CURRENT THERAPY J Oral Maxillofac Surg 49;740-744,1991
Facial Nerve Injuries Associated With Orthognathic Surgery: A Review of Incidence and Management JOHN K. JONES, DMD, MD,* AND JOSEPH E. VAN SICKELS, DDSt While facial nerve injuries associated with both extraoral and intraoral orthognathic surgery are rare, the results of such an injury can be devastating to the patient. A review of the literature shows that the majority of such injuries fall into the first-, second-, and third-degree injury categories. Prevention cannot be stressed enough; however, early recognition of an injury with prompt electrodiagnostic testing can assist with determining prognosis and treatment planning. When close observation is indicated. a variety of medical therapies have been suggested. For more severe injuries, nerve repair and facial reanimation have been reported.
the marginal mandibular nerve following BEVSO. 2 •3 Intraoral ramus osteotomies avoid extraoral scars and minimize risk to the facial nerve; however, damage to the nerve also has been reported with different intraoral procedures. Guralnick and Kelly4 noted a weakness of the lower one third of one side of the face following a bilateral intraoral vertical subcondylar osteotomy (BIVSO). Electrodiagnostic testing indicated a mild neuropathy. Complete resolution of the deficit was seen in 9 weeks. The mechanism of injury was thought to be blunt trauma to the facial nerve trunk due to placement of a retractor behind the posterior border of the ramus. The facial nerve may also be at risk during a bilateral sagittal split osteotomy (BSSO).5-10 Behrman reported a 0.67% incidence of facial nerve injury following BSSO. 5 Dendy" reported unilateral facial paralysis after a large setback without the Hunsuck modification in which spontaneous return of function was seen after 4 months. Maclntosh? reported one case of transient facial paralysis in a patient undergoing BSSO without the Hunsuck modification. Martis" and Karabouta-Voulgaropoulou and Martis'? reported two cases of facial paralysis following BSSO and mandibular setback. One patient had a 12-mm setback and immediate postoperative facial weakness that progressed to complete paralysis by the 7th postoperative day. Full recovery was seen by 5 months. The second patient also had immediate weakness postoperatively that pro-
The incidence and management of sensory nerve injuries associated with orthognathic surgery have been well documented. Although less common, facial nerve injuries also can occur. The purpose of this article is to review facial nerve injuries observed with various orthognathic procedures and to provide current information concerning diagnosis, prognosis, and management. Literature Review
Damage to the marginal mandibular branch of the facial nerve is a well-known complication of extraoral approaches to the mandibular ramus. In 1975, Kline l reported partial axonal degeneration, or axonotemesis, which totally resolved 12 weeks following a bilateral extraoral vertical subcondylar osteotomy (BEVSO). More recent articles also have reported transient and permanent injuries to Received from the Department of Oral and Maxillofacial Surgery, University of Texas Health Science Center at San Antonio. * Resident. t Professor. Address correspondence and reprint requests to Dr Van Sickels: Department of Oral and Maxillofacial Surgery, University of Texas Health Science Center, 7703 Floyd Curl Dr, San Antonio, TX 78284-7908. © 1991 American Association of Oral and Maxillofacial Surgeons 0278-2391/91/4907-0014$3.00/0
740
741
JONES AND VAN SICKELS
gressed to complete paralysis within 2 weeks. Full return of function was noted at 8 months. Although the majority of facial nerve injuries following intraoral procedures have been with BSSO and mandibular setback, in 1982 Piecuch and Lewis" reported unilateral facial paralysis in a patient undergoing a BSSO with mandibular advancement. Surgery was complicated by a proximal segment fracture requiring completion of the medial cut to the posterior border with drills and osteotomes. On the first postoperative day, the patient had difficulty closing his eye. By the second postoperative day this had progressed to complete unilateral facial paralysis. Elcctrornyographic (EMG) testing 5 days postsurgery recorded no action potentials in the right orbicularis oculi, indicating axonotemesis. Spontaneous recovery of function occurred in 11 weeks. Various mechanisms of nerve injury have been proposed. With extraoral approaches to the ramus, the marginal mandibular branch is subject to compression and tension injury during retraction. I1.12 Dendy," in his review of intraoral BSSOs, proposed three mechanisms of injury: 1) compression of the facial nerve by placement of retractors behind the posterior ramus, 2) fracture of the styloid process with posterior displacement! and 3) direct pressure as a result of distal segment setback. Postoperative hematoma formation may also playa role. Types of Injury
