Microvascular decompression (MVD) has been established as a first-line surgical treatment for patients with HFS and has been reported to provide relief from spasms in over 90% of cases.3,5,10 At most centers, intraoperative electromyographic (EMG) monitoring of lateral spread response (LSR) is routinely performed during MVD for HFS. The LSR can be elicited by stimulating one branch of the facial nerve and recording from muscle innervated by other facial branches.14 It is particularly valuable when LSR induced before craniotomy disappears immediately after the culprit vessel is moved off the facial nerve; this is important clinically to help surgeons to confirm whether adequate decompression has been achieved.8,16
Since Møller and Jannetta14 documented that spasms are more likely to persist if LSR is still present at the end of the operation, LSR has been studied as an independent prognostic predictor of surgical outcome. Its value, however, it is still a matter of debate.4,7–9,16,17,21,22,24 In addition, little has been published on whether intraoperative LSR monitoring can significantly improve the cure rate of MVD for HFS. To shed light on these issues, we conducted a prospective study to compare short- and long-term clinical outcomes between 2 cohorts, patients who underwent MVD with intraoperative LSR monitoring and those who underwent MVD with no LSR monitoring.
Method
Patient Population
This study was performed under a protocol approved by the Ruijin Hospital institutional review board. Patients undergoing retromastoid MVD for treatment of HFS at the Ruijin Hospital affiliate to Shanghai Jiao Tong University School of Medicine between November 2013 and July 2014 were enrolled in a prospective study comparing the outcome of MVD performed with or without intraoperative LSR monitoring. Based on coin flip, patients were assigned to either Group A (MVD with LSR monitoring) or Group B (MVD without LSR monitoring). Written informed consent was obtained from all patients prior to their participation in the study. In all cases, HFS was diagnosed based on typical symptoms of unilateral paroxysmal facial muscle contraction, and magnetic resonance tomographic angiography (MRTA) was performed to rule out tumor-related cases.
Intraoperative Monitoring
From the time that patient positioning was completed to dura mater closure, continuous LSR was recorded with paired subdermal needles inserted into the orbicularis oculi and mentalis muscles. With another set of paired needles positioned over the zygomatic branches of the facial nerve, response was evoked using a pulse duration of 0.2 msec and stimulus intensity between 5 and 30 mA. The signals were amplified, filtered, and displayed using a commercial neurophysiological monitoring workstation (Cascade, Caswell). No neuromuscular blockade agents were used except during intubation. Four checkpoints were established in order to identify LSR disappearance or persistence: 1) during CSF drainage period; 2) during dissection of arachnoid membrane; 3) during Teflon implantation; and 4) after dura closure (to check for LSR persistence). In addition, brainstem auditory evoked potential monitoring was performed in all patients in both groups, as presented previously in detail.15,18
Surgical Procedure
All operations were performed by the senior surgeon (W.Z.) using a lateral suboccipital retrosigmoid approach as described previously.14,20 Briefly, after the dura was opened, and CSF was drained slowly to achieve adequate brain relaxation without the need for a brain retractor. The caudal cranial nerve was sharply dissected away from the flocculus cerebelli, the root exit zone (REZ) of the facial nerve was exposed by gentle retraction of the flocculus and choroid plexus, and Teflon was then implanted to make sure of full facial nerve decompression. If LSR persisted after decompression, the entire facial nerve course was re-explored to confirm that there was no visible evidence of neurovascular conflict, and then the surgeon terminated the operation and closed the dura mater routinely despite residual LSR persistence.
Outcome Criteria and Evaluation
Patient characteristics, intraoperative findings, complications, and short- and long-term clinical results were recorded in a prospective patient database. Short-term outcome was assessed on the day of discharge, postoperative Day 7. Long-term outcome was evaluated at 1 year after surgery through telephone surveys carried out by an interviewer who was blinded to the patients’ group assignment (i.e., whether LRS monitoring had been used). Operative results were considered as “good” if the patient had complete relief of spasms or adequate improvement (≥ 90% reduction) and “poor” if the frequency and severity of spasm had not been reduced by at least 90%.
