Otology & Neurotology 36:513Y518 Ó 2014, Otology & Neurotology, Inc.
Facial Nerve Outcomes After Middle Fossa Decompression for Bell’s Palsy *Richard B. Cannon, *Richard K. Gurgel, †Frank M. Warren, and *Clough Shelton *Division of OtolaryngologyYHead and Neck Surgery, University of Utah, Salt Lake City, Utah; and ÞDepartment of Otolaryngology Head and Neck Surgery, Oregon Health & Science University, Portland, Oregon, U.S.A.
I or II) within 1 year after surgery, and 5 of those patients (35.7%) improved to HB I. The remaining 4 patients (28.6%) improved to HB III. Patients older than 60 years (n = 3) had an HB III outcome and did significantly worse than the younger-than-60-years group ( p = 0.002). The difference in preoperative and postoperative pure tone average and word recognition score was 2.1 dB and 0.9%, respectively. There were no major complications. Minor, transient complications occurred in 22.2% of patients. Conclusion: In patients with severe Bell’s palsy at risk for a poor facial nerve outcome, MCF decompression of the facial nerve within 14 days of symptom onset provides good facial nerve outcomes with minimal morbidity. Key Words: Bell’s palsyV Poor prognosisVFacial nerve decompressionVMiddle cranial fossaVSurgical criteriaVLong-term outcomes.
Objective: Evaluate the long-term outcomes of facial nerve decompression via the middle fossa approach for Bell’s palsy patients with poor prognosis based on clinical and electrodiagnostic testing. Study Design: Retrospective case series. Setting: Tertiary-care, academic medical center. Patients: Fourteen patients underwent surgical decompression for Bell’s palsy within 14 days of symptom onset from 2000 to 2012. Surgical criteria included greater than 90% degeneration on ENoG testing and no voluntary EMG potentials. Intervention: Middle cranial fossa (MCF) bony decompression of the facial nerve, including the meatal foramen, labyrinthine segment, and geniculate ganglion. Main Outcome Measures: Long-term facial function, hearing results, and surgical complications. Results: After MCF decompression, 10 patients (71.4%) regained normal or near-normal facial function (House-Brackmann [HB]
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Bell’s palsy is an idiopathic condition of unilateral facial nerve paresis (weakness) or paralysis (complete loss of movement) (1). This disorder affects approximately 23 per 100,000 people per year or approximately 1 in 65 people in a lifetime (2). It affects men and women equally and occurs on both sides of the face in similar frequency. The peak incidence is between ages 10 and 40 years. The exact cause is unknown; however, there is significant evidence that inflammation and edema of the bony intratemporal facial nerve causes constriction and resultant injury (3,4). Particularly, the meatal foramen and labyrinthine segment have been shown to be the narrowest portion of the bony canal and common sites of conduction blockage (5Y8). Herpes simplex virus is the most commonly implicated cause of inflammation (9). The injury due to inflammation causes impaired ability to move facial musculature on the
affected side. A large observational study showed that 70% of patients had complete palsies at initial examination, 85% of patients begin having return of some facial movements within 3 weeks, and overall, approximately 70% of patients return to completely normal facial function without any intervention (10). There is controversy regarding the optimal management of Bell’s palsy. Treatments aim to address the underlying pathophysiology to improve outcomes. Several studies demonstrate the effectiveness of using high-dose steroids, and this treatment has become the standard of care for initial treatment (11Y15). Steroids are started as soon as possible once the diagnosis is made. Normal facial function is recovered after 9 months in 94% of patients treated with prednisolone for 10 days compared with 82% of patients given placebo (11). In addition, time to recovery is significantly shorter in patients who received prednisolone compared with those who did not with a median of 75 days to complete recovery versus 104 days in the placebo group (12). Acyclovir is also commonly prescribed as a treatment; however, there is conflicting evidence regarding efficacy (12,15Y22). Despite the overwhelming majority of patients recovering normal or near normal facial function with observation
Address correspondence and reprint requests to Clough Shelton, M.D., FACS, University of Utah, Division of OtolaryngologyYHead and Neck Surgery, 50 North Medical Dr., SOM 3C-120, Salt Lake City, Utah 84132; E-mail: [email protected] Support/Funding: No sources of support or funding were received for this work. The authors disclose no conflicts of interest.
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or medical management, unfortunately, some patients do not recover good facial function. This long-term facial dysfunction can manifest as persistent paralysis, paresis, or synkinesis and varies from barely noticeable in some patients to significantly disabling in others. These patients can suffer from a dry eye, corneal abrasion, blindness, dysarthria, dysgeusia, oral incompetence, facial contracture, facial spasm, and the significant challenges of facial asymmetry. In fact, there is evidence that patients with Bell’s palsy have significantly increased psychological distress, and this is closely associated with the severity of facial paralysis (23). Identifying this subset of patients with poor long-term prognosis has been an area of intense research, and coupling a function-based clinical grading system with electrodiagnostic testing has shown significant promise (24). The HouseBrackmann (HB) facial nerve grading system is widely accepted as the standard method to evaluate facial nerve palsy, and those patients with persistent, complete paralysis, despite treatment, may benefit from additional electrical testing and surgical treatment (1,25,26). Electroneurography (ENoG) is a tool that provides reliable and objective data to compare the injured face against the patient’s normal side as an internal control. This test measures facial nerve conductivity using surface electrodes to assess electrical depolarization of the facial musculature after the main trunk of the facial nerve is stimulated, and the result is reported as a percentage of the normal side. Patients with significant (990%) ENoG degeneration are at increased risk for incomplete recovery and poor long-term facial outcomes. To be predictive, this testing must be done within 14 days of symptom onset. For patients with greater than 90% degeneration on ENoG, electromyography (EMG) provides complementary information. In this test, needle electrodes are placed into the affected muscles, and both spontaneous depolarizations and voluntary contractions are recorded. Minor contractions that are beyond the ability of the physician to observe can be recorded. Absent voluntary nerve activity on EMG suggests axonal damage, and these patients also have a high probability of prolonged facial dysfunction (26). Therefore, to identify those at risk for an adverse longterm outcome, patients with continued complete facial paralysis (HB VI) during their course of steroids undergo ENoG testing within 14 days of symptom onset. Several studies show that patients with less than 90% degeneration on their ENoG testing have excellent long-term outcomes, with all patients regaining normal or near normal facial function (HB I or II) (26Y28). On the contrary, if patients show greater than 90% degeneration on ENoG testing and have no voluntary EMG motor unit potentials, then they have only a 42% to 50% chance of recovery to normal or near-normal facial function (HB I or II) with steroids alone (26,29,30). For many patients, this rate of recovery is unacceptable, and additional treatment is needed to prevent permanent sequelae. Surgical decompression has been offered to these at-risk patients with reports of 66% to 91% improvement to normal or near-normal facial function (HB I or II) (26,29Y31). The middle fossa approach is used to decompress the meatal
