Neurofunction > Volume 19(2); 2023 > Article
Choi and Koh: Results of microvascular decompression for hemifacial spasm for 23 years

Abstract

Objective

Hemifacial spasm (HFS) is characterized by unilateral tonic and/or clonic contractions of the facial muscles. The most frequent cause of HFS is neurovascular focal compression of the root exit zone of the facial nerve. Microvascular decompression (MVD) works well, with effects that last almost permanently. We analyzed the surgical outcomes and complications from the last 23 years at our institution.

Methods

This study analyzed 244 patients who underwent MVD between June 1998 and July 2021. All patients were followed up for more than 24 months. The preoperative image workups were brain magnetic resonance imaging, magnetic resonance angiography, and constructive interference in steady state (from 2009 onwards). Starting in July 2012, intraoperative monitoring was performed. Surgery was performed through the retrosigmoid approach by a single neurosurgeon.

Results

Out of 244 patients, 160 were female and 84 were male. The average age was 53.8 years (range, 19-78 years). In total, 226 patients (92.6%) completely recovered from HFS, two patients (0.8%) underwent reoperation, and complications occurred in 16 patients (6.6%). In 61 patients with preoperative facial palsy on the affected side, palsy improved in 56 patients (91.8%) and 12 patients (19.7%) had thick arachnoid membranes.

Conclusion

MVD has a durable effect on the improvement of HFS and may also improve HFS and concomitant palsy if preoperative facial palsy is present. Therefore, it is thought to be a treatment method that can be actively recommended to patients.

INTRODUCTION

Ten out of 100,000 people between the ages of 50 and 60 are usually reported to have partial facial spasms (HFS) [1-4]. The symptoms usually progress in frequency and severity, starting with intermittent twitches in the orbicularis oculi muscle, and spreading downward to the ipsilateral facial muscles. The most common cause of HFS is neurovascular compression along the root exit zone (REZ) of the facial nerve and the most common offending vessel is the anterior inferior cerebellar artery or posterior inferior cerebellar artery [5]. HFS is also caused by secondary etiologies such as tumors or vascular malformations [6,7]. Medical treatment of HFS includes administration of anticonvulsants (carbamazepine, clonazepam, gabapentin, etc.), anticholinergic drugs, antipsychotics, or botulinum toxin injections [8-13]. However, medical treatment is increasingly less effective and side effects occur as the dose escalation. Microvascular decompression (MVD) is indicated after unsatisfactory or decreasing effect of medical treatment or becomes intolerable to side effects. In most series, the percentage of patients with total relief ranged between 85% and 90%. In Samii et al.’s reports [14], the rate of symptom resolution following MVD has been reported to be over 92% at 6 months with 90% of patients remaining spasm free at 1 year. Common complications include hearing loss (7-26%), facial nerve injury (2.8-8.3%), and cerebrospinal fluid (CSF) leak (2-3%) [15-20].
We report the surgical outcomes and complications of MVD for HFS in our institute’s last 23 years.

MATERIALS AND METHODS

Two hundred forty-four patients who had got MVD between June 1998 and July 2021 were reviewed retrospectively. All patients followed up for more than 24 months. Preoperative brain magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) were performed in all patients, and constructive interference in steady state (CISS) images were taken after 2009. Institutional Review Board approval and informed consent of the patients were exempted because this study was conducted retrospectively using existing data.

Surgical procedure

The surgical approach was retrosigmoid approach, and all cases were done by one neurosurgeon (HYC). A small craniotomy behind and close to the sigmoid sinus was performed (2.5×2.5 cm square shape just behind sigmoid sinus). The dura was C-shaped opened based on sigmoid sinus. Under binocular microscopy, the cerebellum was depressed spontaneously and progressively helped by CSF aspiration of the cerebellopontine angle and cerebellomedullary cistern. CSF was drained slowly to achieve adequate brain relaxation without the need for a brain retractor. The cranial nerve (CN) IX and X was sharply dissected away from the flocculus cerebelli and the arachnoid dissection around the vessels was performed to cephalad direction until CN VII, VIII complex was seen under arachnoid membrane. Conflict of vascular structure and CN VII exit zone was treated by interposition of Teflon felts and/or liberation vessel or nerve from fibrotic adhesions. Multiple offending vessels were searched in multiple possible affected sites in addition to the REZ of the facial nerve. If lateral spread response (LSR) persisted after decompression, the entire facial REZ was reexplored to confirm that there was no visible evidence of neurovascular conflict. Then the surgeon terminated the decompression despite residual LSR persistence. After that, papaverine and normal saline is filled in cistern, and the dura suture is reinforced with a muscle patch. After reinforcing once more with a hemostat to prevent leakage, the bone defect was reconstructed with hydroxyapatite.

