Anatomie fonctionnelle du nerf vestibulaire

The vestibular system detects head movements such as angular rotation, translation, and head position relative to gravity. It acts to stabilize the eyes and posture through subcortical reflexes. Its signals are also integrated at the cortical level to participate in the elaboration of a body scheme, used for different functions such as spatial orientation and motor control. The vestibular nerve shows a resting discharge rate that is modulated up or down according to head motion or position. Central functioning depends on the detection of an asymmetry between signals coming from a pair of peripheral sensors, one on either side. In pathological cases, unilateral peripheral dysfunction is interpreted by the central system as an asymmetry resulting from a change in head position leading to nystagmus, postural disturbances, and vertigo. The dysfunction can be either a deficit, such as observed in vestibular neuronitis, or hyperactivity such as observed in neurovascular compression syndrome of the VIIIth nerve. Anatomically, the VIIIth nerve has a long Root Entry Zone (REZ) that extends over 10 mm before entering the brainstem. The VIIIth nerve is also physiologically close to numerous vessels at the pontocerebellar angle and internal auditory meatus. Therefore, vestibular syndrome resulting from neurovascular compression syndrome of the VIIIth nerve may exist, but it is very difficult to prove using radiological imagery.     

Neurovascular Compression Syndrome of the Eighth Cranial Nerve. Can the Site of Compression Explain the Symptoms?

Summary  Considerable skepticism still exists concerning the concept of neurovascular compression (NVC) syndromes of the eighth cranial nerve (8th N). If such syndromes exist, the sites of compression of the nerve must explain the symptoms encountered. We recorded compound action potentials of the cochlear nerve (CCAPs) during neurovascular decompression (NVD) to examine the topography of the three components of the 8th N. The sites of compression of the 8th N in cases of NVC syndrome confirmed at surgery were superimposed on the topography of the CN and vestibular nerve (VN) in order to determine the relationship between the sites of compression and the symptoms. CCAPs were clearly and consistently recorded on the caudal surface of the 8th N along the midline. In patients with vertigo and tinnitus there was vascular compression of the rostro-ventral (VN) and caudal surface (CN) of the nerve, respectively. In patients with both vertigo and tinnitus, there was compression of both VN and CN. Our findings clearly demonstrate that the symptoms of NVC of the 8th N depend on the part of the nerve that is compressed by blood vessels, and they support the concept of NVC syndrome of the 8th N.     

Hyperactive rhizopathy of the vagus nerve and microvascular decompression. Case report

A 37-year-old woman underwent microvascular decompression of the superior vestibular nerve for disabling positional vertigo. Immediately following the operation, she noted severe and spontaneous gagging and dysphagia. Multiple magnetic resonance images were obtained but failed to demonstrate a brainstem lesion and attempts at medical management failed. Two years later she underwent exploration of the posterior fossa. At the second operation, the vertebral artery as well as the posterior inferior cerebellar artery were noted to be compressing the vagus nerve. The vessels were mobilized and held away from the nerve with Teflon felt. The patient's symptoms resolved immediately after the second operation and she has remained symptom free. The authors hypothesize that at least one artery was shifted at the time of her first operation, or immediately thereafter, which resulted in vascular compression of the vagus nerve. To the authors' knowledge, this is the first reported case of a hyperactive gagging response treated with microvascular decompression. The case also illustrates the occurrence of a possibly iatrogenic neurovascular compression syndrome.     

Hemifacial spasm associated with other cranial nerve syndromes: Literature review

Hyperactive dysfunction may affect all cranial nerves in the posterior fossa. According to literature review and personal experience, hemifacial spasm was found to be associated not only with the most frequent cranial nerve syndromes, namely: trigeminal neuralgia, vago-glossopharyngeal neuralgia or VIIIth nerve disturbances manifested by vertigo, tinnitus, hearing decrease, but also with rarer syndromes like geniculate neuralgia, masticatory spasm etc. Also, a number of publications have pointed out the relatively high incidence of the coexistence of hemifacial spasm and systemic blood hypertension; both can be cured by vascular decompression of the ventrolateral aspect of the medulla and IX-Xth route entry zone (REZ) together with the facial REZ. Even more complex clinical presentations have been encountered, corresponding to disturbances in several cranial nerve nuclei. Some could be attributed to neurovascular conflicts from elongated arteries invaginated into the brainstem, and cured by microvascular decompression surgery. When confronted with such complex, and therefore misleading, syndrome, it is advised to search for vascular conflicts at the brainstem using high-resolution MRI exploration.     

