scholarly journals Prevalence and severity of neurovascular compression in hemifacial spasm patients

Brain ◽  
2021 ◽  
Author(s):  
Katie S Traylor ◽  
Raymond F Sekula ◽  
Komal Eubanks ◽  
Nallammai Muthiah ◽  
Yue-Fang Chang ◽  
...  
Keyword(s):  
Facial Nerve ◽  
Hemifacial Spasm ◽  
Cranial Nerve ◽  
Odds Ratio ◽  
Imaging Study ◽  
Severe Form ◽  
Vascular Compression ◽  
Neurovascular Compression ◽  
Classical Trigeminal Neuralgia ◽  
Symptomatic Side

Abstract Hemifacial spasm is typically caused by vascular compression of the proximal intracranial facial nerve. Although the prevalence of neurovascular compression has been investigated in a cohort of patients with classical trigeminal neuralgia, the prevalence and severity of neurovascular compression has not been well characterized in patients with hemifacial spasm. We aimed to investigate whether presence and severity of neurovascular compression are correlated to the symptomatic side in patients with hemifacial spasm. All patients in our study were evaluated by a physician who specializes in the management of cranial nerve disorders. Once hemifacial spasm was diagnosed on physical exam, the patient underwent a dedicated cranial nerve protocol magnetic resonance imaging study on a 3 T scanner. Exams were retrospectively reviewed by a neuroradiologist blinded to the symptomatic side. The presence, severity, vessel type, and location of neurovascular compression along the facial nerve was recorded. Neurovascular compression was graded as contact alone (vessel touching the facial nerve) versus deformity (indentation or deviation of the nerve by the culprit vessel). A total of 330 patients with hemifacial spasm were included. The majority (232) were female while the minority (98) were male. The average age was 55.7 years. Neurovascular compression (arterial) was identified on both the symptomatic (97.88%) and asymptomatic sides (38.79%) frequently. Neurovascular compression from an artery along the susceptible/proximal portion of the nerve was much more common on the symptomatic side (96.36%) than on the asymptomatic side (12.73%), odds ratio = 93.00, P < 0.0001. When we assessed severity of arterial compression, the more severe form of neurovascular compression, deformity, was noted on the symptomatic side (70.3%) much more frequently than on the asymptomatic side (1.82%) (odds ratio = 114.00 P < 0.0001). We conclude that neurovascular compression that results in deformity of the susceptible portion of the facial nerve is highly associated with the symptomatic side in hemifacial spasm.

Hemifacial spasm caused by vascular compression of the distal portion of the facial nerve

1998 ◽  
Vol 88 (3) ◽  
pp. 605-609 ◽  
Author(s):  
Hiroshi Ryu ◽  
Seiji Yamamoto ◽  
Kenji Sugiyama ◽  
Kenichi Uemura ◽  
Tsunehiko Miyamoto
Keyword(s):  
Facial Nerve ◽  
Hemifacial Spasm ◽  
Cranial Nerve ◽  
Distal Portion ◽  
Vascular Compression ◽  
Neurovascular Compression ◽  
Content Type ◽  
Seventh Cranial Nerve ◽  
Neurovascular Decompression ◽  
Fine Print

✓ It is generally accepted that hemifacial spasm (HFS) and trigeminal neuralgia are caused by compression of the facial nerve (seventh cranial nerve) or the trigeminal nerve (fifth cranial nerve) at the nerve's root exit (or entry) zone (REZ); thus, neurosurgeons generally perform neurovascular decompression at the REZ. Neurosurgeons tend to ignore vascular compression at distal portions of the seventh cranial nerve, even when found incidentally while performing neurovascular decompression at the REZ of that nerve, because compression of distal portions of the seventh cranial nerve has not been regarded as a cause of HFS. Recently the authors treated seven cases of HFS in which compression of the distal portion of the seventh cranial nerve produced symptoms. The anterior inferior cerebellar artery (AICA) was the offending vessel in five of these cases. Great care must be taken not to stretch the internal auditory arteries during manipulation of the AICA because these small arteries are quite vulnerable to surgical manipulation and the patient may experience hearing loss postoperatively. It must be kept in mind that compression of distal portions of the seventh cranial nerve may be responsible for HFS in cases in which neurovascular compression at the REZ is not confirmed intraoperatively and in cases in which neurovascular decompression at the nerve's REZ does not cure HFS. Surgical procedures for decompression of the distal portion of the seventh cranial nerve as well as decompression at the REZ should be performed when a deep vascular groove is noticed at the distal site of compression of the nerve.