Peripheral nerve injuries have been classified into one of six types depending on the mechanism of injury.I3·14 A first-degree injury is termed neuropraxia, and is caused by increased intraneural pressure with resultant physiologic block. In these injuries the nerve will not be capable of conduction across the effected area; however, if tested it will respond to direct electrical stimulation distal to the site of injury. If compression is relieved, return of function is usually seen within 3 weeks. A second-degree injury is termed axonotemesis. The proposed mechanism for axonotemesis is persistent, increased intraneural pressure. Venous stasis leads to further pressure and eventual disruption of arteriolar flow. The end result is loss ofaxoplasmic flow and loss ofaxons. In axonetemesis, endoneural tubes remain intact and nerve regeneration can begin in 3 weeks to 2 months. If no endoneural tubes are lost, regeneration should be complete and without synkinesis. If intraneural pressure persists and endoneural tubes are lost, a third-degree injury or neurotemesis
results. The loss of endoneural tubes leads to a markedly decreased response to electrical stimulation. With loss of the endoneural tube to guide the developing axonal sprouts, faulty regeneration and synkinesis occur. Return of function is frequently incomplete and delayed, with return in 2 to 4 months. Fourth- and fifth-degree nerve injuries are the result of partial or complete disruption of the perineurium. These are the result of direct trauma to the nerve. With this degree of injury, prognosis for recovery without surgical exploration and repair is
poor.'" Based on clinical experience with nerve injury and repair, MacKinnon and Dellon!" have added a sixth degree of injury that is defined as any combination of first- through fifth-degree injuries in the same peripheral nerve. This category has proven to be very clinically useful as the majority of injuries are mixed rather than pure injuries of a single degree. It allows fascicles and bundles to be considered individually in terms of prognosis and treatment. Diagnosis
Facial nerve injuries as a consequence of orthognathic surgery invariably occur distal to the stylomastoid foramen and are usually the result of tension or compression. Physical examination will reveal the involved branches and distribution. For prognosis and management decisions it is important to establish the degree of injury. Various electrodiagnostic tests are available to assist in this regard. Electrodiagnostic testing of the facial nerve is accomplished using the principles of electroneurography (ENG) and EMG. Electroneurography is the study of peripheral nerve conduction, and consists of measuring nerve conduction velocity (NCV) and conduction latency. Nerve conduction velocity is measured by applying an electrical stimulus toa nerve at proximal and distal sites and measuring the velocity of impulse transmission. Technically, this test requires rather unimpeded access to a segment of peripheral nerve. Conduction latency is a measurement in milliseconds oj the elapsed time between application of a stimulus and response of the muscle. Electromyography records muscle electrical activity at needle insertion, rest, and voluntary contraction. Muscle electrical activity is displayed as a waveform or tracing. As in electrocardiography, observation of the wave morphology and intensity provides information concerning the status of the motor units and their innervation. Anatomic considerations dictate differences in the testing of the facial nerve when compared with
742 other peripheral nerves. Because of the anatomy, the stimulus is usually applied to the distal rather than proximal portion of the nerve. The physiologic basis for nerve testing is that intact nerve distal to the lesion will continue to conduct impulses until axonal degeneration occurs. In first-degree injuries (neuropraxia), stimulation distal to the lesion will continue to elicit a response. In axonotemesis (second degree), neurotemesis (third degree), partial transection (fourth degree), and transection (fifth degree), axonal degeneration will occur, which will result in a loss of nerve transmission when it is stimulated distal to the lesion 3 to 5 days postinjury. The maximal stimulation test (MST) is frequently used in evaluating injuries distal to the stylomastoid foramen. It can be considered a combination of conduction latency and EMG in that if impulse conduction occurs when a stimulus is applied to the nerve, an effect is seen at the muscle (contraction). Rather than measuring elapsed time to response, this test measures stimulus intensity required to elicit a response. With the unaffected side serving as a standard, response can be graded as absent, markedly decreased, minimally decreased, or equal. Patients are optimally tested 3 days postonset and subsequently at days 5, 7, 10, and 14 unless full function returns or becomes completely absent. The maximal stimulation test also can be used to detect and localize transection injuries at the time of surgery or immediately postoperatively. Evoked EMG (EEMG) is similar to the maximal stimulus test, and combines' the principles of EMG