Neurovascular Compression Syndrome of the Eighth Cranial Nerve. What are the Most Reliable Diagnostic Signs?

Summary  Forty-three surgical cases were retrospectively analyzed to establish diagnostic criteria and operative indications for vertigo and tinnitus due to neurovascular compression (NVC) of the eighth cranial nerve (8th N). Many NVC syndromes were mistakenly diagnosed as Ménière's disease or benign paroxysmal positional vertigo. NVC was confirmed in 31 of the 43 patients. Neurovascular decompression (NVD) resulted in complete recovery or marked improvement of subjective symptoms in all 19 cases with vertigo (100%), and in 19 of 29 patients with tinnitus (65.5%). Multiple factor analysis revealed that abnormal caloric responses have high diagnostic value for vertigo due to NVC. Vertigo due to NVC is of short duration (a few sec to a few min.) in the early phase of the disease, which becomes longer and hearing becomes impaired as the history of NVC lengthens. Low pitch pulsatile and high pitch continuous tinnitus are probably due to NVC and are cured by NVD if hearing is still preserved. Tinnitus associated with hemifacial spasm is strongly indicative of NVD. Decompression of the 8th N should be performed in the early phase of disease, since cochlear and vestibular functions are irreversibly impaired if NVC continues for a long period of time.     

Chirurgie des vertiges

Spontaneous recovery or central compensation makes surgical procedures rare in patients with vertigo. Surgery for vertigo proposed after pharmacological or physical therapy fails to eliminate Ménière's disease and some very rare cases of paroxystic positional vertigo. The main target in treating Ménière's disease is to promote vestibular compensation, which is possible only with a nonprogressive and stable deficit leading to readjustment of vestibular reflexes. Surgical procedures can be classified as nondestructive (endolymphatic sac decompression, vestibular nerve decompression, patching of perilymphatic fistulas), selectively destructive (middle fossa or retrosigmoid vestibular neurotomy, lateral semi-circular plugging) and destructive (labyrinthectomy). Surgical indications essentially concern incapacitating vertigo and depend mainly on hearing status. In Ménière's disease, vestibular neurotomy can be regarded as the gold standard considering its good results on vertiginous episodes; however, scoring with functional and quality-of-life scales bring out residual deficiency in some cases.     

Is the root entry/exit zone important in microvascular compression syndromes?

OBJECTIVE: Microvascular compression syndromes such as trigeminal neuralgia, hemifacial spasm, and disabling positional vertigo involve an artery or vein compressing a cranial nerve. A cranial nerve is composed of a central nervous system (CNS) segment and a peripheral nervous system (PNS) segment separated by the root entry/exit zone (REZ). Although vascular compression can occur at any point along the cranial nerve, it has been generally assumed that only vascular contact at the REZ of the affected cranial nerve can cause symptoms. On the basis of personal surgical experience, we propose that vascular compression of the CNS segment alone causes symptoms. This has important repercussions for the future diagnosis and treatment of microvascular compression syndromes, especially the cochleovestibular compression syndrome. METHODS: For the anatomic study, four autopsy specimens and one surgical biopsy specimen of the vestibulocochlear nerve were microscopically and ultramicroscopically analyzed for structural differences between the CNS and PNS segments. For the clinical study, five patients with the clinical picture of cochleovestibular compression syndrome were treated by microsurgical decompression at the level of the CNS segment and not the REZ. One patient underwent reoperation for recurrent symptoms 4 years later, and a 4-mm vestibular neurectomy was performed at that stage. We performed an epidemiological analysis to demonstrate that the known incidences of trigeminal neuralgia, hemifacial spasm, and glossopharyngeal neuralgia are related to the length of their respective CNS segments. RESULTS: Histological differences between the PNS and CNS segments suggest that the PNS segment is more resistant to compression. This was confirmed by neurophysiological data from intraoperative monitoring in posterior fossa surgery and experimental studies. We found a clear epidemiological correlation between the length of the CNS segment, which differed among cranial nerves, and the incidence of the microvascular compression syndrome. Successful decompression of the CNS segment in patients without compression at the REZ of the vestibulocochlear nerve for disabling positional vertigo provides clinical support for this hypothesis. CONCLUSION: The evidence we present supports the hypothesis that vascular compression syndromes arise from vascular contact along the CNS segment of the cranial nerves.     

