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Surgical Neurology 69 (2008) 153 – 157


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Hemifacial Spasm
Microvascular decompression for hemifacial spasm:
analyses of operative complications in 1582 consecutive patients
Ryoong Huh, MD a,1 , In Bo Han, MD a,1 , Ji Young Moon, MD a ,
Jin Woo Chang, MD b , Sang Sup Chung, MD a,⁎
a
Department of Neurosurgery, College of Medicine, Pochun CHA University, Bundang-gu, Sungnam 463-712, South Korea
b
Department of Neurosurgery, Yonsei University College of Medicine, Seoul, South Korea
Received 28 January 2007; accepted 9 July 2007

Abstract Background: Microvascular decompression is the most reliable treatment for HFS, but it may cause
complications. The aim was to identify factors affecting the prognosis after MVD and to establish
appropriate means to reduce complications.
Method: We retrospectively reviewed 1524 patients with HFS who underwent MVD and were
followed for more than 6 months since January 1987. The mean follow-up duration was 30.9 months
(6-197 months).
Results: The effect of MVD was satisfying (excellent or good) in 94.6% (n = 1442). The failure and
recurrence rates were 2.1% (n = 32) and 0.4% (n = 6), respectively. Postoperative complications were
noted in 545 (35.8%) patients. Among them, facial palsy, hearing deficit, and low cranial nerve
palsies were found in 18.6% (n = 283), 7.2% (n = 109), and 2.8% (n = 43), respectively. However,
permanent facial weakness, hearing deficit, and lower cranial nerve palsies such as hoarseness and
dysphagia were encountered in 1.2% (n = 18), 2.1% (n = 32), and 0.1% (n = 2), respectively. The
more immediate and severe the facial palsy was, the more permanent it remained, with statistical
significance (P b .05). There was a trend that the more immediate and severe the hearing deficit was,
the more permanent the deficit remained, without statistical significance (P = .673).
Conclusion: Early (occurrence within 24 hours after operation) and severe cranial nerve
deficits, including facial, hearing, and lower cranial nerve deficits after MVD, entail the risk to
stay permanent.
© 2008 Elsevier Inc. All rights reserved.
Keywords: Facial palsy; Hearing deficit; Hemifacial spasm; Microvascular decompression

1. Introduction decompression is a highly accepted and effective method for


treatment of patients with HFS. It has been reported that
Hemifacial spasm is a disorder characterized by twitching
there is an 85% to 90% cure rate with MVD for HFS and
and spasm of the muscles innervated by the facial nerve. It is
84% success at 10 years from surgery, with an operative
generally believed that HFS is caused by vascular compres-
morbidity of less than 10% [4,9,17,26]. However, the results
sion of the root exit zone of the facial nerve. Microvascular
of MVD surgery were not always satisfactory because of
incomplete cure, recurrence of symptoms, or surgical
complications. The risks of the operation are generally
Abbreviations: BAEP, brainstem auditory evoked potential; CSF, related to the surgical approach and particularly to surgery on
cerebrospinal fluid; EMG, electromyography; HFS, hemifacial spasm; the seventh nerve [15]. The reported complications after
MVD, microvascular decompression.
⁎ Corresponding author. Tel.: +82 31 780 5260; fax: +82 31 780 5269. MVD included facial palsy, hearing impairment, vocal cord
E-mail address: nshanib@naver.com (S.S. Chung). paralysis, intracranial hemorrhage, wound infection, menin-
1
These authors contributed equally to this study. gitis, vertebral artery injury, and CSF leakage. Among them,
0090-3019/$ – see front matter © 2008 Elsevier Inc. All rights reserved.
doi:10.1016/j.surneu.2007.07.027
154 R. Huh et al. / Surgical Neurology 69 (2008) 153–157

