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Contralateral facial palsy following coronoidectomy
Contralateral facial palsy following coronoidectomy Report of a case Robert Chuong, D.M.D., M.D.,* Charlottesville, Va. UNIVERSITY
OF VIRGINIA
MEDICAL
CENTER
Total facial nerve palsy occurring 12 hours after an intraoral procedure on the contralateral described. The differential diagnosis of facial palsy is reviewed, with emphasis on possible factors temporally related to surgery.
F
acial nerve deficit has been reported following surgical procedures on and about the jaws, performed both intraorally and extraorally, and in association with facial trauma, both sharp and blunt. The following is a caseof total facial nerve palsy noted 12 hours after an intraoral procedure on the contralatera1 side. CASE REPORT
A healthy ll-year-old white male patient was initially hospitalized in August, 1982, after he sustained multiple facial fractures in a fall. Injuries included a LeFort II fracture, a left zygomatic complex fracture, and multiple mandibular injuries, including bilateral condylar head and symphyseal fractures. Treatment consisted of open reduction and internal fixation of the left zygomatic complex and symphyseal fractures and closed reduction of the midface and condylar fractures with the aid of frontal suspension. Maxillomandibular fixation was maintained for 8 weeks, and when the patient was first evaluated by the Oral Surgery Service 2 weeks after release from fixation trismus to 6 mm. interincisally was noted. An additional 2 weeks of mouth-opening exercise was instituted, with only slight improvement to an opening of 9 mm. Condylar motion was palpable bilaterally, although lateral excursions were markedly restricted. A scar band was palpable intraorally along the anterior border of the left mandibular ramus. Plain radiographs failed to demonstrate a cause for the trismus; that is, the zygomatic arches were well reduced and there was no obvious new bone formation across the *Formerly AssistantProfessor,Departmentof Plastic and Maxillofacial Surgery, Division of Oral and Maxillofacial Surgery;now
Instructor in Surgery, Departmentof Plastic and Maxillofacial Surgery,Brighamand Women’sHospitalandChildren’sHospital Medical Center,Boston,Mass.
side is mechanical
temporomandibular joints. Tomograms of the joints showed no evidence of bony ankylosis. On Jan 26, 1983, a left coroniodectomy was performed in light of a diagnosis of left temporalis shortening secondary to intramuscular hematoma and subsequent fibrosis induced by the initial injury and/or iatrogenically during fracture reduction. The patient’s head was stabilized in a padded foam cushion. After induction of nasoendotrachealgeneral anesthesia and muscle paralysis, interincisal opening with the aid of a mechanical mouth prop was noted to be 21 mm. Incision through the temporalis insertion at the coronoid process allowed an additional 6 mm. of opening. At completion of the coronoidectomy, the mouth could be opened to 42 mm. A rubber block was placed between the posterior maxillary and mandibular teeth on the right side as the incision was closed. The patient was extubated in the operating room without difficulty. He was alert and responsive. The rubber block remained in place. Throughout the procedure the patient remained in the supine position, and no unusual manipulation of the face or head was carried out. Five hours after the procedure, the patient was tolerating the open-mouth position without problem. There was no evidence of facial nerve deficit. The following morning, 12 hours postoperatively, the patient was noted to be having difficulty closing the right eye. The rubber block had been removed earlier, after a total of approximately 8 hours. Further examination revealed a total right facial palsy (that is, on the side contralateral to the surgical site). There were no other focal neurologic deficits. Hearing and lacrimation were normal. There was no immediate or subsequent skin eruption. A 2-week course of high-dose prednisone was initiated. Follow-up over the next 3 months revealed improved interincisal opening to 35 mm. on a physical therapy 23
24
Chuong
regimen, but restriction of lateral excursionspersisted. There was no clinical improvement in the facial palsy, and the patient declined operative intervention. Nerve excitability testing at 2 and 4 weeks revealed absence of conduction along the peripheral branches of the right facial nerve. Lacrimation and the acoustic reflex remained normal. DISCUSSION