Neurovascular compression findings in hemifacial spasm

2008 ◽  
Vol 109 (3) ◽  
pp. 416-420 ◽  
Author(s):  
Mauricio Campos-Benitez ◽  
Anthony M. Kaufmann
Keyword(s):  
Facial Nerve ◽  
Hemifacial Spasm ◽  
Nerve Root ◽  
Posterior Inferior Cerebellar Artery ◽  
Anterior Inferior Cerebellar Artery ◽  
Vascular Compression ◽  
Neurovascular Compression ◽  
Exit Point ◽  
Root Exit Zone ◽  
Cerebellar Artery

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.

scholarly journals Hemifacial Spasm Caused by Vascular Compression in the Cisternal Portion of the Facial Nerve: Report of Two Cases with Review of the Literature

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Byung-chul Son ◽  
Hak-cheol Ko ◽  
Jin-gyu Choi
Keyword(s):  
Facial Nerve ◽  
Hemifacial Spasm ◽  
Essential Element ◽  
Distal Segment ◽  
Lateral Spread ◽  
Anterior Inferior Cerebellar Artery ◽  
Vascular Compression ◽  
Neurovascular Compression ◽  
Mri Imaging ◽  
Facial Nerves

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.

scholarly journals Hemifacial Spasm and Neurovascular Compression

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Alex Y. Lu ◽  
Jacky T. Yeung ◽  
Jason L. Gerrard ◽  
Elias M. Michaelides ◽  
Raymond F. Sekula ◽  
...  
Keyword(s):  
Facial Nerve ◽  
Hemifacial Spasm ◽  
Nerve Root ◽  
Age Of Onset ◽  
Symptomatic Relief ◽  
Disease Process ◽  
Vascular Compression ◽  
Neurovascular Compression ◽  
Root Entry Zone ◽  
Magnetic Resonance Imaging Mri

Hemifacial spasm (HFS) is characterized by involuntary unilateral contractions of the muscles innervated by the ipsilateral facial nerve, usually starting around the eyes before progressing inferiorly to the cheek, mouth, and neck. Its prevalence is 9.8 per 100,000 persons with an average age of onset of 44 years. The accepted pathophysiology of HFS suggests that it is a disease process of the nerve root entry zone of the facial nerve. HFS can be divided into two types: primary and secondary. Primary HFS is triggered by vascular compression whereas secondary HFS comprises all other causes of facial nerve damage. Clinical examination and imaging modalities such as electromyography (EMG) and magnetic resonance imaging (MRI) are useful to differentiate HFS from other facial movement disorders and for intraoperative planning. The standard medical management for HFS is botulinum neurotoxin (BoNT) injections, which provides low-risk but limited symptomatic relief. The only curative treatment for HFS is microvascular decompression (MVD), a surgical intervention that provides lasting symptomatic relief by reducing compression of the facial nerve root. With a low rate of complications such as hearing loss, MVD remains the treatment of choice for HFS patients as intraoperative technique and monitoring continue to improve.

scholarly journals Hemifacial spasm secondary to middle ear cholesteatoma

2018 ◽  
Vol 97 (6) ◽  
pp. E31-E32
Author(s):  
Maheep Sohal ◽  
Nicholas Karter ◽  
Marc Eisen
Keyword(s):  
Facial Nerve ◽  
Middle Ear ◽  
Hemifacial Spasm ◽  
Final Diagnosis ◽  
Computed Tomographic Angiography ◽  
Vascular Compression ◽  
Computed Tomographic ◽  
Middle Ear Cholesteatoma ◽  
Facial Spasm ◽  
Tomographic Angiography

Hemifacial spasm is a peripheral myoclonus of the VIIth cranial nerve that is characterized by paroxysmal contraction of the muscles of facial expression. It exists in both primary and secondary forms. In rare cases, hemifacial spasm is caused by middle ear pathology. We describe the case of a 90-year-old man with recurrent cholesteatoma and tympanic segment fallopian canal dehiscence manifesting as right-sided hemifacial spasm. His history was significant for a right-sided tympanomastoidectomy for cholesteatoma 6 years earlier. Computed tomographic angiography performed to look for vascular compression of the facial nerve demonstrated a right middle ear opacification. Middle ear exploration revealed a completely dehiscent tympanic segment with cholesteatoma abutting the facial nerve. The overlying keratin debris and matrix were carefully dissected off, and facial nerve function was preserved. The final diagnosis was hemifacial spasm. During 14 months of postoperative follow-up, the patient experienced no further facial spasm.

