Trigeminal Nerve: Mandibular Division (Cranial Nerve V3)

The mandibular division of the trigeminal nerve (CN V3) carries a branchial motor and a general sensory component. The sensory pathway travels via five orocutaneous nerves: auriculotemporal, meningeal, buccal, lingual, and inferior alveolar. Loss of the first two nerves leaves little functional deficit, and compensation readily occurs; however, severe burns to the cutaneous distribution of these nerves may occur with the use of curling irons and other heated hair grooming devices. Patients are instructed to take care in daily hairdressing.

Loss of the buccal, lingual, and inferior alveolar nerves affects the sensory feedback loop of the initial aspects of swallowing. The food bolus is not detected in the nonsensate area, affecting the preparatory phase of oral swallowing. Grafting of these nerves is recommended when possible; however, because these nerves are usually resected intracranially as the nerve exits the dura, it is impossible to identify the appropriate proximal fibers for nerve grafting. Swallowing therapy is the mainstay of rehabilitation, and allows compensation in most patients.

The motor division of CN V3 provides function to six muscles: tensor veli palatini, tensor tympani, medial pterygoid, lateral pterygoid, masseter, and temporalis. The medial pterygoid nerve is the first branch off CV V3 after it exits the foramen ovale. Before it reaches the medial pterygoid muscle, it gives a branch to the tensor veli palatini and to the tensor tympani, both of which pass through the otic ganglion without synapsing. Isolated tensor veli palatini paralysis is compensated for by the action of the levator palatini muscle with minimal palatal dysfunction. Aural attenuation is decreased with loss of tensor tympani function, but is adequately compensated for by the action of the stapedius muscle as long as CN VII has been preserved. Therapy for loss of tensor tympani or stapedius function is usually unnecessary.

Just past the otic ganglion, CN V3 gives off branches to the lateral pterygoid and the masseter muscle. Two or three deep temporal nerve branches arise in the same region and pass up into the temporalis muscle. As the inferior alveolar nerve enters its canal in the mandible, the final motor branches of CN V3 depart from it and go to the mylohyoid muscle and anterior belly of the digastric muscle. If the contralateral muscles of mastication are intact, patients usually compensate with little trismus or chewing dysfunction. Often, early trismus associated with exposure of the temporomandibular joint during surgery in this region may be overcome by propping the mouth open with a stack of tongue depressors for several minutes two or three times daily. The number of tongue depressors is gradually increased until adequate opening is achieved. Shifting of the mandibular arch is usually corrected over time with this therapy and increasing use of the mandible.

Atrophy of the temporalis muscle is an inevitable sequela of CN V3 sacrifice. For this reason, attempts at masseter or temporalis transfer for facial nerve rehabilitation are doomed to failure and should not be attempted. By 1 year, noticeable temporalis wasting occurs, and results in a significant cosmetic defect. Most patients desire placement of a silicone or methylmethacrylate implant beneath the residual temporalis muscle (Fig. 47-2). Care must be taken to contour the implant where it abuts the lateral orbital rim, or else a residual crease results in this region.

FIGURE 47-2 Significant atrophy of temporalis has occurred 1 year after infratemporal fossa dissection with sacrifice of CN V3 and mobilization of temporalis muscle.

(From Netterville JL, Civantos FJ: Rehabilitation of cranial nerve deficits after neurotologic skull base surgery. Laryngoscope 103(Suppl 60):45-54, 1993.)

