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Objectives/hypothesis: Pathologic involvement of the inferior cochlear vein is a mechanism of sensorineural hearing loss in patients with jugular foramen paraganglioma., Study Design: Retrospective case-control study., Methods: The presenting audiograms, magnetic resonance imaging, and computed tomography were reviewed in 46 subjects with jugular foramen paragangliomas. Four-frequency bone conduction average was compared between the tumor and nontumor ears in each subject to establish the presence of sensorineural hearing loss. Imaging findings for each subject were recorded. Univariate and multivariate statistical analyses were performed to determine which radiographic features were associated with sensorineural hearing loss. Hearing data were analyzed as a continuous variable and as a categorical variable., Results: Twenty subjects (43.4%) had a bone-conduction pure-tone asymmetry of greater than 15 dB. Inferior cochlear vein involvement was identified in 19 of the 20 (95%) subjects with sensorineural hearing loss. Inferior cochlear vein involvement was found to be a statistically significant predictor of sensorineural hearing loss using univariate and multivariate analyses. Other imaging findings that were statistically significant predictors of sensorineural hearing loss include Glasscock-Jackson stage, Fisch-Mattox stage, hypoglossal canal involvement, jugulo-carotid spin erosion, and petrous carotid canal erosion., Conclusions: Involvement of the inferior cochlear vein appears to be a plausible mechanism for sensorineural hearing loss in patients with jugular foramen paraganglioma., Level of Evidence: 4 Laryngoscope, 129:67-75, 2019., (© 2018 The American Laryngological, Rhinological and Otological Society, Inc.)

Objectives/hypothesis: The purpose of this study was to investigate possible preventive effects of anti-intercellular adhesion molecule-1 antibody (anti-ICAM-1 Ab) on noise-induced cochlear damage as assessed by changes in auditory thresholds and cochlear blood flow., Study Design: A controlled animal study. Pretreated rats with anti-ICAM-1 Ab or saline control, followed with exposure to 72 continuous hours of broad band noise (107 dB SPL), and 24 hours after noise exposure treated again with anti-ICAM-1 Ab or saline., Methods: Eighteen healthy male Fischer rats (200-250 g) were used. Sixteen were randomly selected to study noise-induced temporary threshold shifts. The remaining two rats were used to study cochlear blood flow (CBF), using laser Doppler flowmetry and blood pressure measurements., Results: Rats treated with anti-ICAM-1 Ab (1.875 mg/kg, intravenously) showed attenuated temporary threshold shifts (TTS) compared to controls. Both groups showed a partial threshold recovery 72 hours following noise exposure, normal for this noise exposure paradigm. Comparisons of baseline and post-treatment measurements of CBF and mean arterial blood pressure revealed no significant changes. Anti-ICAM-1 Ab animals displayed significantly lower mean auditory threshold shifts at all five test frequencies (P < .05) when compared to control., Conclusions: Blocking the cascade of reactive oxygen species (ROS) generation by using anti-ICAM-Ab protects against noise-induced hearing loss.

Objective/hypothesis: The objective of this controlled animal study was to evaluate the effects of intrascalar blood on hearing., Material and Methods: Eight guinea pigs underwent intrascalar administration of their own blood in one ear and control solution in the contralateral ear. Solutions were applied through cochleostomy to the scala tympani. Compound action potential (CAP) thresholds were determined before administration and at different intervals for 2 months thereafter., Results: Immediate deterioration of thresholds was seen mainly in the high-frequency range, averaging 27 dB and 20 dB in the study and control groups, respectively. At day 3, threshold shifts recovered in the control group but remained in the low-frequency range in the study group. An extensive recovery was seen in both groups. However, permanent threshold shifts persisted. There was an enhanced shift of thresholds of up to 7 dB in the study group., Conclusions: Even small amounts of intrascalar blood seem to cause transient and permanent detrimental effects on cochlear function. In procedures involving opening of the otic capsule-like stapes surgery and cochlear implantation with hearing preservation-minimizing surgical blood admixture to intracochlear compartments seems therefore fundamental.

