Surgical Anatomy of the Labyrinthine and Subarcuate Arteries and Clinical Implications.

OBJECTIVE: To study the surgical anatomy of the labyrinthine artery (LA) and the subarcuate artery (SA), their anatomic relationships, and clinical implications, as injury of the LA can result in hearing loss. METHODS: Ten formalin-fixed, latex-colored specimens were studied (20 sides). After retrosigmoid craniotomy and neurovascular dissection under microscopic magnification, 4-mm 0° and 30° endoscopic lenses were used to improve visualization. Results were statistically analyzed. RESULTS: The LA was a constant artery that followed the vestibulocochlear nerve into the internal auditory canal. The SA was an inconstant artery that ended in the dura mater around the subarcuate fossa in 35% of cases. The LA originated from the anterior inferior cerebellar artery in 89.3% of specimens and from the basilar artery in 10.7% of specimens. The SA branched off from the anterior inferior cerebellar artery when present. The origin of the LA was inferomedial to the vestibulocochlear nerve in most cases (71.4%), whereas the SA was usually lateral (70%). The distal portion of the LA was inferomedial to the vestibulocochlear nerve in 71.4% of cases. The distal portion of the SA was superolateral to the nerve in all cases (P < 0.00001). CONCLUSIONS: Knowledge of the different trajectory and anatomic relationship of the LA and the SA with the vestibulocochlear nerve is of paramount importance to differentiate them during surgery. The LA is usually inferomedial to the vestibulocochlear nerve at its distal and proximal aspects, whereas the SA usually originates lateral and ends superolateral to the nerve.

Loop characteristics and audio-vestibular symptoms or hemifacial spasm: is there a correlation? A multiplanar MRI study.

AIM: We investigated if loop characteristics correlate with audio-vestibular symptoms or hemifacial spasm in patients with a vascular loop in the root entry zone (VII and VIII) and in the internal auditory canal. MATERIALS AND METHODS: A retrospective, multicenter study analyzed 2622 consecutive magnetic resonance imaging (MRI) scans of the cerebellopontine angle of patients with asymmetric audio-vestibular symptom or hemifacial spasm; patients' symptoms were confirmed by clinical tests. MRIs displaying vascular loops visible in the axial view were analyzed using multiplanar reconstruction. We evaluated (1) depth of penetration of the loop into the internal auditory canal (IAC); (2) largest diameter of the vessel; (3) nerve(s) involved in the vascular impingement, position of the loop relative to such nerve(s) and number of contacts between vessel and nerve(s); (4) length of such contact. The loop metrics described above were correlated with the patients' audio-vestibular symptoms and hemifacial spasm. RESULTS: Three hundred ninety-nine patients displayed a loop visible in the MRI axial view and out of them only 118 displayed a direct contact between loop and nerve. The cochlear nerve was involved in a contact in 57.7%. Loops in direct nerve contact had a calibre > 0.85 mm, were located in the middle portion of the IAC, and correlated with vertigo (p = 0.002), tinnitus (p = 0.003), and hemifacial spasm (p < 0.001). Asymmetric sensorineural hearing loss (SNHL) correlated with number of contacts (p < 0.001) and length of contact (p < 0.05). The contact was asymptomatic in 41.5% of patients. CONCLUSION: Loop characteristics may help predict whether a vascular impingement is responsible for a symptom and guide the physician to select the best treatment. KEY POINTS: • A vascular loop in the internal auditory canal was observed in 18-20% of the patients in this study; whether a loop can be responsible for a compressive syndrome is still unclear in particular referred to the vestibulocochlear nerve. • Compression by a loop on the facial nerve causes hemifacial spasm; compression by a loop on the cochlear or vestibular nerve may cause audio-vestibular symptoms. • In patients with a loop, the loop calibre, the loop position, and the number of loop-nerve(s) assessed via the multiplanar MRI reconstruction technique may help assess whether the patient will manifest audio-vestibular symptoms or hemifacial spasm.

