Effect of Aspiration of Perilymph during Stapes Surgery on the Endocochlear Potential of Guinea Pig

2011 ◽  
Vol 145 (5) ◽  
pp. 801-805 ◽  
Author(s):  
Ryoukichi Ikeda ◽  
Kazuhiro Nakaya ◽  
Hidetoshi Oshima ◽  
Takeshi Oshima ◽  
Tetsuaki Kawase ◽  
...  

Objective. Suction applied to the vestibule through the oval window during stapes surgery is considered a primary risk for postoperative sensorineural hearing impairment. This study investigated the mechanism of acute phase change in cochlear function caused by aspiration of the opened oval window. Study Design. Guinea pig model. Setting. Academic hospital laboratory. Subjects and Methods. Guinea pigs were divided into 3 groups: stapes footplate removed without suctioning (6 animals), with indirect suctioning (5 animals), and with direct suctioning of the vestibular perilymph (6 animals). Endocochlear potentials (EPs) were measured at the second turn of the cochlea, and temporal bones were examined histologically. Results. Removal of the stapes footplate without suctioning caused little change in the EP (original value, 80.12 ± 3.52 mV), indirect suctioning caused minor decline of the EP of 9.14 ± 1.84 mV, and partial recovery ensued, whereas direct but gentle suctioning, resulting in dry vestibule, caused reduction in the EP of 16.38 ± 6.63 mV. Recovery was not observed or incomplete. No animals showed profound decrease in the EP. Conclusion. Gentle suctioning and removal of the vestibular perilymph can cause a mild decrease in the EP even without damaging the inner ear structures. Therefore, suctioning of the perilymph should be avoided during stapes surgery because acute hearing loss can result even without damaging the inner ear structures. However, hearing loss may not be profound, if suctioning is not vigorous enough to cause damage to the inner ear structures.

2008 ◽  
Vol 139 (2_suppl) ◽  
pp. P101-P101
Author(s):  
Timothy J Hughes ◽  
Gregory J Matz ◽  
Sam J Marzo

Problem Human case reports have been published demonstrating a rapidly progressive sensorineural hearing loss associated with overuse or abuse of acetaminophen/hydrocodone. We hypothesized that hearing loss would result in the guinea pig model if given high, chronic doses of this drug. Methods Sixty female, pigmented guinea pigs were randomly assigned to a control, acetaminophen, hydrocodone, or acetaminophen/hydrocodone group. All guinea pigs were tested with baseline ABRs on day 0, and post drug/placebo administration on days 30, 60, 90, and 120. At the end of the study 5 animals from each group were sacrificed and their cochleae were harvested for histological investigation. Results No significant change in threshold (dB) was seen between the 4 groups. Histological studies of the cochleae revealed no hair cell damage in any of the groups. Conclusion Hydrocodone and acetaminophen/hydrocodone do not have an obvious deleterious effect on guinea pig cochlear function or structure. Significance This study may indicate that human hearing loss seen with abuse of acetaminophen/hydrocodone is multi-factorial and not just related to the drug abuse alone.


2019 ◽  
Vol 98 (6) ◽  
pp. 340-345
Author(s):  
Nisa Oren ◽  
Daniel Thomas Ginat

The purpose of this study is to categorize anomalous tympanic facial nerve (FN) on high-resolution computed tomography (HRCT) and to determinate the significance of associated temporal bone anomalies and congenital syndromes without microtia in patients with hearing loss. A retrospective analysis of HRCT findings in 30 temporal bones in 18 patients with anomalous FN was performed. Abnormalities of the tympanic FN were categorized as follows: category 1: FN medially positioned, but above the oval window; category 2: FN in the oval window niche; and category 3: FN below the oval window. Potential associated findings that were assessed included stapes abnormalities, oval window atresia, and inner ear anomalies, as well as the presence of a known congenital syndrome with hearing loss. The most common type of anomalous tympanic FN was category 1 (67%, n = 20), following by group 2 (20%, n = 6) and group 3 (13%, n = 4). Stapes anomalies were detected in 77% of temporal bones (n = 23), oval window atresia was detected in 43% of temporal bones (n = 13), and inner ear anomalies were detected in 70% of temporal bones (n = 21). Anomalous tympanic facial nerves in temporal bone with conductive hearing loss were often (60%) not associated with oval window atresia. The combination of aberrant tympanic FN and inner ear anomalies was significantly ( P = .038) associated with a known congenital syndrome (6 patients), including CHARGE syndrome, oculo-auriculo-vertebral spectrum, Pierre-Robin sequences, and Down syndrome. Therefore, an anomalous tympanic FN in conjunction with inner ear anomalies appears to be a biomarker for certain congenital syndromes with hearing loss in the absence of microtia.