Abducens Nerve (Cranial Nerve VI)

During lateral transtemporal approaches to the cranial base, the abducens nerve is often encountered in its course along the clivus and medial aspect of the petrous apex. Its sole function is to supply somatic motor innervation to the lateral rectus muscle. After exiting the brainstem, the abducens nerve lies along the clivus and enters Dorello’s canal inferomedial to the root of the trigeminal nerve. It passes beneath (rarely above) the superior sphenopetrous ligament in a sulcus on the petrous apex. It courses through the cavernous sinus lateral to the carotid into the superior orbital fissure. Injury may occur anywhere along this course and result in lateral rectus muscle dysfunction with limitation of lateral gaze with associated diplopia. CN VI is exquisitely sensitive to pressure injury in the cavernous sinus, and great care must be taken not to pack the cavernous sinus vigorously to control bleeding because this may result in permanent lateral rectus palsy despite anatomic integrity of the nerve. If the nerve is known to be intact, treatment is conservative; prism glasses allow compensation until function returns, usually within 3 to 4 months. Botulinum toxin injection into the ipsilateral medial rectus has been used successfully to relieve diplopia by weakening the antagonist action of the medial rectus muscle.⁴ When it seems that permanent palsy has occurred, superior and inferior rectus muscle transposition may be performed to improve lateral gaze function.⁴

Glossopharyngeal Nerve (Cranial Nerve IX)

The glossopharyngeal nerve has branchial motor, visceral motor, visceral sensory, general sensory, and special sensory components. Its branchial motor component is limited to the stylopharyngeus muscle, which elevates the pharynx during swallowing and speech. Isolated loss of motor fibers to this muscle results in little swallowing dysfunction; however, when combined with the loss of general sensory fibers of the glossopharyngeal plexus and vagal motor fibers, severe swallowing deficits result.

The visceral motor component of the glossopharyngeal nerve exerts parasympathetic control over parotid salivary secretion. As CN IX exits the skull base through the pars nervosa of the jugular foramen, it forms superior and inferior ganglia that contain nerve cell bodies that mediate general, visceral, and special sensory function. Parasympathetic fibers leave the inferior ganglion and pass into the middle ear as the tympanic nerve. In the middle ear, these fibers form the tympanic plexus; branches from the tympanic plexus form the lesser petrosal nerve, which passes back up through the floor of the middle cranial fossa, travels intracranially, and descends through the foramen ovale in the greater wing of the sphenoid bone where it synapses at the otic ganglion. Postganglionic fibers travel with the auriculotemporal nerve to reach the parotid gland. Injury to these fibers may occur at many levels and lead to decreased parotid salivary flow; rarely, this leads to chronic parotitis.

The general sensory component provides afferent feedback from the base of tongue and lateral pharyngeal wall, and the external ear and inner aspect of the tympanic membrane. The sensory fibers to the base of tongue and pharynx run in a plexus on the undersurface of the stylopharyngeus muscle and pierce the middle constrictor to reach the mucosa of the base of tongue. Disruption of this glossopharyngeal plexus causes significant delay in the oropharyngeal phase of swallowing on the ipsilateral side. In glomus tumor surgery, the glossopharyngeal nerve is taken at the pars nervosa in the jugular foramen precluding nerve grafting. Isolated, unilateral CN IX deficits are well compensated for with swallowing therapy that focuses on maintaining passage of the food bolus adjacent to the contralateral sensate side of the pharynx using a chin-tuck and head-turn maneuver toward the side of the deficit. When this deficit is combined with the loss of CN X and XII at the skull base, dysfunction becomes severe. Rehabilitation of this combined loss involves correction of glottal incompetence with thyroplasty and intensive swallowing therapy.

The final function of CN IX is visceral sensory from the carotid body and carotid sinus by way of the nerve of Hering. Disruption of CN IX at the skull base causes loss of the carotid sinus reflex on the ipsilateral side and was originally described for the treatment of carotid sinus syndrome.⁵ Unilateral loss does not interfere with the control of blood pressure and pulse, presumably because of the presence of an intact reflex on the contralateral side. When there is bilateral alteration of this system, acute elevation of blood pressure to greater than 220 mm Hg may be seen within a 60 second period. Preoperatively, one should consider the potential for a bilateral deficit in any patient who has had surgery on the contralateral neck where CN IX fibers may have been disrupted, such as in carotid endarterectomy. Appropriate intraoperative management of this scenario includes administration of a pure α-blocker, such as phenoxybenzamine hydrochloride. Sodium nitroprusside may be added for further control. The patient is weaned to clonidine hydrochloride in the postoperative period. Permanent maintenance of blood pressure may be required. Consultation with an intensivist in the preoperative period is strongly recommended if a bilateral loss is anticipated.