Relationship between anterior inferior cerebellar artery and facial-vestibulocochlear nerve complex: an anatomical and magnetic resonance images correlation study.

For the successful microneurosurgical treatment of CP angle located pathologies, an understanding of the relationship and variations between neural and vascular structures and a certain diagnosis are the most valuable factors for surgeons. CP angle lesions have now become a visible area by advances in magnetic resonance imaging (MRI) technology. An evaluation of this area and the decision for a neurosurgical decompression procedure are easier than before. Twenty unfixed adult human cadaver specimens, that have no sign of central nervous system pathology, were obtained and dissected bilaterally at routine autopsy. The facial-vestibulocochlear (VII - VIIIth) nerve complex and the anterior inferior cerebellar artery (AICA) were identified in all specimens. Thirteen of the 40 (32.5 %) AICA were situated ventrally and fourteen (35 %) were located dorsally to the VII - VIIIth nerve complex. Thirteen (32.5 %) passed between the VIIth and the VIIIth nerve fibers. Five of the 40 (12.5 %) AICA had a loop near the nerve complex and then passed the nerves ventrally or dorsally. In an MRI study 74 adult persons (148 sides) were investigated by using three-dimensional Fourier transformation constructive interference in the steady state technique (3D FT-CISS) on a 1.5 Tesla MRI system (Siemens Magnetom, Erlangen, Germany). The results were as follows; 48 AICA (32.4 % of all 148 AICA) were situated ventrally to the VII-VIIIth nerve complex, 45 AICA (30.4 %) were situated dorsally to the VII-VIIIth nerve complex, and the AICA passed between the VIIth and VIIIth nerves in 51 samples (34.5 %). In four of the 148 CP angles (2.7 %), the AICA was not identified. There was an AICA loop coursing to the internal acoustic meatus in 15 patients (10.1 %). In this study, we examined the relations between VIIth and VIIIth nerve complex and the AICA in cadaver and MRI materials for an understanding of the value and reliability of the radiological data. This study also shows the anatomical variation between these structures.     

Neurovascular trauma in athletes

Injuries to neurovascular structures are not the most common injuries seen in athletes and for this reason may often be overlooked. Additionally, diagnosis and management may be more difficult because of inexperience with these injuries. The majority of acute sports-related neurovascular injuries are associated with contact sports such as rugby, wrestling, ice hockey, and especially football. These injuries most commonly occur about the shoulder girdle and brachial plexus, with "burners" syndrome being the most common. Less common injuries include thoracic outlet syndrome, effort-induced thrombosis, axillary artery occlusion, and peripheral nerve injuries, as well as compression syndromes involving the axillary, suprascapular, and long thoracic nerves.     

