Accessory Nerve Injury

Anatomic study of the SAN has long maintained a debate as to the exact contributions of this nerve and other cervical motor nerves to the innervation of the trapezius muscle. In 1933, Bardeen suggested that the origin of motor input to the trapezius muscle was purely from the cervical nerves. Subsequent anatomic study reported a possible plexus composed of both cervical nerves and contributions from the SAN that collectively provided trapezial motor innervation. The classic and much-used Gray’s Anatomy assigned cervical nerves to a proprioceptive sensory role, with only the SAN providing motor innervation to the trapezius.[6, 7]

Current evidence suggests a variable contribution of both cervical and SAN motor innervation to the trapezius. This explains the unpredictable motor and sensory deficits that arise from transection of the nerves to this muscle. For example, significant preservation of trapezial function has been reported even in radical neck dissections where the SAN was intentionally sacrificed.[5] SAN damage that results from radical neck dissection was first described by Ewing and Martin (1952), although Nahum (1961) coined the term "shoulder syndrome," describing the clinical syndrome of pain and shoulder dysfunction that is associated with SAN injury.[8, 9]

Interest in methods for evaluating SAN function and changes after surgical neck dissection have led to the use of various diagnostic modalities, such as electromyography (EMG) and ultrasonography.[9, 10, 11] Likewise, methods of nerve repair following surgical injury have been also been investigated. Harris and Dickey first described a cable grafting technique to restore SAN function.[12] Gou et al have described an alternative technique for SAN reconstruction that used a sternocleidomastoid muscle—greater auricular nerve (GAN) flap, with the advantage of having an interpositioned graft vascularized by fascia and muscle with no donor site morbidity.[13] Diagnostic methods and nerve-salvaging strategies are discussed in further detail in the Workup section.

SAN injury results in shoulder dysfunction that affects the overall quality of life. Currently, several treatment options with predictable results are available to manage patients diagnosed with SAN trauma, provided the appropriate treatment is initiated in a timely fashion. Major pitfalls in early management of SAN injury include failure to recognize or acknowledge the injury and choosing conservative management in the hope that function will return without intervention.[14] The incidence of serious sequelae can be reduced by maintaining a high index of suspicion for SAN injury. Early identification and timely intervention consequently results in better therapeutic outcomes.

Frequency

Iatrogenic SAN injury most commonly occurs following diagnostic lymph node biopsies of the posterior triangle of the neck. Injury rates from these procedures are reportedly 3-8%. Severe functional deficits of the upper extremity have been reported in up to 60-80% of patients who undergo radical neck dissections.[15] A large retrospective series reported clinical evidence of SAN injury in 1.68% of patients who underwent modified radical neck dissection.[16]

Clinical evidence of SAN injury has been reported to be as high as 30% in selective neck dissections that included cervical zones II-IV and V. This percentage is significantly lower if zones II-IV are dissected but zone V is spared.[2]

Reported injury rates vary, however. A retrospective study by Popovski et al found that in radical, selective, and modified neck dissections, postoperative morbidity rates for the SAN were 46.7%, 42.5%, and 25%, respectively.[17]

The dissection of level IIB is also a topic of controversy. It was previously presumed that preservation of zone IIB and consequently reduced manipulation of the SAN in a lateral neck dissection would result in less postoperative shoulder dysfunction. However, reports do not support this assumption. Other, less frequent causes of SAN injury are listed below (see Etiology).

Spinal accessory nerve (SAN) injury may be idiopathic or may have one of the following etiologies:

Iatrogenic

See the list below:

• Lymph node biopsy in the posterior triangle of the neck (a frequent iatrogenic cause of SAN trauma)

• Radical neck dissection (by definition involves the resection of the SAN for complete tumor clearance)

• Neck surgery[18]

  • Excision of benign neck masses

  • Other types of neck dissection (modified or selective neck dissection)

  • Parotidectomy

  • Carotid vessel surgery (eg, endarterectomy)

  • Internal jugular vein manipulation (eg, vein cannulation)

  • Facelift[19]

Traumatic

See the list below:

• Penetrating injury (glass cut or gunshot injury)[9]

• Blunt injury: Sport-induced SAN injury due to external pressure has been reported.[20]

  • A blow from a hockey stick

  • Wrestling

  • A knot in a sling

  • A noose during an unsuccessful hanging

  • A superficial “love bite” to the neck

  • Vigorous movement of the neck from “neck cracking”

  • Severe dislocations of the acromioclavicular joint

  • “Whiplash” injury

Neurologic

See the list below:

• Collet-Sicard syndrome: Involves the lower cranial nerves (IX, X, XI, and XII)[21]

• Vernet syndrome (ie, tumor near jugular foramen): Involves the lower cranial nerves IX, X, and XI[22]

• Poliomyelitis

• Motor neuron disease

• Brachial neuritis

• Syringomyelia

A study by Kassem et al suggested that idiopathic brachial plexitis can affect the spinal accessory nerve and may be sparked by surgical procedures.[23]

Miscellaneous

Spontaneous isolated nerve injury has also been reported.[24]

