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Transtympanic stimulation of the facial nerve to assess nerve integrity in iatrogenic facial nerve paralysis
DRUG/DEVICE CAPSULE RANDAL A. OTTO, MD Drug/Device Capsule Editor
Transtympanic stimulation of the facial nerve to assess nerve integrity in iatrogenic facial nerve paralysis CHARLES J. LIMB, MD, JOHN K. NIPARKO, MD, and DAVID E. TUNKEL, MD, FAAP, FACS, Baltimore, Maryland
Facial nerve paralysis is a well-described complication of head and neck surgical procedures. When the nerve is purposefully transected, the clinical approach is often clear, involving nerve repair, grafting, or substitution. In cases where the extent of facial nerve injury is not obvious, the potential for recovery is often uncertain.1 We present a case of complete ipsilateral facial paralysis after resection of a parapharyngeal space tumor in a child. We used transtympanic stimulation of the tympanic segment of the facial nerve to assess anatomic integrity of the nerve. More experience with this technique may provide valuable information in guiding the management of postoperative facial nerve injury. CASE REPORT A 26-month-old female was evaluated for a right submandibular mass that had enlarged slowly for 5 months. An evaluation for cervical lymphadenopathy, including chest radiograph, serologic tests, and a tuberculin skin test, was unrevealing. Magnetic resonance imaging of the neck showed a 5-cm mass in the right parapharyngeal space, with increased signal intensity on T2-weighted imaging and with some enhancement after administration of gadolinium. The tumor was resected through a transcervical approach. A firm, noncompressible mass was dissected and totally excised without formal identification of the facial nerve. The Xomed NIM-2 (Xomed Surgical Products, Jacksonville, FL) facial nerve monitor was used throughout the case, with recording electrodes placed in orbicularis oris and orbicularis oculi muscles. No recordings were seen suggestive of facial nerve stimulation or injury. The mass was medial to the palpable styloid process at the skull base. Histopathologic examination was diagnostic for aggressive fibromatosis.
From the Department of Otolaryngology–Head and Neck Surgery, Johns Hopkins University School of Medicine. Otolaryngol Head Neck Surg 2001;124:600-2. Copyright © 2001 by the American Academy of Otolaryngology– Head and Neck Surgery Foundation, Inc. 0194-5998/2001/$35.00 + 0 23/75/115403 doi:10.1067/mhn.2001.115403 600
On emergence from anesthesia, the child revealed no motion of the right face in any of the facial nerve divisions. Dexamethasone was administered intravenously, and the patient was observed for 12 hours. When complete peripheral facial nerve palsy was confirmed on serial examinations, plans were made for surgical exploration of the facial nerve using a parotidectomy approach. Nerve conduction velocity of the right facial nerve was normal 24 hours after initial surgery, and electromyography (EMG) recording of facial muscles showed no voluntary motor unit potentials. These results do not distinguish between facial nerve traction injury (neuropraxia) or transection (severe axonotmesis or neurotmesis). On the second postoperative day, she was taken back to the operating room and general anesthesia was induced without neuromuscular blockade. Xomed NIM-2 electrodes were placed in the orbicularis oris and oculi muscles for facial nerve monitoring. A right myringotomy was performed just posterior to the malleus neck, and the Prass monopolar nerve stimulator probe was passed into the middle ear. The stimulator was advanced to a position presumed to be superior and anterior to the oval window. Current was applied at 0.2 mA and increased in 0.1 mA increments, with attention paid to the facial nerve monitor. Current was applied at low levels initially, to prevent nerve injury if the tympanic facial nerve was not bone covered. At 0.5 mA stimulation, EMG activity was recorded from both the eye and lip electrodes, with the event threshold set at 0.1 mV. At 1.0 mA stimulation, subtle movement of frontalis and platysma muscles was directly observed. Transtympanic stimulation of the facial nerve thus suggested an intact facial nerve. The facial nerve trunk was therefore not explored. Steroids were continued for a total of 5 days. Eight days after surgery, no facial motion (HouseBrackmann Grade VI) was seen.2 Examination at 3 weeks after surgery showed a Grade III facial weakness, with near normal frontal movement and eye closure, but weak buccal and marginal branch function. Examination 6 weeks after surgery showed Grade II weakness affecting only marginal branch function. Ten weeks after surgery, facial movement was entirely normal in all divisions (House-Brackmann Grade I). She has been followed for 14 months with no clinical or radiographic evidence of tumor recurrence.
