Eur Arch Otorhinolaryngol DOI 10.1007/s00405-014-3328-4
OTOLOGY
Total facial nerve decompression in severe idiopathic recurrent facial palsy Kai Ai • Mai Sun • Yonggang Liu • Bowen Guo Menjiang Tu • Jiapeng Zhao • Bing Xiao
•
Received: 26 July 2014 / Accepted: 8 October 2014 Ó Springer-Verlag Berlin Heidelberg 2014
Abstract To investigate the role of total facial nerve decompression in severe idiopathic recurrent facial palsy. A consecutive series of 22 cases with severe idiopathic recurrent facial palsy were managed in our hospital between January, 2003 and January, 2011. Either total facial nerve decompression or conservative treatment was provided, and they were divided into surgery group and control group according to their choice of treatment. They were followed up for at least 3 years. Facial palsy recurrence and facial nerve outcomes in the two groups were compared. There were 12 patients in surgery group, who were followed up for 5.3 years (range 3–8 years). In
contrast, there were 10 patients in control group, with an average follow-up of 5.2 years (range 3–7 years). None of the patients (0 %) in surgery group recurred compared to 4 of 10 cases (40 %) in control group (p \ 0.05). In perspectives of facial nerve outcomes, 11 of 12 cases (91.7 %) in surgery group achieved good recovery (HB Grade I or II) in contrast to 3 of 10 cases (30.0 %) in control group (p \ 0.05). For severe idiopathic recurrent facial palsy, total facial nerve decompression could not only prevent further recurrence but also promote facial nerve recovery.
K. Ai M. Tu Department of Urology, The Second Xiangya Hospital of Central South University, Changsha, China
Introduction
M. Sun Department of Otolaryngology, Xiangya School of Medicine, Central South University, Changsha, China Y. Liu Department of Sports Medicine, Hengyang Normal College, Hengyang, China B. Guo Xiangya School of Medicine, Central South University, Changsha, China J. Zhao Department of Neurosurgery, Xiangya School of Medicine, Central South University, Changsha, China B. Xiao (&) Department of Otolaryngology, The Second Xiangya Hospital of Central South University, Changsha 410011, Hunan, People’s Republic of China e-mail: [email protected]
Keywords Recurrent facial palsy Total facial nerve decompression Recurrence Facial nerve
Recurrent facial palsy is usually idiopathic, although it may be associated with Melkersson Rosenthal syndrome, otitis media or facial nerve tumors [1–3]. The ipsilateral recurrence is more common, although the contralateral recurrence is not infrequent [4]. Currently, the etiology of idiopathic recurrent facial palsy is still unclear. Facial nerve outcomes after multiple episodes seem worse compared to a single episode [5]. Good results about prevention of further recurrence of recurrent facial palsy by either total or subtotal facial nerve decompression have been suggested by several reports [6–9], but there are some great limitations in the literatures. First, they are retrospective study with its inherent shortcomings. Second, the case series are too small. Third, there is no control group. To investigate the exact role of total facial nerve decompression in severe idiopathic recurrent facial palsy, we designed a prospective study which included a larger case series.
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Eur Arch Otorhinolaryngol
Materials and methods A consecutive series of patients with severe idiopathic recurrent facial palsy who visited our hospital between January, 2003 and January, 2011 were included in the prospective study. The study passed approval of the local Ethics Committee. Here, ‘‘severe’’ was defined as 95 % or more degeneration of facial nerve on electroneurography, and ‘‘recurrent facial palsy’’ referred to two or more episodes of facial palsy at the ipsilateral side, excluding those at the contralateral side. The patients were excluded from Melkersson Rosenthal syndrome, facial nerve tumors, otitis media, severe hypertension and sarcoidosis. The identification from Melkersson Rosenthal syndrome was dependent on absence of fissured tongue and recurrent orofacial edema. Facial nerve tumors and otitis media were mainly excluded by high-resolution CT of temporal bone. Facial nerve sarcoidosis was excluded according to radiographic manifestations and evidence absence of sarcoidosis in other organs or tissues. Total facial nerve decompression was recommended to all patients, and prednisolone only (oral prednisolone, 1 mg/kg/day, for 10 days) without antiviral drugs was provided to those who refused surgery. The patients were divided into two groups according to their choice of treatment, surgery group and control group. Conservative treatment was provided within 1 week after onset of facial palsy, and surgical decompression was performed between 1 and 2 weeks after facial palsy. In the surgery, we decompressed internal auditory canal segment, labyrinthine segment, geniculate ganglion, tympanic segment and mastoid segment of facial nerve via middle cranial fossa combined with transmastoid approach. The epineurium was slit after nerve exposure. The patients were followed up after surgery. HouseBrackmann grading system [10] was introduced to assess facial nerve function (FNF). Fisher’s exact test was used to compare recurrence rate of facial palsy between the two groups, and t test used to compare mean difference of follow-up, with SPSS 18.0 software involved in statistical analysis.
