Muscle | Origin | Insertion | Innervation | Action |
---|---|---|---|---|
Lower trapezius | T5-T12 SP | Scapular spine | Accessory n. (CN XI) C3 - C4 |
Scapula: Retraction, Depression, Upward rotation, Stabilizes scapula on thorax |
Middle trapezius | Aponeurosis of T1-T4 SP | Acromion | Accessory n. (CN XI) C3 - C4 |
Scapula: Retraction |
Sternocleidomastoid | Manubrium Medial third of Clavicle |
Mastoid process Superior nuchal line |
CN XI Accessory n. Cervical plexus C1 - C4 |
Unilateral: I/L cervical sidebend, C/L cervical rotation Bilateral: Head extension, Cervical Flexion, Assists in respiration, Prevents posterior translation during mastication SCJ stabilization |
Upper trapezius | Occiput SP C1-C7 |
lateral 1/3 of Clavicle | Accessory n. (CN XI) C3 - C4 |
Scapula: Elevation, Upward rotatino Neck: I/L sidebend, C/L Rotation |
CNXI Spinal Accessory Nerve
Overview
CNXI Spinal Accessory Nerve is a purely motor nerve that
Pathway
CNXI originates from the Medulla (cranial part or internal ramus) and the spinal cord (Spinal root or external ramus)1.
Cranial Root (Internal Ramus)
In the medulla, the cranial root arises from the caudal aspect of the nucleus ambiguous1. Specifically, the CNXI’s fibers emerge from the lateral medulla below the roots of the CNX vagus1.
Spinal Root (External Ramus)
The spinal aspect of CNXI arises from the Spinal Accessory Nucleus, which extends from C1 to C6 in the dorsolateral part of the ventral horn of the spinal cord1.
The spinal fibers then pass through the lateral funiculus, leaving between the dentate ligamenta nd the dorsal spinal roots1
The fibers then unite to form the spinal part and ascend together in the subarachnoid space and into the skull via the foramen magnum1
“The cranial and spinal roots unite and exit from the skull through the jugular foramen. The cranial portion then branches off as the internal ramus and joins the vagus nerve to supply the pharynx and larynx. The external ramus enters the neck between the internal carotid artery and the internal jugular vein. It then penetrates and supplies the sternocleidomastoid muscle and emerges near the middle of the posterior border of the muscle. The ramus then crosses the posterior cervical triangle to supply the trapezius muscle. In its course the nerve receives branches from the second, third, and fourth cervical nerves. The innervation of the sternocleidomastoid muscle may be more complex than is usually quoted. For example, there was residual sternocleidomastoid movement in 9 out of 15 cases where a division of the spinal components of the accessory nerve and the upper cervical motor roots was made as treatment for spasmodic torticollis [29]. It is postulated that this residual innervation was likely of vagal origin.”1
“The fibers from the cervical segments merge to form a trunk. The spinal root enters the posterior fossa of the cranium through the foramen magnum. Here, the spinal root briefly joins the cranial (internal) root to form a single nerve trunk, the accessory nerve. The accessory nerve exits the jugular foramen, heading toward the retrostyloid space.7 From here the nerve divides into the cranial and spinal portions of the accessory nerve. The spinal accessory nerve typically passes laterally to the internal jugular vein.9–11 Although less frequent, the nerve can also pass medially,11 through,11,12 or split around11 the internal jugular vein. The nerve then descends in an oblique manner, staying medial to the styloid process, stylohyoid, and digastric muscles.6 From here the nerve most commonly travels through the two heads of the SCM muscle,7 but could also travel between the two heads of the muscle.13 In this region, the nerve merges with fibers from C2 to C4.7,14–16 Then, the nerve travels obliquely through the posterior triangle toward the deep cervical fascia and trapezius muscle, staying in a fat layer in between the trapezius and levator scapulae muscles.6,13”2
Motor Supply
- C1 & C2 levels predominantly innervate the ipsilateral SCM muscle1.
- C3 & C4 levels primarily innervate the ipsilateral trapezius muscle1.