Abnormal postural reflexes in a patient with pontine ischaemia.

The control of body posture is a complex activity that needs a very close relationship between different structures, such as the vestibular system, and the muscle and joint receptors of the neck. Damage of even one of these structures can lead to abnormal postural reflexes. We describe a case of a woman with a left pontine ischaemia who developed a 'dystonic' extensor posture of the left limbs while turned on the right side. This clinical picture differs from previous reports on the subject, and may relate to ischaemic damage of a pontine structure involved in posture control, or of adjacent neural connections to be yet identified. To the best of our knowledge, this is the first case reported in the literature. Clinical examples of an altered interplay between vestibular and neck receptors are rare.

[The clinical manifestations and neurophysiological features of long-lasting paroxysmal vertigo:theanalysis of the original observations].

The objective of the present study was to elucidate specific features of etiology and pathophysiology of recurring chronic vestibular dysfunction. It included 90 patients with this pathology of whom 24 (26.6%) presented with vascular compression of the vestibulocochlear nerve diagnosed by means of high-field MRI. This method revealed the high frequency of positionally-dependent vestibular dysfunction associated with neurovascular interactions. Analysis of the state of vestibular dysfunction during the attack-free periods demonstrated the signs of latent vestibular dysfunction in 20 (83.3%) patients. The results of the study provide additional information on the prevalence of vascular compression of the vestibulocochlear nerve in the patients presenting with recurrent chronic dizziness; moreover, they make it possible to evaluate the state of vestibular function and develop the new diagnostic criteria for vestibular paroxismia.

Labyrinthine artery detection in patients with idiopathic sudden sensorineural hearing loss by 7-T MRI.

OBJECTIVE: To compare the detection rates of the labyrinthine artery in subjects with idiopathic sudden sensorineural hearing loss (ISSHL) and in normal-hearing controls using 7-T magnetic resonance imaging (MRI). STUDY DESIGN: Cross-sectional study. SETTING: Tertiary referral center. SUBJECTS AND METHODS: In 18 patients (9 males, 9 females) with ISSHL and 32 volunteers (21 males, 11 females) with normal hearing, 7-T MRI (Discovery MR950; GE Healthcare, Milwaukee, Wisconsin) was performed with the 3-dimensional time-of-flight spoiled gradient echo (3D TOF SPGR) sequence to compare the detection rates of the labyrinthine artery. RESULTS: The MRI scans were performed from 3 to 54 days after onset. Of the 18 patients with ISSHL, 8 showed complete recovery, 9 showed partial recovery, and the rest showed no recovery. The labyrinthine artery was depicted in 36 of 36 ears (100%) in the ISSHL group and 63 of 64 (98.4%) ears in the normal-hearing group, with no significant difference in detection rates. CONCLUSION: To our knowledge, the present study is the first to report depiction of the labyrinthine artery by 7-T MRI. These preliminary results indicate occlusion of the labyrinthine artery would be rare in the pathogenesis of ISSHL, and they also demonstrate that the labyrinthine artery could be detected by ultra-high-field MRI.

Characterization and inflammatory response of perivascular-resident macrophage-like melanocytes in the vestibular system.

A large number of perivascular cells expressing both macrophage and melanocyte characteristics (named perivascular-resident macrophage-like melanocytes, PVM/Ms), previously found in the intra-strial fluid-blood barrier, are also found in the blood-labyrinth barrier area of the vestibular system in normal adult cochlea, including in the three ampullae of the semicircular canals (posterior, superior, and horizontal), utricle, and saccule. The cells were identified as PVM/Ms, positive for the macrophage and melanocyte marker proteins F4/80 and GSTα4. Similar to PVM/Ms present in the stria vascularis, the PVM/Ms in the vestibular system are closely associated with microvessels and structurally intertwined with endothelial cells and pericytes, with a density in normal (unstimulated) utricle of 225 ± 43/mm(2); saccule 191 ± 25/mm(2); horizontal ampullae 212 ± 36/mm(2); anterior ampullae 238 ± 36/mm(2); and posterior ampullae 223 ± 64/mm(2). Injection of bacterial lipopolysaccharide into the middle ear through the tympanic membrane causes the PVM/Ms to activate and arrange in an irregular pattern along capillary walls in all regions within a 48-h period. The inflammatory response significantly increases vascular permeability and leakage. The results underscore the morphological complexity of the blood barrier in the vestibular system, with its surrounding basal lamina, pericytes, as well as second line of defense in PVM/Ms. PVM/Ms may be important to maintain blood barrier integrity and initiating local inflammatory response in the vestibular system.

