11.1 Introduction

The spinal accessory nerve (SAN) is the main motor innervation of the trapezius and sternocleidomastoid (SCM) muscles. The SAN has a long course through the posterior neck, making it vulnerable to injury. SAN injury has been related to iatrogenic, traumatic, neurologic, and inflammatory injury. Injury may result in shoulder pain (most common) and limited range of motion (ROM). This could result in significant impairment in activities of daily living for patients. Iatrogenic injury during surgery may result in physician stress and management challenges. Early diagnosis and management may decrease these symptoms and reduce further costs. Comprehensive intervention will decrease both physician and patient stress.

11.2 Anatomy

The SAN has a long course originating in the upper cervical portions of the spine and terminating in the neck. The SAN pathway begins with two separate parts. The spinal and motor portions include fibers that originate in the ventral horn, typically from the upper four cervical (C1–C4) segments of the spinal cord. These fibers then ascend adjacent to the spinal cord and enter the skull via the foramen magnum. Following passage into the skull, the fibers then join the second or accessory component of the SAN that begins in the nucleus accumbens brain stem nucleus of the medulla in the posterior fossa. The joined components then exit the skull base through the jugular foramen and with a level of variability separate into the two original components. The components are identified as the superior and inferior branches. The superior branch (accessory branch) joins the vagus directly or via the ganglion nodosum and then contributes to the pharyngeal, laryngeal, and cardiac sympathetic fibers. The inferior branch (spinal branch) is a pure motor nerve and innervates the SCM and trapezius muscles. ¹ The SAN then travels deep to the posterior belly of the digastric muscle and crosses the internal jugular vein (IJV) near the upper limit of the SCM. This relationship of the SAN and IJV is variable—most commonly the nerve passes over the vein, but it infrequently passes deep and rarely the nerve splits around the vein. The SAN joins the second cervical nerve prior to insertion into the SCM. ² The nerve then exits from the posterior aspect of the SCM, and takes an oblique path through the posterior triangle of the neck downward and laterally where it inserts into the trapezius muscle.

11.3 Pathophysiology

SAN injury may result from multiple causes. Unfortunately, the most common source of neuropathy is tumor invasion or iatrogenic injury related to surgical dissection in the region of the SAN. Because of the SAN’s lengthy course around other critical structures from the skull base to the shoulder, it is vulnerable to injury at different locations. If there is malignant invasion anywhere along the nerve, it must be sacrificed for oncologic margins. Additionally, the nerve must be identified, retracted, and sometimes completely skeletonized during a standard surgery to remove cancer from the surrounding neck lymph nodes, referred to as a neck dissection.

Neck dissections can be categorized based on which compartments or “levels” undergo lymph node removal. These levels represent lymph node drainage basins in the submuscular recess along the carotid sheath. Neck levels II to IV are along the IJV from superior near the mastoid tip to inferior at the clavicle. Level V is represented as an area between the posterior border of the SCM, trapezius, and the clavicle.

SAN injury rates following neck dissections vary depending on the extent of disease that requires resection. This decision is frequently made during the surgery based on extent of malignant invasion and the need for oncologic margins.

Traditional radical neck dissection (RND) includes lymphadenectomy of levels II to V plus sacrifice of the SAN, IJV, and SCM in order to obtain oncologic resection of lymph nodes related to malignancies of the head and neck. Unsurprisingly, profound functional deficits have been reported in 60 to 80% of patients undergoing RND. ³

Modified radical neck dissection (MRND) still involves cervical lymphadenectomy of levels II to V, but aims to preserve at least one of the three critical structures if uninvolved by malignant lymphadenopathy. Reported rates of injury following MRND are about 42.5%. ⁴

Furthermore, selective neck dissections of levels II to IV with the aim to preserve all three critical structures without nerve sacrifice still have reported rates of injury as high as 30%. This is likely related to nerve traction or revascularization due to skeletonization. ⁵

Level II is an area of contention. This level is at the upper limit of the SCM, the posterior belly of the digastric muscle, and the IJV. The SAN creates a distinction between level IIa and level IIb. Level IIb is posterior to the nerve, and execution of the dissection may require extensive retraction on the nerve. Some experienced surgeons recommend avoiding level IIb unless clinically indicated as it may result in less morbidity. Frequency of postoperative morbidity following neck dissection decreases significantly from RND (46.7%) and MRND (42.5%) to selective neck dissection (25%). ⁴

The SAN is also vulnerable at the jugular foramen where it exits the skull base. Tumors such as jugular paraganglioma or meningioma may cause direct damage to the lower cranial nerves, or injury may result from surgical resection or radiation to the area.

SAN injury has many other less common causes. Other surgical procedures can lead to injury including excision of lymph nodes in the posterior triangle, neck mass excision, parotidectomy, carotid surgery, jugular vein manipulation, and facelift. ⁶

Traumatic insults can cause SAN. Penetrating and blunt trauma have been associated with SAN injury. Sports injury including hockey stick injury, wrestling, and whiplash can also cause SAN trauma. Neurologic disease processes such as Collet–Sicard syndrome, Vernet’s syndrome, poliomyelitis, motor neuron disease, brachial neuritis, and syringomyelia have been associated with SAN injury. Rarely, spontaneous isolated nerve injury has been reported. ⁷

During any of the events, the nerve could be transected, devascularized, or stretched. The nerve may become transected when exploring, devascularized when there is extensive skeletonization, or stretched during retraction. Ischemia may lead to segmental demyelinization resulting in loss of nerve function. ⁸ SAN injury leads to axonal degeneration resulting in muscle atrophy and contractures. This is evidenced by needle electromyography (EMG) and cicatrix formation. ⁷