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 frontalis, orbicularis oculi, orbicularis oris, 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 millisecond and stimulus intensity between 5 and 30 mA. The signals were amplified, filtered, and displayed using a commercial neurophysiological monitoring workstation (ISIS intraoperative monitoring [IOM] system; Inomed). No neuromuscular blockade agents were used except during intubation. Three checkpoints were established in order to identify LSR disappearance or persistence: 1) during CSF drainage period; 2) during Teflon implantation; and 3) after dura closure (to check for LSR persistence). In addition, brainstem auditory evoked potential monitoring was performed in all patients. IOM was performed after July 2012.

RESULTS

Of the 244 patients, female patients were 160, and male patients were 84. The average age was 53.8 years old (19-78 years old). The average duration of symptoms was 4 years (1 month-20 years). The affected side was left 141 (female:male=82:59) and right 103 (female:male=78:25). Offending vasculatures were anterior inferior cerebellar artery (AICA) 150 (61.5%), posterior inferior cerebellar artery (PICA) 37 (15.2%), vertebral artery (VA) 16 (6.6%), basilar artery (BA) two (0.8%), vein eight (3.3%), AICA+VA eight (3.3%), AICA+BA four (1.6%), AICA+vein two (0.8%), PICA+VA 15 (6.1%), PICA+BA one (0.4%) and VA+vein one (0.4%) (Table 1). Two hundred twenty-six patients (92.6%) completely recovered from HFS, two patients (0.8%) got reoperation, and complications occurred in 16 patients (6.6%) (Table 2).
Total symptom free rate was 92.6%. Before the IOM period (1998.06-2012.06), 96.7% of 150 patients were freed from HFS, and after the IOM period (2012.07-2021.07), 86.2% of 94 patients were freed from HFS (Table 2).
In 61 patients with preoperative facial palsy (female:male=40:21, average age: 55.1 years old, average duration of HFS: 5 years, left:right=36:25) on the affected side, facial palsy was improved to normal in 56 patients (91.8%) and five patients (8.2%) showed slight improvement from House-Brackman Grade (HBG) 3 to 2. There were no patients with worsening paralysis symptoms. Almost patients showed HBG 3. The spasm-free rate of patients with preoperative facial palsy were similar those without preoperative facial palsy (95% versus 92.8%). A peculiarity of the surgical field compared to patients without facial palsy is that the arachnoid thickened more often in patients with facial palsy (12 cases [19.7%] in 61 patients versus four cases [2.2%] in 183 patients, chi-square test: odds ratio 22.16) (Fig. 1). The HFS duration of patients with facial palsy was slightly longer than that of patients without facial palsy (5 years compared to 4.2 years).
Out of 16 complications, wound dehiscence was in three (1.2%), postoperative facial paralysis in five (2.0%), permanent hearing loss four (1.6%), transient hearing impairment in one (0.4%), tinnitus in one (0.4%), hoarseness plus tinnitus plus hearing impairment in one (0.4%), and one patient (0.4%) died from subarachnoid hemorrhage (SAH) that occurred immediately after surgery. There was no CSF leak. Complications in pre-IOM period were wound dehiscence in one patient), facial palsy in two patients, and death in one patient. In post-IOM period wound infection, hearing impairment, facial palsy, tinnitus, and lower CN deficit (hoarseness+tinnitus+hearing impairment) was two, five, three, one, and one, respectively (Table 2). More complications occurred in the post-IOM period compared to the pre-IOM period (chi-square test: odds ratio 6.39).