Assessment of skin microvascular endothelial function in patients with acute unilateral vestibular syndrome.

Abnormalities in labyrinth vasculature, resulting in labyrinth ischemia may be responsible for acute unilateral vestibular syndrome (AVS). However, since no tools for the study of the labyrinth microvasculature are available in clinical settings, labyrinth microvascular abnormalities in AVS patients (AVS-pts) can only be hypothesized on the basis of the their cardiovascular risk profile. Considering that skin microcirculation may mirror vascular function in other body districts, we examined skin endothelial function in 20AVS-pts and in 20 healthy control subjects (CS), with the aim of predicting labyrinth microvascular abnormalities in the same AVS-pts, potentially involved in the pathogenesis of their AVS. AVS-pts and CS underwent laser-Doppler flowmetry measurement of the skin forearm vasodilator response (SVR) to iontophoresis of the endothelial-dependent vasodilator acetylcholine (ACh) and to the endothelial-independent vasodilator sodium nitroprusside (SNP). SVR to ACh was significantly lower than to SNP in AVS patients (p < 0.005, ANOVA for repeated measures), consistent with skin endothelial dysfunction, while no significant differences in SVR between ACh and SNP were observed in CS. Accordingly with an arbitrary cut-off of 30% or greater reduction in SVR to ACh compared to SNP, endothelial dysfunction was found in 4 (20%) of CS, and in 14 (70%) of AVS-pts (6 with associated co-morbidities potentially responsible for endothelial dysfunction, and 8 without these co-morbodities). This study shows that the investigation of skin endothelial function in AVS-pts may be helpful in identifying AVS-pts in whom an ischemic origin of AVS might be more probable, in spite of their low cardiovascular risk profile.

Immunoelectron microscopic analysis of neurotoxic effect of glutamate in the vestibular end organs during ischemia.

CONCLUSION: The excessive glutamate released from the type I and type II hair cells and the supporting cells injure the bouton-type endings and the nerve chalices in 30 min ischemia, and neuronal damage of glutamate was slight in 10 min ischemia. OBJECTIVE: In the present study, we investigated by means of post-embedding immunoelectron microscopic analysis whether neuronal damage in the vestibular end organs is associated with the change of cellular glutamate concentration during ischemia. METHODS: Transient local anoxia (10 min, 30 min) of guinea pig inner ear was induced by pressing the left labyrinthine artery. The right sides were used as controls. The morphological changes of the vestibular end organs and the areal gold particle densities representing glutamate were compared in the ischemia side and the control side. RESULTS: The areal gold particle densities of the type I and type II hair cells and the supporting cells in the ischemic side were lower than those of the control side. There were no remarkable morphological changes compared to the control side in 10 min ischemia. In 30 min ischemia, the bouton-type endings were swollen and intercellular spaces between the type I hair cells and the nerve chalices were enlarged.

Inner ear decompression sickness in compressed-air diving.

