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Idiopathic recurrent facial palsy: Facial nerve decompression via middle cranial fossa approach
AMERI CA N JOURNAL OF OT OLAR YNGOLOGY– H E AD AN D N E CK M EDI CI N E AN D S U RGE RY 3 7 ( 2 0 16 ) 31 – 3 3
Available online at www.sciencedirect.com
ScienceDirect www.elsevier.com/locate/amjoto
Idiopathic recurrent facial palsy: Facial nerve decompression via middle cranial fossa approach☆ Yunhua Zhu, MD a , Yuxin Yang, BM a , Daowen Wang, MD b , Mingmin Dong, MD c,⁎ a b c
Department of Otolaryngology, The First People’s Hospital of Shangqiu, Shangqiu, P.R.C. Department of Otolaryngology Head and Neck Surgery, Peking University Health Science Center, Beijing, P.R.C. Department of Otology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, P.R.C.
ARTI CLE I NFO
A BS TRACT
Article history:
Objective: To introduce our experience of preventing further episodes of idiopathic
Received 22 May 2015
recurrent facial palsy by facial nerve decompression via middle cranial fossa approach. Methods: Twelve cases (surgery group) who had idiopathic recurrent facial palsy underwent facial nerve decompression via middle cranial fossa approach, and 6 cases (control group) who declined surgery accepted conservative treatment. Further episodes of facial palsy and final outcomes of facial nerve were recorded. Facial nerve function was assessed by House– Brackmann facial nerve grade system. Results: Only 8.3% of the patients (one case) in the surgery group had further episodes of facial palsy on the surgical side, but up to 64.7% of the patients (4 cases) in the control group suffered further episodes (p < 0.05). 11 patients (91.7%) in the surgery group recovered to Grade I or Grade II in contrast to 3 cases (50%) in the control group. Conclusions: Facial nerve decompression via middle cranial fossa approach was able to prevent further episodes of idiopathic recurrent facial palsy, and surgical decompression seemed to achieve better outcomes of facial nerve than conservative treatment. © 2015 Published by Elsevier Inc.
1.
Introduction
The incidence of recurrent facial palsy (RFP) is estimated to be 4% to 7% among acute facial palsy, and it may be unilateral or bilateral [1,2]. The cause and mechanism of RFP are still unknown, but it is reported to be associated with Melkersson– Rosenthal syndrome, facial nerve tumors, otitis media, and family history in some study [3–6]. Similar to the dispute on Bell’s palsy, there is no consensus about the management of RFP. Conservative treatment is usually
☆
taken by physicians, but recurrence often affects the patients years later. Moreover, it is revealed that facial nerve function gradually worsens with every attack of facial palsy [7,8], thus it is plausible to prevent further episodes of facial palsy. There have been a few studies demonstrating efficacy of surgical decompression in preventing further episodes of facial palsy in RFP, but the extent of decompression is controversial [9–12]. In the past years, we performed facial nerve decompression on 12 cases of idiopathic RFP via middle cranial fossa approach, and the purpose of this article is to introduce our
Copyright transfer: In consideration of the American Journal of Otolaryngology's reviewing and editing our submission, " Idiopathic recurrent facial palsy: facial nerve decompression via middle cranial fossa approach", the authors undersigned transfer, assign and otherwise convey all copyright ownership to Elsevier Inc. in the event that such work is published in the American Journal of Otolaryngology.Signed by Yunhua Zhu, Yuxin Yang, Daowen Wang, Mingmin Dong ⁎ Corresponding author at: Department of Otology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, P.R.C. E-mail address: [email protected] (M. Dong). http://dx.doi.org/10.1016/j.amjoto.2015.09.004 0196-0709/© 2015 Published by Elsevier Inc.
32
AMERI CAN JOURNAL OF OTOLAR YNGOLOGY– H E AD AN D N E CK M EDI CI N E AN D S U RGE RY 3 7 ( 2 0 16 ) 31 – 3 3
experience of preventing further episodes of idiopathic RFP by middle cranial fossa approach.
