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Fully Endoscopic vascular decompression of the facial nerve for hemifacial spasm
By Joseph B. Eby, M.D., Sung Tae Cha, M.D., Hrayr K. Shahinian, M.D.

Abstract

Hemifacial spasm is an uncommon disorder manifesting as a unilateral, involuntary, sporadic contraction of the musculature innervated by the seventh cranial nerve. Although debated, the etiology of hemifacial spasm is generally accepted as compression of the facial nerve by vessels of the posterior circulation. Early surgical techniques were ineffective and fraught with morbidity. Over the past 25 years microvascular decompression surgery has allowed for the safe and effective treatment of hemifacial spasm. Recent reports combining microsurgical and endoscopic techniques have documented the advantages of the endoscope in exposing the anatomy of this region. Enhanced visualization allows for a less traumatic dissection, and enhances the surgeon's ability to locate nerve-vessel conflicts often difficult to identify with the limited view of the microscope. This article reviews the history of hemifacial spasm and describes the first 3 cases of fully endoscopic vascular decompression for hemifacial spasm, emphasizing the advantages of this novel surgical approach.

Keywords
Endoscopy, hemifacial spasm, vascular decompression.

Introduction

Hemifacial spasm (HFS) is a commonly described as a unilateral, involuntary, paroxysmal contraction of the musculature innervated by the seventh cranial nerve. The incidence of HFS is approximately 0.8 per 100,000 persons.1 Fukushima in 1995 published one of the largest series of patients (2890) undergoing decompressive surgery for HFS.2 This series demonstrated a preponderance of adult females with a F:M ratio of greater than 2:1, and a mean age of 51.2 Crucial to understanding and treating HFS is obtaining a proper diagnosis. The differential diagnosis of HFS includes but is not limited to; Essential Blepharospasm, Facial Myokymia, Focal Seizures, Tardive Dyskinesia, Meige's syndrome, Synkineisis, and Tics, a full discussion of which is beyond the scope of this paper.3-5

Beginning with some of the earliest descriptions of HFS by Shultze in 1875 and Gowers in 1899, the etiology of hemifacial spasm and location of the abnormality have been debated for more than a century.2-4 Oppenheim in 1911 as well as Ehni and Woltman in 1945 reported on patients with hemifacial spasm who sustained contralateral strokes. These patients were left with a facial droop, which did not relieve the spasm; the researchers therefore concluded that the facial nerve nucleus was not the origin of this disorder.3 ,6 Surgical treatment for HFS in the early 20th century included neurolysis, stretching the facial nerve, and high-pressure irrigation of the nerve with lactate ringers solution. While medical regimens of that time involved injection of the nerve with ethanol, electrical stimulation, application toxic compounds (nitrate of silver, zinc, arsenic, bromides) as well as medications such as Dilantin or other anticonvulsants.2-4, 6-8

Watts, McKillop and Lelli in the 1930's and Sutherland in the 1940's studied cadaveric anatomy of the posterior circulation at the cerebellopontine angle, its intimate association, and occasional incidental compression of the cranial nerves.2, 4, 9, 10 Dandy first hypothesized that compression of the trigeminal nerve was the cause of trigeminal neuralgia in 1934.11 Then in 1945 Revilla and Dandy documented their experience with 160 patients having tumors of the cerebellopontine angle and described HFS in 6 of these patients.12 Ehni and Woltman in 1945 analyzed 106 cases of HFS and concluded, that the facial nerve abnormality must lye between the facial nucleus and the stylomastoid foramen.6 A report by Campbell and Keedy in 1947 presented two cases of HFS resulting from an aneurysm of the vertebral artery at the cerebellopontine angle, providing additional evidence that vascular compression of the facial nerve may indeed be the cause of HFS.13

