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Facial nerve paralysis associated with temporal bone masses
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Facial nerve paralysis associated with temporal bone masses Hironobu Nishijima *, Kenji Kondo, Ryoji Kagoya, Hitoshi Iwamura, Kazuo Yasuhara, Tatsuya Yamasoba Department of Otolaryngology- Head and Neck surgery, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo Bunkyo-ku, Tokyo 113-8655, Japan
A R T I C L E I N F O
A B S T R A C T
Article history: Received 5 October 2016 Accepted 10 December 2016 Available online xxx
Objective: To investigate the clinical and electrophysiological features of facial nerve paralysis (FNP) due to benign temporal bone masses (TBMs) and elucidate its differences as compared with Bell’s palsy. Methods: FNP assessed by the House–Brackmann (HB) grading system and by electroneurography (ENoG) were compared retrospectively. Results: We reviewed 914 patient records and identified 31 patients with FNP due to benign TBMs. Moderate FNP (HB Grades II–IV) was dominant for facial nerve schwannoma (FNS) (n = 15), whereas severe FNP (Grades V and VI) was dominant for cholesteatomas (n = 8) and hemangiomas (n = 3). The average ENoG value was 19.8% for FNS, 15.6% for cholesteatoma, and 0% for hemangioma. Analysis of the correlation between HB grade and ENoG value for FNP due to TBMs and Bell’s palsy revealed that given the same ENoG value, the corresponding HB grade was better for FNS, followed by cholesteatoma, and worst in Bell’s palsy. Conclusions: Facial nerve damage caused by benign TBMs could depend on the underlying pathology. Facial movement and ENoG values did not correlate when comparing TBMs and Bell’s palsy. When the HB grade is found to be unexpectedly better than the ENoG value, TBMs should be included in the differential diagnosis. © 2017 Elsevier B.V. All rights reserved.
Keywords: Facial nerve paralysis Electroneurography Temporal bone tumor Schwannoma Bell palsy,
1. Introduction Facial nerve paralysis (FNP) associated with benign temporal bone masses (TBMs) is a relatively rare clinical disease. It occurs due to various pathological disorders, including facial nerve schwannoma (FNS) [1–3], cholesteatoma [4–8], and hemangioma [9–11], FNP due to benign TBMs is thought to develop through one of the following mechanisms: direct physical pressure on the facial nerve, ischemia of the nerve due to the compression of the vessels, or invasion into the nerve [12,13]. In the absence of imaging studies, FNP due to benign TBMs is often initially misdiagnosed as Bell’s palsy,
* Corresponding author. Fax: +81 3 3814 9486. E-mail address: [email protected] (H. Nishijima).
and even if the benign TBMs are revealed by imaging studies, it can be difficult to make a correct diagnosis before operative exploration. Based on the pathogenesis of different benign TBMs, it is possible that FNP can have clinical and electrophysiological features that are distinct from those of Bell’s palsy. Such information would be useful for diagnosing the etiology of FNP at initial evaluation. Indeed, some previous studies have reported characteristic clinical symptoms of FNP based on the underlying benign TBM. However, the clinical and electrophysiological findings caused by different benign TBMs and differences of FNP between benign TBMs and Bell’s palsy have not been compared earlier. This study therefore aimed to examine the clinical and electrophysiological features of FNP due to benign TBMs, focusing on three benign TBMs: FNS, cholesteatoma, and
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Please cite this article in press as: Nishijima H, et al. Facial nerve paralysis associated with temporal bone masses. Auris Nasus Larynx (2017), http://dx.doi.org/10.1016/j.anl.2016.12.006
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hemangioma. We also evaluated the diagnostic value of electroneurography (ENoG) for FNP due to benign TBMs, comparing the clinical and electrophysiological correlation between FNS, cholesteatoma, and Bell’s palsy. 2. Materials and methods We reviewed patient records at the Facial Nerve Clinic, Department of Otolaryngology, Head and Neck Surgery, the University of Tokyo Hospital. Patients are referred to our clinic if they have diseases related to the facial nerve, including patients with temporary or residual FNP, and perioperative patients with temporal bone tumors. At initial assessment, the severity of neural damage of the facial nerve is assessed for all patients using the House–Brackmann (HB) grading system [14], ENoG, and the blink reflex (BR). We identified 914 patients with peripheral FNP between 2005 and 2013; of these, 31 patients were identified as having FNP due to benign TBMs and were included in the study. Of 31 patients, 26 patients received surgical treatments after our initial assessment and benign TBMs were diagnosed retrospectively by postoperative pathological findings. Five cases of FNS that were diagnosed as possible FNS with computed tomography (CT) and magnetic resonance imaging (MRI). All benign TBMs were included irrespective of the time of onset of FNP. The average time from FNP development to consultation at our clinic was 86 days (4 to 200 days, median = 90 days). Steroid treatment for FNP had been administered for all patients prior to referral. The data collected included age, gender, HB grade, ENoG results, FNP development patterns, BR results, CT and MRI images, treatment modality, and pathological diagnosis. We also collected the data of 30 patients with Bell’s palsy who visited our clinic within 14 days of symptom onset. This allowed comparison of the data for benign TBMs with the most common FNP. All patients with Bell’s palsy received steroid treatment during the study period, and CT or MRI images were performed in all 30 patients to confirm the absence of benign TBMs. The primary outcome measures were the clinical and electrophysiological features of FNP due to the benign TBMs at initial evaluation, which included facial movement evaluated by the HB system, ENoG findings, FNP development patterns, synkinetic potential measured by visual assessment and BR testing, and the location and size of the benign TBMs. The secondary outcome measure was the comparison of the HB grade and ENoG value between cases with benign TBMs and Bell’s palsy. ENoG and BR were performed using a Neuropack electromyography system (Nihon kohden, Japan). On ENoG, 0.2-ms supramaximal stimulation was provided through bipolar surface electrodes that were placed with the anode just outside the stylomastoid foramen and the cathode in front of the ear lobe and manipulated to obtain the maximal compound action potential amplitude. For recording, the surface disc electrodes were placed on the nasolabial fold. Peak-to-peak ENoG response amplitudes on the affected side were compared with those on the unaffected side. The ENoG value was the percentage of the response amplitude
