Magnetic resonance imaging of the facial nerve during Bell’s palsy TERRENCE P. MURPHY, MD, and DAVID C. TELLER, MD, CPT, Atlanta, Georgia, and Ft. Sam Houston, Texas
Twenty-five patients with Bell’s palsy were evaluated to assess the efficacy of gadolinium (Gd+)-enhancedMRI in determining: (1) the site of facial nerve enhancement, (2) the relationship between EMG findings and Gd+ MRls, and (3) the usefulness of Gd + MRI in predictingrecovery of facial function. Eighteen of twenty-five patients had enhancement of the facial nerve during Gd+ MRI whereas seven did not. The most common areas of facial nerve enhancement were the labyrinthine, geniculate ganglion, and proximal tympanic segments of the facial nerve. EMGs were performed on ten patients who lost nerve excitability. The segments of facial nerve enhanced during Gd + MRI varied in locationand intensity in patients who maintained nerve excitability and in patients who lost nerve excitability. There was no correlation between EMG findings and location of facial nerve enhancement in patients who lost nerve excitability. The location of facial nerve enhancement during Gd+ MRI was not useful in predicting recovery of facial paralysis. (OTOLARYNGOL HEAD NECKSURG 1991;105:667.)
Gadolinium is an intravenous paramagnetic agent that does not enhance normal brain or cranial nerves. In the presence of inflammation or edema, gadolinium is absorbed into these tissues, resulting in an increased signal intensity and enhancement in T-1 weighted images. Initial interest in this subject arose because of the following case. This patient’s MRI scans and clinical course provided the impetus for this study to understand the affect of Bell’s palsy on Gd+ MRI. CASE REPORT
A 60-year-old man came to the ENT clinic in December 1988 with a facial paralysis of House grade IV/VI. The severity of the paralysis fluctuated over the next 6 weeks, so a CAT scan was obtained that demonstrated a widened fallopian canal at the meatal foramen and labyrinthine facial nerve (Fig. 1). This appears to be consistent with a facial nerve tumor, so an MRI was ordered for further confirmation. The G d +
From the ENT Department, Brooke Army Medical Center. The opinions or assertions contained herein are the private views of the authors and are not to be construed as reflecting the views of the Department of the A m y or the Department of Defense. Presented at the Annual Meeting of the American Academy of Otolaryngology-Head and Neck Surgery, San Diego, Calif., Sept. 9-13, 1990. Received for publication Sept. 26, 1990; accepted Feb. 20, 1991. Reprint requests: Terrence P. Murphy, MD, 993-F Johnson Ferry Rd., N.E., Suite 300, Atlanta, GA 30342. 23/1/29O50
MRI demonstrated an enhancement of the facial nerve (Fig. 2). The CAT, MRI, and clinical course of the facial paralysis all seem consistent with a facial nerve tumor. After extensive discussion with the patient, a middle fossa exploration of the facial nerve was performed. The labyrinthine facial nerve was identified and found mildly inflamed and swollen, but no facial nerve neuroma or hemangioma was identified. Further nerve exploration was carried out through the mastoid, and the nerve was found to be normal in appearance from the cochleariformis process to the stylomastoid foramen. The patient was followed for the next year with MRIs every 6 months. He had a full recovery of facial function at 10 months. His MRIs demonstrated residual enhancement at the geniculate ganglion at 6 months and no enhancement of the facial nerve at 12 months. Previous studies have noted the presence of facial nerve enhancement with Gd+ MRI in patients with facial nerve neuromas, traumatic facial paralysis, Bell’s palsy, and lyme disease.14 The purpose of this study is to determine: (1) the location of facial nerve enhancement, (2) the relationship between Gd + MRI during Bell’s palsy and EMG findings in patients who lost nerve excitability, and (3) if Gd+ MRI is useful in predicting the recovery of facial paralysis.
METHODS AND MATERIAL Ten of the patients used in this study were previously reported on in an earlier study.4 An additional fifteen patients with a final diagnosis of Bell’s palsy were evaluated with Gd+ MRI. Twenty-five patients with facial paralysis were evaluated at Brooke Army Medical Center, San Antonio, 667
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Fig. 1. CAT scan demonstrates widened labyrinthinesegment of the facial nerve, Table 1. MRI during Bell's palsy Tlme Interval
from
(wk,mo)
Facial grade at time of MRI
Location of facial nerve enhancement
Final grade of facial recovery
8 wk 10 wk 5 wk 6 wk 7 wk 6 wk 6 wk 10 wk 10 wk 4 wk 13 wk 7 wk 7 wk 10 wk 6 wk 7 wk 12 wk 5 wk 7 wk 1 wk 5 mo 5 wk 10 wk 10 wk 1 wk
Ill-IVIVI VIIVI VIIVI IlllVl IIIIVI IIVI llVl VIIVI VIIVI llVl VIIVI IIVI IIIVI IIIVI IIIIVI IIVI VIIVI VIIVI VIVI VIIVI I/VI IIIIVI VIIVI VIVI VIVI
L. G. PT L, G. PT L, G, PT L, G, PT L, G, PT None L, G. PT L. G , PT, M L, G, PT. M None G, IAC G None IAC M, Basal ganglia None None Both G L, G , PT Both G None G L. G. PT IAC, L, G, PT None
llVl II V I lIVl llVl lIVl llVl IIVI Il-IIIIVI Il-IIIIVI IIVI IIIIVI IIVI IIVI IIVI IIVI IIVI IVIVI IIIIVI IIVI IIVI IIVI llVl IIIIVI IIIVI I/VI
Patient no.