foramen and labyrinthine segment. As discussed previously, several studies support the location of greatest constriction and nerve conduction blockage to be at the meatal foramen and along the labyrinthine segment. Therefore, this site must be accessed and decompressed during surgery. Transmastoid decompression of the facial nerve for Bell’s palsy has been abandoned because it is ineffective (31Y33). In the past, there was significant variability in the timing of surgery for Bell’s palsy in the literature. Some studies insist on decompression within 2 weeks of symptom onset, whereas others perform surgery up to 3 months (26,29Y35). Based on the presumed pathophysiology, an earlier decompression should confer added benefit over a later decompression by relieving the site of constriction before irreversible neural injury. Currently, most experts agree that decompression should be done within 14 days of onset to be effective (24,26,28,29). Research of surgical decompression has been hampered by the limited number of patients who meet surgical decompression criteria. There are only a few studies available to guide treatment, and they have not been widely reproduced. The main purpose of this study is to further characterize the surgical decompression of Bell’s palsy via the middle fossa approach for patients with poor prognosis based on clinical and electrodiagnostic testing. This study also evaluates the long-term outcomes of the middle fossa facial nerve decompression, particularly in regard to long-term facial function outcomes, safety, and hearing results. MATERIALS AND METHODS With institutional review board approval, we searched our institutional database for patients who underwent a middle fossa craniotomy for the diagnosis of Bell’s palsy. Patients who underwent surgery for recurrent Bell’s palsy were excluded. The medical records of 15 consecutive patients with Bell’s palsy treated with a middle cranial fossa surgical decompression from May 19, 2000, to April 11, 2012, at the University of Utah Hospital were retrospectively reviewed. There was 1 patient who was lost to follow-up after the 4-week postoperative visit and was excluded from analysis. All patients received a course of high-dose steroids when the Bell’s palsy was initially identified. Those who had complete facial paralysis (HB VI) underwent ENoG testing. If the patients had greater than 90% degeneration on ENoG testing, no voluntary EMG motor unit potentials, and presented within 14 days of symptom onset, then surgical decompression via the middle fossa approach was recommended. For further comparison, an additional analysis was performed on the 5 consecutive patients treated before 2000, when surgical decompression was offered to patients up to 1 month after the onset of their paralysis. For patients electing to have surgical decompression, a standard middle cranial fossa approach to the internal auditory canal (IAC) was performed. The facial nerve was identified in the lateral IAC, exposed from the labyrinthine segment and meatal foramen to the geniculate ganglion and a portion of the tympanic segment. The fibrous ligament at the meatal foramen of the fallopian canal and exposed nerve sheath (epineurium) was incised. The patient’s clinical course was followed including their HB grade, preoperative and postoperative hearing results, and both surgical and longterm complications. Final HB grade was assessed at the last available clinic visit within 1 year of surgery, and the final hearing result was assessed at a clinic visit between 3 months and 1 year
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MIDDLE FOSSA DECOMPRESSION FOR BELL_S PALSY
FIG. 1. Final facial nerve HB grade based on the day of decompression after paralysis.
after surgery. The results were compiled and statistically analyzed with the W2 test and regression analysis with a best fit linear trend line, R2 value, and p value.
RESULTS There are 14 patients who met the inclusion criteria. The average time from onset of facial paralysis to decompression was 11.3 days (range, 7Y14 d; median, 10 d). Average duration of follow-up was 15.3 months. The majority of patients, 71.4% (10/14), regained normal or near normal facial function (HB I or II) by their last clinic visit within 1 year after surgery. Of these patients, 35.7% (5/14) improved to normal (HB I), 35.7% (5/14) improved to near normal (HB II), and all remaining patients improved to a HB III, 28.6% (4/14). Analyzing the final facial nerve grade based on the number of days from the beginning of facial paralysis to surgical decompression demonstrated a weak correlation (R2 = 0.047; p = 0.23) (Fig. 1). Regression analysis with a best fit linear trend line shows a tendency toward worse outcomes the more days to decompression, but this was not statistically significant within our 14-day time frame. There was no difference in final facial nerve outcome depending on the patient’s sex or side of paralysis. All patients older than 60 years (n = 3) had an HB III facial outcome. Patients younger than 60 years were significantly more likely to regain normal or near-normal facial function (HB I or II), 90.9% (10/11) versus 0% (0/3), respectively (p = 0.002) (Fig. 2). To compare patients decompressed within 14 days with those decompressed after 14 days, an additional analysis was performed. The 5 consecutive patients treated before 2000 were compared with the modern criteria because surgical decompression was offered to these patients up to 1 month after the onset of their paralysis. Stratifying these 2 groups based on the timing of surgery, those patients decompressed within 14 days were more likely to regain normal or near normal facial function (HB I or II) compared with those decompressed after 14 days, 71.4% (10/14) versus 20.0% (1/5), respectively ( p = 0.046) (Fig. 3). In addition, the only patients to have complete recovery (HB I) were decompressed within 14 days, 35.7% (5/14) versus 0.0%
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FIG. 2. Final facial nerve HB grade after decompression based on the patient’s age.
