Scott P. Steinmann
Gilbert Csuja
Clinical Evaluation
History
Accurate recognition and diagnosis of potential neurologic injury about the shoulder is paramount for proper treatment of a patient's condition. In a patient presenting with complaints of shoulder pain or weakness, obtaining a thorough history should be the first step to establish an accurate diagnosis.
The patient should be questioned about pain, weakness, numbness, onset of symptoms, progression, timing of symptomatic episodes, and any improvement with time. The quality, level, and timing of pain are important factors to document. A visual scale to have the patient estimate his or her pain during the day and night, and compare this with the other noninvolved extremity may, be a useful adjunct.
In the emergency room setting, an accurate neurologic examination should be attempted. If all or part of the neurologic examination is unable to be completed, adequate documentation of this should be made. A cursory exam with documentation of “neurovascularly intact” may attract future litigation. Diagnosis of nerve injury may be delayed until the patient regains consciousness and becomes cooperative.
Physical Examination
The initial part of the neurologic exam of the shoulder and arm is examining the extremity for muscle atrophy. This can be done only with the shoulder completely exposed, to be able to view the shoulder and scapula.
An accurate neurologic examination should be able to be performed on any patient who is coherent, even in the setting of shoulder trauma. Starting the examination at the level of the fingers and hand is recommended, for most of this part of the exam should be able to be done with minimal discomfort to the patient. Assessing median, ulnar, and radial nerve motor and sensory functions should take little time and should include two-point discrimination measurements to both aspects of all fingers and thumb. Elbow flexion and extension can determine musculocutaneous nerve and high radial nerve function by testing for biceps, brachialis, brachioradialis, and triceps activity. Axillary nerve function is determined by testing shoulder abduction, specifically by looking at deltoid contraction with the arm at the patient's side. Loss of motor or sensory function in the distal extremity can also be helpful in locating the area of injury more proximally. If radial nerve dysfunction is seen distally in combination with axillary nerve injury (both nerves being branches of the posterior cord), this is an indication that the injury may have occurred at the level of the posterior cord of the brachial plexus.
More proximally, pectoralis major function tests lateral pectoral nerve (clavicular head) and medial pectoral nerve (sternal head) function. Latissimus dorsi is innervated by the thoracodorsal nerve and is tested by extending the arm, or contraction with coughing. Serratus anterior is supplied by the long thoracic nerve and is tested for by examining presence of winging while the patient forward flexes the arm such as in a wall push-up. The rhomboids are tested by scapular adduction and observing for muscle atrophy. The rhomboids, major and minor, are innervated by the dorsal scapular nerve.
Full arc abduction of the shoulder can be accomplished is some patients with both deltoid and supraspinatus separately. Supraspinatus and infraspinatus muscles are supplied by the suprascapular nerve and are tested by looking at external rotation strength and midrange abduction of the shoulder.
Examination of the neck should be considered an integral part of any shoulder and upper extremity examination. Just as brachial plexus injury can affect function of the muscles about the shoulder and arm, injury of the spinal cord and exiting nerve roots can do the same. Being able to illicit the patient's symptoms with flexion, extension of the neck, or with the Spurling maneuver indicates probable cervical radiculopathy. In upper motor neuron lesions, deep tendon reflexes may be hyperreflexic, there may be increased tone, and pathologic reflexes may be present.
Referred pain of cardiac or other intrathoracic origins such as gall bladder pain should be excluded as a cause of shoulder pain.
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Much of the above shoulder examination is dependent on a healthy shoulder joint. It is often difficult to elicit whether the patient's pain (and weakness) on testing supraspinatus is caused by rotator cuff injury, internal joint pathology, or true neurologic injury. In these cases, lidocaine injection of the subacromial space may provide some benefit in decreasing pain to the area and obtaining a better examination.
Finally, patients with secondary gain issues commonly have nonphysiologic examination findings. However these patients cannot stop the latissimus from contracting while coughing when testing for latissimus function.