on the affected side compared to that on the unaffected side. In BR testing, a 0.2-ms 18-mA stimulation was applied via the supraorbital margin, and the responses of the orbicularis oculi and orbicularis oris were recorded. We evaluated synkinesis by visual assessment and BR results [15]; when abnormal reflex waves were observed in the orbicularis oris, with similar latency to the BR of the orbicularis oculi, we diagnosed synkinesis [16]. The anatomical locations of the benign TBMs were identified by CT and/or MRI and subdivided into five segments as follows: internal auditory canal, labyrinthine, geniculate ganglion, tympanic, and mastoid portion. Benign TBMs spanning multiple segments were counted for each segment. The size of each benign TBM was measured at its largest part, as identified by axial CT or MRI. Test results were statistically evaluated using the StatMate IV (ATMS, Tokyo, Japan). For statistical analyses, the differences were evaluated using the Mann–Whitney U test. The statistical significance was set at p < 0.05. All procedures were performed in accordance with the guidelines of the University of Tokyo, and the study was approved by the institutional review board (approval no. 2487). 3. Results We identified 31 patients with FNP due to benign TBMs, including 17 men and 14 women, with an age range of 16–75 years (median, 51 years; mean, 52 years). The three most common causes of FNP in this series were FNS, cholesteatoma, and hemangioma (Table 1). The detailed clinical and electrophysiological data on patients with FNP due to FNS, cholesteatoma, and hemangioma are summarized consecutively in Tables 2. In the FNS group, 12 patients (80%) showed moderate paralysis (HB Grades II–IV), and 3 patients (20%) showed severe paralysis (Grades V–VI). In the cholesteatoma group, only two patients (25%) showed moderate paralysis, and six (75%) showed severe paralysis. In the hemangioma group, one patient (33%) showed moderate paralysis, and two patients (67%) showed severe paralysis. Significant differences were observed in the HB grade between the FNS and cholesteatoma groups (p < 0.001); the average HB grade in the patients with FNS was 3.3 (median = 4), while the average grade in patients with cholesteatoma and hemangioma were 4.8 (median = 5) and 5.0 (median = 6), respectively. The average ENoG values were 19.8% (median = 23.4%), 15.6% (median = 9.4%), and 0% (median = 0%) in the FNS, Table 1 Causes of temporal bone masses. Cause
No. of Cases (n = 31)
Facial nerve schwannoma Cholesteatoma Hemangioma Wegener’s granuloma Cholesterin granuloma Meningioma Meningoencephalocele
15 8 3 2 1 1 1
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Table 2 Patients with temporal bone tumors. Diagnosis
Age/Sex
HB grade
ENoG value (%)
FNP development
Facial nerve schwannoma
50/M 48/M 21/F 63/F 50/F 16/M 53/M 31/M 36/F 75/F 29/F 45/F 58/F 49/F 51/M
III II IV II IV IV IV II IV V II V II II V
25.6 39.5 10.7 58.4 4.4 24.4 3.5 23.4 0.2 4 25.6 1.7 38.3 37.1 0.19
A A A A A R R R P P P P R A A
61/F 37/M 69/M 67/M 54/F 63/F 66/M 63/M
VI II IV V VI V V V
2.4 48.2 39 2.2 12.3 13.1 6.4 1.3
P A P P R A P P
60/M 45/M 62/M
VI VI III
0 0 No data
P P R
Cholesteatoma
Hemangioma
Synkinesis
Location
Size (mm)
GG, TYM, MAS GG, TYM, MAS TYM, MAS GG GG, TYM, MAS IAC, LAB,GG IAC, LAB,GG, TYM, MAS TYM, MAS IAC, LAB,GG, TYM GG, TYM MAS GG, TYM, MAS IAC IAC
16 11 15.4 7 2.7 16.7 14 32.8 28 19.9 24 8 22 20 7
–
LAB,GG IAC, TYM TYM LAB,GG LAB,GG TYM IAC, LAB,GG TYM
10.4 8 14 11.6 15 8 7 3
+
GG, TYM, MAS GG GG, TYM
11.9 6 14.7
+
+ + + +
+ + +
A: the paralysis of acute onset, P: progressive worsening without improvement, R: repeated improvements and exacerbations, plus sign (+), minus sign ( ), IAC: internal auditory canal, LAB: labyrinthine, GG: geniculate ganglion, TYM: tympanic portion, MAS: mastoid portion.
cholesteatoma, and hemangioma groups, respectively. No significant differences were observed in the ENoG values between the FNS and cholesteatoma groups (p = 0.77). The patterns of FNP development were categorized into three groups: acute onset, progressive worsening without improvement, and repeated improvements and exacerbations. Acute onset was predominant in the FNS group, while progressive worsening was predominant in the cholesteatoma and hemangioma groups. Synkinesis was observed in eight patients (53%) in the FNS group and one patient (33%) in the hemangioma group. No synkinesis was demonstrated for the seven patients in the FNS group, all eight patients in the cholesteatoma group, and the two patients in the hemangioma group. Using Fisher’s exact test, we found that the prevalence of synkinesis in the FNS group was significantly higher than that in the cholesteatoma groups. The most frequently involved locations in the FNS group were the geniculate ganglion and the tympanic segment (60%), followed by the mastoid segment (53%). The most frequently involved segments in the cholesteatoma group were the labyrinthine segment (50%) and geniculate ganglion (50%) followed by the tympanic segment (38%). The most frequently involved segments in the hemangioma group were the geniculate ganglion (100%) followed by the tympanic segment (66%). The average size of the masses was 16.3 mm, 9.6 mm, and 10.9 mm for FNS, cholesteatomas, and hemangiomas, respectively.