Otolaryngology– Head and Neck Surgery Volume 124 Number 5
DISCUSSION
The facial nerve can be inadvertently injured as part of many otologic, skull base, and head and neck procedures. During otologic procedures, the labyrinthine, tympanic, and mastoid segments of the facial nerve are most likely to be injured, with the tympanic segment having the highest incidence of injury.3 Skull base procedures may require exposure and surgical risk to the extracanalicular and intracanalicular portions of the facial nerve. Resection of neck and parotid masses can lead to injury to the extratemporal facial nerve and more distal branches. Intraoperative facial nerve monitoring has been used to assist in identification of the facial nerve and its branches to decrease the risk of surgical injury.1 Intraoperative facial nerve monitoring uses EMG recording to detect activity of facial muscles from mechanical or electrical stimulation of the facial nerve. The Xomed-2 Nerve Integrity Monitor is often used during otologic and neck procedures to record EMG activity from orbicularis oris and oculi areas during procedures where facial nerve identification is necessary or facial nerve injury is possible. In skull base procedures, proximal stimulation of the facial nerve at the brainstem has been used to assess prognosis for facial function. For example, in cases of facial nerve compression by acoustic neuroma, stimulation of the facial nerve at the site of tumor removal has been used as a reasonable predictor of postoperative facial function.4,5 Factors that affect prognosis for recovery of facial function after iatrogenic facial nerve injury include the degree of direct injury, disruption of vascular supply to the facial nerve, and presence of thermal injury (particularly laser induced).6 Interestingly, percent degeneration of the facial nerve is not clearly related to percent function of the facial nerve, unless total transection has occurred.7 Fisch8 noted that trauma to neural connective tissue (especially the endoneurium) likely carries more prognostic relevance than axonal injury. Tears in the epineurium may result in herniation of the facial nerve, with subsequent intraneural fibrosis and paralysis.8 EMG and electroneuronography (ENoG) tests can be used to assign prognosis for recovery in patients with idiopathic and other forms of facial paralysis. Guidelines for the interpretation of results obtained with such methods have been described.7,8 These methods measure nerve and muscle activity distal to a presumed site of injury and therefore have had mixed utility for determining prognosis. In most cases of iatrogenic facial nerve injury, trauma to the facial nerve occurs at proximal locations, so stimulation distal to the site of injury may not be helpful. The ideal timing for repair of a transected facial nerve has been debated, but the ability to use nerve stimulators to identify branches distal to a severed nerve is an
LIMB et al
601
obvious advantage for repair of a transected nerve.1 Distal nerve stimulation diminishes within several days of nerve transection, and would not be useful by the time ENoG or EMG information indicates nerve transection.8 The child reported here had a complete facial paralysis after a surgical procedure that involved dissection and retraction near the facial nerve and where the facial nerve had not been identified definitively during the surgery. Although neuromuscular blockade was not used, it is unclear why the facial nerve monitor (which was functioning properly) did not sound during the initial procedure. To evaluate the integrity of the facial nerve during the second procedure, the tympanic segment of the nerve was approached through a myringotomy and stimulated at a site proximal to the presumed location of a facial nerve injury (near the stylomastoid foramen). Successful stimulation of the facial muscles supplied by both the upper and lower divisions of the facial nerve, as seen by EMG activity at low levels of stimulation and movement at higher levels of stimulation, provided evidence of a mixture of injured and responsive fibers, ostensibly within an intact nerve. The probable explanation for these findings is that a significant percentage of facial nerve fibers were intact with varying degrees of neuropraxia, axonotmesis, and neurotmesis. Fisch8 stated that facial muscle denervation of <90% indicates a reasonable prognosis for recovery and that at least 25% of facial nerve fibers must be functional for normal facial expression. Kartush et al9 pointed out that the range of 80% to 95% degeneration of facial nerve fibers is when determination of prognosis is most difficult and subject to clinically significant errors in management. We note that inability to evoke facial activity through this approach would not help to prognosticate facial nerve