Axillary Nerve
The axillary nerve is a terminal branch of the posterior cord. It crosses over the anteroinferior aspect of the subscapularis muscle near its insertion, then turns posteriorly to cross the quadrilateral space, where it is in close contact with the inferior joint capsule. It has been reported to be as close as 10 mm inferior to the inferior glenoid labrum. When the nerve exits the quadrilateral space, it branches into two trunks. The posterior trunk branches to supply teres minor and posterior deltoid, then terminates as the superior lateral brachial cutaneous nerve. The anterior trunk travels subfascially, then enters the middle and anterior deltoid to innervate those muscles. The position of the anterior trunk is reported to be as close as 4 cm inferior to the anterolateral acromion. Internal topography studies of the axillary nerve show that on its exit from the posterior cord, the nerve is monofascicular, but by the time it exits the quadrangular space, the nerve has distinct fascicles. The deltoid motor fascicles run superolateral, and the teres minor and sensory fascicle run inferomedially.
Axillary nerve paralysis is the most common peripheral nerve injury to affect the shoulder. It is most commonly seen as a complication of shoulder dislocation, proximal humerus fracture, or blunt trauma to the shoulder. The literature reports 5% to 10% incidence of clear axillary nerve injury with glenohumeral dislocation. However, at least one study reports electromyography/nerve conduction study (EMG/NCS) findings in as many as 54% of dislocations, most patients being subclinical. Fortunately, most patients recover from their injury spontaneously. Patients who are at a higher risk of permanent injury are those older than 50 years of age and patients whose shoulder stays dislocated for >12 hours. The mechanism of injury is that of direct compression of the dislocated humeral head against the nerve. Because of the short length of the axillary nerve from its origin in the posterior cord of the brachial plexus and its attachment at the deltoid, traction injury may also result at the infraclavicular brachial plexus.
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Figure 41-1 An 18-year-old male who dislocated his right shoulder 3 months prior, with no recovery of axillary nerve function. At surgery the axillary nerve was found to be torn. It was repaired with sural nerve grafts. |
The axillary nerve may also be injured from blunt trauma to the shoulder without glenohumeral dislocation. Most reports of this kind of injury show a mechanism of posteriorly directed force from collisions in football and hockey with similar symptomatology; however, no isolated axillary nerve ruptures of this type were found reported (Fig. 41-1).
There is at least one report in the literature of rotator cuff tears associated with neuropathies. Of the 15 patients evaluated with this combination of injuries, 12 had EMG-demonstrable axillary nerve injury. Interestingly, only 2 of these 12 patients had decreased sensation over the lateral shoulder. This study reported that since the cause of nerve injury was thought to be a traction neurapraxia, treatment was recommended of rotator cuff repair followed by a monitored physical therapy protocol. Follow-up EMGs were reported to have shown significant nerve recovery in the study patients.
Quadrilateral nerve syndrome has been described as a compression of the axillary nerve (and posterior humeral circumflex artery) in the quadrilateral space. Symptoms may present as deltoid weakness, vague posterior shoulder pain, and tingling and numbness in lateral shoulder distribution. Compression of the nerve is presumed to be caused by anomalous fibrous bands, muscle hypertrophy, and mass effect. Treatment is mostly conservative, with most cases resolving spontaneously. Exploration and release of impinging structures are rarely needed.
Paralysis of the muscles innervated by the axillary nerve is also seen as one of many nerves injured in brachial plexus trauma. In these cases, avulsion or stretch injury of roots, trunks, or cords of the brachial plexus is the usual site of injury. Isolated axillary nerve injury in brachial plexus trauma has a reported incidence between 3% and 6% in the literature.
The axillary nerve is also at significant risk during some shoulder open and arthroscopic procedures (Fig. 41-2). These procedures include open rotator cuff repair, open and arthroscopic Bankart procedures, arthroscopic capsular release, arthroscopic thermal capsulodesis, open reduction internal fixation, and humeral nail placement for humeral head and neck fractures. The mechanism of injury varies to include traction injuries, incision or cautery of the nerve, screw placement through the nerve, and capturing the nerve with sutures intended to tighten the joint capsule. Incidence of iatrogenic nerve palsies after plate fixation is reported between 0% and 5%, whereas incidence of nerve injury after intramedullary nail placement is between 0% and 4%.
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Figure 41-2 A 21-year-old man underwent prior arthroscopic instability repair. He awoke with severe axillary neuropathy. At surgical exploration, a suture was found compressing the axillary nerve. The suture can be seen dividing the axillary nerve. The suture was removed, and the patient achieved excellent recovery. |
Albritton et al. suggested a significant risk to the axillary nerve with blind placement of screws for flexible nail insertion and recommended blunt dissection through the deltoid, direct visualization of lateral humeral cortex, and use of soft tissue guides for drilling to protect the nerve.