Results Summary of the patients is listed in Tables 1 and 2. There were 15 female and 7 male. The median age was 27.5 ± 7.8 years (range 16–41 years). There was no predilection of the affected side. 12 patients accepted surgical decompression, and 10 patients selected conservative treatment. They were followed up for 5.3 ± 1.5 years (range 3–8 years) and 5.2 ± 1.3 years (range 3–7 years), respectively, without significant difference (p [ 0.05).
123
During the follow-up, facial palsy recurrence affected none of the patients in surgery group (0.0 %), while 4 of 10 cases (40 %) in control group suffered palsy recurrence (p \ 0.05). The patients in surgery group gained better recovery. It was shown that 91.7 % cases in surgery group restored to Grade I or Grade II compared to 30.0 % in control group (p \ 0.05). None of the patients developed noticeable complications.
Discussions It is common that recurrent facial palsy recurs after conservative treatment or self-resolution. According to Pitts et al. [11] report, the risk of recurrence rises from 15 percent on the second episode to 50 percent on the fourth attack. Another report [12] reveals that the mean interval between the first and second recurrence is shortened by almost 50 % when compared to the interval between the first facial palsy and the first recurrence. FNF appears to deteriorate progressively as multiple episodes [9, 13, 14], and the loss of action potential amplitude in cases of recurrent facial palsy is greater than that in cases of a single attack [4]. If further episodes of facial palsy are successfully prevented, potential damage of facial nerve may be avoided. It appears that there is no inconsistency about the effect of total facial nerve decompression in preventing further episodes of idiopathic recurrent facial palsy. Graham and Kartush [15] attempted total facial nerve decompression on six patients who had recurrent facial palsy, and they reported no recurrence within the next 3–8 years. Recently, Li Y et al. [16] found that recurrence affected only 1 of 16 patients with idiopathic recurrent facial palsy after total facial nerve decompression within an average period of 4.9 years while 4 of 8 patients who accepted prednisolone treatment only recurred. However, their study demonstrated that total facial nerve decompression was ineffective to promote facial nerve recovery. In our study, further recurrence of facial palsy was noticed in none of the patients in surgery group, while 40 % patients in control group were conflicted with further episodes of facial palsy during the follow-up. The difference was significant (p \ 0.05), indicating total facial nerve decompression was effective to prevent further episodes of idiopathic recurrent facial palsy. The most important factor affecting recurrence rate was thought to be follow-up. There was no significant difference between surgery group and control group in the mean follow-up. Thereby our conclusion was relatively convincing. Surgical intervention is controversial for Bell’s palsy, but most authors advocate the benefits of surgical decompression when the percentage of facial nerve degeneration
Eur Arch Otorhinolaryngol Table 1 Summary of 12 patients who underwent total facial nerve decompression Patient No.