“The supranuclear innervation of the trapezius and sternocleidomastoid muscles probably originates in the lower precentralgyrus. The corticobulbar fibers to the trapezius are crossed, and thus one cerebral hemisphere supplies the contralateral trapezius muscle. The course of the fibers controlling the sternocleidomastoid muscle is unknown, but the fibers are thought to terminate chiefly in the ipsilateral nuclei. Three alternative pathways for this ipsilateral innervation have been postulated, as follows [26]:”1
- “The innervation may be truly ipsilateral with fibers descending ipsilaterally from hemisphere to nuclei”1
- “The pathway may start in one hemisphere and cross the corpus callosum to the opposite hemisphere, which, in turn, controls movement on the contralateral side.”1
- “A double decussation may exist. The pathway to the sternocleidomastoid muscle may cross from the hemisphere to the opposite pons and then return, below the first cervical level, to the side of the cord ipsilateral to the hemisphere of origin”1
“Others have suggested that the sternal head of the sternocleidomastoid (which turns the head to the contralateral side) receives bilateral cortical innervation, mainly from the ipsilateral cortex with a double decussation, whereas the clavicular head of the muscle (which tilts the head to the ipsilateral side) appears to have a distinct cortical representation [20]. These findings support the concept that each cerebral hemisphere controls muscles that result in movements toward the contralateral hemispace rather than simply controlling the contralateral muscle groups [20]. For example, only mild weakness of the right sternocleidomastoid muscle was noted with Wada testing of the right carotid artery; therefore, bilateral hemispheric innervation of the sternocleidomastoid must be present [19]. A weakness of only the sternocleidomastoid ipsilateral to the side of the carotid injection suggests that the ipsilateral hemisphere is more involved in the cortical innervation of the ipsilateral sternocleidomastoid muscle than the contralateral muscle [19]”1
DeToledo and David noted the following1:
- “The XI nucleus has a rostral and a caudal portion”
- “Analogous to the VII nerve nucleus, the rostral portion receives projections from both cerebral hemispheres, whereas the caudal portion is innervated preferentially by the contralateral hemisphere”1
- “The caudal XI nucleus innervates the ipsilateral cleidomastoid and trapezius with a predominantly crossed corticonuclear innervation”1
- “The rostral XI nucleus innervates both sternomastoids. Each rostral portion receives projections from both cerebral hemispheres”1
“Contrary to the long-held view that the representation of the neck muscles in the motor strip is close to that of the face, Thompson et al. found that the projection to both the ipsilateral and contralateral sternocleidomastoid muscles arises from an area of the cortex high up on the cerebral convexity close to the trunk representation and at a comparable level to the sensory innervation of the neck in the postcentral cortex [71]. The origin of corticomotor projections to this muscle lies in a region of the cortex located between the representation of the trunk and the upper limb. The authors noted that the corticomotor projection to the sternocleidomastoid muscle follows both a fast conducting monosynaptic contralateral pathway and an ipsilateral pathway that may be disynaptic [71].”1
“The spinal accessory, or simply the accessory, nerve is formed by the union of CN XI (see Cranial Nerves) and the spinal nerve roots of C3 and C4, and innervates the trapezius and the SCM muscles. Thus, dysfunction of this nerve causes paralysis of the SCM and the trapezius muscles.”3
“Isolated lesions to this nerve result from forces acting across the glenohumeral (G-H) joint. Combined lesions of the spinal accessory and the axillary nerve result from forces acting broadly across the scapulothoracic joint. These lesions are usually associated with fractures of the clavicle and/or scapula and subclavian vascular lesions.26–28”3
Dysfunction
“The corticobulbar fibers to the sternocleidomastoid are located in the brainstem tegmentum, whereas fibers to the trapezius are located in the ventral brainstem [44]. Thus, a ventral pontine lesion can cause supranuclear paresis of the trapezius with sparing of the sternocleidomastoid muscle.”1
Clinical Presentation
“The superficial course of the nerve also makes it susceptible to injury during operative procedures or blunt trauma,27 and to stretch-type injuries, such as during a manipulation of the shoulder under anesthesia.29 However, the stretch-type injuries do not always involve the SCM. Accessory nerve paresis can also result from a serious pathology such as a tumor at the base of the skull, or from surgery.26–28 Clinical findings for this condition include:”3
Examination
“A confirmatory test includes resisted adduction of the scapula while the clinician applies counterpressure at the medial border of the inferior scapular angle. This will highlight weakness on the affected side.”3
Localization of Lesions
Lesions to the spinal accessory nerve are rare. Most lesions to this nerve are iatrogenic, caused during radical neck dissection, modified radical neck dissection, or functional neck dissection2. These surgeries are commonly performed to remove cervical lymph nodes secondary to head and neck metastatic cancers2.
