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At least 361 records · Page 20Linked to original sources
PubMed1994

Unilateral mimicking bilateral benign paroxysmal positioning vertigo.

BACKGROUND: Unilateral benign paroxysmal positioning vertigo (BPPV) may mimic bilateral BPPV if the diagnostic positioning maneuver is executed without appropriate alignment of the head and neck with the trunk. OBSERVATIONS: Appropriate alignment is achieved by adjusting the plane of the affected posterior semicircular canal so that it is parallel to the plane of diagnostic head tilt, ie, 45 degrees horizontal head rotation to the left before a head tilt to the right in suspected right-sided BPPV. With inappropriate head alignment and head tilt to the side of the unaffected ear, a free-floating clot within the long arm of the uppermost posterior canal may gravitate toward the cupula and become settled on it. This causes ampullopetal cupulolithiasis, evoking geotropic nystagmus, which may mimic BPPV of the unaffected ear. CONCLUSION: This hypothesis explains the seemingly paradoxical observation of immediate relief from "bilateral BPPV" following unilateral surgical canal occlusion on the "more symptomatic" side.

Calculi↗
PubMed1998

Photochemically induced focal cochlear lesions in the guinea pig: I. DAB staining and SEM study.

A photochemical reaction was used to produce focal microcirculation disorders in the guinea pig cochlea. Temporal bones were removed at various intervals between 5 minutes and 1 month after infusion of rose bengal (RB) and illumination. Infused but unilluminated contralateral cochleae served as controls. Dissected cochlear structures were stained by 3,3'-diaminobenzidine (DAB) peroxidase substrate medium. After observation by light microscopy (LM), the same specimens were processed and observed by scanning electron microscopy (SEM). Dilation of strial capillaries and destruction of strial epithelial cells became apparent at 1 hour after illumination. Tightly packed red blood cells were found filling the severed end of markedly dilated strial capillaries at 24 hours after the procedure. DAB staining of the osseous spiral lamina indicated vascular change with vessel dilation in the illuminated area. At 1 week after illumination, the lesion area of the stria vascularis and spiral prominence was replaced by a layer of larger, flat cells. At 1 month after illumination, all vascular supply to the cochlear lateral wall disappeared at the site of illumination. All lesions remained focal and showed no sign of expansion or reduction throughout the observation period. The cochlear duct of the guinea pig appears to be segmentally nourished by the capillary system. Observation of DAB stained tissue by LM and SEM proved to be informative in the study of microcirculation disorders of the inner ear.

3,3'-Diaminobenzidine↗
PubMed1998

Photochemically induced focal cochlear lesions in the guinea pig: II. A transmission electron microscope study.

Photochemically induced focal lesions in guinea pig cochleas were studied by light microscopy and transmission electron microscopy. The lesions were induced in the second cochlear turns of 35 adult guinea pigs by illumination for 10 minutes with a focused green light immediately after a rose bengal solution was injected into the jugular vein. The cochlear lateral wall and organ of Corti were examined 5, 10, 20, 30, and 90 minutes, 12 and 24 hours, and 3, 7, and 30 days after the procedure. Aggregations of platelets and red blood cells were found in strial capillaries at 5 minutes after illumination. After 30 minutes, marginal cell surfaces protruded into the endolymphatic space; surface membranes were ruptured and the cytoplasm was expelled into the space. In outer hair cells, disruption of the cellular membrane was found near the cuticular plate 12 hours after the procedure. All cellular elements of the lateral wall and organ of Corti were markedly degenerated in the 30-day specimens. Histological changes found in the stria vascularis were consistent with cell damage caused by active oxygen species. It is likely that the stria vascularis is more sensitive to the photochemical reaction than other parts of the cochlea. Cell damage in other parts of the cochlea seemed to have been caused by local microvascular ischemia in addition to the action of active oxygen species induced by the photochemical reaction.

Animals↗
PubMed2003

Transient cochlear ischemia causes delayed cell death in the organ of Corti: an experimental study in gerbils.