DISCUSSION

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 [5,21,22]. However, although MVD is a reliable treatment method, general anesthesia and the difficulty of handling the area around the brainstem are still reasons for reluctance to perform surgery. We aimed to investigate the results of MVD for HFS, and to evaluate the outcome and morbidity of this treatment. We retrospectively studied 244 patients who underwent retrosigmoid MVD last 23 years.
In our series, the female patients were 160 and male patients were 84. The proportion of female patients was about twice as high, and the average age of the patients was also in their mid-fifties as already known. The left and right incidence rates were the same in the entire patient group, but when the analysis was performed separately for female and male, the left side was more affected in male.
MRI is the gold standard for neurovascular conflicts diagnosis MRI, focusing on the facial nerve trajectory, was performed to diagnose and localize the offenders, and to exclude tumors or other vascular malformations. Improvement in imaging modalities since 1990 would result in overestimation of discordance. Recently, for better information, neurovascular conflicts are documented by MRI with three-dimensional constructive CISS, alone or together with three-dimensional time-of-flight MRA [23,24].
In about offending vessels the most common conflict vessels was AICA 150 (62.3%), followed by PICA 37 (15.2%), VA 16 (6.5%), BA two (0.8%), vein eight (3.3%), and AICA+VA eight (3.3%), AICA+BA 4 (1.6%), PICA+VA 15 (6.1%), PICA+BA 1 (0.4%) and VA+vein 1 (0.4%). Most of the vessels colliding with facial REZ were AICA and PICA.
We were interested in the changes in the surgical outcome and postoperative paralysis symptoms of 61 patients with facial paralysis before surgery. Almost patients showed HBD 3. A peculiarity of the surgical field compared to patients without facial palsy is that the arachnoid thickened more often in patients with facial palsy (12 cases [19.7%] in 61 patients versus four cases [2.2%] in 183 patients). We believe that the reason for the thick arachnoid membrane observed in patients with facial paralysis before surgery suggests the possibility of some previously unknown inflammation.
The overall rate of symptom-free without complications after MVD was 92.6%. This result is similar to previous reports. Out of 16 complications, wound dehiscence was in three (1.2%), postoperative facial paralysis in five (2.0%), permanent hearing loss four (1.6%), transient hearing impairment in one (0.4%), tinnitus in one (0.4%), hoarseness plus tinnitus plus hearing impairment in one (0.4%), and one patient (0.4%) died from SAH that occurred immediately after surgery. Our results also showed a complication rate similar to that previously known. The risk of permanent CN deficit was 1-2% for facial palsy, 2-3% for non-functional hearing loss, 0.5-1% for lower CN dysfunction. Risk of stroke was at 0.1% and mortality at 0.1%.
We analyzed the surgical results and complications before and after IOM. Before IOM, one serious complication, death, occurred, but the complication rate was 2.7%. After IOM, there were no serious complications, but the complication rate was 12.7%. It is thought that the introduction of the IOM has led to an increase in the incidence of complications even though the operator or surgical method has not changed. It is thought that the cause of the problem is that the vascular and nerve structures are further manipulated until the loss of the LSR is confirmed. 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 [25,26]. Since Møller and Jannetta [27] 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 [28-34]. In Wei et al.’s report [35] in 2018 patients who underwent MVD with intraoperative LSR monitoring did not exhibit better clinical outcomes than those who underwent MVD without intraoperative LSR monitoring at the 1-week or 1-year follow-up examination. In most of their cases (all but 18), LSR monitoring did not play a guiding role during surgery. A meta-analysis conducted by Sekula et al. [36] indicated that the chance of a cure if the LSR disappeared during Teflon implantation was 4.2 times greater than if the LSR persisted. Hatem et al. [21] 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 [27,37,38]. However, LSR could also be due to hyperactivity of the facial nucleus [39]. As such, there are various causes of LSR, so manipulating blood vessels and nerves and inserting more Teflon until the LSR disappears in the surgical field can only increase the possibility of complications.

CONCLUSION

MVD has a durable effect on the improvement of HFS and also improve HFS and simultaneous palsy if preoperative facial palsy is present. When using an IOM, it is better to use it at a level that prevents or predicts complications rather than relying solely on LSR loss.

NOTES

CONFLICTS OF INTEREST

No potential conflict of interest relevant to this article was reported.