Age (yr)/sex/slde of paralysis
Grade of paralysls at presentation
paralysls to MRI
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25
59lMlR 67lMIL 69lFlL 36lMIR 31 /FIR 18IMlL 6OlFlL 54lFlR 52lFlR 19IFlR 60lFlR 16fFIR 69lMlL 62lFlR 67lMlR 57lFIL 61 I F I L 34lMlL 34lFlR 75lMIR i- L 50lFlL 48lMlR 54lFlR 61 /FIR 33lMlR
VIIVI VIIVI VIIVI VllVl VIIVI IV/VI IlIlVI VllVl VIIVI VIIVI VIIVI IIIIVI VI I V I VllVl VIIVI lllIVl VIIVI VIIVI VIIVI VIIVI V/VI VIIVI VIIVI VllVl IIIIVI
Tlme elapsed from paralysis to recovery
(mo) 10 mo 10 rno 10 mo 3 mo 2.5 mo 1.5 mo 1.5 mo 12 rno 24 rno 1 mo 4 mo 2 rno 2 mo 3 mo 1.5 mo 2 rno 4.5 rno 8 mo 8 mo 2.5 rno 1 mo 2 rno 4 mo 4 mo 1 rno
L, Labyrinthine segment; G, geniculate ganglion; P T. proximal tympanic segment; M. mastoid segment, IAC, internal auditory canal segment.
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Fig. 2. MRI demonstrates enhancement of the facial nerve at the lateral end of the internal auditory canal, labyrinthine facial nerve.
Table 2. Data on patients who lost nerve excitability In
Patient no.
1
2 8 9 11 17 18
19 23 24
Age (yr)/sex/slde of paralysis
location of facial nerve enhancement
59IMIR 67lMIL 54lFlR 521FlR
L. G. PT L. G. PT L, G. PT. M L, G, PT. M G, IAC None Both G L. G, PT L. G, PT L , G. PT. IAC
GOIFIR 61 I F I L
34lMiL 34lFIL 54lFlR 61 /FIR
= 10)
lime interval to completlon of MRI (wk)
EMG findings
8 wk 10 w k
ID ID
10 w k 10 wk 13 wk 12 w k 5 wk 7 wk 10 wk 10 wk
CD CD ID ID MD
ID ID ID
lime after paralysis EMG was performed (wk. mol
4 3 8 3
wk wk wk wk 4 wk 5 rno 4 wk 4 wk 4 wk 4 wk
Final grade of facial recovery
Grade I at 10 rno Grade I at 10 rno Grade 11-111 at 12 rno Grade 11-111 at 24 rno Grade ill at 8 rno Grade IV at 5 rno Grade 111 at 8 rno Grade I at 8 rno Grade 111 at 4 rno Grade 111 at 4 rno
L, Labyrinthine segment: G. geniculale ganglion. PT, proximal lympanic segrnenl. M , masloid segment, IAC. internal auditory Canal segment. ID. incomplete denervation. CD.complete denervalion, MD, minimal denervalion
Texas, from December 1988 to August 1990. All of these patients had a final diagnosis of Bell's palsy. All patients underwent a complete otologic and neurologic history and physical examination. They also underwent audiornetric evaluation, Schirmer's testing. Hilger nerve stimulation, and G d + MRI. MRIs were performed with a 0.35 magnet with 3-11lnl sections. The
time interval from the onset of the paralysis to the completion of the initial MRI ranged from 1 week to 5 months. Facial function was assessed at the time of presentation and at the time of each MRI scan according to the House-Brackmann facial nerve classification sysEMGs were performed on ten patients who lost response to Hilger nerve stimulation at 9 niA. The time
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Fig. 3. Gad + MRI demonstrates e n h a n c e m e n t of the labyrinthine, geniculate, a n d proximal iyrn-
panic segments of t h e facial nerve.