To elucidate whether ischemia-reperfusion can cause delayed cell death in the cochlea, the effects of transient cochlear ischemia on hearing and on neuronal structures in the cochlea were studied in Mongolian gerbils. Ischemia was induced by bilaterally occluding the vertebral arteries for 5 minutes in gerbils, which lack posterior cerebral communicating arteries. In gerbils, the labyrinthine arteries are fed solely by the vertebral arteries. Occlusion of the vertebral arteries caused a remarkable increase in the threshold of compound action potentials (CAPs), which recovered over the following day. However, 7 days after the onset of reperfusion, the threshold began to increase again. Morphologic changes in the hair cell stereocilia were revealed by electron microscopy. The number of nuclear collapses was counted in cells stained for DNA and F-actin to evaluate the degree of cell death in the organ of Corti. Changes in spiral ganglion cell (SGC) neuron number were detected, whether or not progressive neuronal death occurred in the SGC. These studies showed that sporadic fusion of hair cells and the disappearance of hair cell stereocilia did not begin until 4 days after ischemia. On subsequent days, the loss of hair cells, especially inner hair cells (IHCs), and the degeneration of SGC neurons became apparent. Ten days after ischemia, the mean percentage cell loss of IHCs was 6.4% in the basal turn, 6.4% in the second turn, and 0.8% in the apical turn, respectively, and the number of SGC neurons had decreased to 89% of preischemic status. These results indicate that transient ischemia causes delayed hearing loss and cell death in the cochlea by day 7 after ischemia.

Action Potentials↗
PubMed2004

Calpain activity in the amikacin-damaged rat cochlea.

The principal aim of this study was to investigate the involvement of calpain in the degeneration of hair cells and ganglion neurons in the amikacin-poisoned rat cochlea. An antibody designed against fodrin-breakdown products (FBDP), which result exclusively from cleavage by calpain, was used. In addition, the involvement of both caspases and protein kinase C (PKC) was studied using, respectively, antibodies against activated caspase 3 and PKCgamma. The results demonstrate the accumulation of FBDP in the degenerating hair cells, in some supporting cells such as Deiters cells, and, later, in the affected ganglion neurons that had been deprived of their sensory targets. Activated caspase 3 was evidenced in a few dying hair cells and ganglion neurons. PKCgamma was highly expressed in all ganglion neurons, sometimes after the loss of hair cells. We conclude that calpain plays a role in the degradation of both the sensory cells and neurons after amikacin ototoxicity. In the poisoned hair cells, calpain and caspase 3 may have synergistic effects in the process of apoptosis. In the ganglion neurons deprived of their sensory elements, calpain may have a prominent role in cell degradation. By contrast, in these ganglion neurons PKCgamma may be implicated in a survival process. Finally, we suggest that calpain is involved in the remodeling of Deiters cells during the scarring process that follows hair cell loss.

Age Factors↗
PubMed2006

Lipopolysaccharide-activated SHP-1-deficient motheaten microglia release increased nitric oxide, TNF-alpha, and IL-1beta.

Accumulating evidence suggests a deleterious role for activated microglia in facilitating neuronal death by producing neurocytotoxic substances during injury, infection, or neurodegenerative diseases. After cochlear ablation, abnormal microglial activation accompanied by increased neuronal loss within the auditory brainstem occurs in motheaten (me/me) mice deficient in the protein tyrosine phosphatase SHP-1. To determine whether abnormally activated microglia contribute to neuronal death in me/me mice, primary microglial cultures from me/me and wild-type mouse cortices were stimulated by the bacterial endotoxin lipopolysaccharide (LPS) to evaluate the secretion of the neurotoxic mediators nitric oxide (NO), tumor necrosis factor-alpha (TNF-alpha), and interleukin-1beta (IL-1beta). Me/me microglia release significantly greater amounts of all three mediators compared with wild-type microglia. However, the increased release of these compounds in microglia lacking SHP-1 does not appear to occur through activation of extracellular signal-regulated kinase (ERK), p38 kinase subgroups of mitogen-activated protein (MAP) kinases, or increases in NF-kappaB-inducing kinase (NIK). These results suggest that abnormal microglial activation and release of neurotoxic compounds may potentiate neuronal death in deafferented cells and can thus potentiate neurodegeneration in the me/me brainstem. Our data also indicate that SHP-1 is engaged in signaling pathways in LPS-activated microglia, but not through regulation of the ERK and p38 MAP kinases.