2.
Materials and methods
A retrospective chart review of 18 cases with idiopathic RFP (at least 2 episodes of facial palsy on the same side), which were excluded from Melkersson–Rosenthal syndrome, facial nerve tumors and otitis media by physical examination and imaging techniques (including CT of temporal bone and MRI), was carried out. There were 14 females and 4 males. They were aged 16 to 46 years, with a mean of 27 years. The age at the first onset of facial palsy varied from 4 to 35 years. Electroneurography was performed on the patients with complete paralysis within 2 weeks after the last onset. Internal auditory canal segment, meatal foramen, labyrinthine segment and geniculate ganglion were decompressed in 12 cases within 3 weeks after the last episode via middle cranial fossa approach, and conservative treatment (oral prednisolone, 1 mg/kg/d for 10 days) was provided to the 6 cases rejecting surgery. The patients were thereby divided into surgery group and control group accordingly. The patients in the surgery group and the control group were followed up for 5.8 ± 1.3 years and 5.5 ± 1.0 years, respectively. Facial nerve function was assessed by House– Brackmann facial nerve grading system [13]. SPSS 18.0 software was used for data analysis. t-test was employed to compare the initial facial nerve function, and Fisher’s exact test was used to compare recurrence rate between the surgery group and the control group. P < 0.05 was deemed as significant difference.
3.
Results
The cases of the study are listed in Table 1. Further episodes of facial palsy on the surgical side occurred in only one patient (8.3%) in the surgery group, while 4 of 6 cases (64.7%) in the control group had further episodes on the ipsilateral side (the side at which there were at least two episodes of facial palsy) (p < 0.05). Electroneurography indicated that the two cases with complete paralysis at the last onset before treatment showed over 95% maximal degeneration of facial nerve. The initial mean facial nerve function of the surgery group and the control group was 3.5 ± 1.2 and 3.7 ± 1.4, respectively, without significant difference (p > 0.05). After treatment, 11 patients (91.7%) in the surgery group recovered to Grade I or Grade II, among which 6 patients totally recovered. Only one patient finally recovered to Grade III, as was caused by further episode of facial palsy on the surgical side. In contrast, only 3 cases (50%) in the control group recovered to Grade I or Grade II, and the other 3 cases returned to Grade III or worse level due to further episodes of facial palsy. Hearing was preserved in all patients, and there was no severe complication.
4.
Discussion
RFP is uncommon, and its pathogenesis is not well-known; it tends to recur after prednisolone treatment or self-resolution. It is demonstrated that the risk of recurrence increases with every recurrence, from 15% chance of recurrence on the second attack to 50% chance of recurrence on the fourth
Table 1 – Summary of 18 cases with idiopathic recurrent facial palsy. Patient No.
FPE before treatment
FPE after treatment
Side
Initial FNF
Final FNF
Age at the first onset
Age
Follow-up (yr)
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18
2 3 3 4 2 6 2 2 3 4 2 5 3 2 3 2 3 4
0 0 0 0 0 1 0 0 0 0 0 0 2 0 0 1 3 3
L R L R L L R L R L L L R R L L L R
II V III IV III VI II III IV IV II IV IV III III II IV VI
I I II II I III I I II II I II III I II I IV V
20 35 10 16 4 4 30 34 11 12 12 13 13 16 12 15 13 18
29 46 17 29 27 27 33 46 16 24 28 22 27 26 25 22 25 32
5 5 6 6 7 4 7 5 4 8 7 5 7 5 4 6 6 5
FPE, facial palsy episode; FNS, facial nerve function. Case 1–12 accepted surgical decompression, and Case 13–18 accepted prednisolone treatment only. Case 4 suffered right-sided facial palsy four times and left-sided facial palsy once, and underwent decompression of the rightsided facial nerve; case 5 suffered left-sided facial palsy twice and right-sided facial palsy once, and underwent decompression of the left-sided facial nerve; case 6 suffered left-sided facial palsy six times and right-sided facial palsy twice, and underwent decompression of the left-sided facial nerve. Case 16 suffered facial palsy twice on the left side and once on the right side before treatment. Case 18 suffered facial palsy three times on the right side and once on the left side after treatment.