Statistical Analysis
Statistical analysis was performed with SPSS version 20.0 (IBM Corp.). Chi-square tests and Mann-Whitney U-tests were used to assess the group differences in binary and ordinal variables, respectively; outcomes were compared between the 2 groups using the Fisher exact test. All probability values reported here are 2 tailed, and p < 0.05 was considered statistically significant.
Results
A total of 300 patients were included in this study; 162 underwent MVD with intraoperative LSR monitoring (Group A) and 138 underwent MVD without LSR monitoring (Group B). Data from 17 (10.49%) of the patients in Group A were excluded from analysis (Fig. 1). In 4 of these patients (2.47% of the 162 patients originally assigned to Group A), LSR was not observed before dura opening but only emerged after initiation of subarachnoid dissection or nerve decompression. In the other 13 patients (8.02%), LSR was not induced despite reduction of the minimal alveolar concentration of sevoflurane and increase of the stimulus intensity to 30 mA.
Flow diagram for this study. pts = patients.
Table 1 lists the clinical features of Group A and Group B. No statistically significant difference was found in clinical characteristics (age, sex, side of HFS, and history of botulinum toxin treatment) or surgical findings (type and number of culprit vessels) between the 2 groups.
Demographic data for patients undergoing MVD with (Group A) or without (Group B) intraoperative LSR monitoring
| Characteristics | Group A (n = 145) | Group B (n = 138) | p Value |
|---|---|---|---|
| Age in yrs, mean | 51.8 ± 10.19 | 51.99 ± 9.74 | 0.871 |
| Sex | 0.702 | ||
| Female | 97 | 96 | |
| Male | 48 | 42 | |
| Side | 0.812 | ||
| Left | 77 | 71 | |
| Right | 68 | 67 | |
| Follow-up in mos, mean | 18.04 ± 2.57 | 18.41 ± 2.46 | 0.141 |
| Duration in yrs, mean | 5.27 ± 3.8 | 6.34 ± 3.24 | 0.361 |
| BTA history | 0.526 | ||
| Yes | 14 | 10 | |
| No | 131 | 128 | |
| Culprit vessel | |||
| AICA | 89 (61.38%) | 93 (67.34%) | |
| PICA | 64 (44.14%) | 48 (34.78%) | |
| VA | 31 (21.38%) | 25 (18.12%) | |
| No. of culprit vessels | 0.121 | ||
| 1 | 106 | 112 | |
| >1 | 39 | 26 |
AICA = anterior inferior cerebellar artery; BTA = botulinum-A injection; PICA = posterior inferior cerebellar artery; VA = vertebral artery.
Values represent number of patients (%) unless otherwise indicated. Mean values are given with SDs.
Differences in Outcomes According to LSR Monitoring
In Group A (MVD with LSR monitoring), 1-week follow-up evaluation showed reduction in spasms by 90% or more in 127 patients (87.59%). At the 1-year follow-up examination, 135 patients (93.1%) showed adequate spasm relief, and only 10 patients (6.9%) had no significant improvement (Table 2).
Comparison of clinical results of MVD with (Group A) and without (Group B) intraoperative LSR monitoring
| Time Point & Outcome | Group A (n = 145) | Group B (n = 138) | p Value |
|---|---|---|---|
| 1 wk | 0.317 | ||
| Good | 127 (87.59%) | 115 (83.33%) | |
| Poor | 18 (12.41%) | 23 (16.67%) | |
| 1 yr | 0.809 | ||
| Good | 135 (93.1%) | 130 (94.2%) | |
| Poor | 10 (6.9%) | 8 (5.8%) |
Data are number of patients (%). Good outcome was defined as at least 90% reduction in hemifacial spasm. Poor outcome was defined as lack of at least 90% reduction.