Direct injury to the peripheral branches of the facial nerve by extraoral dissection in the temporal, preauricular, or submandibular regions to approach the jaws and contiguous structures is well recognized. Less common is facial nerve injury secondary to intraoral surgical procedures on the mandibular ramus. Facial nerve injury has been reported following sagittal osteotomy’~’ and intraoral oblique osteotomy of the mandible, in each instance presumed to be secondary to compression of the nerve trunk by retractors or mobilized bony segments against the mastoid or by styloid process fracture. Other considerations in the differential diagnosis of facial palsy occurring in close temporal relationship to surgery include (1) compression from hematoma; (2) external compression at the stylomatoid foramen by unusual positioning during surgery, perhaps with prolonged pressure applied by a firm head-stabilizing device or during induction of anesthesia*; (3) ischemic lesions of the central nervous system, such as stroke from hemorrhage, thrombosis, or embolus, or a mass lesion, such as an acoustic neuroma, aneurysm, cholesteatoma, etc. (a central ischemic event during a general anesthetic must be ruled out by thorough neurologic evaluation); (4) aural pathosis (acute or chronic otitis media can causefacial palsy, as can “malignant external otitis,” that is, infection, usually by Pseudomonas, in the external canal extending to the base of the skull causing facial palsy); (5) systemic diseases associated with an increased incidence of facial paralysis, such as diabetes, hypothyroidism, collagen vascular diseases,sarcoidosis, and Wegener’s granulomatosis, among others; (6) Bell’s palsy (primary idiopathic facial paralysis) occurring coincidentally. (Bell’s palsy is defined as “a lower motor neurone facial paresis, of acute onset, unaccompanied by evidence of aural or neurological disease and without other local cause.“5) There is evidence that a viral origin underlies Bell’s palsy. Adour found a high correlation with herpes simplex virus and believes that reactivation of a latent herpes virus with a resultant acute cranial *Mayumi and associate9 have reported facial nerve palsy following general anesthesia by mask.
Oral Surg. Januar>. I 984
polyneuritis accounts for this phenomenon. The neuritis may result in edema, secondarily causing nerve compression within the bony canal. Gussen’ subscribes to a vasospastic etiology leading to vascular distention, nerve compression, and resultant ischemia. McGovern and Estevez*present evidence of an immunologic mechanism of nerve injury mediated through IgE antibody and mast cell degranulation. They report successfulearly use of cromolyn sodium, an inhibitor of mast cell degranulation, in the prevention of nerve degeneration. Bell’s palsy occurs in seventeenor eighteen cases per 100,000.9 It tends to occur in middle-aged women, often after exposure to cold, and occurs with greater frequency during pregnancy and in persons with diabetes. Often other cranial nerves (V, VIII, IX, X) are involved, supporting Adour’s concept of a cranial polyneuritis. In the present case the patient had no underlying systemic diseasepredisposing him to Bell’s palsy, and there was no evidence of aural pathosis or evidence of extrinsic nerve compression. There was no direct trauma to the nerve trunk, since the surgical procedure was carried out on the contralateral side and, 5 hours postoperatively, there was no nerve deficit. A delayed onset of neurologic deficit suggests that inflammation and secondary edema or hemorrhage, rather than disruption of the nerve trunk, were the mechanisms of injury. The g-hour period of forced mouth opening must be considered as a possible cause of stretching or compression of the nerve, with delayed onset of palsy, or of compression of the nerve trunk between the posterior border of the ramus and the mastoid which, in the absence of gross dislocation of the condyles, is anatomically impossible. There was no evidence of dislocation of the condyles intra- OF postoperatively. Stretching of the nerve trunk by mouth opening to 40 OF 50 mm. in the absence of condylar dislocation OF acute fracture is not explainable mechanically. Review of the facial radiographs showed no unusual bone fragment that might have been dislodged posteriorly by forceful mouth opening. Facial nerve injury in the absence of temporal bone fracture has been reported in association with mandibular fractures, usually fractures of the condyle with or without dislocation.“-I4 Injury may result from severance of the nerve by fracture segments, or neuropraxia or axonotmesis may occur secondary to lateral dislocation of the ipsilateral condyle from the glenoid fossa, resulting in nerve stretching.14A second fracture, usually of the body with lateral dislocation of the condyle on the affected