INTRODUCTION: Inner ear decompression sickness (IEDCS) has become more frequently reported in recreational diving. METHODS: We examined 34 divers after IEDCS and analyzed their dive profiles, pattern of symptoms, time of symptom onset and the association with a right-to left shunt (r/l shunt). RESULTS: Four divers used mixed gas and were excluded from the analysis. Of the remaining 30 divers, 25 presented with isolated IEDCS alone, while five divers had additional skin and neurological symptoms. All divers presented with vertigo (100%), and 12 divers reported additional hearing loss (40%). All symptoms occurred within 120 minutes (median 30 minutes) of ascent. Twenty-two of 30 divers (73.3%) showed a r/l shunt. CONCLUSION: A possible explanation for the frequent association of a r/l shunt and the dominance of vestibular rather than cochlear symptoms could be attributed to the different blood supply of the inner ear structures and the different size of the labyrinthine compartments. The cochlea has a blood supply up to four times higher than the vestibular part of the inner ear, whereas the vestibular fluid space is 30% larger. The higher prevalence of symptoms referrable to the less well-perfused vestibular organ provides further evidence that persistent local inert gas supersaturation may cause growth of incoming arterial bubbles and may therefore be an important pathophysiological factor in IEDCS.

Abnormal cervical vestibular-evoked myogenic potential in anterior inferior cerebellar artery territory infarction: frequency, pattern, and a determinant.

BACKGROUND: There has been no systematic study that carefully investigates the characteristic features of abnormal cervical vestibular-evoked myogenic potential (cVEMP) response associated with the AICA territory infarction. OBJECTIVES: To investigate the frequency, the characteristic patterns of abnormal cVEMP associated with AICA territory infarction, and the crucial site for producing abnormal cVEMP response in the AICA territory infarction. METHODS: We studied 16 consecutive cases of unilateral AICA territory infarction diagnosed by brain MRI. VEMP was induced by a short click sound and was recorded in contracting sternocleidomastoid muscle. Each patient underwent a quantitative audiovestibular evaluation, including bithermal caloric test and pure tone audiogram. RESULTS: Eight patients (50%) exhibited abnormal cVEMP response on the side of the AICA territory infarction. All patients with abnormal cVEMP showed an absent or decreased response in amplitude but no difference in latency. Patients with abnormal VEMP were significantly more likely to have canal paresis (CP), sensorineural hearing loss, or both compared with patients who had normal cVEMP. Conversely, abnormal cVEMP was more frequently observed among patients with CP than among those without CP. There was no difference in lesion sites according to brain MRI among patients with or without abnormal cVEMP response. CONCLUSIONS: Our findings suggest that the peripheral vestibular structure with the inner ear probably plays a crucial role in producing abnormal cVEMP response associated with AICA territory infarction.

Vestibular tributaries to the vein of the vestibular aqueduct.

CONCLUSION: The vein of the vestibular aqueduct drains blood from areas extensively lined by vestibular dark cells (VDCs). A possible involvement in the pathogenesis of an impaired endolymphatic homeostasis can be envisioned at the level of the dark cells area. OBJECTIVES: The aim of this study was to investigate the vascular relationship between the vein of the vestibular aqueduct and the vestibular apparatus, with focus on the VDCs. METHODS: Sixteen male Wistar rats were divided into groups of 6 and 10. In the first group, 2 µm thick sections including the vein of the vestibular aqueduct, utricle, and crista ampullaris of the lateral ampulla were examined by light microscopy and computer-generated three-dimensional imaging. In the second group, ultrathin sections including venules and VDCs were examined by transmission electron microscopy. RESULTS: A microvascular network was observed in close relation to the VDCs in the utricle and the crista ampullaris of the lateral semicircular canal in the vestibular apparatus. One major vein emanated from these networks, which emptied into the vein of the vestibular aqueduct. Veins draining the saccule and the common crus of the superior and posterior semicircular canals were likewise observed to merge with the vein of the vestibular aqueduct.

Contribution of intracranial vertebral artery asymmetry to vestibular neuropathy.