(0/5), respectively ( p = 0.12). All remaining patients in both groups improved to a HB III, 28.6% (4/14) of those decompressed within 14 days versus 80.0% (4/5) of those decompressed after 14 days. The average ENoG observed was 96% degeneration, with 35.7% (5/14) of patients having an ENoG of 100% degeneration and 64.3% (9/14) having greater than 95% degeneration. There was no difference in final facial function outcome depending on the patient’s preoperative ENoG degeneration. The average preoperative pure tone average (PTA) was 10.1 dB (range, 0Y22 dB), and average postoperative PTA was 12.2 dB (range, 3Y29 dB). Average preoperative word recognition score (WRS) was 99.7% (range, 96%Y100%), and average postoperative WRS was 98.8% (range, 92%Y100%). There were no significant changes in final hearing results (98 dB loss or 98% decrease in WRS) in any patient. There were no major postoperative complications, based on a standardized classification of surgical complications, which includes life-threatening complications (i.e., death, cerebrovascular accident, cardiopulmonary insult, multiorgan dysfunction); complication requiring further surgery, endoscopy, or radiologic intervention; and complication requiring unanticipated pharmacological treatment, Grades IV, III, and II, respectively (36). Minor complications (Grade I) occurred in 22.2% of patients and were largely limited to the postoperative period. Temporary morbidity observed was
FIG. 3. Final facial nerve HB grade after decompression based on the timing of surgery. Otology & Neurotology, Vol. 36, No. 3, 2015
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facial numbness/tingling, nausea/vomiting, dizziness, periorbital ecchymosis, and pruritus. Gustatory hyperlacrimation was a late complication observed in 3 patients. DISCUSSION Treatment of Bell’s palsy is complex. The vast majority of cases recover completely with observation or medical therapy alone; however, long-term facial paresis, paralysis, and synkinesis are still grave outcomes in a small portion of patients with Bell’s palsy. Standardized algorithms have been shown to successfully identify these high-risk patients based on clinical exam and electrical testing. Fisch and Esslen helped to develop and popularize the use of ENoG and EMG testing for Bell’s palsy and set the stage to stratify patients into high- and low-risk groups (27). Gantz et al. also showed that patients with less than 90% degeneration on ENoG (n = 54), all regained normal or near-normal facial function (HB I or II), with 89% achieving a HB I (26). These low-risk patients, therefore, clearly do not need further intervention. In addition, EMG is a complimentary modality in patients with 100% degeneration on ENoG. Patients with persistent motor unit potentials on EMG are likely to recover with a good prognosis.Therefore, for Bell’s palsy, using the HB grading system coupled with electrical testing, patients with complete facial paralysis (HB VI), greater than 90% degeneration on ENoG, and absent voluntary EMG potentials have been shown to represent a subset of patients who are at increased risk for a poor long-term outcome. The pathophysiology of Bell’s palsy is likely due to neural edema compressing the facial nerve at its most narrow course in the bony fallopian canal. Despite this presumed etiology, surgical decompression of the mastoid segment of the facial nerve has not shown any benefit in multiple studies, including a recent Cochrane review (32,33,37). This operation fails to address the known site of greatest constriction, the meatal foramen, where axonal injury occurs. However, using a middle cranial fossa approach to identify and decompress the proximal facial nerve accomplishes this goal. This surgical technique has been shown to be safe when done by appropriately trained surgeons and effective at improving long-term facial motor function in this high-risk subset of patients. Using the above surgical criteria, Gantz et al. identified high risk Bell’s palsy patients and demonstrated high-level evidence (caseYcontrol study) for decompression via a middle cranial fossa approach (26). This study showed that 91% of patients (n = 34) who underwent decompression within 14 days improved to normal or near-normal facial function (HB I or HB II) compared with only 42% of patients (n = 36) who were treated with steroids only. The researchers demonstrated during surgery that the conduction blockage was medial to the geniculate ganglion in 17 of 19 patients on intraoperative evoked EMG. This study also demonstrated that the timing of surgical decompression was critical. Those patients decompressed before 14 days had a high probability of a good outcome (HB I or II); after 14 days, outcomes were significantly worse. Decompressed patients had significantly improved outcomes compared with
nonsurgical controls, despite similar prognosis on electrophysiologic testing. In 2013, the American Academy of OtolaryngologyYHead and Neck Surgery assembled a multi-specialty clinical practice guideline (CPG) committee to give evidence-based recommendations pertaining to Bell’s palsy (1). Ultimately, the committee made no recommendation (neither for nor against) regarding surgical decompression of Bell’s palsy patients because of the variable quality of the aggregate evidence. They report the aggregate evidence as Grade D and state that the risks of surgery may outweigh the potential benefits, but concern for long-term facial deformity may make some patients willing to pursue a major operation for an increased chance of complete recovery. Although the CPG development process has strict methods for reviewing existing evidence, Eibling et al. observed that the lack of consideration of current standard treatment and expert opinion may reduce their value (38). The current study supports MCF facial nerve decompression in Bell’s palsy patients who are at high risk for poor facial nerve outcomes. In this group of patients that met the electrodiagnostic criteria for severe dysfunction and were treated with surgery within 14 days from onset of facial paralysis, their chances of regaining HB I or II function was 71.4%, with 35.7% obtaining a HB I outcome. This rate is significantly higher than the published standards for this subset with poor prognosis treated with steroids alone, with only 42% to 50% recovering to HB I or II, and is similar to other surgical decompression studies that report 66% to 91% improvement to HB I or II in these at-risk patients (26,29Y31). Also, in our additional analysis, we again showed that patients must be decompressed within 14 days because of significantly improved results. We have shown that age is related to facial nerve recovery; in our study, all patients older than 60 years (n = 3) had a poor (HB III) facial function outcome, a finding which is supported by several other studies. Adour showed that of the 446 patients, those younger than 60 years had an 11% chance of a poor outcome with persistent weakness, contractures, or synkinesis compared with 51% of those older than 60 years (39). In addition, Adour showed that those older than 60 years had an increased rate of complete paralysis during their course of Bell’s palsy, 55% versus 32%, respectively. Prescott also reported that of 879 patients, those with incomplete recovery were on average 14 years older than those with complete recovery, suggesting that older patients have a significantly poorer prognosis than younger patients (40). Katusic et al. showed that of 208 patients with Bell’s palsy, those older than 55 years (n = 64) were significantly more likely to have incomplete recovery, 21% versus 10% (41). More recently, Peitersen showed in an observational study of 1701 cases of Bell’s palsy, patients older than 60 years had worse prognosis (10). Only about one-third of these older patients returned to normal function, compared with children who had a 90% chance of full recovery, and patients aged 15 to 44 years who had a 75% to 84% chance of return to normal function. Several studies in other surgical fields, particularly for carpal tunnel decompression and cervical spinal nerve