Author(s):  
Sergey Armakov

Sensorineural hearing loss is a disorder associated with the damage to the inner ear structures: the cochlea (cortical organ), dysfunctioning of the vestibule-cochlear nerve or the central part of the auditory analyser (brain stem and cortical representation of the cortical temporal lobe). In recent years, there has been a steady increase in ensorineural hearing loss patients; they account for ca. 70% among the total patients with impaired hearing. The disease has numerous causes and a complex pathogenesis. Among the main factors contributing to hearing loss are genetic predisposition, perinatal pathology, including hypoxia at childbirth, exposure to infectious and toxic agents and metabolic disorders, injuries (mechanical, acoustic and altitude trauma). Vascular-rheological disorders in the vertebro-basilar system play an important part because blood is supplied to the inner ear from the anterior inferior cerebellar artery. There are sudden, acute and chronic sensorineural hearing loss. The ensorineural hearing loss isdiagnosed by examinations that allow to verify the diagnosis and to determine the sound analyser damage level. This complex includes audiometric examinations, including the tuning fork examination, speech audiometry, and acoustic impedancemetry. If necessary, ultrasound Doppler imaging of the main blood vessels of the brain, computed tomography of the temporal bones, and MRI of the brain are prescribed. The pattern of comprehensive treatment should include, first of all, the elimination of the disease cause and anti-hypoxic drugs, anti-oxidants and a number of physiotherapy procedures.


2019 ◽  
Vol 98 ◽  
pp. 139-152
Author(s):  
Hoda H. Hussein Abd El Raouf ◽  
Rania A. Galhom ◽  
Mona H. Mohammed Ali ◽  
Wael Amin Nasr El-Din

2018 ◽  
Vol 2018 ◽  
pp. 1-10
Author(s):  
Bu-Sheng Tong ◽  
Zi-Yu He ◽  
Chen-Ru Ding ◽  
Juan-Mei Yang ◽  
Jing Wang ◽  
...  

Defective acoustic transmission in the cochlea is closely related with various auditory and vestibular symptoms. Among them, semicircular canal dehiscence (SCD) with a defective semicircular bone is typical. Currently, the pathogenesis of SCD is usually explained by the third window hypothesis; however, this hypothesis fails to explain the variability in the symptoms and signs experienced by superior SCD (SSCD) patients. We evaluated the mechanism of hearing loss in a guinea pig model of bony dehiscence with various sizes and locations along the superior semicircular canal. Auditory brainstem responses (ABRs) and laser Doppler velocimetry were used to measure hearing loss and vibration changes before and after fenestration, as well as after restorative patching. ABR thresholds at low frequencies (e.g., 1000 Hz) increased after fenestration and decreased back to the normal range after we repaired the defect. Energy leakage from the surgically introduced third window was detected in the range of 300–1500 Hz, accompanied by increased vibration at the umbo, stapes head, and the dehiscence site, while decreased vibration was observed at the round window membrane in the same frequency range. After the patching procedure, the deviant vibrations were recovered. The degree of postfenestration energy leakage was proportional to the size of fenestration and the proximity of the fenestration site to the oval window. These results suggest that the bony fenestration of the superior semicircular canal mimics the hearing loss pattern of patients with SSCD. The decrease in perilymph wave impedance likely accounts for the auditory changes.