Although thermal capsular shrinkage procedures are on a sharp decline, the close proximity of the axillary nerve to the inferior glenohumeral joint capsule puts the nerve at a significant risk of injury owing to high temperatures. These injuries are thought to be caused by high temperatures in the shoulder joint with the nerve running as close as 1 cm to the inferior joint capsule. The reported incidence is 1% to 2% with spontaneous recovery in most cases.
As previously discussed, most axillary nerve injuries resulting from blunt trauma resolve spontaneously, so in these cases, it is recommended that nerve recovery should be observed for at least 3 months prior to considering surgical intervention. It is recommended that a baseline EMG/NCS be obtained at 3 to 4 weeks and repeated at 1 to 2 month intervals to assess nerve recovery. Physical therapy should be initiated to prevent loss of motion to the shoulder joint. There are no studies to show that electrical nerve or muscle stimulation speed recovery. If there are no signs of recovery by 6 months, surgical exploration with possible nerve grafting is indicated. Because of its short course through the axilla, cable grafting is the preferred choice of surgical repair. The axillary nerve is approached via a combined anterior/posterior incision. The nerve is identified anteriorly at its origin off the posterior cord and followed posteriorly through the quadrilateral space. It is then found posteriorly as it branches to innervate the deltoid and followed anteriorly. Neurolysis is done in cases where the nerve is shown to conduct with intraoperative direct electrical stimulation. Nerve grafting is done with preferred use of sural nerve graft if the nerve is ruptured, retracted, or if neuroma scarring is too great. Leechavengvongs reported nerve to long head triceps grafted to axillary nerve deltoid motor branches to reinnervate an otherwise nonrepairable axillary nerve with excellent results and rapid recovery.
Mackinnon advocates transfer of nerve to medial head triceps to very proximal axillary nerve to accomplish the same goal with inclusion of grafting to the teres minor motor branch.
Following surgical repair, the shoulder is immobilized in neutral abducted position for 2 to 3 weeks, followed by progressive active and active-assist therapy to regain shoulder range of motion. Maximal recovery of the nerve is expected at 12 to 18 months from surgery. One study with 25 patients with axillary nerve repair (most treated by sural nerve grafting) reported 23 patients obtaining M4 or M5 strength postoperatively. Neurotization of the nerve is usually done in massive brachial plexus trauma with thoracodorsal, spinal accessory, phrenic, and intercostal nerves. These patients have less optimal recovery.
Spinal Accessory Nerve
The spinal accessory nerve (cervical nerve [CN] XI) supplies motor function to the trapezius and sternocleidomastoid muscles, which is a major scapular stabilizer. It enters the neck through the jugular foramen and after passing through the sternocleidomastoid, it crosses the posterior cervical triangle obliquely to innervate the trapezius on its underside. The posterior cervical triangle is bordered anteriorly by the sternocleidomastoid, posteriorly by the trapezius and inferiorly by the clavicle. Although most motor function to the trapezius is derived from the spinal accessory nerve, at least some have dual innervation of the upper portion of the muscle from cervical roots 3 and 4.
The trapezius muscle takes its origins from the ligamentum nuchae superiorly and from the spinous processes of C7–T12. The muscle can be divided into three portions: upper, middle, and inferior. It is the upper portion of the muscle that originates from the ligamentum nuchae, rotating around to become the posterior border of the posterior cervical triangle, and finally attaching to the posterior aspect of the lateral third of the clavicle. This part of the muscle may have alternate innervation from cranial nerves 3 and 4 and may still remain functional after spinal accessory nerve injury. The upper portion elevates and upwardly rotates scapula. The middle portion of the muscle inserts on the medial acromion and the lateral aspect of the scapular spine and adducts and retracts the scapula. The most inferior portion of the muscle's origin is mostly thoracic spinous processes as far inferior as T12, and insertion is on the medial spine of the scapula. This portion mainly depresses and rotates the scapula downward. The spinal accessory nerve gives off branches to innervate these
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different parts sequentially, which is important in brachial plexus reconstruction for using the lower branches to neurotize injured nerves, without losing the elevating function of the upper trapezius and while preserving neck contour. In this situation, the rhomboids and serratus can partly compensate for the lost inferior sections with continued retraction of the scapula.