Objective: This animal study aimed to investigate effects of glucocorticoids on the functional recovery of outer hair cells (OHCs) after transient ischemia., Methods: Distortion-product otoacoustic emission (DPOAE) was examined before, during, and after transient cochlear ischemia of 30 minutes using albino guinea pigs., Results: DPOAE decreased to noise level during ischemia. On recirculation, DPOAE initially recovered with time until 20 minutes after the onset of reperfusion, but thereafter, the DPOAE level gradually decreased toward the noise level in the control animals. Prednisolone and methylprednisolone significantly improved the DPOAE level 60 minutes after the onset of reperfusion., Conclusions: The present findings suggest that glucocorticoids possess protective effects against ischemia-reperfusion injury of OHCs.

Objectives: The aim of this study was to observe the effects of mannitol, administered topically at the round window (RW), on cochlear blood flow (CBF) and distortion-product otoacoustic emission (DPOAE) after repeated episodes of cochlear ischemia., Methods: Ten young rabbits were used for this study. Reversible ischemic episodes within the cochlea were induced by directly compressing the internal auditory artery (IAA). CBF was measured using a laser-Doppler (LD) probe positioned at the RW niche. DPOAEs were measured at 4, 8, and 12 kHz geometric mean frequency (GMF) using 60 dB sound pressure level (SPL) primary tone stimuli. In five test ears, mannitol was administered topically at the RW for 30 minutes before the IAA compressions. In five control ears, the IAA compressions were undertaken without application of RW medication. Each ear underwent three 5 minute IAA compressions with a 60 minute rest period between compressions., Results: In the control animals, it was observed that a progressive reduction in DPOAE level followed each successive IAA compression at all three test frequencies. The reduction in DPOAE amplitudes was consistently greater at the higher test frequencies. In the test rabbits, the RW administration of mannitol resulted in significantly less reduction in DPOAE level measures after repeated IAA compressions. For example, 30 minutes after reperfusion at 12 kHz GMF, DPOAE levels in the control ears were reduced by 1.5, 6.0, and 16 dB, compared with 1.5, 4.0, and 6.0 dB in the mannitol test ears., Conclusions: Mannitol appears to exert a protective effect on cochlear function after periods of ischemia. The RW appears to be an efficacious route for topical administration of mannitol into the inner ear.

Objective/hypothesis: Examine and compare in detail the time courses of the auditory brainstem response (ABR) wave I amplitude and latency to the distortion-product otoacoustic emission (DPOAE) amplitude and phase measured in the rabbit model following deliberate obstruction of cochlear blood flow (CBF)., Methods: Using a posterior fossa craniotomy in five rabbits, the internal auditory artery (IAA) was compressed with a probe. ABR and otoacoustic emission were continuously monitored before, during, and after the compressions., Results: ABR wave I amplitudes demonstrated measurable decreases at a mean of 28.3 s after IAA compression, whereas DPOAE amplitudes decreased after a mean of 14.8 s. Wave I latencies began to increase at a mean of 18.3 s after occlusion, while DPOAE phase measures changed after a mean of only 4.8 s following IAA compression. The time-course patterns were similar for the amplitudes of both ABR wave I and DPOAE., Conclusions: ABR wave I amplitude follows a similar, though delayed (by approximately 10 s) time-course pattern to that of the DPOAE following IAA compression. The implication of these findings for intraoperative auditory monitoring is that changes in many currently employed measures will lag actual surgically induced alterations in CBF by at least 20 to 30 s.

Distortion-product otoacoustic emissions (DPOAEs) have been shown to be ideally sensitive to interruptions of the cochlear blood flow. However, a 15- to 30-second latency typically occurs between cessation of circulation and measurable DPOAE level changes. DPOAEs can also be characterized by phase measures. The aim of the present study was to determine in 10 rabbits the effects on DPOAE phase of repetitively compressing the internal auditory artery. In contrast to the delays measured by DPOAE level, phase changes were detected 1 to 5 seconds after internal auditory artery compression. These data suggest that the essentially "real time" monitoring of cochlear function with DPOAE phase can be used to ensure hearing preservation during surgery involving the porus acousticus and skull base.

The postcapillary venule is known to be the preferred site of lymphocyte migration into the extravascular compartment. In this study, induction of these high endothelial venule (HEV)-like vessels has been investigated by inoculation of live cytomegalovirus or inactivated virus into scala tympani of guinea pig cochleas. Endothelial cells of the spiral modiolar vein (SMV) were evaluated histologically 2 to 6 days following inoculation. The experimental group endothelial cells had larger nuclei and increased amounts of cytoplasm. In addition, many lymphocytes were adherent to and present within the vascular wall. Control SMV endothelia showed normal structure and morphology throughout the study. These findings reiterate that nonlymphoid tissues may develop HEV-like characteristics and suggest that HEV-like morphology may be acquired during an acute inflammatory condition in the cochlea.

