scholarly journals Hemifacial spasm caused by the brainstem developmental venous anomaly: A case report and review of the literature

2020 ◽  
Vol 11 ◽  
pp. 141
Author(s):  
George Grigoryan ◽  
Andrey Sitnikov ◽  
Yuri Grigoryan
Keyword(s):  
Facial Nerve ◽  
Hemifacial Spasm ◽  
Cranial Nerves ◽  
Rare Condition ◽  
Cerebellar Hemisphere ◽  
Vascular Compression ◽  
Developmental Venous Anomaly ◽  
Venous Anomaly ◽  
Effective Treatment Option ◽  
Main Trunk

Background: Hemifacial spasm (HFS) is usually caused by vascular compression of the root exit zone (REZ) of the facial nerve. Dual compression of the REZ by veins and arteries is also associated with HFS, but venous origin alone is rarely reported. We present a rare case of HFS caused by the brainstem developmental venous anomaly (DVA) treated with microvascular decompression (MVD). Case Description: A 30-year-old women presented with the left-sided HFS since the age of 18 years. The brainstem DVA was diagnosed by magnetic resonance imaging (MRI) and followed by two attempts of MVD at some other clinics without any improvement. At our hospital, MVD was performed through a left retromastoid craniotomy. Intraoperatively, after detaching the strong adhesions between the cerebellar hemisphere, petrosal dura and lower cranial nerves, and removing the Teflon sponge inserted during the previous operations, the compressing large vein was found, separated from facial nerve REZ and MVD was completed. The postoperative computed tomography angiography and MRI showed the thrombosis of the main trunk of DVA and decompression of the facial nerve REZ. Complete cessation of HFS with hearing preservation was observed with only slight weakness of mimic muscles which disappeared within 3 months after surgery. Conclusion: HFS associated with brainstem DVA is a very rare condition. MVD of the facial nerve REZ with transposition of the large draining vein should be considered as an effective treatment option.

Endoscopic-Assisted Microvascular Decompression

2018 ◽  
pp. 139-154
Author(s):  
M. Yashar S. Kalani ◽  
Michael R. Levitt ◽  
Celene B. Mulholland ◽  
Charles Teo ◽  
Peter Nakaji
Keyword(s):  
Trigeminal Neuralgia ◽  
Minimally Invasive ◽  
Effective Treatment ◽  
Hemifacial Spasm ◽  
Microvascular Decompression ◽  
Patient Population ◽  
Surgical Intervention ◽  
Cranial Nerves ◽  
Vascular Compression ◽  
Ephaptic Transmission

Diseases of ephaptic transmission are commonly caused by vascular compression of cranial nerves. The advent of microvascular decompression has allowed for surgical intervention for this patient population. This chapter highlights the technique of endoscopic-assisted microvascular decompression for trigeminal neuralgia and hemifacial spasm. Endoscopy and keyhole techniques have resulted in a minimally invasive and effective treatment of symptoms for patients with neuralgia.

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.

Microvascular decompression for hemifacial spasm

1991 ◽  
Vol 75 (3) ◽  
pp. 388-392 ◽  
Author(s):  
Shinji Nagahiro ◽  
Akira Takada ◽  
Yasuhiko Matsukado ◽  
Yukitaka Ushio
Keyword(s):  
Hemifacial Spasm ◽  
Microvascular Decompression ◽  
Posterior Inferior Cerebellar Artery ◽  
Cranial Nerves ◽  
Anterior Inferior Cerebellar Artery ◽  
Vascular Compression ◽  
Content Type ◽  
Seventh Cranial Nerve ◽  
Cerebellar Artery

✓ To determine the causative factors of unsuccessful microvascular decompression for hemifacial spasm, the follow-up results in 53 patients were assessed retrospectively. The mean follow-up period was 36 months. There were 32 patients who had compression of the seventh cranial nerve ventrocaudally by an anterior inferior cerebellar artery (AICA) or a posterior inferior cerebellar artery. Of these 32 patients, 30 (94%) had excellent postoperative results. Of 14 patients with more severe compression by the vertebral artery, nine (64%) had excellent results, three (21%) had good results, and two (14%) had poor results; in this group, three patients with excellent results experienced transient spasm recurrence. There were seven patients in whom the meatal branch of the AICA coursed between the seventh and eighth cranial nerves and compressed the dorsal aspect of the seventh nerve; this was usually associated with another artery compressing the ventral aspect of the nerve (“sandwich-type” compression). Of these seven patients, five (71%) had poor results including operative failure in one and recurrence of spasm in four. The authors conclude that the clinical outcome was closely related to the patterns of vascular compression.

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.