and ENG. The testing is accomplished as described for the maximal stimulation test with the difference being the direct recording of muscle action potentials via EMG rather than by observation for strength of contraction. This test is more objective and allows more reliable quantification of the degree of deficit. Conduction latency testing can be accomplished when the lesion is distal to the stylomastoid foramen. An increased latency, or loss of conduction, indicates axonal degeneration. This test has not been particularly helpful in determining prognosis for acute palsies, but is quite useful in evaluating peripheral neuropathies associated with systemic diseases. Electromyography is very useful in evaluating both traumatic injuries and the potential for recovery once significant nerve degeneration has occurred. In suspected traumatic nerve injuries, the presence of voluntary motor unit action potentials indicates the nerve has not been completely transected. This helps with decisions concerning
FACIAL NERVE INJURIES AND ORTHOGNATHIC SURGERY
Prognosis
The majority of experience and data concerning prognosis for return of facial nerve function are derived from patients with temporal bone fractures and idiopathic (Bell's) palsies. This information is extrapolated to traumatic injuries distal to the stylomastoid foramen based on a common pathophysiology of injury. The best prognostic indicator for full return of function is delayed or incomplete loss of function initially. Even when delayed paresis subsequently proceeds to complete paralysis, the prognosis for recovery of function is very good.!" Prognosis for recovery is worst when the deficit is immediate and complete. When this is the case, electrodiagnostic testing should be done early. Maximal stimulus testing, EEMG, EMG, and conduction latency testing are optimally initiated at I to 2 days postinjury and serve as a baseline. If axonal degeneration occurs there will be a gradual decrease in responsiveness starting with the 3rd to 5th day. No decrease over time indicates neuropraxia, which has an excellent prognosis for complete recovery. A decrease indicates a more severe injury. A MST with minimally decreased response (>25% normal) or an EEMG with greater than 25% normal function at 5 days indicates a mild injury with favorable prognosis. An EEMG with 10% or less of normal function at 14 days indicates severe injury. An EMG evaluation indicating voluntary motor unit potentials within 10 days of onset on injury rules out transection. In first- and second-degree injuries, complete recovery is usually seen within I to 6 months, and occurs without faulty regeneration and synkinesis. Spontaneous recovery of third-, fourth-, and fifthdegree injuries begins to occur within 3 to 4 months, but will result in incomplete recovery with faulty regeneration and synkinesis.!? Our review of cases following orthognathic surgery showed that most of the injuries were in the first- and second-degree cat· egories, although there were several in the thirdand fourth-degree categories. Treatment
Spontaneous recovery can be expected in cases where the nerve is intact at the completion of the procedure. Examination in the recovery room in questionable cases provides prognostic information since any function noted postoperatively would exclude transection. It is worthwhile to remember that local anesthetics may complicate these examinations. When local anesthesia was used. the exarni-
743
JONES AND VAN SICKELS
tively, it should be documented and the patient should be observed for return of function. If no return of function is noted at 24 hours, consideration should be given to electrodiagnostic testing (Fig I). Clinical management of the patient with a paralysis will vary depending on the branches involved and the type of injury. When eyelid closure is difficult, an eye patch and methylcellulose drops may be helpful. Physical therapy such as heat, facial massage, and facial exercise performed twice a day have been suggested. 18 Facial cream should be massaged into the skin around the eyes and mouth and over the midface ideally using an electric vibrator. Exercises consist of having the patient stand in front of a mirror watching his face while raising the eyebrows, blowing the cheeks, and grinning. Even though no facial movement may be noted, intact nerve fibers will be activated and exercise will help to maintain muscle tone. Steroids have been given intraorally, intramuscularly, and intravenously for facial nerve paralysis. In Piecuch and Lewis's case," peri operative steroids were maintained for an additional 3 days. Whether this decreased the severity of injury is unknown. Exploration and repair is only indicated for severe fourth- and fifth-degree injuries. If transection is noted at surgery, or if a postoperative MST indicates a transection, the nerve should be immediately explored and primarily repaired. No return of POSTOPERATIVE EVALUATION:
WITHIN 24 HOURS:
1-2 DAYS:
3·5 DAYS:
4·S!MONTHS:
1 'rEAR::
FIGURE I. Algorithm for testing, liming, and Ireatment options for facial nerve repair.
