosses the posterior cervical triangle. The posterior cervical triangle is bordered anteriorly by the sternocleidomastoid muscle, posteriorly by the trapezius, and inferiorly by the clavicle. The nerve lies on the floor of the posterior triangle with only the overlying fascia as protection against injury.⁶² It abuts the posterior cervical lymph nodes. The nerve enters the anterior surface of the trapezius and travels inferiorly, parallel to the medial border of the scapula.⁶³ The trapezius has a broad origin from the ligamentum nuchae to the 12th thoracic vertebra and inserts over the lateral part of the clavicle, acromion, and spine of the scapula. The upper trapezius is the prime elevator of the scapula and acts to upwardly rotate the lateral aspect of the bone.

Diagnosis

If the spinal accessory nerve is injured, the diagnosis is often missed, and appropriate treatment may be delayed.⁵⁷ Patients usually have vague shoulder pain as their primary complaint. Loss of motion may be a secondary concern. Unless trapezius function is specifically tested, the diagnosis might not be recognized. Because of the common occurrence of anterior shoulder pain in these patients, with occasionally only slight visible wasting of the trapezius muscle, the pain may be assumed to represent postoperative pain or be misinterpreted as resulting from another condition associated with shoulder pain, such as rotator cuff pathology. The trapezius receives some innervation from the upper cervical nerve roots, so complete atrophy of the muscle might not occur.

The spinal accessory nerve supplies the sole innervation to the lateral portion of the muscle, which is critical in supporting abduction of the shoulder. If the patient is carefully observed, the scapula appears to be rotated forward at the shoulder. The shoulder might hang lower or droop in comparison to the contralateral side; this finding can even cause symptoms of thoracic outlet syndrome. Winging of the scapula often occurs but is not as dramatic as that associated with injury to the long thoracic nerve. Usually, a shoulder shrug produces the deformity, but a strong levator scapulae can compensate well, and only minimal deformity may be noted. The patient might not be able to abduct the arm fully with the forearm either pronated or supinated.

Some of the pain that patients experience might come from strain of the other parascapular muscles as they attempt to compensate for the lack of trapezius function. Additionally, because the scapula cannot properly rotate the acromion away from the humerus as the arm is elevated, impingement of the rotator cuff can cause secondary rotator cuff tendinopathy. If attention is directed only at the rotator cuff, the underlying nerve pathology will be missed. In addition, the spinal accessory nerve, though mainly a motor nerve, still has sensory fibers. Injury to the nerve can also produce neuropathic pain. Finally, one should also examine for possible concomitant injury to other neighboring nerves such as the cervical plexus or great auricular nerve.

Operative Treatment

Whenever possible, surgical exploration of the nerve should be performed by 6 months. Although surgical reconstruction of the nerve may be considered up to a year after injury, better results occur with treatment as soon after injury as possible.^57,^58,⁶⁰ We favor early exploration of these nerve injuries when they occur immediately after surgery, especially when the nerve was not identified and protected as part of the operation.

Surgical options include neurolysis, direct repair, or nerve grafting, depending on intraoperative observations and electrophysiologic testing. During surgical reconstruction, it is important to consider the acromion–mastoid distance in the anesthetized patient. If direct repair of the nerve is performed with the head tilted toward the operated shoulder, when the patient is awakened after surgery and transported to the recovery room, significant traction can occur and disrupt the repair. If the nerve ends are found to have retracted at surgery, it is best to use an intervening graft such as a sural nerve or the great auricular nerve to put less tension on the repair (Fig. 27-4).

FIGURE 27-4 Spinal accessory nerve paralysis. A, The spinal accessory nerve was transected. A neuroma (inset) can be seen. A suture marks the distal stump. B, An interpositional graft repair (backgrounds) was performed using the sural nerve.

Nerve Transfer

Nerve transfer using a pectoral branch can be performed in cases of proximal injury to the accessory nerve, inability to identify proximal stump, or late referral.⁶⁴ If more than 12 to 18 months have passed since injury to the spinal accessory nerve, nonoperative treatment may be considered if the patient has compensated reasonably well. The degree of disability varies from patient to patient, even despite aggressive physical therapy. Some have only a persistent ache in the shoulder, whereas others feel and act completely disabled with respect to the upper extremity. Braces have been advocated as adjunctive treatment, but they are bulky and not used consistently by patients.⁶⁵ A patient symptomatic enough to attempt to use a brace is potentially a candidate for surgical reconstruction.