facial palsy and hearing deficit are not uncommon 1 week. In case of facial palsy, physical therapy was
complications resulting from disturbance adjacent to the performed to facial muscles starting from 5 to 7 days
facial nerve or auditory nerve [2,10,25,26]. Although most after operation.
cases of postoperative facial weakness and hearing impair- Descriptive statistics were performed with SPSS 10.0
ment are transient, permanent facial weakness and hearing software (SPSS, Chicago, Ill). Significance was assigned
impairment may develop. In this study, we evaluated the when probability was less than .05.
long-term follow-up results and postoperative complications
and tried to determine the prognostic factors related to cranial
3. Results
nerve deficits after MVD.
The mean age of patients was 49.2 years (range, 15-78
years), and the ratio of male to female patients was 1:3.6. The
2. Methods mean duration of symptoms was 7.9 years (range, 7 months-
40 years). There was no statistically significant difference in
A total of 1582 patients with HFS underwent MVD. A the laterality. The mean follow-up duration was 30.9 months
total of 1609 operations was performed by the senior (range, 2.4-196.8 months).
author (SS Chung) at the Severance Hospital, Yonsei Excellent surgical outcome was obtained in 90.3% and
University, Seoul, Korea (September 1978-February 2003), good in 4.3%. The overall success rate was 94.6%. The
and at the Bundang CHA Hospital, Pochon CHA failure rate of MVD was 2.1% (n = 32), and spasm
University, Sungnam, Korea (March 2003-September recurrence was noted in 0.4% (n = 6). Of the patients with
2005). Modern microsurgical technique has been per- persistent or recurrent HFS, 13 (0.9%) patients who had
formed since 1987 in our institutes [1,2]. We retro- compressing vessels identified on postoperative 3-dimen-
spectively reviewed 1524 patients who were followed for sional magnetic resonance angiography underwent repeated
more than 6 months since January 1987. Patients with MVD. Eleven had excellent results with the second MVD, 1
symptomatic HFS secondary to tumors or vascular had a good result, and 1 had a fair outcome.
malformation were excluded from this study. Preopera- The operative complications are summarized in Table 1.
tively, 3-dimensional magnetic resonance angiography Postoperative complications were noted in 35.8% (n = 545),
(3D = TOF MRA) has been used since 1992, and pure but permanent deficits were encountered in 3.6% (n = 55).
tone audiometry (PTA) and facial EMG were performed There was no operation-related mortality in this study.
before operation. Brainstem auditory evoked potential has Postoperative permanent hearing deficit was more
been monitored during operation since 1983, but facial common than facial weakness (2.1% vs 1.2%). The onset
EMG was not performed intraoperatively. The clinical of permanent facial weakness occurred within 24 hours in
results for each patient were assessed in a personal 88.9% (n = 16). Delayed facial weakness was noted in 94
interview or by telephone. All patients received a (6.2%) patients. The onset of delayed facial weakness
questionnaire addressing the persistence of any operative occurred between postoperative days 8 and 28 (mean, 13.1
complications. days). Among them, 92 (97.9%) patients improved to
The patients were classified into the following 5 grades, complete recovery, and the mean time to recovery was
on the basis of the degree of HFS present: (1) “excellent” if 8.6 weeks (range, 0.7-43.7 weeks). However, 2 patients
there was no residual spasm; (2) “good” if the HFS was more remained with permanent severe facial weakness. Immediate
than 90% resolved; (3) “fair” for spasm relief of 50% to 90%; facial weakness was encountered in 66.8% (n = 189). Of the
(4) “poor” if the HFS was less than 50% resolved; and (5) patients with immediate facial weakness, permanent facial
“failure” for all remaining results. weakness was found in 8.5% (n = 16). When analyzed on the
Among the postoperative complications, the “immedi-
ate” cranial nerve deficit was assigned to the occurrence of
deficit within 24 hours. The occurrence 24 hours after
Table 1
operation was defined as “delayed.” Facial palsies were The complications of MVD and their frequencies
classified into the following 3 grades: (1) “mild” for facial
Complications No. of patients (%)
palsy of House-Brackmann grade I or II; (2) “moderate”
for grade III; and (3) “severe” for grade IV or V. Hearing Transient (%) Permanent (%) Total
deficits were also classified into 4 grades, on the basis Facial palsy 265 (17.4) 18 (1.2) 283
of PTA: (1) “mild” for 26 to 40 dB hearing loss (HL); Hearing impairment 77 (5.1) 32 (2.1) 109
Hemorrhage 35 (2.3) 0 (0) 35
(2) “moderate” for 41 to 70 dB HL; (3) “severe” for
Lower CN palsy 41 (2.7) 2 (0.1) 43
71 to 90 dB HL; and 4) “deafness” for more than 91 dB Infection 38 (2.5) 3 (0.2) 41
HL. When cranial nerve dysfunction developed post- CSF leakage 17 (1.1) 0 (0) 17
operatively, steroid medication (dexamethasone, 20 mg/d) Others 17 (1.1) 0 (0) 17
was initiated, and this was gradually discontinued over Total 490 (32.2)* 55 (3.6)* 545*
2 weeks. Naloxone (6 mg/d), IV, was also administered for n = 1524. CN indicates cranial nerve.
R. Huh et al. / Surgical Neurology 69 (2008) 153–157 155

