Microvascular decompression for cochlear symptoms

2000 ◽  
Vol 93 (3) ◽  
pp. 421-426 ◽  
Author(s):  
Tomomi Okamura ◽  
Yasushi Kurokawa ◽  
Norio Ikeda ◽  
Seisho Abiko ◽  
Makoto Ideguchi ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Microvascular Decompression ◽  
Cranial Nerve ◽  
Cochlear Nerve ◽  
Auditory Brainstem Responses ◽  
Neurovascular Compression ◽  
Minimal Risk ◽  
Eighth Cranial Nerve ◽  
Content Type ◽  
Fine Print

Object. The object of this study was to evaluate the efficacy of a new neurovascular decompression technique in relieving symptoms of cochlear nerve dysfunction.Methods. Nineteen patients with slowly progressive hearing loss, low-frequency fluctuating hearing loss, and high-pitched tinnitus due to neurovascular compression (NVC) of the eighth cranial nerve in a triangular space between the seventh and eighth cranial nerves (the VII–VIII triangle) of the cerebellopontine angle (CPA) were treated using a new technique for microvascular decompression that was developed by anatomical study in 24 cadaver specimens of the CPA. In 12 of 19 patients the anterior inferior cerebellar artery (AICA) was observed to cause compression in the VII–VIII triangle and this vessel was easily mobilized medially for placement of a silicone sponge or Teflon cushion between the compressing artery and nerve. Postoperatively, hearing loss of 20 dB or more that was present in 11 of the 19 patients with NVC improved by more than 5 dB in seven (64%), including the patient with the most severe hearing loss. Of 18 patients presenting with tinnitus preoperatively, eight (44%) had no tinnitus and an additional nine (for a total of 94%) had good improvement in tinnitus after surgery and at long-term follow up.Conclusions. The microvascular decompression technique described is highly successful in treating symptoms due to direct or indirect compression of the cochlear nerve, with minimal risk of complications. Recordings of auditory brainstem responses confirmed the clinical diagnosis of NVC of the eighth cranial nerve and correlated with clinical results after microvascular decompression of the cochlear nerve.

Microvascular decompression of cranial nerves: lessons learned after 4400 operations

1999 ◽  
Vol 90 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Mark R. McLaughlin ◽  
Peter J. Jannetta ◽  
Brent L. Clyde ◽  
Brian R. Subach ◽  
Christopher H. Comey ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Trigeminal Neuralgia ◽  
Hemifacial Spasm ◽  
Microvascular Decompression ◽  
Cranial Nerve ◽  
Glossopharyngeal Neuralgia ◽  
Complication Rates ◽  
Content Type ◽  
Csf Leakage ◽  
Fine Print

Object. Microvascular decompression has become an accepted surgical technique for the treatment of trigeminal neuralgia, hemifacial spasm, glossopharyngeal neuralgia, and other cranial nerve rhizopathies. The senior author (P.J.J.) began performing this procedure in 1969 and has performed more than 4400 operations. The purpose of this article is to review some of the nuances of the technical aspects of this procedure.Methods. A review of 4415 operations shows that numerous modifications to the technique of microvascular decompression have occurred during the last 29 years. Of the 2420 operations performed for trigeminal neuralgia, hemifacial spasm, and glossopharyngeal neuralgia before 1990, cerebellar injury occurred in 21 cases (0.87%), hearing loss in 48 (1.98%), and cerebrospinal fluid (CSF) leakage in 59 cases (2.44%). Of the 1995 operations performed since 1990, cerebellar injuries declined to nine cases (0.45%), hearing loss to 16 (0.8%), and CSF leakage to 37 (1.85% p < 0.01, test for equality of distributions). The authors describe slight variations made to maximize surgical exposure and minimize potential complications in each of the six principal steps of this operation. These modifications have led to decreasing complication rates in recent years.Conclusions. Using the techniques described in this report, microvascular decompression is an extremely safe and effective treatment for many cranial nerve rhizopathies.