interval between the onset of facial paralysis and the final recovery was also recorded, as well as the last grading of facial function. RESULTS
Twenty-four patients with unilateral Bell's palsy and one patient with simultaneous bilateral Bell's palsy were evaluated from December I988 to August 1990. Seventeen patients were 48 to 75 years of age, whereas the other eight patients ranged in age from 16 to 36 years. Ten patients were men and fifteen were women. Eighteen of twenty-five patients had areas of enhancement of the facial nerve on the bide of their paralysis. whereas seven had none. Six of the seven patients who showed no enhancement of the facial nerve on MRI had complete recovery of facial function in 4 to 8 weeks. Only patient 17. whose facial nerve did not enhance, has not had full recovery of facial function (Table I ) . This patient is the only patient without nerve enhancement that lost nerve excitability with Hilger stimulation. Of the eighteen patients with facial nerve enhanccnicnt during G d + MRI, eight had the enhancement localized to the labyrinthine. geniculate ganglion, and
proximal tympanic portions of the facial nerve (Table I ) (Fig. 3). Four patients had enhancement only at the geniculate ganglion. whereas three patients had involvement of the internal auditory canal segment. with and without other facial nerve seginents (Fig. 4).Two patients had enhancement of the labyrinthine, geniculate ganglion, proximal tympanic, and mastoid portions of the facial nerve, whereas patient 15 had enhancement of only the mastoid segment of the facial nerve and the basal ganglion (Fig. 5). Patients who lost electrical excitability during Hilger stimulation of the facial nerve did not have uniform areas of enhancement of the facial nerve during Gd MRI (Table 2 and Fig. 6). Sonie had enhancement of the IAC, labyrinthine. geniculate ganglion, and proximal tympanic. whereas other patients' facial nerves enhanced only in one or two of the segments. Patient 17, who had no response to Hilger stimulation. showed no areas of facial nerve enhancement, The fifteen patients who maintained nerve excitability also had varied facial nerve segments enhance during G d + MRI (Table 3 and Fig. 7). Six of the fifteen patients who maintained nerve excitability had no area of facial nerve enhancement with Gd MRI. Recovery
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Fig. 4. Gad + MRI of patient with enhancement of the internal auditory canal segment of the facial nerve.
Table 3. Data on patients who maintained nerve excitability (n = 15) Patient no.
Age (yr) /sex
Location of nerve enhancement
3 4
69iF 36lM 31 I F 18lM 6OlF 19lF 16lF 69lM 62lF 67lM 57lF 75lM 50/F 48lM 33lM
L. G, PT L. G. PT L. G. PT None L. G. PT None G None IAC M. Basal ganglia None Both G None G None
5 6 7 10 12 13 14 15 16 20 21 22 25
Facial recovery
Grade Grade Grade Grade Grade Grade Grade Grade Grade Grade Grade Grade Grade Grade Grade
I
I I I I I
I
I I I I I I I I
Time to recovery (mo)
10 rno 3 mo 2 5 rno 1 5 mo 1 5 rno I rno 1 75 mo 2 rno 3 rno 1 5 rno
2 mo 25 rno 1 mo
2 mo 1 rno
L Labyrinthine segrnenl G geniculate ganglion PT proximal tympanic segment M rnasloid s?yrnenl IAC interrial auditory canal segmenl
of facial function was complete in all liltccn patients who continued to have nornial responses to Hilger stimulation (Table 3). Eight of ten patients who lost electrical excitability
with Hilger stimulation Iiavc. as o f yct. incompletc rcturn of facial function. Eight of ten of these patients dcmonstrutcd severe but incorllplcte dcnervation during EMG. whereas two patients l i d complete dcncrvation.
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Fig. 5. Gad+ MRI of patient demonstrates enhancement of the mastoid segment of the facial nerve.
The two patients with complete denervation have House grade 11-III/VI results at I and 2 years after their initial paralysis. Of the eight patients with severe but incomplete denervation on EMG, two have normal facial function after 10 months and six have incomplete return of facial function as of this writing. For these six patients it has been 4 to 8 months since the onset of their paralyses (Table 3). DISCUSSION
MRI is currently used to evaluate the facial nerve to exclude the presence of facial neuromas. Its role and value in evaluation of inflammation of the facial nerve is still being defined. This study hopes to define the role of Gd MRI in assessing: ( I ) the location and duration of facial nerve enhancement, (2) the relationship between MRI findings and EMG data, and (3) if G d + MRI is useful in predicting recovery of facial function in Bell's palsy. In our study, eighteen of twenty-five patients with facial paralysis demonstrated an increased signal intensity of the facial nerve, whereas seven did not. Of the
+
+
seven patients with n o enhancement during Gd MRI, four patients had normal facial function and one had a grade II/VI facial function at the time of the MRI. These five patients had complete return of facial function in 4 to 8 weeks (Table 1). Patient 17 had MRI performed 12 weeks after the onset of facial paralysis and had a loss of nerve excitability. At the time of the MRI, she still exhibited a grade VI/VI total facial paralysis. Why she did not demonstrate enhancement of the facial nerve remains unclear, although it may be that the lengthy time interval between her paralysis and the MRI scan was a factor. The most common site of facial nerve enhancement with G d + MRI was the area of the labyrinthine, geniculate ganglion, and proximal tympanic segments of the facial nerve. This finding was present in eight of the twenty-five patients with enhancement of the facial nerve. This was found in both patient groups that maintained and lost nerve excitability (Tables 2 and 3, Figs. 6 and 7). Three patients showed enhancement of the facial nerve in the internal auditory canal segment.