Rarely, the spinal accessory nerve (SAN) is inadvertently transected during exploration of the posterior cervical triangle. Alternatively, a small branch of the SAN that innervates the upper trapezius muscle may be transected if it is not clearly identified during neck dissection. In nerve-sparing procedures, the proposed mechanism of SAN injury is traction, skeletonization, and devascularization of the nerve during neck dissection. The result of these insults is proposed to be segmental demyelinization due to local ischemia, leading to diminished or complete loss of nerve function.[25] SAN injury results in axonal degeneration, as evidenced by needle EMG and scar formation that are responsible for muscle atrophy and contractures.[24]

Stretch or traction on the SAN compromises intraneural microvascular flow, leading to ischemia and consequently axonal rupture and degeneration. In general, when stress on the SAN due to traction is distributed over longer periods of time, it is tolerated better than rapid and large stretches of the nerve (eg, as seen in sudden acceleration-deceleration injuries).[20]

Evaluation of patients to detect SAN injury requires an organized clinical examination that may be supplemented with electrophysiologic nerve and muscle studies, as described in the Workup section.[26]

An understanding of the clinical presentation that arises from complete SAN resection during a radical neck dissection procedure gives insight into the spectrum of signs and symptoms that manifest during lesser injuries. The term "shoulder syndrome" is used to describe the pain and shoulder dysfunction that can follow radical neck dissection.[27] Most of the following presenting symptoms and signs are attributable to denervation of the upper trapezius muscle:

Symptoms

Shoulder pain (the most common presenting symptom)

• Pain can radiate to the neck and upper back and occasionally to the ipsilateral arm.

• Pain may worsen when the weight of the involved shoulder is not supported, placing strain upon the shoulder joint.

• The etiology of pain is multifactorial and can include the straining of supporting muscles (rhomboids and levator scapulae) with subsequent traction on the brachial plexus.[2, 20]

• Diminished strength when performing regular daily activities (eg, placing dishes in overhead shelves, exercises that involve bearing weight on the shoulders).

Signs

Limited or loss of sustained abduction of the shoulder is the most common sign.

A full passive range of motion may eventually progress to decreased passive range of motion due to adhesive capsulitis (frozen shoulder).

The ipsilateral shoulder may droop.

Scapular winging or prominence of the medial border of the scapula and protraction may be found.

Internal rotation of the humeral head may be found.

Atrophy of trapezius muscle may be found.

Sternoclavicular joint hypertrophy or subluxation may be caused by abnormal stress on the medial clavicular head after the loss of the trapezius muscle support.[28]

 

Differentials

The differential diagnoses of SAN injury are as follows:

• Lesions of the long thoracic nerve of Bell: Scapular winging in lesions of the long thoracic nerve is accentuated by forward flexion of the affected upper extremity as opposed to accentuation by abduction in SAN injury.[1, 20]

• Myofascial pain syndromes of the shoulder girdle region: The absence of significant muscular atrophy and weakness and the absence of scapular winging differentiate this syndrome from SAN injury.

• Whiplash injury: In whiplash injuries, symptoms are limited to the neck and include neck pain, headache, cervical spine rigidity, and limitation of neck motion.[20]

The indications for spinal accessory nerve repair are as follows:

• Iatrogenic intraoperative injury or transection of the nerve (eg, radical neck dissection)[2]

• Delayed diagnosis of intraoperative SAN injury associated with signs and symptoms of shoulder syndrome (The type of SAN repair depends on the time interval from the injury to diagnosis; see Surgical treatment.)

• Patients with known SAN injury who do not demonstrate improvement with conservative management as evidenced by serial clinical examinations or by lack of electrical regeneration on EMG conduction studies and also exhibit a dense stable neurologic deficit[14]

The spinal accessory nerve (SAN) is formed by 2 parts. The spinal or motor portion includes fibers that originate in the ventral horn of the upper 4 or more cervical segments of the spinal cord. The fibers may originate from as low as the fifth and rarely the seventh cervical segment. These fibers ascend lateral and parallel to the spinal cord, entering the skull through the foramen magnum. These fibers join the second or accessory component of the SAN that originates in the nucleus accumbens brain stem nucleus of the medulla oblongata in the posterior fossa. The 2 parts of the SAN, now joined, leave the skull through the jugular foramen in the same dural compartment as the vagus nerve. The nerve passes through the jugular foramen and then divides variably into the 2 original components.

The superior branch, also known as the accessory or internal branch, joins the vagus either directly or through the ganglion nodosum and then contributes to the pharyngeal, laryngeal, and cardiac sympathetic fibers.