function should be expected for 4 to 8 months, and return can take as long as 2 years. Faulty regeneration and synkinesis can be expected. No return of function at 8 months is an indication for reexploration. Treatment decisions regarding exploration and repair of suspected transections are most difficult when the patient is 1 to 4 months postonset of deficit because optimal results for primary repair are obtained in the first month; however, after 4 months, spontaneous recovery can begin. Even in this interval, exploration may be indicated if paralysis is complete and MST, EEMG, and EMG indicate complete disruption. Experiences with resection of large segments of the facial nerve during parotid tumor removal have shown as much as a 25% incidence of some spontaneous recovery of function. The mechanism for this is unknown, and return of function is unpredictable. When treatment is indicated, the best results are obtained with end-to-end facial nerve anastomosis. In the event that immediate or delayed facial nerve end-to-end anastomosis is not possible, facial reanimation can be considered. Various facial reanimation procedures have been described. The best results are obtained with facial nerve grafting. This requires access to the proximal stump. If this is not possible, various nerve crossovers can be used, with the hypoglossal probably being the most used. With these techniques, some evidence of return of function should be seen within 4 to 8 months. Reanimation procedures involving nerve repair should be done within I year of injury. After 1 year, nerve and muscle atrophy lead to poor results and consideration should be given to muscle transfers. Discussion
The incidence of severe facial nerve injury as a complication of orthognathic surgery is low for both extraoral and intraoral procedures. Extraoral procedures have greater potential for damage to the marginal mandibular nerve. Although classically described as a single nerve branch, studies by Nelson and Gingrass'" indicate that this nerve actually has several separate branches in the region of the submandibular triangle. There are discrete branches to the depressor anguli oris, depressor labii inferioris, and mentalis. The extremely low incidence of permanent deficits indicates that the majority of injuries are secondary to blunt trauma during flap retraction. Intraoral procedures carry a small risk of damage to the nerve. The mechanism of injury is thought to be blunt trauma secondary to the placement of retractors posterior to the ramus, fracture of the sty-
744 loid process, or distal segment pressure secondary to large mandibular setbacks. Careful retraction and use of the Hunsuck modification with large setbacks should minimize nerve injuries. Fortunately, all of the reported injuries with intraoral procedures spontaneously resolved after a variable length of time. Immediate and complete facial nerve deficits carry the worst prognosis, and should be evaluated by .electrodiagnostic testing, beginning on the 1st and 2nd postoperative day and following by serial testing. If initial and subsequent testing is consistent with nerve transection, surgical exploration and repair is indicated. If testing indicates axonal disruption without transection, medical management is implemented while awaiting return of spontaneous function. Steroids are frequently used intraoperatively and postoperatively. Although there is no evidence for efficacy in preventing or minimizing nerve injuries, a presumed benefit is decreased edema with resultant decreased intraneural pressure. If there is no evidence for return of function at 4 to 8 months, reexploration with nerve grafting or reanimation should be considered. References I. Kline SN: Electrical testing for injuries of the seventh nerve. J Oral Surg 33:215, 1975 2. Egyedi P; Houwing M, Juten E: The oblique subcondylar osteotomy. Report of results of 100 cases. J Oral Surg 39:871, 1981 3. Tomes K, Gilhuus-Moe OT: The surgical technique of vertical subcondylar osteotomy for correction of mandibular
FACIAL NERVE INJURIES AND ORTHOGNATHIC SURGERY
4.
5.
6. 7.
8. 9. 10. II.
12. 13. 14.
15. 16. 17. 18.
prognathism. A 10 year survey. Acta Odont Scand 45:203, 1987 Guralnick W, Kelly JP: Palsy of the facial nerve after intraoral oblique osteotomies of the mandible. J Oral Surg 37:743, 1979 Behrman S: Complications of sagittal osteotomy of the mandibular ramus. J Oral Surg 30:554, 1972 Dendy RA: Facial nerve paralysis following sagittal split mandibular osteotomy. A care report. Br J Oral Surg 11:101,1973 Maclntosh RB: Experience with the sagittal osteotomy of the mandibular ramus. A 13 year review. J Maxillofac Surg 9:151,1981 Piecuch JF, Lewis RA: Facial nerve injury as a complication of sagittal split ramus osteotomy. J Oral Maxillofac Surg 40:309, 1982 Martis CS: Complication of sagittal split ramus osteotomy. J Oral Maxillofac Surg 42: 101, 1984 Karabouta-Voulgaropoulav I, Martis CS: Facial paresis following sagittal split osteotomy. Report of two cases. Oral Surg Oral Med Oral Pathol 57:600, 1984 Nelson DW, Gingrass RP: Anatomy of the mandibular branches of the facial nerve. Plast Reconstr Surg 64:479, 1979 May M: Anatomy of the facial nerve for the clinician, in May M (ed): The Facial Nerve. New York, NY, Thieme, 1986, pp 21-63 Sunderland S (ed): Nerve and Nerve Injuries. London, Churchill Livingston, 1978 MacKinnon SE, Dellon AL: Classification of nerve injuries as the bases for treatment, ill MacKinnon SE, Dellon AL: Surgery of the Peripheral Nerve. New York, NY, Thieme, 1988, pp 35-39 May M: Microanatomy and pathophysiology of the facial nerve, ill May M (ed): The Facial Nerve. New York, NY, Thieme, 1986, pp 63-74 Blumenthal F, May M: Electrodiagnosis, in May M (ed): The Facial Nerve. New York. NY, Thieme, 1986, pp 241-263 May M, Weit RJ: Iatrogenic injury-Prevention and management, ill May M (ed): The Facial Nerve. New York, NY, Thieme, 1986, pp 549-560 May M: Office medical management of acute facial palsies, in May M (ed): The Facial Nerve. New York, NY, Thieme, 1986. pp 333-338
Facial Nerve Injuries Associated With Orthognathic Surgery: A Review of Incidence and Management JOHN K. JONES, DMD, MD,* AND JOSEPH E. VAN SICKELS, DDSt While facial nerve injuries associated with both extraoral and intraoral orthognathic surgery are rare, the results of such an injury can be devastating to the patient. A review of the literature shows that the majority of such injuries fall into the first-, second-, and third-degree injury categories. Prevention cannot be stressed enough; however, early recognition of an injury with prompt electrodiagnostic testing can assist with determining prognosis and treatment planning. When close observation is indicated. a variety of medical therapies have been suggested. For more severe injuries, nerve repair and facial reanimation have been reported.