PreFPE
PosFPE
Side
Initial FNF
Final FNF
Age at the first onset
Age
Frequency (times/year)
Follow-up (year)
1
2
0
L
V
I
14
26
2/12
6
2
3
0
L
VI
II
20
34
3/14
4
3
4
0
L
VI
II
5
23
4/18
5
4
2
0
R
V
I
28
35
2/7
7
5
2
0
L
VI
II
8
16
2/8
4
6
5
0
L
VI
III
20
33
5/13
8
7 8
7 2
0 0
L/R L
VI VI
II I
15 30
33 40
7/18 2/10
5 6
9
3
0
R
VI
II
13
21
3/8
3
10a
5
0
L/R
VI
II
10
24
5/14
5
11
3
0
L
VI
II
6
17
3/11
4
12
4
0
L
V
II
15
19
4/4
7
a
PreFPE preoperative facial palsy episode, PosFPE postoperative facial palsy episode, FNF facial nerve function, R right, L left a
Case 7 suffered left-sided facial palsy for five times and right-sided facial palsy for twice and underwent decompression of the left-sided facial nerve followed by final recovery of Grade II; Case 10 suffered left-sided facial palsy for four times and right-sided facial palsy for once, and underwent decompression of the left-sided facial nerve followed by final recovery of Grade II
Table 2 Summary of 10 patients who selected prednisolone treatment
FPE facial palsy episode, T treatment, FNF facial nerve function, L left, R right, FU follow-up a
Case 5 suffered right-sided facial palsy for twice and leftsided facial palsy for five times, followed by left-sided facial palsy for three times and final recovery of Grade IV during the follow-up
Patient No.
FPE before T
FPE after T
Side
Initial FNF
Final FNF
Age at the first onset
Age
Frequency (times/year)
FU (year)
1
3
0
L
V
II
28
40
3/12
6
2
2
0
L
VI
III
22
33
2/11
4
3
4
2
R
VI
III
7
20
4/13
5
4
5
1
R
V
III
14
28
5/14
3
5a
7
3
L/R
VI
IV
12
19
7/7
7
6
3
1
L
VI
III
9
22
3/13
5
7
2
0
R
VI
III
30
41
2/11
7
8
2
0
L
VI
I
21
30
2/9
5
9
4
0
L
VI
II
8
22
4/14
4
10
3
2
R
VI
III
18
30
3/12
6
reaches 90–95 % or above on electroneurography. According to Fisch [17], patients lost 50 % of chance to obtain a satisfactory spontaneous recovery of facial nerve, when 95 % or more maximal degeneration was reached within 2 weeks of onset. Gantz et al. [18] performed facial nerve decompression on patients who had [90 % degeneration on electroneurography and no voluntary motor unit potentials on electromyography within 14 days of complete paralysis, and found: 91 % of the patients in surgical group recovered to Grade I or II in contrast to 42 % of the nonoperated patients. In our study, all patients had over 95 % degeneration of facial nerve before treatment. 91.7 % cases in surgery group versus 30.0 % in control group recovered to Grade I or Grade II, and the difference was statistically significant (p \ 0.05), further documenting the benefits of surgical decompression in promoting facial nerve recovery
of those patients who had more than 95 % nerve degeneration. As mentioned above, Li Y et al. [16] claimed that total facial nerve decompression was ineffective to promote facial nerve recovery of idiopathic recurrent facial palsy. The reason for the different finding was that our study enrolled only those patients who had over 95 % nerve degeneration while there was alternative enrollment standard in their study. Fisch used intraoperative electrical stimulation in three patients who underwent total facial nerve decompression, and found nerve conduction block in the region proximal to the geniculate ganglion, consistent with their gross anatomic observations of swelling of the facial nerve proximal to the geniculate ganglion. Thus, he proposed that the most likely site of neural compression in Bell’s palsy was at the meatal foramen (the narrowest point) [19]. Therefore, we
123
Eur Arch Otorhinolaryngol
selected total facial nerve decompression. Interestingly, it seemed that subtotal facial nerve decompression from stylomastoid foramen to geniculate ganglion or labyrinthine segment or decompression from meatal foramen to geniculate ganglion was also effective to prevent further episodes of recurrent facial palsy [6, 9, 20]. But the enrolled cases were smaller, and further research was required to draw a relatively convincing conclusion. Our study demonstrated that total facial nerve decompression was not only able to prevent further recurrence of facial palsy but also able to promote facial nerve recovery of the patients who had severe idiopathic recurrent facial palsy. Whereas there were also some limits in the study. First, the patients were not randomized for the choice of treatment. Second, longer