Hemifacial Spam: Endoscopic Assistance in Facial Nerve Decompression With Lateral Spread Response Corroboration: 2-Dimensional Operative Video

2020 ◽  
Author(s):  
Cameron J Brimley ◽  
Raghuram Sampath

Abstract This video depicts the case of a 48-yr-old female with 3 yr of progressive left hemifacial spasm (HFS) refractory to medication. Magnetic resonance imaging showed a large anterior inferior cerebellar artery (AICA) and also a labyrinthine artery loop around the facial nerve (FN) root exit zone. A large bony eminence was also noted in the superior and lateral aspects of the porous acousticus (PA). She preferred surgery if “cure” was possible in lieu of Botox injections. A left retro sigmoid craniotomy was performed with brainstem auditory evoked responses (BAERs) and FN monitoring along with lateral spread response (LSR) assessment. The large bony prominence was drilled in its lateral aspect. Despite this, visualization was still limited and therefore we utilized a 30-degree-angled endoscope to observe the vessels caudal and cranial to the FN. This view prompted us to then drill further at the PA to decompress the FN as well as mobilize the labyrinthine artery away from the nerve. The LSR showed a dramatic improvement when FN decompression was accomplished, and then a further improvement with arterial mobilization and Teflon pledget placement. The BAERS remained at baseline throughout. FN function and hearing were intact on postoperative clinical assessment. Her symptomatic improvement was recorded at 12 mo after surgery. This video illustrates a more complex case of microvascular decompression with skull base concepts and techniques. The patient provided consent for the procedure and use of her images and operative video for publication.

2019 ◽  
Vol 80 (S 03) ◽  
pp. S312-S313
Author(s):  
James K. Liu ◽  
Vincent N. Dodson

In this operative video atlas manuscript, the authors demonstrate the operative nuances and surgical technique for endoscopic-assisted microvascular decompression of a large ectatic vertebral artery causing hemifacial spasm. A retrosigmoid approach was performed and a large ectatic vertebral artery was transposed away from the root exit zone of cranial nerve VII (Fig. 1). The lateral spread response disappeared, signifying adequate decompression of the facial nerve (Fig. 2). The use of endoscopic-assistance during the microsurgical decompression was very useful to confirm the origin and also the resolution of neurovascular conflict. Postoperatively, the patient experienced immediate resolution of hemifacial spasm with normal facial nerve and hearing function. Written consent was obtained from the patient to publish videos, photographs, and images from the surgery.The link to the video can be found at: https://youtu.be/RlMz44uCDCw.


2018 ◽  
Vol 80 (S 03) ◽  
pp. S294-S295
Author(s):  
Yu-Wen Cheng ◽  
Chun-Yu Cheng ◽  
Zeeshan Qazi ◽  
Laligam N. Sekhar

This 68-year-old woman presented with repeated episodes of bilateral hemifacial spasm with headache for 5 years and with recent progression of left sided symptoms. Preoperative imaging showed a left sided tentorial meningioma with brain stem and cerebellar compression. Left facial nerve was compressed by the vertebral artery (VA) and the right facial nerve by the anterior inferior cerebellar artery (AICA). This patient underwent left side retrosigmoid craniotomy and mastoidectomy. The cisterna magna was drained to relax the brain. The tumor was very firm, attached to the tentorium and had medial and lateral lobules. The superior cerebellar artery was adherent to the lateral lobule of the tumor and dissected away. The tumor was detached from its tentorial base; we first removed the lateral lobule. Following this, the medial lobule was also completely dissected and removed. The root exit zone of cranial nerve (CN) VII was dissected and exposed. The compression was caused both by a prominent VA and AICA. Initially, the several pieces of Teflon felt were placed for the decompression. Then vertebropexy was performed by using 8–0 nylon suture placed through the VA media to the clival dura. A further piece of Teflon felt was placed between cerebellopontine angle region and AICA. Her hemifacial spasm resolved postoperatively, and she discharged home 1 week later. Postoperative imaging showed complete tumor removal and decompression of left CN VII. This video shows the complex surgery of microsurgical resection of a large tentorial meningioma and microvascular decompression with a vertebropexy procedure.The link to the video can be found at: https://youtu.be/N5aHN9CRJeM.