the marginal mandibular nerve following BEVSO. 2 •3 Intraoral ramus osteotomies avoid extraoral scars and minimize risk to the facial nerve; however, damage to the nerve also has been reported with different intraoral procedures. Guralnick and Kelly4 noted a weakness of the lower one third of one side of the face following a bilateral intraoral vertical subcondylar osteotomy (BIVSO). Electrodiagnostic testing indicated a mild neuropathy. Complete resolution of the deficit was seen in 9 weeks. The mechanism of injury was thought to be blunt trauma to the facial nerve trunk due to placement of a retractor behind the posterior border of the ramus. The facial nerve may also be at risk during a bilateral sagittal split osteotomy (BSSO).5-10 Behrman reported a 0.67% incidence of facial nerve injury following BSSO. 5 Dendy" reported unilateral facial paralysis after a large setback without the Hunsuck modification in which spontaneous return of function was seen after 4 months. Maclntosh? reported one case of transient facial paralysis in a patient undergoing BSSO without the Hunsuck modification. Martis" and Karabouta-Voulgaropoulou and Martis'? reported two cases of facial paralysis following BSSO and mandibular setback. One patient had a 12-mm setback and immediate postoperative facial weakness that progressed to complete paralysis by the 7th postoperative day. Full recovery was seen by 5 months. The second patient also had immediate weakness postoperatively that pro-
The incidence and management of sensory nerve injuries associated with orthognathic surgery have been well documented. Although less common, facial nerve injuries also can occur. The purpose of this article is to review facial nerve injuries observed with various orthognathic procedures and to provide current information concerning diagnosis, prognosis, and management. Literature Review
Damage to the marginal mandibular branch of the facial nerve is a well-known complication of extraoral approaches to the mandibular ramus. In 1975, Kline l reported partial axonal degeneration, or axonotemesis, which totally resolved 12 weeks following a bilateral extraoral vertical subcondylar osteotomy (BEVSO). More recent articles also have reported transient and permanent injuries to Received from the Department of Oral and Maxillofacial Surgery, University of Texas Health Science Center at San Antonio. * Resident. t Professor. Address correspondence and reprint requests to Dr Van Sickels: Department of Oral and Maxillofacial Surgery, University of Texas Health Science Center, 7703 Floyd Curl Dr, San Antonio, TX 78284-7908. © 1991 American Association of Oral and Maxillofacial Surgeons 0278-2391/91/4907-0014$3.00/0
740
741
JONES AND VAN SICKELS
gressed to complete paralysis within 2 weeks. Full return of function was noted at 8 months. Although the majority of facial nerve injuries following intraoral procedures have been with BSSO and mandibular setback, in 1982 Piecuch and Lewis" reported unilateral facial paralysis in a patient undergoing a BSSO with mandibular advancement. Surgery was complicated by a proximal segment fracture requiring completion of the medial cut to the posterior border with drills and osteotomes. On the first postoperative day, the patient had difficulty closing his eye. By the second postoperative day this had progressed to complete unilateral facial paralysis. Elcctrornyographic (EMG) testing 5 days postsurgery recorded no action potentials in the right orbicularis oculi, indicating axonotemesis. Spontaneous recovery of function occurred in 11 weeks. Various mechanisms of nerve injury have been proposed. With extraoral approaches to the ramus, the marginal mandibular branch is subject to compression and tension injury during retraction. I1.12 Dendy," in his review of intraoral BSSOs, proposed three mechanisms of injury: 1) compression of the facial nerve by placement of retractors behind the posterior ramus, 2) fracture of the styloid process with posterior displacement! and 3) direct pressure as a result of distal segment setback. Postoperative hematoma formation may also playa role. Types of Injury
Peripheral nerve injuries have been classified into one of six types depending on the mechanism of injury.I3·14 A first-degree injury is termed neuropraxia, and is caused by increased intraneural pressure with resultant physiologic block. In these injuries the nerve will not be capable of conduction across the effected area; however, if tested it will respond to direct electrical stimulation distal to the site of injury. If compression is relieved, return of function is usually seen within 3 weeks. A second-degree injury is termed axonotemesis. The proposed mechanism for axonotemesis is persistent, increased intraneural pressure. Venous stasis leads to further pressure and eventual disruption of arteriolar flow. The end result is loss ofaxoplasmic flow and loss ofaxons. In axonetemesis, endoneural tubes remain intact and nerve regeneration can begin in 3 weeks to 2 months. If no endoneural tubes are lost, regeneration should be complete and without synkinesis. If intraneural pressure persists and endoneural tubes are lost, a third-degree injury or neurotemesis