follow-up was required to provide a more solid conclusion. Conflict of interest The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References 1. Greene RM, Rogers RS III (1989) Melkersson-Rosenthal syndrome: a review of 36 patients. J Am Acad Dermatol 21: 1263–1270 2. Kim J, Jung GH, Park SY, Lee WS (2012) Facial nerve paralysis due to chronic otitis media: prognosis in restoration of facial function after surgical intervention. Yonsei Med J 53(3):642–648 3. Scholz E, Langer J, Begall K (2007) Recurrent facial paresis with facial neurinoma. Laryngorhinootologie 86(6):443–447 4. Mamoli B, Neumann H, Ehrmann L (1977) Recurrent Bell’s palsy. Etiology, frequency, prognosis. J Neurol 216(2):119–125 5. Van Amstel AD, Devriese PP (1988) Clinical experiences with recurrences of Bell’s palsy. Arch Otorhinolaryngol 245(5): 302–306
123
6. Yetiser S, Satar B, Kazkayasi M (2002) Immunologic abnormalities and surgical experiences in recurrent facial nerve paralysis. Otol Neurotol 23(5):772–778 7. Canale TJ, Cox RH (1974) Compression of the facial nerve in Melkersson syndrome. Arch Otolarngol 100(5):373–374 8. Dutt SN, Mirza S, Irving RM, Donaldson I (2000) Total decompression of facial nerve for Melkersson Rosental syndrome. J Laryngol Otol 114(11):870–873 9. Doshi J, Irving R (2010) Recurrent facial nerve palsy: the role of surgery. J Laryngol Otol 124(11):1202–1204 10. Hous JW, Brackmann DE (1985) Facial nerve grading system. Otolaryngol Head Neck Surg 93(2):146–147 11. Pitts DB, Adour KK, Hilsinger RL Jr (1988) Recurrent Bell’s palsy: analysis of 140 patients. Laryngoscope 98(5):535–540 12. Crego F, Galindo J, Quesada P, Naches S, Pin˜as J, Vila J et al (1998) Recurrent peripheral facial paralysis. Our case load from 1995. Acta Otorrinolaringol Esp 49(4):280–282 13. Boddie HG (1972) Recurrent Bell’s Palsy. J Laryngol Otol 86:117–120 14. Ralli G, Magliulo G (1988) Bell’s Palsy and its recurrences. Arch Otorhinolaryngol 244:387–390 15. Graham MD, Kartush JM (1989) Total facial nerve decompression for recurrent facial paralysis: an update. Otolaryngol Head Neck Surg 101(4):442–444 16. Li Y, Li Z, Yan C, Hui L (2014) The effect of total facial nerve decompression in preventing further recurrence of idiopathic recurrent facial palsy. Eur Arch Otorhinolaryngol 2014 Feb 4 (online) 17. Fisch U (1981) Surgery for Bell’s palsy. Arch Otolaryngol 107:1–11 18. Gantz BJ, Rubinstein JT, Gidley P, Woodworth GG (1999) Surgical management of Bell’s palsy. Laryngoscope 109(8): 1177–1188 19. Fisch U, Esslen E (1972) Total intratemporal exposure of the facial nerve. Pathologic findings in Bell’s palsy. Arch Otolaryngol 95(4):335–341 20. Dai C, Li J, Yang S, Zhao L, Feng S, Li Y et al (2014) Subtotal facial nerve decompression for recurrent facial palsy in Melkersson Rosenthal syndrome. Acta Otolaryngol 134(4):425–428
OTOLOGY
Total facial nerve decompression in severe idiopathic recurrent facial palsy Kai Ai • Mai Sun • Yonggang Liu • Bowen Guo Menjiang Tu • Jiapeng Zhao • Bing Xiao
•
Received: 26 July 2014 / Accepted: 8 October 2014 Ó Springer-Verlag Berlin Heidelberg 2014
Abstract To investigate the role of total facial nerve decompression in severe idiopathic recurrent facial palsy. A consecutive series of 22 cases with severe idiopathic recurrent facial palsy were managed in our hospital between January, 2003 and January, 2011. Either total facial nerve decompression or conservative treatment was provided, and they were divided into surgery group and control group according to their choice of treatment. They were followed up for at least 3 years. Facial palsy recurrence and facial nerve outcomes in the two groups were compared. There were 12 patients in surgery group, who were followed up for 5.3 years (range 3–8 years). In
contrast, there were 10 patients in control group, with an average follow-up of 5.2 years (range 3–7 years). None of the patients (0 %) in surgery group recurred compared to 4 of 10 cases (40 %) in control group (p \ 0.05). In perspectives of facial nerve outcomes, 11 of 12 cases (91.7 %) in surgery group achieved good recovery (HB Grade I or II) in contrast to 3 of 10 cases (30.0 %) in control group (p \ 0.05). For severe idiopathic recurrent facial palsy, total facial nerve decompression could not only prevent further recurrence but also promote facial nerve recovery.