Although patients with FNS had significantly better facial movement under the HB grading system than those with cholesteatoma, no significant differences were observed in the ENoG values between the FNS and cholesteatoma groups. Moreover, ENoG value seems to be too low compared to empirically-predicted value derived from HB grade in clinical practice. To analyze this finding, we plotted the HB grades and ENoG values of each patient in the FNS, cholesteatoma, and extracted Bell’s palsy groups on the X and Y axes, respectively (Fig. 1). This showed that the plots for benign TBM cases were consistently in the area under the diagonal line from the upper left to the lower right, whereas those of Bell’s palsy were spread over a wider area. Fig. 1 also indicates that, for a given ENoG value, the corresponding HB grade was most favorable in the FNS group, followed by the cholesteatoma group, and worst in the Bell’s palsy group. This trend was also observed between acute FNP cases of FNS and Bell’s palsy (Fig. 2). 4. Discussion Our study demonstrated that, of more than 900 patients with FNP within an eight-year period, only 31 patients (3.4%) presented with FNP due to benign TBMs. Their pathologies included FNS in 15 cases (1.6%), cholesteatoma in 8 cases (0.9%), and hemangioma in 3 cases (0.3%). Latack et al. reported that FNS is the most common neoplasm to cause FNP, but that it accounts for less than 5% of all cases of FNP [2]. The
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Fig. 1. The correlation between HB grade and ENoG value. The r-values of the regression curves were 0.86 (p < 0.01), 0.55, and 0.41 (p < 0.01) for the FNS, cholesteatoma, and Bell’s palsy groups, respectively, as determined using the Spearman’s correlation coefficient. Given the same ENoG value, the HB grade was best in FNS, followed by cholesteatoma, and was worst in Bell’s palsy.
Fig. 2. The correlation between HB grade and ENoG values in case of acute onset. The r-values of the regression curves were 0.93 (p < 0.01) and 0.41 (p < 0.01) for the FNS and Bell’s palsy groups, respectively, as determined using the Spearman’s correlation coefficient. Given the same ENoG value, the HB grade was higher in the FNS group compared with that in the Bell’s palsy group.
incidence of FNP due to cholesteatoma varies widely. Peitersen reported that the incidence of peripheral FNP presenting with cholesteatoma was 0.9% [17], while the incidence of FNP in cases of petrous apex cholesteatoma is reported to be between 50% and 60% [7,8]. FNP caused by hemangioma appears to be extremely rare, with hemangiomas arising adjacent to the facial nerve accounting for 0.7% of intratemporal tumors according to a series of 1,430 patients over a 20-year period [11]. In our case series, facial movement assessed by HB grade was best in cases of FNS, followed by cholesteatoma, and then hemangioma. The severities of FNP for the benign TBMs in our study were consistent with those reported previously. McRackan et al. reported that 65% of patients with FNP due to FNS showed moderate paralysis (HB Grades II–IV), whereas 35% presented with severe paralysis (Grades V and VI) [1]. The severity of FNP due to cholesteatoma varies. Quaranta et al. reported that clinically moderate paralysis occurred in 53% of their patients with cholesteatoma, while 47% had severe paralysis [4]. In contrast, hemangioma frequently presents with moderate to severe FNP and an HB Grade of III–VI [9]. It is also reported that hemangiomas present with FNP and hemifacial spasm at an earlier stage than FNS because they invade the nerve rather than simply compressing it [18]. FNS has a variety of clinical courses. McRacken reported that 82.1% of FNS cases resulted in permanent weakness, whereas 17.9% were transient [1]. In our cases, 7 of 15 FNS cases showed acute onset, 4 of 15 FNS cases showed
progressive worsening without improvement, and the remaining 4 of 15 showed repeated improvements and exacerbations. Furthermore, 4 of 15 FNS cases showed synkinesis despite not having had a previous episode of subjective FNP. These findings suggest that both clinical and subclinical nerve fiber degeneration and regeneration occurs in cases of FNS. In contrast, the cholesteatoma and hemangioma groups predominantly showed a pattern of progressive worsening without improvement. Even with a history of FNP, synkinesis was not observed in most cases of cholesteatoma and hemangioma. This is likely because the nerve damage is progressive, and nerve regeneration does not occur. The location of the benign TBMs differed according to the specific lesion. FNS lesions were located mainly at the geniculate ganglion and the mastoid portion of temporal bone in this study. Kertesz et al. reported that the geniculate ganglion (68.2%) and labyrinthine (52.3%) segments were the most likely to develop FNS followed by the mastoid segment [3]. In our series, cholesteatoma was mainly located at the apex of petrous part of temporal bone, although the most common location of cholesteatoma is typically the tympanic cavity. Hemangioma with FNP in the geniculate ganglion occurred similar to the descriptions in previous reports [10]. The average sizes of the benign TBMs were 16.3 mm, 9.6 mm, and 10.9 mm in the FNS, cholesteatoma, and hemangioma groups, respectively. Although the average size of TBMs was smaller in the cholesteatoma and hemangioma