2014 ◽  
Vol 316 ◽  
pp. 82-93 ◽  
Author(s):  
Chiemi Tanaka ◽  
Anh Nguyen-Huynh ◽  
Katherine Loera ◽  
Gemaine Stark ◽  
Lina Reiss

1992 ◽  
Vol 101 (2) ◽  
pp. 176-182 ◽  
Author(s):  
Lorne S. Parnes ◽  
Kathleen C. M. Campbell

To improve understanding of the pathophysiology of perilymph fistulas, a predictable animal model of a chronic fistula was developed. Our findings suggest that guinea pig fistulas do not remain patent for prolonged periods. By extrapolating these findings to humans, we postulate that the symptoms and signs of perilymph fistula are possibly due not to one prolonged constant fistula, but rather a series of “blowouts” from an inherent congenital or posttraumatic weak spot in either the round or oval window. We feel that a diagnosis of perilymph fistula must be considered in any patient presenting with a Meniere's-like symptom set concomitant with a congenital inner ear deformity or a history of inner ear trauma.


1998 ◽  
Vol 118 (5) ◽  
pp. 703-708 ◽  
Author(s):  
Eugene N. Myers ◽  
Shingo Murakami ◽  
Kiyofumi Gyo ◽  
Richard L. Goode

Velocity of malleus, umbo, and stapes footplate in response to stepwise increases up to +400 mm H2O in hydrostatic pressure of the inner ear was investigated in 10 fresh human temporal bones by using a laser Doppler interferometer. The sound-pressure input was 114 dB SPL, and the frequency range was 0.4 to 5.0 kHz. Static displacement of these sites was also measured by a video measuring system. When the inner ear pressure was increased, the malleus and stapes moved outward. Amplitude of umbo velocity decreased below 1.0 kHz with a slight increase around 2.0 kHz, whereas stapes velocity decreased at all frequencies with the major effect below 1.0 kHz. The phase angle of malleus umbo velocity advanced markedly in response to the increased inner ear pressure between 1.0 and 1.4 kHz. Change in the vibration of the umbo was thought to be primarily caused by an increased stiffness of the middle ear conduction system, and that of the stapes was caused by distention of the annular ligament and increased cochlear impedance produced by the increased inner ear pressure. These changes in TM vibration and its phase angle may help detect indirectly an elevation of inner ear pressure. (Otolaryngol Head Neck Surg 1998;118:703–8.)


2009 ◽  
Vol 1257 ◽  
pp. 108-116 ◽  
Author(s):  
Anna Rita Fetoni ◽  
Roberto Piacentini ◽  
Antonella Fiorita ◽  
Gaetano Paludetti ◽  
Diana Troiani

1981 ◽  
Vol 89 (2) ◽  
pp. 343-351 ◽  
Author(s):  
Dennis R. Elonka ◽  
Edward L. Applebaum

This study sought correlations between sensorineural hearing loss and otosclerotic endosteal involvement in 29 temporal bones examined histologically. The sensorineural hearing loss of the affected parts of the cochlea was determined by the last antemortum bone conduction audiogram available. There were eight temporal bones with only stapes footplate involvement, six with one discrete focus of otosclerotic endosteal involvement, and 15 with two or more foci of endosteal involvement. Analysis of audiometric data showed that the group of bones with two or more foci of endosteal involvement had a similar incidence of 45 dB sensorineural loss (9 of 15 or 60%) as did the group with no endosteal involvement (5 of 8 or 62%). The group with two or more foci had a greater incidence of 60 dB or greater sensorineural loss (46%) compared with the groups with none (12%) or one focus (16%) involved. Correlation between hearing toss and involvement of cochlear endosteum was poor. Correlation existed in only 2 of 15 ears with two or more foci involving the cochlear endosteum. There was no correlation in the other groups. It appears that cochlear endosteal involvement alone may not be sufficient explanation for the sensorineural hearing loss found with otosclerosis, except in the most severely involved ears.


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