Microvascular decompression for hemifacial spasm outcome

Microvascular decompression for hemifacial spasm outcome

Microvascular decompression is an effective treatment for hemifacial spasm. Given that postoperative delayed cure was unavoidable, even with accurate identification of the offending vessel and sufficient decompression of the root exit zone, the delayed cure should be considered in patients undergoing reoperation due to lack of remission or relapse after the operation. Additionally, the timing of efficacy assessments should be delayed 1).

The definitive treatment for hemifacial spasm is microvascular decompression (MVD), which cures the disease in 85% to 95% of patients according to reported series. In expert hands, the MVD procedure can be done with relatively low morbidity.

Post-operatively, there may be episodes of mild HFS, however they usually begin to diminish 2–3 days following MVD. Severe spasm that does not abate suggests failure to achieve adequate decompression, and reoperation should be considered.

Surgical results of MVD depends on the duration of symptoms (shorter duration has better prognosis) as well as on the age of the patient (elderly patients do less well). Complete resolution of HFS occurred in 44 (81%) of 54 patients undergoing MVD, however, 6 of these patients had relapse 2). 5 patients (9%) had partial improvement, and 5 (9%) had no relief.


Complete resolution of spasm occurs in ≈ 85–93% 3) 4) 5) 6) 7). Spasm is diminished in 9%, and unchanged in 6% 8). Of 29 patients with complete relief, 25 (86%) had immediate post-op resolution, and the remaining 4 patients took from 3 mos to 3 yrs to attain quiescence.

Recurrence

References

1)

Li MW, Jiang XF, Wu M, He F, Niu C. Clinical Research on Delayed Cure after Microvascular Decompression for Hemifacial Spasm. J Neurol Surg A Cent Eur Neurosurg. 2019 Oct 10. doi: 10.1055/s-0039-1698461. [Epub ahead of print] PubMed PMID: 31600810.
2)

Auger RG, Peipgras DG, Laws ER. Hemifacial Spasm: Results of Microvascular Decompression of the Facial Nerve in 54 Patients. Mayo Clin Proc. 1986; 61:640–644
3)

Rhoton AL. Comment on Payner T D and Tew J M: Recurren ce of Hemifacial Spasm After Microvascular Decompression. Neurosurgery. 1996; 38
4)

Jannetta PJ. Neurovascular Compression in Cranial Nerve and Systemic Disease. Ann Surg. 1980; 192:518–525
5)

Loeser JD, Chen J. Hemifacial Spasm: Treatment by Microsurgical Facial Nerve Decompression. Neurosurgery. 1983; 13:141–146
6)

Huang CI, Chen IH, Lee LS. Microvascular Decompression for Hemifacial Spasm: Analyses of Operative Findings and Results in 310 Patients. Neurosurgery. 1992; 30:53–57
7) , 8)

Payner TD, Tew JM. Recurrence of Hemifacial Spasm After Microvascular Decompression. Neurosurgery. 1996; 38:686–691

Hemifacial spasm etiology

Hemifacial spasm etiology

Although classical hemifacial spasm (HFS) has been attributed to an atraumatic pulsatile vascular compression around the root exit zone (REZ) of the facial nerve, rare tumor-related HFS associated with meningiomas, epidermoid tumors, lipomas, and schwannomas in the cerebellopontine angle have been reported. The exact mechanism and the necessity of microvascular decompression for tumor-induced HFS is not clear, especially for vestibular schwannomas.

In clinical pediatric neurosurgery practice, fourth ventricle tumor and cerebellar tumors are not rare. However, reports of secondary refractory hemifacial spasm are very rare. No report is currently available on the treatment of hemifacial spasm secondary to fourth ventricle and cerebellar tumors in China. Zamponi et al. [Childs Nerv Syst 2011 Jun;27(6):1001-5] reported that these lesions can occur in neonates and infants, and surgical resection is effective 1).


Imaging data of 341 patients with a HFS who underwent microvascular decompression were reviewed retrospectively and compared with 360 controls. The hemodynamics of typical anatomical variations of the vertebral artery (VA) were analyzed using computational fluid dynamics (CFD) software.

Asymmetry of the left and right VAs was prevalent, and the left VA was the most dominant VA. A dominant VA was more prevalent in the HFS group than in the control group (p=0.026). A Left HFS had a significantly higher proportion of a left dominant VA, and a right HFS had a significantly higher proportion of right dominant VA (p<0.001). CFD models showed that angulation and tortuosity of vessels caused remarkable pressure difference between vascular walls of opposite sides. Dynamic clinical observations showed the mode of vessel transposition coincided with biomechanical characteristics.