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groups, the FNP observed in these groups was more severe than that in the FNS group. Chan et al. reported FNS, even when of a considerable size, does not necessarily induce FNP [12]. The ENoG value is thought to represent the percentage of intact or neurapraxic axons of total axons [19], and it has been established as the most useful method for evaluating the severity of neural damage in cases of Bell’s palsy or Ramsay– Hunt syndrome [20–22]. Interestingly, we found that although there was no significant difference between the FNS and cholesteatoma groups regarding the ENoG values, the degree of facial movement was significantly better in the FNS group compared with the cholesteatoma and hemangioma groups. Moreover, in FNS groups, ENoG value was too low compared to empirically-predicted value derived from HB grade in clinical practice. We therefore compared the correlation of HB grade and ENoG value between the FNS, cholesteatoma, and Bell’s palsy groups. When we plotted the HB grades and ENoG values on the X and Y axes, respectively, FNPs due to benign TBMs and Bell’s palsy existed in different areas. The regression curves of each disease revealed that, given the same ENoG value, HB grade was best for FNS, followed by cholesteatoma, and worst for Bell’s palsy. This trend was observed between acute FNP cases of FNS and Bell’s palsy. This result indicates that the correlations of facial movement and ENoG values were not equivalent for FNP due to Bell’s palsy and that due to benign TBMs. The reason for this is unclear, but it is possible that the remaining nerve fibers work sufficiently because benign TBMs tend to induce physical compression of the facial nerve, and the border between the damaged and intact nerve remains distinct. In contrast, the nerve fibers are typically uniformly damaged in Bell’s palsy, where the acute nerve inflammation and subsequent edema probably cause the facial nerve damage [23]; indeed, even though some fibers survive the damage, they may easily become neuropraxia. Therefore, when the ENoG values are the same, it is possible that more nerve fibers continue to function normally in benign TBMs when compared with Bell’s palsy. Whatever the exact mechanism is, this difference in the correlation of ENoG values to HB grade may be an interesting electrophysiological characteristic of benign TBMs. It may be clinically useful to exclude benign TBMs by imaging when the HB grade is unexpectedly better than the ENoG value in cases of undiagnosed FNP at the initial assessment. This study has several limitations. First, the average time interval for consultation to our clinic was long for FNP due to benign TBMs. In the case of Bell’s palsy, ENoG should be performed within four weeks of onset to maximize its diagnostic value for nerve severity [24]. However, the diagnostic value of ENoG of FNP due to benign TBMs has not been evaluated in previous studies. In spite of the delay between ENoG and onset of FNP in TBMs group, the correlation of ENoG value and HB grade in TBMs group (i.e. better facial movement compared to ENoG value.) never happens in any period of Bell’s palsy group. Second, the disparity between HB grade and ENoG value is just one of the characteristics of FNP due to benign TBMs. Imaging studies should be considered for cases with atypical histories and clinical courses and should not rely only on the ENoG and HB
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grade association. In spite of these limitations, we believe the information provided in this study has merit in helping clinicians decide the most appropriate diagnostic and/or therapeutic strategy for their patients. In fact, we experienced that recurrence of cholesteatoma, which was suggested based on the disparity of HB grade and ENoG value but not confirmed by imaging, was often confirmed during exploratory surgery. 5. Conclusion The patterns of FNP development due to benign TBMs appears to be dependent on the underlying pathology. Facial movement assessed by HB grade was best in those with FNS, followed by those with cholesteatoma, and was worst in those with hemangioma. Facial movement and ENoG values did not correlate equivalently between FNP caused by Bell’s palsy and that caused by benign TBMs, which represents an important electrophysiological characteristic of benign TBMs. We propose that it is clinically useful to exclude the diagnosis of benign TBM when the HB grade is unexpectedly better than the ENoG value in cases of undiagnosed FNP. Disclosure of funding received for this work None. Disclosure statement None of the authors have any conflicts of interest, financial or otherwise. Acknowledgment None. References [1] McRackan TR, Rivas A, Wanna GB, Yoo MJ, Bennett ML, Dietrich MS, et al. Facial nerve outcomes in facial nerve schwannomas. Otol Neurotol 2012;33:78–82. [2] Latack JT, Gabrielsen TO, Knake JE, Kemink JL, Graham MD, Gebarski SS, et al. Facial nerve neuromas: radiologic evaluation. Radiology 1983;149:731–9. [3] Kertesz TR, Shelton C, Wiggins RH, Salzman KL, Glastonbury CM, Harnsberger R. Intratemporal facial nerve neuroma: anatomical location and radiological features. Laryngoscope 2001;111:1250–6. [4] Quaranta N, Cassano M, Quaranta A. Facial paralysis associated with cholesteatoma: a review of 13 cases. Otol Neurotol 2007;28:405–7. [5] Yetiser S, Tosun F, Kazkayasi M. Facial nerve paralysis due to chronic otitis media. Otol Neurotol 2002;23:580–8. [6] Ikeda M, Nakazato H, Onoda K, Hirai R, Kida A. Facial nerve paralysis caused by middle ear cholesteatoma and effects of surgical intervention. Acta Otolaryngol 2006;126:95–100. [7] Siddiq MA, Hanu-Cernat LM, Irving RM. Facial palsy secondary to cholesteatoma: analysis of outcome following surgery. J Laryngol Otol 2007;121:114–7. [8] Magliulo G, Terranova G, Sepe C, Cordeschi S, Cristofar P. Petrous bone cholesteatoma and facial paralysis. Clin Otolaryngol Allied Sci 1998;23:253–8. [9] Semaan MT, Slattery WH, Brackmann DE. Geniculate ganglion hemangiomas: clinical results and long-term follow-up. Otol Neurotol 2010;31:665–70.