Volume 57 Number I
Contralateral
side, is the most likely combination of events accounting for such a mechanism of injury. No lateral dislocating forces were applied to the mandible in the case reported here. Bell’s palsy, perhaps incited by the manipulations about the face, is the most likely explanation of the problem reported here. Many of the factors that appear to be related to the onset of herpes labialis, such as cold exposure and manipulation about the mouth, appear to be related to the onset of spontaneous facial palsy.6 Onset of facial paralysis following dental extractions or other short procedures in the mouth has been reported. In these instances a latent virus is presumably activated and an inflammatory response is initiated. This may be only one of the factors involved in the pathogenesis of Bell’s palsy. Most commonly, hyperacusis is noted with Bell’s palsy as a result of involvement of the stapedial branch from the pyramidal segment of the facial nerve within the facial canal. A decreasein taste and dryness of the ipsilateral eye are usually noted and are due to involvement of the chorda tympani and the greater superficial petrosal nerve, respectively. The pattern of denervation in the case reported here demonstrates a lesion that is more distal than is usually seen in Bell’s palsy but not inconsistent with this diagnosis. SUMMARY
Contralateral facial palsy has been described as an unusual complication following coronoidectomy. The differential diagnosis of facial palsy is reviewed. An idiopathic Bell’s palsy, coincident with the surgical procedure, is the most likely diagnosis in the absence of dislocation or acute fracture involving the ipsilatera1 condyle.
facial palsy following
coronoidectomy
25
REFERENCES I. Dendy, R. A.: Facial Nerve Paralysis Following Sagittal Split Mandibular Osteotomy: Case Report, Br. J. Oral Surg. 11: 101-105, 1973. 2. Behrman, S. J.: Complications of Sagittal Osteotomy of the Mandibular Ramus, j. Oral Surg. 30: 554-561, 1972. 3. Guralnick. W. C.. and Kellv. J. P.: Palsv of the Facial Nerve After intraoral Oblique Os
Surgery
OF VIRGINIA
MEDICAL
CENTER
Total facial nerve palsy occurring 12 hours after an intraoral procedure on the contralateral described. The differential diagnosis of facial palsy is reviewed, with emphasis on possible factors temporally related to surgery.
F
acial nerve deficit has been reported following surgical procedures on and about the jaws, performed both intraorally and extraorally, and in association with facial trauma, both sharp and blunt. The following is a caseof total facial nerve palsy noted 12 hours after an intraoral procedure on the contralatera1 side. CASE REPORT
A healthy ll-year-old white male patient was initially hospitalized in August, 1982, after he sustained multiple facial fractures in a fall. Injuries included a LeFort II fracture, a left zygomatic complex fracture, and multiple mandibular injuries, including bilateral condylar head and symphyseal fractures. Treatment consisted of open reduction and internal fixation of the left zygomatic complex and symphyseal fractures and closed reduction of the midface and condylar fractures with the aid of frontal suspension. Maxillomandibular fixation was maintained for 8 weeks, and when the patient was first evaluated by the Oral Surgery Service 2 weeks after release from fixation trismus to 6 mm. interincisally was noted. An additional 2 weeks of mouth-opening exercise was instituted, with only slight improvement to an opening of 9 mm. Condylar motion was palpable bilaterally, although lateral excursions were markedly restricted. A scar band was palpable intraorally along the anterior border of the left mandibular ramus. Plain radiographs failed to demonstrate a cause for the trismus; that is, the zygomatic arches were well reduced and there was no obvious new bone formation across the *Formerly AssistantProfessor,Departmentof Plastic and Maxillofacial Surgery, Division of Oral and Maxillofacial Surgery;now
Instructor in Surgery, Departmentof Plastic and Maxillofacial Surgery,Brighamand Women’sHospitalandChildren’sHospital Medical Center,Boston,Mass.