“Lesions of the spinal accessory nerve result in paresis and atrophy of the sternocleidomastoid and the trapezius muscles. Unilateral paresis of the sternocleidomastoid does not affect the position of the head at rest. There is weakness in turning the head to the opposite side, and when the patient flexes the head, it rotates slightly toward the unaffected side because the action of the opposite sternocleidomastoid muscle is unopposed. Bilateral sternocleidomastoid paresis causes weakness of neck flexion, with the head tending to fall backward when the patient attempts to stand erect.”1
“:Unilateral trapezius paresis due to spinal accessory nerve lesions affects predominantly the upper trapezius fibers (the part not supplied by the cervical plexus). The shoulder is lower on the affected side at rest, and the scapula is displaced downward and laterally with its vertebral border slightly winged. There is paresis of shoulder elevation and retraction, and the patient cannot raise the arm above the horizontal after it has been abducted by the supraspinatus and deltoid muscles. Trapezius atrophy often develops with chronic accessory nerve injury; rarely, neurogenic hypertrophy of the trapezius muscle may develop with accessory nerve injury, perhaps due to excessive spontaneous muscle activity [52]. Bilateral trapezius paresis results in weakness of neck extension, with the head tending to fall forward when the patient attempts to stand erect.”1
“Because the spinal accessory nerve is a purely motor nerve (except for some proprioceptive afferent fibers), nerve lesions do not result in sensory disturbance.”1
Supranuclear Lesions
“In hemispheric lesions resulting in contralateral hemiplegia, the trapezius muscle on the side of the hemiplegia is paretic. However, the head is turned away from the hemiplegic side indicating paresis of the sternocleidomastoid muscle on the side opposite the hemiplegia (i.e., ipsilateral to the cerebral lesion). Focal seizures, particularly those arising in areas 8 and 9 of the cerebral cortex, cause contraction of the ipsilateral sternocleidomastoid muscle as the head turns to the side contralateral to the epileptogenic lesion (adversive seizures). Head turning without head tilting, the most common pattern observed, has been explained as an isolated contraction of the sternomastoid portion of the muscle, with less contribution from the cleidomastoid portion, which tilts the axis of the head forward and toward the ipsilateral side while exerting less rotational force [34]. Because the sternocleidomastoid muscle receives a strong input from the ipsilateral cerebral hemisphere, cortical, capsular, and high brainstem lesions affecting corticobulbar fibers may result in decreased strength on the head turning away from the side of the lesion [51,77].”1
“Bender et al. suggest that the pathway for sternocleidomastoid control crosses from the hemisphere to the opposite pons and then returns to the side of the cord ipsilateral to the hemisphere of origin [5]. Geschwind points out that this second decussation may well be located in the decussation of the pyramids and that the side of sternocleidomastoid paresis in relation to the side of the hemiplegia may be of localizing significance [26]. That is, when the hemiplegic side is contralateral to the paretic sternocleidomastoid muscle, a hemispheric lesion is likely, the descending pathway being affected above its double decussation. On the other hand, hemiplegia associated with ipsilateral (to the hemiplegia) sternocleidomastoid paresis implies a lesion at or below the pontine level (i.e., after the first decussation on the descending pathway). Thus, medullary lesions affecting corticobulbar fibers may result in decreased strength on the head turning toward the lesion [51].”1
“Cases of dissociated weakness of the sternocleidomastoid and trapezius muscles with neurologic lesions have been described, including several syndromes that are of localizing value [49]:”1
- “Weakness of the trapezius on one side associated with weakness of the sternocleidomastoid on the other side (dissociated weakness) indicates an upper motor neuron lesion ipsilateral to the weak sternocleidomastoid and above the oculomotor complex.”1