Retrolabyrinthine section of the vestibular nerve

When symptoms of dizziness and episodic vertigo cannot be controlled through medical management or drainage procedures such as endolymphatic subarachnoid shunt operations, selective vestibular nerve section may be necessary. In the 1920s eighth cranial nerve sections were performed by neurosurgeons through the suboccipital approach but were frequently associated with hearing loss and facial paralysis. The middle fossa approach has been popularized by Dr. William House and others as a method of selectively sectioning the vestibular nerve and preserving facial and cochlear function. More recently the suboccipital retrolabyrinthine approach has been described as a method of selectively sectioning the vestibular nerve. We have reviewed 42 cases of suboccipital retrolabyrinthine selective section of the vestibular nerve performed at the Otologic Medical Group over the past 2 years. The shortest follow-up on these patients has been 6 months. Thirty-two patients had preoperative diagnosis of Meniere's disease, and of these patients 25 had had previous endolymphatic subarachnoid shunt surgery. Eighty-five percent (27 patients) experienced complete relief of vertigo following surgery, while 6% (two patients) stated they were improved. Three patients reported no relief. There were 10 patients with dizziness who had a diagnosis other than Meniere's disease. In this diverse group three experienced complete relief of vertigo, five were improved, and two reported no improvement of vertigo following surgery. None of the patients lost his hearing as a result of the surgery and there was no facial weakness. One patient had postoperative CSF rhinorrhea and another had meningitis.     

Neurovascular compression (conflict)]

Since Dandy first reported vascular compression of the trigeminal nerve, the concept of neurovascular compression syndrome for trigeminal neuralgia and hemifacial spasm (HFS) has been accepted, and neurovascular decompression has been performed for this condition. The further investigations indicated that some other clinical syndromes such as glossopharyngeal neuralgia, disabling positional vertigo, tinnitus, geniculate neuarlgia, spasmodic torticolis, essential hypertension, cyclic oculomotor spasm with paresis and superior oblique myokymia also may be initiated by vascular compression of the glossopharyngeal, cochleovestibular, intermediate, accessory, oculomotor and trochlear nerves or the ventrolateral medulla oblongata. In this study several hypotheses regarding the development of cranial nerves vascular compression syndromes are presented. It is alsoemphasized the value of high-resolution magnetic resonance tomographic angiography for visualization of vascular compression. The most frequent clinical syndromes caused by vascular compressionof the cranial nerves are discussed regarding the pathogenesis, symptomes and therapy. We present our series of 124 patients with preoperative evidently positive finding of vascular compression to the trigeminal nerve (MRI). Microvascular decompression (MVD) was performed in all of them. Initial postoperative result was excellent in 110/124 (89%) patients,while in 11/124 (9%) patients the pain relief was satisfactory. In the remaining three patients MVD failed. Recurrence of pain after two years reached 19%. Complications were related to diplopia associated with transient fourth nerve dysfunction in 5 (4%) patients, facial motor dysfunction in 4 (3%) patients, transient facial hypesthesia in 27 (22%) patients and partially hearing loss in 4 (3%) patients. Cerebellar hemorrhagic infarction occurred in 1 (0.8%) patient and cerebrospinal fluid leaks appeared in two (1.6%) cases. There was no lethal outcome.     

Surgical labyrinthectomy in the older patient

OBJECTIVE: Ablation of vestibular function is a highly efficacious option in the treatment of disabling vertigo arising from unilateral labyrinthine dysfunction. Regardless of the method used to ablate vestibular function, permanent posttreatment impairment of the balance function will develop in a number of treated patients. Many physicians who are involved in the care of the older patient with episodic vertigo are reluctant to recommend or perform a vestibular ablation procedure, because this treatment may result in permanent disequilibrium, which may be more detrimental to the older patient than the episodic vertigo. This study evaluates the outcome in older patients who underwent unilateral surgical labyrinthine ablation. METHODS: A retrospective analysis was done of the cases of 30 patients, all more than 60 years old, who underwent unilateral vestibular ablation because of disabling episodic vertigo by either transmastoid labyrinthectomy (n = 22) or transcanal labyrinthectomy (n = 8). RESULTS: Episodic vertigo was controlled in 95.5% of the patients in the transmastoid labyrinthectomy group and in 100% of those in the transcanal labyrinthectomy group. Postoperative imbalance was present in 22.7% of patients in the transmastoid labyrinthectomy group and in 62.5% of those in the transcanal labyrinthectomy group. CONCLUSIONS: Vestibular ablation is a viable option in the treatment of disabling vertigo in the older patient. A transmastoid labyrinthectomy may be preferable to a transcanal labyrinthectomy because the incidence of permanent posttreatment imbalance is less with a transmastoid labyrinthectomy. (Otolaryngol Head Neck Surg 1998;118:739-42.)     