The inferior branch, also known as the spinal or lateral branch, is essentially a pure motor nerve and innervates the sternocleidomastoid (SCM) and trapezius muscles.[29] It passes beneath the posterior belly of the digastric and the upper end of the SCM muscle along the internal jugular vein. It may travel either anterior or posterior to the occipital artery, and it communicates with the second cervical nerve before it enters the SCM.[30]

The nerve emerges from the posterior border of the SCM and obliquely crosses the posterior cervical triangle downward before entering the trapezius (see the image below). The posterior or lateral cervical triangle is bordered ventrally by the SCM, dorsally by the trapezius muscle, and caudally by the clavicle.[9] The length of the SAN can vary from 4-5 cm when it is lax (chin pointing forward) to 9-10 cm when it is extended (chin pointing to the opposite shoulder).[6, 31]

The coiled and redundant nature of the nerve as it traverses the posterior triangle allows for this variability in length. A recent cadaveric study compared this distal portion of the spinal accessory nerve with the less redundant proximal segment between the skull base and sternocleidomastoid muscle. The authors concluded that this coiled, redundant appearance was purely a functional characteristic of the nerve, as the 2 segments were identical under electron microscopy.[32]

Connections to the SAN are as follows:

• Greater auricular nerve (C2, C3): The greater auricular nerve may serve as a conduit between the SAN and the lesser occipital nerve and lower divisions of the trigeminal nerve.[6]

• Cervical roots (C2, C3, C4): The cervical nerve plexus connects the SAN to the hypoglossal nerve (via the ansa hypoglossi), stellate ganglion, and mandibular branch of the facial nerve. One to three branches of the cervical plexus run to the middle and lower trapezius independent of the SAN and rarely intermingle with it.[2]

• The SAN has a single fine branch that runs to the upper trapezius without any communication with cervical nerves. This branch does not communicate with the main trunk of the nerve that runs caudally and provides independent innervation to the upper muscle fibers of the trapezius.[2]

• Phrenic nerve

• Brachial plexus

In the posterior neck, the SAN has a superficial and unpredictable course beneath the superficial cervical fascia that makes it vulnerable to injury. It is embedded in fibrofatty tissue and is found in relation to a group of 5-10 superficial nodes.[9] Several anatomic landmarks and important variations in its course require careful consideration while identifying the nerve.

Important anatomic landmarks and variations of the SAN are as follows:

• Surface anatomy - Draw a line from the angle of the mandible to the tip of the mastoid process. The course of the SAN is indicated by bisecting this line at a right angle and extending the second line downward across the posterior triangle.[14]

• The greater auricular nerve has been used as a landmark to identify the SAN as it emerges from the posterior margin of the SCM muscle. The SAN is always found above the greater auricular nerve within a distance of 10.7 mm, with a standard deviation of 6.3 mm.[33]

• In the upper neck, 2 arrangements of the SAN have been described in relation to the internal jugular vein (IJV). In the more common (75-90%) anterior variant, the SAN nerve crosses in front of the IJV; in the less common (10-25%) variant, the nerve crosses behind the vein (see the first image below). Rarely, the SAN may traverse a divided IJV and appear to travel through the lumen of the vein (see the second image below).[34, 35] The SAN may also be palpable as a cord as it runs through the upper neck beneath the SCM muscle, dividing zone II into levels IIA and IIB. This often serves as a guide to the surgeon to begin nerve identification.

  Relationship of internal jugular vein to the spinal accessory nerve (SAN).

  Spinal accessory nerve (SAN) posterior to the internal jugular vein.

  Spinal accessory nerve (SAN) traversing a bifurcated internal jugular vein (IJV). (* = carotid artery, yellow arrow = SAN)

• As the nerve approaches the sternocleidomastoid muscle (SCM), it may perforate the cleidomastoid portion of the SCM (80%) or run posterior to it (20%).[36] The following 3 types of SAN innervation of the SCM have been described:

  • Type A, the nonpenetrating type

  • Type B, the partially penetrating type

  • Type C, the completely penetrating type

• The SAN is known to form a plexus prior to its insertion into the trapezius. Shiozaki et al described 5 types of innervation of the trapezius by the main trunk of the SAN and its branches, in which the number of branches that innervate the muscle ranged from 0-4.[29] More importantly, greater branching in the nerves seems to be associated with a thinner main trunk.

• Another important landmark for the surgeon is the relationship of the clavicle to the point of insertion of the SAN into the trapezius muscle. The SAN can be identified approximately 51.3 mm (standard deviation 17 mm) above the clavicle as it enters the anterior border of the trapezius. This is a constant landmark and is often helpful in identifying the distal end of the nerve.[33, 37]

• The superficial cervical vein, a branch of the external jugular vein, vascularizes the anterior margin of the trapezius muscle close to the site at which the main trunk of the SAN innervates the trapezius muscle. The superficial cervical vein is therefore a useful anatomic landmark that runs slightly inferior to the SAN.[29]

Cardinal symptoms associated with SAN injury

These include the following:

• Pain over the muscle
• Heaviness of the arm
• Depressed motor functions that consist of an inability to lift the shoulder girdle and abduct the arm ^[14]
• Late sequelae - Shoulder syndrome that consists of shoulder droop, atrophic trapezius, loss of abduction, paresthesias, and adhesive capsulitis resulting in a frozen shoulder

Clinical signs associated with SAN injury

Pain around the shoulder and neck can be assessed on a 10-point visual analogue scale (VAS). The mean intensity associated with SAN-related shoulder syndrome can average around 7 (range, 6-9).[36]

The affected shoulder is depressed, with inferior rotation of the lateral angle of the scapula.

Scapular “winging” can be accentuated by abduction of the arm.