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Figure 41-3 Spinal accessory nerve. (From Steinmann SP, Spinner RJ. Nerve problems about the shoulder. In: Rockwood CA Jr, ed. The Shoulder. Vol. 2. 3rd ed. Philadelphia: WB Saunders; 2004:1015 , with permission.) |
The trapezius muscle is the predominant stabilizer of the scapula, with its action of elevating, rotating, and retracting the shoulder blade. Loss of this function causes the shoulder to droop and allows the scapula to rotate downward, outward, and away from the midline. This causes winging of the scapula and decreases strength and range of motion in the planes of abduction and forward flexion. As the shoulder assumes this new position, subacromial impingement now becomes more likely, as does development of rotator cuff tendinopathy. Other shoulder stabilizers are overworked, which causes pain and spasm. The decreased range of motion can also result in a stiff shoulder and may advance to frank adhesive capsulitis. This, in turn, causes still active shoulder stabilizers and rotator cuff muscles to work even harder to compensate, worsening the patient's pain and spasm. In addition to the drooping shoulder, atrophy of upper trapezius fibers may cause a considerable change in the contours of the patient's neckline, which usually results in significant self-image problems.
Spinal accessory nerve injury, although initially seemingly benign, has significant morbidity, resulting in pain, disability, and a significantly altered physical appearance. Injury to the spinal accessory nerve can occur after penetrating trauma to the shoulder. Blunt trauma to the shoulder and neck region may also injure the nerve, causing trapezius palsy. However, the most common cause is iatrogenic laceration after cervical lymph node biopsy, which is reported to be as high as 3% to 8% in the literature.
The spinal accessory nerve is intimately involved with the cervical lymph nodes in the posterior triangle of the neck. During lymph node dissection, the nerve can easily be injured because of sharp laceration, clipping of nerve thought to be a vessel, or cautery of fibers.
The initial presentation of a patient with recent injury to the spinal accessory nerve is usually a painful shoulder with some decreased shoulder range of motion. Patients and treating physicians may attribute these complaints to postoperative pain. Initially the trapezius may show minimal wasting, and winging may not be appreciated. The levator scapulae muscle may be able to compensate and produce a normal-appearing shoulder shrug. Also, the possibility of a secondary innervation of the trapezius from upper cervical nerves may confuse the initial physical examination. As the trapezius becomes more atrophied, the appearance of the shoulder becomes more obvious, as discussed above.
The patient's history of recent surgical procedure and history of the above symptoms should make the astute physician think of the possibility of spinal accessory nerve injury. The condition is best diagnosed by EMG/NCS done, at the earliest, 3 to 4 weeks after injury. If the nerve injury is recognized within 6 months of the injury, the recommended plan is exploration with planned neurolysis versus repair of the nerve, either in primary fashion or with the use of (sural) nerve graft, depending on intraoperative findings. It is recommended to have intraoperative electrophysiologic testing available during the procedure. The preferred timing for surgery is as soon as possible after injury to the spinal accessory nerve for preservation of best nerve function; however, successful recovery of trapezius function has been reported as far out as 1 year.
In the more uncommon presentations of trapezius palsy resulting from blunt trauma, initial EMG/NCS should be done 3 to 4 weeks after injury as a baseline and the patient followed up every 2 to 3 months, looking for resolution of symptoms or improved EMG/NCS results. If no sign of recovery occurs by the 4- to 6-month time frame, surgical exploration is an option (Fig. 41-3).
Commonly, patients present late (>12 months from injury) with a history of multiple consultations without a clear diagnosis. After 12 months, primary repair of the nerve is generally not useful because of motor end plates degeneration. If the patient compensated well for his or
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her condition, continued observation is a reasonable option. Some patients, however, have severe disability and are unable to function with their resultant level of function. Braces may be offered to these patients, but they tend to be cumbersome.
Many static stabilization procedures have been attempted in the past with modest results, for the large torsion forces on the scapula usually tend to stretch and tear such repairs. The current standard for trapezius reconstruction is the Eden-Lange procedure. This procedure involves dynamic transfer of the levator scapulae, rhomboid major, and rhomboid minor muscles. The levator is transferred to the lateral scapular spine, the rhomboid major as lateral as possible onto the infraspinatus fossa, and the rhomboid minor either to the scapular spine or the supraspinatus fossa. Multiple authors reported good results with this procedure. The salvage operations such as scapulothoracic fusion should be reserved for patients who either have failed all the above attempts at stabilization or have fascioscapulohumeral dystrophy with global loss of shoulder function. This is an operation with potentially very high complication rates.