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Facial nerve paralysis associated with temporal bone masses Hironobu Nishijima *, Kenji Kondo, Ryoji Kagoya, Hitoshi Iwamura, Kazuo Yasuhara, Tatsuya Yamasoba Department of Otolaryngology- Head and Neck surgery, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo Bunkyo-ku, Tokyo 113-8655, Japan
A R T I C L E I N F O
A B S T R A C T
Article history: Received 5 October 2016 Accepted 10 December 2016 Available online xxx
Objective: To investigate the clinical and electrophysiological features of facial nerve paralysis (FNP) due to benign temporal bone masses (TBMs) and elucidate its differences as compared with Bell’s palsy. Methods: FNP assessed by the House–Brackmann (HB) grading system and by electroneurography (ENoG) were compared retrospectively. Results: We reviewed 914 patient records and identified 31 patients with FNP due to benign TBMs. Moderate FNP (HB Grades II–IV) was dominant for facial nerve schwannoma (FNS) (n = 15), whereas severe FNP (Grades V and VI) was dominant for cholesteatomas (n = 8) and hemangiomas (n = 3). The average ENoG value was 19.8% for FNS, 15.6% for cholesteatoma, and 0% for hemangioma. Analysis of the correlation between HB grade and ENoG value for FNP due to TBMs and Bell’s palsy revealed that given the same ENoG value, the corresponding HB grade was better for FNS, followed by cholesteatoma, and worst in Bell’s palsy. Conclusions: Facial nerve damage caused by benign TBMs could depend on the underlying pathology. Facial movement and ENoG values did not correlate when comparing TBMs and Bell’s palsy. When the HB grade is found to be unexpectedly better than the ENoG value, TBMs should be included in the differential diagnosis. © 2017 Elsevier B.V. All rights reserved.
Keywords: Facial nerve paralysis Electroneurography Temporal bone tumor Schwannoma Bell palsy,
1. Introduction Facial nerve paralysis (FNP) associated with benign temporal bone masses (TBMs) is a relatively rare clinical disease. It occurs due to various pathological disorders, including facial nerve schwannoma (FNS) [1–3], cholesteatoma [4–8], and hemangioma [9–11], FNP due to benign TBMs is thought to develop through one of the following mechanisms: direct physical pressure on the facial nerve, ischemia of the nerve due to the compression of the vessels, or invasion into the nerve [12,13]. In the absence of imaging studies, FNP due to benign TBMs is often initially misdiagnosed as Bell’s palsy,
* Corresponding author. Fax: +81 3 3814 9486. E-mail address: [email protected] (H. Nishijima).
and even if the benign TBMs are revealed by imaging studies, it can be difficult to make a correct diagnosis before operative exploration. Based on the pathogenesis of different benign TBMs, it is possible that FNP can have clinical and electrophysiological features that are distinct from those of Bell’s palsy. Such information would be useful for diagnosing the etiology of FNP at initial evaluation. Indeed, some previous studies have reported characteristic clinical symptoms of FNP based on the underlying benign TBM. However, the clinical and electrophysiological findings caused by different benign TBMs and differences of FNP between benign TBMs and Bell’s palsy have not been compared earlier. This study therefore aimed to examine the clinical and electrophysiological features of FNP due to benign TBMs, focusing on three benign TBMs: FNS, cholesteatoma, and
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hemangioma. We also evaluated the diagnostic value of electroneurography (ENoG) for FNP due to benign TBMs, comparing the clinical and electrophysiological correlation between FNS, cholesteatoma, and Bell’s palsy. 2. Materials and methods We reviewed patient records at the Facial Nerve Clinic, Department of Otolaryngology, Head and Neck Surgery, the University of Tokyo Hospital. Patients are referred to our clinic if they have diseases related to the facial nerve, including patients with temporary or residual FNP, and perioperative patients with temporal bone tumors. At initial assessment, the severity of neural damage of the facial nerve is assessed for all patients using the House–Brackmann (HB) grading system [14], ENoG, and the blink reflex (BR). We identified 914 patients with peripheral FNP between 2005 and 2013; of these, 31 patients were identified as having FNP due to benign TBMs and were included in the study. Of 31 patients, 26 patients received surgical treatments after our initial assessment and benign TBMs were diagnosed retrospectively by postoperative pathological findings. Five cases of FNS that were diagnosed as possible FNS with computed tomography (CT) and magnetic resonance imaging (MRI). All benign TBMs were included irrespective of the time of onset of FNP. The average time from FNP development to consultation at our clinic was 86 days (4 to 200 days, median = 90 days). Steroid treatment for FNP had been administered for all patients prior to referral. The data collected included age, gender, HB grade, ENoG results, FNP development patterns, BR results, CT and MRI images, treatment modality, and pathological diagnosis. We also collected the data of 30 patients with Bell’s palsy who visited our clinic within 14 days of symptom onset. This allowed comparison of the data for benign TBMs with the most common FNP. All patients with Bell’s palsy received steroid treatment during the study period, and CT or MRI images were performed in all 30 patients to confirm the absence of benign TBMs. The primary outcome measures were the clinical and electrophysiological features of FNP due to the benign TBMs at initial evaluation, which included facial movement evaluated by the HB system, ENoG findings, FNP development patterns, synkinetic potential measured by visual assessment and BR testing, and the location and size of the benign TBMs. The secondary outcome measure was the comparison of the HB grade and ENoG value between cases with benign TBMs and Bell’s palsy. ENoG and BR were performed using a Neuropack electromyography system (Nihon kohden, Japan). On ENoG, 0.2-ms supramaximal stimulation was provided through bipolar surface electrodes that were placed with the anode just outside the stylomastoid foramen and the cathode in front of the ear lobe and manipulated to obtain the maximal compound action potential amplitude. For recording, the surface disc electrodes were placed on the nasolabial fold. Peak-to-peak ENoG response amplitudes on the affected side were compared with those on the unaffected side. The ENoG value was the percentage of the response amplitude
