Rehabilitation of Lower Cranial Nerve Deficits after Neurotologic Skull Base Surgery

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Chapter 47 Rehabilitation of Lower Cranial Nerve Deficits after Neurotologic Skull Base Surgery

James L. Netterville, Christopher A. Sullivan

Before the advent of modern skull base surgery, the treatment of cranial base lesions was associated with significant perioperative complications and long-term morbidity. Rapid advances in medical imaging have made possible early detection of lesions and preservation of vital structures at the time of surgery. The development of advanced microsurgical techniques has made the removal of most skull base tumors not only possible, but also feasible. Today, the major source of short-term and long-term morbidity results from the loss of cranial nerves at the time of resection. Innovative approaches to cranial nerve rehabilitation have allowed many of these patients productive and enjoyable lives after cranial base surgery.

The lower cranial nerves function in concert to facilitate speech, swallowing, and airway protection (Fig. 47-1). Interruption of the complex interactions of these nerves results in articulation deficits, inanition, and aspiration. With speech and swallowing therapy, most patients are able to compensate for the loss of a single lower cranial nerve. The loss of multiple nerves, particularly in an elderly patient, may result in permanent inability to swallow despite intensive therapy. Paradoxically, preoperative loss of cranial nerve function from tumor compression allows most patients to compensate slowly over time, and may predict better postoperative speech and swallowing rehabilitation. Patient age and preoperative cranial nerve function are important factors in the decision to proceed with complete surgical resection, partial resection, or radiation therapy.

FIGURE 47-1 Function of upper aerodigestive tract is coordinated by complex interaction of lower cranial nerves in speech and swallowing.

PATIENT EVALUATION

When lateral skull base surgery is elected, CN V3 to XII and the sympathetic trunk are at risk. A careful head and neck examination including cranial nerve evaluation and flexible fiberoptic examination of the hypopharynx and larynx should be performed at the bedside on the 1st postoperative day to confirm known deficits and to determine the extent of any additional cranial nerve deficits. The state of the airway, vocal fold function and cord position, pooling of secretions, and the ability to clear secretions by coughing should be noted. A modified barium swallow is the “gold standard” for evaluating aspiration, and should be performed as soon as the patient is awake and alert enough to cooperate with the study. The level of oropharyngeal dysphagia may be identified and addressed by the speech and language pathologist at the time of this study. Flexible videoendoscopic evaluation has been described to evaluate swallowing at the bedside, but is not the study of choice because it cannot identify aspiration during the pharyngeal phase of swallowing, which is the most significant component of swallowing dysfunction in lateral skull base surgery.¹

After thorough evaluation has been completed, efforts are directed at rehabilitation. The remainder of this chapter describes the pertinent regional cranial nerve anatomy and function,^2,³ associated postoperative deficits, and methods for rehabilitation.

LOWER CRANIAL NERVE DEFICITS AND REHABILITATION

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.