Suprascapular Nerve
The suprascapular nerve is an important contributor to rotator cuff function. Its injury causes significant morbidity with loss of abduction and external rotation of the involved shoulder.
The suprascapular nerve takes its origin from the upper trunk of the brachial plexus; it courses through the posterior triangle of the neck following the omohyoid under the anterior border of the trapezius. The nerve enters the supraspinatus fossa through the suprascapular notch (under the superior transverse scapular ligament), where it gives off branches to innervate the supraspinatus muscle. Upon exiting the supraspinatus fossa through the spinoglenoid notch, the nerve splits off a sensory branch to innervate the posterior joint capsule and turns medial to innervate the infraspinatus muscle.
Major locations where the suprascapular nerve may be tethered are its origin off the upper trunk (the Erb point) and at the suprascapular notch, where it is noted to be relatively fixed. It may also be compressed at the level the spinoglenoid ligament as the nerve courses around the spine of the scapula. It is also here that the nerve may be as close as 20 mm to the superoposterior glenoid edge.
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Figure 41-4 Suprascapular nerve compression. Nerve loop holds the suprascapular nerve being compressed by a large ganglion at the suprascapular notch in a 50-year-old man. The cyst was resected, and he achieved excellent recovery. |
The suprascapular nerve can be injured as a result of blunt trauma sustained to the shoulder, often in occasional with a fracture of the scapula. A common cause of compression of the nerve is a ganglion cyst either at the suprascapular notch or at the spinoglenoid notch. The presumptive origin of these cysts is from degenerative glenoid labral tears (Fig. 41-4). The literature also cites many sports as potential predisposing factors for repetitive-type injury to the suprascapular nerve. The literature often cites volleyball players as the most commonly affected patients, but reports have also implicated baseball, tennis, and weight lifting as possible activities aggravating chronic injury. Parsonage-Turner syndrome is also a cause of idiopathic supraspinatus palsy. This condition has certain identifying characteristics and will be discussed later in the chapter.
Signs and symptoms of suprascapular nerve palsy are nearly identical to those of a rotator cuff tear initially. However, specific symptoms are dependent on the location of the injury or compression. When the injury level is at the suprascapular notch or proximally, patients complain of pain over the posterior and lateral aspects of the shoulder. They also note significant weakness of abduction and external rotation. When the site of injury is more distal, such as the spinoglenoid notch, there is usually less pain (owing to the fact that the sensory nerve may have split off the main nerve) and only loss of external rotation strength may be found. Later as significant muscle atrophy develops, the condition declares itself more clearly. Even then, supraspinatus atrophy is never observed owing to the bulk of the overlying trapezius.
MRI may rule out rotator cuff tear (RCT) as a cause and show fatty degeneration and atrophy of the involved muscles in the absence of massive RCT. Although acutely denervated muscles may not show any significant changes, MRI findings of subacute denervation are characterized by high signal intensity distributed homogeneously throughout the denervated muscle on T2-weighed images.
For cases of suprascapular neuropathy, where a compressive mass of the nerve is known, surgical exploration is recommended. Most ganglions at the spinoglenoid notch can be reached and debrided via shoulder arthroscopy, at which time the labral tear may also be debrided or repaired. A single ganglion noted on MRI with no neurologic involvement does not need operative resection. Repair of any associated symptomatic labral tear may be considered, but the ganglion itself does not need to be debrided. Repair of the labral tear will often cause the ganglion to resorb over time.
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Musculocutaneous Nerve
The musculocutaneous nerve is a branch off the medial cord of the brachial plexus. It courses through the coracobrachialis in an oblique medial to lateral direction, entering the coracobrachialis approximately 5 cm below the coracoid. The nerve then travels in a lateral direction to send motor branches to first the biceps and then to the brachialis muscles. Distal to these branches, the nerve becomes the lateral antebrachial cutaneous nerve to supply the lateral forearm.
Musculocutaneous nerve injury is occasionally seen with glenohumeral dislocations and is occasionally seen as a result of penetrating trauma (such as knife wounds).