on the affected side compared to that on the unaffected side. In BR testing, a 0.2-ms 18-mA stimulation was applied via the supraorbital margin, and the responses of the orbicularis oculi and orbicularis oris were recorded. We evaluated synkinesis by visual assessment and BR results [15]; when abnormal reflex waves were observed in the orbicularis oris, with similar latency to the BR of the orbicularis oculi, we diagnosed synkinesis [16]. The anatomical locations of the benign TBMs were identified by CT and/or MRI and subdivided into five segments as follows: internal auditory canal, labyrinthine, geniculate ganglion, tympanic, and mastoid portion. Benign TBMs spanning multiple segments were counted for each segment. The size of each benign TBM was measured at its largest part, as identified by axial CT or MRI. Test results were statistically evaluated using the StatMate IV (ATMS, Tokyo, Japan). For statistical analyses, the differences were evaluated using the Mann–Whitney U test. The statistical significance was set at p < 0.05. All procedures were performed in accordance with the guidelines of the University of Tokyo, and the study was approved by the institutional review board (approval no. 2487). 3. Results We identified 31 patients with FNP due to benign TBMs, including 17 men and 14 women, with an age range of 16–75 years (median, 51 years; mean, 52 years). The three most common causes of FNP in this series were FNS, cholesteatoma, and hemangioma (Table 1). The detailed clinical and electrophysiological data on patients with FNP due to FNS, cholesteatoma, and hemangioma are summarized consecutively in Tables 2. In the FNS group, 12 patients (80%) showed moderate paralysis (HB Grades II–IV), and 3 patients (20%) showed severe paralysis (Grades V–VI). In the cholesteatoma group, only two patients (25%) showed moderate paralysis, and six (75%) showed severe paralysis. In the hemangioma group, one patient (33%) showed moderate paralysis, and two patients (67%) showed severe paralysis. Significant differences were observed in the HB grade between the FNS and cholesteatoma groups (p < 0.001); the average HB grade in the patients with FNS was 3.3 (median = 4), while the average grade in patients with cholesteatoma and hemangioma were 4.8 (median = 5) and 5.0 (median = 6), respectively. The average ENoG values were 19.8% (median = 23.4%), 15.6% (median = 9.4%), and 0% (median = 0%) in the FNS, Table 1 Causes of temporal bone masses. Cause
No. of Cases (n = 31)
Facial nerve schwannoma Cholesteatoma Hemangioma Wegener’s granuloma Cholesterin granuloma Meningioma Meningoencephalocele
15 8 3 2 1 1 1
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Table 2 Patients with temporal bone tumors. Diagnosis
Age/Sex
HB grade
ENoG value (%)
FNP development
Facial nerve schwannoma
50/M 48/M 21/F 63/F 50/F 16/M 53/M 31/M 36/F 75/F 29/F 45/F 58/F 49/F 51/M
III II IV II IV IV IV II IV V II V II II V
25.6 39.5 10.7 58.4 4.4 24.4 3.5 23.4 0.2 4 25.6 1.7 38.3 37.1 0.19
A A A A A R R R P P P P R A A
61/F 37/M 69/M 67/M 54/F 63/F 66/M 63/M
VI II IV V VI V V V
2.4 48.2 39 2.2 12.3 13.1 6.4 1.3
P A P P R A P P
60/M 45/M 62/M
VI VI III
0 0 No data
P P R
Cholesteatoma
Hemangioma
Synkinesis
Location
Size (mm)
GG, TYM, MAS GG, TYM, MAS TYM, MAS GG GG, TYM, MAS IAC, LAB,GG IAC, LAB,GG, TYM, MAS TYM, MAS IAC, LAB,GG, TYM GG, TYM MAS GG, TYM, MAS IAC IAC
16 11 15.4 7 2.7 16.7 14 32.8 28 19.9 24 8 22 20 7
–
LAB,GG IAC, TYM TYM LAB,GG LAB,GG TYM IAC, LAB,GG TYM
10.4 8 14 11.6 15 8 7 3
+
GG, TYM, MAS GG GG, TYM
11.9 6 14.7
+
+ + + +
+ + +
A: the paralysis of acute onset, P: progressive worsening without improvement, R: repeated improvements and exacerbations, plus sign (+), minus sign ( ), IAC: internal auditory canal, LAB: labyrinthine, GG: geniculate ganglion, TYM: tympanic portion, MAS: mastoid portion.
cholesteatoma, and hemangioma groups, respectively. No significant differences were observed in the ENoG values between the FNS and cholesteatoma groups (p = 0.77). The patterns of FNP development were categorized into three groups: acute onset, progressive worsening without improvement, and repeated improvements and exacerbations. Acute onset was predominant in the FNS group, while progressive worsening was predominant in the cholesteatoma and hemangioma groups. Synkinesis was observed in eight patients (53%) in the FNS group and one patient (33%) in the hemangioma group. No synkinesis was demonstrated for the seven patients in the FNS group, all eight patients in the cholesteatoma group, and the two patients in the hemangioma group. Using Fisher’s exact test, we found that the prevalence of synkinesis in the FNS group was significantly higher than that in the cholesteatoma groups. The most frequently involved locations in the FNS group were the geniculate ganglion and the tympanic segment (60%), followed by the mastoid segment (53%). The most frequently involved segments in the cholesteatoma group were the labyrinthine segment (50%) and geniculate ganglion (50%) followed by the tympanic segment (38%). The most frequently involved segments in the hemangioma group were the geniculate ganglion (100%) followed by the tympanic segment (66%). The average size of the masses was 16.3 mm, 9.6 mm, and 10.9 mm for FNS, cholesteatomas, and hemangiomas, respectively.