- “Weakness of the trapezius on one side with sparing of the sternocleidomastoid muscles indicates a ventral brainstem lesion (the supranuclear fibers to the trapezius are ventral to those to the sternocleidomastoid), a lower cervical cord lesion (due to the somatotopic arrangement of the lower motor neurons and nuclear cell column of the trapezius being below that of the sternocleidomastoid), or a lower spinal accessory root lesion (sparing upper roots to the sternocleidomastoid).”1
- “Weakness of the sternocleidomastoid with trapezius sparing indicates a lesion of the lower brainstem tegmentum (sparing ventral supranuclear fibers to the trapezius) or upper cervical accessory roots (sparing lower cervical roots to the trapezius).”1
- “Weakness of the sternocleidomastoid and the trapezius muscles on the same side indicates a contralateral brainstem lesion, an ipsilateral high cervical cord lesion, or an accessory nerve lesion before the nerve divides into its sternocleidomastoid and trapezius branches.”1
- “Weakness in one muscle only (sternocleidomastoid or trapezius) may occur with lesions of the accessory nerve distal to its bifurcation (e.g., lesion of the branch of the accessory nerve to the trapezius).”1
“Head-turning movements have been analyzed in relation to the actions of the two divisions of the sternocleidomastoid muscle: the sternomastoid division and the cleidomastoid division [32]. The sternomastoid division runs obliquely and posteriorly from the sternum to insert on the occiput; it acts mainly on the atlantoaxial joint to rotate the head around a vertical axis so that the face points upward and outward over the contralateral shoulder. The cleidomastoid division originates from the clavicle and runs vertically to insert into the mastoid; it acts mainly on the middle cervical joints below C4 to tilt the axis of the head forward and toward the ipsilateral side, exerting little rotational force. Cleidomastoid contraction thus causes the face to point downward to the same side. When both divisions are activated simultaneously, there is an ipsiversive downward head tilt together with a contraversive rotation of the face. In 12 (75%) of 16 patients with surgically confirmed lateralized seizure foci, the face rotated upward and contraversive to the hemisphere of seizure origin, consistent with activation of the ipsilateral sternomastoid muscle. One patient showed a sustained, downward ipsiversive head tilt consistent with activation of the ipsilateral cleidomastoid muscle, and three patients had a combined ipsiversive head tilt and contraversive face rotation. No patient exhibited ipsiversive upward face rotation or contraversive head tilting, as would be expected if the contralateral sternocleidomastoid were activated. These findings indicate that hemispheric seizure foci activate one or both divisions of the ipsilateral sternocleidomastoid muscle and that accurate lateralization of the seizure focus is possible only when ictal head deviation is assessed in the context of the different actions of the two divisions [34].”1
Nuclear Lesions
“These relatively rare lesions result in paresis with prominent atrophy and fasciculations that affect the trapezius and sternocleidomastoid muscles. The motor neurons may be preferentially attacked (e.g., motor neuron disease) or may be involved by intraparenchymal high cervical cord-low medulla lesions (e.g., intraparenchymal tumor, syringomyelia). A nuclear localization is suggested by associated medullary or upper cervical cord dysfunction (see Chapters 5 and 15 ).”1
Infranuclear Lesions
Lesions within the Skull and Foramen Magnum