AMERI CA N JOURNAL OF OT OLAR YNGOLOGY– H E AD AN D N E CK M EDI CI N E AN D S U RGE RY 3 7 ( 2 0 16 ) 31 – 3 3
attack [2], and the mean interval between the first and second recurrence was dramatically shortened compared to that between the first episode and the first recurrence [14]. As mentioned before, facial nerve function gradually worsens with every attack [7,8]. It is also documented by an electrophysiological study, which shows loss of action potential amplitude in cases of RFP compared to those which have only a single episode [15]. Thereby it is necessary to prevent further episodes of facial palsy. Some earlier authors attempt either total or subtotal facial nerve decompression in a few cases with RFP, and it appears effective to prevent further attacks [9–12,16], but these studies do not provide a robust evidence of the efficacy of surgical decompression due to the absence of a control group. Recently, Li Y et al. [17] carried out a retrospective study involving 24 cases, in which 16 cases underwent total facial nerve decompression and 8 accepted prednisolone treatment only, proving that total facial nerve decompression was effective to prevent further episodes of facial palsy in idiopathic RFP. Fisch and Esslen utilized direct intraoperative stimulation and demonstrated that nerve conduction was situated before the geniculate ganglion, at the meatal foramen, the narrowest site of facial nerve [18]. Therefore, we decompressed the internal auditory canal segment, meatal foramen, labyrinthine segment and geniculate ganglion of the facial nerve. In our study, surgical decompression via middle cranial fossa approach successfully prevented further attacks of facial palsy on the surgical side in 91.7% of the patients during a long period of 4 to 8 years. In contrast, 64.7% of the patients who accepted conservative treatment had further episodes during the follow-up. Given that the average follow-up of surgery group and control group was almost identical (5.8 ± 1.3 years versus 5.5 ± 1.0 years), our study demonstrated that facial nerve decompression via middle cranial fossa approach was able to prevent further episodes of idiopathic RFP. It seemed that better outcomes of facial nerve were also obtained by our surgical approach. In the current study, it was showed that 91.7% of the cases in the surgery group recovered completely or almost completely while half of the patients in the control group finally obtained poor recovery due to further attacks. What’s more, the initial facial nerve function difference between the two groups was not statistically significant. The better outcomes of surgery group were probably caused by the fact that deterioration of facial nerve caused by repetitive episodes was avoided in the vast majority cases. According to the discussion above, both facial nerve decompression via middle cranial fossa and total facial nerve decompression are capable of preventing further episodes of RFP. Interestingly, it is reported that subtotal facial nerve decompression from stylomastoid approach till labyrinthine segment is also effective [19]. We thereby speculate that decompression of labyrinthine segment and geniculate ganglion may be the key to prevent further
33
episodes of facial palsy. Of course, further study is required to verify our assumption.