In Group B (MVD without LSR monitoring), 115 patients (83.33%) experienced spasm relief at the 1-week follow-up examination. At 1 year after operation, the spasms had resolved in 130 of 138 patients (94.2%), whereas 8 patients (5.8%) still had the symptoms. There was no significant difference of spasm relief ratio between Group A and Group B at 1-week (87.59% vs 83.33%, p = 0.317) and at 1-year (93.1% vs 94.2%, p = 0.809) follow-up examination.
Differences in Outcomes According to LSR Disappearance
A complete elimination of LSR was observed in 131 (90.34%) of 145 patients. It occurred in 5 patients (3.45%) during CSF drainage, in 28 patients (19.31%) during dissection of arachnoid membrane, and in 98 patients (67.59%) during implantation of Teflon. At completion of dura closure, 14 patients (9.66%) still had LSR persistence.
Table 3 lists the clinical outcomes of the patients in Group A. At the 1-week follow-up examination, 118 (90.08%) of 131 patients who suffered LSR disappearance and 9 (64.29%) of 14 patients with residual LSR exhibited complete spasm relief. However, at the 1-year follow-up evaluation, complete spasm relief was achieved in 123 (93.9%) of 131 patients who experienced LSR disappearance and in 12 (85.71%) of 14 patients who had persistence of LSR. Data analysis showed that the difference in clinical outcomes between patients with disappearance of LSR and those without LSR disappearance was statistically significant at 1 week after surgery (p = 0.017) but not at the 1-year follow-up evaluation (p = 0.249).
Comparison of clinical results in patients who had disappearance or persistence of LSR at the end of the surgical procedure
| Time Point & Outcome | LSR Disappearance (n = 131) | LSR Persistence (n = 14) | p Value |
|---|---|---|---|
| 1 wk | 0.017 | ||
| Good | 118 (90.08%) | 9 (64.29%) | |
| Poor | 13 (9.92%) | 5 (35.71%) | |
| 1 yr | 0.249 | ||
| Good | 123 (93.9%) | 12 (85.71%) | |
| Poor | 8 (6.1%) | 2 (14.29%) |
Data are number of patients (%).
Complications
In the overall group of 283 patients, the most common complications were transient hearing impairment (occurring in 13 patients [4.59%]), permanent hearing loss (in 3 patients [1.06%]), slight hoarseness and gagging/coughing on eating or drinking (in 9 patients [3.18%]), and immediate postoperative facial paralysis (in 4 patients [1.41%]). There were no deaths, hemorrhages, or CSF leakage in our series.
Discussion
MVD has become popular worldwide as an effective method for treating HFS, and a variety of methods, including electrophysiological monitoring, are employed in an effort to increase its effectiveness. Previous studies of intraoperative LSR monitoring have generally demonstrated its utility, although the use of this method remains a topic of debate, with some studies showing conflicting results. Detection of the disappearance of LSR has been reported to be helpful in identification of culprit vessels and confirmation of adequate decompression14,16 and also to be a reliable predictor for excellent clinical outcomes.11,26
However, in this study, patients who underwent MVD with intraoperative LSR monitoring (Group A) did not exhibit better clinical outcomes than those who underwent MVD without intraoperative LSR monitoring (Group B) at the 1-week or 1-year follow-up examination. In most of our cases (all but 18), LSR monitoring did not play a guiding role during surgery. We speculate that there are 3 likely causes. This lack of utility for guidance may be largely due to the pattern of LSR disappearance during MVD in this study. Several studies have suggested that LSR frequently disappears during CSF drainage, which might be due to a slight shift in the compressive site, equivalent to decompression.2,16 In our study, 33 patients (22.76%) in whom LSR disappeared during the CSF drainage or arachnoid membrane dissection period did not show recurrence through the end of operation. None of these patients benefited from intraoperative LSR monitoring. Mooij et al.16 reported that intraoperative EMG monitoring played a guiding role in 33.8% of the 74 patients in their series (the monitoring guided the surgery by demonstrating that the initially suspected vessel was not the actual culprit). However, the corresponding rate in our study was lower. In our study compressive vessels could be identified just on the basis of the surgeon’s experience in most cases. LSR monitoring played a guiding role (guiding the surgery by demonstrating that the initially suspected vessel was not the actual culprit) in only 18 (12.41%) of the cases. However, all operations in our study were performed by a surgeon with unusually extensive experience with this procedure, and this may have contributed to the lack of difference between the groups. A third factor may be LSR waveform confusion in difficult cases. In some cases, the posterolateral sulcus of the medulla oblongata can be excessively depressed into the midline or the flocculus cerebelli may be very large and may cover the proximal part of the facial nerve. In order to achieve satisfactory REZ exposure, it may be necessary to retract the flocculus, resulting in a noisy EMG output signal, leading in turn to a failure of monitoring for purposes of guidance. It should be emphasized that all operations were performed by a neurosurgeon who is very experienced with the procedure, and thus disparity in surgical outcome due to variability in surgical proficiency can be ruled out in this series.
