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IntroductionHydropic ear disease, initially described by and named after Prosper Meniere, is one of the most frequent vertigo disorders and one of the most frequent inner ear disorders. It is the syndrome of endolymphatic hydrops ...
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IntroductionHydropic ear disease, initially described by and named after Prosper Meniere, is one of the most frequent vertigo disorders and one of the most frequent inner ear disorders. It is the syndrome of endolymphatic hydrops which until 2007 could be diagnostically confirmed only by post-mortem histology. In the past, various attempts to formulate clinical diagnostic criteria have been undertaken but were hampered by the inability to ascertain the diagnosis in living patients. With the milestone achievement of endolymphatic hydrops imaging, today the pathology can be ascertained. In this study, we have performed a detailed analysis of the clinical features of hydropic ear disease for the first time by examining a large cohort of patients with morphologically confirmed endolymphatic hydrops using a detailed physician-administered neurotologic face-to-face interview.ResultsDuring a hydropic vertigo attack, the patients report nausea, vomiting, sweating, urge to defecate, urge to urinate, phosphenes, headache, photophobia, phonophobia and even transient loss of consciousness. A third of the patients does not experience auditory symptoms during the vertigo attacks. Vertigo attacks last less than 20min in more than one-fourth of the patients. Audiometric hearing loss has its greatest diagnostic value at the frequencies of 1kHz and below. Cochleovestibular symptom onset simultaneity is associated with a high frequency of drop-attacks. Migraine and autoimmune disorders are not associated with hydropic ear disease.ConclusionThis study marks the beginning of the clinical characterization of hydropic ear disease. The findings have important implications for the future formulation of clinical diagnostic criteria.
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Human hearing is rather insensitive for very low frequencies (i.e. below 100 Hz). Despite this insensitivity, low-frequency sound can cause oscillating changes of cochlear gain in inner ear regions processing even much higher freq...
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Human hearing is rather insensitive for very low frequencies (i.e. below 100 Hz). Despite this insensitivity, low-frequency sound can cause oscillating changes of cochlear gain in inner ear regions processing even much higher frequencies. These alterations outlast the duration of the low-frequency stimulation by several minutes, for which the term 'bounce phenomenon' has been coined. Previously, we have shown that the bounce can be traced by monitoring frequency and level changes of spontaneous otoacoustic emissions (SOAEs) over time. It has been suggested elsewhere that large receptor potentials elicited by low-frequency stimulation produce a net Ca2+ influx and associated gain decrease in outer hair cells. The bounce presumably reflects an underdamped, homeostatic readjustment of increased Ca2+ concentrations and related gain changes after low-frequency sound offset. Here, we test this hypothesis by activating the medial olivocochlear efferent system during presentation of the bounce-evoking low-frequency (LF) sound. The efferent system is known to modulate outer hair cell Ca2+ concentrations and receptor potentials, and therefore, it should modulate the characteristics of the bounce phenomenon. We show that simultaneous presentation of contralateral broadband noise (100 Hz-8 kHz, 65 and 70 dB SPL, 90 s, activating the efferent system) and ipsilateral low-frequency sound (30 Hz, 120 dB SPL, 90 s, inducing the bounce) affects the characteristics of bouncing SOAEs recorded after low-frequency sound offset. Specifically, the decay time constant of the SOAE level changes is shorter, and the transient SOAE suppression is less pronounced. Moreover, the number of new, transient SOAEs as they are seen during the bounce, are reduced. Taken together, activation of the medial olivocochlear system during induction of the bounce phenomenon with low-frequency sound results in changed characteristics of the bounce phenomenon. Thus, our data provide experimental support for the hypothesis that outer hair cell calcium homeostasis is the source of the bounce phenomenon.
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Loss of neural structures (such as hair cells or neurones within the spiral ganglion) has been proposed to be involved in MeniSre's disease (MD) (Spoendlin et al. Acta oto-laryngologica Supplementum 499:1-21, 1; Merchant et al. Eu...