basis of grade of facial palsy, of the patients with severe Table 3


facial weakness, immediate facial weakness was noted in Classification by the severity of hearing impairment
81.2% (n = 13), and permanent facial weakness was found in Postoperative day Before 24 h After 24 h Total (n)
61.5% (n = 8) of patients with immediate facial weakness. Mild Transient 43 6 49
In the moderate facial weakness group, permanent facial Permanent 6 0 6
weakness was noted in only 5 (9.6%) patients with Moderate Transient 11 3 14
Permanent 4 2 6
immediate moderate facial weakness. In the mild group,
Severe Transient 12 0 12
permanent facial weakness was found in only 3 (2.4%) Permanent 11 1 12
patients with immediate mild facial weakness. These Deaf Transient 0 0 0
indicated that permanent facial weakness frequently occurred Permanent 9 1 10
within 24 hours after operation, and the more severe the Total (n) 96 13 109
facial palsy was, the more permanent the facial palsy For total transient disorders, n = 75; total permanent disorders, n = 34; and
remained, with statistical significance (P b .05) (Table 2). total, n = 109. P = .673.
The mean time to recovery from transient facial palsy was
6 weeks (mean, 4 weeks; SD, 7.1 weeks). Most of the
patients recovered within 2 months. Among 4 patients who cranial nerve palsies was 26.6 weeks and was longer than
recovered 8 months after operation, 2 patients had mild that of facial palsy or hearing impairment.
facial palsy, and 2 patients had moderate facial palsy.
Of the 109 (7.2%) patients with hearing deficit,
4. Discussion
immediate hearing deficit was noted in 88.1% (n = 96),
but delayed occurrence was encountered in 13 patients. To The cranial nerve injuries during MVD may lead to
exclude temporary conduction hearing impairment related to postoperative facial weakness, hearing impairment, or lower
middle ear fluid rather than neurosensory loss, postoperative cranial nerve palsy such as dysphagia and hoarseness, and
PTA was performed. As shown in Table 3, permanent these complications can decrease the patient's subjective
hearing deficit occurred immediately in 88.2% (n = 30) of satisfaction despite the complete disappearance of facial
patients with permanent hearing deficit. Permanent hearing spasm [3-5,11,16-18,21,23].
deficit was encountered in 62.5% (n = 20) of patients in the The efficacy of MVD in treating HFS in our patients
immediate severe or deaf group. These suggested that the was similar to that reported in other published series,
onset of permanent hearing deficit usually occurred within especially concerning the high rate of long-term success,
24 hours after operation, and the more severe the hearing together with the low rates of recurrence and operative
deficit was, the more permanent the deficit remained, but complication [1,8,12,14,22,26]. There was no operation-
this trend did not reach statistical significance (P = .673) related death. Postoperative facial weakness was more
(Table 3). The mean time to recovery from transient common than hearing deficit. Of 109 patients with hearing
hearing impairment was 10 weeks (mean, 4 weeks; SD, deficit, 22 (20.2%) suffered deafness or severe permanent
13.9 weeks). This indicated that the recovery from damage loss of hearing, whereas only 3.5% (n = 10) of 283
to the auditory nerve after operation was slower than patients with facial weakness remained with severe
recovery from damage to the facial nerve. permanent facial weakness. The mean time to recovery
The lower cranial nerve (IX-X) deficits, such as from transient hearing impairment was longer than that of
hoarseness and dyspahgia, were encountered in 2.8% (n = facial palsy. This indicated that the time to recovery from
43). Among them, complete recovery was achieved in 95.3% auditory nerve dysfunction was slower than that of facial
(n = 41). Two patients remained with mild permanent palsy nerve dysfunction. We believe that this can be attributed to
(Table 1). The mean time to recovery from transient lower the fact that the motor nerves (facial nerves) are less
susceptible than the cochlear nerve to traction and/or
ischemic traumas.
The transient facial palsy improved within 8 months, and
Table 2 hearing impairment improved within 12 months. Therefore,
Relationship between the severities and the time of occurrence of facial palsy
1-year or longer follow-up monitoring is required before
Postoperative day Before 24 h After 24 h Total (n) determination of “permanence” with respect to cranial nerve
Mild Transient 121 60 181 dysfunction. When facial palsy developed within 24 hours
Permanent 3 0 3 after operation, and the initial grade of facial palsy was
Moderate Transient 47 31 78
severe, there was a high possibility of permanent facial palsy
Permanent 5 0 5
Severe Transient 5 1 6 (P b .05). Although there was no statistical significance (P =
Permanent 8 2 10 .673), permanent hearing impairment developed more
Total (n) 189 94 283 frequently in patients who had immediate and severe hearing
For total transient disorders, n = 265; total permanent disorders, n = 18; and impairment. Consequently, when cranial nerve palsies
total, n = 283. P b .05. immediately occurred, and the initial grade of palsies was
156 R. Huh et al. / Surgical Neurology 69 (2008) 153–157