Anatomical variations and hemodynamics of the vertebrobasilar arterial system are likely to contribute to vascular compression formation in a HFS2).


Liu et al. retrospectively analyzed 10 patients with vestibular schwannomas out of 5218 cases of hemifacial spasm between 2004 and 2014.

Hemifacial spasm occurred ipsilateral to the vestibular schwannoma in 9 patients and contralateral to the lesion in 1 patient. The mean follow-up period was 86 months (range, 22-140 months). All patients underwent surgery for resection of the vestibular schwannoma. Following the principle of neurovascular compression, offending vessels were found in 7 patients, no offending vessels in 2 patients, and a tumor with the displacement of brain stem contributing to contralateral facial nerve compression in 1 patient. HFS was relieved immediately postoperatively in 9 patients, whereas it improved gradually and then resolved after one month in one patient with a contralateral vestibular schwannoma.

For HFS induced by vestibular schwannomas in this study, the majority of cases are caused by a combination of tumor and vascular co-compression at the REZ. Surgical intervention resulted in resolution of symptoms. For HFS with ipsilateral vestibular schwannoma, exploration of the facial nerve root for vascular compression should be performed routinely after tumor resection. It is critical to check that no vessel is contact with the entire nerve root 3).


During the period from October 1984 to October 2008, Han et al. treated 6,910 HFS patients using a microsurgical procedure. Of these HFS patients, 55 cases were associated with cerebellopontine angle tumors. A small craniectomy was performed in order to excise the tumor. All tumors were found to compress the root exit zone (REZ) of the facial nerve to different extents, but concomitant vascular compression of the facial nerve was observed in a majority of cases, and microvascular decompression of the facial nerve at REZ was conducted in 43 of 55 patients (78.2%) by displacing the co-compressing vasculature away from the REZ and retaining it using a Teflon pad. Intraoperative findings and postoperative pathological examinations suggested that the tumors were epidermoid cysts, meningiomas, and Schwannomas. Follow-up in 48 of 55 patients for 4-230 months after surgery showed that the clinical symptoms of HFS disappeared in 43 cases, improved in two cases, and recurred in three cases. Ten patients had sequelae associated with the operation. They concluded from this study that the majority of cases of tumor-related HFS are caused by combined tumor and vascular co-compression at the REZ, and tumor removal and microvascular decompression are required in order to relieve the symptoms 4).


Kindling-like hyperactivity of the facial motor nucleus induced by constant stimulation of compressing artery is considered as the predominant mechanism underlying the pathogenesis of Hemifacial spasm (HFS).

Trigeminal neuralgia, hemifacial spasm, vestibulocochlear neuralgia and glossopharyngeal neuralgia represent the most common neurovascular compression syndromes.

In nearly all cases, primary hemifacial spasm is related to arterial compression of the facial nerve at root exit zone (REZ). The offending arterial loops originate from the posterior inferior cerebellar artery (PICA), anterior inferior cerebellar artery (AICA), or vertebrobasilar artery (VB). In as many as 40% of the patients, neurovascular conflicts are multiple. The cross-compression is almost always seen on magnetic resonance imagingcombined with magnetic resonance angiography.


Hemifacial spasm (HFS) associated with type 1 Chiari malformation is particularly uncommon and is limited to isolated case report.

Li et al retrospectively evaluated 13 patients who had simultaneously HFS and type 1 Chiari malformation among 675 HFS patients. Clinical features and radiological findings were collected from each patient and analyzed. All these 13 patients were surgically treated with MVD through retro-mastoid microsurgical approach, and postoperative outcomes were evaluated. A review of literature about this association was also provided. In this study, the frequency of type 1 Chiari malformation in HFS patients was 1.9 %. The clinical profile of this series of patients did not differ from typical form of primary HFS. MVD achieved satisfactory results in 11 patients (85 %) in short- and long-term follow-up. There was no mortality or severe complication occurred postoperatively. Although rare, clinician should be aware of the association of HFS and type 1 Chiari malformation and consider MVD as an effective surgical management 5).