results. The loss of endoneural tubes leads to a markedly decreased response to electrical stimulation. With loss of the endoneural tube to guide the developing axonal sprouts, faulty regeneration and synkinesis occur. Return of function is frequently incomplete and delayed, with return in 2 to 4 months. Fourth- and fifth-degree nerve injuries are the result of partial or complete disruption of the perineurium. These are the result of direct trauma to the nerve. With this degree of injury, prognosis for recovery without surgical exploration and repair is
poor.'" Based on clinical experience with nerve injury and repair, MacKinnon and Dellon!" have added a sixth degree of injury that is defined as any combination of first- through fifth-degree injuries in the same peripheral nerve. This category has proven to be very clinically useful as the majority of injuries are mixed rather than pure injuries of a single degree. It allows fascicles and bundles to be considered individually in terms of prognosis and treatment. Diagnosis
Facial nerve injuries as a consequence of orthognathic surgery invariably occur distal to the stylomastoid foramen and are usually the result of tension or compression. Physical examination will reveal the involved branches and distribution. For prognosis and management decisions it is important to establish the degree of injury. Various electrodiagnostic tests are available to assist in this regard. Electrodiagnostic testing of the facial nerve is accomplished using the principles of electroneurography (ENG) and EMG. Electroneurography is the study of peripheral nerve conduction, and consists of measuring nerve conduction velocity (NCV) and conduction latency. Nerve conduction velocity is measured by applying an electrical stimulus toa nerve at proximal and distal sites and measuring the velocity of impulse transmission. Technically, this test requires rather unimpeded access to a segment of peripheral nerve. Conduction latency is a measurement in milliseconds oj the elapsed time between application of a stimulus and response of the muscle. Electromyography records muscle electrical activity at needle insertion, rest, and voluntary contraction. Muscle electrical activity is displayed as a waveform or tracing. As in electrocardiography, observation of the wave morphology and intensity provides information concerning the status of the motor units and their innervation. Anatomic considerations dictate differences in the testing of the facial nerve when compared with
742 other peripheral nerves. Because of the anatomy, the stimulus is usually applied to the distal rather than proximal portion of the nerve. The physiologic basis for nerve testing is that intact nerve distal to the lesion will continue to conduct impulses until axonal degeneration occurs. In first-degree injuries (neuropraxia), stimulation distal to the lesion will continue to elicit a response. In axonotemesis (second degree), neurotemesis (third degree), partial transection (fourth degree), and transection (fifth degree), axonal degeneration will occur, which will result in a loss of nerve transmission when it is stimulated distal to the lesion 3 to 5 days postinjury. The maximal stimulation test (MST) is frequently used in evaluating injuries distal to the stylomastoid foramen. It can be considered a combination of conduction latency and EMG in that if impulse conduction occurs when a stimulus is applied to the nerve, an effect is seen at the muscle (contraction). Rather than measuring elapsed time to response, this test measures stimulus intensity required to elicit a response. With the unaffected side serving as a standard, response can be graded as absent, markedly decreased, minimally decreased, or equal. Patients are optimally tested 3 days postonset and subsequently at days 5, 7, 10, and 14 unless full function returns or becomes completely absent. The maximal stimulation test also can be used to detect and localize transection injuries at the time of surgery or immediately postoperatively. Evoked EMG (EEMG) is similar to the maximal stimulus test, and combines' the principles of EMG and ENG. The testing is accomplished as described for the maximal stimulation test with the difference being the direct recording of muscle action potentials via EMG rather than by observation for strength of contraction. This test is more objective and allows more reliable quantification