Vagus Nerve (Cranial Nerve X)

Of the lower cranial nerves, the vagus is most intimately involved in control of the airway and swallowing function. Isolated loss of vagal function yields a far greater deficit than the loss of any other single lower cranial nerve. The vagus nerve carries general sensory, visceral sensory, visceral motor, and branchial motor fibers. The general sensory component provides afferent signals from the external auditory canal, tympanic membrane, supraglottic larynx, and lateral pharyngeal wall. Two ganglia are formed as it exits the skull base through the pars nervosa of the jugular foramen: the superior (jugular) ganglion lies in the jugular foramen, and the inferior (nodose) ganglion is located 1 to 2 cm outside the foramen. The sensory fibers from the supraglottic larynx form the superior laryngeal nerve, which passes deep to the external and internal carotid arteries to join the vagus at the level of the inferior ganglion. Isolated loss of this nerve can result in swallowing difficulties; it is grafted on rare occasions in selected patients. Most often, the vagus is resected so proximally at the skull base that grafting is technically impossible. With time and swallowing therapy, compensation for the sensory loss occurs.

The visceral sensory and branchial motor components of CN X provide afferent sensory and parasympathetic function to the pharynx, larynx, trachea, esophagus, thoracic viscera, and abdominal viscera distally to the level of the splenic flexure of the colon. Unilateral loss of vagal function may cause decreased gastroesophageal motility, loss of lower esophageal sphincter tone, and delayed gastric emptying owing to inadequate pyloric sphincter function. Subsequent regurgitation during the early postoperative period is common, and may limit adequate nutrition, cause transient increases in intracranial pressure and potential for cerebrospinal fluid leak, and lead to life-threatening aspiration pneumonia. Pain medication and anticholinergic drying agents add further to gastric stasis. Treatment consists of administration of a motility agent, such as metoclopramide hydrochloride, and a temporary decrease in feeding rate. Over time, these symptoms gradually improve. If feeding intolerance continues, a jejunal feeding tube may be necessary. Rarely, usually in cases of bilateral vagal injury, total loss of lower esophageal sphincter tone can occur and may require Nissen fundoplication.

The branchial motor component of CN X provides motor function to the palate, pharynx, and larynx, with the exception of the stylopharyngeus muscle (CN IX) and the tensor veli palatini muscle (CN V3). These fibers depart the vagus in three distinct bundles: the pharyngeal branch, the external branch of the superior laryngeal nerve, and the recurrent laryngeal nerve. The pharyngeal branch departs the vagus as the inferior (nodose) ganglion passes over the internal carotid, deep to the external carotid artery, and enters the pharynx at the upper border of the middle constrictor. Damage to this branch results in unilateral palatal and pharyngeal paralysis, which causes a loss of lateral wall motion on the affected side and an ineffective sphincter for closing the nasopharyngeal port; this leads to nasal regurgitation and hypernasal speech. In the early postoperative period, unilateral palatal paralysis causes no significant morbidity relative to more immediate concerns regarding airway and swallowing function. The pharyngeal dysfunction responds well to swallowing therapy. Subsequent velopharyngeal insufficiency (VPI) resulting in nasal regurgitation and hypernasal speech is embarrassing and quite bothersome to most patients.