Muscle Transfer

Modern surgical procedures currently involve dynamic muscle transfer techniques. Earlier historical procedures, however, initially involved mostly static repairs. Henry and others advocated static stabilization of the medial aspect of the scapula to the vertebral spine with strips of fascia lata.⁶⁶^–⁶⁸ Dewar and Harris described lateral transfer of the levator scapulae to the lateral part of the scapula combined with a static fascial sling from the vertebral spine to the medial part of the scapula.⁶⁹ Static repairs with fascia, tendon, or artificial materials, however, tend to stretch out or rupture over time.⁷⁰

Dynamic transfer of the levator scapulae along with the rhomboid major and rhomboid minor was described in Germany by Eden and Lange.⁷¹^–⁷³ Bigliani reported good results with this technique.^61,^74,⁷⁵

The surgical approach for an Eden–Lange transfer involves a vertical incision midway between the vertebral spine and the medial edge of the scapula. The atrophied trapezius is divided, and the levator scapulae and rhomboids are released from the medial part of the scapula, with a small piece of bone containing their insertions. This release can be accomplished with a small saw or an osteotome. The levator scapulae is passed subcutaneously to a horizontal incision over the lateral spine of the scapula, near the acromion. The levator should be placed as far laterally as possible on the spine of the scapula, usually 5 to 7 cm medial to the posterolateral edge of the acromion. The rhomboid major and minor can be elevated individually or together from the medial edge of the scapula. The dorsal scapular nerve is potentially at risk during this part of the procedure.

The infraspinatus is partially elevated off of the scapula in a medial-to-lateral direction. The rhomboids are then placed as far lateral as possible–at least 4 cm–on the posterior aspect of the scapula and secured in place via suture and drill holes through the scapula. Alternatively, the rhomboid minor can be transferred cephalad to the spine of the scapula into the supraspinatus fossa. The infraspinatus is then sutured back in position over the transferred rhomboids.

Postoperatively, patients are placed in a shoulder abduction brace that holds the arm at approximately 70 degrees of abduction for 4 weeks. This brace will relieve tension on the transferred muscles while healing takes place. At 4 weeks, a gradual strengthening program can begin.

This technique has shown good results, probably because it involves dynamic transfer of muscle rather than a static transfer, which might stretch or possibly wear out over time.⁷³ If an Eden–Lange procedure or a static transfer fails and a salvage situation exists, scapulothoracic fusion becomes a potential option. Scapulothoracic fusion should be reserved primarily for patients with facioscapulohumeral dystrophy and global loss of shoulder muscle function. Different techniques have been used to perform scapulothoracic fusion, but most involve passing wires through the scapula and around several ribs with a broad iliac crest bone graft or metallic plate for support. The complication rate can be high, with the potential for pneumothorax or hardware failure.

LONG THORACIC NERVE

Anatomy

The serratus anterior originates from the upper nine ribs and inserts on the anteromedial border of the scapula. This insertion is only a few millimeters wide at the midportion of the scapula, but it becomes more substantial at the inferior pole of the scapula. It is the inferior portion of the muscle that is important in maintaining protraction and upward rotation of the scapula during forward elevation of the shoulder. The long thoracic nerve has a relatively long course after taking origin from the C5, C6, and C7 nerve roots. After crossing over the first rib, it travels 10 to 20 cm to its motor end plate in the serratus anterior. It is vulnerable to blunt trauma over the first rib along the lateral chest wall and can be crushed by forceful displacement of the scapula.

Etiology

The nerve is rarely injured as a result of penetrating trauma, but injury can occur from thoracic outlet surgery in the region of the first rib, breast surgery, or lateral chest wall procedures such as axillary node dissection.^76,⁷⁷ Spontaneous cases of entrapment at the scalenus medius have been described.⁷⁸ Probably, the most common cause of serratus anterior dysfunction is Parsonage–Turner syndrome. In fact, this condition is most likely the underlying cause of dysfunction attributed to overexertion, including athletic activities.

Clinical Manifestation

Isolated injury to the long thoracic nerve is usually manifested as winging of the scapula. Velpeau first described injury to the long thoracic nerve causing paralysis of the serratus anterior in 1837.⁷⁹ However, winging of the scapula has multiple causes, with multidirectional instability probably being the most common cause of mild winging. Spinal accessory nerve injury can also cause winging, but this injury tends to be milder and results in more of a rotational deformity of the scapula. Additionally, some patients have volitional control over the scapula and can demonstrate significant winging at will.