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673
L0,fT,IAC 0 ,lAC 1
c3 1
L0.W 4
I=labyrln. g=gonlwluh pt-prox.tpp.
m=ma.fold. lac=lnt.aud.
Fig. 6. Location of facial nerve enhancement in 10 patients (with EMGs) who lost nerve excitability
1
Fig. 7. Location of facial nerve enhancement in 15 patients who maintained nerve excitability
whereas patient I 1 also had involvement o f the geniculate ganglion. Patient 24 demonstrated enhancement in four areas: the labyrinthine, geniculate, proximal tympanic, and internal auditory canal segments. Four patients' facial nerve enhancement was limited to the geniculate ganglion. Enhancement of the mastoid segment of the facial nerve was seen in three patients, two of whom-patients 8 and 9-also showed enhancement of the labyrinthine. geniculate. and proximal tympanic segments of their facial nerve.
In general, a short duration of paralysis appears to be consistent with less facial nerve enhancement and a more rapid recovery of facial nerve function. Most patients who do not have an enhancement of the facial nerve on MRI can anticipate a rapid and complete recovery of facial nerve function, although there can be exceptions. as was demonstrated by patient 17. Demonstration of facial nerve enhancement with Gd + MRI is best accomplished with axial and coronal 3-mm T- I weighted sections. Axial sections best deni-
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onstrate the internal auditory, labyrinthine, geniculate ganglion, and proximal tympanic segments of the facial nerve, whereas coronal sections are most useful for displaying the mastoid segment of the facial nerve. Coronal studies can be difficult to perform and are not always successful in demonstrating the mastoid segment of the facial nerve. MRIs were performed on patients who lost nerve excitability and had EMG performed (Table 2). Eight of ten patients had multiple segments of the facial nerve enhance during G d + MRI (Fig. 6). Patient 18 had enhancement limited to the geniculate ganglion. This patient’s EMG demonstrated minimal denervation. In spite of these findings, patient 18 has had a slow recovery of facial function. Patient 17 had no area of enhancement during G d + MRI and also is having a slow recovery of facial function. Patients 8 and 9, who had inflammation of the mastoid segment of the facial nerve, have had incomplete recovery of facial function. The remaining six patients had multiple areas of facial nerve enhancement during G d + MRI. While enhancement of the mastoid segment was found in two patients with complete degeneration on EMG, it was also found in patient 15, who had a complete recovery of facial function (Tables 2 and 3). No other patients who experienced loss of electrical excitability and had EMGs performed had enhancement of the mastoid segment of the facial nerve. While MRIs supply information concerning the location of facial nerve inflammation, location of enhancement was variable and was no different in patients with loss or maintenance of nerve excitability. Location of facial nerve enhancement during Gd + MRI was not useful in predicting recovery of facial paralysis in Bell’s palsy (Tables 2 and 3). Loss of electrical excitability during Hilger stimulation more
accurately predicted a delay in the recovery of facial function than did the location of nerve enhancement. Lack of enhancement during Gd MRI was in general a good sign, and six of seven patients had early and complete return of facial function. There was an exception to this, as seen with patient 17, who had no enhancement but still lost nerve excitability.
+
CONCLUSIONS
1. The intensity and location of facial nerve enhancement varies among patients. 2 . The labyrinthine, geniculate ganglion, and proximal tympanic segments are the most common areas to enhance during G d + MRI. 3. There is no direct correlation between EMG findings and the segment of facial nerve enhancement during G d + MRI. 4. The location of facial nerve enhancement with Gd MRI is not useful in predicting the recovery of facial function in Bell’s palsy.
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REFERENCES
1. Millen SJ, Daniels DL, Meyer GA. Gadolinium-enhanced magnetic resonance imaging in temporal bone lesions. Laryngoscope 1989;99:257-60. 2. Millen SJ, Daniels DL, Meyer GA. Gadolinium-enhanced magnetic imaging in facial nerve lesions. OTOLARYNGOL HEADNECK SURG1990;lO2:26-33. 3. Schwaber MK, Zealear D, Netterville G , et al. The use of magnetic resonance imaging with high-resolution CT in the evaluation of facial paralysis. OTOLARYNGOL HEAD NECK SURG 1989;101:449-58. 4. Murphy TP. MRI of the facial nerve during paralysis. OTOLARYNGOL HEADNECKSURG 1991;104:47-51. 5. House J, Brackmann DE. Facial nerve grading system. OTOLARYNGOL HEADNECKSURG 1985;92:146. 6. Fisch U, Mattox D. Microsurgery of the skull base. New York: Thieme, 1988.