K. Ai M. Tu Department of Urology, The Second Xiangya Hospital of Central South University, Changsha, China
Introduction
M. Sun Department of Otolaryngology, Xiangya School of Medicine, Central South University, Changsha, China Y. Liu Department of Sports Medicine, Hengyang Normal College, Hengyang, China B. Guo Xiangya School of Medicine, Central South University, Changsha, China J. Zhao Department of Neurosurgery, Xiangya School of Medicine, Central South University, Changsha, China B. Xiao (&) Department of Otolaryngology, The Second Xiangya Hospital of Central South University, Changsha 410011, Hunan, People’s Republic of China e-mail: [email protected]
Keywords Recurrent facial palsy Total facial nerve decompression Recurrence Facial nerve
Recurrent facial palsy is usually idiopathic, although it may be associated with Melkersson Rosenthal syndrome, otitis media or facial nerve tumors [1–3]. The ipsilateral recurrence is more common, although the contralateral recurrence is not infrequent [4]. Currently, the etiology of idiopathic recurrent facial palsy is still unclear. Facial nerve outcomes after multiple episodes seem worse compared to a single episode [5]. Good results about prevention of further recurrence of recurrent facial palsy by either total or subtotal facial nerve decompression have been suggested by several reports [6–9], but there are some great limitations in the literatures. First, they are retrospective study with its inherent shortcomings. Second, the case series are too small. Third, there is no control group. To investigate the exact role of total facial nerve decompression in severe idiopathic recurrent facial palsy, we designed a prospective study which included a larger case series.
123
Eur Arch Otorhinolaryngol
Materials and methods A consecutive series of patients with severe idiopathic recurrent facial palsy who visited our hospital between January, 2003 and January, 2011 were included in the prospective study. The study passed approval of the local Ethics Committee. Here, ‘‘severe’’ was defined as 95 % or more degeneration of facial nerve on electroneurography, and ‘‘recurrent facial palsy’’ referred to two or more episodes of facial palsy at the ipsilateral side, excluding those at the contralateral side. The patients were excluded from Melkersson Rosenthal syndrome, facial nerve tumors, otitis media, severe hypertension and sarcoidosis. The identification from Melkersson Rosenthal syndrome was dependent on absence of fissured tongue and recurrent orofacial edema. Facial nerve tumors and otitis media were mainly excluded by high-resolution CT of temporal bone. Facial nerve sarcoidosis was excluded according to radiographic manifestations and evidence absence of sarcoidosis in other organs or tissues. Total facial nerve decompression was recommended to all patients, and prednisolone only (oral prednisolone, 1 mg/kg/day, for 10 days) without antiviral drugs was provided to those who refused surgery. The patients were divided into two groups according to their choice of treatment, surgery group and control group. Conservative treatment was provided within 1 week after onset of facial palsy, and surgical decompression was performed between 1 and 2 weeks after facial palsy. In the surgery, we decompressed internal auditory canal segment, labyrinthine segment, geniculate ganglion, tympanic segment and mastoid segment of facial nerve via middle cranial fossa combined with transmastoid approach. The epineurium was slit after nerve exposure. The patients were followed up after surgery. HouseBrackmann grading system [10] was introduced to assess facial nerve function (FNF). Fisher’s exact test was used to compare recurrence rate of facial palsy between the two groups, and t test used to compare mean difference of follow-up, with SPSS 18.0 software involved in statistical analysis.
