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Rehabilitation of Lower Cranial Nerve Deficits After Neurotologic Skull Base Surgery
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 enabled the 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 is the loss of cranial nerves at the time of resection. Innovative approaches to cranial nerve (CN) rehabilitation have allowed many of these patients to lead productive and enjoyable lives after cranial base surgery.
The lower CNs function in concert to facilitate speech, swallowing, and airway protection ( Fig. 42.1 ). Interruption of the complex interactions of these nerves results in articulation deficits, inanition, and aspiration. With speech and swallowing therapy, most patients can compensate for the loss of a single lower CN. The loss of multiple nerves, particularly in an elderly patient, may result in the permanent inability to swallow despite intensive therapy. Paradoxically, the preoperative loss of CN 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 CN function are important factors in the decision to proceed with complete surgical resection, partial resection, or radiation therapy.
The function of the upper aerodigestive tract is coordinated by complex interactions of the lower cranial nerves in speech and swallowing.
Patient Evaluation
When lateral skull base surgery is elected, CN V 3 to XII and the sympathetic trunk are at risk. A careful head and neck examination, including CN evaluation and flexible fiberoptic examination of the hypopharynx and larynx, should be performed at the bedside on the first postoperative day to confirm the known deficits and to determine the extent of any additional CN deficits. The state of the airway, vocal fold function, 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.
After thorough evaluation has been completed, efforts are directed at rehabilitation. The remainder of this chapter describes the pertinent regional CN anatomy and function, , associated postoperative deficits, and methods for rehabilitation.
Lower Cranial Nerve Deficits and Rehabilitation
Trigeminal Nerve: Mandibular Division (Cranial Nerve V 3 )
The mandibular division of the trigeminal nerve (CN V 3 ) carries a branchial motor and a general sensory component. The sensory pathway travels via five orocutaneous nerves: auriculotemporal, meningeal, buccal, lingual, and inferior alveolar. The 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.
The 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 V 3 provides function to six muscles: the tensor veli palatini, tensor tympani, medial pterygoid, lateral pterygoid, masseter, and temporalis. The medial pterygoid nerve is the first branch arising from CN V 3 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 the 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 V 3 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 V 3 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 V 3 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 the placement of a silicone or methyl methacrylate implant beneath the residual temporalis muscle ( Fig. 42.2 ). Care must be taken to contour the implant where it abuts the lateral orbital rim; otherwise a residual crease results in this region.
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