Cranial nerve XI, the spinal accessory nerve (SAN), is vulnerable to injury, owing to its long and superficial course in the posterior cervical neck.  An important landmark in the neck, the SAN is considered to contribute most motor innervation to the trapezius muscle. Injury to the SAN results in varying degrees of shoulder dysfunction. This article reviews the important surgical landmarks and anatomic variations of the SAN, etiologies of SAN injury, and outcomes of surgical repair. Early identification of SAN injury and appropriate treatment can have a significant impact on overall shoulder function and, consequently, quality of life. (See the image below.)
History of the Procedure
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. 
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.  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. [4, 5]
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. [5, 6, 7] 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.  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.  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.  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.
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.  A large retrospective series reported clinical evidence of SAN injury in 1.68% of patients who undergo modified radical neck dissections as well.  Studies report that even in nerve-sparing procedures such as functional neck dissections, the reported incidence of SAN-related disability is approximately 30-40%. 
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.  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:
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)
See the list below:
Penetrating injury (glass cut or gunshot injury) 
Blunt injury: Sport-induced SAN injury due to external pressure has been reported. 
- A blow from a hockey stick
- 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
See the list below:
Collet-Sicard syndrome: Involves the lower cranial nerves (IX, X, XI, and XII) 
Vernet syndrome (ie, tumor near jugular foramen): Involves the lower cranial nerves IX, X, and XI 
Motor neuron disease
Spontaneous isolated nerve injury has also been reported. 
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.  SAN injury results in axonal degeneration, as evidenced by needle EMG and scar formation that are responsible for muscle atrophy and contractures. 
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). 
Evaluation of patients to detect SAN injury requires an organized clinical examination that may be supplemented with electrophysiologic nerve and muscle studies, as described below in the Workup section.
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.  Most of the following presenting symptoms and signs are attributable to denervation of the upper trapezius muscle:
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.
Diminished strength when performing regular daily activities (eg, placing dishes in overhead shelves, exercises that involve bearing weight on the shoulders).
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. 
The differential diagnoses of SAN injury are as follows:
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.
The indications for spinal accessory nerve repair are as follows:
Iatrogenic intraoperative injury or transection of the nerve (eg, radical neck dissection) 
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 
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.  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.
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.  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). 
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. 
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. 
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. 
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. 
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.  Several anatomic landmarks and important variations in its course require careful consideration while identifying the nerve.
Important anatomic landmarks and variations of the SAN (see the image below) are as follows:
See the list below:
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. 
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. 
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). [27, 28] 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.
As the nerve approaches the sternocleidomastoid muscle (SCM), it may perforate the cleidomastoid portion of the SCM (80%) or run posterior to it (20%).  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.  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. [26, 30]
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. 
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