recovery, as other factors (probe position relative to the tympanic facial, thickness of the fallopian canal, etc) could lead to failure to stimulate an intact nerve through a myringotomy. If facial stimulation had not been demonstrated, we would have explored the facial nerve from the stylomastoid foramen to the pes anserinus to assess nerve integrity and repair any damage to the nerve. In addition, the possibility remains that retrograde stimulation of the facial nerve via the chorda tympani, rather than stimulation of the tympanic segment of the facial nerve itself, resulted in facial movement, because we did not visualize the facial nerve itself during transtympanic stimulation. Cervical approaches to the parapharyngeal space can be performed with or without mandibulotomy via neck incisions that can extend to the preauricular area.11,12 Olsen11 described routine identification of the facial nerve early in surgery. Mattox13 noted that for tumors of neural or salivary origin restricted to the parapharyngeal
602
Otolaryngology– Head and Neck Surgery May 2001
LIMB et al
space medial to the mandible, formal facial nerve dissection is not necessary. Facial nerve injury has been reported after parapharyngeal space surgery, but permanent facial paralysis in the absence of parotid malignancy is rare.11 In Olsen’s series11 of 44 tumors of the parapharyngeal space, facial paresis occurred in 22.3% of patients, and in all cases the marginal branch of the facial nerve was the affected branch. Of 137 parapharyngeal space tumors, Hughes et al14 reported tumor involvement of the facial nerve in 19 (13.9%) cases that required sacrifice of the nerve. Stell et al12 reported an incidence of 16% of patients with temporary facial palsy postoperatively after removal of parapharyngeal space tumors, all in the distribution of the marginal mandibular branch. The child reported here had a cervical approach without mandibulotomy or facial nerve dissection. Although the dissection was medial to the mandible inferiorly and to the styloid posterosuperiorly, facial nerve paralysis developed after surgery. We postulate that the firm noncompressible nature of the fibromatosis tumor required aggressive retraction for dissection, which caused either pressure or traction injury to the facial nerve. The more common salivary tumors of the parapharyngeal space, such as pleomorphic adenoma, are more compressible and require less vigorous retraction. Of course, in retrospect, early identification of the facial nerve during tumor resection would have ensured nerve integrity. In summary, we applied the technique of proximal facial nerve stimulation in combination with a commercially available facial nerve monitor in a novel fashion to test nerve integrity after iatrogenic paralysis. Additional experi-
ence with the technique of transtympanic facial nerve stimulation may help to identify that subset of patients with facial paralysis in which a significant percentage of nerve fibers remain responsive to direct electrical stimulation and further surgical intervention is unnecessary. REFERENCES 1. Prass RL. Iatrogenic facial nerve injury. Otolaryngol Clin N Am 1996;29:265-75. 2. House JW, Brackmann DE. Facial nerve grading system. Otolaryngol Head Neck Surg 1985;93:146-7. 3. Green JD Jr, Shelton C, Brackmann DE. Iatrogenic facial nerve injury during otologic surgery. Laryngoscope 1994;104:922-6. 4. Selesnick SH, Carew JF, Victor JD, et al. Predictive value of facial nerve electrophysiologic stimulation thresholds in cerebellopontine-angle surgery. Laryngoscope 1996;106:633-8. 5. Zeitouni AG, Hammerschlag PE, Cohen NL. Prognostic significance of intraoperative facial nerve stimulus thresholds. Am J Otol 1997;18:494-7. 6. Sampath P, Holliday MJ, Brem H, et al. Facial nerve injury in acoustic neuroma (vestibular schwannoma) surgery: etiology and prevention. J Neurosurg 1997;87:60-6. 7. Silverstein H, McDaniel AB, Hyman SM. Evoked serial electromyography in the evaluation of the paralyzed face. Am J Otol 1985;Suppl:80-7. 8. Fisch U. Prognostic value of electrical tests in acute facial paralysis. Am J Otol 1984;5:494-8. 9. Esslen E. The acute facial palsies. Berlin: Springer Verlag, 1977. 10. Kartush JM, Lilly DJ, Kemink JL. Facial electroneurography: clinical and experimental investigations. Otolaryngol Head Neck Surg 1985;93:516-23. 11. Olsen KD. Tumors and surgery of the parapharyngeal space. Laryngoscope 1994;Suppl:1-28. 12. Stell PM, Mansfield AO, Stoney PJ. Surgical approaches to tumors of the parapharyngeal space. Am J Otolaryngol 1985;6:92-7. 13. Mattox DE. Excision of parapharyngeal space tumors. In: Johns ME, Price JC, Mattox DE, eds. Atlas of head and neck surgery, vol 1. Philadelphia: BC Decker Inc, 1990. 14. Hughes KV III, Olsen KD, McCaffrey TV. Parapharyngeal space neoplasms. Head Neck 1995;17:124-30.