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Twenty-five patients with Bell’s palsy were evaluated to assess the efficacy of gadolinium (Gd+)-enhancedMRI in determining: (1) the site of facial nerve enhancement, (2) the relationship between EMG findings and Gd+ MRls, and (3) the usefulness of Gd + MRI in predictingrecovery of facial function. Eighteen of twenty-five patients had enhancement of the facial nerve during Gd+ MRI whereas seven did not. The most common areas of facial nerve enhancement were the labyrinthine, geniculate ganglion, and proximal tympanic segments of the facial nerve. EMGs were performed on ten patients who lost nerve excitability. The segments of facial nerve enhanced during Gd + MRI varied in locationand intensity in patients who maintained nerve excitability and in patients who lost nerve excitability. There was no correlation between EMG findings and location of facial nerve enhancement in patients who lost nerve excitability. The location of facial nerve enhancement during Gd+ MRI was not useful in predicting recovery of facial paralysis. (OTOLARYNGOL HEAD NECKSURG 1991;105:667.)
Gadolinium is an intravenous paramagnetic agent that does not enhance normal brain or cranial nerves. In the presence of inflammation or edema, gadolinium is absorbed into these tissues, resulting in an increased signal intensity and enhancement in T-1 weighted images. Initial interest in this subject arose because of the following case. This patient’s MRI scans and clinical course provided the impetus for this study to understand the affect of Bell’s palsy on Gd+ MRI. CASE REPORT
A 60-year-old man came to the ENT clinic in December 1988 with a facial paralysis of House grade IV/VI. The severity of the paralysis fluctuated over the next 6 weeks, so a CAT scan was obtained that demonstrated a widened fallopian canal at the meatal foramen and labyrinthine facial nerve (Fig. 1). This appears to be consistent with a facial nerve tumor, so an MRI was ordered for further confirmation. The G d +
From the ENT Department, Brooke Army Medical Center. The opinions or assertions contained herein are the private views of the authors and are not to be construed as reflecting the views of the Department of the A m y or the Department of Defense. Presented at the Annual Meeting of the American Academy of Otolaryngology-Head and Neck Surgery, San Diego, Calif., Sept. 9-13, 1990. Received for publication Sept. 26, 1990; accepted Feb. 20, 1991. Reprint requests: Terrence P. Murphy, MD, 993-F Johnson Ferry Rd., N.E., Suite 300, Atlanta, GA 30342. 23/1/29O50
MRI demonstrated an enhancement of the facial nerve (Fig. 2). The CAT, MRI, and clinical course of the facial paralysis all seem consistent with a facial nerve tumor. After extensive discussion with the patient, a middle fossa exploration of the facial nerve was performed. The labyrinthine facial nerve was identified and found mildly inflamed and swollen, but no facial nerve neuroma or hemangioma was identified. Further nerve exploration was carried out through the mastoid, and the nerve was found to be normal in appearance from the cochleariformis process to the stylomastoid foramen. The patient was followed for the next year with MRIs every 6 months. He had a full recovery of facial function at 10 months. His MRIs demonstrated residual enhancement at the geniculate ganglion at 6 months and no enhancement of the facial nerve at 12 months. Previous studies have noted the presence of facial nerve enhancement with Gd+ MRI in patients with facial nerve neuromas, traumatic facial paralysis, Bell’s palsy, and lyme disease.14 The purpose of this study is to determine: (1) the location of facial nerve enhancement, (2) the relationship between Gd + MRI during Bell’s palsy and EMG findings in patients who lost nerve excitability, and (3) if Gd+ MRI is useful in predicting the recovery of facial paralysis.
METHODS AND MATERIAL Ten of the patients used in this study were previously reported on in an earlier study.4 An additional fifteen patients with a final diagnosis of Bell’s palsy were evaluated with Gd+ MRI. Twenty-five patients with facial paralysis were evaluated at Brooke Army Medical Center, San Antonio, 667
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Fig. 1. CAT scan demonstrates widened labyrinthinesegment of the facial nerve, Table 1. MRI during Bell's palsy Tlme Interval
from
(wk,mo)
Facial grade at time of MRI
Location of facial nerve enhancement
Final grade of facial recovery
8 wk 10 wk 5 wk 6 wk 7 wk 6 wk 6 wk 10 wk 10 wk 4 wk 13 wk 7 wk 7 wk 10 wk 6 wk 7 wk 12 wk 5 wk 7 wk 1 wk 5 mo 5 wk 10 wk 10 wk 1 wk
Ill-IVIVI VIIVI VIIVI IlllVl IIIIVI IIVI llVl VIIVI VIIVI llVl VIIVI IIVI IIIVI IIIVI IIIIVI IIVI VIIVI VIIVI VIVI VIIVI I/VI IIIIVI VIIVI VIVI VIVI
L. G. PT L, G. PT L, G, PT L, G, PT L, G, PT None L, G. PT L. G , PT, M L, G, PT. M None G, IAC G None IAC M, Basal ganglia None None Both G L, G , PT Both G None G L. G. PT IAC, L, G, PT None
llVl II V I lIVl llVl lIVl llVl IIVI Il-IIIIVI Il-IIIIVI IIVI IIIIVI IIVI IIVI IIVI IIVI IIVI IVIVI IIIIVI IIVI IIVI IIVI llVl IIIIVI IIIVI I/VI
Patient no.