severe, the prognosis was poor, and there was more frequent [2] Barker FG, Jannette PJ, Bissonette DJ. Microvascular decompression
occurrence of permanent palsy. for hemifacial spasm. J Neurosurg 1995;82:201-10.
[3] Chung SS, Chang JH, Park YG. Microvascular decompression for
The pathophysiologic mechanism of postoperative facial hemifacial spasm: a long-term follow-up of 1,169 consecutive cases.
weakness is still unclear, particularly because it can occur Stereotact Funct Neurosurg 2001;77:190-3.
some days after operation. It has been suggested that a viral [4] Elston JS. Botulinum toxin treatment of hemifacial spasm. J Neurol
cause could be involved. The manipulation of the nerve Neurosurg Psychiatry 1986;49:827-9.
could stimulate a dormant virus, possibly localized in the [5] Hanakita J, Kondo A. Serious complications of microvascular
decompression operations for trigeminal neuralgia and hemifacial
geniculate ganglion. In addition, it has been reported that spasm. Neurosurgery 1998;22:348-52.
possible causes include facial nerve exit zone injury via the [6] Hatem J, Sindou M, Vial C. Intraoperative monitoring of facial EMG
Teflon felt, delayed facial nerve edema, or a microcirculation responses during microvascular decompression for hemifacial spasm.
disturbance due to vasospasm. Despite the uncertain cause, Prognostic value for long-term outcome: a study in a 33-patient series.
the facial weakness can resolve spontaneously, with Br J Neurosurg 2001;15:496-9.
[7] Hengstman GJ, Gons RA, Menovsky T. Delayed cranial neuropathy
excellent outcomes [5,7,13,15,20,23,24]. after neurosurgery caused by herpes simplex virus reactivation: report
The cranial nerve injuries during MVD might result from of three cases. Surg Neurol 2005;64:67-70.
direct nerve damage or traction injuries. In our series, to [8] Illingworth RD, Porter DG, Jakubowski J. Hemifacial spasm: a
avoid direct nerve damage, the best exposure for HFS has prospective long term follow up of 83 cases treated by microvascular
decompression at two neurosurgical centres in the United Kingdom.
been achieved from below upward, that is, “approaching the
J Neurol Neurosurg Psychiatry 1992;60:72-7.
ninth nerve to expose the area of compression at the seventh [9] Jannetta PJ, Kassam A. Hemifacial spasm. J Neurol Neurosurg
exit zone,” since 1987, and the incidence of facial palsy and Psychiatry 1999;66:255-6.
hearing impairment significantly decreased below the level [10] Jannette PJ. Typical or atypical hemifacial spasm. J Neurosurg 1998;
of 5%, compared with the early period (between 1978 and 89:346-7.
1986). Many neurosurgeons prefer to carry out MVD [11] Kalkanis SN, Eskandar EN, Carter BS. Microvascular decompression
surgery in the United States, 1996 to 2000: mortality rates, morbidity
without any fixed retractor, primarily using withdrawal of rates, and the effects of hospital and surgeon volumes. Neurosurgery
CSF and gentle exposure of pertinent anatomy with their 2003;52:1251-61.
handheld suction. In our patients, however, the retraction of [12] Kondo A. Follow-up results of microvascular decompression in trige-
the cerebellum was performed. The eighth nerve has the minal neuralgia and hemifacial spasm. Neurosurgery 1997;40:46-52.
longest extracerebral central part of all the nerves in the [13] Kuroki A, Itagaki S, Nagai O. Delayed facial palsy after microvascular
decompression for hemifacial spasm. Facial Nerve Res 1991;11:
cerebellopontine angle and is highly vulnerable to traction. 147-50.
Therefore, the retraction was done in a direction perpendi- [14] Lovely TJ. Efficacy and complications of microvascular decompres-
cular rather than longitudinal to the axis of the eighth nerve sion: a review. Neurosurg Q 1998 [In press].
to minimize risk of postoperative hearing impairment. [15] Lovely TJ, Getch CC, Jannetta PJ. Delayed facial weakness after