Declaration of interest The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
REFERENCES
[1] Yanagihara N, Mori H, Kozawa T, et al. Bell’s palsy. Nonrecurrent v recurrent and unilateral v bilateral. Arch Otolaryngol 1984;110:374–7. [2] Pitts DB, Adour KK, Hilsinger Jr RL. Recurrent Bell’s palsy: analysis of 140 patients. Laryngoscope 1988;98:535–40. [3] Greene RM, Rogers III RS. Melkersson–Rosenthal syndrome: a review of 36 patients. J Am Acad Dermatol 1989;21:1263–70. [4] Scholz E, Langer J, Begall K. Recurrent facial paresis with facial neurinoma. Laryngorhinootologie 2007;86:443–7. [5] Schwenzfeier CW. Recurrent facial paralysis associated with bouts of otitis media. Am J Otol 1991;12:466–7. [6] Hageman G, Ippel PF, Jansen EN, et al. Familial, alternating Bell’s palsy with dominant inheritance. Eur Neurol 1990;30:310–3. [7] Boddie HG. Recurrent Bell’s palsy. J Laryngol Otol 1972;86:117–20. [8] Ralli G, Magliulo G. Bell’s palsy and its recurrences. Arch Otorhinolaryngol 1988;244:387–90. [9] Yetiser S, Satar B, Kazkayasi M. Immunologic abnormalities and surgical experiences in recurrent facial nerve paralysis. Otol Neurotol 2002;23:772–8. [10] Canale TJ, Cox RH. Compression of the facial nerve in Melkersson syndrome. Arch Otolaryngol 1974;100:373–4. [11] Dutt SN, Mirza S, Irving RM, et al. Total decompression of facial nerve for Melkersson Rosenthal syndrome. J Laryngol Otol 2000;114:870–3. [12] Doshi J, Irving R. Recurrent facial nerve palsy: the role of surgery. J Laryngol Otol 2010;124:1202–4. [13] Hous JW, Brackmann DE. Facial nerve grading system. Otolaryngol Head Neck Surg 1985;93:146–7. [14] Crego F, Galindo J, Quesada P, et al. Recurrent peripheral facial paralysis. Our case load from 1995. Acta Otorrinolaringol Esp 1998;49:280–2. [15] Mamoli B, Neumann H, Ehrmann L. Recurrent Bell’s palsy. Etiology, frequency, prognosis. J Neurol 1977;216:119–25. [16] Graham MD, Kartush JM. Total facial nerve decompression for recurrent facial paralysis: an update. Otolaryngol Head Neck Surg 1989;101:442–4. [17] Li Y, Li Z, Yan C, et al. The effect of total facial nerve decompression in preventing further recurrence of idiopathic recurrent facial palsy. Eur Arch Otorhinolaryngol 2015;272: 1087–90. [18] Fisch U, Esslen E. Total intratemporal exposure of the facial nerve. Pathologic findings in Bell’s palsy. Arch Otolaryngol 1972;95:335–41. [19] Wu SH, Chen X, Wang J, et al. Subtotal facial nerve decompression in preventing further recurrence and promoting facial nerve recovery ofsevere idiopathic recurrent facial palsy. Eur Arch Otorhinolaryngol 2015;272:3295–8.
Available online at www.sciencedirect.com
ScienceDirect www.elsevier.com/locate/amjoto
Idiopathic recurrent facial palsy: Facial nerve decompression via middle cranial fossa approach☆ Yunhua Zhu, MD a , Yuxin Yang, BM a , Daowen Wang, MD b , Mingmin Dong, MD c,⁎ a b c
Department of Otolaryngology, The First People’s Hospital of Shangqiu, Shangqiu, P.R.C. Department of Otolaryngology Head and Neck Surgery, Peking University Health Science Center, Beijing, P.R.C. Department of Otology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, P.R.C.
ARTI CLE I NFO
A BS TRACT
Article history:
Objective: To introduce our experience of preventing further episodes of idiopathic
Received 22 May 2015
recurrent facial palsy by facial nerve decompression via middle cranial fossa approach. Methods: Twelve cases (surgery group) who had idiopathic recurrent facial palsy underwent facial nerve decompression via middle cranial fossa approach, and 6 cases (control group) who declined surgery accepted conservative treatment. Further episodes of facial palsy and final outcomes of facial nerve were recorded. Facial nerve function was assessed by House– Brackmann facial nerve grade system. Results: Only 8.3% of the patients (one case) in the surgery group had further episodes of facial palsy on the surgical side, but up to 64.7% of the patients (4 cases) in the control group suffered further episodes (p < 0.05). 11 patients (91.7%) in the surgery group recovered to Grade I or Grade II in contrast to 3 cases (50%) in the control group. Conclusions: Facial nerve decompression via middle cranial fossa approach was able to prevent further episodes of idiopathic recurrent facial palsy, and surgical decompression seemed to achieve better outcomes of facial nerve than conservative treatment. © 2015 Published by Elsevier Inc.
1.