Most musculocutaneous nerve palsies present as a mixed motor and sensory situation with symptoms of weakness of elbow flexion and with pain and numbness along the radial forearm. However, a pure sensory syndrome of lateral antebrachial nerve compression may also be seen, with symptoms exacerbated by vigorous activity and elbow extension. The sensory nerve is thought to be compressed between the biceps and brachialis on its exit just lateral to the distal biceps tendon or by fascial bands in the antebrachial fossa. Treatment is usually conservative with rest, nonsteroidal anti-inflammatories, and posterior splint to limit hyperextension of the elbow.
If musculocutaneous nerve injury is suspected, either resulting from traumatic or from iatrogenic origin, and no recovery is seen by the 3 to 4-week mark postinjury, an EMG/NCS can be performed both for diagnostic purposes and to establish a baseline for following recovery of the nerve. Since most musculocutaneous nerve injuries are traction related versus sharp lacerations of the nerve, spontaneous recovery is expected within the first 3 to 6 months after initial injury. If no biceps recovery is seen by 6 months, or if initial injury is suspected to be a frank division of the nerve, surgical exploration should be performed. After exploration and neurolysis of the involved nerve segment where the nerve appears to be intact and intraoperative EMG shows conduction across the nerve segment involved, a further period of observation for recovery is recommended. If, however, neuroma scarring or complete laceration of the nerve is found, excision of scarred nerve segments with interpositional nerve grafting is the preferred treatment option.
In cases where the musculocutaneous nerve is injured as part of brachial plexus injury, or there may be no proximal segment to graft the nerve into, other reconstructive options for recovery of biceps function exist. The Oberlin transfer, which transfers one or two ulnar nerve (wrist flexion) fascicles to the motor branch to the biceps, is an excellent choice for rapid recovery of biceps function, owing to the short distance of reinnervation. Recovery of the biceps has been reported as soon as 3 months from the procedure, with ultimate biceps strength of M4 in >90% of patients. For patients who do not have the ulnar or median nerve available because of more extensive brachial plexus trauma, neurotization procedures from intercostals, spinal accessory, phrenic, and medial pectoral nerves may be an available option.
When patients are referred >1 year from their initial injury, the chance of successful muscle function recovery with nerve repairs and transfers is significantly decreased. For these patients, tendon transfer such as the Steindler flexorplasty is recommended. This procedure requires a functioning brachioradialis (radial nerve), which is transferred more proximally on the humerus with the plan of improving elbow flexion. Tendon transfers such as triceps, latissimus, and pectoralis major and minor are have also been described.
Another salvage technique of recovering elbow flexion is free muscle transfer. Many of these procedures have been performed with reasonable success, primarily using gracilis to supplement biceps function. This muscle has a proximal neurovascular pedicle and shape that is optimal for restoring biceps function. The proximal vessels are usually connected to the thoracoacromial trunk, with the obturator nerve branch connected to the spinal accessory nerve with sural graft extension. The proximal muscle is usually attached through bone sutures to the distal clavicle and acromion, while distally it is woven into biceps tendon.
Long Thoracic Nerve
The long thoracic nerve is a pure motor nerve, formed from proximal contributions from cervical roots 5, 6, and 7. The nerve has a long course along the lateral thorax (26 cm) to its insertion on the serratus anterior. This muscle originates from the lateral aspect of the upper nine ribs and inserts along anteromedial scapula, with the inferior component of the muscle being the most important, inserting over the inferomedial corner of the scapula. This insertion is important in stabilizing the scapula on the chest wall and protracting the scapula in forward flexion and abduction. If this function is lost, scapular winging is seen with actions such as wall push-ups and overhead activities (Fig. 41-5). This winging is different than that caused by spinal accessory nerve injury in that, with the loss of serratus stabilization, the vertebral border and inferior pole of the scapula become more prominent This deformity becomes accentuated with forced forward flexion of the arm.
Patients affected by this injury complain of decreased forward flexion and abduction as well as pain and weakness about the shoulder. The pain is usually posterior and may result from spasm and overuse of other scapular stabilizers such as the rhomboids and levator scapulae. Complaints of initial severe pain followed by atrophy and winging is commonly seen in Parsonage-Turner syndrome.
Although plain radiographs should always be included in the diagnostic workup for any patient who presents with scapular winging, the best diagnostic test for long thoracic nerve injury is EMG/NCS. Radiographs, however, may detect the occasional osteochondroma that may cause compression of the nerve as well as other neoplasms inside and outside the thoracic cavity. CT scan and MRI are seldom useful except in cases of neoplasm or cervical disk herniation to make or refine the diagnosis.