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Loss of neural structures (such as hair cells or neurones within the spiral ganglion) has been proposed to be involved in MeniSre's disease (MD) (Spoendlin et al. Acta oto-laryngologica Supplementum 499:1-21, 1; Merchant et al. Eur Arch Oto-Rhino-Laryngol Off J Eur Feder Oto-Rhino-Laryngol Soc (EUFOS) Affil German Soc Oto-Rhino-Laryngol Head Neck Surg 252(2):63-75, 2; Tsuji et al. Ann Otol Rhinol Laryngol Suppl 81:26-31, 3; Kariya, Otol Neurotol Off Publ Am Otol Soc Am Neurotol Soc Eur Acad Otol Neurotol 28(8):1063-1068, 4; Megerian Laryngoscope 115(9):1525-1535, 5) but this has yet to be confirmed. Therefore, the aim of this study was to investigate morphometric changes of VIIth and VIIIth cranial nerve in MD. MD is characterized by episodic vertigo, tinnitus, fluctuating hearing loss, and aural fullness. The exact pathophysiological mechanisms involved such as viral infections, autoimmune processes, genetic predisposition, cellular apoptosis, and oxidative stress are still not clear. Using a T2-weighted 3D-GE "constructive interference in steady state" (CISS) 3T magnetic resonance imaging (MRI) sequence, we evaluated the properties of the VIIth and VIIIth cranial nerves as they passed from the cerebellopontine angle to the inner ear modiolus. 21 patients with MD were examined along with 39 normal controls. Bidirectional nerve diameters and cross-sectional areas (CSA) were measured in a transverse plane. The comparison of study and control group showed statistically significant (P < 0.000595 after Bonferroni correction) differences between the CSA measurements. The facial, cochlear, superior vestibular, and inferior vestibular nerves (FN, CN, SVN, IVN) of MD patients were significantly larger than those of the control group, both on the MD-affected side and on the healthy side. Thus for example, the cochlear nerve CSA measurements were 0.69 +/- 0.14 mm(2) (P < 0.0001) in the affected ears of the unilateral MD group, 0.70 +/- 0.12 mm(2) (P < 0.0001) in the affected ears of the cohort including the bilateral MD group, 0.71 +/- 0.13 mm(2) (P < 0.0001) in the non-affected ears of the MD patients, as compared to 0.46 +/- 0.14 mm(2) in the control group. The perpendicular nerve diameters were found to vary according to site of measurement and type of measurement used. For example a statistically significant enlargement of the short diameter measurements of the SVN at the level of the meatus was found, but not of long diameter measurements at the same site. Although cellular death would theoretically be expected to lead to a decreased nerve thickness, our data showed a swelling of cranial nerves VII and VIII within the study group compared to our normal hearing control group. The similar reaction of the facial nerve supports mediator-based theories of MD pathophysiology.
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To determine whether vestibular evoked myogenic potential (VEMP) measurements that combine the VEMP 500/1000 Hz frequency tuning ratio and the inter-aural asymmetry ratio can reliably detect unilateral Meniere's disease ears as co...
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To determine whether vestibular evoked myogenic potential (VEMP) measurements that combine the VEMP 500/1000 Hz frequency tuning ratio and the inter-aural asymmetry ratio can reliably detect unilateral Meniere's disease ears as compared to healthy controls. Forty-two consecutive patients with certain unilateral Meniere's disease (as confirmed using a locally enhanced inner ear MRI (LEIM)) were assessed. Cervical vestibular evoked myogenic potentials (cVEMP) and ocular vestibular evoked myogenic potentials (oVEMP) were recorded at 500 and 1000 Hz. The VEMP amplitudes, asymmetry ratios, and the 500/1000 Hz amplitude ratios were compared with those of 21 age-matched healthy controls. A multi-frequency VEMPs score that combined: (1) the cVEMP 500/1000 Hz amplitude ratio, (2) the oVEMP 500/1000 Hz amplitude ratio, (3) the 500 Hz cVEMP asymmetry ratio, (4) the 1000 Hz cVEMP asymmetry ratio, produced a ROC curve with an area under the curve (AUC) of 0.814. The inclusion of audiology data further improved the result to 0.906. This score can be used to discriminate with a good degree of clinical accuracy between Meniere's ears (unilateral) and those of healthy controls. Multi-frequency VEMP analysis offers a simple, cost-effective solution to the diagnostic difficulties presented by Meniere's disease.
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The presentation of intense, low-frequency (LF) sound to the human ear can cause very slow, sinusoidal oscillations of cochlear sensitivity after LF sound offset, coined the "Bounce" phenomenon. Changes in level and frequency of s...