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MIDDLE FOSSA DECOMPRESSION FOR BELL_S PALSY decompression, show that peripheral motor nerve regeneration and recovery is inversely related to age and is markedly worse in patients older than 60 years (42Y45). A systematic review of the peripheral nerve repair literature reiterated this result, stating that holding all other variables constant, older age predicts poorer outcomes (44). Mondelli et al. showed that patients older than 60 years had more severe clinical and electrophysiological findings preoperatively and argued that their reduced improvement after surgical decompression is likely due to lower repair capacity (45). Basic science studies have elucidated multiple molecular reasons why nerve repair is reduced in older patients (46Y50). These researchers demonstrate that each phase of nerve regeneration is affected. After nerve injury, the early repair process is delayed because of decreased macrophage recruitment, which slows Wallerian degeneration (46). Older patients also have fewer Schwann cells and reduced secretion of trophic factors. This change decreases axonal sprout formation, slows axon regeneration rates, and decreases nerve density after restoration (47). Axonal transport slows as we age, and this delays nerve repair (48). Also, regenerated axons in older patients are more often unmyelinated, which decreases synaptic responsiveness to nerve stimulation, resulting in clinically incomplete reinnervation (49). These age-related changes are not linearly progressive; normal function is maintained throughout the majority of human life but then begins to decline in the fifth and sixth decades (50). These cellular factors likely result in the observed worse outcomes reported in our study for patients older than 60 years. The middle fossa surgical approach requires a craniotomy, and it is commonly used to approach the medial temporal bone. The safety of this technique has been shown in numerous studies to approach the facial nerve, remove acoustic neuromas, and repair superior canal dehiscence (51,52). Our results were similar. There were no significant changes in final hearing results (98 dB loss or 98% decrease in WRS) in any patient. There were no major postoperative complications, and minor postoperative complications were transient and largely limited to the immediate postoperative period. For Bell’s palsy patients, the data available support the efficacy of middle cranial fossa surgical decompression of the labyrinthine segment and meatal foramen in high-risk patients. Our results further support this thesis. This surgery is safe and effective, preserves hearing, and should be performed within 14 days of the onset of facial paralysis. Decompression in patients older than 60 years should be performed cautiously, and these patients should be warned of their likely worse overall prognosis. In summary, middle fossa surgical decompression offers good facial nerve outcomes for patients with Bell’s palsy and poor prognosis on electrical testing. CONCLUSION In patients with severe Bell’s palsy at risk for a poor facial nerve outcome, middle cranial fossa decompression of the facial nerve provides good long-term facial function
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outcomes with few complications. Surgical decompression is reserved for those patients with HB VI, greater than 90% degeneration on ENoG, and absent voluntary EMG potentials and should be performed within 14 days of the onset of facial paralysis. This series further supports the safety and efficacy of this operative technique, demonstrating good facial nerve outcomes and minimal morbidity in these at-risk Bell’s palsy patients. REFERENCES 1. Baugh RF, Basura GJ, Ishii LE, et al. Clinical practice guideline: Bell’s palsy. Otolaryngol Head Neck Surg 2013;149:S1Y27. 2. Marson AG, Salinas R. Bell’s palsy. Western J Med 2000;173:266Y8. 3. Pulec JL. Early decompression of the facial nerve in Bell’s palsy. Ann Otol Rhinol Laryngol 1981;90:570Y7. 4. Yamamoto E, Fisch U. Experimentally induced facial nerve compression in cats. Acta Otolaryngol 1975;79:390Y5. 5. Burmeister HP, Baltzer PA, Volk GF, et al. Evaluation of the early phase of Bell’s palsy using 3 T MRI. Eur Arch Otorhinolaryngol 2011;268:1493Y500. 6. Fisch U, Esslen E. Total intratemporal exposure of the facial nerve. Pathologic findings in Bell’s palsy. Arch Otolaryngol 1972;95:335Y41. 7. Gantz BJ, Gmur A, Fisch U. Intraoperative evoked electromyography in Bell’s palsy. Am J Otolaryngol 1982;3:273Y8. 8. Ge XX, Spector GJ. Labyrinthine segment and geniculate ganglion of facial nerve in fetal and adult human temporal bones. Ann Otol Rhinol Laryngol Suppl 1981;90:1Y12. 9. Murakami S, Mizobuchi M, Nakashiro Y, et al. Bell palsy and herpes simplex virus: identification of viral DNA in endoneurial fluid and muscle. Ann Intern Med 1996;124:27Y30. 10. Peitersen E. Bell’s palsy: the spontaneous course of 2,500 peripheral facial nerve palsies of different etiologies. Acta Otolaryngol Suppl 2002;549:4Y30. 11. Sullivan FM, Swan IR, Donnan PT, et al. Early treatment with prednisolone or acyclovir in Bell’s palsy. N Engl J Med 2007;357:1598Y607. 12. Engstrom M, Berg T, Stjernquist-Desatnik A, et al. Prednisolone and valaciclovir in Bell’s palsy: a randomised, double-blind, placebocontrolled, multicentre trial. Lancet Neurol 2008;7:993Y1000. 13. Sullivan FM, Swan IR, Donnan PT, et al. A randomised controlled trial of the use of aciclovir and/or prednisolone for the early treatment of Bell’s palsy: the BELLS study. Health Technol Assess 2009;13:iiiYiv, ixYxi, 1Y130. 14. Hazin R, Azizzadeh B, Bhatti MT. Medical and surgical management of facial nerve palsy. Curr Opin Ophthalmol 2009;20:440Y50. 15. Axelsson S, Berg T, Jonsson L, et al. Bell’s palsy - the effect of prednisolone and/or valaciclovir versus placebo in relation to baseline severity in a randomised controlled trial. Clin Otolaryngol 2012;37:283Y90. 16. Alberton DL, Zed PJ. Bell’s palsy: a review of treatment using antiviral agents. Ann Pharmacother 2006;40:1838Y42. 17. Allen D, Dunn L. Aciclovir or valaciclovir for Bell’s palsy (idiopathic facial paralysis). Cochrane Database Syst Rev 2004:CD001869. 18. Browning GG. Bell’s palsy: a review of three systematic reviews of steroid and anti-viral therapy. Clin Otolaryngol 2010;35:56Y8. 19. Lockhart P, Daly F, Pitkethly M, et al. Antiviral treatment for Bell’s palsy (idiopathic facial paralysis). Cochrane Database Syst Rev 2009:CD001869. 20. Adour KK. Combination treatment with acyclovir and prednisone for Bell palsy. Arch Otolaryngol Head Neck Surg 1998;124:824. 21. Adour KK, Ruboyianes JM, Von Doersten PG, et al. Bell’s palsy treatment with acyclovir and prednisone compared with prednisone alone: a double-blind, randomized, controlled trial. Ann Otol Rhinol Laryngol 1996;105:371Y8. 22. Goudakos JK, Markou KD. Corticosteroids vs corticosteroids plus antiviral agents in the treatment of Bell palsy: a systematic review and meta-analysis. Arch Otolaryngol Head Neck Surg 2009;135:558Y64. 23. Huang B, Xu S, Xiong J, et al. Psychological factors are closely associated with the Bell’s palsy: a caseYcontrol study. J Huazhong Univ Sci Technol 2012;32:272Y9. Otology & Neurotology, Vol. 36, No. 3, 2015
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Facial Nerve Outcomes After Middle Fossa Decompression for Bell’s Palsy *Richard B. Cannon, *Richard K. Gurgel, †Frank M. Warren, and *Clough Shelton *Division of OtolaryngologyYHead and Neck Surgery, University of Utah, Salt Lake City, Utah; and ÞDepartment of Otolaryngology Head and Neck Surgery, Oregon Health & Science University, Portland, Oregon, U.S.A.