VIIIth nerve cavernous hemangioma mimicking a stage 1 acoustic schwannoma

ObjectiveTo report a case of VIIIth nerve cavernous hemangioma, a very rare differential diagnosis among the various pathologies presenting as small enhancing entities into the internal auditory canal. It is one of the most challenging when imaging is not able to differentiate it from an intrameatal vestibular schwannoma.Methods and resultsWe report a cavernous hemangioma extruding from the internal auditory canal, diagnosed after a left translabyrinthine resection in a 45-year-old man complaining of profound sensorineural hearing loss, with no facial paresis or dizziness. The preoperative differential diagnosis of a vestibular schwannoma was impossible, due to the absence of calcifications that usually characterize temporal bone hemangiomas. Clinical presentation, radiological features and treatment considerations are discussed along with up-to-date review of pertinent literature.ConclusionsWhen considering an apparent small intra-auditory canal schwannoma, otoneurologists should be aware of the rare possibility of a cavernous hemangioma. Early diagnosis and surgical treatment may improve the functional outcome, possibly preserving neural integrity.     

Quadrilateral space syndrome: diagnosis, pathology, and treatment

Quadrilateral space syndrome is an infrequent, recently established neurovascular compression syndrome affecting young active adults. With this syndrome, the neurovascular bundle, consisting of the posterior humeral circumflex artery (PHCA) and the axillary nerve, is compressed by fibrotic bands as it traverses the quadrilateral space. Symptoms result from compression of the axillary nerve, not from PHCA occlusion. Because of the vague, often nonspecific, clinical presentation of patients with quadrilateral space syndrome, diagnosis is challenging and requires a high index of suspicion from the orthopedist. Subclavian arteriography confirms the diagnosis. Treatment is usually conservative; operative management is reserved for selected patients. A posterior approach with detachment of the deltoid and teres minor muscles is recommended for surgical decompression and for lysis of fibrous tissue. We report two cases of persistent quadrilateral space syndrome in young adults, treated surgically, with 2-year follow-up. In the present report, diagnostic criteria, pathology, management, operative technique, and recent literature are also reviewed.     

Costo-clavicular outlet syndrome]

Syndromes caused by the compression of the neurovascular bundle are not a rare pathology, though their exact frequency cannot be assessed. Neurovascular bundle in the upper limbs may be compressed at the costo-clavicular space, interscalene triangle or at the insertion of the minor pectoralis muscle into the coracoid process. More than 90% of patients present neurological symptoms and 10% also have vascular problems. Diagnosis depends on a careful clinical and instrumental study of the patients. Arteriography, phlebography and Doppler tests were of value in the diagnostic approach, showing the compression of the subclavian artery and vein using the arm abduction manoeuvre. Electromyography is of value in differential diagnosis of the carpal tunnel syndrome showing the entity and site of nerve compression. The best form of surgical treatment is resection of the first rib according to Roos, using an extrapleural and transaxillary route.     

Characteristics and Management of Superior Semicircular Canal Dehiscence

Objectives To review the characteristic symptoms of superior semicircular canal dehiscence, testing and imaging of the disease, and the current treatment and surgical options.Results and Conclusions Symptoms of superior semicircular canal dehiscence (SSCD) include autophony, inner ear conductive hearing loss, Hennebert sign, and sound-induced episodic vertigo and disequilibrium (Tullio phenomenon), among others. Potential etiologies noted for canal dehiscence include possible developmental abnormalities, congenital defects, chronic otitis media with cholesteatoma, fibrous dysplasia, and high-riding jugular bulb. Computed tomography (CT), vestibular evoked myogenic potentials, Valsalva maneuvers, and certain auditory testing may prove useful in the detection and evaluation of dehiscence syndrome. Multislice temporal bone CT examinations are normally performed with fine-cut (0.5- to 0.6-mm) collimation reformatted to the plane of the superior canal such that images are parallel and orthogonal to the plane. For the successful alleviation of auditory and vestibular symptoms, a bony dehiscence can be surgically resurfaced, plugged, or capped through a middle fossa craniotomy or the transmastoid approach. SSCD should only be surgically treated in patients who exhibit clinical manifestations.     

