Delayed Hearing Loss after Neurovascular Decompression

Neurosurgery ◽  
1990 ◽  
Vol 27 (6) ◽  
pp. 997-1003 ◽  
Author(s):  
Dennis E. McDonnell ◽  
Bahman Jabbari ◽  
Giovana Spinella ◽  
Gustave H. Mueller ◽  
Peter M. Klara
Keyword(s):  
Hearing Loss ◽  
Facial Nerve ◽  
Hemifacial Spasm ◽  
Cerebellopontine Angle ◽  
Unilateral Hearing Loss ◽  
Neurovascular Compression ◽  
Bilateral Hearing Loss ◽  
First Case ◽  
Neurovascular Decompression ◽  
Vascular Decompression

Abstract We report two unusual cases of delayed hearing loss after neurovascular decompression of structures within the cerebellopontine angle. In the first case, the patient noted a unilateral hearing loss 3 weeks after undergoing vascular decompression of the trigeminal nerve for tic douloureux. This gradually improved over an 18-month period. In the second case, the patient awoke on the 4th day after vascular decompression of the facial nerve for hemifacial spasm with a bilateral hearing loss that has remained unchanged after the onset. These are examples of delayed acoustic dysfunction occurring with a shift in surgically freed vessels and may have been induced by newly directed neurovascular compression or distortion.

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.

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.

Hemifacial Spasm: Endoscopic Vascular Decompression

1997 ◽  
Vol 117 (4) ◽  
pp. 308-314 ◽  
Author(s):  
J. Magnan ◽  
F. Caces ◽  
P. Locatelli ◽  
A. Chays
Keyword(s):  
Hemifacial Spasm ◽  
Marked Improvement ◽  
Cerebellopontine Angle ◽  
Posterior Inferior Cerebellar Artery ◽  
Endoscopic Examination ◽  
Anterior Inferior Cerebellar Artery ◽  
Cerebellar Artery ◽  
The Mean ◽  
Vascular Decompression

Sixty patients with primitive hemifacial spasm were treated by means of a minimally invasive retrosigmoid approach in which endoscopic and microsurgical procedures were combined. Intraoperative endoscopic examination of the cerebellopontine angle showed that for 56 of the patients vessel-nerve conflict was the cause of hemifacial spasm. The most common offending vessel was the posterior inferior cerebellar artery (39 patients), next was the vertebral artery (23 patients), and last was the anterior inferior cerebellar artery (16 patients). Nineteen of the patients had multiple offending vascular loops. In one patient, another cause of hemifacial spasm was an epidermoid tumor of the cerebellopontine angle. For three patients, it was not possible to determine the exact cause of the facial disorder. Follow-up information was reviewed for 54 of 60 patients; the mean follow-up period was 14 months. Fifty of the patients were in the vessel-nerve conflict group. Forty of the 50 were free of symptoms, and four had marked improvement. The overall success rate was 88%, and there was minimal morbidity (no facial palsy, two cases of severe hearing loss).

scholarly journals Fully Endoscopic Vascular Decompression of the Facial Nerve for Hemifacial Spasm

Skull Base ◽  
2001 ◽  
Vol 11 (03) ◽  
pp. 189-198 ◽  
Author(s):  
Joseph B. Eby ◽  
Sung Tae Cha ◽  
Hrayr K. Shahinian
Keyword(s):  
Facial Nerve ◽  
Hemifacial Spasm ◽  
Vascular Decompression

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.

Acoustic Schwannoma Presenting as a Tumor of the External Auditory Canal

1987 ◽  
Vol 96 (4) ◽  
pp. 415-418 ◽  
Author(s):  
Patrice Tran Ba Huy ◽  
Jean Michel Hassan ◽  
Michel Wassef ◽  
Jacqueline Mikol ◽  
Claude Thurel
Keyword(s):  
Hearing Loss ◽  
External Auditory Canal ◽  
Cerebellopontine Angle ◽  
Internal Auditory Canal ◽  
Unilateral Hearing Loss ◽  
Acoustic Neurinoma ◽  
History Of ◽  
Acoustic Schwannoma ◽  
Initial Episode ◽  
Central Compensation

An acoustic neurinoma involving the internal auditory canal, the vestibule, the cochlea, the middle ear, and extending into the cerebellopontine angle and the external auditory canal, is described in a 56-year-old woman. An initial episode of vertigo was followed by a 27-year history of progressive unilateral hearing loss leading to complete deafness and areflexia with central compensation. The tumor was removed by a two-step surgical procedure, and the histologic features were those of a schwannoma.

