Cranial nerves are attached to the brain and then travel outside the skull via foramina to innervate various structures. Cranial nerve XI is also known as the accessory nerve. According to the morphology characteristics of the cranial root of the accessory nerve, it is made of the union of two to four short filaments, making the cranial roots of the accessory nerve then two to nine rootlets join the spinal root to form the nerve. The cranial roots of CN XI could be possibly considered as part of the vagus nerve when factoring in the function of the two nerves, not only morphology. Both the cranial roots of the accessory nerve and the vagus nerve originate from nucleus ambiguus and dorsal nucleus of the vagus nerve and travel to the laryngeal muscles, supplying the motor fibers. As the accessory nerve travels down and away from the brain, the cranial and spinal pieces of the nerve come together to form the spinal accessory nerve (SAN). The SAN is formed by the fusion of cranial and spinal contributions within the skull base and exits the skull through the jugular foramen adjacent to the vagus nerve. The SAN descends alongside the internal jugular vein, coursing posterior to the styloid process, posterior belly of the digastric muscle, and sternocleidomastoid muscle (SCM) prior to entering the posterior cervical triangle. As the accessory nerve leaves through the jugular foramen along with glossopharyngeal nerve (CN IX) and vagus nerve (CN X), accessory nerve travels to the SCM, either superficial or deep, and then enters trapezius muscle, where a major trunk of the accessory nerve converges with C2, C3, or both. The traveling pathway of this nerve provides a functional significance to the structures in the posterior neck. However, the accessory nerve is prone and vulnerable to injury due to its long and superficial nature, Injury to the accessory nerve could be from blunt trauma, incidental, or most commonly, iatrogenic reasons.
The most common cause for cranial nerve 11 injury is iatrogenic, such as lymph node biopsies that involve the posterior triangle of the neck, neck surgeries including removal of tumor, carotid or internal jugular vein surgeries, neck dissection (including radical, selective, and modified), or cosmetic surgery (e.g., facelift) from the mechanical stress exerted on the neck due to positioning throughout the procedure. Other causes are penetrating trauma such as knife or gunshot trauma, blunt trauma from pressure, stress to the neck area, due to a vigorous movement, or acromioclavicular joint dislocation affecting SCM. Other possible sources of injury are neurological causes in which the nerve or the foramen it passes through are affected, leading to CN XI palsy. Examples are a tumor at jugular foramen which causes cranial nerve palsies such as Collet-Sicard syndrome, involving the lower cranial nerves IX, X, XI, and XII, and Vernet syndrome, involving the lower cranial nerves IX, X, and XI. Syringomyelia, brachial neuritis, poliomyelitis, and motor neuron disease are other possible causes of CN XI injury. Other examples are traction palsies to brachial plexus and thoracic outlet. Due to the various causes of this nerve injury, the age of presentation could be anywhere between a couple of months old to the elderly.
Cranial nerve XI injury mostly occurs due to iatrogenic causes that involve posterior and lateral cervical triangles surgeries such as lymph biopsy from the area. The high likelihood of SAN injury with posterior and lateral neck surgeries led to exploring the various options with neck dissections such as radical, selective, and modified neck dissections in different studies. According to a retrospective study by Popovski et al., SAN injury rate postoperatively is the highest, with radical neck dissections at 46.7% compared to selective neck dissections at 42.5% and 25% in modified neck dissections. Other studies suggest preservation of other structures such as the nerve, muscles, and veins would lead to fewer dysfunctions compared to more extensive procedures in the neck zones in which only the nerve preserved. Although other causes of cranial nerve XI injury are uncommon, they are explored as part of etiology.
The most common and primary complaint of SAN injury is pain, more specifically, shoulder pain and weakness. Radiation of pain is to the upper back, neck, and ipsilateral arm. Pain is exacerbated with weight on the injured shoulder without being supported. The traction and straining of the muscles rhomboids and levator scapulae that work to compensate for the nerve injury could lead to more pain and decreased strength in the injured side. The combination of the pain and decreased strength would limit the range of motion of the involved shoulder.
The most common sign is the noticeable asymmetry on inspection of the shoulder and upper back. The patient would present with a diminished ability to hold the shoulder in abduction motion, involved-shoulder drooping, and ipsilateral scapular winging (in which medial side of the scapula is more prominent than the unaffected side). A limited active range of motion might eventually progress to a worsening of the passive range of motion causing adhesive capsulitis. Other possible findings are atrophy of trapezius (depending on the length of time of the injury) and internally rotation of the humeral head.
Ultrasound such as high-resolution ultrasonography (HRUS) has been used to confirm the target nerve and visualize the structures surrounding the nerve. Ultrasound is meaningful in detecting some change to the muscles, such as atrophy, and reducing possible damage during the administration of injections and medication to the affected area by guiding to correct targeted area while visualizing with the ultrasound. Ultrasonography is not helpful in detecting the actual transection of the nerve.
Moreover, electromyography (EMG) and nerve conduction studies are unnecessary for the diagnosis; however, it would be helpful to distinguish and quantify the degree of damage by doing serial EMGs.
Electromyography (EMG) has shown that the trapezius muscle is the main muscle responsible for shoulder elevation and, by means of its upper bundle, it participates in the arm elevation movement. Nonetheless, this movement also involves the participation of the deltoid, supra-spinal, and infra-spinal muscles. For these reasons, arm elevation paresis secondary to spinal nerve mononeuropathy may be missed by clinicians because the movement may be compensated by the action of the other muscles responsible for arm elevation.
The algorithm for management is divided between immediate therapy and delayed management. The severity and the cause of the SAN injury would be factors in determining whether the treatment is surgical, such as reanastomosis and nerve grafting, or nonsurgical, such as nonsteroidal anti-inflammatory drugs (NSAIDs), nerve stimulation and local/ regional nerve blocking and physical therapy and rehabilitation. Immediate therapy should be considered for severe presentation such as penetrating traumas and iatrogenic traumas. In a study in which half of the patients received primary nerve repair and half of the patients received nerve graft, it was found that the recovery time ranged between 4 to 10 months. However, one of the most important contributors to a better prognosis is early referral and intervention which leads to a more accurate diagnosis. Also, early operative intervention has better results in regaining functionality; whereas, delayed diagnosis and treatment run the risk of less effective treatment and less predictable results.
A patient with injury to the SAN may present with neck pain, asymmetrical shoulders, inability shrug the shoulder or weakness in the neck area. It is important for the nurse practitioner and primary care provider to refer this patient to a neurologist to determine the cause and treatment. Coordination of care for the patient is crucial, with physical therapy and occupational therapy play a significant role in better recovery and improved outcomes.
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