Nonsurgical approaches to VPI have included speech and swallowing therapy, palatal lift prostheses, and palatal obturators. Various surgical procedures have been described for the treatment of VPI secondary to cleft palate, including pharyngeal augmentation and pharyngoplasty. The most popular of the pharyngoplasty techniques is the superiorly based pharyngeal flap as described by Jackson.⁶ Vagal injury at or above the jugular foramen causes paralysis of not only the palate, but also the pharyngeal constrictors, resulting in loss of lateral wall motion on the affected side. Superiorly based flaps and pharyngeal augmentation are used to address VPI in cleft palate patients and are designed to leave an open lateral port. Lateral pharyngoplasty techniques⁷ are adynamic, and do not recreate lateral pharyngeal wall movement. A simple alternative technique that addresses the palatal and pharyngeal component of VPI in skull base patients is to close the lateral port by adhering the palate on the affected side to the posterior pharyngeal wall. The chief advantage of this procedure in patients who may already have multiple cranial nerve deficits and abnormal swallowing is that it does not alter pharyngeal anatomy with long mucosal flaps, and does not carry the risk of pharyngeal stenosis. Unilateral palatal adhesion successfully eliminates hypernasality and nasal regurgitation, and has become the procedure of choice for the correction of velopharyngeal incompetence in neurotologic skull base patients.^8,9

Palatal adhesion is usually performed several months after resection when swallowing function has stabilized, and when it is certain that an injured but intact vagus nerve has not recovered. Preoperative assessment by nasopharyngoscopy with either a rigid or a flexible scope shows unilateral closure of the nasopharynx. Under general anesthesia, the palate is exposed with a Dingman mouth gag. The paralyzed hemipalate and posterior pharyngeal wall are injected with epinephrine. Care is taken to inject just below any residual adenoid tissue. A transpalatal incision is performed in the area of the palatal crease that forms with normal palatal elevation, and the posterior pharyngeal wall is viewed through this incision (Fig. 47-3). A similar incision is created into the posterior pharyngeal wall down to the prevertebral fascia. The pharyngeal mucosa is elevated for just a few millimeters all around to create an edge to which the nasopharyngeal mucosa of the palate is sewn. Multiple deep mattress sutures are used to suture the nasopharyngeal surface of the palate to the posterior pharyngeal wall (Fig. 47-4). The oral surface of the palate is closed on itself, creating a unilateral palatal adhesion (Figs. 47-5 to 47-7).

FIGURE 47-3 Transpalatal incision is made in area of palatal crease that forms with normal palatal elevation, and posterior pharyngeal wall is viewed.

FIGURE 47-4. Incisions are made in palate and posterior pharyngeal wall. Multiple mattress stitches are placed to complete adhesion.

FIGURE 47-5. Superior endoscopic view of left-sided palatal adhesion.

FIGURE 47-6 Sagittal view of completed palatal adhesion.

FIGURE 47-7. A and B, Endoscopic view from above of right-sided palatal adhesion during quiet respiration (A), and showing complete closure during production of pressure consonant (B).

FIGURE 47-8. Alar window is positioned as shown, taking care to preserve inferior alar strut.

FIGURE 47-9. Depth gauge is used to medialize true vocal fold based on auditory and visual feedback.

Postoperatively, the patient is immediately allowed to take a liquid diet and is discharged from the hospital as soon as pain control is adequate. The only complication that has occurred from this procedure is a wound dehiscence that granulates over several months, producing a secondary adhesion with minimal VPI. Sleep apnea has not been seen as a complication of this procedure. Improvement of nasal regurgitation and reduction in hypernasal speech occur in all patients.^8,9

The effect of paralysis of the superior, middle, and inferior constrictor muscles causes more morbidity than the palatal dysfunction. As the food bolus passes into the oropharynx, the paralyzed side dilates laterally and forms a pseudopocket that collects the bolus. The normal contraction on the contralateral side pushes the bolus into this region, rather than down into the hypopharynx. This delay interrupts the normal timing of the swallowing event so that when the larynx reopens, the food bolus, which should have been in the esophagus, is still partially in the hypopharynx, where it is then aspirated. Treatment is centered around an intensive swallowing therapy program in which a head positioning technique is used to obliterate physically the paralyzed side and force the food bolus onto the normal side. Avoidance of a tracheotomy, if possible, further hastens recovery of swallowing function because the tracheotomy would interfere with laryngeal elevation. Loss of cricopharyngeal relaxation combined with an indwelling tracheotomy tube (particularly a cuffed tube) further hinders the passage of the food bolus through the esophageal inlet and encourages aspiration.