microvascular decompression of cranial nerve VII. Surg Neurol 1998;
It has been reported that particular change in “lateral
50:449-52.
spread reflex” and BAEP monitoring can be used to predict [16] Lovely TJ, Lowry DW, Jannetta PJ. Functional outcome and the effect
postoperative function. However, the role of intraoperative of cranioplasty after retromastoid craniectomy for microvascular
BAEP and facial EMG in preventing cranial nerve deficit is decompression. Surg Neurol 1999;51:191-7.
uncertain [6,17,19,20,24,26]. We did not perform facial [17] McLaughlin MR, Jannetta PJ, Clyde BL. Microvascular decompres-
EMG during operation, and BAEP has been monitored since sion of cranial nerves: lessons learned after 4400 operations.
J Neurosurg 1999;90:1-8.
1983. The rate of hearing impairment after operation began [18] Moller AR. Vascular compression of cranial nerves II. Pathophysiol-
to decrease from 1987, at the end of learning period, and the ogy. Neurol Res 1999;21:439-43.
improvement in the late period could be due to the [19] Moller MB, Moller AR. Loss of auditory function in microvascular
improvement on the neurosurgeon's learning curve. decompression for hemifacial spasm. Results in 143 consecutive cases.
J Neurosurg 1985;63:17-20.
4.1. Conclusion [20] Polo G, Fischer C, Sindou MP. Brainstem auditory evoked potential
monitoring during microvascular decompression for hemifacial spasm:
When cranial nerve palsies occur within 24 hours after intraoperative brainstem auditory evoked potential changes and
operation and when the initial grade of the cranial palsies is warning values to prevent hearing loss—prospective study in a
severe, the prognosis is poor, and there is a high possibility consecutive series of 84 patients. Neurosurgery 2004;54:97–106.
[21] Rhee DJ, Kong DS, Park K. Frequency and prognosis of delayed facial
of permanent cranial nerve dysfunction. To determine the palsy after microvascular decompression for hemifacial spasm. Acta
permanence, a 2-year wait minimum would be best, Neurochir (Wien) 2006;148:839-43.
especially considering that lower cranial nerve palsy may [22] Roh SW, Chung SS, Park YG, Rhim SC, Lee KC. Significance of
improve during this time span. brainstem auditory evoked potentials in posterior fossa surgery.
J Korean Neurosurg Soc 1987;16:1061-72.
[23] Samii M, Gunther T, Iaconetta. Microvascular decompression to treat
References hemifacial spasm: long-term results for a consecutive series of 143
patients. Neurosurgery 2002;50:712-8.
[1] Auger RG, Piepgras DG, Laws Jr ER. Hemifacial spasm: results of [24] Sindou MP. Microvascular decompression for primary hemifacial
microvascular decompression of the facial nerve in 54 patients. Mayo spasm. Importance of intraoperative neurophysiological monitoring.
Clin Proc 1986;61:640-4. Acta Neurochir (Wien) 2005;147:1019-26.
R. Huh et al. / Surgical Neurology 69 (2008) 153–157 157

[25] Wang A, Jankovic J. Hemifacial spasm: clinical findings and treatment. 2003. Dr P J Jannetta introduced the MVD for HFS in the
Muscle Nerve 1998;21:1740-8. Journal of Neurosurgery in 1977. In this current article,
[26] Wilkins RH. Hemifacial spasm: a review. Surg Neurol 1991;36:
251-77.
the surgery was performed only by Dr S S Chung, and his
long experience is expressed in this article. His data will
serve as preoperative explanation for a patient. I would like
to congratulate him for his great effort and good results.
Commentary
Masashi Fukui, MD
The authors analyzed surgical complications of MVD Department of Neurosurgery
surgery for HFS. The data plural is based on their 1582 Sasebo Kyosai Hospital
patients and 1609 surgeries during the period from 1978 to Sasebo 857-8575, Japan

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