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PubMed1994

Potassium circulation in the perilymph of guinea pig cochlea.

To determine whether any differences exist in potassium circulation between the scala vestibuli and scala tympani, we recorded the change in K+ activity in both scalae of the guinea pig cochlea at the basal and third turns, using a double-barrelled, K(+)-sensitive microelectrode after perfusion with artificial perilymph containing 20 mM KCl and 130 mM NaCl. K+ activity increased immediately after the start of perfusion and decreased after its completion. The rates of decrease of K+ activities were approximately 1.0 mEq/l per min in the scala vestibuli of the basal and third turns, also 1.0 mEq/l per min in the scala tympani of the basal turn, and approximately 0.5 mEq/l per min in the scala tympani of the third turn. The rate of decrease of K+ activity in the scala tympani was significantly slower in the third turn than in the basal turn. Blockage of the cochlear aqueduct depressed the rate of decrease of K+ activity in the scala tympani more in the basal turn than in the third turn. These results suggest that there is a difference in potassium circulation between the scala vestibuli and scala tympani, and that the cochlear aqueduct plays an important role in potassium circulation in the perilymph of the scala tympani.

Animals↗

PubMed1996

A human temporal bone study of acute bacterial meningogenic labyrinthitis.

It is well established that sensorineural hearing loss (SNHL) is an important sequela of acute bacterial meningitis. Previous human temporal bone histopathologic studies have suggested that such hearing loss is due to labyrinthitis. This study involved a detailed and systematic evaluation of the auditory and vestibular end-organs in 41 human temporal bones from patients with acute bacterial meningitis, aimed at describing the spectrum of histopathologic changes within the labyrinth, ascertaining likely routes for spread of infection from the meninges to the inner ear, and comparing the data from humans with those described in a rabbit model of meningogenic labyrinthitis. Our study revealed the following: (a) Suppurative labyrinthitis occurred in 20 (49%) bones. Of these 20 bones, the cochlea was affected in all, whereas the vestibular organs were involved in 10. Eosinophilic staining of inner ear fluids without the presence of inflammatory cells (so-called "serous" labyrinthitis) occurred in 14 of the remaining 21 bones. This staining occurred primarily within the vestibular system. Its significance and pathogenesis remains unknown; (b) Sensory and neural structures of the inner ear appeared intact in the majority of specimens, including bones with suppurative labyrinthitis and those with eosinophilic staining of inner ear fluids. This finding raises the possibility of preventing or reversing SNHL by therapeutic intervention. Spiral ganglion cells were severely degenerated in 12% of bones, indicating a retrocochlear site of hearing loss in addition to the cochlea. This subset of patients may perform poorly after cochlear implantation; (c) It has been traditionally assumed that irreversible and permanent SNHL is caused by suppurative labyrinthitis, whereas reversible SNHL is caused by serous labyrinthitis. Our findings question the validity of these assumptions; (d) The data were consistent with the hypothesis that both the cochlear modiolus and cochlear aqueduct can serve as potential pathways for spread of infection from the meninges to the inner ear; (e) There were many similarities in the histopathology of the inner ear in humans when compared with the rabbit model of meningogenic labyrinthitis. A notable difference was that the cochlear aqueduct appeared to be the sole pathway for spread of infection in the rabbit, whereas in the human, both the modiolus and aqueduct were possible pathways.

Adolescent↗

PubMed1996

Is perilymphatic pressure altered in tinnitus?

Tinnitus is characterized by the continuous or intermittent auditory perception of various sounds (buzzing, whistling, etc.) in the absence of any external stimulus. Perilymphatic hyperpressure is one of the numerous mechanisms which could hypothetically be involved in tinnitus generation. In the present experiment, perilymphatic pressure was measured indirectly using the tympanic membrane displacement technique. Twenty-five tinnitus patients were investigated at 10, 15 and 20 dB above the acoustic reflex threshold with ipsilateral stimulation. The variables Vi (inward tympanic displacement), Vm (mean tympanic displacement) and their variations according to stimulus level were compared between tinnitus sufferers and age-matched or hearing-matched controls. Tympanic displacement was measured in sitting and supine positions so as to evaluate cochlear aqueduct patency. No systemic changes in response occurred in tinnitus patients, except at a high stimulation level, perhaps due to hearing impairment.

Adult↗

PubMed1990

The relationship between intracranial pressure and tympanic membrane displacement.