Introduction
The incidence of recurrent facial palsy (RFP) is estimated to be 4% to 7% among acute facial palsy, and it may be unilateral or bilateral [1,2]. The cause and mechanism of RFP are still unknown, but it is reported to be associated with Melkersson– Rosenthal syndrome, facial nerve tumors, otitis media, and family history in some study [3–6]. Similar to the dispute on Bell’s palsy, there is no consensus about the management of RFP. Conservative treatment is usually
☆
taken by physicians, but recurrence often affects the patients years later. Moreover, it is revealed that facial nerve function gradually worsens with every attack of facial palsy [7,8], thus it is plausible to prevent further episodes of facial palsy. There have been a few studies demonstrating efficacy of surgical decompression in preventing further episodes of facial palsy in RFP, but the extent of decompression is controversial [9–12]. In the past years, we performed facial nerve decompression on 12 cases of idiopathic RFP via middle cranial fossa approach, and the purpose of this article is to introduce our
Copyright transfer: In consideration of the American Journal of Otolaryngology's reviewing and editing our submission, " Idiopathic recurrent facial palsy: facial nerve decompression via middle cranial fossa approach", the authors undersigned transfer, assign and otherwise convey all copyright ownership to Elsevier Inc. in the event that such work is published in the American Journal of Otolaryngology.Signed by Yunhua Zhu, Yuxin Yang, Daowen Wang, Mingmin Dong ⁎ Corresponding author at: Department of Otology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, P.R.C. E-mail address: [email protected] (M. Dong). http://dx.doi.org/10.1016/j.amjoto.2015.09.004 0196-0709/© 2015 Published by Elsevier Inc.
32
AMERI CAN JOURNAL OF OTOLAR YNGOLOGY– H E AD AN D N E CK M EDI CI N E AN D S U RGE RY 3 7 ( 2 0 16 ) 31 – 3 3
experience of preventing further episodes of idiopathic RFP by middle cranial fossa approach.
2.
Materials and methods
A retrospective chart review of 18 cases with idiopathic RFP (at least 2 episodes of facial palsy on the same side), which were excluded from Melkersson–Rosenthal syndrome, facial nerve tumors and otitis media by physical examination and imaging techniques (including CT of temporal bone and MRI), was carried out. There were 14 females and 4 males. They were aged 16 to 46 years, with a mean of 27 years. The age at the first onset of facial palsy varied from 4 to 35 years. Electroneurography was performed on the patients with complete paralysis within 2 weeks after the last onset. Internal auditory canal segment, meatal foramen, labyrinthine segment and geniculate ganglion were decompressed in 12 cases within 3 weeks after the last episode via middle cranial fossa approach, and conservative treatment (oral prednisolone, 1 mg/kg/d for 10 days) was provided to the 6 cases rejecting surgery. The patients were thereby divided into surgery group and control group accordingly. The patients in the surgery group and the control group were followed up for 5.8 ± 1.3 years and 5.5 ± 1.0 years, respectively. Facial nerve function was assessed by House– Brackmann facial nerve grading system [13]. SPSS 18.0 software was used for data analysis. t-test was employed to compare the initial facial nerve function, and Fisher’s exact test was used to compare recurrence rate between the surgery group and the control group. P < 0.05 was deemed as significant difference.
3.
Results
The cases of the study are listed in Table 1. Further episodes of facial palsy on the surgical side occurred in only one patient (8.3%) in the surgery group, while 4 of 6 cases (64.7%) in the control group had further episodes on the ipsilateral side (the side at which there were at least two episodes of facial palsy) (p < 0.05). Electroneurography indicated that the two cases with complete paralysis at the last onset before treatment showed over 95% maximal degeneration of facial nerve. The initial mean facial nerve function of the surgery group and the control group was 3.5 ± 1.2 and 3.7 ± 1.4, respectively, without significant difference (p > 0.05). After treatment, 11 patients (91.7%) in the surgery group recovered to Grade I or Grade II, among which 6 patients totally recovered. Only one patient finally recovered to Grade III, as was caused by further episode of facial palsy on the surgical side. In contrast, only 3 cases (50%) in the control group recovered to Grade I or Grade II, and the other 3 cases returned to Grade III or worse level due to further episodes of facial palsy. Hearing was preserved in all patients, and there was no severe complication.