The second motor branch of CN X is the superior laryngeal nerve. It provides motor control to the ipsilateral cricothyroid muscle. Loss of this nerve results in decreased vocal range, which is usually a problem only for professional voice patients. Because the vagus is usually resected or injured at the skull base, patients have superior and recurrent laryngeal nerve paralyses, which are rehabilitated at the same time with silicone elastomer (Silastic) medialization thyroplasty and arytenoid adduction.

The third motor branch of the vagus is the recurrent laryngeal nerve, which provides innervation to the intrinsic laryngeal musculature and the cricopharyngeus muscle. True vocal fold paralysis and lack of cricopharyngeal relaxation result from resection or neural injury at the time of surgery. The resultant glottal incompetence leads to a weak, breathy voice and an inefficient cough. This deficit combined with lack of cricopharyngeal relaxation results in aspiration and poor pulmonary hygiene. Tracheotomy has been universally performed to protect the airway until early swallowing rehabilitation can be accomplished. From an airway perspective, most patients with high vagal injury tolerate a unilateral vocal fold paralysis, making tracheotomy generally unnecessary; for the reasons discussed earlier, tracheotomy prolongs swallowing rehabilitation and adds morbidity to the postoperative course. Silastic medialization with arytenoid adduction has been the procedure of choice for addressing vocal fold paralysis in these patients.¹⁰ Although cricopharyngeal myotomy is not routinely necessary in these patients, it has been shown to decrease aspiration and promote early swallowing.¹¹

The primary goal for vocal fold medialization in skull base patients is (1) to provide glottal competence, (2) to provide an efficient mechanism for coughing, and (3) to give support and volume to the voice. Generally, most patients with a unilateral vocal fold paralysis undergo a absorbable gelatin sponge (Gelfoam) injection postoperatively regardless of whether the nerve was taken. This injection lasts approximately 6 to 8 weeks, and greatly facilitates speech and swallowing rehabilitation while the nerve regains function or until Silastic medialization and arytenoid adduction may be performed. It is prudent to wait 2 to 3 months before proceeding with thyroplasty because denervation vocal fold atrophy occurs over several weeks, which alters the size of the Silastic implant and the degree of arytenoid adduction necessary to achieve good voice and airway results. Several weeks postoperatively, the patient should return for airway evaluation, videostroboscopy, and airflow measurements. A Silastic medialization under local anesthesia is performed. The technique is outlined in the following paragraphs and has been described elsewhere.^10,12–14

Under local anesthesia, a midline horizontal incision or an extension of the cervical portion of the skull base incision is made overlying the midpoint of the thyroid cartilage. The sternohyoid muscle is divided at its medial attachments to the hyoid bone superiorly. A perichondrial flap is created from the midline back to the posterior edge of the thyroid cartilage, elevating the remaining attachments of the sternohyoid muscle and the thyrohyoid muscle with the flap, and exposing the inferior edge of the thyroid ala. A rectangular window is outlined so that the anterior extent lies 5 mm back from the anterior commissure in women and 7 mm back in men. The window is placed as low as possible, leaving an inferior 3 mm thyroid cartilage strut that is wide enough not to fracture when the implant is placed (Fig. 47-8).

The final outline of the window is usually 6 mm in height and 13 mm in length. The location of the implant relative to the anterior commissure is based on the angle of the thyroid ala. With an increased thyroid cartilage angle as seen in women, the implant must be brought closer to the anterior commissure, and must have an increased slope to compensate for the wider angle. If the implant is placed too far anteriorly, overmedialization of the anterior commissure occurs, producing a strained quality to the voice. Using 4× loupes, a high-speed drill with a 2 mm cutting burr is employed to drill away the outline of the window. The cartilage may be partially ossified, particularly inferiorly and posteriorly. The window is usually 3 to 4 mm thick anteriorly and 5 to 7 mm thick posteriorly.