In 1960 Gardner published a case report of a patient with HFS treated by vascular decompression, and demonstrating an excellent result with 5-year follow up.14 Then in 1962 reporting on a series of 19 patients operated on for HFS Gardner noted that aneurysms, AVMs, or ectatic vessels were intimately associated with the facial nerve in the majority of cases.8 From this he concluded: "hemifacial spasm is the expression of a reversible pathologic state commonly (in 13 of 19 cases) produced by mild, long continuing compression of the 7th cranial nerve by a vascular structure in the cerebellopontine angle".8 Treatment of HFS at this time was primarily medical or involved neurolysis.2-4, 6, 7 Gardner's excellent results in his first study, showing immediate relief in 12 patients, delayed relief in 5, and 2 failures (where nerve was not compressed by any visible structure) supported his opinion that vascular compression was the likely cause of HFS.2, 8, 15 Gardner's early success however, was met with significant operative complications in later reports; as a result his decompression operation lost much of its early appeal.2

Additional advances in understanding the etiology and improving the treatment of HFS did not occur until the mid-seventies.16, 17 Jannetta's 1977 article documented 47 cases of HFS all decompressed using the operating microscope, and illustrated nerve-vessel conflicts (or cholesteatoma in one case) to be located at the root exit zone (REZ) of the facial nerve in all cases.17 The REZ is where the central glial axonal insulation of the nerve ends and the peripheral axonal myelination begins. Biopsies of the REZ reported by Ruby and Jannetta demonstrated degeneration of axons, denuded axis cylinder and interrupted myelin.18 Janneta's results strengthened the theory that vascular compression was the primary cause of HFS, and proposed a specific region of the facial nerve (REZ) where the effects of longstanding compression results in nerve dysfunction. Moreover, this paper demonstrated that by using the operating microscope to guide decompression of the nerve, a safer and more complete operation could be performed.16, 17

Three theories exist to explain the facial nerve dysfunction found in HFS. Gardner first proposed ephaptic transmission in 1962.19 ,20 Work by Digre and Corbett, as well as Nielsen and Moller support this theory, which proposed that normal electrical activity can cross from one demyelinated neuron to another resulting in a false synapse. The second theory involves abnormal axonal activity at the REZ secondary to compressive damage/demyelination. The third theory or "Kindling theory" involves increased excitability of the facial nerve nucleus due to feedback from a damaged facial nerve.3-5, 21-23

The mainstay of medical therapy for HFS in the 21st century involves injection of the muscle with botulinum toxin, while additional treatments include the use of anticonvulsants such as Carbamazepine or Dilantin.3, 4

In the past 25 years following the introduction of the operating microscope, ample evidence from several large series reports has reinforced the position that compression of the facial nerve by ectatic vessels of the posterior fossa is the principle cause of HFS.1-5, 8, 15-18, 22, 24-41 Overall, microvascular decompression yields an "excellent result" (complete resolution of symptoms) for 70-95% of patients undergoing this procedure with minimal morbidity.1-5, 17, 24-32, 35-38, 40-42 The dramatic improvement in symptoms and minimal complications have led some authors to claim that HFS is primarily a surgical disease, and as such recommend early operative decompression.2 ,20 However, this procedure is not without its limitations, as several reports have documented the failures, recurrences, and complications related to microscopic decompression.42-47

Recently, some publications have documented combined microscopic and endoscopic approach to vascular decompression.33 Additionally, several papers and an anatomic atlas have also described the endoscopic anatomy of the posterior fossa.33, 34, 48, 49 However, no published reports have documented a completely endoscopic approach to vascular decompression of the facial nerve for hemifacial spasm.

In this paper we present three cases of patients suffering from hemifacial spasm who underwent a fully endoscopic vascular decompression of the facial nerve. All patients had full resolution of their symptoms postoperatively.

Case Reports

Prior to performing the procedures, the protocol was reviewed and approved by the hospital's Institutional Review Board Committee, and informed consent to perform fully endoscopic vascular decompression was obtained from each patient.

Case 1

History: 72-year-old female with 6-year history of left hemifacial spasm treated with repeated botulinum toxin injection. The patient presented for definitive therapy, as she was unhappy with the pain of the injections, the temporary period of relief (3- 4 months), as well as the slight facial weakness she experienced secondary to these injections.

Examination/Preoperative Testing: Revealed frequent involuntary contractions of muscles of the left face primarily involving the orbicularis occuli and orbicularis oris muscles.