Neurovascular decompression of the eighth cranial nerve in patients with hemifacial spasm and incidental tinnitus: an alternative way to study tinnitus

1998 ◽  
Vol 88 (2) ◽  
pp. 232-236 ◽  
Author(s):  
Hiroshi Ryu ◽  
Seiji Yamamoto ◽  
Kenji Sugiyama ◽  
Kenichi Uemura ◽  
Michihiko Nozue
Keyword(s):  
Hemifacial Spasm ◽  
Cranial Nerve ◽  
Diagnostic Value ◽  
Sensorineural Hearing ◽  
Neurovascular Compression ◽  
Eighth Cranial Nerve ◽  
Chi Square ◽  
Content Type ◽  
Neurovascular Decompression ◽  
Fine Print

Object. The authors sought to clarify the clinical characteristics of tinnitus resulting from neurovascular compression (NVC) of the eighth cranial nerve. Methods. The authors explored the eighth cranial nerve in the cerebellopontine cistern during neurovascular decompression (NVD) of the facial nerve in 10 patients with hemifacial spasm who suffered from incidental tinnitus on the same side. The diagnosis of NVC of the eighth cranial nerve was confirmed in all patients. This condition was found in only seven of 114 patients with hemifacial spasm alone, indicating that NVC of the eighth cranial nerve is one of the causes of tinnitus (p < 0.001, chi-square test). The tinnitus resolved or was markedly improved after NVD of the eighth cranial nerve in eight patients (80%). Both pulsatile and continuous tinnitus responded well to NVD. All patients experienced various degrees of sensorineural hearing disturbance, but other neurotological examinations provided poor diagnostic value. Conclusions. It is the authors' opinion that sensorineural hearing loss and positive findings on magnetic resonance imaging are the most reliable evidence for the presence of tinnitus caused by NVC of the eighth cranial nerve.

Diagnosis and surgical treatment of disabling positional vertigo

1986 ◽  
Vol 64 (1) ◽  
pp. 21-28 ◽  
Author(s):  
Margareta B. Møller ◽  
Aage R. Møller ◽  
Peter J. Jannetta ◽  
Laligam Sekhar
Keyword(s):  
Hearing Loss ◽  
Differential Diagnosis ◽  
Surgical Treatment ◽  
Microvascular Decompression ◽  
Social Life ◽  
Eighth Cranial Nerve ◽  
Content Type ◽  
Positional Vertigo ◽  
Normal Work ◽  
Fine Print

✓ This report reviews the characteristic symptoms of disabling positional vertigo (DPV), and the tests used to reach a differential diagnosis of this disorder. Twenty-one patients were operated on consecutively for management of DPV between March, 1983, and September, 1984. In all patients one or more arteries or veins was found to be compressing the eighth cranial nerve when the nerve was exposed for microvascular decompression to relieve the symptoms of DPV. After the operation, 16 of the 21 patients were free of symptoms, or symptoms were so much improved that the patients returned to normal work or social life. Two patients had no improvement and three had limited relief of symptoms postoperatively. None of the patients experienced hearing loss as a result of the operation to relieve DPV, but one patient suffered a cerebellar contusion during the operation.

Correlation between auditory function and internal auditory canal pressure in patients with vestibular schwannomas

2002 ◽  
Vol 96 (5) ◽  
pp. 872-876 ◽  
Author(s):  
Samir B. Lapsiwala ◽  
G. Mark Pyle ◽  
Ann W. Kaemmerle ◽  
Frank J. Sasse ◽  
Behnam Badie
Keyword(s):  
Hearing Loss ◽  
Tumor Growth ◽  
Tumor Size ◽  
Internal Auditory Canal ◽  
Auditory Evoked Potential ◽  
Cochlear Nerve ◽  
Content Type ◽  
Vascular Compromise ◽  
Brainstem Response ◽  
Fine Print