Nonoperative Treatment

In our opinion, in idiopathic or nonpenetrating trauma cases, observation is the standard therapy. No specific physical therapy protocol has been found to be especially helpful other than continued use of the shoulder as tolerated. Braces have been advocated to help hold the scapula against the chest wall.⁸⁰ Though somewhat effective, braces are usually found to be awkward and are not well tolerated by patients. Most patients with a nontraumatic or idiopathic cause tend to recover from the paralysis and regain serratus anterior function within 6 months to 1 year.⁸¹

Operative Treatment

Potential surgical options are available for treating injury to the long thoracic nerve in the early stages. Some have favored neurolysis of the nerve with decompression at the level of the scalenus medius.⁷⁸ However, because it is difficult to be certain where the lesion resides or if compression (rather than inflammation, for example) is responsible for the dysfunction, we do not recommend this approach for most patients. In cases where no spontaneous recovery has occurred, another strategy is to perform neurotization (or nerve transfer) using one or two intercostal nerves or the thoracodorsal nerve.^82,⁸³ Because it is not usually clear where the damaged section is, the nerve can be connected with the donor nerve close to the motor end plate. This technique has been helpful in a small number of reported cases.^82,⁸³ Many patients with atraumatic lesions recover spontaneously, so we do not routinely recommend surgery to the average patient before 6 or 9 months after the nerve deficit develops.

If a patient does not recover serratus anterior function and use of the shoulder is compromised, a number of reconstructive options are available (Fig. 27-5).^76,⁸⁴^–⁹⁵ Scapulothoracic fusion has been performed when the scapula is fixed to the underlying ribs. Although this technique can eliminate winging of the scapula, it will decrease shoulder girdle motion by at least 30%, with mostly forward elevation and extension affected.⁹⁶ Pneumothorax is a risk with this technique, and the pseudarthrosis rate is not insignificant. For these reasons, scapulothoracic fusion should be reserved for the salvage situation or for patients with symptomatic facioscapulohumeral dystrophy.

FIGURE 27-5 Long thoracic nerve palsy. A complete long thoracic nerve paralysis from Parsonage– Turner syndrome developed in this 36-year-old man. His winged scapula did not improve after 3 years. He had persistent pain in his shoulder and disability when performing overhead maneuvers. A, Prominent right scapula winging is noted preoperatively. B, Postoperatively, the winging has disappeared after pectoralis major transfer. The posterior incision has healed well. C, Postoperatively, his shoulder arc of motion has improved as well.

Tendon Transfer

Tendon transfers provide dynamic control of a winging scapula and are now our preferred method in patients who have had a neurologic deficit for 1 year or more. Tubby described transfer of the pectoralis major to the serratus anterior in 1904.⁹⁴ Although this transfer might offer initial relief of the winging, the paralyzed serratus anterior tends to stretch out with time, and this procedure is not recommended today. Other techniques described include transfer of the pectoralis minor, rhomboids, or levator scapulae.^85,^88,⁹⁷

Pectoralis Major Transfer

The technique that seems to give the most consistent result is transfer of the pectoralis major to the scapula with tendon graft augmentation. Durman, Ober, and Marmor ^90,^98,⁹⁹ each described successful transfer of the pectoralis major with a fascial extension graft in a few cases. More recent studies have demonstrated the excellent ability of this tendon transfer procedure to control winging of the scapula.^86,^89,^91,^92,^100,¹⁰¹ The pectoralis major is ideally suited as a transfer to substitute for the paralyzed serratus anterior. The direction of pull of the pectoralis major is similar to the path of the serratus anterior, and the bulk of the pectoralis major provides enough strength to resist winging of the scapula. The technique has been used with transfer of the entire pectoralis major or with only the sternal head (Fig. 27-6). Equally good results have been reported with both procedures. However, the sternal head of the pectoralis major is much more in line with the direction of pull of the serratus anterior than the clavicular head is, and it also provides for a less bulky transfer. Moreover, the sternal head is more substantial than the clavicular head and provides a stronger tendon transfer. Potential concerns of cosmesis or visible deformity of the anterior chest wall should be minimal. In most instances, regardless of whether the entire pectoralis major or the sternal head is transferred, there is little change in the normal contour of the anterior chest.