Fig. 1.
(A) The operative field of a patient who preoperatively had facial palsy and hemifacial spasm shows a thick, opaque arachnoid membrane (red star) between cranial nerves X-IX (sky-blue arrows) and the VII-VIII complex (yellow arrow). (B) The operative field of a patient with only hemifacial spasm shows a clear and transparent arachnoid membrane (yellow-green star) between cranial nerves X-IX (sky-blue arrows) and VII-VIII complex (yellow arrow).
jksfn-2023-00073f1.jpg
Table 1.
Offending vessels
Offending vessel (n) Thick arachnoid membrane (n)
Single
 AICA 150 6
 PICA 37 7
 VA 16 2
 BA 2
 Vein 8 2
Complex
 AICA+VA 8
 AICA+BA 4
 AICA+vein 2 2
 PICA+VA 15
 PICA+BA 1
 VA+vein 1

AICA: anterior inferior cerebellar artery, PICA: posterior inferior cerebellar artery, VA: vertebral artery, BA: basilar artery.

Table 2.
Surgical outcomes and complications
Total (n=244) Pre-IOM (n=150) Post-IOM (n=94)
Symptom-free without complications 226 (92.6) 145 (96.7) 81 (86.2)
Re-operation 2 1 1
Occurrence of complications
 Wound problem 3 1 2
 Facial nerve paralysis 5 2 3
 Transient cochlear nerve 1 1
 Permanent cochlear nerve 4 4
 Transient vestibular nerve 1 1
 Lower cranial nerve dysfunction 1 1
 Death 1 1

Values are presented as number (%) or number only. IOM: intraoperative monitoring.