Wasting of the trapezius may be evident in the upper part of the neck.[20]

Range of motion (ROM) can be restricted, as follows:

• Active abduction (30°-140° range)
• Active forward flexion (50°-180° range) ^[38]

Serial clinical examinations and electromyographic studies that fail to show an improvement in function are a clinical sign associated with SAN injury.

A dual or contributing nerve supply from the cervical plexus to the trapezius muscle that results in some retained motor function after SAN injury can make the diagnosis of an SAN injury difficult.

Subjective symptoms that result from trapezial dysfunction secondary to myofascial pain syndromes, contralateral paresthesias, and radiculitis can make diagnosis difficult.

Variations in presentations can also be attributed to the anatomic level of SAN injury, amount of collateral tissue damage, and subjective pain thresholds.[14]

High-resolution ultrasonography (HRUS) allows visualization of the normal SAN, as well as changes after accessory nerve injury. The SAN appears as a singular small (approximately 1 cm in diameter on ultrasound), hypoechoic tubular structure in the transverse plane and as a hypoechoic linear structure in the longitudinal plane. It is best identified in the posterior cervical triangle. In addition, HRUS is able to demonstrate hyperechoic and atrophic changes in the trapezius muscle, granuloma formation, and scar entrapment of the SAN in the region of the injury and the normal course of the nerve beyond. However, the actual transection of the SAN is not readily visualized by HRUS.[9]

A retrospective study by Powell et al indicated that, preoperatively, SAN injuries can more accurately be characterized by ultrasonography than by magnetic resonance imaging (MRI). SAN injuries in the study, most of which were iatrogenic, were surgically confirmed as stump neuromas and incomplete nerve injuries. The investigators determined that 95% of the preoperative ultrasonography reports, versus 24% of those derived from MRI, agreed with the surgical diagnosis.[39]  However, ultrasonography is operator dependent, so when ultrasonographic results are in doubt, MRI should still be considered.

Electrodiagnostic tests

Electrodiagnostic tests are most sensitive for the detection of nerve conduction impairment.[2]

Nerve conduction studies reveal prolonged latencies in nerve injury, while electromyography (EMG) may reveal signs of denervation or reinnervation, depending on the timing of the study.[20]

Electrophysiologic integrity of the SAN does not correlate well with the clinical symptoms and outcome measures for shoulder dysfunction.[3]

However, EMG has shown a positive correlation with range-of-motion (ROM) tests, particularly active shoulder abduction with contralateral head rotation as a test of strength. Consequently, this physical examination maneuver serves as a reliable and cost-effective tool for evaluating the degree of upper trapezius denervation.

Electrodiagnostic tests can be used in the management of SAN injury as follows:

• To monitor upper trapezius recovery of function

• To plan a physical therapy course to reduce postoperative morbidity[2]

• To confirm suspicions of SAN trauma that are related to traction or stretch injury of the nerve

• To monitor the SAN nerve intraoperatively for identification and preservation[3]

A retrospective study by Kim et al indicated that in a nerve conduction study of the SAN, the best recording site for the upper trapezius “is the midpoint between the C7 spinous process and the acromion,” while the optimal recording site for the middle trapezius is “the junction of middle and lateral thirds of the line between the root of scapular spine and the vertebral spine.”[40]

Some patients with severe SAN injury do not experience the degree of dysfunction that one would expect from their evaluations by EMG. In contrast, patients treated with nerve-sparing neck procedures often present with symptoms and signs suggestive of nerve impairment. These apparently contradictory results can be explained by the influence of several factors, including age, gender, dominant hand, presence of concurrent myopathy or neuropathy, condition of other synergistic shoulder girdle muscles, preoperative or postoperative radiotherapy, and anatomic variations of SAN contributions to trapezius muscle innervation.[15, 41]

Clinical evaluation of shoulder function

Clinical evalution of shoulder function includes the following:

• ROM assessment by goniometry to evaluate flexion and abduction of the shoulder joint
• Manual measure of muscle strength in the motions of elevation, flexion, and abduction ^[4]

The constant shoulder scale is as follows:

• This weighted test takes 10 minutes to perform and combines patient symptom scores (35%) and objective measures of active shoulder function (65%) and is a validated clinical assessment with established accuracy across many diseases that affect the shoulder.

• Scores range from 0-100, with higher scores indicating better shoulder function.[42]

The disease-specific quality-of-life (QOL) questionnaires are sensitive tools to evaluate shoulder function. Some more common questionnaires that have been validated for shoulder specific evaluations include the following:

• The University of Washington QOL scale – shoulder domain

• The neck dissection impairment index

• The shoulder disability questionnaire (SDQ)[43]

Intraoperative diagnosis is intuitive. A provoked movement of the shoulder in response to cautery or dissection must be carefully reviewed. Clinically examining the patient’s motor function postoperatively is best; in addition, widely explore the area during surgery to rule out an inadvertent injury.[14]

The approach to management of spinal accessory nerve (SAN) injury and trapezius muscle dysfunction is a multidisciplinary approach that involves conservative management, physical therapy, and surgical repair. See below for an algorithm regarding the management of SAN injury.