Animals↗
PubMed1991

On the pathomechanism of cochlear dysfunction in experimental perilymph fistulas.

The mechanism leading to hearing impairment in perilymph fistulas was investigated in guinea pigs with perforated round window membranes (RWM) by analyzing alterations of inner ear fluid pressure, changes of auditory function following manipulations to get presumed air bubbles out of the cochlea ("positional audiometry"), and temporal bone sections. The instantaneous loss of normal positive inner ear fluid pressure after RWM perforation had no immediate effect on auditory function. Inner ear pressure was restored 4 days following RWM perforation. "Positional audiometry" was negative in guinea pigs with perforated RWM. All ears in which auditory thresholds had increased had additional iatrogenic lesions at the spiral lamina. Fistulas in the RWM per se do not affect auditory thresholds. The question of the surgical repair of fistulas was not directly addressed; it only can be concluded that there are no direct sequelae of an isolated fistula which induce auditory impairment and which could be prevented by surgical repair of the fistula.

Acoustic Stimulation↗
PubMed1996

Some ideas on the origin of otoacoustic emissions.

The presence of a basal activity in the cochlea is postulated. This activity is generated by the OHCs which are made to vibrate at their intrinsic resonant frequency by Brown's motion. In keeping with the chaos theory clusters vibrating in phase at one and the same frequency aggregate in the process. These clusters alternate with one another. Minor pathology enhances OHC synchronization so that the clusters become larger. As a result, more energy is projected back into the outer ear canal. This energy is high enough for being picked up as SOAE by current measuring tools.

Adult↗
PubMed1996

Intracochlear schwannoma.

In the case reported evaluation of unilateral endocochlear deafness in a 44-year-old man led to a diagnosis of a small intracanalicular neurinoma of the cochlear nerve which had invaded the first turn of the cochlear spiral.

Adult↗
PubMed1993

Structure and composition of stereocilia cross-links in normal and hydropic cochleas of the guinea pig.

Structure and composition of stereocilia cross-links were investigated cytochemically in normal and hydropic cochleas of the guinea pig. The electron-dense markers colloidal thorium and cationized ferritin were used for visualization. Side links as well as tip links were visualized using both markers. Cationized ferritin allowed a better visualization of the delicate cross-link substructure than did colloidal thorium. Following digestion with neuraminidase, cross-link reactivity for colloidal thorium was virtually abolished. However, the basic structure of the cross-links could still be observed as a result of routine post-fixation and contrast staining. In both 3- and 6-month hydropic cochleas glycocalyx reactivity of the stereocilia appeared to be unaltered, provided that stereocilia were still present. However, loss of cross-links of the outer hair cells - resulting in disarrangement of the stereociliary bundles - was observed in hydropic cochleas. Our results suggest that cross-links are a separate morphological and cytochemical entity, which is different from the glycocalyx. Furthermore, loss of stereocilia cross-links, with concomitant disarrangement of the outer hair cell stereociliary bundle, appears to be one of the early pathological features of surgically induced endolymphatic hydrops, which might be responsible for permanent sensorineural hearing loss.

Animals↗
PubMed1994

H and B human blood-group antigen expression in cochlear hair cells is modulated by thyroxine.

The presence of human blood-group antigens in developing and adult hypothyroid rat cochleas was analyzed using antibodies directed against antigens H and B. During postnatal development, hypothyroid rat cochleas exhibited a highly selective expression of both B and H antigens, mainly at the hair cell level. Labeling for antigen B was found throughout the hair cells, whereas the antibody directed against antigen H selectively labeled the apical part of these cells. These immunostaining patterns were similar to those found in normal (euthyroid) rat cochleas, but antigenic expression periods were clearly prolonged. Thus, whereas in normal rat cochleas, the B and H antigenic expression disappears from postnatal day (PD) 9 on, in cochleas of hypothyroid rats the reactivity was intense until PD15; it decreased from this developmental stage, and was negative or only faintly positive at PD30. Therefore, in congenital hypothyroidism, hair cell immunoreactivity is present at developmental stages that are negative in normal rat cochleas. These results suggest that human blood-group antigen expression on the developing cochlear hair cells of rats is modulated by thyroxine and that thyroxine is necessary for the temporal expression pattern and secretion of normal glycoproteins.