The transient expression of stress proteins in cells exposed to adverse environmental conditions is thought to provide a survival advantage. In the present study, the expression of the major mammalian stress protein, Hsp72, was characterized in the rat peripheral auditory system following varying periods of unilateral cochlear ischemia and reperfusion. Western blot analysis of whole cochlear homogenates revealed Hsp72 expression after as little as 5 minutes of cochlear ischemia. Cochlear Hsp72 immunoreactivity following 10 minutes of ischemia was observed within 2 hours, remained evident through 6 hours, and decreased toward control levels by 12 hours. Preliminary immunocytochemical localization data revealed Hsp72 expression in the outer hair cells. The characterization of Hsp72 expression following transient ischemia represents the first step toward understanding the role that stress proteins have in the protection of the mammalian auditory system.

The vessels emerging from one side of the basilar artery are supplied exclusively by the homolateral vertebral artery. Since blood flow is laminar through the vertebrobasilar system, mixing between two sides does not normally occur. Based on this fact, an experimental model for research on cochlear hypoxia is proposed and described. The animal's own blood flow in the vertebral artery is completely replaced by a stream of poorly oxygenated blood injected retrogradely through the ipsilateral axillary artery. In this way, the territory supplied by the vessels emerging from this side of the basilar artery, including the ear, is rendered hypoxic. The changes in the cochlear action potentials induced by the reduced oxygen supply are recorded by a chronically implanted electrode and analyzed.

Circulatory disorders, which are well documented in most parts of the human body, are not well documented in the inner ear, although they are expected to occur. It has been previously shown that experimental occlusion of the labyrinthine artery in animals results in severe degenerative changes, fibrosis, and new bone formation in the cochlea. Accordingly, this paper presents presumptive evidence that depriving the human cochlea of its blood supply after surgical removal of an acoustic tumor results in severe degenerative changes that progress to total ossification of the cochlear spaces. This paper also discusses similar changes seen in temporal bones of two patients with sudden sensorineural hearing impairment. Based on these observations, the author concludes that occlusive arterial disease, whether thrombotic, embolic, or spastic, plays a role in some sudden sensorineural hearing losses. Cochlea ossification, detected by polytomography, suggests a vascular etiology of the hearing impairment. Treatment with vasodilator drugs and anticoagulants is justified in these cases until a better diagnostic protocol is developed to eliminate other causes.

A relatively restricted area, including the ear, was perfused in guinea pigs with hypoxic blood having a pO2 of 10, 20, and 30 mm Hg, respectively. The changes induced to the cochlear action potentials were analyzed and the results compared with those obtained in a previous study in which the guinea pigs were rendered hypoxemic by ventilating them with air entrapped in a closed circuit from which the CO2 was continuously absorbed. The changes induced to the cochlear action potentials by both methods were very similar. However, while using the territorial model for inducing hypoxia, 75% of the animals showed a threshold shift at a blood pO2 of 20 mm Hg and with the general model all the animals showed a threshold shift at 25 mm Hg blood pO2. In other words, if the hypoxic condition affected the whole body, other factors such as a slight, but continuous tendency to acidosis with significant increase in blood lactic acid concentration could join the oxygen deficit in affecting cochlear function.

The later stages of development (16-40 weeks in utero) of the periotic duct and its adjacent areas in the human fetus indicate that the critical stages of development occur in four specific time related stages over a six-week period (20-26 weeks). First, the petrous apex ossifies to separate th inferior cochlear vein into the canal of Cotugno and forms the medial wall of the cochlear aqueduct (22 weeks); second, the canalicular otic capsule fuses with the cochlear otic capsule to obliterate Hyrtl fissure and forms of the lateral wall of the cochlear aqueduct (24 weeks); third, progressive bone deposition to the medial surface of the membranous labyrinth and cochlea at the petrous apex elongates the periotic duct and cochlear aqueduct (32 weeks in utero); and fourth, active arachnoid tissue ingrowth into the periotic duct occurs at 20-24 weeks and 34-40 weeks in utero. The terminal event is widening of the CNS opening of the periotic duct at 32 weeks in utero. The periotic duct and cochlear aqueduct length increase with gestation from 25 weeks until term. The periotic duct width remains the same throughout the gestation. The cochlear aqueduct width diminishes with gestational age. The periotic duct remains patent throughout 16-40 weeks in utero.