Transtympanic stimulation of the facial nerve to assess nerve integrity in iatrogenic facial nerve paralysis CHARLES J. LIMB, MD, JOHN K. NIPARKO, MD, and DAVID E. TUNKEL, MD, FAAP, FACS, Baltimore, Maryland
Facial nerve paralysis is a well-described complication of head and neck surgical procedures. When the nerve is purposefully transected, the clinical approach is often clear, involving nerve repair, grafting, or substitution. In cases where the extent of facial nerve injury is not obvious, the potential for recovery is often uncertain.1 We present a case of complete ipsilateral facial paralysis after resection of a parapharyngeal space tumor in a child. We used transtympanic stimulation of the tympanic segment of the facial nerve to assess anatomic integrity of the nerve. More experience with this technique may provide valuable information in guiding the management of postoperative facial nerve injury. CASE REPORT A 26-month-old female was evaluated for a right submandibular mass that had enlarged slowly for 5 months. An evaluation for cervical lymphadenopathy, including chest radiograph, serologic tests, and a tuberculin skin test, was unrevealing. Magnetic resonance imaging of the neck showed a 5-cm mass in the right parapharyngeal space, with increased signal intensity on T2-weighted imaging and with some enhancement after administration of gadolinium. The tumor was resected through a transcervical approach. A firm, noncompressible mass was dissected and totally excised without formal identification of the facial nerve. The Xomed NIM-2 (Xomed Surgical Products, Jacksonville, FL) facial nerve monitor was used throughout the case, with recording electrodes placed in orbicularis oris and orbicularis oculi muscles. No recordings were seen suggestive of facial nerve stimulation or injury. The mass was medial to the palpable styloid process at the skull base. Histopathologic examination was diagnostic for aggressive fibromatosis.
From the Department of Otolaryngology–Head and Neck Surgery, Johns Hopkins University School of Medicine. Otolaryngol Head Neck Surg 2001;124:600-2. Copyright © 2001 by the American Academy of Otolaryngology– Head and Neck Surgery Foundation, Inc. 0194-5998/2001/$35.00 + 0 23/75/115403 doi:10.1067/mhn.2001.115403 600
On emergence from anesthesia, the child revealed no motion of the right face in any of the facial nerve divisions. Dexamethasone was administered intravenously, and the patient was observed for 12 hours. When complete peripheral facial nerve palsy was confirmed on serial examinations, plans were made for surgical exploration of the facial nerve using a parotidectomy approach. Nerve conduction velocity of the right facial nerve was normal 24 hours after initial surgery, and electromyography (EMG) recording of facial muscles showed no voluntary motor unit potentials. These results do not distinguish between facial nerve traction injury (neuropraxia) or transection (severe axonotmesis or neurotmesis). On the second postoperative day, she was taken back to the operating room and general anesthesia was induced without neuromuscular blockade. Xomed NIM-2 electrodes were placed in the orbicularis oris and oculi muscles for facial nerve monitoring. A right myringotomy was performed just posterior to the malleus neck, and the Prass monopolar nerve stimulator probe was passed into the middle ear. The stimulator was advanced to a position presumed to be superior and anterior to the oval window. Current was applied at 0.2 mA and increased in 0.1 mA increments, with attention paid to the facial nerve monitor. Current was applied at low levels initially, to prevent nerve injury if the tympanic facial nerve was not bone covered. At 0.5 mA stimulation, EMG activity was recorded from both the eye and lip electrodes, with the event threshold set at 0.1 mV. At 1.0 mA stimulation, subtle movement of frontalis and platysma muscles was directly observed. Transtympanic stimulation of the facial nerve thus suggested an intact facial nerve. The facial nerve trunk was therefore not explored. Steroids were continued for a total of 5 days. Eight days after surgery, no facial motion (HouseBrackmann Grade VI) was seen.2 Examination at 3 weeks after surgery showed a Grade III facial weakness, with near normal frontal movement and eye closure, but weak buccal and marginal branch function. Examination 6 weeks after surgery showed Grade II weakness affecting only marginal branch function. Ten weeks after surgery, facial movement was entirely normal in all divisions (House-Brackmann Grade I). She has been followed for 14 months with no clinical or radiographic evidence of tumor recurrence.