Several studies have demonstrated the positive effect of LSR abolition in predicting surgical outcomes.4,11,17,19,26 It has been suggested that patients with disappearance of LSR after decompression have better outcomes than those with abolition of LSR before decompression.8 A meta-analysis conducted by Sekula et al.19 indicated that the chance of a cure if the LSR disappeared during Teflon implantation was 4.2 times greater than if the LSR persisted. We found this interesting, but we are concerned that these statistics may be somewhat misleading because the patients in whom LSR disappeared during CSF drainage or manipulation of cerebellum were excluded from the analysis. Furthermore, operative result evaluations varied in the included studies and the timelines of the pooled data were also discordant. In our series, even after sufficient decompression, 14 patients still had persistence of LSR after closure, but 12 (85.71%) of these 14 patients nevertheless had complete relief of spasm at the 1-year evaluation. Kiya et al.9 reported that 17 patients with persistence of LSR at the end of MVD had complete disappearance of spasm within 3 months. Moreover, a study evaluating the outcomes of 293 MVD procedures with intraoperative LSR monitoring in the University of Pittsburgh Medical Center, the largest such study to date, showed a significant difference in spasm relief between the LSR disappearance group and the LSR persistence group within 24 hours of surgery and at discharge, but not at follow-up, and the authors concluded that there was no statistically significant association between intraoperative LSR monitoring and long-term outcomes.21
Hatem et al.3 demonstrated that an excellent result is still likely to be obtained in patients with LSR persistence after successful decompression, and delayed spasm relief strongly supports the hypothesis that HFS is not only due to the neurovascular compression but also to severe nerve demyelination and/or hyperactivity of the facial nucleus. Although LSR exists in almost all patients with typical HFS, the exact mechanism of this phenomenon has not yet been well elucidated. It was presumed to be related to cross-transmission between axons at the lesion site because LSR disappeared immediately in most cases after the offending vessel was separated from the facial nerve.6,12,14 However, LSR could also be due to hyperactivity of the facial nucleus.1,13 Yamakami et al.25 found that an abnormal EMG response similar to LSR could be induced in rats by chronic electrical stimulation to the facial nerve nucleus. We used resting-state functional MRI to investigate spontaneous changes of brain activity in patients with HFS; our results show not only that the facial nucleus and motor cortex were excessively excited, but also that the facial motor inhibitory cortex was dysfunctional.23 Therefore, it is feasible that LSR could represent a combined electrophysiological phenomenon of ephaptic transmission at REZ and disturbance of the facial motor control system. We concluded that the persistence of LSR after decompression might be due to interindividual differences in the hyperexcitation of the facial nucleus or motor cortex facilitated by pulsatile compression. If this excitation declines or is suppressed immediately after decompression, then the LSR will disappear soon, otherwise the LSR will persist. The LSR will not disappear until the subsequent remyelination of the facial nerve or increase of the firing threshold. It seems that the cessation of facial muscle contraction does not always occur synchronously with the recovery of myoelectric potential. Consequently, it is unreliable to predict the long-term outcomes of spasm by recording the intraoperative changes of LSR.