side is mechanical
temporomandibular joints. Tomograms of the joints showed no evidence of bony ankylosis. On Jan 26, 1983, a left coroniodectomy was performed in light of a diagnosis of left temporalis shortening secondary to intramuscular hematoma and subsequent fibrosis induced by the initial injury and/or iatrogenically during fracture reduction. The patient’s head was stabilized in a padded foam cushion. After induction of nasoendotrachealgeneral anesthesia and muscle paralysis, interincisal opening with the aid of a mechanical mouth prop was noted to be 21 mm. Incision through the temporalis insertion at the coronoid process allowed an additional 6 mm. of opening. At completion of the coronoidectomy, the mouth could be opened to 42 mm. A rubber block was placed between the posterior maxillary and mandibular teeth on the right side as the incision was closed. The patient was extubated in the operating room without difficulty. He was alert and responsive. The rubber block remained in place. Throughout the procedure the patient remained in the supine position, and no unusual manipulation of the face or head was carried out. Five hours after the procedure, the patient was tolerating the open-mouth position without problem. There was no evidence of facial nerve deficit. The following morning, 12 hours postoperatively, the patient was noted to be having difficulty closing the right eye. The rubber block had been removed earlier, after a total of approximately 8 hours. Further examination revealed a total right facial palsy (that is, on the side contralateral to the surgical site). There were no other focal neurologic deficits. Hearing and lacrimation were normal. There was no immediate or subsequent skin eruption. A 2-week course of high-dose prednisone was initiated. Follow-up over the next 3 months revealed improved interincisal opening to 35 mm. on a physical therapy 23
24
Chuong
regimen, but restriction of lateral excursionspersisted. There was no clinical improvement in the facial palsy, and the patient declined operative intervention. Nerve excitability testing at 2 and 4 weeks revealed absence of conduction along the peripheral branches of the right facial nerve. Lacrimation and the acoustic reflex remained normal. DISCUSSION
Direct injury to the peripheral branches of the facial nerve by extraoral dissection in the temporal, preauricular, or submandibular regions to approach the jaws and contiguous structures is well recognized. Less common is facial nerve injury secondary to intraoral surgical procedures on the mandibular ramus. Facial nerve injury has been reported following sagittal osteotomy’~’ and intraoral oblique osteotomy of the mandible, in each instance presumed to be secondary to compression of the nerve trunk by retractors or mobilized bony segments against the mastoid or by styloid process fracture. Other considerations in the differential diagnosis of facial palsy occurring in close temporal relationship to surgery include (1) compression from hematoma; (2) external compression at the stylomatoid foramen by unusual positioning during surgery, perhaps with prolonged pressure applied by a firm head-stabilizing device or during induction of anesthesia*; (3) ischemic lesions of the central nervous system, such as stroke from hemorrhage, thrombosis, or embolus, or a mass lesion, such as an acoustic neuroma, aneurysm, cholesteatoma, etc. (a central ischemic event during a general anesthetic must be ruled out by thorough neurologic evaluation); (4) aural pathosis (acute or chronic otitis media can causefacial palsy, as can “malignant external otitis,” that is, infection, usually by Pseudomonas, in the external canal extending to the base of the skull causing facial palsy); (5) systemic diseases associated with an increased incidence of facial paralysis, such as diabetes, hypothyroidism, collagen vascular diseases,sarcoidosis, and Wegener’s granulomatosis, among others; (6) Bell’s palsy (primary idiopathic facial paralysis) occurring coincidentally. (Bell’s palsy is defined as “a lower motor neurone facial paresis, of acute onset, unaccompanied by evidence of aural or neurological disease and without other local cause.“5) There is evidence that a viral origin underlies Bell’s palsy. Adour found a high correlation with herpes simplex virus and believes that reactivation of a latent herpes virus with a resultant acute cranial *Mayumi and associate9 have reported facial nerve palsy following general anesthesia by mask.