Outcome following retrosigmoid microvascular decompression of the facial nerve for hemifacial spasm

2005 ◽  
Vol 119 (10) ◽  
pp. 779-783 ◽  
Author(s):  
D A Moffat ◽  
V S P Durvasula ◽  
A Stevens King ◽  
R De ◽  
D G Hardy
Keyword(s):  
Hearing Loss ◽  
Facial Nerve ◽  
Hemifacial Spasm ◽  
Microvascular Decompression ◽  
Retrospective Review ◽  
Facial Palsy ◽  
Complete Resolution ◽  
Symptom Control ◽  
Short Term

This paper evaluates the outcome of retrosigmoid microvascular decompression of the facial nerve in a series of patients suffering from hemifacial spasm who had been referred to the skull-base team (comprising senior authors DAM and DGH). The paper is a retrospective review of 15 patients who underwent retrosigmoid microvascular decompression of the facial nerve at Addenbrooke's Hospital between 1985 and 1995. In this series it was possible to obtain complete resolution of hemifacial spasm in 93.3 per cent of cases in the short term and in 80 per cent in the long term. Twelve patients (80 per cent) were symptom-free post-operatively. Two patients had minor recurrence of symptoms occurring within six months of the procedure. One patient with no identifiable vascular impingement of the facial nerve had no improvement following surgery. Three patients suffered sensorineural hearing loss. Two patients complained of post-operative tinnitus, and transient facial palsy was noted in one patient.Retrosigmoid microvascular decompression of the facial nerve provides excellent long-term symptom control in a high percentage of patients with hemifacial spasm.

CEREBELLOPONTINE ANGLE ARACHNOID CYST: A CASE OF HEMIFACIAL SPASM CAUSED BY AN ORGANIC LESION OTHER THAN NEUROVASCULAR COMPRESSION

Neurosurgery ◽  
2009 ◽  
Vol 65 (6) ◽  
pp. E1205-E1205 ◽  
Author(s):  
Luciano Mastronardi ◽  
Raymond Taniguchi ◽  
Manuela Caroli ◽  
Francesco Crispo ◽  
Luigi Ferrante ◽  
...  
Keyword(s):  
Arachnoid Cyst ◽  
Hemifacial Spasm ◽  
Cerebellopontine Angle ◽  
Rare Case ◽  
Magnetic Resonance Imaging Scan ◽  
Neurovascular Compression ◽  
Resonance Imaging ◽  
Organic Lesion ◽  
History Of ◽  
Preoperative Magnetic Resonance

Abstract OBJECTIVE A rare case of cerebellopontine angle arachnoid cyst manifesting as hemifacial spasm (HFS) is reported. The patient is a 42-year-old woman with 10-month history of left HFS. A preoperative magnetic resonance imaging scan showed a well-demarcated area, hypointense on T1-weighted imaging and hyperintense on T2-weighted imaging, in the left cerebellopontine angle, without contrast enhancement, resembling an arachnoid cyst. METHODS The cyst was excised with microneurosurgical technique and the facial, vestibular, and acoustic nerves were completely decompressed from the arachnoid wall. RESULTS The postoperative course was uneventful, and the left HFS disappeared immediately. Histologically, the cyst wall was a typical arachnoidal membrane. Ten months after surgery, the patient is symptom free. CONCLUSION It is well-known that in approximately 10% of cases, trigeminal neuralgia can be caused by a space-occupying mass. However, the fact that HFS can also be caused by organic lesions as well as neurovascular compression is less well-known. Although the occurrence of tumor compression causing HFS has been previously recognized, cerebellopontine angle cysts have very rarely been described. The observation of a patient with a cerebellopontine angle arachnoid cyst causing HFS prompted us to review the literature relative to HFS caused by an organic lesion rather than neurovascular compression.

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