Treatment of serratus anterior palsy is usually conservative, for most cases, idiopathic or resulting from closed
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injury, resolve spontaneously. Physical therapy is initiated to preserve motion and for shoulder-strengthening exercises. Braces are not considered effective. If there is no improvement seen clinically or with EMG/NCS after 9 months, and the patient is severely affected by his or her loss of scapular protraction or by pain, operative intervention in the form of muscle transfers is a potential option.
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Figure 41-5 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. (From Steinmann SP, Spinner RJ. Nerve problems about the shoulder. In: Rockwood CA Jr, ed. The Shoulder. Vol. 2. 3rd ed. Philadelphia: WB Saunders; 2004:1016 , with permission.) |
The preferred procedure is pectoralis major sternal head muscle transfer via tendon interposition graft to the scapula. Graft choices are autograft or allograft and include fascia lata or hamstring tendons. Allograft Achilles tendon is a great option, as its proximal portion drapes over the pectoralis muscle and tendon and its distal tendon portion provides strong attachment to the scapula.
Scapulothoracic fusion is usually reserved for patients who failed tendon transfer procedures and continue to be severely disabled by their condition and for patients with multimuscle atrophy and weakness such as patients with fascioscapulohumeral dystrophy. This procedure has a high reported complication rate and may be disabling in itself owing to severely decreased shoulder motion and variable pain relief.
Parsonage-Turner Syndrome
Parsonage-Turner syndrome, also known as brachial neuritis, is thought to be an uncommon condition. Men are more likely to be affected, with a reported male-to-female ratio ranging between 2:1 and 11:1. Age of presentation is variable, but most patients present in the third to seventh decades of life.
The cause of this condition remains unclear but is thought to be inflammatory or immune mediated. Brachial neuritis is described following a viral illness, immunization, surgery, extreme exercise, and pregnancy. There is also thought to be an inherited form of the syndrome known as hereditary neuralgic amyotrophy. Patients affected with this disorder usually present at an earlier age and may have
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recurrent episodes of what typically appears to be Parsonage-Turner syndrome.
Onset of the syndrome is somewhat typical in that patients describe an initial onset of severe shoulder pain with no apparent cause. The pain is commonly described as intense and burning in quality and may last from days to weeks. This painful episode is followed by progressive muscle atrophy with accompanying weakness and sensory loss. Fewer patients with atypical presentation complain of motor and sensory loss but are fortunate enough not to have the initial painful onset. Muscles innervated by C5 and C6 are most commonly involved, and the most typically affected nerves include the suprascapular, axillary, long thoracic, anterior interosseous, and radial nerves. Brachial neuritis can affect individual nerves or involve many nerves of the brachial plexus and the cervical region (such as the spinal accessory nerve) at the same time. Approximately 10% of the cases have bilateral presentation.
The diagnosis of Parsonage-Turner syndrome is primarily made on history, a thorough physical examination, and ruling out other conditions that may be responsible for the patient's symptoms. Some orthopaedic conditions that may have similar presentations and symptoms include herniated cervical disk, perilabral ganglia, rotator cuff tear, impingement syndrome, shoulder bursitis, calcific tendonitis, and adhesive capsulitis. Neurologic conditions that may mimic this condition include entrapment syndromes also known as inflammatory demyelinating polyneuropathy, transverse myelitis, and mononeuritis multiplex. EMG/NCS will identify nerves and muscles involved and will initially show acute denervation, with fibrillation and positive waves seen at the 3- to 4-week mark. MRI is useful more to exclude other diagnoses and will typically show a picture of selective involved muscle atrophy with increased signal on T2-weighed scans.
As in the case of other idiopathic nerve syndromes such as Bell palsy, most patients show spontaneous improvement with time. However, recovery can be variable, with most patients having residual effects such as winging. Most patients recover within 3 to 6 months, but complete recovery may take >12 months. Treatment is supportive, with nonsteroidal anti-inflammatory medications and other analgesics. The use of steroids and immunoglobulin therapy has not been shown to be effective. Physical therapy is recommended to regain range of motion and to strengthen shoulder girdle muscles. As in all other cases of permanent deficits described earlier in this chapter, tendon transfers may be of use to treat long-term disability.
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