I or II) within 1 year after surgery, and 5 of those patients (35.7%) improved to HB I. The remaining 4 patients (28.6%) improved to HB III. Patients older than 60 years (n = 3) had an HB III outcome and did significantly worse than the younger-than-60-years group ( p = 0.002). The difference in preoperative and postoperative pure tone average and word recognition score was 2.1 dB and 0.9%, respectively. There were no major complications. Minor, transient complications occurred in 22.2% of patients. Conclusion: In patients with severe Bell’s palsy at risk for a poor facial nerve outcome, MCF decompression of the facial nerve within 14 days of symptom onset provides good facial nerve outcomes with minimal morbidity. Key Words: Bell’s palsyV Poor prognosisVFacial nerve decompressionVMiddle cranial fossaVSurgical criteriaVLong-term outcomes.
Objective: Evaluate the long-term outcomes of facial nerve decompression via the middle fossa approach for Bell’s palsy patients with poor prognosis based on clinical and electrodiagnostic testing. Study Design: Retrospective case series. Setting: Tertiary-care, academic medical center. Patients: Fourteen patients underwent surgical decompression for Bell’s palsy within 14 days of symptom onset from 2000 to 2012. Surgical criteria included greater than 90% degeneration on ENoG testing and no voluntary EMG potentials. Intervention: Middle cranial fossa (MCF) bony decompression of the facial nerve, including the meatal foramen, labyrinthine segment, and geniculate ganglion. Main Outcome Measures: Long-term facial function, hearing results, and surgical complications. Results: After MCF decompression, 10 patients (71.4%) regained normal or near-normal facial function (House-Brackmann [HB]
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Bell’s palsy is an idiopathic condition of unilateral facial nerve paresis (weakness) or paralysis (complete loss of movement) (1). This disorder affects approximately 23 per 100,000 people per year or approximately 1 in 65 people in a lifetime (2). It affects men and women equally and occurs on both sides of the face in similar frequency. The peak incidence is between ages 10 and 40 years. The exact cause is unknown; however, there is significant evidence that inflammation and edema of the bony intratemporal facial nerve causes constriction and resultant injury (3,4). Particularly, the meatal foramen and labyrinthine segment have been shown to be the narrowest portion of the bony canal and common sites of conduction blockage (5Y8). Herpes simplex virus is the most commonly implicated cause of inflammation (9). The injury due to inflammation causes impaired ability to move facial musculature on the
affected side. A large observational study showed that 70% of patients had complete palsies at initial examination, 85% of patients begin having return of some facial movements within 3 weeks, and overall, approximately 70% of patients return to completely normal facial function without any intervention (10). There is controversy regarding the optimal management of Bell’s palsy. Treatments aim to address the underlying pathophysiology to improve outcomes. Several studies demonstrate the effectiveness of using high-dose steroids, and this treatment has become the standard of care for initial treatment (11Y15). Steroids are started as soon as possible once the diagnosis is made. Normal facial function is recovered after 9 months in 94% of patients treated with prednisolone for 10 days compared with 82% of patients given placebo (11). In addition, time to recovery is significantly shorter in patients who received prednisolone compared with those who did not with a median of 75 days to complete recovery versus 104 days in the placebo group (12). Acyclovir is also commonly prescribed as a treatment; however, there is conflicting evidence regarding efficacy (12,15Y22). Despite the overwhelming majority of patients recovering normal or near normal facial function with observation
Address correspondence and reprint requests to Clough Shelton, M.D., FACS, University of Utah, Division of OtolaryngologyYHead and Neck Surgery, 50 North Medical Dr., SOM 3C-120, Salt Lake City, Utah 84132; E-mail: [email protected] Support/Funding: No sources of support or funding were received for this work. The authors disclose no conflicts of interest.
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or medical management, unfortunately, some patients do not recover good facial function. This long-term facial dysfunction can manifest as persistent paralysis, paresis, or synkinesis and varies from barely noticeable in some patients to significantly disabling in others. These patients can suffer from a dry eye, corneal abrasion, blindness, dysarthria, dysgeusia, oral incompetence, facial contracture, facial spasm, and the significant challenges of facial asymmetry. In fact, there is evidence that patients with Bell’s palsy have significantly increased psychological distress, and this is closely associated with the severity of facial paralysis (23). Identifying this subset of patients with poor long-term prognosis has been an area of intense research, and coupling a function-based clinical grading system with electrodiagnostic testing has shown significant promise (24). The HouseBrackmann (HB) facial nerve grading system is widely accepted as the standard method to evaluate facial nerve palsy, and those patients with persistent, complete paralysis, despite treatment, may benefit from additional electrical testing and surgical treatment (1,25,26). Electroneurography (ENoG) is a tool that provides reliable and objective data to compare the injured face against the patient’s normal side as an internal control. This test measures facial nerve conductivity using surface electrodes to assess electrical depolarization of the facial musculature after the main trunk of the facial nerve is stimulated, and the result is reported as a percentage of the normal side. Patients with significant (990%) ENoG degeneration are at increased risk for incomplete recovery and poor long-term facial outcomes. To be predictive, this testing must be done within 14 days of symptom onset. For patients with greater than 90% degeneration on ENoG, electromyography (EMG) provides complementary information. In this test, needle electrodes are placed into the affected muscles, and both spontaneous depolarizations and voluntary contractions are recorded. Minor contractions that are beyond the ability of the physician to observe can be recorded. Absent voluntary nerve activity on EMG suggests axonal damage, and these patients also have a high probability of prolonged facial dysfunction (26). Therefore, to identify those at risk for an adverse longterm outcome, patients with continued complete facial paralysis (HB VI) during their course of steroids undergo ENoG testing within 14 days of symptom onset. Several studies show that patients with less than 90% degeneration on their ENoG testing have excellent long-term outcomes, with all patients regaining normal or near normal facial function (HB I or II) (26Y28). On the contrary, if patients show greater than 90% degeneration on ENoG testing and have no voluntary EMG motor unit potentials, then they have only a 42% to 50% chance of recovery to normal or near-normal facial function (HB I or II) with steroids alone (26,29,30). For many patients, this rate of recovery is unacceptable, and additional treatment is needed to prevent permanent sequelae. Surgical decompression has been offered to these at-risk patients with reports of 66% to 91% improvement to normal or near-normal facial function (HB I or II) (26,29Y31). The middle fossa approach is used to decompress the meatal