Indications for nonsurgical management include the following:[14]

• Serial clinical evaluation that shows improvement in shoulder function

• Demonstrable clinical/electromyography (EMG) improvement that indicates electrical regeneration

• Mild, tolerable subjective symptoms; pain; and minimal scapulohumeral dysfunction

Short-term options for nonsurgical therapy include the following:

• Nonsteroidal anti-inflammatory drugs (NSAIDs)

• Transcutaneous nerve stimulation

• Regional nerve-blocking procedures with local anesthetics

These options may have short-term benefits for relieving shoulder pain and improving function. The major drawbacks of short-term treatment options are that the efficacy is highly variable and short lived and nerve-blocking procedures require frequent repeat injections. This makes nerve-blocking procedures unfeasible for long-term management.[44]

Rehabilitation

Rehabilitation in the form of physical and occupational therapy can provide significant functional benefit and improvement of pain. The goal of rehabilitation is to promote wide passive range of motion and gradually active motion to prevent shoulder dysfunction due to adhesive capsulitis or frozen shoulder.[5]

Maintaining proper shoulder alignment is extremely important for effective rehabilitation because it reduces the mechanical tension on the scapula and shoulder girdle. Elevation and medialization of the scapula reduces the level of functional deficit of the trapezius muscle.[45]

The affected limb can be "unloaded" with the following recommendations to the patient:[20]

• Avoid carrying heavy weights on the affected side.

• Hook the thumb in a pants pocket or put the hand of the affected side in the pocket, which can provide significant relief.

• Use an arm sling to reduce pain; however, this can be counterproductive because it can prevent functional activities of the affected arm.

Orthoses (the Akman-Sari orthosis; see the image below) have been used for rehabilitation.

An orthosis provides pain relief and corrects malalignment, promoting appropriate positioning and better functioning of the remaining scapular musculature.

In one study, use of the orthosis has been associated with improvement, in terms of pain and ability to resume daily activities, in shoulder dysfunction after radical neck dissection in which the SAN was resected. In spite of this apparent improvement, the active shoulder abduction improved by only 5-25°; therefore, the improvement must not be mistaken for a return of trapezial function.[45]

Physical therapy (PT)

PT is a crucial component of recovery from SAN injury and shoulder dysfunction. It is essential both for patients who decline or are ineligible for surgical intervention and for those who are planning to undergo surgical repair of the SAN.

The goal of PT is to maintain or regain passive ROM about the shoulder. This serves to limit or prevent stiffness of the shoulder capsule and ligaments that can arise with malalignment of the shoulder and adhesive capsulitis. A PT protocol as suggested by Salerno et al is described as follows:[5]

• Passive forward elevation of the arm in the plane of the scapula in supine and half-sitting positions

• Passive forward elevation with the hands locked in supine and half-sitting positions and subsequent stretching movements

• External rotation with the elbow at the side and flexed at 90°

• Internal rotation with the hand placed behind the back

The investigators assigned physical therapy to one study group (PT group) and compared that group’s findings with the findings of another group that did not undergo physical therapy (non-PT group).[5] All patients had undergone neck dissection with anatomic preservation of the SAN. A significant improvement in mobility, pain, quality of life, and return to previous occupation was seen in the PT group. Approximately 63% of the PT group, as compared with 10% of the non-PT group, was able to achieve what is known as the zero position: 165° flexion at the shoulder joint in a plane 45° anterior to the coronal plane. Achievement of this position is necessary for common daily activities.

Note that the benefits of PT were not evident 1 month after initiating therapy but were significant after 6 months of aggressive PT.[5] The authors of this study emphasized early and prolonged PT, beginning within 1 month of surgery and lasting, on average, 3 months. Optimally, PT should be instituted within 1 month surgery and continue for at least 3 months; however, recent literature suggests that PT is also effective for late-diagnosed SAN injury.[46]

A randomized, controlled trial by McGarvey et al suggested that scapular strengthening exercises following SAN injury in neck dissection can, at least in the short-term, maximize shoulder abduction. In the study, patients who had undergone neck dissection received either 12 weeks of progressive scapular strengthening exercises or usual care. At 3-month follow-up, carried out on 52 patients (53 shoulders), shoulder abduction in the PT group was greater than in the usual-care patients by a statistically significant amount (+26.6 degrees).[47]

Ultimately, if nonsurgical management of the shoulder syndrome is pursued, aggressive PT is vital to long-term preservation of shoulder function and reduction of pain. Serial clinical examinations and EMG monitoring is useful to monitor SAN function. However, with a dense, stable clinical and electrical neural deficit, early operative intervention yields the best results.[14]

The decision to undergo surgical intervention in the absence of an obvious nerve injury or resection should be made only after sequential evaluations following the initial trauma fail to show spontaneous improvement in trapezius muscle function and confirm stable neurologic deficits.