2008 ◽  
Vol 109 (3) ◽  
pp. 416-420 ◽  
Author(s):  
Mauricio Campos-Benitez ◽  
Anthony M. Kaufmann

Object It is generally accepted that hemifacial spasm (HFS) is caused by pulsatile vascular compression upon the facial nerve root exit zone. This 2–3 mm area, considered synonymous with the Obersteiner–Redlich zone, is a transition zone (TZ) between central and peripheral axonal myelination that is situated at the nerve's detachment from the pons. Further proximally, however, the facial nerve is exposed on the pontine surface and emerges from the pontomedullary sulcus. The incidence and significance of neurovascular compression upon these different segments of the facial nerve in patients with HFS has not been previously reported. Methods The nature of neurovascular compression was determined in 115 consecutive patients undergoing their first microvascular decompression (MVD) for HFS. The location of neurovascular compression was categorized to 1 of 4 anatomical portions of the facial nerve: RExP = root exit point; AS = attached segment; RDP = root detachment point that corresponds to the TZ; and CP = distal cisternal portion. The severity of compression was defined as follows: mild = contact without indentation of nerve; moderate = indentation; and severe = deviation of the nerve course. Success in alleviating HFS was documented by telephone interview conducted at least 24 months following MVD surgery. Results Neurovascular compression was found in all patients, and the main culprit was the anterior inferior cerebellar artery (in 43%), posterior inferior cerebellar artery (in 31%), vertebral artery (in 23%), or a large vein (in 3%). Multiple compressing vessels were found in 38% of cases. The primary culprit location was at RExP in 10%, AS in 64%, RDP in 22%, and CP in 3%. The severity of compression was mild in 27%, moderate in 61%, and severe in 12%. Failure to alleviate HFS occurred in 9 cases, and was not related to compression location, severity, or vessel type. Conclusions The authors observed that culprit neurovascular compression was present in all cases of HFS, but situated at the RDP or Obersteiner–Redlich zone in only one-quarter of cases and rarely on the more distal facial nerve root. Since the majority of culprit compression was found more proximally on the pontine surface or even pontomedullary sulcus origin of the facial nerve, these areas must be effectively visualized to achieve consistent success in performing MVD for HFS.


2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Byung-chul Son ◽  
Hak-cheol Ko ◽  
Jin-gyu Choi

Although primary hemifacial spasm (HFS) is mostly related to a vascular compression of the facial nerve at its root exit zone (REZ), its occurrence in association with distal, cisternal portion has been repeatedly reported during the last two decades. We report two patients with typical HFS caused by distal neurovascular compression, in which the spasm was successfully treated with microvascular decompression (MVD). Vascular compression of distal, cisternal portion of the facial nerve was identified preoperatively in the magnetic resonance imaging (MRI). It was confirmed again with intraoperative findings of compression of cisternal portion of the facial nerve by the meatal loop of the anterior inferior cerebellar artery (AICA) and absence of any offending vessel in the REZ of the facial nerve. Immediate disappearance of lateral spread response (LSR) after decompression and resolution of spasm after the operation again validated that HFS in the current patients originated from the vascular compression of distal, cisternal portion of the facial nerves. According to our literature review of 64 patients with HFS caused by distal neurovascular compression, distal compression can be classified by pure distal neurovascular compression (31 cases, 48.4%) and double compression (both distal segment and the REZ of the facial nerves, 33 cases [51.6%]) according to the presence or absence of simultaneous offender in the REZ. Eighty-four percent of 64 identified distal offenders were the AICA, especially its meatal and postmeatal segments. Before awareness of distal neurovascular compression causing HFS and sophisticated MRI imaging (before 2000), the rate of reoperation was high (58%). Preoperative MRI and intraoperative monitoring of LSR seems to be an essential element in determination of real offending vessel in MVD caused by distal offender.


