Sustained improvements in surgical technique now allow safe resection of JP with minimal mortality. Yet a major cause of morbidity remains the cranial nerve deficits resulting from both tumor growth and surgical extirpation [1]. These impairments may dramatically influence multiple defining elements of the human condition: vision, hearing, speech, and deglutition. Recovery may be incomplete and often requires a prolonged period of rehabilitation. When multiple cranial nerves are affected, the effects on overall quality of life can be devastating. While those deficits produced by tumor growth generally occur progressively over many months, the acute postsurgical deficit is not nearly as well tolerated.

In the past, studies of JP treatment have focused on traditional end points, such as completeness of tumor removal, response to radiation, survival, and local control. More recently, investigators have begun to appreciate the importance of quality of life (QOL) outcomes in the setting of skull base surgery (composed of composite speech, swallowing, and symptom-specific domains) [2]. The impact of surgery on QOL outcomes in skull base paragangliomas directly relates to the speech and swallowing deficits that can occur with treatment [3]. Although in the largest series to date 98% of patients returned to their previous occupations within 2 years after surgery, only 75% returned to their preoperative baseline overall QOL levels owing to sustained swallowing deficits. These results stand in contrast to the results of patients undergoing surgical resection for acoustic neuroma (AN) where infrequent low QOL scores were specifically associated with postoperative headache symptoms after surgical excision [4], while study of 105 surgically resected skull base meningiomas [5] that showed persistent impairments at 1 year were attributed to physical handicaps and low energy levels.

A detailed understanding of the unique speech and swallowing deficits following surgical excision of paraganglioma is critical to help surgeons improve the initial multidisciplinary assessment and postoperative management of these patients. It allows identification of specific impediments as early as possible during follow-up and allows application of appropriate medical interventions to patients with increased risk of poor outcome. Equally as critical, providing patients detailed information about their disease and the expected outcomes of therapy prior to any intervention can markedly improve patients’ satisfaction with their treatment decisions.

The lower cranial nerves function as a complex team orchestrating the function of the upper aerodigestive tract. Thus, the primary dysfunction, with the loss of these nerves, is alterations in swallowing, speech, and airway protection. Many surgical procedures are available as adjuncts to rehabilitation of lower cranial nerve defects. With therapy most patients compensate for damage to any one of these cranial nerves in isolation. However, damage to more than one nerve significantly prolongs the period of recovery and impairs the overall outcome of rehabilitation.

The function of the glossopharyngeal nerve (IX ) is broad in scope. It possesses fibers responsible for brachial motor function (stylopharyngeus), a general sensory component (afferent feedback from the ipsilateral oropharynx), and a visceral sensory component (feedback from the carotid body and carotid sinus).

Its brachial motor function is restricted to the stylopharyngeus, generating pharyngeal elevation during swallowing and speech. Isolated loss of function of this muscle would have little effect on swallowing. However, when its loss is combined with damage to the vagus nerve, it further compounds swallowing rehabilitation.

The glossopharyngeal nerve also carries a visceral motor component responsible for the parasympathetic control of the parotid gland. As cranial nerve IX exits the skull base through the jugular foramen, the parasympathetic motor fibers depart from the ninth cranial nerve and pass through the tympanic plexus in the middle ear, progressing back up through the middle fossa floor, then descend through the foramen ovale to the otic ganglion. From the otic ganglion, they travel with the auriculotemporal nerve to reach the parotid gland. Injury to these fibers can occur at many levels and result in a decrease in parotid salivary flow. Infrequently, this may lead to chronic parotitis.

The general sensory component provides afferent feedback from the base of the tongue and lateral pharyngeal wall. A small branch also provides sensory fibers to the external ear and the inner aspect of the tympanic membrane. These fibers make up the extracranial portion of cranial nerve IX as it runs on the deep surface of the stylopharyngeus muscle, passing through the middle constrictor to reach the mucosa of the base of the tongue. Loss of this sensory feedback results in significant alterations in the oropharyngeal phase of swallowing, with the food bolus being delayed on the involved side. When this defect is combined with the loss of cranial nerves X or XII, dysfunction becomes severe. Therapy for oropharyngeal sensory loss from glossopharyngeal nerve injury involves extended swallowing therapy to try to maintain passage of the food bolus adjacent to the contralateral sensate side of the pharynx.

The final function of the glossopharyngeal nerve is visceral sensory , providing feedback from the carotid body and carotid sinus. It appears that unilateral loss of this feedback loop does not alter the integrity of the system, but bilateral loss results in marked abnormalities in postoperative blood pressure and pulse. This can occur when the patient has undergone a previous contralateral cervical dissection where the nerve fibers could have been resected or injured. In this situation the postoperative course is remarkably similar to a patient with an existing pheochromocytoma. If bilateral loss can be predicted ahead of time, preoperative planning in conjunction with an intensivist can greatly facilitate the patient’s postoperative course.

The vagus nerve is the most complex of the lower cranial nerves. Comprised of general sensory, visceral sensory, visceral motor, and branchial motor components, loss of its function is far reaching and creates a greater functional defect in speech and swallowing than isolated loss of the other cranial nerves.