Indications for surgical management are as follows:[14]

• Dense paralysis

• Absence of clinical or electrophysiologic improvement on serial examinations

• Distressing subjective symptoms, pain or severe scapulohumeral dysfunction

• Intraoperative identification of a nerve-in-continuity that does not show contractions on direct stimulation (nerve resection and reconstruction should be considered.)[38]

The surgical options are as follows:

• Neurolysis

• Primary nerve anastomosis

• Cable graft (autograft, biosynthetic nerve guide or Neurotube)

• Eden-Lange muscle transfer

Although serial examinations may differentiate patients who are appropriate for surgical reconstruction of the SAN from those patients who may be managed conservatively, in the case of clear SAN transection, immediate reconstruction at the time of nerve injury is recommended. In patients who present with trapezius muscle palsy with or without a history of neck surgery, the evaluating surgeon must determine the length of time that has elapsed from the initial onset of symptoms.

Previous studies have emphasized that the best outcomes of surgical repair occur if the surgery is performed within 3 months of the injury.[48, 49] Although this is a rational stance, other studies have reported good outcomes of SAN repair in patients with symptom duration of less than 20 months. Maldonado and Spinner reported on the successful use of a lateral pectoral nerve transfer, employing a supraclavicular approach, for SAN repair in two patients who presented 8 and 10 months postinjury.[50] The Eden-Lange muscle transfer procedure is recommended for cases of spontaneous trapezius palsy or cases in which the elapsed symptomatic time is greater than 20 months.[38]

Neurolysis

Neurolysis is an option for improving nerve function if no anatomical break in continuity of the nerve is found intraoperatively and conduction of electrical impulses is present. Intraoperative stimulation of the SAN should demonstrate transmission of an action potential to the neuromuscular junction, as indicated by trapezius muscle contraction. If the SAN is able to conduct nerve impulses, an extrafascicular neurolysis may be performed.[14, 38] While performing a neurolysis of a scarred segment of the nerve (neuroma), the surgeon must exercise extreme caution because of the risk of damage to underlying functional nerve fibers.

The completion of the neurolysis can be gauged by identifying redundant functional nerve fibers also known as the "bands of Fontana." Under normal circumstances, these bands protect nerve function through their redundancy by permitting physiological nerve stretching. Consequently, preserving these bands during a neurolysis is important. In addition, intraoperative nerve conduction studies, both proximal and distal to the scarred segment of nerve, aid in identification of functional nerve fascicles.[51]

In summary, minimal dissection and neurolysis of a neuroma facilitated by the above techniques is preferred to protect underlying functional nerve fascicles, while nonfunctional fascicles can be bypassed with grafting procedures similar to the ones described below.[51]

Nerve repair

If the SAN is in continuity and without electrically demonstrable transmission upon direct nerve stimulation, a resection of the nerve with the associated scar or neuroma is performed. This is followed by a primary end-to-end anastomosis. Nerve grafting is performed if the primary anastomosis produces unacceptable tension.

The basic surgical principles of both primary nerve anastomosis and nerve grafting are one and the same, as elegantly outlined in Dvali and Mackinnon in 2003, as follows:[51]

• Preoperative quantification of motor and sensory function

• Use of microsurgical technique, including magnification, instrumentation, and microsutures

• Emphasis on tension-free repair[52]

• Use of interpositional grafting when tension-free primary anastomosis is not possible

• Primary repair (anastomosis) when possible

• Delay in repair for approximately 3 weeks in cases in which primary repair is not optimal (eg, severe crush injury, stretch, or loss of nerve tissue) (This allows the surgeon to identify the true extent of the injured area, which is not always evident in the period immediately subsequent to injury.)

• Promoting early protected range of motion to facilitate nerve gliding and to prevent contracture formation.

Surgical loupes (with a minimum 4X magnification) and/or operating microscopes should be used for nerve repair. Usually, 9-0 or 10-0 nylon sutures are recommended for nerve anastomosis.[51]

Primary anastomosis and principle of tension avoidance

The proximal and distal free nerve endings are cut cleanly with a No. 15 surgical blade on a firm, flat background, or with a micro scissor, to prepare the ends for re-approximation. One epineural interrupted suture is loosely placed to bring the nerve ends together. The proximal and distal ends of the nerve fascicles are aligned with trimming, when necessary, so that the ends are not buckling. That is, the fascicle ends should lightly approximate one another in one line, rather than tight approximation leading to misdirected fibers. Subsequent interrupted sutures are placed.

Nerve elasticity causes retraction of the proximal and distal nerve segments after injury. This, in addition to the actual nerve injury, may create tension along the site of anastomosis. This tension must be avoided because it will lead to gaps between approximated fascicular ends. Ischemia and increased scarring are also complications of excess tension.[51] Of note, fixed positioning of the limb to alleviate tension is not recommended because stiffness of the joint may result, as well as nerve scarring and gapping when limb movement is eventually restarted.