Results Summary of the patients is listed in Tables 1 and 2. There were 15 female and 7 male. The median age was 27.5 ± 7.8 years (range 16–41 years). There was no predilection of the affected side. 12 patients accepted surgical decompression, and 10 patients selected conservative treatment. They were followed up for 5.3 ± 1.5 years (range 3–8 years) and 5.2 ± 1.3 years (range 3–7 years), respectively, without significant difference (p [ 0.05).
123
During the follow-up, facial palsy recurrence affected none of the patients in surgery group (0.0 %), while 4 of 10 cases (40 %) in control group suffered palsy recurrence (p \ 0.05). The patients in surgery group gained better recovery. It was shown that 91.7 % cases in surgery group restored to Grade I or Grade II compared to 30.0 % in control group (p \ 0.05). None of the patients developed noticeable complications.
Discussions It is common that recurrent facial palsy recurs after conservative treatment or self-resolution. According to Pitts et al. [11] report, the risk of recurrence rises from 15 percent on the second episode to 50 percent on the fourth attack. Another report [12] reveals that the mean interval between the first and second recurrence is shortened by almost 50 % when compared to the interval between the first facial palsy and the first recurrence. FNF appears to deteriorate progressively as multiple episodes [9, 13, 14], and the loss of action potential amplitude in cases of recurrent facial palsy is greater than that in cases of a single attack [4]. If further episodes of facial palsy are successfully prevented, potential damage of facial nerve may be avoided. It appears that there is no inconsistency about the effect of total facial nerve decompression in preventing further episodes of idiopathic recurrent facial palsy. Graham and Kartush [15] attempted total facial nerve decompression on six patients who had recurrent facial palsy, and they reported no recurrence within the next 3–8 years. Recently, Li Y et al. [16] found that recurrence affected only 1 of 16 patients with idiopathic recurrent facial palsy after total facial nerve decompression within an average period of 4.9 years while 4 of 8 patients who accepted prednisolone treatment only recurred. However, their study demonstrated that total facial nerve decompression was ineffective to promote facial nerve recovery. In our study, further recurrence of facial palsy was noticed in none of the patients in surgery group, while 40 % patients in control group were conflicted with further episodes of facial palsy during the follow-up. The difference was significant (p \ 0.05), indicating total facial nerve decompression was effective to prevent further episodes of idiopathic recurrent facial palsy. The most important factor affecting recurrence rate was thought to be follow-up. There was no significant difference between surgery group and control group in the mean follow-up. Thereby our conclusion was relatively convincing. Surgical intervention is controversial for Bell’s palsy, but most authors advocate the benefits of surgical decompression when the percentage of facial nerve degeneration
Eur Arch Otorhinolaryngol Table 1 Summary of 12 patients who underwent total facial nerve decompression Patient No.
PreFPE
PosFPE
Side
Initial FNF
Final FNF
Age at the first onset
Age
Frequency (times/year)
Follow-up (year)
1
2
0
L
V
I
14
26
2/12
6
2
3
0
L
VI
II
20
34
3/14
4
3
4
0
L
VI
II
5
23
4/18
5
4
2
0
R
V
I
28
35
2/7
7
5
2
0
L
VI
II
8
16
2/8
4
6
5
0
L
VI
III
20
33
5/13
8
7 8
7 2
0 0
L/R L
VI VI
II I
15 30
33 40
7/18 2/10
5 6
9
3
0
R
VI
II
13
21
3/8
3
10a
5
0
L/R
VI
II
10
24
5/14
5
11
3
0
L
VI
II
6
17
3/11
4
12
4
0
L
V
II
15
19
4/4
7
a
PreFPE preoperative facial palsy episode, PosFPE postoperative facial palsy episode, FNF facial nerve function, R right, L left a
Case 7 suffered left-sided facial palsy for five times and right-sided facial palsy for twice and underwent decompression of the left-sided facial nerve followed by final recovery of Grade II; Case 10 suffered left-sided facial palsy for four times and right-sided facial palsy for once, and underwent decompression of the left-sided facial nerve followed by final recovery of Grade II
Table 2 Summary of 10 patients who selected prednisolone treatment
FPE facial palsy episode, T treatment, FNF facial nerve function, L left, R right, FU follow-up a
Case 5 suffered right-sided facial palsy for twice and leftsided facial palsy for five times, followed by left-sided facial palsy for three times and final recovery of Grade IV during the follow-up
Patient No.