Retrolabyrinthine vestibular neurectomy with simultaneous monitoring of eighth nerve and brain stem auditory evoked potentials

We have used retrolabyrinthine vestibular neurectomy in 36 of 49 cases as the primary surgical procedure to relieve vertigo. Most of the patients (46 of 49) had Meniere's disease. Results indicate that 71% (35 of 49) of the patients had no vertigo after the operation, while 22% (11 of 49) had much improvement. Hearing was maintained within 20 dB of the preoperative level in 78% (38 of 49) of the patients. During surgery in the last 23 patients, direct nerve potentials were recorded from the middle ear promontory and the intracranial cochlear nerve. Brain stem auditory evoked responses were simultaneously recorded in the last 10 patients. It appears that the intraoperative direct cochlear nerve potentials can be used as a sensitive monitor of trauma to the cochlear nerve during and after vestibular neurectomy. If the latency of the eighth nerve action potential changes less than 0.3 msec and the waveform does not change after vestibular neurectomy, there is an excellent chance that hearing at 1 month after surgery will be within 15 dB of the level before surgery. The retrolabyrinthine vestibular neurectomy has replaced the middle fossa vestibular neurectomy and the endolymphatic subarachnoid shunt procedure in our clinic.     

Neurovascular compression in the thoracic outlet: changing management over 50 years.

SUMMARY BACKGROUND DATA: During the past five decades, significant improvements have been made in the diagnosis and treatment of thoracic outlet syndrome (TOS) secondary to sports activities, breast implants, or median sternotomy. METHODS, RESULTS, AND CONCLUSIONS: Of more than 15,000 patients evaluated for TOS, 3914 underwent primary neurovascular decompression procedures and 1221 underwent second surgical procedures for recurrent symptoms. Of 2210 consecutive patients, 250 had symptoms of upper plexus compression only (median nerve), 1508 had symptoms of lower plexus compression only (ulnar nerve), and 452 patients had symptoms of both. Ulnar and median nerve conduction velocities confirmed the clinical diagnosis. Transaxillary first rib removal alone for neurovascular decompression relieved both upper and lower plexus symptoms (without a combined transaxillary and supraclavicular approach). There are two reasons for this: most upper compression mechanisms attach to the first rib, and the median nerve is also supplied by C8 and T1 as well as C5, C6, and C7 nerve roots. Axillary subclavian artery aneurysm or occlusion was treated successfully in 240 patients. Dorsal sympathectomy was performed concomitantly in 71 patients for occlusion or embolectomy. It was combined with first rib resection in 1974 patients for sympathetic maintained pain syndrome and causalgia that did not improve with conservative therapy. Of 264 patients with effort thrombosis (Paget-Schroetter syndrome), 211 were treated by urokinase thrombolysis and prompt first rib resection with excellent long-term results. Recurrent TOS symptoms required a second procedure using the posterior approach in 1221 patients with brachial plexus neurolysis and dorsal sympathectomy. The use of hyaluronic acid significantly reduced recurrent scarring.     

Introduction to primary hemifacial spasm: A neurosurgical disease

Primary hemifacial spasm is a hyperactive cranial nerve syndrome. The cause is always a neurovascular compression, generally at the root exit zone from the brainstem. Its curative treatment is microvascular decompression, that may be performed as a first option, or secondarily when botulinum toxin injections fail.     

Surgical treatment for vertigo: patient survey of vertigo, imbalance, and time course for recovery.

OBJECTIVES: To assess surgical treatment of vertigo by patient ratings of postoperative vertigo, imbalance, and timing of symptom improvement. METHODS: A total of 3637 surgeries for vertigo were performed since 1974. Questionnaires sent to a random sample of patients operated since 1994 were completed by 28 endolymphatic sac shunt (ES), 54 vestibular nerve section (VNS), and 14 labyrinthectomy patients. RESULTS: All groups rated current vertigo characteristics and AAO-HNS disability as improved (all P 相似文献