Classification of neurovascular compression in typical hemifacial spasm: three-dimensional visualization of the facial and the vestibulocochlear nerves

2007 ◽  
Vol 107 (6) ◽  
pp. 1154-1163 ◽  
Author(s):  
Ramin Naraghi ◽  
Levent Tanrikulu ◽  
Regina Troescher-Weber ◽  
Barbara Bischoff ◽  
Martin Hecht ◽  
...  
Keyword(s):  
Mr Imaging ◽  
Facial Nerve ◽  
Volume Rendering ◽  
Hemifacial Spasm ◽  
Three Dimensional ◽  
Neurosurgical Procedures ◽  
Neurovascular Compression ◽  
Direct Volume Rendering ◽  
Vestibulocochlear Nerve ◽  
Cerebellar Artery

Object In this paper, the authors introduce a method of noninvasive anatomical analysis of the facial nerve–vestibulocochlear nerve complex and the depiction of the variable vascular relationships by using 3D volume visualization. With this technique, a detailed spatial representation of the facial and vestibulocochlear nerves was obtained. Patients with hemifacial spasm (HFS) resulting from neurovascular compression (NVC) were examined. Methods A total of 25 patients (13 males and 12 females) with HFS underwent 3D visualization using magnetic resonance (MR) imaging with 3D constructive interference in a steady state (CISS). Each data set was segmented and visualized with respect to the individual neurovascular relationships by direct volume rendering. Segmentation and visualization of the facial and vestibulocochlear nerves were performed with reference to their root exit zone (REZ), as well as proximal and distal segments including corresponding blood vessels. The 3D visualizations were interactively compared with the intraoperative situation during microvascular decompression (MVD) to verify the results with the observed microneurosurgical anatomy. Results Of the 25 patients, 20 underwent MVD (80%). Microvascular details were recorded on the affected and unaffected sides. On the affected sides, the anterior inferior cerebellar artery (AICA) was the most common causative vessel. The posterior inferior cerebellar artery, vertebral artery, internal auditory artery, and veins at the REZ of the facial nerve (the seventh cranial nerve) were also found to cause vascular contacts to the REZ of the facial nerve. In addition to this, the authors identified three distinct types of NVC within the REZ of the facial nerve at the affected sides. The authors analyzed the varying courses of the vessels on the unaffected sides. There were no bilateral clinical symptoms of HFS and no bilateral vascular compression of the REZ of the facial nerve. The authors discovered that the AICA is the most common vessel that interferes with the proximal and distal portions of the facial nerve without any contact between vessels and the REZ of the facial nerve on the unaffected sides. Conclusions Three-dimensional visualization by direct volume rendering of 3D CISS MR imaging data offers the opportunity of noninvasive exploration and anatomical categorization of the facial nerve–vestibulocochlear nerve complex. Furthermore, it proves to be advantageous in establishing the diagnosis and guiding neurosurgical procedures by representing original MR imaging patient data in a 3D fashion. This modality provides an excellent overview of the entire neurovascular relationship of the cerebellopontine angle in each case.

Neurovascular contact plays no role in trigeminal neuralgia secondary to multiple sclerosis

Cephalalgia ◽  
2020 ◽  
pp. 033310242097435
Author(s):  
Navid Noory ◽  
Emil Andonov Smilkov ◽  
Jette Lautrup Frederiksen ◽  
Tone Bruvik Heinskou ◽  
Anne Sofie Schott Andersen ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Trigeminal Neuralgia ◽  
Odds Ratio ◽  
Morphological Changes ◽  
3.0 Tesla ◽  
Classical Trigeminal Neuralgia ◽  
Mri Scans ◽  
Low Prevalence ◽  
Headache Center ◽  
Symptomatic Side

Introduction A demyelinating plaque and neurovascular contact with morphological changes have both been suggested to contribute to the etiology of trigeminal neuralgia secondary to multiple sclerosis (TN-MS). The aim of this study was to confirm or refute whether neurovascular contact with morphological changes is involved in the etiology of TN-MS. Methods We prospectively enrolled consecutive TN-MS patients from the Danish Headache Center. Clinical characteristics were collected systematically. MRI scans were done using a 3.0 Tesla imager and were evaluated by the same experienced blinded neuroradiologist. Results Sixty-three patients were included. Fifty-four patients were included in the MRI analysis. There was a low prevalence of neurovascular contact with morphological changes on both the symptomatic side (6 (14%)) and the asymptomatic side (4 (9%)), p = 0.157. Demyelinating brainstem plaques along the trigeminal afferents were more prevalent on the symptomatic side compared to the asymptomatic side (31 (58%) vs. 12 (22%), p < 0.001). A demyelinating plaque was highly associated with the symptomatic side (odds ratio = 10.6, p = 0.002). Conclusion The primary cause of TN-MS is demyelination along the intrapontine trigeminal afferents. As opposed to classical trigeminal neuralgia, neurovascular contact does not play a role in the etiology of TN-MS. Microvascular decompression should generally not be offered to patients with TN-MS. The study was registered at ClinicalTrials.gov (number NCT04371575)