Although patients with FNS had significantly better facial movement under the HB grading system than those with cholesteatoma, no significant differences were observed in the ENoG values between the FNS and cholesteatoma groups. Moreover, ENoG value seems to be too low compared to empirically-predicted value derived from HB grade in clinical practice. To analyze this finding, we plotted the HB grades and ENoG values of each patient in the FNS, cholesteatoma, and extracted Bell’s palsy groups on the X and Y axes, respectively (Fig. 1). This showed that the plots for benign TBM cases were consistently in the area under the diagonal line from the upper left to the lower right, whereas those of Bell’s palsy were spread over a wider area. Fig. 1 also indicates that, for a given ENoG value, the corresponding HB grade was most favorable in the FNS group, followed by the cholesteatoma group, and worst in the Bell’s palsy group. This trend was also observed between acute FNP cases of FNS and Bell’s palsy (Fig. 2). 4. Discussion Our study demonstrated that, of more than 900 patients with FNP within an eight-year period, only 31 patients (3.4%) presented with FNP due to benign TBMs. Their pathologies included FNS in 15 cases (1.6%), cholesteatoma in 8 cases (0.9%), and hemangioma in 3 cases (0.3%). Latack et al. reported that FNS is the most common neoplasm to cause FNP, but that it accounts for less than 5% of all cases of FNP [2]. The
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Fig. 1. The correlation between HB grade and ENoG value. The r-values of the regression curves were 0.86 (p < 0.01), 0.55, and 0.41 (p < 0.01) for the FNS, cholesteatoma, and Bell’s palsy groups, respectively, as determined using the Spearman’s correlation coefficient. Given the same ENoG value, the HB grade was best in FNS, followed by cholesteatoma, and was worst in Bell’s palsy.
Fig. 2. The correlation between HB grade and ENoG values in case of acute onset. The r-values of the regression curves were 0.93 (p < 0.01) and 0.41 (p < 0.01) for the FNS and Bell’s palsy groups, respectively, as determined using the Spearman’s correlation coefficient. Given the same ENoG value, the HB grade was higher in the FNS group compared with that in the Bell’s palsy group.
incidence of FNP due to cholesteatoma varies widely. Peitersen reported that the incidence of peripheral FNP presenting with cholesteatoma was 0.9% [17], while the incidence of FNP in cases of petrous apex cholesteatoma is reported to be between 50% and 60% [7,8]. FNP caused by hemangioma appears to be extremely rare, with hemangiomas arising adjacent to the facial nerve accounting for 0.7% of intratemporal tumors according to a series of 1,430 patients over a 20-year period [11]. In our case series, facial movement assessed by HB grade was best in cases of FNS, followed by cholesteatoma, and then hemangioma. The severities of FNP for the benign TBMs in our study were consistent with those reported previously. McRackan et al. reported that 65% of patients with FNP due to FNS showed moderate paralysis (HB Grades II–IV), whereas 35% presented with severe paralysis (Grades V and VI) [1]. The severity of FNP due to cholesteatoma varies. Quaranta et al. reported that clinically moderate paralysis occurred in 53% of their patients with cholesteatoma, while 47% had severe paralysis [4]. In contrast, hemangioma frequently presents with moderate to severe FNP and an HB Grade of III–VI [9]. It is also reported that hemangiomas present with FNP and hemifacial spasm at an earlier stage than FNS because they invade the nerve rather than simply compressing it [18]. FNS has a variety of clinical courses. McRacken reported that 82.1% of FNS cases resulted in permanent weakness, whereas 17.9% were transient [1]. In our cases, 7 of 15 FNS cases showed acute onset, 4 of 15 FNS cases showed
progressive worsening without improvement, and the remaining 4 of 15 showed repeated improvements and exacerbations. Furthermore, 4 of 15 FNS cases showed synkinesis despite not having had a previous episode of subjective FNP. These findings suggest that both clinical and subclinical nerve fiber degeneration and regeneration occurs in cases of FNS. In contrast, the cholesteatoma and hemangioma groups predominantly showed a pattern of progressive worsening without improvement. Even with a history of FNP, synkinesis was not observed in most cases of cholesteatoma and hemangioma. This is likely because the nerve damage is progressive, and nerve regeneration does not occur. The location of the benign TBMs differed according to the specific lesion. FNS lesions were located mainly at the geniculate ganglion and the mastoid portion of temporal bone in this study. Kertesz et al. reported that the geniculate ganglion (68.2%) and labyrinthine (52.3%) segments were the most likely to develop FNS followed by the mastoid segment [3]. In our series, cholesteatoma was mainly located at the apex of petrous part of temporal bone, although the most common location of cholesteatoma is typically the tympanic cavity. Hemangioma with FNP in the geniculate ganglion occurred similar to the descriptions in previous reports [10]. The average sizes of the benign TBMs were 16.3 mm, 9.6 mm, and 10.9 mm in the FNS, cholesteatoma, and hemangioma groups, respectively. Although the average size of TBMs was smaller in the cholesteatoma and hemangioma