The activity of adenylate cyclase and the steady state levels of cyclic AMP (cAMP) were determined in stria vascularis (SV) and organ of Corti (OC) of the guinea pig cochlea. The activities are 12 and 19 pmoles/mg dry weight/minute for OC and SV, respectively. The activity was increased two to four-fold by NaF. The base level of cAMP is 4.2 and 4.4 nmoles/g dry weight in OC and SV, respectively. In contrast to brain, neither ischemia nor barbiturates produced major changes of the steady state levels of cAMP. No in vitro effect of cAMP upon the state of activation of glycogen phosphorylase was noticeable in either tissue. cAMP did not exert a significant in vitro inhibition of strial Na+K+-ATPase. Perilymphatic perfusion of cAMP (10-3 M) and of theophylline (5 times 10-3 M) did not produce changes in the endolymphatic potential (EP), but dibutyryl cAMP (10-3 M) led to a significant increase of EP. The alpha adrenergic blocking agent, phentolamine, produced very complex changes of the cochlear potentials. A possible role of catecholamines and cAMP in the secretory phenomena of the SV and in the transduction and/or transmission processes of the auditory sense organ are discussed.

Systemic blood flow, blood flow to the peripheral skin, middle ear, and temporal bone, and that to the inner ear of normal volunteers was manipulated selectively through the use of vasodilator drugs. The effect of selective vasodilation was monitored via changes in the temporal course of the slow-phase velocity of nystagmus evoked by bithermal caloric irrigation. Drug influenced eye velocities were compared with control values measured before drug administration. Eye velocities measured after niacin (a peripheral vasodilator) administration generally were greater than control values, whereas eye velocities measured after papaverine (a central vasodilator) and histamine (a systemic vasodilator) administration typically were less than control values. These findings, with the exception of the cool caloric/niacin condition, are consistent with a model of vestibular dynamics and measurements of cochlear blood flow in animal models.

The purpose of this research is to establish in laboratory animals whether a relationship exists among noise exposure, hypertension, and hyperlipoproteinemia. A discussion of the historical background leading to this work is presented. Previous investigations dealing with each of the three variable, noise, hypertension, and hyperlipoproteinemia, as they relate to hearing, are discussed. Methodology, including new methods developed during this study, will be presented. Results support the concept that a significant relationship does exist among noise, hypertension, hyperlipoproteinemia, and hearing loss.

By means of vascular perfusion via the anterior inferior cerebellar artery with a blood substitute containing the perfluorochemical FC 47 as oxygen carrier, it is possible to maintain normal or near normal levels of the cochlear microphonics and the endolymphatic potential of the guinea pig for perios of 90 min, or longer. Following 60 min. of perfusion with artificial blood, the levels of ATP and 5' AMP in the stria vascularis and the organ of Corti are comparable to those of nonperfused control animals maintained at optimal metabolic conditions. Following the same period of perfusion, the appearance of the organ of Corti is normal, but small vacuoles, presumably deposits of FC 47, are visible in the marginal cells of the stria vascularis. Preliminary experiments concerning the survival time and the revival time of the cochlear potentials, as well as the response to furosemide, ouabain, and mersalyl are presented to illustrate the value of this method in elucidating various biochemical and pharmacological problems of the cochlea.

Using a model previously described, prolonged emotional stress was induced in guinea pigs. Under this condition, arterial blood gases, blood glucose level, PO2 and PCO2 in the expired air, and the heat irradiated by the animals were measured and compared to those of the anesthetized guinea pigs. From the present study, two important findings should be mentioned. First, the metabolic rate of the animals under stress was 30% higher than in the anesthetized group. Second, the arterial PO2 level of the animals under stress was significantly lower than that in the anesthetized ones. Evaluating the noxious effect of severe and/or prolonged emotional stress, one should not neglect the increased oxygen demand resulting from the high metabolic rate of the subject. This factor, together with the decreased arterial blood PO2 level, reinforce the hypoxic effects on the cochlear function, caused by the vasoconstriction of the labyrinthine vessels.