Age (yr)/sex/slde of paralysis
Grade of paralysls at presentation
paralysls to MRI
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25
59lMlR 67lMIL 69lFlL 36lMIR 31 /FIR 18IMlL 6OlFlL 54lFlR 52lFlR 19IFlR 60lFlR 16fFIR 69lMlL 62lFlR 67lMlR 57lFIL 61 I F I L 34lMlL 34lFlR 75lMIR i- L 50lFlL 48lMlR 54lFlR 61 /FIR 33lMlR
VIIVI VIIVI VIIVI VllVl VIIVI IV/VI IlIlVI VllVl VIIVI VIIVI VIIVI IIIIVI VI I V I VllVl VIIVI lllIVl VIIVI VIIVI VIIVI VIIVI V/VI VIIVI VIIVI VllVl IIIIVI
Tlme elapsed from paralysis to recovery
(mo) 10 mo 10 rno 10 mo 3 mo 2.5 mo 1.5 mo 1.5 mo 12 rno 24 rno 1 mo 4 mo 2 rno 2 mo 3 mo 1.5 mo 2 rno 4.5 rno 8 mo 8 mo 2.5 rno 1 mo 2 rno 4 mo 4 mo 1 rno
L, Labyrinthine segment; G, geniculate ganglion; P T. proximal tympanic segment; M. mastoid segment, IAC, internal auditory canal segment.
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Fig. 2. MRI demonstrates enhancement of the facial nerve at the lateral end of the internal auditory canal, labyrinthine facial nerve.
Table 2. Data on patients who lost nerve excitability In
Patient no.
1
2 8 9 11 17 18
19 23 24
Age (yr)/sex/slde of paralysis
location of facial nerve enhancement
59IMIR 67lMIL 54lFlR 521FlR
L. G. PT L. G. PT L, G. PT. M L, G, PT. M G, IAC None Both G L. G, PT L. G, PT L , G. PT. IAC
GOIFIR 61 I F I L
34lMiL 34lFIL 54lFlR 61 /FIR
= 10)
lime interval to completlon of MRI (wk)
EMG findings
8 wk 10 w k
ID ID
10 w k 10 wk 13 wk 12 w k 5 wk 7 wk 10 wk 10 wk
CD CD ID ID MD
ID ID ID
lime after paralysis EMG was performed (wk. mol
4 3 8 3
wk wk wk wk 4 wk 5 rno 4 wk 4 wk 4 wk 4 wk
Final grade of facial recovery
Grade I at 10 rno Grade I at 10 rno Grade 11-111 at 12 rno Grade 11-111 at 24 rno Grade ill at 8 rno Grade IV at 5 rno Grade 111 at 8 rno Grade I at 8 rno Grade 111 at 4 rno Grade 111 at 4 rno
L, Labyrinthine segment: G. geniculale ganglion. PT, proximal lympanic segrnenl. M , masloid segment, IAC. internal auditory Canal segment. ID. incomplete denervation. CD.complete denervalion, MD, minimal denervalion
Texas, from December 1988 to August 1990. All of these patients had a final diagnosis of Bell's palsy. All patients underwent a complete otologic and neurologic history and physical examination. They also underwent audiornetric evaluation, Schirmer's testing. Hilger nerve stimulation, and G d + MRI. MRIs were performed with a 0.35 magnet with 3-11lnl sections. The
time interval from the onset of the paralysis to the completion of the initial MRI ranged from 1 week to 5 months. Facial function was assessed at the time of presentation and at the time of each MRI scan according to the House-Brackmann facial nerve classification sysEMGs were performed on ten patients who lost response to Hilger nerve stimulation at 9 niA. The time
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Fig. 3. Gad + MRI demonstrates e n h a n c e m e n t of the labyrinthine, geniculate, a n d proximal iyrn-
panic segments of t h e facial nerve.