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groups, the FNP observed in these groups was more severe than that in the FNS group. Chan et al. reported FNS, even when of a considerable size, does not necessarily induce FNP [12]. The ENoG value is thought to represent the percentage of intact or neurapraxic axons of total axons [19], and it has been established as the most useful method for evaluating the severity of neural damage in cases of Bell’s palsy or Ramsay– Hunt syndrome [20–22]. Interestingly, we found that although there was no significant difference between the FNS and cholesteatoma groups regarding the ENoG values, the degree of facial movement was significantly better in the FNS group compared with the cholesteatoma and hemangioma groups. Moreover, in FNS groups, ENoG value was too low compared to empirically-predicted value derived from HB grade in clinical practice. We therefore compared the correlation of HB grade and ENoG value between the FNS, cholesteatoma, and Bell’s palsy groups. When we plotted the HB grades and ENoG values on the X and Y axes, respectively, FNPs due to benign TBMs and Bell’s palsy existed in different areas. The regression curves of each disease revealed that, given the same ENoG value, HB grade was best for FNS, followed by cholesteatoma, and worst for Bell’s palsy. This trend was observed between acute FNP cases of FNS and Bell’s palsy. This result indicates that the correlations of facial movement and ENoG values were not equivalent for FNP due to Bell’s palsy and that due to benign TBMs. The reason for this is unclear, but it is possible that the remaining nerve fibers work sufficiently because benign TBMs tend to induce physical compression of the facial nerve, and the border between the damaged and intact nerve remains distinct. In contrast, the nerve fibers are typically uniformly damaged in Bell’s palsy, where the acute nerve inflammation and subsequent edema probably cause the facial nerve damage [23]; indeed, even though some fibers survive the damage, they may easily become neuropraxia. Therefore, when the ENoG values are the same, it is possible that more nerve fibers continue to function normally in benign TBMs when compared with Bell’s palsy. Whatever the exact mechanism is, this difference in the correlation of ENoG values to HB grade may be an interesting electrophysiological characteristic of benign TBMs. It may be clinically useful to exclude benign TBMs by imaging when the HB grade is unexpectedly better than the ENoG value in cases of undiagnosed FNP at the initial assessment. This study has several limitations. First, the average time interval for consultation to our clinic was long for FNP due to benign TBMs. In the case of Bell’s palsy, ENoG should be performed within four weeks of onset to maximize its diagnostic value for nerve severity [24]. However, the diagnostic value of ENoG of FNP due to benign TBMs has not been evaluated in previous studies. In spite of the delay between ENoG and onset of FNP in TBMs group, the correlation of ENoG value and HB grade in TBMs group (i.e. better facial movement compared to ENoG value.) never happens in any period of Bell’s palsy group. Second, the disparity between HB grade and ENoG value is just one of the characteristics of FNP due to benign TBMs. Imaging studies should be considered for cases with atypical histories and clinical courses and should not rely only on the ENoG and HB
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grade association. In spite of these limitations, we believe the information provided in this study has merit in helping clinicians decide the most appropriate diagnostic and/or therapeutic strategy for their patients. In fact, we experienced that recurrence of cholesteatoma, which was suggested based on the disparity of HB grade and ENoG value but not confirmed by imaging, was often confirmed during exploratory surgery. 5. Conclusion The patterns of FNP development due to benign TBMs appears to be dependent on the underlying pathology. Facial movement assessed by HB grade was best in those with FNS, followed by those with cholesteatoma, and was worst in those with hemangioma. Facial movement and ENoG values did not correlate equivalently between FNP caused by Bell’s palsy and that caused by benign TBMs, which represents an important electrophysiological characteristic of benign TBMs. We propose that it is clinically useful to exclude the diagnosis of benign TBM when the HB grade is unexpectedly better than the ENoG value in cases of undiagnosed FNP. Disclosure of funding received for this work None. Disclosure statement None of the authors have any conflicts of interest, financial or otherwise. Acknowledgment None. References [1] McRackan TR, Rivas A, Wanna GB, Yoo MJ, Bennett ML, Dietrich MS, et al. Facial nerve outcomes in facial nerve schwannomas. Otol Neurotol 2012;33:78–82. [2] Latack JT, Gabrielsen TO, Knake JE, Kemink JL, Graham MD, Gebarski SS, et al. Facial nerve neuromas: radiologic evaluation. Radiology 1983;149:731–9. [3] Kertesz TR, Shelton C, Wiggins RH, Salzman KL, Glastonbury CM, Harnsberger R. Intratemporal facial nerve neuroma: anatomical location and radiological features. Laryngoscope 2001;111:1250–6. [4] Quaranta N, Cassano M, Quaranta A. Facial paralysis associated with cholesteatoma: a review of 13 cases. Otol Neurotol 2007;28:405–7. [5] Yetiser S, Tosun F, Kazkayasi M. Facial nerve paralysis due to chronic otitis media. Otol Neurotol 2002;23:580–8. [6] Ikeda M, Nakazato H, Onoda K, Hirai R, Kida A. Facial nerve paralysis caused by middle ear cholesteatoma and effects of surgical intervention. Acta Otolaryngol 2006;126:95–100. [7] Siddiq MA, Hanu-Cernat LM, Irving RM. Facial palsy secondary to cholesteatoma: analysis of outcome following surgery. J Laryngol Otol 2007;121:114–7. [8] Magliulo G, Terranova G, Sepe C, Cordeschi S, Cristofar P. Petrous bone cholesteatoma and facial paralysis. Clin Otolaryngol Allied Sci 1998;23:253–8. [9] Semaan MT, Slattery WH, Brackmann DE. Geniculate ganglion hemangiomas: clinical results and long-term follow-up. Otol Neurotol 2010;31:665–70.
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