MRI/MRA T1 sagittal, coronal, and thin-section axial pre- and post- gadolinium images with fat saturation, as well as T2 axial proton density images were obtained. This study demonstrated a tortuous left anterior inferior cerebellar artery in close proximity to the cisternal portion of the left facial nerve.

Operation: A completely endoscopic surgical procedure was performed via a retrosigmoid keyhole approach as outlined in the surgical technique section. At the time of operation, a loop of the anterior inferior cerebellar artery and the main left vertebral artery were both compressing the REZ of the left facial nerve (Figure 1). These structures were separated and Teflon pledgets were placed between the nerve and arteries to provide complete decompression.

Postoperative Course: The patient was taken to the surgical intensive care unit for overnight neurologic monitoring. The following day the patient was transferred to the floor and subsequently discharged home on post-operative day number three. The patient had complete resolution of her facial spasm with no facial weakness. At seven months follow-up, she has had no recurrence of her hemifacial spasm.

Case 2

History: 70 year-old-male with 15 yr history of right-sided hemifacial spasm. The patient had undergone more than 5 botulinum toxin injections over a 4-year period with only a temporary improvement in his symptoms.

Examination/Preoperative Testing: The patient exhibited active involuntary facial twitching, primarily in the orbicularis oculi and right upper cheek. The patient also had mild facial asymmetry, with a mild right lower facial droop thought to be secondary to multiple botulinum injections.

Facial Nerve EMG: Revealed some evidence of deinnervated facial musculature.

MRI: Pre-operatively T1 and T2 parasagittal, coronal, and axial slices in proton-density were obtained. This study demonstrated ectatic vertebral and basilar arteries located in the right cerebellopontine angle.

Operation: A completely endoscopic surgical procedure was performed via a retrosigmoid keyhole approach as outlined in the surgical technique section. At the time of operation a tortuous loop of the anterior inferior cerebellar artery and the main right vertebral artery were both compressing the REZ of the right facial nerve. These structures were separated and Teflon pledgets were placed between the nerve and arteries to provide complete decompression.

Postoperative Course: The patient was transferred to the surgical intensive care unit and extubated within 12 hours following the operation. The patient was neurologically intact but lethargic, a CT scan demonstrated tension pneumocephalus. This was treated with bed rest and Oxygen. Repeat CT within 24 hours showed >50% reduction in the amount of intracranial air. The patient experienced complete resolution of his hemifacial spasm. Immediately after surgery the patient exhibited mild gait instability, and mild nystagmus L>R gaze. Prior to discharge both of these findings improved significantly. The patient remained in the hospital for acute rehabilitation and was discharged home on post-operative day seven. Follow-up at one year reveals no hemifacial spasm, complete resolution of gait disturbance, and no remaining nystagmus or facial weakness.

Case 3

History: 51 year-old female with 6 yr. History of right-sided hemifacial spasm. The patient has had multiple botulinum toxin injections over her six-year history, most of which provide relief for a period of approximately 3 months.

Examination/Preoperative Testing: Revealed multiple paroxysms of right facial spasm involving the entire facial nerve distribution. The patient also demonstrated mild right facial weakness.

Operation: A completely endoscopic surgical procedure was performed via a retrosigmoid keyhole approach as outlined in the surgical technique section. At the time of operation, a complex compression of the facial nerve by the anterior inferior cerebellar artery, which pierced the acousticofacial bundle between the facial nerve and the vestibulocochlear nerve was noted. The AICA was dissected free from the facial nerve, and two three-millimeter Teflon pledgets were placed between them.

Postoperative Course: The patient was taken to the surgical intensive care unit overnight; her hemifacial spasm was completely resolved. The patient was transferred to the floor on post-operative day number one, and discharged on post-operative day three. Immediately after surgery the patient demonstrated grade III-IV facial paresis, which completely resolved by her 4-week follow-up visit. At six months follow-up she reports no recurrence of her hemifacial spasm.