REFERENCES

1. Auger RG, Whisnant JP. Hemifacial spasm in Rochester and Olmsted County, Minnesota, 1960 to 1984. Arch Neurol 1990;47:1233-4
crossref pmid
2. Nilsen B, Le KD, Dietrichs E. Prevalence of hemifacial spasm in Oslo, Norway. Neurology 2004;63:1532-3
crossref pmid
3. Wu Y, Davidson AL, Pan T, Jankovic J. Asian over-representation among patients with hemifacial spasm compared to patients with cranial-cervical dystonia. J Neurol Sci 2010;298:61-3
crossref pmid
4. Poungvarin N, Devahastin V, Viriyavejakul A. Treatment of various movement disorders with botulinum A toxin injection: an experience of 900 patients. J Med Assoc Thai 1995;78:281-8
pmid
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 2010;33:325-34
crossref pmid pdf
6. Tan EK, Chan LL. Young onset hemifacial spasm. Acta Neurol Scand 2006;114:59-62
crossref pmid
7. Miller LE, Miller VM. Safety and effectiveness of microvascular decompression for treatment of hemifacial spasm: a systematic review. Br J Neurosurg 2012;26:438-44
crossref pmid
8. Yaltho TC, Jankovic J. The many faces of hemifacial spasm: differential diagnosis of unilateral facial spasms. Mov Disord 2011;26:1582-92
crossref pmid pdf
9. Bandini F, Mazzella L. Gabapentin as treatment for hemifacial spasm. Eur Neurol 1999;42:49-51
crossref pmid pdf
10. Defazio G, Abbruzzese G, Girlanda P, Vacca L, Currà A, De Salvia R, et al. Botulinum toxin A treatment for primary hemifacial spasm: a 10-year multicenter study. Arch Neurol 2002;59:418-20
crossref pmid
11. Costa J, Espírito-Santo C, Borges A, Ferreira JJ, Coelho M, Moore P, et al. Botulinum toxin type A therapy for hemifacial spasm. Cochrane Database Syst Rev 2005;2005:CD004899
crossref pmid pmc
12. Jost WH, Kohl A. Botulinum toxin: evidence-based medicine criteria in blepharospasm and hemifacial spasm. J Neurol 2001;248 Suppl 1:21-4
crossref pmid pdf
13. Frei K, Truong DD, Dressler D. Botulinum toxin therapy of hemifacial spasm: comparing different therapeutic preparations. Eur J Neurol 2006;13 Suppl 1:30-5
crossref pmid
14. Samii M, Günther T, Iaconetta G, Muehling M, Vorkapic P, Samii A. Microvascular decompression to treat hemifacial spasm: long-term results for a consecutive series of 143 patients. Neurosurgery 2002;50:712-8
crossref pmid pdf
15. Hanakita J, Kondo A. Serious complications of microvascular decompression operations for trigeminal neuralgia and hemifacial spasm. Neurosurgery 1988;22:348-52
crossref pmid
16. Sindou M, Fobé JL, Ciriano D, Fischer C. Hearing prognosis and intraoperative guidance of brainstem auditory evoked potential in microvascular decompression. Laryngoscope 1992;102:678-82
crossref pmid
17.  Jannetta PJ. Cranial rhizopathies. In: Youmans JR (ed). Neurological Surgery. 3rd ed. WB Saunders, 1990
18. Lovely TJ, Getch CC, Jannetta PJ. Delayed facial weakness after microvascular decompression of cranial nerve VII. Surg Neurol 1998;50:449-52
crossref pmid
19. Rhee DJ, Kong DS, Park K, Lee JA. Frequency and prognosis of delayed facial palsy after microvascular decompression for hemifacial spasm. Acta Neurochir (Wien) 2006;148:839-43
crossref pmid pdf
20. Lee MH, Jee TK, Lee JA, Park K. Postoperative complications of microvascular decompression for hemifacial spasm: lessons from experience of 2040 cases. Neurosurg Rev 2016;39:151-8
crossref pmid pdf
21. 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 2001;15:496-9
crossref pmid
22. 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) 2012;154:773-8
crossref pmid pdf
23. Iijima K, Horiguchi K, Yoshimoto Y. Microvascular decompression of the root emerging zone for hemifacial spasm: evaluation by fusion magnetic resonance imaging and technical considerations. Acta Neurochir (Wien) 2013;155:855-62
crossref pmid pdf
24. El Refaee E, Langner S, Baldauf J, Matthes M, Kirsch M, Schroeder HW. Value of 3-dimensional high-resolution magnetic resonance imaging in detecting the offending vessel in hemifacial spasm: comparison with intraoperative high definition endoscopic visualization. Neurosurgery 2013;73:58-67
crossref pmid
25. 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 2010;67:1581-8
crossref pdf
26. Mooij JJ, Mustafa MK, van Weerden TW. Hemifacial spasm: intraoperative electromyographic monitoring as a guide for microvascular decompression. Neurosurgery 2001;49:1365-70
crossref pmid pdf
27. Møller AR, Jannetta PJ. Microvascular decompression in hemifacial spasm: intraoperative electrophysiological observations. Neurosurgery 1985;16:612-8
crossref pmid pdf
28. Huang BR, Chang CN, Hsu JC. Intraoperative electrophysiological monitoring in microvascular decompression for hemifacial spasm. J Clin Neurosci 2009;16:209-13
crossref pmid
29. 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 2008;15:1335-9
crossref pmid
30. 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) 2001;143:365-8
crossref pmid pdf
31. 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 2009;80:1375-80
crossref pmid
32. 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 2011;28:56-66
crossref pmid
33. 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) 2014;54:474-82
crossref pmid
34. 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 2014;75:198-203
crossref pmid pmc
35. Wei Y, Yang W, Zhao W, Pu C, Li N, Cai Y, et al. Microvascular decompression for hemifacial spasm: can intraoperative lateral spread response monitoring improve surgical efficacy? J Neurosurg 2018;128:885-90
crossref pmid
36. 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 2009;27:E10
crossref pmc
37. 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 1997;86:654-61
crossref pmid
38. Møller AR. The cranial nerve vascular compression syndrome: II. A review of pathophysiology. Acta Neurochir (Wien) 1991;113:24-30
crossref pmid pdf
39. Fernández-Conejero I, Ulkatan S, Sen C, Deletis V. Intra-operative neurophysiology during microvascular decompression for hemifacial spasm. Clin Neurophysiol 2012;123:78-83
crossref pmid


ABOUT
BROWSE ARTICLES
EDITORIAL POLICY
FOR CONTRIBUTORS
Editorial Office
Department of Neurosurgery, Yonsei University College of Medicine
50 Yonsei-ro, Seodaemun-gu, Seoul 03722, Korea
Tel: +82-2-2228-2150    Fax: +82-2-393-9979    E-mail: changws@yonsei.ac.kr / changws0716@yuhs.ac                

Copyright © 2024 The Korean Society of Stereotactic and Functional Neurosurgery.

Developed in M2PI

Close layer
prev next