Object. Hearing loss is the most common presenting symptom in patients who harbor a vestibular schwannoma (VS). Although mechanical injury to the cochlear nerve and vascular compromise of the auditory apparatus have been proposed, the exact mechanism of this hearing loss remains unclear. To test whether pressure on the cochlear nerve from tumor growth in the internal auditory canal (IAC) is responsible for this clinical finding, the authors prospectively evaluated intracanalicular pressure (ICaP) in patients with VS and correlated this with preoperative brainstem response. Methods. In 40 consecutive patients undergoing a retrosigmoid—transmeatal approach for tumor excision, ICaP was measured by inserting a pressure microsensor into the IAC before any tumor manipulation. Pressure recordings were correlated with tumor size and preoperative auditory evoked potential (AEP) recordings. The ICaP, which varied widely among patients (range 0–45 mm Hg), was significantly elevated in most patients (median 16 mm Hg). Although these pressure measurements directly correlated to the extension of tumor into the IAC (p = 0.001), they did not correlate to total tumor size (p = 0.2). In 20 patients in whom baseline AEP recordings were available, the ICaP directly correlated to wave V latency (p = 0.0001), suggesting that pressure from tumor growth in the IAC may be responsible for hearing loss in these patients. Conclusions. Tumor growth into the IAC results in elevation of ICaP and may play a role in hearing loss in patients with VS. The relevance of these findings to the surgical treatment of these tumors is discussed.

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.

The significance for postoperative hearing of preserving the labyrinth in acoustic neurinoma surgery

1992 ◽  
Vol 77 (5) ◽  
pp. 677-684 ◽  
Author(s):  
Marcos Tatagiba ◽  
Madjid Samii ◽  
Cordula Matthies ◽  
Mowaffak El Azm ◽  
Robert Schonmayr
Keyword(s):  
Hearing Loss ◽  
Inner Ear ◽  
Semicircular Canal ◽  
Semicircular Canals ◽  
Cochlear Nerve ◽  
Acoustic Neurinoma ◽  
Content Type ◽  
Acoustic Neurinomas ◽  
A Prospective Study ◽  
Fine Print

✓ Among 186 patients with preoperative hearing, a total of 189 acoustic neurinomas were removed through a lateral suboccipital approach with anatomical preservation of the cochlear nerve. Functional hearing was preserved in 92 (49%) of these patients; despite anatomical preservation of the cochlear nerve, deafness was the result in 51 % of the series. Many factors have been considered to cause hearing loss in patients whose cochlear nerve was intact after surgery; these include nerve retraction, nerve or cochlear ischemia, overheating and vibration damage to the nerve, and opening of the labyrinth. To evaluate the significance of injury to the labyrinth in postoperative hearing loss, a prospective study was undertaken. High-resolution computerized tomography studies through the inner ear with bone algorithm were performed pre- and postoperatively. The postoperative status of the labyrinth was classified into three patterns: intact, fenestrated, and widely opened. Injury to the labyrinth occurred in 30% of the cases. The most frequently injured labyrinth structures were the crus commune of the posterior and superior semicircular canals (52%), the posterior semicircular canal (23%). the vestibule (21%), and the superior semicircular canal (4%). A statistically significant relationship was found between injury to the labyrinth and deafness, elevated thresholds, and lower discrimination values at pure-tone audiograms and speech audiometry (p < 0.0001). The degree of the injury (comparison between fenestration and wide opening of the labyrinth) was also significantly related to postoperative deafness (p < 0.0001). Disturbance of the inner-ear fluids was considered to be the cause of the hearing loss. In 12 patients labyrinth injury was not associated with deafness. This finding may support the existence of mechanisms of cochlear protection. The homeostatic function of the endolymphatic sac was considered to play an important role in recovery of damaged hearing in these 12 cases.