Oral Surg. Januar>. I 984
polyneuritis accounts for this phenomenon. The neuritis may result in edema, secondarily causing nerve compression within the bony canal. Gussen’ subscribes to a vasospastic etiology leading to vascular distention, nerve compression, and resultant ischemia. McGovern and Estevez*present evidence of an immunologic mechanism of nerve injury mediated through IgE antibody and mast cell degranulation. They report successfulearly use of cromolyn sodium, an inhibitor of mast cell degranulation, in the prevention of nerve degeneration. Bell’s palsy occurs in seventeenor eighteen cases per 100,000.9 It tends to occur in middle-aged women, often after exposure to cold, and occurs with greater frequency during pregnancy and in persons with diabetes. Often other cranial nerves (V, VIII, IX, X) are involved, supporting Adour’s concept of a cranial polyneuritis. In the present case the patient had no underlying systemic diseasepredisposing him to Bell’s palsy, and there was no evidence of aural pathosis or evidence of extrinsic nerve compression. There was no direct trauma to the nerve trunk, since the surgical procedure was carried out on the contralateral side and, 5 hours postoperatively, there was no nerve deficit. A delayed onset of neurologic deficit suggests that inflammation and secondary edema or hemorrhage, rather than disruption of the nerve trunk, were the mechanisms of injury. The g-hour period of forced mouth opening must be considered as a possible cause of stretching or compression of the nerve, with delayed onset of palsy, or of compression of the nerve trunk between the posterior border of the ramus and the mastoid which, in the absence of gross dislocation of the condyles, is anatomically impossible. There was no evidence of dislocation of the condyles intra- OF postoperatively. Stretching of the nerve trunk by mouth opening to 40 OF 50 mm. in the absence of condylar dislocation OF acute fracture is not explainable mechanically. Review of the facial radiographs showed no unusual bone fragment that might have been dislodged posteriorly by forceful mouth opening. Facial nerve injury in the absence of temporal bone fracture has been reported in association with mandibular fractures, usually fractures of the condyle with or without dislocation.“-I4 Injury may result from severance of the nerve by fracture segments, or neuropraxia or axonotmesis may occur secondary to lateral dislocation of the ipsilateral condyle from the glenoid fossa, resulting in nerve stretching.14A second fracture, usually of the body with lateral dislocation of the condyle on the affected
Volume 57 Number I
Contralateral
side, is the most likely combination of events accounting for such a mechanism of injury. No lateral dislocating forces were applied to the mandible in the case reported here. Bell’s palsy, perhaps incited by the manipulations about the face, is the most likely explanation of the problem reported here. Many of the factors that appear to be related to the onset of herpes labialis, such as cold exposure and manipulation about the mouth, appear to be related to the onset of spontaneous facial palsy.6 Onset of facial paralysis following dental extractions or other short procedures in the mouth has been reported. In these instances a latent virus is presumably activated and an inflammatory response is initiated. This may be only one of the factors involved in the pathogenesis of Bell’s palsy. Most commonly, hyperacusis is noted with Bell’s palsy as a result of involvement of the stapedial branch from the pyramidal segment of the facial nerve within the facial canal. A decreasein taste and dryness of the ipsilateral eye are usually noted and are due to involvement of the chorda tympani and the greater superficial petrosal nerve, respectively. The pattern of denervation in the case reported here demonstrates a lesion that is more distal than is usually seen in Bell’s palsy but not inconsistent with this diagnosis. SUMMARY
Contralateral facial palsy has been described as an unusual complication following coronoidectomy. The differential diagnosis of facial palsy is reviewed. An idiopathic Bell’s palsy, coincident with the surgical procedure, is the most likely diagnosis in the absence of dislocation or acute fracture involving the ipsilatera1 condyle.
facial palsy following
coronoidectomy
25
REFERENCES I. Dendy, R. A.: Facial Nerve Paralysis Following Sagittal Split Mandibular Osteotomy: Case Report, Br. J. Oral Surg. 11: 101-105, 1973. 2. Behrman, S. J.: Complications of Sagittal Osteotomy of the Mandibular Ramus, j. Oral Surg. 30: 554-561, 1972. 3. Guralnick. W. C.. and Kellv. J. P.: Palsv of the Facial Nerve After intraoral Oblique Os
Surgery