References

1)

Cai Y, Ge M, Qi X, Sun H, Zhang D. Ocular Dyskinesia and Hemifacial Spasm Secondary to Fourth Ventricular Tumor: Report of 4 Cases and Review of the Literature. Pediatr Neurosurg. 2019 Aug 22:1-8. doi: 10.1159/000501915. [Epub ahead of print] PubMed PMID: 31437843.
2)

Wang QP, Yuan Y, Xiong NX, Fu P, Huang T, Yang B, Liu J, Chu X, Zhao HY. Anatomical variation and hemodynamic evolution of vertebrobasilar arterial system may contribute to the development of vascular compression in hemifacial spasm. World Neurosurg. 2018 Dec 26. pii: S1878-8750(18)32897-3. doi: 10.1016/j.wneu.2018.12.074. [Epub ahead of print] PubMed PMID: 30593967.
3)

Liu J, Liu P, Zuo Y, Xu X, Liu H, Du R, Yu Y, Yuan Y. Hemifacial Spasm as Rare Clinical Presentation of Vestibular Schwannomas. World Neurosurg. 2018 Aug;116:e889-e894. doi: 10.1016/j.wneu.2018.05.124. Epub 2018 May 28. PubMed PMID: 29852302.
4)

Han H, Chen G, Zuo H. Microsurgical treatment for 55 patients with hemifacial spasm due to cerebellopontine angle tumors. Neurosurg Rev. 2010 Jul;33(3):335-9; discussion 339-40. doi: 10.1007/s10143-010-0250-0. Epub 2010 Mar 9. PubMed PMID: 20217169.
5)

Li N, Zhao WG, Pu CH, Yang WL. Hemifacial spasm associated with type 1 Chiari malformation: a retrospective study of 13 cases. Neurosurg Rev. 2016 Jul 15. [Epub ahead of print] PubMed PMID: 27422274.

Recurrent hemifacial spasm after microvascular decompression

Recurrent hemifacial spasm after microvascular decompression

Microvascular decompression (MVD) is a highly effective treatment for hemifacial spasm (HFS), but even if the root exit zone (REZ) from the brainstem is adequately decompressed, residual spasms after surgery or early reappearance of spasms are not uncommon 1) 2) 3) 4) 5)

Return of symptoms after a period of complete resolution of hemifacial spasm occurs in up to 10% of patients, 86% of recurrences happen within 2 yrs of surgery, and the risk of developing recurrence after 2 yrs of post-op relief is only ≈ 1% 6).


Among more than 2500 patients who underwent microvascular decompression for hemifacial spasm, 23 patients received a second MVD in the Kyung Hee University Hospital from January 2002 to December 2017. Three-dimensional time of flight magnetic resonance angiography and reconstructed imaging were used to identify the culprit vessel and its conflict upon root exit zone (REZ) of the facial nerve. They reviewed patients’ medical records and operation videos to identify the missing points of the first surgery.

8 patients had incomplete decompression, such as single-vessel decompression of multiple offending vessels. Teflon was not detected at the REZ, but was found in other locations in 12 patients. Three patients had severe adhesion with previous Teflon around the REZ. Nineteen patients had excellent surgical outcomes at immediate postoperative evaluation; 20 patients showed spasm disappearance at 1 year after surgery and 3 patients showed persistent symptoms. Neuro-vascular contacts around REZ of facial nerve were revealed on MRI of incomplete decompression and Teflon malposition patient groups. There were no clear neuro-vascular contacts in the patients with severe Teflon adhesion.

The decision on secondary MVD for persistent or recurrent spasm is troubling. However, if the neurovascular contact was observed in the MRI of the patient and there were offending vessels, the surgical outcome might be favorable 7).

References

1)

Fukushima T: Microvascular decompression for hemifacial spasm: results in 2890 cases, in Carter LP, Spetzler RF, editors. (eds): Neurovascular Surgery. New York, McGraw-Hill, 1995, pp 1133–1145
2)

Huang CI, Chen IH, Lee LS: Microvascular decompression for hemifacial spasm: analyses of operative findings and results in 310 patients. Neurosurgery 30: 53– 56; discussion 56–57, 1992.
3)

Ishikawa M, Nakanishi T, Takamiya Y, Namiki J: Delayed resolution of residual hemifacial spasm after microvascular decompression operations. Neurosurgery 49: 847– 854; discussion 854–856, 2001.
4)

Li CS: Varied patterns of postoperative course of disappearance of hemifacial spasm after microvascular decompression. Acta Neurochir (Wien) 147: 617– 620; discussion 620, 2005.
5)

Shin JC, Chung UH, Kim YC, Park CI: Prospective study of microvascular decompression in hemifacial spasm. Neurosurgery 40: 730– 734; discussion 734–735, 1997.
6)

Payner TD, Tew JM. Recurrence of Hemifacial Spasm After Microvascular Decompression. Neurosurgery. 1996; 38:686–691
7)

Park CK, Lee SH, Park BJ. Surgical Outcomes of Revision Microvascular Decompression for Persistent or Recurrent Hemifacial Spasm after Surgery: Analysis of radiological and intraoperative findings. World Neurosurg. 2019 Aug 2. pii: S1878-8750(19)32107-2. doi: 10.1016/j.wneu.2019.07.191. [Epub ahead of print] PubMed PMID: 31382068.
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