Next, the long and short phonosurgery intralaryngeal elevators (Xomed, Jacksonville, MS) are used to elevate the inner perichondrium in all directions except anteriorly. Medialization is attempted, but it is rarely possible to achieve the required medialization with the inner perichondrium intact. The superior, posterior, and inferior margins of the perichondrium are incised discretely without injuring the lateral fascia of the thyroarytenoid muscle just deep to this. Branches of the superior laryngeal artery and vein can usually be seen lying just under this fascia. Although some surgeons fear that dividing the perichondrium leads to implant extrusion, this has not occurred in several hundred medialization procedures using this technique.¹³

The depth gauge is used to medialize the cord, and voice quality and cord position are assessed (Fig. 47-9). Based on these visual and auditory data, an implant is carved to appropriate dimensions from a preformed Silastic block (Fig. 47-10). Its inferior border is thicker than the superior border, and the posterior border is thicker than the anterior border. This creates an even medialization of the vocal fold with the point of maximum medialization at the lower edge of the window. Good alignment of the true vocal cord in the midline is usually obtained with little medialization of the false cord. All edges of the Silastic block are beveled to allow ease of insertion through the window. The average size of the block that is used when performing this under general anesthesia is 2 to 3 mm thick anteriorly and 5 to 7 mm at the point of maximal medialization, with an overall length of 13 to 18 mm. The block is inserted in the window by placing the lower flange behind the lower window strut while compressing the upper flange until it expands under the cartilage. Some 4-0 polypropylene (Prolene) sutures are used to stabilize the implant to the inferior strut of thyroid cartilage (Fig. 47-11).

FIGURE 47-10 Preformed Silastic block is trimmed to fit auditory and visual feedback.

FIGURE 47-11. Final position of vocal cord after placement of Silastic implant.

FIGURE 47-12. Exposure is achieved by rotating thyroid cartilage upward with a hook. A Kerrison rongeur is used to remove posterior thyroid ala. Muscular process is palpated and moved on its plane of abduction and adduction.

FIGURE 47-13. Arytenoid stitch is placed to mimic vector of force that rotates vocal process downward and inward.

All patients are given 10 mg of dexamethasone at the time of the procedure and at least three doses every 6 hours postoperatively. Patients are treated with glycopyrrolate, 0.2 mg every 6 hours, for 3 days postoperatively to decrease salivary secretions.

High vagal injury with loss of the superior laryngeal nerve is usually best addressed with medialization and arytenoid adduction. Arytenoid adduction has been described elsewhere,^15,16 and is performed at the time of Silastic medialization. When the cartilage window has been created, the voice is assessed using the depth gauge as described earlier, and the decision to proceed with arytenoid adduction is made.

Exposure of the arytenoid cartilage is achieved by first placing a hook beneath the posterior border of the thyroid cartilage and rotating the larynx forward. The perichondrium at the posterior border is divided, and the piriform sinus mucosa is elevated away from the inner surface of the thyroid cartilage. A 5 mm Kerrison rongeur is used to remove the posterior border of the thyroid cartilage, exposing the paraglottic space lateral to the muscular process of the arytenoid. Patients are then asked to purse their lips and blow out to confirm the location of the piriform mucosa so that dissection may be carried out anteriorly to expose the posterior cricoarytenoid muscle. The muscular process is palpated and moved in its plane of abduction and adduction while observing the monitor (Fig. 47-12).