Vertebral artery pexy for microvascular decompression of the facial nerve in the treatment of hemifacial spasm

2011 ◽  
Vol 114 (6) ◽  
pp. 1800-1804 ◽  
Author(s):  
Manuel Ferreira ◽  
Brian P. Walcott ◽  
Brian V. Nahed ◽  
Laligam N. Sekhar
Keyword(s):  
Facial Nerve ◽  
Vertebral Artery ◽  
Hemifacial Spasm ◽  
Microvascular Decompression ◽  
Cranial Nerve ◽  
Anterior Inferior Cerebellar Artery ◽  
Careful Study ◽  
Venous Compression ◽  
Select Group ◽  
Far Lateral Approach

Object Hemifacial spasm (HFS) is caused by arterial or venous compression of cranial nerve VII at its root exit zone. Traditionally, microvascular decompression of the facial nerve has been an effective treatment for posterior inferior and anterior inferior cerebellar artery as well as venous compression. The traditional technique involves Teflon felt or another construct to cushion the offending vessel from the facial nerve, or cautery and division of the offending vein. However, using this technique for severe vertebral artery (VA) compression can be ineffective and fraught with complications. The authors report the use of a new technique of VA pexy to the petrous or clival dura mater in patients with HFS attributed to a severely ectatic and tortuous VA, and detail the results in a series of patients. Methods Six patients with HFS due to VA compression underwent a retrosigmoid craniotomy, combined with a far-lateral approach in some patients. On identification of the site of VA compression, the vessel was mobilized adequately for the decompression. Great care was taken to avoid kinking the perforating vessels arising from the VA. Two 8-0 nylon sutures were passed through to the wall of the VA and then through the clival or petrous dura, and then tied to alleviate compression on cranial nerve VII. Results Patients were followed for at least 1 year postoperatively (mean 2.7 years, range 1–4 years). All 6 patients had complete resolution of their HFS. Facial function was tested postoperatively, and was stable when compared with the preoperative baseline. Two of the 3 patients with preoperative tinnitus had resolution of this symptom after the procedure. Postoperative imaging demonstrated VA decompression of the facial nerve and no evidence of stroke in all patients. One patient suffered from hearing loss, another developed a postoperative transient unilateral vocal cord paralysis, and a third patient developed a pseudomeningocele that resolved with the placement of a lumbar drain. Conclusions Hemifacial spasm and other neurovascular syndromes are effectively treated by repositioning the compressing artery. Careful study of the preoperative MR images may identify a select group of patients with HFS due to an ectatic VA. Rather than traditional decompression with only pledget placement, these patients may benefit from a VA pexy to provide an effective, safe, and durable resolution of their symptoms while minimizing surgical complications.

A “Sling Swing Transposition” Technique With Pedicled Dural Flap for Microvascular Decompression in Hemifacial Spasm

2012 ◽  
Vol 71 (suppl_1) ◽  
pp. ons25-ons31 ◽  
Author(s):  
Hui Ming Khoo ◽  
Toshiki Yoshimine ◽  
Takuyu Taki
Keyword(s):  
Facial Nerve ◽  
Hemifacial Spasm ◽  
Microvascular Decompression ◽  
Cerebellopontine Angle ◽  
Symptom Relief ◽  
Neurovascular Compression ◽  
Posterior Surface ◽  
Anatomic Structure ◽  
Compression Syndrome ◽  
Root Exit Zone

Abstract BACKGROUND: The key to successful microvascular decompression of the neurovascular compression syndrome is maintaining the separation between the nerve and the offending vessel. OBJECTIVE: We describe a transposition technique in which a local pedicled dural flap, fashioned from the petrous posterior surface, is used to retract the offending vessel away from the root exit zone of the facial nerve in hemifacial spasm cases. METHODS: We conducted a retrospective review of microvascular decompression operations in which the offending vessel was transposed and then retained by a local pedicled dural flap made from the dura of the petrous posterior surface. RESULTS: This technique was used in 7 consecutive cases of the most recently operated series. Postoperatively, complete symptom relief was achieved in 100% of the patients without any significant surgical complications. CONCLUSION: To our knowledge, this is the first report in which an autologous anatomic structure in the cerebellopontine angle, such as petrous dura mater, is used in the microvascular decompression of the facial nerve. This is a simple yet robust method and can be considered an option for the treatment of hemifacial spasm caused by arterial compression.

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