Chapter 47 Rehabilitation of Lower Cranial Nerve Deficits after Neurotologic Skull 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.
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)
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.
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 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.