“Lesions of the spinal accessory nerve at the foramen magnum and within the skull also involve neighboring cranial nerves IX (glossopharyngeal), X (vagus), and XII (hypoglossal). Thus, the trapezius and sternocleidomastoid paresis is associated with dysphonia and dysphagia, loss of taste on the ipsilateral posterior third of the tongue, ipsilateral palatal paresis, an ipsilateral depressed gag reflex, ipsilateral vocal cord paralysis, and ipsilateral tongue paresis and atrophy (the protruded tongue deviates to the side of the lesion). A mass lesion in this location may also directly compress the upper cervical cord or lower medulla, resulting in “intramedullary” dysfunction. The most common etiologies for spinal accessory nerve involvement within the skull and foramen magnum include extramedullary neoplasms, meningitis, and trauma.”1
Jugular Foramen Syndrome (Vernet Syndrome) and Associated Syndromes
The spinal accessory nerve enters the jugular foramen accompanied by cranial nerve IX (glossopharyngeal nerve) and cranial nerve X (vagus nerve). Therefore, lesions at the jugular foramen (e.g., basal skull fracture, tumors, infections, sarcoidosis) [14,28,40,57,70] result in a syndrome (Vernet syndrome) characterized by the following:
- “Ipsilateral trapezius and sternocleidomastoid paresis and atrophy”1
- “Dysphonia and dysphagia with an absent or depressed gag reflex and a palatal droop on the affected side; paralysis of the homolateral vocal cord”1
- “Loss of taste over the posterior third of the tongue on the involved side”1
- “Depressed sensation (e.g., anesthesia) on the posterior third of the tongue, soft palate, uvula, pharynx, and larynx”1
“Lesions affecting the spinal accessory nerve just after it leaves the skull (in the retroparotid or retropharyngeal space) may also involve cranial nerves IX, X, and XII and the nearby sympathetic chain in variable combinations. The resulting syndromes vary and may also be seen with lesions of multiple cranial nerves within the skull and even with intramedullary lesions. Involvement of all four of the lower cranial nerves (IX through XII) results in the Collet–Sicard syndrome (all findings are ipsilateral to the site of injury), which consists of the following:”1
- “Paralysis of the trapezius and sternocleidomastoid (cranial nerve XI)”1
- “Paralysis of the vocal cord (cranial nerve X) and pharynx (cranial nerve IX)”1
- “Hemiparalysis of the tongue (cranial nerve XII)”1
- “Loss of taste on the posterior third of the tongue (cranial nerve IX)”1
- “Hemianesthesia of the palate, pharynx, and larynx (cranial nerves IX and X)”1
“A case of Collet–Sicard syndrome has been described associated with traumatic atlas fractures and congenital basilar invagination [32].”1
“Lesions of the retroparotid or retropharyngeal spaces may cause Villaret syndrome (affecting cranial nerves IX, X, XI, and XII, the sympathetic chain, and occasionally cranial nerve VII). Villaret syndrome has been described due to a carotid-artery dissection and an associated aneurysm [10].”1
“The descriptions of other syndromes involving cranial nerves IX through XII and the sympathetic chain vary widely in the literature; Table 13 1 describes some of these syndromes. Cranial nerves IX, X, XI, and XII may also be variably involved with neuralgic amyotrophy (Parsonage–Turner syndrome) [60].”1
Syndrome (Eponym) | Nerves Affected | Location of Lesion |
---|---|---|
Collet-Sicard | CN IX, X, XI, XII1 | Retroparotid space usually Lesion may be intracranial or extracranial1 |
Villaret | CN IX, X, XI, XII Plus the sympathetic chain CN VII is occassionally involved1 |
Retroparotid or retropharyngeal space1 |
Schmidt | CN IX & X1 | Usually intracranial before nerve fibers leave the skull; Occassionally inferior margin of jugular foramen1 |
Jackson | CN IX, X, & XI1 | May be intraparenchymal (medulla); Usually intracranial before nerve fibers leave the skull1 |
Tapia | CN X & XII (CNXI and the sympathetic chain are occassionally involved)1 |
Usually high in the neck1 |
Garcin (hemibase syndrome) | All Cranial Nerves on one side (often incomplete)1 |
Often infiltrative; Arising from base of skull (especially nasopharyngeal carcinoma)1 |
Lesions of the Spinal Accessory Nerve within the Neck
Isolated CNXI Spinal Accessory nerve palsy can occur in the neck due to Iatrogenic causes1. Surgery or internal jugular vein cannulation in the posterior triangle, carotid endarterectomy, surgery for cervicofacial lift, and coronary artery bypass surgery1. Radiation therapy has also been shown to cause CNXI Palsy1.