Surgical technique: Under general anesthesia without paralysis, the patient is placed in a park bench position, their head secured in mild flexion to expose the affected mastoid region. Intraoperative facial nerve monitoring is performed in all cases. A 3cm retroauricular scalp incision is made, and the dissection is carried down to the cranium where a 1.5 cm retrosigmoid craniotomy is performed. The dura is incised and CSF is drained allowing the structures of the posterior fossa to fall away without retraction. A 4mm 0 degree rigid endoscope (Karl Storz of America, Culver City, CA) is introduced into the posterior fossa between the posterior aspect of the petrous bone and the cerebellum, and then advanced slowly to visualize the cerebellopontine angle. The acousticofacial bundle is visualized and the facial nerve stimulated and positively identified. Once identified the surrounding vascular structures are surveyed, to identify any nerve-vessel conflicts or other compression on the facial nerve. (In all cases one or more offending vessels were identified) Using microdissection and gentle manipulation the adhesions and compressions on the facial nerve from the vessel(s) are lysed and the nerve and vessel(s) are freed from one another. Following this dissection, a Teflon pledget is placed between the two structures and secured in place with fibrin glue. The dura is re-approximated and sutured providing a watertight closure. The craniotomy is reconstructed using the bone plug, while the soft tissues and skin are re-approximated using sutures. The patient is awoken from general anesthesia, extubated and taken to the surgical intensive care unit for observation.

Results

Each of the above three outlined cases demonstrated one or more nerve-vessel conflicts. Upon relieving the facial nerve compression complete resolution of their hemifacial spasm was achieved. The endoscope was used to perform the vascular decompression in each case. The anatomy of the cerebellopontine angle, and the area of nerve-vessel conflicts were well visualized with the endoscope alone. The improved visualization enhanced the surgeon's ability to perform the surgical dissection and assess the adequacy of the decompression, both of which are often difficult to appreciate using the operating microscope.

Complications of this procedure were limited to mild temporary facial weakness, and one patient who experienced post-operative tension pneumocephalus, which resolved with medical management and time. There were no cases of hearing loss, permanent facial paresis, or other neurological deficits. All patients were discharged within one week following surgery. Follow-up examinations show complete resolution of their hemifacial spasm.

Discussion

Although tumors, bony abnormalities, aneurysms, AVMs, and plaques from Multiple Sclerosis have all been described as causing hemifacial spasm, these abnormalities account for less than ten percent of cases. The overwhelming majority of cases of HFS are due to abnormal compression of the facial nerve by ectatic vessels of the posterior cerebral and/or cerebellar circulation.1-5, 8, 15-18, 22, 24-41

The key aspects of a safe and effective vascular decompression operation for HFS includes optimal visualization of the cerebellopontine angle to identify normal and abnormal anatomic relationships, identification of significant nerve-vessel conflicts, atraumatic dissection and separation of these structures, as well as placement of a permanent barrier to ensure that the compression does not reoccur.

Access to the posterior cranial fossa via a retrosigmoid approach, was first described by Magnan and Bremond in 1974.15 In the late seventies Jannetta introduced the current standard treatment for this disorder involving microscope-assisted vascular decompression.16, 17 The complex anatomy of the posterior fossa, as well as the limited size of the craniotomy makes adequate visualization of the facial nerve using an operating microscope difficult.15, 33, 34, 48, 49 Jannetta, in his initial article describing the use of the operative microscope for vascular decompression pointed out some of the microscope's limitations: "The facial nerve may not be clearly visualized medially at this time because the offending arterial loop, flocculonodular lobe of the cerebellum or choroid plexus of the lateral recess may be in the way."17

The earliest recognized use of endoscopy for surgery of the posterior fossa is in 1917 when Doyen used endoscopes to perform trigeminal root neurectomy.50 Following this early report not much was written about an endoscopic approach to this region. Then in 1993 O‘Donoghue and O'Flynn operating on cadavers documented the anatomy of the cerebellopontine angle, and highlighted the advantages of the endoscope over the operating microscope.48 In this article they comment: " The microscope has distinct limitations: the operator can only visualize objects directly ahead and is unable to see around objects or down narrow, tortuous pathways; therefore, access to the side of disease may need wide exposure and retraction of adjacent structures."48 Retraction injury of the cerebellum or brainstem during decompressive surgery for HFS can be a considerable source of morbidity.44 During our procedures we found the unimpeded view of endoscope provided excellent panoramic views of the posterior fossa, cerebellopontine angle, as well as the root exit zone of the facial nerve, and allowed identification of the nerve-vessel conflicts in all cases without the need for brain retraction.