foramen and labyrinthine segment. As discussed previously, several studies support the location of greatest constriction and nerve conduction blockage to be at the meatal foramen and along the labyrinthine segment. Therefore, this site must be accessed and decompressed during surgery. Transmastoid decompression of the facial nerve for Bell’s palsy has been abandoned because it is ineffective (31Y33). In the past, there was significant variability in the timing of surgery for Bell’s palsy in the literature. Some studies insist on decompression within 2 weeks of symptom onset, whereas others perform surgery up to 3 months (26,29Y35). Based on the presumed pathophysiology, an earlier decompression should confer added benefit over a later decompression by relieving the site of constriction before irreversible neural injury. Currently, most experts agree that decompression should be done within 14 days of onset to be effective (24,26,28,29). Research of surgical decompression has been hampered by the limited number of patients who meet surgical decompression criteria. There are only a few studies available to guide treatment, and they have not been widely reproduced. The main purpose of this study is to further characterize the surgical decompression of Bell’s palsy via the middle fossa approach for patients with poor prognosis based on clinical and electrodiagnostic testing. This study also evaluates the long-term outcomes of the middle fossa facial nerve decompression, particularly in regard to long-term facial function outcomes, safety, and hearing results. MATERIALS AND METHODS With institutional review board approval, we searched our institutional database for patients who underwent a middle fossa craniotomy for the diagnosis of Bell’s palsy. Patients who underwent surgery for recurrent Bell’s palsy were excluded. The medical records of 15 consecutive patients with Bell’s palsy treated with a middle cranial fossa surgical decompression from May 19, 2000, to April 11, 2012, at the University of Utah Hospital were retrospectively reviewed. There was 1 patient who was lost to follow-up after the 4-week postoperative visit and was excluded from analysis. All patients received a course of high-dose steroids when the Bell’s palsy was initially identified. Those who had complete facial paralysis (HB VI) underwent ENoG testing. If the patients had greater than 90% degeneration on ENoG testing, no voluntary EMG motor unit potentials, and presented within 14 days of symptom onset, then surgical decompression via the middle fossa approach was recommended. For further comparison, an additional analysis was performed on the 5 consecutive patients treated before 2000, when surgical decompression was offered to patients up to 1 month after the onset of their paralysis. For patients electing to have surgical decompression, a standard middle cranial fossa approach to the internal auditory canal (IAC) was performed. The facial nerve was identified in the lateral IAC, exposed from the labyrinthine segment and meatal foramen to the geniculate ganglion and a portion of the tympanic segment. The fibrous ligament at the meatal foramen of the fallopian canal and exposed nerve sheath (epineurium) was incised. The patient’s clinical course was followed including their HB grade, preoperative and postoperative hearing results, and both surgical and longterm complications. Final HB grade was assessed at the last available clinic visit within 1 year of surgery, and the final hearing result was assessed at a clinic visit between 3 months and 1 year
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MIDDLE FOSSA DECOMPRESSION FOR BELL_S PALSY
FIG. 1. Final facial nerve HB grade based on the day of decompression after paralysis.
after surgery. The results were compiled and statistically analyzed with the W2 test and regression analysis with a best fit linear trend line, R2 value, and p value.
RESULTS There are 14 patients who met the inclusion criteria. The average time from onset of facial paralysis to decompression was 11.3 days (range, 7Y14 d; median, 10 d). Average duration of follow-up was 15.3 months. The majority of patients, 71.4% (10/14), regained normal or near normal facial function (HB I or II) by their last clinic visit within 1 year after surgery. Of these patients, 35.7% (5/14) improved to normal (HB I), 35.7% (5/14) improved to near normal (HB II), and all remaining patients improved to a HB III, 28.6% (4/14). Analyzing the final facial nerve grade based on the number of days from the beginning of facial paralysis to surgical decompression demonstrated a weak correlation (R2 = 0.047; p = 0.23) (Fig. 1). Regression analysis with a best fit linear trend line shows a tendency toward worse outcomes the more days to decompression, but this was not statistically significant within our 14-day time frame. There was no difference in final facial nerve outcome depending on the patient’s sex or side of paralysis. All patients older than 60 years (n = 3) had an HB III facial outcome. Patients younger than 60 years were significantly more likely to regain normal or near-normal facial function (HB I or II), 90.9% (10/11) versus 0% (0/3), respectively (p = 0.002) (Fig. 2). To compare patients decompressed within 14 days with those decompressed after 14 days, an additional analysis was performed. The 5 consecutive patients treated before 2000 were compared with the modern criteria because surgical decompression was offered to these patients up to 1 month after the onset of their paralysis. Stratifying these 2 groups based on the timing of surgery, those patients decompressed within 14 days were more likely to regain normal or near normal facial function (HB I or II) compared with those decompressed after 14 days, 71.4% (10/14) versus 20.0% (1/5), respectively ( p = 0.046) (Fig. 3). In addition, the only patients to have complete recovery (HB I) were decompressed within 14 days, 35.7% (5/14) versus 0.0%
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FIG. 2. Final facial nerve HB grade after decompression based on the patient’s age.