Otolaryngology– Head and Neck Surgery Volume 124 Number 5
DISCUSSION
The facial nerve can be inadvertently injured as part of many otologic, skull base, and head and neck procedures. During otologic procedures, the labyrinthine, tympanic, and mastoid segments of the facial nerve are most likely to be injured, with the tympanic segment having the highest incidence of injury.3 Skull base procedures may require exposure and surgical risk to the extracanalicular and intracanalicular portions of the facial nerve. Resection of neck and parotid masses can lead to injury to the extratemporal facial nerve and more distal branches. Intraoperative facial nerve monitoring has been used to assist in identification of the facial nerve and its branches to decrease the risk of surgical injury.1 Intraoperative facial nerve monitoring uses EMG recording to detect activity of facial muscles from mechanical or electrical stimulation of the facial nerve. The Xomed-2 Nerve Integrity Monitor is often used during otologic and neck procedures to record EMG activity from orbicularis oris and oculi areas during procedures where facial nerve identification is necessary or facial nerve injury is possible. In skull base procedures, proximal stimulation of the facial nerve at the brainstem has been used to assess prognosis for facial function. For example, in cases of facial nerve compression by acoustic neuroma, stimulation of the facial nerve at the site of tumor removal has been used as a reasonable predictor of postoperative facial function.4,5 Factors that affect prognosis for recovery of facial function after iatrogenic facial nerve injury include the degree of direct injury, disruption of vascular supply to the facial nerve, and presence of thermal injury (particularly laser induced).6 Interestingly, percent degeneration of the facial nerve is not clearly related to percent function of the facial nerve, unless total transection has occurred.7 Fisch8 noted that trauma to neural connective tissue (especially the endoneurium) likely carries more prognostic relevance than axonal injury. Tears in the epineurium may result in herniation of the facial nerve, with subsequent intraneural fibrosis and paralysis.8 EMG and electroneuronography (ENoG) tests can be used to assign prognosis for recovery in patients with idiopathic and other forms of facial paralysis. Guidelines for the interpretation of results obtained with such methods have been described.7,8 These methods measure nerve and muscle activity distal to a presumed site of injury and therefore have had mixed utility for determining prognosis. In most cases of iatrogenic facial nerve injury, trauma to the facial nerve occurs at proximal locations, so stimulation distal to the site of injury may not be helpful. The ideal timing for repair of a transected facial nerve has been debated, but the ability to use nerve stimulators to identify branches distal to a severed nerve is an
LIMB et al
601
obvious advantage for repair of a transected nerve.1 Distal nerve stimulation diminishes within several days of nerve transection, and would not be useful by the time ENoG or EMG information indicates nerve transection.8 The child reported here had a complete facial paralysis after a surgical procedure that involved dissection and retraction near the facial nerve and where the facial nerve had not been identified definitively during the surgery. Although neuromuscular blockade was not used, it is unclear why the facial nerve monitor (which was functioning properly) did not sound during the initial procedure. To evaluate the integrity of the facial nerve during the second procedure, the tympanic segment of the nerve was approached through a myringotomy and stimulated at a site proximal to the presumed location of a facial nerve injury (near the stylomastoid foramen). Successful stimulation of the facial muscles supplied by both the upper and lower divisions of the facial nerve, as seen by EMG activity at low levels of stimulation and movement at higher levels of stimulation, provided evidence of a mixture of injured and responsive fibers, ostensibly within an intact nerve. The probable explanation for these findings is that a significant percentage of facial nerve fibers were intact with varying degrees of neuropraxia, axonotmesis, and neurotmesis. Fisch8 stated that facial muscle denervation of <90% indicates a reasonable prognosis for recovery and that at least 25% of facial nerve fibers must be functional for normal facial expression. Kartush et al9 pointed out that the range of 80% to 95% degeneration of facial nerve fibers is when determination of prognosis is most difficult and subject to clinically significant errors in management. We note that inability to evoke facial activity through this approach would not help to prognosticate facial nerve