Magnan in a 1994 article also demonstrated the utility of the endoscope in exposure of the cerebellopontine angle wherein he stated that the endoscope yields, "magnified high resolution images and provides an unobstructed view of all nervous and vascular structures in the area.".34 In 1997 he then utilized the endoscope to assist microscopic vascular decompression of the facial nerve for HFS, and demonstrated an additional 72% accuracy rate in identifying nerve-vessel conflicts.15

Microscopically assisted vascular decompression for HFS is reported to have a mortality rate of 0.2%, and an overall complication rate of approximately 5-25% for temporary dysfunction and 2-10% for permanent neurologic impairment.1-5, 15, 17, 24-32, 35-38, 40-42 Most complications involve auditory or facial nerve dysfunction. The reported rate of auditory nerve impairment is 3-5% for temporary disturbance and 2-3% permanent hearing loss. Facial nerve dysfunction occurs temporarily in approximately 4% of patients, while 1-2% experience permanent facial nerve deficit.1, 2, 4, 17, 26, 27, 31, 32, 35-38, 41 Facial nerve monitoring, as well as the use of brainstem auditory evoked potentials have been shown in to help reduce these major complications.41, 46, 47

Facial nerve monitoring was performed in all of our cases, while brainstem auditory evoked potentials were performed in 2 out of 3 cases. One patient in our group experienced mild temporary facial nerve weakness. There were no cases of hearing loss or permanent facial nerve weakness.

We found the endoscope provided improved visualization of the cerebellopontine angle, and avoided the need for retraction; both factors should reduce the number of complications resulting from dissection in this region.

Hemifacial spasm treated by microscopic decompression has an initial failure rate of approximately 3-5% and a recurrence rate of approximately 10-20%.1-5, 15, 17, 24-32, 35-38, 40-42 Kureshi in a 1998 review of cases of recurrent HFS found 37.5% of patients re-explored were found to have an artery or vein compressing the facial nerve.42 This study also noted an extremely high (75%) complication rate for patients undergoing re-operation for HFS.42 As discussed above several studies have shown that endoscopy identifies a significant number of nerve-vessel conflicts, which are not appreciated using the operating microscope alone.15, 33, 49 Endoscopic identification of the often-obscure areas of nerve compression during the primary operation should lead to improved rates of initial success, and avoid the morbidity of re-exploration for missed neuro-vascular conflicts.

Previous reports have documented the use of endoscopy at the cerebellopontine angle, and have utilized endoscopy as an adjunct to microscopic dissection. The results of the current study demonstrate that the endoscope can be used exclusively to obtain visualization of the neuro-vascular conflicts leading to hemifacial spasm, allowing for safe and complete decompression of the facial nerve. We propose that additional studies involving a larger series of patients will reveal endoscopic vascular decompression of the facial nerve for hemifacial spasm to be a safer, more complete operation, with a lower incidence of complications and recurrence.

Conclusions

Hemifacial spasm is a benign disorder characterized by involuntary, recurrent contraction of the facial musculature on the side of the affected facial nerve. Although an indolent disorder, patients who suffer from HFS bare the emotional trauma of society's negative response to facial disfigurement and therefore seek out definitive medical or surgical treatment.

The prevailing theory as to the cause of HFS is that of vascular compression of the facial nerve. Microsurgical vascular decompression first is the current standard surgical treatment for HFS. Advances in endoscopic technology have allowed for its implementation in the surgical treatment of many disorders. Recent reports utilizing combined microscopic dissection with endoscopic assistance have documented beneficial aspects of the endoscope. However, this report documents the first series of patients treated by fully endoscopic vascular decompression. The early results of our study documents complete resolution of facial spasm, with minimal morbidity and no mortality.

Throughout the past century, hemifacial spasm like many other illnesses has undergone an evolution in both understanding the underlying etiology, as well as vast improvements in the methods of treatment. We believe that routine and exclusive use of the endoscope for vascular decompression of the facial nerve represents a step forward in the safe and effective treatment of hemifacial spasm.

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