OBJECTIVES: To test the hypothesis that vertebral artery hypoplasia (VAH) may affect the lateralisation of vestibular neuropathy (VN), probably through haemodynamic effect on the vestibular labyrinth. METHODS: 69 patients with unilateral VN were examined with a magnetic resonance angiographic (MRA) and caloric test. 50 healthy subjects served as controls. The diagnosis of intracranial VAH was based on MRA if <0.22 cm in VA diameter and a diameter asymmetry index >40%. The authors then correlated the canal paretic side with the VAH side. RESULTS: MRA study revealed 29 VAH (right/left: 23/6) in VN subjects and six VAH in controls (right/left: 5/1). The RR of VAH in VN subjects compared with controls was elevated (RR=2.2; 95% CI 1.8 to 2.8). There was a high accordance rate between the side of VAH and VN. Among 29 patients with unilateral VAH, 65.5% (N=19) had an ipsilateral VN, in which left VAH showed a higher accordance rate (83.3%) than the right side (60.9%). VN subjects with vascular risk factors also had a higher VAH accordance rate (81%) than those without (25%). CONCLUSIONS: VAH may serve as a regional haemodynamic negative contributor and impede blood supply to the ipsilateral vestibular labyrinth, contributing to the development of VN, which could be enhanced by atherosclerotic risk factors and the left-sided location.

Gross anatomy and arterial vascularization of the tympanic cavity and osseous labyrinth in mid-gestational bovine fetuses.

This study aims to determine morphological features of certain aural formations, varietal characteristics, and arterial supply in fetal development period in cattle. For this purpose, ears of 10 bovine fetuses in mid-gestation were evaluated. Organ morphology and vascularization in prenatal life were investigated by using corrosion cast technique. It was observed that some aspects of osseous formation and vascular organization in middle and inner ears were not developed completely in the first half of gestation; in addition, cochlea did not its snail-like structure yet, lateral semicircular canal was rather low compared to others and auditory ossicles did not take its final shape. The feeding blood vessels of inner ear were found to demonstrate three different distribution patterns, whereas feeding pattern in middle ear was very similar in many specimens. The presence of stapedial artery was also identified. Differences and similarities with other some species were assessed in terms of both general morphological structure and vascular organization. From this regard, it is thought that this study will constitute a comparative model for both humans and other species and provide morphological contributions since there is not sufficient literature on species-specific ear morphology in the field of veterinary anatomy in contrast to the abundance of studies on humans.

Gamma knife surgery of vestibular schwannomas: volumetric dosimetry correlations to hearing loss suggest stria vascularis devascularization as the mechanism of early hearing loss.

OBJECTIVE: Determine which variables are correlated with early hearing changes after gamma knife surgery of vestibular schwannomas (VSs). STUDY DESIGN: Prospective clinical study of hearing outcomes, radiation dosimetry, conformity, and tumor size of all sporadic unilateral VS patients treated between June 2000 and July 2009. SETTING: Tertiary referral center. PATIENTS: : Fifty-nine VS patients with at least 6 months of follow-up data were studied. INTERVENTIONS: Audiometry and imaging were performed to determine auditory thresholds, speech discrimination, and tumor size. Radiation doses to 5 volumes were measured. MAIN OUTCOME MEASURES: Pretreatment and posttreatment comparisons were performed with regard to change in tumor size; radiation dose to specific volumes including the internal auditory canal, cochlea, basal turn of the cochlea, and modiolus; and conformity of the treatment. RESULTS: The mean follow-up was 63.76 months (standard deviation, ±29.02 mo; range, 9-109 mo). The median follow-up was 65.5 months. A statistically significant association between maximum radiation dose to the cochlea volume and 3-frequency pure-tone average in patients starting with 50 dB or lesser PTA3 was demonstrated using linear regression analysis. CONCLUSION: Longitudinal changes in hearing occur over time, with the largest changes seen in the first 12 months after treatment. With our study outcomes as basis, limiting the dose of radiation to the cochlea to no more than 4 Gy would likely reduce vascular injury to the stria vascularis and improve hearing outcomes. Shielding the cochlea during the treatment planning process would be one mechanism to accomplish this goal.

Effect of treatment with betahistine dihydrochloride on the postural stability in patients with different duration of benign paroxysmal positional vertigo.