(0/5), respectively ( p = 0.12). All remaining patients in both groups improved to a HB III, 28.6% (4/14) of those decompressed within 14 days versus 80.0% (4/5) of those decompressed after 14 days. The average ENoG observed was 96% degeneration, with 35.7% (5/14) of patients having an ENoG of 100% degeneration and 64.3% (9/14) having greater than 95% degeneration. There was no difference in final facial function outcome depending on the patient’s preoperative ENoG degeneration. The average preoperative pure tone average (PTA) was 10.1 dB (range, 0Y22 dB), and average postoperative PTA was 12.2 dB (range, 3Y29 dB). Average preoperative word recognition score (WRS) was 99.7% (range, 96%Y100%), and average postoperative WRS was 98.8% (range, 92%Y100%). There were no significant changes in final hearing results (98 dB loss or 98% decrease in WRS) in any patient. There were no major postoperative complications, based on a standardized classification of surgical complications, which includes life-threatening complications (i.e., death, cerebrovascular accident, cardiopulmonary insult, multiorgan dysfunction); complication requiring further surgery, endoscopy, or radiologic intervention; and complication requiring unanticipated pharmacological treatment, Grades IV, III, and II, respectively (36). Minor complications (Grade I) occurred in 22.2% of patients and were largely limited to the postoperative period. Temporary morbidity observed was
FIG. 3. Final facial nerve HB grade after decompression based on the timing of surgery. Otology & Neurotology, Vol. 36, No. 3, 2015
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facial numbness/tingling, nausea/vomiting, dizziness, periorbital ecchymosis, and pruritus. Gustatory hyperlacrimation was a late complication observed in 3 patients. DISCUSSION Treatment of Bell’s palsy is complex. The vast majority of cases recover completely with observation or medical therapy alone; however, long-term facial paresis, paralysis, and synkinesis are still grave outcomes in a small portion of patients with Bell’s palsy. Standardized algorithms have been shown to successfully identify these high-risk patients based on clinical exam and electrical testing. Fisch and Esslen helped to develop and popularize the use of ENoG and EMG testing for Bell’s palsy and set the stage to stratify patients into high- and low-risk groups (27). Gantz et al. also showed that patients with less than 90% degeneration on ENoG (n = 54), all regained normal or near-normal facial function (HB I or II), with 89% achieving a HB I (26). These low-risk patients, therefore, clearly do not need further intervention. In addition, EMG is a complimentary modality in patients with 100% degeneration on ENoG. Patients with persistent motor unit potentials on EMG are likely to recover with a good prognosis.Therefore, for Bell’s palsy, using the HB grading system coupled with electrical testing, patients with complete facial paralysis (HB VI), greater than 90% degeneration on ENoG, and absent voluntary EMG potentials have been shown to represent a subset of patients who are at increased risk for a poor long-term outcome. The pathophysiology of Bell’s palsy is likely due to neural edema compressing the facial nerve at its most narrow course in the bony fallopian canal. Despite this presumed etiology, surgical decompression of the mastoid segment of the facial nerve has not shown any benefit in multiple studies, including a recent Cochrane review (32,33,37). This operation fails to address the known site of greatest constriction, the meatal foramen, where axonal injury occurs. However, using a middle cranial fossa approach to identify and decompress the proximal facial nerve accomplishes this goal. This surgical technique has been shown to be safe when done by appropriately trained surgeons and effective at improving long-term facial motor function in this high-risk subset of patients. Using the above surgical criteria, Gantz et al. identified high risk Bell’s palsy patients and demonstrated high-level evidence (caseYcontrol study) for decompression via a middle cranial fossa approach (26). This study showed that 91% of patients (n = 34) who underwent decompression within 14 days improved to normal or near-normal facial function (HB I or HB II) compared with only 42% of patients (n = 36) who were treated with steroids only. The researchers demonstrated during surgery that the conduction blockage was medial to the geniculate ganglion in 17 of 19 patients on intraoperative evoked EMG. This study also demonstrated that the timing of surgical decompression was critical. Those patients decompressed before 14 days had a high probability of a good outcome (HB I or II); after 14 days, outcomes were significantly worse. Decompressed patients had significantly improved outcomes compared with
nonsurgical controls, despite similar prognosis on electrophysiologic testing. In 2013, the American Academy of OtolaryngologyYHead and Neck Surgery assembled a multi-specialty clinical practice guideline (CPG) committee to give evidence-based recommendations pertaining to Bell’s palsy (1). Ultimately, the committee made no recommendation (neither for nor against) regarding surgical decompression of Bell’s palsy patients because of the variable quality of the aggregate evidence. They report the aggregate evidence as Grade D and state that the risks of surgery may outweigh the potential benefits, but concern for long-term facial deformity may make some patients willing to pursue a major operation for an increased chance of complete recovery. Although the CPG development process has strict methods for reviewing existing evidence, Eibling et al. observed that the lack of consideration of current standard treatment and expert opinion may reduce their value (38). The current study supports MCF facial nerve decompression in Bell’s palsy patients who are at high risk for poor facial nerve outcomes. In this group of patients that met the electrodiagnostic criteria for severe dysfunction and were treated with surgery within 14 days from onset of facial paralysis, their chances of regaining HB I or II function was 71.4%, with 35.7% obtaining a HB I outcome. This rate is significantly higher than the published standards for this subset with poor prognosis treated with steroids alone, with only 42% to 50% recovering to HB I or II, and is similar to other surgical decompression studies that report 66% to 91% improvement to HB I or II in these at-risk patients (26,29Y31). Also, in our additional analysis, we again showed that patients must be decompressed within 14 days because of significantly improved results. We have shown that age is related to facial nerve recovery; in our study, all patients older than 60 years (n = 3) had a poor (HB III) facial function outcome, a finding which is supported by several other studies. Adour showed that of the 446 patients, those younger than 60 years had an 11% chance of a poor outcome with persistent weakness, contractures, or synkinesis compared with 51% of those older than 60 years (39). In addition, Adour showed that those older than 60 years had an increased rate of complete paralysis during their course of Bell’s palsy, 55% versus 32%, respectively. Prescott also reported that of 879 patients, those with incomplete recovery were on average 14 years older than those with complete recovery, suggesting that older patients have a significantly poorer prognosis than younger patients (40). Katusic et al. showed that of 208 patients with Bell’s palsy, those older than 55 years (n = 64) were significantly more likely to have incomplete recovery, 21% versus 10% (41). More recently, Peitersen showed in an observational study of 1701 cases of Bell’s palsy, patients older than 60 years had worse prognosis (10). Only about one-third of these older patients returned to normal function, compared with children who had a 90% chance of full recovery, and patients aged 15 to 44 years who had a 75% to 84% chance of return to normal function. Several studies in other surgical fields, particularly for carpal tunnel decompression and cervical spinal nerve