recovery, as other factors (probe position relative to the tympanic facial, thickness of the fallopian canal, etc) could lead to failure to stimulate an intact nerve through a myringotomy. If facial stimulation had not been demonstrated, we would have explored the facial nerve from the stylomastoid foramen to the pes anserinus to assess nerve integrity and repair any damage to the nerve. In addition, the possibility remains that retrograde stimulation of the facial nerve via the chorda tympani, rather than stimulation of the tympanic segment of the facial nerve itself, resulted in facial movement, because we did not visualize the facial nerve itself during transtympanic stimulation. Cervical approaches to the parapharyngeal space can be performed with or without mandibulotomy via neck incisions that can extend to the preauricular area.11,12 Olsen11 described routine identification of the facial nerve early in surgery. Mattox13 noted that for tumors of neural or salivary origin restricted to the parapharyngeal
602
Otolaryngology– Head and Neck Surgery May 2001
LIMB et al
space medial to the mandible, formal facial nerve dissection is not necessary. Facial nerve injury has been reported after parapharyngeal space surgery, but permanent facial paralysis in the absence of parotid malignancy is rare.11 In Olsen’s series11 of 44 tumors of the parapharyngeal space, facial paresis occurred in 22.3% of patients, and in all cases the marginal branch of the facial nerve was the affected branch. Of 137 parapharyngeal space tumors, Hughes et al14 reported tumor involvement of the facial nerve in 19 (13.9%) cases that required sacrifice of the nerve. Stell et al12 reported an incidence of 16% of patients with temporary facial palsy postoperatively after removal of parapharyngeal space tumors, all in the distribution of the marginal mandibular branch. The child reported here had a cervical approach without mandibulotomy or facial nerve dissection. Although the dissection was medial to the mandible inferiorly and to the styloid posterosuperiorly, facial nerve paralysis developed after surgery. We postulate that the firm noncompressible nature of the fibromatosis tumor required aggressive retraction for dissection, which caused either pressure or traction injury to the facial nerve. The more common salivary tumors of the parapharyngeal space, such as pleomorphic adenoma, are more compressible and require less vigorous retraction. Of course, in retrospect, early identification of the facial nerve during tumor resection would have ensured nerve integrity. In summary, we applied the technique of proximal facial nerve stimulation in combination with a commercially available facial nerve monitor in a novel fashion to test nerve integrity after iatrogenic paralysis. Additional experi-
ence with the technique of transtympanic facial nerve stimulation may help to identify that subset of patients with facial paralysis in which a significant percentage of nerve fibers remain responsive to direct electrical stimulation and further surgical intervention is unnecessary. REFERENCES 1. Prass RL. Iatrogenic facial nerve injury. Otolaryngol Clin N Am 1996;29:265-75. 2. House JW, Brackmann DE. Facial nerve grading system. Otolaryngol Head Neck Surg 1985;93:146-7. 3. Green JD Jr, Shelton C, Brackmann DE. Iatrogenic facial nerve injury during otologic surgery. Laryngoscope 1994;104:922-6. 4. Selesnick SH, Carew JF, Victor JD, et al. Predictive value of facial nerve electrophysiologic stimulation thresholds in cerebellopontine-angle surgery. Laryngoscope 1996;106:633-8. 5. Zeitouni AG, Hammerschlag PE, Cohen NL. Prognostic significance of intraoperative facial nerve stimulus thresholds. Am J Otol 1997;18:494-7. 6. Sampath P, Holliday MJ, Brem H, et al. Facial nerve injury in acoustic neuroma (vestibular schwannoma) surgery: etiology and prevention. J Neurosurg 1997;87:60-6. 7. Silverstein H, McDaniel AB, Hyman SM. Evoked serial electromyography in the evaluation of the paralyzed face. Am J Otol 1985;Suppl:80-7. 8. Fisch U. Prognostic value of electrical tests in acute facial paralysis. Am J Otol 1984;5:494-8. 9. Esslen E. The acute facial palsies. Berlin: Springer Verlag, 1977. 10. Kartush JM, Lilly DJ, Kemink JL. Facial electroneurography: clinical and experimental investigations. Otolaryngol Head Neck Surg 1985;93:516-23. 11. Olsen KD. Tumors and surgery of the parapharyngeal space. Laryngoscope 1994;Suppl:1-28. 12. Stell PM, Mansfield AO, Stoney PJ. Surgical approaches to tumors of the parapharyngeal space. Am J Otolaryngol 1985;6:92-7. 13. Mattox DE. Excision of parapharyngeal space tumors. In: Johns ME, Price JC, Mattox DE, eds. Atlas of head and neck surgery, vol 1. Philadelphia: BC Decker Inc, 1990. 14. Hughes KV III, Olsen KD, McCaffrey TV. Parapharyngeal space neoplasms. Head Neck 1995;17:124-30.