4.
Discussion
RFP is uncommon, and its pathogenesis is not well-known; it tends to recur after prednisolone treatment or self-resolution. It is demonstrated that the risk of recurrence increases with every recurrence, from 15% chance of recurrence on the second attack to 50% chance of recurrence on the fourth
Table 1 – Summary of 18 cases with idiopathic recurrent facial palsy. Patient No.
FPE before treatment
FPE after treatment
Side
Initial FNF
Final FNF
Age at the first onset
Age
Follow-up (yr)
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18
2 3 3 4 2 6 2 2 3 4 2 5 3 2 3 2 3 4
0 0 0 0 0 1 0 0 0 0 0 0 2 0 0 1 3 3
L R L R L L R L R L L L R R L L L R
II V III IV III VI II III IV IV II IV IV III III II IV VI
I I II II I III I I II II I II III I II I IV V
20 35 10 16 4 4 30 34 11 12 12 13 13 16 12 15 13 18
29 46 17 29 27 27 33 46 16 24 28 22 27 26 25 22 25 32
5 5 6 6 7 4 7 5 4 8 7 5 7 5 4 6 6 5
FPE, facial palsy episode; FNS, facial nerve function. Case 1–12 accepted surgical decompression, and Case 13–18 accepted prednisolone treatment only. Case 4 suffered right-sided facial palsy four times and left-sided facial palsy once, and underwent decompression of the rightsided facial nerve; case 5 suffered left-sided facial palsy twice and right-sided facial palsy once, and underwent decompression of the left-sided facial nerve; case 6 suffered left-sided facial palsy six times and right-sided facial palsy twice, and underwent decompression of the left-sided facial nerve. Case 16 suffered facial palsy twice on the left side and once on the right side before treatment. Case 18 suffered facial palsy three times on the right side and once on the left side after treatment.
AMERI CA N JOURNAL OF OT OLAR YNGOLOGY– H E AD AN D N E CK M EDI CI N E AN D S U RGE RY 3 7 ( 2 0 16 ) 31 – 3 3
attack [2], and the mean interval between the first and second recurrence was dramatically shortened compared to that between the first episode and the first recurrence [14]. As mentioned before, facial nerve function gradually worsens with every attack [7,8]. It is also documented by an electrophysiological study, which shows loss of action potential amplitude in cases of RFP compared to those which have only a single episode [15]. Thereby it is necessary to prevent further episodes of facial palsy. Some earlier authors attempt either total or subtotal facial nerve decompression in a few cases with RFP, and it appears effective to prevent further attacks [9–12,16], but these studies do not provide a robust evidence of the efficacy of surgical decompression due to the absence of a control group. Recently, Li Y et al. [17] carried out a retrospective study involving 24 cases, in which 16 cases underwent total facial nerve decompression and 8 accepted prednisolone treatment only, proving that total facial nerve decompression was effective to prevent further episodes of facial palsy in idiopathic RFP. Fisch and Esslen utilized direct intraoperative stimulation and demonstrated that nerve conduction was situated before the geniculate ganglion, at the meatal foramen, the narrowest site of facial nerve [18]. Therefore, we decompressed the internal auditory canal segment, meatal foramen, labyrinthine segment and geniculate ganglion of the facial nerve. In our study, surgical decompression via middle cranial fossa approach successfully prevented further attacks of facial palsy on the surgical side in 91.7% of the patients during a long period of 4 to 8 years. In contrast, 64.7% of the patients who accepted conservative treatment had further episodes during the follow-up. Given that the average follow-up of surgery group and control group was almost identical (5.8 ± 1.3 years versus 5.5 ± 1.0 years), our study demonstrated that facial nerve decompression via middle cranial fossa approach was able to prevent further episodes of idiopathic RFP. It seemed that better outcomes of facial nerve were also obtained by our surgical approach. In the current study, it was showed that 91.7% of the cases in the surgery group recovered completely or almost completely while half of the patients in the control group finally obtained poor recovery due to further attacks. What’s more, the initial facial nerve function difference between the two groups was not statistically significant. The better outcomes of surgery group were probably caused by the fact that deterioration of facial nerve caused by repetitive episodes was avoided in the vast majority cases. According to the discussion above, both facial nerve decompression via middle cranial fossa and total facial nerve decompression are capable of preventing further episodes of RFP. Interestingly, it is reported that subtotal facial nerve decompression from stylomastoid approach till labyrinthine segment is also effective [19]. We thereby speculate that decompression of labyrinthine segment and geniculate ganglion may be the key to prevent further
33
episodes of facial palsy. Of course, further study is required to verify our assumption.