Nevertheless, we do not deny that there is a role for intraoperative LSR monitoring; it may be useful as an aid in learning as well as in confirming the successful decompression to enhance surgeon self-confidence and ascertaining recurrence of HFS.6 However, it needs to be emphasized that the disappearance of LSR should not be pursued in all operations after verified and complete decompression; any excessive additional exploration is likely not necessary and might put the adjacent nerve and vascular structures at risk.
Conclusions
MVD for HFS with intraoperative LSR monitoring does not show greater efficacy than MVD without LSR monitoring when the surgery is performed by a skilled MVD surgeon. Residual LSR does not always correlate with a poor long-term outcome. Therefore, the disappearance of LSR should not be pursued in all patients after complete and satisfactory decompression.
Disclosures
The authors report no conflict of interest concerning the materials or methods used in this study or the findings specified in this paper.
Author Contributions
Conception and design: Zhao, Wei. Acquisition of data: Wei, Yang. Analysis and interpretation of data: Wei. Drafting the article: Wei. Critically revising the article: Zhao, Pu. Reviewed submitted version of manuscript: Zhao, Pu, Li, Cai, Shang. Approved the final version of the manuscript on behalf of all authors: Zhao. Statistical analysis: Wei. Administrative/technical/material support: all authors. Study supervision: Zhao.
References
- 1↑
Fernández-Conejero I, Ulkatan S, Sen C, Deletis V: Intra-operative neurophysiology during microvascular decompression for hemifacial spasm. Clin Neurophysiol 123:78–83, 2012
- 2↑
Haines SJ, Torres F: Intraoperative monitoring of the facial nerve during decompressive surgery for hemifacial spasm. J Neurosurg 74:254–257, 1991
- 3↑
Hatem J, Sindou M, Vial C: Intraoperative monitoring of facial EMG responses during microvascular decompression for hemifacial spasm. Prognostic value for long-term outcome: a study in a 33-patient series. Br J Neurosurg 15:496–499, 2001
- 4↑
Huang BR, Chang CN, Hsu JC: Intraoperative electrophysiological monitoring in microvascular decompression for hemifacial spasm. J Clin Neurosci 16:209–213, 2009
- 5↑
Hyun SJ, Kong DS, Park K: Microvascular decompression for treating hemifacial spasm: lessons learned from a prospective study of 1,174 operations. Neurosurg Rev 33:325–334, 2010
- 6↑
Ishikawa M, Ohira T, Namiki J, Kobayashi M, Takase M, Kawase T, et al.: Electrophysiological investigation of hemifacial spasm after microvascular decompression: F waves of the facial muscles, blink reflexes, and abnormal muscle responses. J Neurosurg 86:654–661, 1997
- 7
Joo WI, Lee KJ, Park HK, Chough CK, Rha HK: Prognostic value of intra-operative lateral spread response monitoring during microvascular decompression in patients with hemifacial spasm. J Clin Neurosci 15:1335–1339, 2008
- 8↑
Kim CH, Kong DS, Lee JA, Park K: The potential value of the disappearance of the lateral spread response during microvascular decompression for predicting the clinical outcome of hemifacial spasms: a prospective study. Neurosurgery 67:1581–1588, 2010
- 9↑
Kiya N, Bannur U, Yamauchi A, Yoshida K, Kato Y, Kanno T: Monitoring of facial evoked EMG for hemifacial spasm: a critical analysis of its prognostic value. Acta Neurochir (Wien) 143:365–368, 2001
- 10↑
Kondo A, Date I, Endo S, Fujii K, Fujii Y, Fujimaki T, et al.: A proposal for standardized analysis of the results of microvascular decompression for trigeminal neuralgia and hemifacial spasm. Acta Neurochir (Wien) 154:773–778, 2012