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MIDDLE FOSSA DECOMPRESSION FOR BELL_S PALSY decompression, show that peripheral motor nerve regeneration and recovery is inversely related to age and is markedly worse in patients older than 60 years (42Y45). A systematic review of the peripheral nerve repair literature reiterated this result, stating that holding all other variables constant, older age predicts poorer outcomes (44). Mondelli et al. showed that patients older than 60 years had more severe clinical and electrophysiological findings preoperatively and argued that their reduced improvement after surgical decompression is likely due to lower repair capacity (45). Basic science studies have elucidated multiple molecular reasons why nerve repair is reduced in older patients (46Y50). These researchers demonstrate that each phase of nerve regeneration is affected. After nerve injury, the early repair process is delayed because of decreased macrophage recruitment, which slows Wallerian degeneration (46). Older patients also have fewer Schwann cells and reduced secretion of trophic factors. This change decreases axonal sprout formation, slows axon regeneration rates, and decreases nerve density after restoration (47). Axonal transport slows as we age, and this delays nerve repair (48). Also, regenerated axons in older patients are more often unmyelinated, which decreases synaptic responsiveness to nerve stimulation, resulting in clinically incomplete reinnervation (49). These age-related changes are not linearly progressive; normal function is maintained throughout the majority of human life but then begins to decline in the fifth and sixth decades (50). These cellular factors likely result in the observed worse outcomes reported in our study for patients older than 60 years. The middle fossa surgical approach requires a craniotomy, and it is commonly used to approach the medial temporal bone. The safety of this technique has been shown in numerous studies to approach the facial nerve, remove acoustic neuromas, and repair superior canal dehiscence (51,52). Our results were similar. There were no significant changes in final hearing results (98 dB loss or 98% decrease in WRS) in any patient. There were no major postoperative complications, and minor postoperative complications were transient and largely limited to the immediate postoperative period. For Bell’s palsy patients, the data available support the efficacy of middle cranial fossa surgical decompression of the labyrinthine segment and meatal foramen in high-risk patients. Our results further support this thesis. This surgery is safe and effective, preserves hearing, and should be performed within 14 days of the onset of facial paralysis. Decompression in patients older than 60 years should be performed cautiously, and these patients should be warned of their likely worse overall prognosis. In summary, middle fossa surgical decompression offers good facial nerve outcomes for patients with Bell’s palsy and poor prognosis on electrical testing. CONCLUSION In patients with severe Bell’s palsy at risk for a poor facial nerve outcome, middle cranial fossa decompression of the facial nerve provides good long-term facial function
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outcomes with few complications. Surgical decompression is reserved for those patients with HB VI, greater than 90% degeneration on ENoG, and absent voluntary EMG potentials and should be performed within 14 days of the onset of facial paralysis. This series further supports the safety and efficacy of this operative technique, demonstrating good facial nerve outcomes and minimal morbidity in these at-risk Bell’s palsy patients. REFERENCES 1. Baugh RF, Basura GJ, Ishii LE, et al. Clinical practice guideline: Bell’s palsy. Otolaryngol Head Neck Surg 2013;149:S1Y27. 2. Marson AG, Salinas R. Bell’s palsy. Western J Med 2000;173:266Y8. 3. Pulec JL. Early decompression of the facial nerve in Bell’s palsy. Ann Otol Rhinol Laryngol 1981;90:570Y7. 4. Yamamoto E, Fisch U. Experimentally induced facial nerve compression in cats. Acta Otolaryngol 1975;79:390Y5. 5. Burmeister HP, Baltzer PA, Volk GF, et al. Evaluation of the early phase of Bell’s palsy using 3 T MRI. Eur Arch Otorhinolaryngol 2011;268:1493Y500. 6. Fisch U, Esslen E. Total intratemporal exposure of the facial nerve. Pathologic findings in Bell’s palsy. Arch Otolaryngol 1972;95:335Y41. 7. Gantz BJ, Gmur A, Fisch U. Intraoperative evoked electromyography in Bell’s palsy. Am J Otolaryngol 1982;3:273Y8. 8. Ge XX, Spector GJ. Labyrinthine segment and geniculate ganglion of facial nerve in fetal and adult human temporal bones. Ann Otol Rhinol Laryngol Suppl 1981;90:1Y12. 9. Murakami S, Mizobuchi M, Nakashiro Y, et al. Bell palsy and herpes simplex virus: identification of viral DNA in endoneurial fluid and muscle. Ann Intern Med 1996;124:27Y30. 10. Peitersen E. Bell’s palsy: the spontaneous course of 2,500 peripheral facial nerve palsies of different etiologies. Acta Otolaryngol Suppl 2002;549:4Y30. 11. Sullivan FM, Swan IR, Donnan PT, et al. Early treatment with prednisolone or acyclovir in Bell’s palsy. N Engl J Med 2007;357:1598Y607. 12. Engstrom M, Berg T, Stjernquist-Desatnik A, et al. Prednisolone and valaciclovir in Bell’s palsy: a randomised, double-blind, placebocontrolled, multicentre trial. Lancet Neurol 2008;7:993Y1000. 13. Sullivan FM, Swan IR, Donnan PT, et al. A randomised controlled trial of the use of aciclovir and/or prednisolone for the early treatment of Bell’s palsy: the BELLS study. Health Technol Assess 2009;13:iiiYiv, ixYxi, 1Y130. 14. Hazin R, Azizzadeh B, Bhatti MT. Medical and surgical management of facial nerve palsy. Curr Opin Ophthalmol 2009;20:440Y50. 15. Axelsson S, Berg T, Jonsson L, et al. Bell’s palsy - the effect of prednisolone and/or valaciclovir versus placebo in relation to baseline severity in a randomised controlled trial. Clin Otolaryngol 2012;37:283Y90. 16. Alberton DL, Zed PJ. Bell’s palsy: a review of treatment using antiviral agents. Ann Pharmacother 2006;40:1838Y42. 17. Allen D, Dunn L. Aciclovir or valaciclovir for Bell’s palsy (idiopathic facial paralysis). Cochrane Database Syst Rev 2004:CD001869. 18. Browning GG. Bell’s palsy: a review of three systematic reviews of steroid and anti-viral therapy. Clin Otolaryngol 2010;35:56Y8. 19. Lockhart P, Daly F, Pitkethly M, et al. Antiviral treatment for Bell’s palsy (idiopathic facial paralysis). Cochrane Database Syst Rev 2009:CD001869. 20. Adour KK. Combination treatment with acyclovir and prednisone for Bell palsy. Arch Otolaryngol Head Neck Surg 1998;124:824. 21. Adour KK, Ruboyianes JM, Von Doersten PG, et al. Bell’s palsy treatment with acyclovir and prednisone compared with prednisone alone: a double-blind, randomized, controlled trial. Ann Otol Rhinol Laryngol 1996;105:371Y8. 22. Goudakos JK, Markou KD. Corticosteroids vs corticosteroids plus antiviral agents in the treatment of Bell palsy: a systematic review and meta-analysis. Arch Otolaryngol Head Neck Surg 2009;135:558Y64. 23. Huang B, Xu S, Xiong J, et al. Psychological factors are closely associated with the Bell’s palsy: a caseYcontrol study. J Huazhong Univ Sci Technol 2012;32:272Y9. Otology & Neurotology, Vol. 36, No. 3, 2015
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