FPE before T
FPE after T
Side
Initial FNF
Final FNF
Age at the first onset
Age
Frequency (times/year)
FU (year)
1
3
0
L
V
II
28
40
3/12
6
2
2
0
L
VI
III
22
33
2/11
4
3
4
2
R
VI
III
7
20
4/13
5
4
5
1
R
V
III
14
28
5/14
3
5a
7
3
L/R
VI
IV
12
19
7/7
7
6
3
1
L
VI
III
9
22
3/13
5
7
2
0
R
VI
III
30
41
2/11
7
8
2
0
L
VI
I
21
30
2/9
5
9
4
0
L
VI
II
8
22
4/14
4
10
3
2
R
VI
III
18
30
3/12
6
reaches 90–95 % or above on electroneurography. According to Fisch [17], patients lost 50 % of chance to obtain a satisfactory spontaneous recovery of facial nerve, when 95 % or more maximal degeneration was reached within 2 weeks of onset. Gantz et al. [18] performed facial nerve decompression on patients who had [90 % degeneration on electroneurography and no voluntary motor unit potentials on electromyography within 14 days of complete paralysis, and found: 91 % of the patients in surgical group recovered to Grade I or II in contrast to 42 % of the nonoperated patients. In our study, all patients had over 95 % degeneration of facial nerve before treatment. 91.7 % cases in surgery group versus 30.0 % in control group recovered to Grade I or Grade II, and the difference was statistically significant (p \ 0.05), further documenting the benefits of surgical decompression in promoting facial nerve recovery
of those patients who had more than 95 % nerve degeneration. As mentioned above, Li Y et al. [16] claimed that total facial nerve decompression was ineffective to promote facial nerve recovery of idiopathic recurrent facial palsy. The reason for the different finding was that our study enrolled only those patients who had over 95 % nerve degeneration while there was alternative enrollment standard in their study. Fisch used intraoperative electrical stimulation in three patients who underwent total facial nerve decompression, and found nerve conduction block in the region proximal to the geniculate ganglion, consistent with their gross anatomic observations of swelling of the facial nerve proximal to the geniculate ganglion. Thus, he proposed that the most likely site of neural compression in Bell’s palsy was at the meatal foramen (the narrowest point) [19]. Therefore, we
123
Eur Arch Otorhinolaryngol
selected total facial nerve decompression. Interestingly, it seemed that subtotal facial nerve decompression from stylomastoid foramen to geniculate ganglion or labyrinthine segment or decompression from meatal foramen to geniculate ganglion was also effective to prevent further episodes of recurrent facial palsy [6, 9, 20]. But the enrolled cases were smaller, and further research was required to draw a relatively convincing conclusion. Our study demonstrated that total facial nerve decompression was not only able to prevent further recurrence of facial palsy but also able to promote facial nerve recovery of the patients who had severe idiopathic recurrent facial palsy. Whereas there were also some limits in the study. First, the patients were not randomized for the choice of treatment. Second, longer follow-up was required to provide a more solid conclusion. Conflict of interest The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References 1. Greene RM, Rogers RS III (1989) Melkersson-Rosenthal syndrome: a review of 36 patients. J Am Acad Dermatol 21: 1263–1270 2. Kim J, Jung GH, Park SY, Lee WS (2012) Facial nerve paralysis due to chronic otitis media: prognosis in restoration of facial function after surgical intervention. Yonsei Med J 53(3):642–648 3. Scholz E, Langer J, Begall K (2007) Recurrent facial paresis with facial neurinoma. Laryngorhinootologie 86(6):443–447 4. Mamoli B, Neumann H, Ehrmann L (1977) Recurrent Bell’s palsy. Etiology, frequency, prognosis. J Neurol 216(2):119–125 5. Van Amstel AD, Devriese PP (1988) Clinical experiences with recurrences of Bell’s palsy. Arch Otorhinolaryngol 245(5): 302–306
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