Declaration of interest The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
REFERENCES
[1] Yanagihara N, Mori H, Kozawa T, et al. Bell’s palsy. Nonrecurrent v recurrent and unilateral v bilateral. Arch Otolaryngol 1984;110:374–7. [2] Pitts DB, Adour KK, Hilsinger Jr RL. Recurrent Bell’s palsy: analysis of 140 patients. Laryngoscope 1988;98:535–40. [3] Greene RM, Rogers III RS. Melkersson–Rosenthal syndrome: a review of 36 patients. J Am Acad Dermatol 1989;21:1263–70. [4] Scholz E, Langer J, Begall K. Recurrent facial paresis with facial neurinoma. Laryngorhinootologie 2007;86:443–7. [5] Schwenzfeier CW. Recurrent facial paralysis associated with bouts of otitis media. Am J Otol 1991;12:466–7. [6] Hageman G, Ippel PF, Jansen EN, et al. Familial, alternating Bell’s palsy with dominant inheritance. Eur Neurol 1990;30:310–3. [7] Boddie HG. Recurrent Bell’s palsy. J Laryngol Otol 1972;86:117–20. [8] Ralli G, Magliulo G. Bell’s palsy and its recurrences. Arch Otorhinolaryngol 1988;244:387–90. [9] Yetiser S, Satar B, Kazkayasi M. Immunologic abnormalities and surgical experiences in recurrent facial nerve paralysis. Otol Neurotol 2002;23:772–8. [10] Canale TJ, Cox RH. Compression of the facial nerve in Melkersson syndrome. Arch Otolaryngol 1974;100:373–4. [11] Dutt SN, Mirza S, Irving RM, et al. Total decompression of facial nerve for Melkersson Rosenthal syndrome. J Laryngol Otol 2000;114:870–3. [12] Doshi J, Irving R. Recurrent facial nerve palsy: the role of surgery. J Laryngol Otol 2010;124:1202–4. [13] Hous JW, Brackmann DE. Facial nerve grading system. Otolaryngol Head Neck Surg 1985;93:146–7. [14] Crego F, Galindo J, Quesada P, et al. Recurrent peripheral facial paralysis. Our case load from 1995. Acta Otorrinolaringol Esp 1998;49:280–2. [15] Mamoli B, Neumann H, Ehrmann L. Recurrent Bell’s palsy. Etiology, frequency, prognosis. J Neurol 1977;216:119–25. [16] Graham MD, Kartush JM. Total facial nerve decompression for recurrent facial paralysis: an update. Otolaryngol Head Neck Surg 1989;101:442–4. [17] Li Y, Li Z, Yan C, et al. The effect of total facial nerve decompression in preventing further recurrence of idiopathic recurrent facial palsy. Eur Arch Otorhinolaryngol 2015;272: 1087–90. [18] Fisch U, Esslen E. Total intratemporal exposure of the facial nerve. Pathologic findings in Bell’s palsy. Arch Otolaryngol 1972;95:335–41. [19] Wu SH, Chen X, Wang J, et al. Subtotal facial nerve decompression in preventing further recurrence and promoting facial nerve recovery ofsevere idiopathic recurrent facial palsy. Eur Arch Otorhinolaryngol 2015;272:3295–8.