Another tension-relieving technique that is now less popular involves extensive freeing of the proximal and distal nerve ends from surrounding soft tissue. Nerve mobilization less than 2 cm has been reported as acceptable and will not increase the risk of nerve devascularization.[53]

The intraoperative matching of corresponding proximal and distal nerve fascicles using anatomical, histochemical, and electrophysiological analysis is not fully described here. The reader is directed to Dvali and Mackinnon (2003) for an in-depth description of these techniques.[51]

Nerve grafting (autografts or biosynthetic nerve guides)

Several options are available for nerve repair when primary anastomosis will produce unacceptable tension. Grafting with nonvascularized or vascularized autologous nerves are both viable options. An example of a vascularized graft for SAN repair includes creation of a local flap in which the nerve graft is composed of the proximal sternocleidomastoid muscle and the greater auricular nerve. In this instance, the muscle and surrounding fascia provide vascularization to the nerve graft.[13]

Alternatives to autologous grafting include synthetic nerve guides or conduits. Also, nerve allografting with temporary recipient immunosuppression has been effectively used. However, autologous nerve grafting remains the criterion standard.[51]

The first description of cable grafting for repair of the SAN was reported more than 40 years ago.[2]

Immediate reconstruction of the nerve with microsurgical techniques and cable grafts can result in significant restoration of shoulder function.[54]

Cable grafts are recommended to bridge gaps greater than 2-3 cm.[38, 55]

The average size of grafts can vary from 2-5 cm.[38]

Longer intervals between injury and repair are associated with larger gaps due to nerve scarring and retraction. Longer grafts are associated with worse outcomes due to increased fiber misdirection and defective pruning.[36]

An autograft consists of a nerve segment taken from another nerve within the same patient to be interposed between the 2 cut ends of the SAN. Common donor grafts include the following:

• Greater auricular nerve

• Sural nerve

• Anterior branch of the medial antebrachial cutaneous nerve

• Lateral anti-brachial cutaneous nerve

• Thoraco-dorsal nerve

The advantages of biosynthetic nerve guides or Neurotube include the following:

• Avoidance of a nerve harvesting procedure with associated donor site morbidity

• High availability of nerve guides in various desired sizes

• Transparency of the nerve guides (allows easy nerve-end visualization)

• Rapid and simple procedure

• Outcomes similar to those of formal nerve repair, without associated donor site morbidity.[56, 57]

The principles of primary nerve anastomosis also apply to graft interpositioning. Both proximal and distal nerve ends must be cleanly cut so that the fascicles are visible. The nerve graft is interpositioned in the reverse direction (ie, the proximal graft end attached to the distal free end of the nerve and vice versa). Nerve fascicles progressively branch and diverge distally, so reverse interpositioning promotes "funneling" of the regenerating axons from proximal to distal through the graft.[51]

Mayer et al described an SAN repair procedure using nerve fascicles from the upper trunk that are associated with axillary nerve function. In the study’s five patients, the investigators found improvement in the active ROM in shoulder abduction from a mean 55° preoperatively to 151° postoperatively. Moreover, the average pain level, reported as 6.8 preoperatively on the visual analogue scale, fell to 0.8 following surgery.[58]

Because grafting requires nerve axons to regenerate across 2 sites (proximal and distal), outcomes were previously believed to be inferior to those with primary anastomosis (ie, with only one site of end approximation). However, this hypothesis has been disproved; a tension free graft inter-positioning will lead to superior outcomes when compared with a tension-laden primary anastomosis. In addition, thinner nerve grafts such as cutaneous nerve grafts are more easily revascularized than thicker grafts, thus leading to better outcomes.[51]

Eden-Lange procedure

Indications for this procedure include the following:

• A time interval of over 20 months after SAN injury

• Failed surgical reconstruction of the SAN

• Delayed diagnosis of a spontaneous trapezius palsy[38]

The principles of the procedure are as follows:

• The scapula is stabilized using the levator scapulae and rhomboid muscles, which consequently reinforce the action of the denervated trapezius.

• The levator scapulae and rhomboid muscles normally insert medially on the scapula. These insertion points are surgically transferred to more lateral scapular targets.[59] As a result, when these muscles contract, the traction stabilizes the scapula, particularly during abduction and anterior flexion of the shoulder (see the image below).

• Eden-Lange procedure.

As discussed above, rapid diagnosis and management of SAN injury is critical because surgical outcomes are dependent on the time that elapses from the initial onset of symptoms or nerve injury to surgical therapy. Physical therapy is always recommended to maintain passive range of motion (ROM) about the shoulder joint and prevent adhesive capsulitis. Surgery is indicated if serial clinical examinations as well as electromyelography (EMG) do not demonstrate SAN function. Electrodiagnostic testing at 12 weeks after onset of SAN injury will show recovering function if the nerve is simply neurapraxic rather than transected.[55] If SAN injury is discovered at the time of the initial operation, immediate surgical repair is recommended.

Specific recommendations related to each type of surgical repair have been discussed in previous sections (see Surgical therapy). Some additional recommendations include the following:

• A generous incision and wide surgical exposure facilitate identification of the nerve.[60]

• Anatomic landmarks are critical in identifying the proximal and distal ends of the SAN.

• Intraoperative nerve stimulation can be a useful tool to identify the SAN.

• Dissection of the distal stump of the nerve under the deep cervical fascia is relatively avascular and allows direct visualization of the nerve branches as they enter the trapezius. Efforts should be made to identify at least 1-3 branches.