1987 ◽  
Vol 66 (5) ◽  
pp. 681-685 ◽  
Author(s):  
Aage R. Møller ◽  
Peter J. Jannetta

✓ Facial electromyographic (EMG) responses were monitored intraoperatively in 67 patients with hemifacial spasm who were operated on consecutively by microvascular decompression of the facial nerve near its exit from the brain stem. At the beginning of the operation, electrical stimulation of the temporal or the zygomatic branch of the facial nerve gave rise to a burst of EMG activity (autoexcitation) and spontaneous EMG activity (spasm) that could be recorded from the mentalis muscle in all patients. In some patients, the spontaneous activity and the autoexcitation disappeared after the dura was incised or when the arachnoid was opened, but stimulation of the temporal branch of the facial nerve caused electrically recordable activity in the mentalis muscle (lateral spread) with a latency of about 10 msec that lasted until the facial nerve was decompressed in all but one patient, in whom it disappeared when the arachnoidal membrane was opened. When the facial nerve was decompressed, this lateral spread of antidromic activity disappeared totally in 44 cases, in 16 it was much reduced, and in seven it was present at the end of the operation at about the same strength as before craniectomy. In four of these last seven patients there was still very little improvement of the spasm 2 to 6 months after the operation; these four patients underwent reoperation. In two of the remaining three patients, the spasm was absent at the 3- and 7-month follow-up examination, respectively, and one had mild spasm. Of the 16 patients in whom the lateral spread response was decreased as a result of the decompression but was still present at the end of the operation, 14 had no spasm and two underwent reoperation and had mild spasm at the last examination. Of the 44 patients in whom the lateral spread response disappeared totally, 42 were free from spasm and two had occasional mild spasm at 6 and 13 months, respectively, after the operation. Monitoring of facial EMG responses is now used routinely by the authors during operations to relieve hemifacial spasm, and is performed simultaneously with monitoring of auditory function for the purpose of preserving hearing. The usefulness of monitoring both brain-stem auditory evoked potentials recorded from electrodes placed on the scalp and compound action potentials recorded directly from the eighth cranial nerve is evaluated.


Life ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 40
Author(s):  
Ryan Wing-Yuk Chan ◽  
Yung-Hsiao Chiang ◽  
Yi-Yu Chen ◽  
Yi-Chen Chen ◽  
Jiann-Her Lin ◽  
...  

Recent studies have shown the evocation of lateral spread response (LSR) due to the compression of the facial nerve in hemifacial spasm (HFS). Intraoperative monitoring (IOM) of LSR could help locate neurovascular conflicts and confirm adequate micro-vascular decompression (MVD) while treatment of hemifacial spasm (HFS). However, studies on early LSR loss before decompression in HFS surgery are sparse, indicating the need to understand various perceptions on it. Therefore, we retrospectively analyzed 50 adult HFS patients who underwent MVD during the period of September 2018–June 2021. We employed IOM combining traditional LSR (tLSR) and dual LSR (dLSR). One patient was excluded owing to the lack of LSR induction throughout the surgery, while 49 were divided into groups A (n = 14) and B (n = 35), designated as with or without early LSR loss groups, respectively, and offending vessels were analyzed. The mean age of group A patients was significantly younger (47.8 ± 8.6) than that of group B (53.9 ± 10.6) (p = 0.0393). The significant predominating offending vessel in group A was the anterior inferior cerebellar artery (AICA, 78.57%). However, group B included those with AICA (28.57%), posterior inferior cerebellar artery (PICA, 22.86%), vertebral artery (VA) involved (25.71%), and combined AICA and PICA (22.86%). Group B exhibited poorer clinical outcomes with more complications. Conclusively, early LSR loss might occur in the younger population, possibly due to the AICA offending vessel. The compression severity of offending vessels may determine the occurrence of early LSR loss.


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