interval between the onset of facial paralysis and the final recovery was also recorded, as well as the last grading of facial function. RESULTS
Twenty-four patients with unilateral Bell's palsy and one patient with simultaneous bilateral Bell's palsy were evaluated from December I988 to August 1990. Seventeen patients were 48 to 75 years of age, whereas the other eight patients ranged in age from 16 to 36 years. Ten patients were men and fifteen were women. Eighteen of twenty-five patients had areas of enhancement of the facial nerve on the bide of their paralysis. whereas seven had none. Six of the seven patients who showed no enhancement of the facial nerve on MRI had complete recovery of facial function in 4 to 8 weeks. Only patient 17. whose facial nerve did not enhance, has not had full recovery of facial function (Table I ) . This patient is the only patient without nerve enhancement that lost nerve excitability with Hilger stimulation. Of the eighteen patients with facial nerve enhanccnicnt during G d + MRI, eight had the enhancement localized to the labyrinthine. geniculate ganglion, and
proximal tympanic portions of the facial nerve (Table I ) (Fig. 3). Four patients had enhancement only at the geniculate ganglion. whereas three patients had involvement of the internal auditory canal segment. with and without other facial nerve seginents (Fig. 4).Two patients had enhancement of the labyrinthine, geniculate ganglion, proximal tympanic, and mastoid portions of the facial nerve, whereas patient 15 had enhancement of only the mastoid segment of the facial nerve and the basal ganglion (Fig. 5). Patients who lost electrical excitability during Hilger stimulation of the facial nerve did not have uniform areas of enhancement of the facial nerve during Gd MRI (Table 2 and Fig. 6). Sonie had enhancement of the IAC, labyrinthine. geniculate ganglion, and proximal tympanic. whereas other patients' facial nerves enhanced only in one or two of the segments. Patient 17, who had no response to Hilger stimulation. showed no areas of facial nerve enhancement, The fifteen patients who maintained nerve excitability also had varied facial nerve segments enhance during G d + MRI (Table 3 and Fig. 7). Six of the fifteen patients who maintained nerve excitability had no area of facial nerve enhancement with Gd MRI. Recovery
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MRI of facial nerve during Bell's palsy 671
Fig. 4. Gad + MRI of patient with enhancement of the internal auditory canal segment of the facial nerve.
Table 3. Data on patients who maintained nerve excitability (n = 15) Patient no.
Age (yr) /sex
Location of nerve enhancement
3 4
69iF 36lM 31 I F 18lM 6OlF 19lF 16lF 69lM 62lF 67lM 57lF 75lM 50/F 48lM 33lM
L. G, PT L. G. PT L. G. PT None L. G. PT None G None IAC M. Basal ganglia None Both G None G None
5 6 7 10 12 13 14 15 16 20 21 22 25
Facial recovery
Grade Grade Grade Grade Grade Grade Grade Grade Grade Grade Grade Grade Grade Grade Grade
I
I I I I I
I
I I I I I I I I
Time to recovery (mo)
10 rno 3 mo 2 5 rno 1 5 mo 1 5 rno I rno 1 75 mo 2 rno 3 rno 1 5 rno
2 mo 25 rno 1 mo
2 mo 1 rno
L Labyrinthine segrnenl G geniculate ganglion PT proximal tympanic segment M rnasloid s?yrnenl IAC interrial auditory canal segmenl
of facial function was complete in all liltccn patients who continued to have nornial responses to Hilger stimulation (Table 3). Eight of ten patients who lost electrical excitability
with Hilger stimulation Iiavc. as o f yct. incompletc rcturn of facial function. Eight of ten of these patients dcmonstrutcd severe but incorllplcte dcnervation during EMG. whereas two patients l i d complete dcncrvation.
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Fig. 5. Gad+ MRI of patient demonstrates enhancement of the mastoid segment of the facial nerve.
The two patients with complete denervation have House grade 11-III/VI results at I and 2 years after their initial paralysis. Of the eight patients with severe but incomplete denervation on EMG, two have normal facial function after 10 months and six have incomplete return of facial function as of this writing. For these six patients it has been 4 to 8 months since the onset of their paralyses (Table 3). DISCUSSION
MRI is currently used to evaluate the facial nerve to exclude the presence of facial neuromas. Its role and value in evaluation of inflammation of the facial nerve is still being defined. This study hopes to define the role of Gd MRI in assessing: ( I ) the location and duration of facial nerve enhancement, (2) the relationship between MRI findings and EMG data, and (3) if G d + MRI is useful in predicting recovery of facial function in Bell's palsy. In our study, eighteen of twenty-five patients with facial paralysis demonstrated an increased signal intensity of the facial nerve, whereas seven did not. Of the
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seven patients with n o enhancement during Gd MRI, four patients had normal facial function and one had a grade II/VI facial function at the time of the MRI. These five patients had complete return of facial function in 4 to 8 weeks (Table 1). Patient 17 had MRI performed 12 weeks after the onset of facial paralysis and had a loss of nerve excitability. At the time of the MRI, she still exhibited a grade VI/VI total facial paralysis. Why she did not demonstrate enhancement of the facial nerve remains unclear, although it may be that the lengthy time interval between her paralysis and the MRI scan was a factor. The most common site of facial nerve enhancement with G d + MRI was the area of the labyrinthine, geniculate ganglion, and proximal tympanic segments of the facial nerve. This finding was present in eight of the twenty-five patients with enhancement of the facial nerve. This was found in both patient groups that maintained and lost nerve excitability (Tables 2 and 3, Figs. 6 and 7). Three patients showed enhancement of the facial nerve in the internal auditory canal segment.