The effect of betahistine dihydrochloride on the postural stability after repositioning Epley's maneuver (EM) in patients with BPPV was evaluated by static posturography in open and closed eyes conditions. Ninety patients were divided into four groups by duration (less and above 60 days of BPPV) and by treatment (with and without treatment with betahistine). The investigation was made one hour after the positive Dix-Hallpike test, 10 and 20 days after the treatment with EM. "Sway velocity" (SV) was calculated to evaluate postural stability. The results show dependence between efficacy of treatment with betahistine applied after EM and duration of BPPV. Betahistine normalized postural stability of patients with duration of BPPV less than 60 days after 10 days of treatment and had less effect on patients with duration of BPPV above 60 days. We assume that after removing the otoconia betahistine plays an important role for improving blood flow in the inner ear. The short presence of otoconia didn't damage sensory receptor, and restoring the normal function of motion-sensitive hairs cells and stabilizing the posture was observed.

A potential portal flow in the inner ear.

OBJECTIVES/HYPOTHESIS: The aim of the present study was to visualize the flow direction of blood in the extraosseous part of the vein of the vestibular aqueduct (VVA) and to explore the effect of an induced obstruction in the distal part of the VVA before it merges with the sigmoid sinus. The endolymphatic sac has been implicated as a potential endocrine gland, which venules drain to the VVA. A reversal of the direction of flow in the VVA toward the inner ear could, through vestibular arteriovenous anastomosis, cause portal circulation in the inner ear. STUDY DESIGN: The authors conducted an experimental animal study using in vivo fluorescence microscopy. RESULTS: Obstructing the distal part of the VVA just before it empties into the sigmoid sinus immediately reverses the flow of blood in the VVA toward the inner ear. CONCLUSIONS: After an obstruction of the VVA, the drained venous blood from the endolymphatic sac may enter a portal circulation in the inner ear, which could cause disturbances in the endolymph homeostasis and potentially symptoms as seen in Meniere disease.

Acute peripheral vestibular syndrome of a vascular cause.

BACKGROUND: Acute peripheral vestibular syndrome (APVS) is an idiopathic peripheral vestibulopathy characterized by prolonged vertigo (over 24 h), nausea, vomiting, and postural instability. There has been no previous report of APVS presumably of a vascular cause. OBJECTIVES: To describe APVS presumably resulting from a vascular disturbance with embolic cerebral infarction. PATIENT: A 67-year-old woman developed sudden onset of severe isolated vertigo, nausea, and vomiting, which lasted for 3 days. Ten days earlier, she had had 4 episodes of transient vertigo lasting a few minutes. She had a spontaneous right-beating horizontal nystagmus with a torsional component, in the primary position and on gaze to the right or left. Caloric test showed a decreased response on the left side. Diffusion-weighted brain MRI showed 2 tiny acute infarcts in the left hippocampus and basal ganglia. Magnetic resonance angiogram showed no abnormalities. Continuous electrocardiographic monitoring for 24 h showed paroxysmal atrial fibrillation. CONCLUSION: In this patient, clinical and laboratory findings were consistent with APVS. Considering the simultaneous onset of acute silent infarcts on brain MRI, the definite cardioembolic source with atrial fibrillation, and the episodic transient vertigo attacks before APVS, we speculate that small emboli arising from the heart may have lodged selectively in the anterior vestibular artery, producing APVS.

[Vertigo and peripheral ischemic cochleovestibular syndrome caused by circulatory insufficiency in the vertebrobasilar system].

We studied characteristics of vestibular and acoustic disorders in patients with arterial hypertension, atherosclerosis and vascular dystonia; correlation between peripheral cochleovestibular syndromes (PCVS) and circulation in the major and intracranial arteries, central hemodynamics, organic changes in the brain. We discovered that anomalies and asymmetry in vertebral arteries diameters, stenoses, reduced stroke and minute blood volumes play an essential role in development of PCVS. The latter are rarely accompanied with ischemic foci in the brain. Medication of vascular vertigo consists in administration of an adequate drug. We believe that betaserk is most effective.