of the degree of deficit. Conduction latency testing can be accomplished when the lesion is distal to the stylomastoid foramen. An increased latency, or loss of conduction, indicates axonal degeneration. This test has not been particularly helpful in determining prognosis for acute palsies, but is quite useful in evaluating peripheral neuropathies associated with systemic diseases. Electromyography is very useful in evaluating both traumatic injuries and the potential for recovery once significant nerve degeneration has occurred. In suspected traumatic nerve injuries, the presence of voluntary motor unit action potentials indicates the nerve has not been completely transected. This helps with decisions concerning
FACIAL NERVE INJURIES AND ORTHOGNATHIC SURGERY
Prognosis
The majority of experience and data concerning prognosis for return of facial nerve function are derived from patients with temporal bone fractures and idiopathic (Bell's) palsies. This information is extrapolated to traumatic injuries distal to the stylomastoid foramen based on a common pathophysiology of injury. The best prognostic indicator for full return of function is delayed or incomplete loss of function initially. Even when delayed paresis subsequently proceeds to complete paralysis, the prognosis for recovery of function is very good.!" Prognosis for recovery is worst when the deficit is immediate and complete. When this is the case, electrodiagnostic testing should be done early. Maximal stimulus testing, EEMG, EMG, and conduction latency testing are optimally initiated at I to 2 days postinjury and serve as a baseline. If axonal degeneration occurs there will be a gradual decrease in responsiveness starting with the 3rd to 5th day. No decrease over time indicates neuropraxia, which has an excellent prognosis for complete recovery. A decrease indicates a more severe injury. A MST with minimally decreased response (>25% normal) or an EEMG with greater than 25% normal function at 5 days indicates a mild injury with favorable prognosis. An EEMG with 10% or less of normal function at 14 days indicates severe injury. An EMG evaluation indicating voluntary motor unit potentials within 10 days of onset on injury rules out transection. In first- and second-degree injuries, complete recovery is usually seen within I to 6 months, and occurs without faulty regeneration and synkinesis. Spontaneous recovery of third-, fourth-, and fifthdegree injuries begins to occur within 3 to 4 months, but will result in incomplete recovery with faulty regeneration and synkinesis.!? Our review of cases following orthognathic surgery showed that most of the injuries were in the first- and second-degree cat· egories, although there were several in the thirdand fourth-degree categories. Treatment
Spontaneous recovery can be expected in cases where the nerve is intact at the completion of the procedure. Examination in the recovery room in questionable cases provides prognostic information since any function noted postoperatively would exclude transection. It is worthwhile to remember that local anesthetics may complicate these examinations. When local anesthesia was used. the exarni-
743
JONES AND VAN SICKELS
tively, it should be documented and the patient should be observed for return of function. If no return of function is noted at 24 hours, consideration should be given to electrodiagnostic testing (Fig I). Clinical management of the patient with a paralysis will vary depending on the branches involved and the type of injury. When eyelid closure is difficult, an eye patch and methylcellulose drops may be helpful. Physical therapy such as heat, facial massage, and facial exercise performed twice a day have been suggested. 18 Facial cream should be massaged into the skin around the eyes and mouth and over the midface ideally using an electric vibrator. Exercises consist of having the patient stand in front of a mirror watching his face while raising the eyebrows, blowing the cheeks, and grinning. Even though no facial movement may be noted, intact nerve fibers will be activated and exercise will help to maintain muscle tone. Steroids have been given intraorally, intramuscularly, and intravenously for facial nerve paralysis. In Piecuch and Lewis's case," peri operative steroids were maintained for an additional 3 days. Whether this decreased the severity of injury is unknown. Exploration and repair is only indicated for severe fourth- and fifth-degree injuries. If transection is noted at surgery, or if a postoperative MST indicates a transection, the nerve should be immediately explored and primarily repaired. No return of POSTOPERATIVE EVALUATION:
WITHIN 24 HOURS:
1-2 DAYS:
3·5 DAYS:
4·S!MONTHS:
1 'rEAR::
FIGURE I. Algorithm for testing, liming, and Ireatment options for facial nerve repair.
