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Intratumoral hemorrhage in vestibular schwannomas is rare. Symptoms often have an acute onset and include headache, nausea, vomiting, vertigo, and depressed consciousness. Intratumoral hemorrhage is probably caused by vascular fragility associated with tumor characteristics and growth. With hemorrhage in VS being rare, repeated hemorrhage has only been reported twice, and on clinical grounds only. The present report details the case of acute neurological deterioration in a patient with repeated intratumoral hemorrhage inside a vestibular schwannoma with computed tomography and magnetic resonance imaging confirmation. To our knowledge, repeated hemorrhage in vestibular schwannoma with radiological confirmation has not been reported before.

We report a patient with anterior and posterior inferior cerebellar artery infarction, which manifested as profound deafness, transient vertigo, and minimal cerebellar signs. We suspect that ischaemia of the left internal auditory artery, which originates from the anterior inferior cerebellar artery, caused the deafness and transient vertigo. A small lesion in the middle cerebellar peduncle in the anterior inferior cerebellar artery territory and no lesion in the dentate nucleus in the posterior inferior cerebellar artery territory are thought to explain the minimal cerebellar signs despite the relatively large size of the infarction. Thus a relatively large infarction of the vertebral-basilar territory can manifest as sudden deafness with vertigo. Neuroimaging, including magnetic resonance imaging, is strongly recommended for patients with sudden deafness and vertigo to exclude infarction of the vertebral-basilar artery territory.

Sensitivity to sound and vertigo are often components of migraine. Recent studies suggest that plasma extravasation from intradural blood vessels may contribute to migraine pain. This study documented plasma extravasation in the mouse inner ear after intravenous administration of serotonin (5-HT). Horseradish peroxidase (HRP) was injected intravenously to trace protein extravasation in mice, followed 15 min later by intravenous 5-HT or saline. Forty-five minutes later, mice were euthanized. HRP extravasation was visualized immunohistochemically and quantified densitometrically. Baseline and evoked extravasation in stria vascularis and tectorial membrane were indistinguishable from skin, dura mater and tympanic membrane. Brain parenchyma, Scarpa's ganglion, basal spiral ganglion and modiolus, and the central vestibular nerve segment showed no significant 5-HT-induced extravasation. In contrast, 5-HT produced extravasation in the apical spiral ganglion, modiolus, and intralabyrinthine superior and inferior vestibular nerve. Thus, inner ear plasma extravasation is a potential mechanism for migraine-associated vertigo and sound sensitivity.

A perfect knowledge of the anatomy of the vestibuloacusticofacial pedicle is required to preserve hearing and facial functions during cerebellopontine angle surgery for vestibular schwannoma. A clarification of the anatomy of this pedicle, in particular of its blood supply, is presented here, based on a review of the available literature, as well as on the author's data issued from anatomical dissections on latex-injected fresh specimens, and from radiological images of the cerebellopontine angle. The blood supply to the vestibuloacusticofacial bundle arises from the meatal loop of the anterior inferior cerebellar artery most often exhibited at the porus of the internal acoustical meatus. The labyrinthine artery is particularly exposed to injury between the cochlear and facial nerves. In addition, dissection in between these two nerves is likely to sever vessels directed to these nerves even though the labyrinthine artery is not interrupted. Thus, aside from a direct injury to the labyrinth, auditory function can be impaired through two distinct ischemic lesion types. Although the facial nerve is supplied through three main arterial systems (from the labyrinthine, the middle meningeal, and the stylomastoid arteries), its labyrinthine portion is more likely to suffer from ischemic damage as it is only supplied by meatal arteries. A refinement of our anatomical knowledge of the vestibuloacusticofacial pedicle, from a functional point of view, could arise from laser Doppler measurements of labyrinthine and facial blood flow during surgery, in an attempt to improve our functional preservation rate during therapeutic procedures for vestibular schwannoma.

The authors present pilot experience with transcranial duplex scanning (TCDS) of the cerebral vessels in 17 patients with secondary cochleovestibular neuritis combined with chronic leptomeningitis (primarily of the posterior cranial fossa). This method has determined extra- and intracranial hemodynamics, characterized arterial and venous blood flow qualitatively and quantitatively, outlined possible genetically determined factors in development of dyscirculatory disorders. Finally, hemodynamic defects of two types were revealed in 12 patients. Type 1 (3 patients) was characterized by asymmetric circulation in the territory of the middle, anterior and posterior cerebral arteries, by the absence of venous congestion. Type 2 (9 patients) was characterized by impaired venous outflow manifesting as higher speed of the blood flow and its phase response along the intracranial veins and sinuses. In 7 patients these defects combined with asymmetric circulation along brain stem arteries. These patients were diagnosed to have perilymphatic labyrinthine hydrops.

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.