• Reinnervation of the upper portion of the trapezius is vital for correction of shoulder droop and is of high priority. This prevents the dragging pain associated with shoulder syndrome. The paralysis of the middle and lower portions of the trapezius is partially compensated for by the levator scapulae and rhomboid muscles.[36]

The postoperative rehabilitation can vary depending on individual preferences and institutional protocols. However, the goal of postoperative care is early rehabilitation gradually graded from passive to active physiotherapy, along with shoulder immobilization for 2-4 weeks (or up to 6 weeks with casting following the Eden-Lange procedure), to facilitate appropriate shoulder alignment.[61]

Initial follow-up intervals should be every week for approximately 6 weeks and then every month thereafter. Documentation of symptoms and functional recovery should be made at each visit.[14] Aggressive physical therapy is vital after surgery in order to avoid fibrosis of the shoulder capsule and to maximize functional improvement. Physical therapy should continue for at least 3 months following surgery. At 6 weeks postsurgery, recovery of function is expected to be noticeable. On average, maximal recovery is evident at 6.5 months (range, 5-12 mo).[14, 55]

Nerve graft complications include neuroma formation or fibrotic ingrowth along the graft, preventing proximal axon sprouting and causing failure of graft. This complication may be found in patients who received radiotherapy postoperatively or in patients in which a long and nonvascular graft was used. Another complication is morbidity of the donor site that is associated with harvesting the autologous nerve graft.

Several factors affect spinal accessory nerve (SAN) function after injury such as the extent of injury, type of neck dissection, radiation therapy, interval between injury and repair, length or the vascularity of the graft.[41] Nerve repair with rehabilitation reduces pain, improves shoulder function, and quality of life.[1] Maintaining a high index of suspicion and accepting iatrogenic trauma as a possible cause of persistent shoulder symptoms is important. This approach will lead to early intervention, improved outcomes, and a better patient-physician relationship.

A study by Eickmeyer et al found that in 5-year, disease-free survivors of head and neck cancer, those who underwent SAN-sparing neck dissection had a higher level of functioning than did patients who were treated with SAN-sacrificing neck dissection, with shoulder flexion and abduction being poorest in the latter group. In addition, a correlation was found between reduced scores on quality-of-life measures and decreased shoulder flexion and abduction. Patients in the study who underwent no neck dissection had the highest level of function.[62]

A study by Park et al of patients who sustained iatrogenic SAN injury during lymph node biopsy found that, among 41 patients who underwent end-to-end repair and 82 patients treated with graft repair, 90% and 85%, respectively, achieved at least grade 3 recovery, as measured using the Louisiana State University Health Science Center (LSUHSC) grading system. Among 29 patients who underwent neurolysis—all of whom were treated with this modality when the SAN “was found in continuity with recordable nerve action potential (NAP) across the lesion”—more than 95% achieved LSUHSC grade 3 recovery or above.[63]

A study by Göransson et al found that at an average 10.2 years postoperatively, patients who had undergone either neurolysis, direct nerve repair, or nerve grafting for SAN injury achieved improvement in the mean active range of shoulder movement of, respectively, 44° (43%), 59° (71%), and 30° (22%). Atrophy of the trapezius muscle was absent or modest in, respectively, 75%, 44%, and 50% of patients, while pain was absent or controllable in, respectively, 63%, 56%, and 50% of patients. The study involved a total of 37 patients, with postinjury time to surgery ranging from 2-120 months.[64]

Performing a diagnostic biopsy on lymph nodes in the posterior triangle is controversial. Most isolated enlarged lymph nodes in young, healthy patients are reactive in nature. Even in established cases of head and neck cancer, only a small percentage of patients present with isolated metastasis to the posterior triangle.[60] Observation or fine-needle aspiration biopsy for persistent lymphadenopathy is reasonable. However, noting that persistent lymphadenopathy may represent relevant pathology such as lymphoma is important. The authors have found diagnostic lymph node biopsies to be very useful in our experience.

The surgeon performing a neck node biopsy must explain to the patient the potential for SAN paresis or palsy. Loupe magnification and bipolar coagulation have been recommended as the standard of care while performing surgery on neck nodes.[55] However, the importance of good surgical technique, knowledge of surgical landmarks, and relevant anatomic variations of the SAN cannot be overemphasized.

A study by Lanišnik et al indicated that intraoperative nerve monitoring of the SAN during modified radical neck dissection can lead to reduced postoperative shoulder disability, benefiting surgeons at the start of their learning curve and as they become familiar with the anatomical variation of the SAN. In the study, patients undergoing the dissection procedure were monitored on one side of the neck but not on the other, with the trapezius muscle demonstrating better EMG scores at 6 months postoperatively on the monitored sides than on the unmonitored sides.[65, 66, 67]

In the authors’ experience, indications for cervical lymph node biopsy include persistent lymphadenopathy after a trial of antibiotics, persistent lymphadenopathy associated with an inconclusive fine-needle aspirate, or the presence of risk factors for head and neck cancer or lymphoma.[14]

A future management measure may involve brief electrical stimulation (BES), which is used to improve recovery after peripheral nerve injury. Barber et al studied the use of intraoperative BES therapy on suspected spinal nerve injury (based on electromyographic changes) in patients who underwent level IIb and/or level V oncologic neck dissection. They found a decreased rate of clinically significant shoulder weakness in individuals treated intraoperatively with BES.[68]