Delayed and Progressive Hearing Loss after Microvascular Decompression of Cranial Nerves

1996 ◽  
Vol 105 (2) ◽  
pp. 158-161 ◽  
Author(s):  
Takeo Fuse ◽  
Margareta B. Møller
Keyword(s):  
Hearing Loss ◽  
Evoked Potentials ◽  
Brain Stem ◽  
Microvascular Decompression ◽  
Cranial Nerve ◽  
Auditory Evoked Potentials ◽  
Cranial Nerves ◽  
Reflex Response ◽  
Eighth Cranial Nerve ◽  
Progressive Hearing Loss

An unusual case of unilateral delayed and progressive hearing loss following a microvascular decompression operation on cranial nerves V, VII, and VIII on the left side is reported. Preoperative and postoperative audiologic evaluation revealed a mild high-frequency hearing loss for both ears, normal thresholds for the acoustic middle ear reflex response, and normal brain stem auditory evoked potentials. Three years after this microvascular decompression procedure, the patient noticed slowly decreasing hearing in her left ear, and subsequent serial audiograms revealed a progressive sensorineural hearing loss and a decrease in her speech discrimination score. Brain stem auditory evoked potentials showed progressive changes. Because of the patient's increasing symptoms of vertigo and tinnitus in the left ear, reexploration of the eighth cranial nerve was performed 5½ years after the initial procedure. This second operation revealed reactive tissue around the eighth cranial nerve that was atrophic and yellow. We interpret the delayed and progressive hearing loss to be a result of reactive scar tissue and progressive atrophy of the auditory nerve.

Microvascular decompression for trigeminal neuralgia caused by vertebrobasilar compression

1994 ◽  
Vol 81 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Mark E. Linskey ◽  
Hae Dong Jho ◽  
Peter J. Jannetta
Keyword(s):  
Hearing Loss ◽  
Trigeminal Neuralgia ◽  
Trigeminal Nerve ◽  
Microvascular Decompression ◽  
Sensory Loss ◽  
Vascular Compression ◽  
Content Type ◽  
Root Section ◽  
Vascular Decompression ◽  
Fine Print

✓ Thirty-one (2%) of 1404 consecutive patients with typical trigeminal neuralgia who underwent microvascular decompression between 1972 and 1993 were found to have vascular compression by the vertebral artery (VA) or the basilar artery (BA). Compared to the remaining 1373 patients, this subgroup was older (mean age 62 vs. 55 years, p < 0.001), was predominantly male (68% vs. 39%, p < 0.002), demonstrated left-sided predominance (65% vs. 39%, p < 0.002), was more likely to be hypertensive (65% vs. 18%, p < 0.001), and was more likely to have ipsilateral hemifacial spasm (16% vs. 0.6%, p < 0.001). The trigeminal nerve was compressed by the VA in 18 cases (the VA alone in three and the VA plus other vessels in 15), the BA in 12 cases (the BA alone in four and the BA plus other vessels in eight), and the vertebrobasilar junction in one case. Twenty-nine of the 31 patients underwent vascular decompression of the trigeminal nerve, one had a complete trigeminal root section, and one underwent partial root section with vascular decompression of the remaining nerve. All 31 patients were pain-free, off medication immediately after surgery, and this pain-free, medication-free status was maintained at 1 year after surgery in 96% of cases, at 3 years in 92%, and at 10 years in 86%, based on life-table analysis. Minor trigeminal hypesthesia/hypalgesia was present preoperatively in 52%. New or worsened minor hypesthesia/hypalgesia developed in 41% of patients, while transient diplopia as well as hearing loss developed in 23% and 13% in the overall series, respectively. No patient developed major trigeminal sensory loss or masseter weakness after vascular decompression alone. There was no operative mortality. Vascular decompression is an effective treatment for patients with trigeminal neuralgia who have vertebrobasilar compression of the trigeminal nerve. Patients should be warned that decompression of a tortuous vertebrobasilar system carries a higher risk of mild trigeminal dysfunction, diplopia, and hearing loss than standard microvascular decompression.