- 11↑
Kong DS, Park K, Shin BG, Lee JA, Eum DO: Prognostic value of the lateral spread response for intraoperative electromyography monitoring of the facial musculature during microvascular decompression for hemifacial spasm. J Neurosurg 106:384–387, 2007
- 12↑
Møller AR: The cranial nerve vascular compression syndrome: II. A review of pathophysiology. Acta Neurochir (Wien) 113:24–30, 1991
- 13↑
Møller AR: Vascular compression of cranial nerves: II: pathophysiology. Neurol Res 21:439–443, 1999
- 14↑
Møller AR, Jannetta PJ: Microvascular decompression in hemifacial spasm: intraoperative electrophysiological observations. Neurosurgery 16:612–618, 1985
- 15↑
Møller AR, Møller MB: Does intraoperative monitoring of auditory evoked potentials reduce incidence of hearing loss as a complication of microvascular decompression of cranial nerves? Neurosurgery 24:257–263, 1989
- 16↑
Mooij JJ, Mustafa MK, van Weerden TW: Hemifacial spasm: intraoperative electromyographic monitoring as a guide for microvascular decompression. Neurosurgery 49:1365–1371, 2001
- 17↑
Neves DO, Lefaucheur JP, de Andrade DC, Hattou M, Ahdab R, Ayache SS, et al.: A reappraisal of the value of lateral spread response monitoring in the treatment of hemifacial spasm by microvascular decompression. J Neurol Neurosurg Psychiatry 80:1375–1380, 2009
- 18↑
Polo G, Fischer C, Sindou MP, Marneffe V: Brainstem auditory evoked potential monitoring during microvascular decompression for hemifacial spasm: intraoperative brainstem auditory evoked potential changes and warning values to prevent hearing loss—prospective study in a consecutive series of 84 patients. Neurosurgery 54:97–106, 2004
- 19↑
Sekula RF Jr, Bhatia S, Frederickson AM, Jannetta PJ, Quigley MR, Small GA, et al.: Utility of intraoperative electromyography in microvascular decompression for hemifacial spasm: a meta-analysis. Neurosurg Focus 27(4):E10, 2009
- 20↑
Sindou MP: Microvascular decompression for primary hemifacial spasm. Importance of intraoperative neurophysiological monitoring. Acta Neurochir (Wien) 147:1019–1026, 2005
- 21↑
Thirumala PD, Shah AC, Nikonow TN, Habeych ME, Balzer JR, Crammond DJ, et al.: Microvascular decompression for hemifacial spasm: evaluating outcome prognosticators including the value of intraoperative lateral spread response monitoring and clinical characteristics in 293 patients. J Clin Neurophysiol 28:56–66, 2011
- 22↑
Tobishima H, Hatayama T, Ohkuma H: Relation between the persistence of an abnormal muscle response and the long-term clinical course after microvascular decompression for hemifacial spasm. Neurol Med Chir (Tokyo) 54:474–482, 2014
- 23↑
Tu Y, Wei Y, Sun K, Zhao W, Yu B: Altered spontaneous brain activity in patients with hemifacial spasm: a resting-state functional MRI study. PLoS One 10:e0116849, 2015
- 24↑
von Eckardstein K, Harper C, Castner M, Link M: The significance of intraoperative electromyographic “lateral spread” in predicting outcome of microvascular decompression for hemifacial spasm. J Neurol Surg B Skull Base 75:198–203, 2014
- 25↑
Yamakami I, Oka N, Higuchi Y: Hyperactivity of the facial nucleus produced by chronic electrical stimulation in rats. J Clin Neurosci 14:459–463, 2007
- 26↑
Ying TT, Li ST, Zhong J, Li XY, Wang XH, Zhu J: The value of abnormal muscle response monitoring during microvascular decompression surgery for hemifacial spasm. Int J Surg 9:347–351, 2011