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Volume 105 Number 5 November 1991
MRI of facial nerve during Bell's palsy
673
L0,fT,IAC 0 ,lAC 1
c3 1
L0.W 4
I=labyrln. g=gonlwluh pt-prox.tpp.
m=ma.fold. lac=lnt.aud.
Fig. 6. Location of facial nerve enhancement in 10 patients (with EMGs) who lost nerve excitability
1
Fig. 7. Location of facial nerve enhancement in 15 patients who maintained nerve excitability
whereas patient I 1 also had involvement o f the geniculate ganglion. Patient 24 demonstrated enhancement in four areas: the labyrinthine, geniculate, proximal tympanic, and internal auditory canal segments. Four patients' facial nerve enhancement was limited to the geniculate ganglion. Enhancement of the mastoid segment of the facial nerve was seen in three patients, two of whom-patients 8 and 9-also showed enhancement of the labyrinthine. geniculate. and proximal tympanic segments of their facial nerve.
In general, a short duration of paralysis appears to be consistent with less facial nerve enhancement and a more rapid recovery of facial nerve function. Most patients who do not have an enhancement of the facial nerve on MRI can anticipate a rapid and complete recovery of facial nerve function, although there can be exceptions. as was demonstrated by patient 17. Demonstration of facial nerve enhancement with Gd + MRI is best accomplished with axial and coronal 3-mm T- I weighted sections. Axial sections best deni-
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onstrate the internal auditory, labyrinthine, geniculate ganglion, and proximal tympanic segments of the facial nerve, whereas coronal sections are most useful for displaying the mastoid segment of the facial nerve. Coronal studies can be difficult to perform and are not always successful in demonstrating the mastoid segment of the facial nerve. MRIs were performed on patients who lost nerve excitability and had EMG performed (Table 2). Eight of ten patients had multiple segments of the facial nerve enhance during G d + MRI (Fig. 6). Patient 18 had enhancement limited to the geniculate ganglion. This patient’s EMG demonstrated minimal denervation. In spite of these findings, patient 18 has had a slow recovery of facial function. Patient 17 had no area of enhancement during G d + MRI and also is having a slow recovery of facial function. Patients 8 and 9, who had inflammation of the mastoid segment of the facial nerve, have had incomplete recovery of facial function. The remaining six patients had multiple areas of facial nerve enhancement during G d + MRI. While enhancement of the mastoid segment was found in two patients with complete degeneration on EMG, it was also found in patient 15, who had a complete recovery of facial function (Tables 2 and 3). No other patients who experienced loss of electrical excitability and had EMGs performed had enhancement of the mastoid segment of the facial nerve. While MRIs supply information concerning the location of facial nerve inflammation, location of enhancement was variable and was no different in patients with loss or maintenance of nerve excitability. Location of facial nerve enhancement during Gd + MRI was not useful in predicting recovery of facial paralysis in Bell’s palsy (Tables 2 and 3). Loss of electrical excitability during Hilger stimulation more
accurately predicted a delay in the recovery of facial function than did the location of nerve enhancement. Lack of enhancement during Gd MRI was in general a good sign, and six of seven patients had early and complete return of facial function. There was an exception to this, as seen with patient 17, who had no enhancement but still lost nerve excitability.
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CONCLUSIONS
1. The intensity and location of facial nerve enhancement varies among patients. 2 . The labyrinthine, geniculate ganglion, and proximal tympanic segments are the most common areas to enhance during G d + MRI. 3. There is no direct correlation between EMG findings and the segment of facial nerve enhancement during G d + MRI. 4. The location of facial nerve enhancement with Gd MRI is not useful in predicting the recovery of facial function in Bell’s palsy.
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REFERENCES
1. Millen SJ, Daniels DL, Meyer GA. Gadolinium-enhanced magnetic resonance imaging in temporal bone lesions. Laryngoscope 1989;99:257-60. 2. Millen SJ, Daniels DL, Meyer GA. Gadolinium-enhanced magnetic imaging in facial nerve lesions. OTOLARYNGOL HEADNECK SURG1990;lO2:26-33. 3. Schwaber MK, Zealear D, Netterville G , et al. The use of magnetic resonance imaging with high-resolution CT in the evaluation of facial paralysis. OTOLARYNGOL HEAD NECK SURG 1989;101:449-58. 4. Murphy TP. MRI of the facial nerve during paralysis. OTOLARYNGOL HEADNECKSURG 1991;104:47-51. 5. House J, Brackmann DE. Facial nerve grading system. OTOLARYNGOL HEADNECKSURG 1985;92:146. 6. Fisch U, Mattox D. Microsurgery of the skull base. New York: Thieme, 1988.
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