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The presentation of intense, low-frequency (LF) sound to the human ear can cause very slow, sinusoidal oscillations of cochlear sensitivity after LF sound offset, coined the "Bounce" phenomenon. Changes in level and frequency of spontaneous otoacoustic emissions (SOAEs) are a sensitive measure of the Bounce. Here, we investigated the effect of LF sound level and frequency on the Bounce. Specifically, the level of SOAEs was tracked for minutes before and after a 90-s LF sound exposure. Trials were carried out with several LF sound levels (93 to 108 dB SPL corresponding to 47 to 75 phons at a fixed frequency of 30 Hz) and different LF sound frequencies (30, 60, 120, 240 and 480 Hz at a fixed loudness level of 80 phons). At an LF sound frequency of 30 Hz, a minimal sound level of 102 dB SPL (64 phons) was sufficient to elicit a significant Bounce. In some subjects, however, 93 dB SPL (47 phons), the lowest level used, was sufficient to elicit the Bounce phenomenon and actual thresholds could have been even lower. Measurements with different LF sound frequencies showed a mild reduction of the Bounce phenomenon with increasing LF sound frequency. This indicates that the strength of the Bounce not only is a simple function of the spectral separation between SOAE and LF sound frequency but also depends on absolute LF sound frequency, possibly related to the magnitude of the AC component of the outer hair cell receptor potential.
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PURPOSE: Contrast enhanced ultrasound (CE-US) is a promising imaging modality for non-invasive analysis of functional vascularisation. Lesions of the parotid gland are associated with a vascularisation that differs from normal gla...
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PURPOSE: Contrast enhanced ultrasound (CE-US) is a promising imaging modality for non-invasive analysis of functional vascularisation. Lesions of the parotid gland are associated with a vascularisation that differs from normal gland tissue. The aim of this clinical study was to further analyse the perfusion in parotid gland lesions with CE-US. The new quantification software VueBox (Bracco, Italy) was used to assess the perfusion, based on DICOM datasets of CE-US examination.
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Background: Cochlear implantation is an important method of hearing rehabilitation. Earlier studies have shown the influence of implantation on the vestibular system. However, until now, the effect of hearing rehabilitation with c...
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Background: Cochlear implantation is an important method of hearing rehabilitation. Earlier studies have shown the influence of implantation on the vestibular system. However, until now, the effect of hearing rehabilitation with cochlear implants (CI) on postural control and body stability has not been sufficiently studied. Objective: To analyse the effect of hearing rehabilitation with activated CI and different sound inputs (music, speech text, and white noise) on postural control and risk of falls after implantation. Methods: This was a prospective clinical trial that included 33 adult patients with at least 6 months' use of a CI (mean time after implantation = 23 months). All patients underwent a standard or geriatric (for patients >60 years) balancing deficit test protocol with a mobile posturography system (VertiGuard (R)) in different situations (CI deactivated/activated and different sound inputs). As the main outcome measure, the risk of falls (%) after each protocol was calculated by evaluating body sway both forward to backward and side to side (degrees/s). Results: With the CI deactivated, the mean risk of falls was 45.5%. After activation of the CI, there was a small decrease in the mean risk of falls, but it was statistically significant. With an additional sound input (music or speech text) this decrease was more pronounced: 42.0 and 42.4%, respectively. This effect seems to be more pronounced in older patients. Regarding the individual patients, 72% had an improvement in the risk of falls with an activated CI, and 28% had a slight deterioration. An activated CI accompanied by sound input (music) further improved the individual risk of falls. Conclusions: Compared with prior research, this study found that the risk of falls after implantation decreased over a longer time period. Furthermore, the use of a CI and different sound inputs had a positive effect on postural control. These findings support the need for optimal hearing rehabilitation, especially in elderly patients. Although this effect is relatively small, it is important to consider for further studies that rehabilitation with CI may reduce the risk of falls. While the auditory system supposedly contributes to postural control only to a small degree and the mechanism is still poorly understood, further studies with bigger samples are warranted to clarify these effects.
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Objective:To characterize the short-, middle-, and long-term occurrence of vertigo attacks in a large population of Meniere's disease (MD) and to investigate the relationship between the extent of endolymphatic hydrops (ELH) and t...
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Objective:To characterize the short-, middle-, and long-term occurrence of vertigo attacks in a large population of Meniere's disease (MD) and to investigate the relationship between the extent of endolymphatic hydrops (ELH) and the severity of audiovestibular symptoms.
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Intense, low-frequency sound presented to the mammalian cochlea induces temporary changes of cochlear sensitivity, for which the term 'Bounce' phenomenon has been coined. Typical manifestations are slow oscillations of hearing thr...
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Intense, low-frequency sound presented to the mammalian cochlea induces temporary changes of cochlear sensitivity, for which the term 'Bounce' phenomenon has been coined. Typical manifestations are slow oscillations of hearing thresholds or the level of otoacoustic emissions. It has been suggested that these alterations are caused by changes of the mechano-electrical transducer transfer function of outer hair cells (OHCs). Shape estimates of this transfer function can be derived from low-frequency biased distortion product otoacoustic emissions (DPOAE).
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