function should be expected for 4 to 8 months, and return can take as long as 2 years. Faulty regeneration and synkinesis can be expected. No return of function at 8 months is an indication for reexploration. Treatment decisions regarding exploration and repair of suspected transections are most difficult when the patient is 1 to 4 months postonset of deficit because optimal results for primary repair are obtained in the first month; however, after 4 months, spontaneous recovery can begin. Even in this interval, exploration may be indicated if paralysis is complete and MST, EEMG, and EMG indicate complete disruption. Experiences with resection of large segments of the facial nerve during parotid tumor removal have shown as much as a 25% incidence of some spontaneous recovery of function. The mechanism for this is unknown, and return of function is unpredictable. When treatment is indicated, the best results are obtained with end-to-end facial nerve anastomosis. In the event that immediate or delayed facial nerve end-to-end anastomosis is not possible, facial reanimation can be considered. Various facial reanimation procedures have been described. The best results are obtained with facial nerve grafting. This requires access to the proximal stump. If this is not possible, various nerve crossovers can be used, with the hypoglossal probably being the most used. With these techniques, some evidence of return of function should be seen within 4 to 8 months. Reanimation procedures involving nerve repair should be done within I year of injury. After 1 year, nerve and muscle atrophy lead to poor results and consideration should be given to muscle transfers. Discussion
The incidence of severe facial nerve injury as a complication of orthognathic surgery is low for both extraoral and intraoral procedures. Extraoral procedures have greater potential for damage to the marginal mandibular nerve. Although classically described as a single nerve branch, studies by Nelson and Gingrass'" indicate that this nerve actually has several separate branches in the region of the submandibular triangle. There are discrete branches to the depressor anguli oris, depressor labii inferioris, and mentalis. The extremely low incidence of permanent deficits indicates that the majority of injuries are secondary to blunt trauma during flap retraction. Intraoral procedures carry a small risk of damage to the nerve. The mechanism of injury is thought to be blunt trauma secondary to the placement of retractors posterior to the ramus, fracture of the sty-
744 loid process, or distal segment pressure secondary to large mandibular setbacks. Careful retraction and use of the Hunsuck modification with large setbacks should minimize nerve injuries. Fortunately, all of the reported injuries with intraoral procedures spontaneously resolved after a variable length of time. Immediate and complete facial nerve deficits carry the worst prognosis, and should be evaluated by .electrodiagnostic testing, beginning on the 1st and 2nd postoperative day and following by serial testing. If initial and subsequent testing is consistent with nerve transection, surgical exploration and repair is indicated. If testing indicates axonal disruption without transection, medical management is implemented while awaiting return of spontaneous function. Steroids are frequently used intraoperatively and postoperatively. Although there is no evidence for efficacy in preventing or minimizing nerve injuries, a presumed benefit is decreased edema with resultant decreased intraneural pressure. If there is no evidence for return of function at 4 to 8 months, reexploration with nerve grafting or reanimation should be considered. References I. Kline SN: Electrical testing for injuries of the seventh nerve. J Oral Surg 33:215, 1975 2. Egyedi P; Houwing M, Juten E: The oblique subcondylar osteotomy. Report of results of 100 cases. J Oral Surg 39:871, 1981 3. Tomes K, Gilhuus-Moe OT: The surgical technique of vertical subcondylar osteotomy for correction of mandibular
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prognathism. A 10 year survey. Acta Odont Scand 45:203, 1987 Guralnick W, Kelly JP: Palsy of the facial nerve after intraoral oblique osteotomies of the mandible. J Oral Surg 37:743, 1979 Behrman S: Complications of sagittal osteotomy of the mandibular ramus. J Oral Surg 30:554, 1972 Dendy RA: Facial nerve paralysis following sagittal split mandibular osteotomy. A care report. Br J Oral Surg 11:101,1973 Maclntosh RB: Experience with the sagittal osteotomy of the mandibular ramus. A 13 year review. J Maxillofac Surg 9:151,1981 Piecuch JF, Lewis RA: Facial nerve injury as a complication of sagittal split ramus osteotomy. J Oral Maxillofac Surg 40:309, 1982 Martis CS: Complication of sagittal split ramus osteotomy. J Oral Maxillofac Surg 42: 101, 1984 Karabouta-Voulgaropoulav I, Martis CS: Facial paresis following sagittal split osteotomy. Report of two cases. Oral Surg Oral Med Oral Pathol 57:600, 1984 Nelson DW, Gingrass RP: Anatomy of the mandibular branches of the facial nerve. Plast Reconstr Surg 64:479, 1979 May M: Anatomy of the facial nerve for the clinician, in May M (ed): The Facial Nerve. New York, NY, Thieme, 1986, pp 21-63 Sunderland S (ed): Nerve and Nerve Injuries. London, Churchill Livingston, 1978 MacKinnon SE, Dellon AL: Classification of nerve injuries as the bases for treatment, ill MacKinnon SE, Dellon AL: Surgery of the Peripheral Nerve. New York, NY, Thieme, 1988, pp 35-39 May M: Microanatomy and pathophysiology of the facial nerve, ill May M (ed): The Facial Nerve. New York, NY, Thieme, 1986, pp 63-74 Blumenthal F, May M: Electrodiagnosis, in May M (ed): The Facial Nerve. New York. NY, Thieme, 1986, pp 241-263 May M, Weit RJ: Iatrogenic injury-Prevention and management, ill May M (ed): The Facial Nerve. New York, NY, Thieme, 1986, pp 549-560 May M: Office medical management of acute facial palsies, in May M (ed): The Facial Nerve. New York, NY, Thieme, 1986. pp 333-338