Objective: To study the pathophysiology of labyrinthine infarction., Background: The syndrome of sudden onset vertigo or hearing loss is commonly attributed to inner ear vascular disease, yet histologic studies of isolated labyrinthine infarction in humans have been rare and have not included a complete examination of the vertebrobasilar vascular system., Methods: Temporal bones, brainstem, cerebellum, and the supplying blood vessels were subjected to gross and microscopic postmortem examinations in a 92-year-old woman who had a sudden onset of vertigo and hearing loss in the right ear 7 years before death., Results: There were prominent atherosclerotic changes at the vertebrobasilar junction, but the internal auditory artery and its branches were patent on both sides. Histologic studies showed degenerative changes in the cochlea and vestibular labyrinth on the right. The posterior canal ampulla and saccular macule were relatively preserved showing partial areas of intact sensory epithelium with underlying nerve fibers. The right vestibulocochlear nerve showed a fibrotic scar and multiple patchy areas of degeneration. These findings are most consistent with a transient period of reduced perfusion of the internal auditory artery., Conclusion: The partial sparing of the inferior vestibular labyrinth may indicate a decreased vulnerability to ischemia because of its better collateral blood supply.

Vascular casting has so far been used mainly for observation of the vascular system of the inner ear in experimental animals. In the present study, this method was applied to analysis of the three-dimensional vascular structure in the inner ear in humans. To date there has been no comparative study of overall pictures of blood vessels in the human inner ear. Seven cases were observed mainly by means of scanning electron microscopy. Even with this new method, the results in many respects obtained confirmed those of previous reports. However, the following findings which have not been previously reported or are currently in dispute, were observed: i) In two cases, spring coil-like structures of blood vessels were found in the internal auditory canal; ii) We corroborated the pattern of arrangement of cochlear arteries previously described in words and schemata, i.e., the following two types were confirmed: the first type showing the cochlear branch of vestibulocochlear artery and the spiral modiolar artery running into the cochlea, and the second type showing the cochlea supported by arteries derived from the artery corresponding to the vestibulocochlear artery, alone; and iii) A right-angled arteriolar branch of the spiral modiolar artery was found to further bifurcate to form radiating arterioles extending in two directions: both over the scala vestibuli and along the spiral lamina.

Cochleovestibular nerve compression syndrome (CNCS) is the term used to describe a group of audiovestibular symptoms thought to be due to a vessel compressing the cochleovestibular nerve. These symptoms include recurrent vertigo, continuous disequilibrium and acquired motion intolerance. Recently, Moller reported that CNCS can be diagnosed based on abnormalities in the auditory brainstem response (ABR). After specifically excluding all other vestibular disorders, 63 patients with symptoms suggestive of CNCS were identified. These patients were systematically evaluated with a standard neurotologic test battery, and the results were reviewed retrospectively. Hearing loss was found in 51 (81%) of 63 cases, including 33 cases of unilateral high-frequency loss and 14 cases of middle-frequency loss. ABR data were interpreted with respect to Moller's criteria, and abnormal studies were found in 42 (75%) of 56 cases. Abnormal electronystagmograms were found in 57 (93%) of 61 cases. Thirteen of the patients subsequently underwent a posterior fossa procedure for vertigo and, vessels were found in contact with the cochleovestibular nerve in 11 of 13 cases. The results of this study suggest that the majority of CNCS patients have neurotologic test findings that suggest an abnormality of the cochleovestibular nerve. The results and their implications are discussed.

Histological and morphometrical investigations of the vestibular nerve were performed on surgical specimens from 19 patients suffering from Ménière's disease and on 5 autopsy preparations from patients without inner ear disease. The number of lipofuscin granules and vacuoles in the ganglion cells of specimens from Ménière patients was not increased compared with control specimens of a similar age, nor did the amount of endoneuronal connective tissue in the vestibular nerve specimens differ between the two groups. The density of capillaries in Scarpa's ganglion and vestibular nerve was significantly increased in the Ménière patients compared with the control specimens. Furthermore, the ratio of nerve fibres with a larger diameter was higher in specimens from Ménière patients than in control preparations. There was no difference in the density of myelinated fibres between the two groups.

Permanent or transient reduction of blood flow to the end-organs and to the hindbrain is the single major cause of vestibular disorders and a common cause of sensorineural hearing loss. New imaging modalities have become available which allow the recognition of focal areas of hindbrain ischemia in the prestroke stage. The correlation between focal ischemic pathology and clinical findings opens a new approach to the mapping of central pathology. In addition a detailed knowledge of the vascular anatomy of the hindbrain is indispensable for the development of new microvascular surgical techniques aimed at the restoration of sufficient blood supply.

Fluorescence microscopy was used to examine the perivascular adrenergic innervation in the eighth nerve and vestibular end-organ specimens from 13 patients with otoneurological diseases. It was observed that all the blood vessels accompanying the cochlear and vestibular nerves from patients with acoustic neuroma or Meniere's disease were devoid of specifically fluorescent fibers, while several adrenergic fibers were seen around the arterioles accompanying the inferior vestibular nerve from the patient with sudden deafness.

Considerable interest has developed in otology concerning the relationship between the vascular loop and compression of the eighth nerve, producing vertigo. Several authors have described the radiographic findings relative to the anatomy of these vascular loops. Few previous articles have dealt with cases that have had surgical confirmation or repair of the defect. Our presentation concerns 27 patients who were studied by air CT cisternography of the cerebellopontine angle cistern and internal auditory canal followed by surgical repair. We postulate dampened pulsation as the reason for being able to visualize the vessels on the air study. The diversity of vessel-eighth nerve defects is illustrated. Compression of the vestibular nerve by a vascular loop should be considered one of the causes of intractable vertigo and motion intolerance and is a differential diagnosis in Meniere disease. Air CT cisternography is useful in diagnosing this condition in patients who do not respond to medical treatment.