Microvascular Decompression in Patient With Atypical Features of Hemifacial Spasm Secondary to Compression by a Tortuous Vertebrobasilar System

Neurosurgery ◽  
2010 ◽  
Vol 66 (6) ◽  
pp. E1212-E1212 ◽  
Author(s):  
David H. Perlmutter ◽  
Anthony L. Petraglia ◽  
Richard Barbano ◽  
Jason M. Schwalb
Keyword(s):  
Hearing Loss ◽  
Botulinum Toxin ◽  
Hemifacial Spasm ◽  
Microvascular Decompression ◽  
Cranial Nerves ◽  
Vascular Compression ◽  
Vertebrobasilar System ◽  
The Face ◽  
Grade 3 ◽  
The Right

Abstract OBJECTIVE We report a case of hemifacial spasm in a patient who had associated hearing loss, numbness throughout the face, tinnitus, and vertigo, all of which occurred when turning his head to the left. To our knowledge, these symptoms have not occurred in this pattern and with a single trigger. CLINICAL PRESENTATION A 45-year-old man presented with a 3-year history of right-sided hemifacial spasm initially treated with botulinum toxin. One month before presentation, he had an episode of acute hearing loss in the right ear when turning his head to the left, followed by multiple episodes of transient hearing loss in his right ear, numbness in his right face in all distributions of the trigeminal nerve, tinnitus, and vertigo. He was found to have decreased sensation in nerves V1 to V3 and House-Brackmann grade 3/6 weakness in his right face, despite not having botulinum toxin injections in more than a year. Magnetic resonance imaging/angiography showed an ectatic vertebrobasilar system causing compression of the fifth, seventh, and eighth cranial nerves. INTERVENTION The patient underwent a retromastoid craniotomy and microvascular decompression. Postoperatively, he had complete resolution of his symptoms except for his facial weakness. The benefit has been long-lasting. CONCLUSION Multiple, simultaneous cranial neuropathies from vascular compression are rare, but this case is an example of safe and effective treatment with microvascular decompression with durable results.

THROMBOSED BRAINSTEM DEVELOPMENTAL VENOUS ANOMALY CAUSING HYDROCEPHALUS

2015 ◽  
Vol 86 (11) ◽  
pp. e4.99-e4
Author(s):  
Katherine Dodd ◽  
Emily Pegg ◽  
Sachin Mathur ◽  
Chhetri Suresh
Keyword(s):  
Posterior Fossa ◽  
Drainage System ◽  
Venous Drainage ◽  
Cerebellar Hemisphere ◽  
Cerebral Peduncle ◽  
Developmental Venous Anomaly ◽  
Venous Anomaly ◽  
Venous Infarction ◽  
Heparin Infusion ◽  
The Right

Developmental venous anomaly (DVA) is a commonly encountered congenital abnormality of the venous drainage system. Spontaneous thrombosis of DVA is rare. We present a case of thrombosed brainstem DVA leading to venous infarction and oedema within the posterior fossa.A 49 year old, previously fit gentleman presented to the local hospital with a one day history of headache, slurred speech and incoordination. Examination demonstrated GCS of 13/15, cerebellar dysarthria, horizontal nystagmus to the left, mild right sided pyramidal weakness, right sided cerebellar ataxia and bilateral extensor plantars.CT venogram revealed a cerebellar DVA with thrombosis of one of the veins. There was surrounding venous infarction and oedema within the posterior fossa, causing compression of the fourth ventricle and dilatation of the lateral ventricles. MRI demonstrated extensive T2 change in the right cerebellar hemisphere, dorsal pons and right cerebral peduncle. No underlying thrombotic tendency was identified. He was treated successfully with intravenous heparin infusion. He improved over the next 3 weeks, and was discharged on warfarin with mild right sided ataxia and cerebellar dysarthria.Our case demonstrates that DVAs, generally considered as common insignificant anatomical variants, can uncommonly lead to significant complications.

Outcome of Endoscope-Assisted Microvascular Decompression in Patients With Hemifacial Spasm Caused by Severe Indentation of the Brain Stem at the Pontomedullary Sulcus by the Posterior Inferior Cerebellar Artery

2021 ◽  
Author(s):  
Ehab El Refaee ◽  
Steffen Fleck ◽  
Marc Matthes ◽  
Sascha Marx ◽  
Joerg Baldauf ◽  
...  
Keyword(s):  
Facial Nerve ◽  
Brain Stem ◽  
Hemifacial Spasm ◽  
Microvascular Decompression ◽  
Posterior Inferior Cerebellar Artery ◽  
Transitional Zone ◽  
Effective Treatment Option ◽  
Cerebellar Artery ◽  
The Brain

Abstract BACKGROUND Microvascular decompression (MVD) is the most effective treatment option for hemifacial spasm (HFS). However, deeply located forms of compression would require proper identification to allow for adequate decompression. OBJECTIVE To describe the usefulness of endoscopic visualization in one of the most challenging compression patterns in HFS, where the posterior inferior cerebellar artery (PICA) loop is severely indenting the brain stem at the proximal root exit zone of facial nerve along the pontomedullary sulcus. METHODS Radiological and operative data were checked for all patients in whom severe indentation of the brainstem by PICA at pontomedullary sulcus was recorded and endoscope-assisted MVD was performed. Clinical correlation and outcome were analyzed. RESULTS A total of 58 patients with HFS were identified with radiological and surgical evidence proving brainstem indentation at the VII transitional zone. In 31 patients, PICA was the offending vessel to the facial nerve. In 3 patients, the PICA loop was mobilized under visualization of a 45° endoscope. A total of 31 patients had a mean follow-up duration of 52.1 mo. The mean duration between start of complaints and surgery was 7.2 yr. In the last follow-up, all patients had remarkable spasm improvement. A total of 5 patients had more than 90% disappearance of spasms and 26 patients experienced spasm-free outcome. CONCLUSION Although severe indentation of brain stem implies morphological damage, outcome after MVD is excellent. A 45° endoscope is extremely helpful to identify compression down at the pontomedullary sulcus. Deeply located compression site can easily be missed with microscopic inspection alone.

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.

Sign in / Sign up

Export Citation Format

Share Document