Bee stings can cause CNXI Palsy1.
Trauma can also cause isolated CNXI palsy such as: blunt trauma to the shoulder, attempted hanging, gunshot injury, shoulder dislocation, with other trauma, or after nerve stretch (i.e., quickly turning the head while the shoulders are tractioned by heavy hand-held objects)1.
Presentation
- Nerve injury in the neck proximal to the SCM results in ipsilateral weakness of the sternocleidomastoid and trapezius muscles without affecting other cranial nerves1.
- Nerve injury in the neck distal to the SCM result in trapezius weakness occurs in isolation1.
- Traction or other injuries to the posterior cervical triangle can cause CNXI injury distal to the SCM1
“Iatrogenic injury to the spinal accessory nerve is, thus, not uncommon during neck surgery involving the posterior cervical triangle, because its superficial course here makes it susceptible [11]. In a retrospective review of 111 patients with spinal accessory nerve injury, the most frequent injury mechanism was iatrogenic (103 patients, 93%), and 82 (80%) of these injuries involved lymph node biopsies [42]. Eight injuries were caused by stretch (five patients) and laceration (three patients).”1
“Patients may develop manifestations of neurovascular compression upon arm abduction, associated with unilateral droopy shoulder and trapezius muscle weakness caused by iatrogenic spinal accessory neuropathies following cervical lymph node biopsies [1]. One patient developed a cold, numb hand with complete axillary artery occlusion when his arm was abducted to 90 degree. Another patient complained of paresthesias in digits 4 and 5 of the right hand, worsened by elevation of the arm, with nerve conduction findings of right lower trunk plexopathy. These two cases demonstrate that unilateral droopy shoulder secondary to trapezius muscle weakness may cause compression of the thoracic outlet structures [1].”1
“Neuromyotonia of accessory nerve, characterized by transient involuntary tonic contractures of the sternocleidomastoid muscle with head movements, has been described after radiation therapy [76]. These head movements, which occur either spontaneously or are triggered by movements, are associated with muscle hypertrophy and delayed relaxation of the affected muscle.”1
“Weakness of neck extension against gravity with or without involvement of neck flexion has been called the floppy head syndrome [45], the dropped head syndrome [30,68], or head ptosis [74]. The etiologies for this syndrome include myasthenia gravis (which often affects neck flexors more than extensors), Lambert–Eaton myasthenic syndrome, motor neuron disease, chronic inflammatory demyelinating polyneuropathy, syringomyelia, polymyositis, dermatomyositis, facioscapulohumeral muscular dystrophy, carnitine deficiency, LMNArelated congenital muscular dystrophy (L CMD) (a disorder characterized by infantile-onset myopathy due to mutations in the lamin A/C [LMNA] gene), adult-onset nemaline myopathy, primary amyloidosis, hypothyroidism, hyperparathyroidism, Parkinson disease, choreoacanthocytosis, Huntington disease, after radiotherapy for Hodgkin disease, with selumetinib (a selective non-ATP competitive small-molecule inhibitor of mitogen-activated protein kinase) treatment for uveal melanoma and non-small cell lung cancer, and a restrictive noninflammatory myopathy predominantly affecting the cervical paraspinal muscles, resulting in relatively isolated neck extensor weakness (isolated neck extensor myopathy)”1
Intervention
“Conservative intervention for this condition involves patient education to avoid traction to the nerve, specific upper, middle, and lower trapezius strengthening, neuromuscular electrical stimulation to the upper and lower trapezius, cervical proprioceptive neuromuscular facilitation (PNF) techniques, scapular PNF techniques, prone-on-elbows scapular stabilization exercises (see Chapter 25), and shoulder elevation strengthening. McConnell taping is also used to facilitate the middle and lower trapezius muscle.29”3