ABO Blood-Group System↗
PubMed1992

Specificity of auditory brainstem response audiometry criteria in acoustic neuroma screening as a function of deviations of reference values in patients with cochlear hearing loss.

On the basis of 79 patients with cochlear hearing loss, the statistical distribution of two criteria commonly used in auditory brainstem response audiometry (ABR) was analyzed: the interaural V latency difference (ILD V) and the interaural difference of I-V interpeak interval (ID I-V). The distribution of both criteria was Gaussian. By evaluating their standard deviations the percentages of statistical false-positives were estimated. The estimated results were 24% false-positive findings using the decision criterion ILD V greater than 0.2 ms and 5.4% false-positive findings using ID I-V greater than 0.3 ms. This corresponds closely to the actual false-positive ABR rates obtained in this sample: 21.5% and 6.3%, respectively. In a separate series of 301 unselected cases with asymmetric sensorineural hearing loss, 29 ABRs were suspect for retrocochlear pathology. In 20 patients, ABRs were absent due to severe hearing loss. Retrocochlear pathology could be confirmed in only 2 cases (both from the group with ABR present). Thus, 47 ABRs (15.7% of 299) were false-positive.

Cochlear Diseases↗
PubMed1994

Effects of acoustic overstimulation on cochlear evoked potentials.

Guinea pigs were exposed to 2 kHz pure-tone or octave-band pass noise at an intensity of 100 dBSPL for 30 min. The effects of sound exposure on cochlear microphonics (CM) and compound action potential (AP) were studied using a test condition devised to complete the measurement of the sensitivity of both potentials for the frequency from 1 to 7 kHz within several minutes. The loss of CM sensitivity was limited to around 5 dB for all test frequencies in animals exposed either to pure-tone or band noise. In contrast, the loss of AP in both exposure conditions was significantly greater than that of the CM, and the magnitude of the AP losses reflected the frequency characteristics of the exposure sounds. From these observations, the AP is considered to be a more sufficient index than the CM in studying the effects of acoustic overstimulation.

Animals↗
PubMed2003

[Prognostic factors in hearing recovery following sudden unilateral deafness].

A perilymph fistula is a possible cause for sudden unilateral sensory deafness. In this retrospective study the data of 73 patients with unilateral sudden deafness were analyzed. All of them underwent an exploratory tympanotomy during which both windows were packed with soft tissue. Postoperatively all patients received rheological therapy with pentoxifyllin and steroids. The following possible prognostic indicators were analyzed: age, sex, tinnitus, vertigo, vomiting, spontaneous nystagmus, positive fistula test, time between onset of symptoms and therapy, intraoperative proof of a perilymph fistula, and signs of barotrauma in the patient's history. A significant postoperative recovery of the hearing loss (>20%) was found in 29 patients (39.7%) (group 1), and 44 patients (60.3%) showed only an increase of <20% (group 2). The statistical analyses showed the following significant difference: The symptoms vertigo (p=0.002) and spontaneous nystagmus (p=0.014) occurred more frequently in group 2 (patients with a poor hearing recovery) than in group 1. Patients with a barotrauma,however, had an overproportionally good outcome (50-100% hearing recovery). A perilymph fistula was seen intraoperatively equally often in both groups. In summary, the symptoms vertigo and spontaneous nystagmus are indicators of complex damage in cases of sudden deafness and are associated with a worse prognosis concerning hearing recovery. Exploratory tympanotomy in combination with drug treatment is a reasonable therapy as an ultima ratio in every case of unilateral sudden deafness.

Adolescent↗