A double-armed 4-0 Prolene suture is passed through the lateral edge of the muscular process in a figure-eight fashion to secure the arytenoid (Fig. 47-13). The goal of this stitch is to mimic the vector of force that rotates the vocal process of the arytenoid down (inferior) and in (medial) during phonation. To accomplish this, one end of the suture is brought through the paraglottic space and out through the cartilage just anterior to the window. The other end of the suture is passed from the window below the lower cartilage strut and then through the cricothyroid membrane soft tissue in the midline. Gentle traction is applied to the arytenoid, and its motion is observed on the monitor. The implant is carved and placed. Both arytenoid sutures pass deep to the implant. Final adjustments are made to the arytenoid stitch, and it is tied down. The perichondrium and strap muscles are laid back into position, and the wound is closed with absorbable suture.

Spinal Accessory Nerve (Cranial Nerve XI)

The spinal accessory nerve has only a branchial motor component. Its lower motor neuron cell bodies arise in the spinal cord, and its motor fibers ascend into the cranium and then descend through the pars nervosa of the jugular foramen, passing superficial to (70%), posterior to (27%), or through (3%) the jugular vein to innervate the sternocleidomastoid and trapezius muscles.¹⁷ Loss of sternocleidomastoid function results in weakness when turning the head away from the operated side, although this is rarely noticed by most patients. Loss of trapezius function results in downward and lateral rotation of the scapula with a shoulder droop. This causes severe shoulder disability secondary to weakness and pain. Whether the nerve may be grafted successfully or not, a shoulder exercise program that emphasizes strengthening of the levator, scalene, and rhomboid muscles should be administered by a qualified physical therapist. This program should continue indefinitely to maintain the strength and support of the shoulder girdle.

Hypoglossal Nerve (Cranial Nerve XII)

The hypoglossal nerve provides somatic motor control to all the intrinsic and extrinsic muscles of the tongue except the palatoglossus. The nerve exits the skull base through the hypoglossal canal medial to the jugular foramen. As it passes laterally, it shares fibers with the vagus nerve near the inferior (nodose) ganglion. Separation of these fibers leads to vocal fold paresis or paralysis and should be avoided.¹⁸ In time, most patients can compensate for unilateral tongue paralysis. The deficit is characterized by difficulty in positioning the bolus during the oral phase of swallowing. Often the bolus becomes lodged beneath the tongue on the paralyzed side. With swallowing therapy and lingual exercise, patients learn to position the bolus on the nonparalyzed side.

Cervical Sympathetic Chain

The sympathetic innervation to the head and neck structures originates in the upper thoracic segment of the spinal column. The preganglionic fibers ascend in the sympathetic chain to exit through one of its four ganglia (superior, middle, vertebral, and stellate). The superior cervical ganglion lies on the surface of the longus capitus muscle at the level of the second or third cervical vertebra, deep to the internal carotid artery at the most distal or superior point of the cervical sympathetic chain. From this ganglion, postganglionic fibers typically reach the first three or four cervical rootlets. They also communicate with CN IX, X, XI, and XII as part of the pharyngeal plexus. Finally, they form the sympathetic plexus that ascends along the internal carotid artery.^2,19

Damage to the superior cervical ganglion or the internal carotid plexus results in Horner’s syndrome, consisting of ptosis, miosis, and anhidrosis. For most patients, there is little functional deficit. Rarely, visual fields may be partially obstructed because of the ptosis. More commonly, it is a cosmetic nuisance. Elevation of the eyelid to its normal open position can be accomplished by either levator shortening or resection of Müller’s muscle.²⁰

The other significant sequela from injury to the cervical sympathetics at the skull base is loss of sympathetic innervation to the parotid gland. This complication is frequently seen with resection of high vagal paragangliomas when the sympathetic chain is either resected or damaged. In this setting, a prolonged course of cramping pain is associated with the first bite of each meal and has been named “firstbite syndrome.”¹⁸ Patients usually describe this pain as a spasm over the parotid region that begins with the first bite and subsides within the next several bites. The intensity of the pain is increased with strong sialogogues, such as vinegar or lemon. In the early postoperative period, the pain can be so severe as to limit oral intake. Early management consists of dietary modification with bland foods and oral carbamazepine (100 to 200 mg twice daily). Slowly, over time, the symptoms improve.