Temporal pattern of cochlear nerve degeneration following compression injury: a quantitative experimental observation

2002 ◽  
Vol 97 (4) ◽  
pp. 929-934 ◽  
Author(s):  
Norihito Shimamura ◽  
Tetsuji Sekiya ◽  
Akinori Yagihashi ◽  
Shigeharu Suzuki
Keyword(s):  
Temporal Pattern ◽  
Time Window ◽  
Cochlear Nerve ◽  
Nerve Degeneration ◽  
Compression Injury ◽  
Eighth Cranial Nerve ◽  
Content Type ◽  
Pattern Of Injury ◽  
Precise Knowledge ◽  
Fine Print

Object. It has been empirically recognized that the cochlear nerve is highly vulnerable to traumatic stress resulting from surgical procedures; therefore, careful manipulation of the cochlear nerve is mandatory in preventing trauma-induced hearing loss during cerebellopontine angle (CPA) surgery. There is, however, no precise knowledge about the temporal pattern of cochlear nerve degeneration following trauma. This study was performed to determine the temporal pattern of injury that occurs after cochlear nerve trauma, knowledge of which is indispensable not only to neurosurgeons but also to all those who manage lesions involving the cochlear nerve. Methods. Right suboccipital craniectomies were performed in groups of rats with the aid of a surgical microscope, and the seventh and eighth cranial nerve trunks were identified at the internal auditory meatus. The cochlear nerve was quantifiably compressed while compound action potentials of the cochlear nerve were monitored and recorded. Following injury, one group of rats was killed for histological examination at the end of each week for 4 weeks. Data from this study disclosed that the degeneration of the compressed cochlear nerve progressed in a relatively rapid manner and was complete within 1 week after the insult. The main pathophysiological mechanisms responsible for cochlear neuronal death in this experimental setting appeared to be necrosis, and an apoptotic mechanism seemed to play a subsidiary role. Conclusions. Accurate knowledge about the temporal profile of trauma-induced cochlear nerve degeneration is closely linked with the problem of the therapeutic time window. The results of the present study indicated that any measures to ameliorate cochlear nerve degeneration following trauma should be started as early as possible (within 1 week) after an injury.

Neurovascular compression in trigeminal neuralgia: a clinical and anatomical study

1992 ◽  
Vol 76 (6) ◽  
pp. 948-954 ◽  
Author(s):  
Peter J. Hamlyn ◽  
Thomas T. King
Keyword(s):  
Trigeminal Neuralgia ◽  
Cranial Nerve ◽  
Operative Procedure ◽  
Anatomical Study ◽  
Vascular Compression ◽  
Neurovascular Compression ◽  
Content Type ◽  
Simple Contact ◽  
Neurovascular Decompression ◽  
Fine Print

✓ Neurovascular decompression is a widely practiced tec hnique for the treatment of trigeminal neuralgia, and yet there is still debate as to whether the beneficial effect results from relieving the nerve of compression by an anatomically abnormal vessel or from the manipulation and trauma the nerve undergoes during the procedure. The development of this operation has been hampered by the lack of adequate anatomical studies in normal controls. The authors present a combined study of clinical and anatomical material employing standardized definitions of the neurovascular relationships in both groups. Detailed simulations of the operative procedure were carried out on fresh cadavers matched for age, sex, and side, and a technique of in situ blood vessel perfusion was developed that enabled the normal neurovascular arrangement to be observed post mortem at physiological pressures. Neurovascular compression, typified by a large vessel distorting and creating a groove in the fifth cranial nerve, was found in 37 of the 41 cases of trigeminal neuralgia; recurrence of pain did not relate to the site of compression. A follow-up study was carried out for a median of 53 months (range 12 to 103 months). No distortion was found in a total of 50 normal cadaveric dissections; however, on perfusion to physiological pressures, the percentage of nerves with vessels adjacent or in simple contact increased from 16% to 40%. This study using this new technique confirms that vascular compression of the fifth cranial nerve is an anatomical abnormality specific to trigeminal neuralgia.

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