Transmission of intracranial pressure (ICP) to the perilymph of the cochlea may occur via the cochlear aqueduct and possibly other routes. Indirect measurement of perilymphatic pressure may be investigated by observing tympanic membrane (TM) displacement during stapedial reflex contraction. In a previous study we investigated the effects of changes in ICP on perilymphatic fluid pressure in three patients who underwent ventriculo/lumbar-peritoneal shunt operations. The TM displacement technique proved extremely sensitive and revealed marked changes in cochlear fluid pressure brought about by changes in ICP (Marchbanks et al., 1987). The study has been extended to 58 patients with hydrocephalus, intracranial tumours and other neurological conditions associated with abnormal ICP. Significant differences in the TM displacement were found between patients with raised and normal ICP. We have shown that changes in ICP can affect the hydrostatic pressure of the cochlea and influence the peripheral auditory system. The finding that ICP can be correlated with TM displacement strengthens the association between an abnormal TM displacement and abnormal cochlear hydrostatic status, irrespective of cochlear aqueduct patency. We suggest that the TM displacement technique provides a useful non-invasive method for the assessment of perilymphatic fluid pressure.

Acoustic Stimulation↗

PubMedDate not supplied

Gradients of organic substances between fluid compartments of the cochlea.

We have previously demonstrated the presence of steep gradients of amino acids between cochlear endolymph and perilymph of scala vestibuli. However, only recently have we succeeded in developing a sampling technique which is capable of providing amino acid levels in scala tympani which are representative of the in vivo situation under physiological circumstances. This is achieved by sampling perilymph in a closed system, which precludes unphysiological contamination by CSF via the cochlear aqueduct. It is also shown that amino acids which exhibit very steep gradients between CSF and perilymph, such as glycine and alanine, can be used as endogenous markers to assess the degree of artifactual admixture of CSF when perilymph is sampled by conventional techniques in the open system. Moreover, pilot experiments indicate that net production of perilymph is very low when the cochlear aqueduct is blocked.

Amino Acids↗

PubMed1999

Time course of hearing loss in an animal model of pneumococcal meningitis.

A leading cause of morbidity from bacterial meningitis is an irreversible, usually profound sensorineural hearing loss, with an incidence as high as 30% in some studies. Bacterial meningitis remains the most common cause of acquired postnatal sensorineural deafness. Although several clinical studies have examined the long-term outcome of hearing in meningitis, few studies have examined the time course of hearing loss during the acute course of the disease. We have developed an animal model of meningogenic hearing loss in the rat and have plotted the time course of that hearing loss. Serial auditory brain stem responses (ABRs) were measured in rats inoculated in the cisterna magna (subarachnoid space) with Streptococcus pneumoniae (10(5) to 10(7) colony-forming units). All rats injected developed meningitis as evidenced by increased cerebrospinal fluid (CSF) white cell counts and positive CSF cultures. Serial ABR measurements taken 6, 12, 15, 18, 21, and 24 hours after inoculation demonstrated significant threshold shifts and eventual loss of the ABR waveform as compared with measurements in control rats injected with sterile culture medium. Hearing loss began approximately 12 to 15 hours after inoculation and progressed to complete loss by 24 hours (17 of 18 animals). No correlation was found between the magnitude of hearing loss and CSF white cell count or bacterial titer. Temporal bone histology of rats with meningitis shows a dense inflammatory cell infiltrate throughout the subarachnoid space. Labyrinthine inflammatory cells were confined to the scala tympani. The cochlear aqueduct is the proposed route of infection from the meninges to the labyrinth (scala tympani). Endolymphatic hydrops was also noted throughout the cochlea. These experiments both establish a reproducible animal model of meningogenic hearing loss and support the hypothesis that this hearing loss is progressive rather than abrupt in onset and is related to the duration of untreated infection. CSF inflammatory cells appear to enter the cochlea through the cochlear aqueduct. This reliable animal model will enable future studies directed toward further understanding the pathogenesis and pathophysiology of this hearing loss.

Acute Disease↗

PubMedDate not supplied

Otologic manifestations of the hydantoin syndrome.

The temporal bones of a newborn infant with hydantoin syndrome showed multiple middle ear and inner ear anomalies. There was a constellation of bony and membranous defects involving the oval and round windows, cochlear ducts, cochlear aqueducts, endolymphatic ducts and sacs, and vestibular labyrinths. To the authors' knowledge, supernumerary vestibular sensory epithelial structures and an inner ear epidermoid cyst have not been previously reported. Wide communications between the subarachnoid space and inner ear were of surgical relevance.

Abnormalities, Drug-Induced↗

PubMed2001

Progressive fluctuant hearing loss, enlarged vestibular aqueduct, and cochlear hypoplasia in branchio-oto-renal syndrome.

OBJECTIVE: To study the results of petrosal bone imaging and audiometric long-term follow-up of two patients with branchio-oto-renal (BOR) syndrome and relate them to the clinical features, including caloric responses. STUDY DESIGN: Longitudinal case study. SETTING: Tertiary referral center. PATIENTS: A father and son with the BOR syndrome. MAIN OUTCOME MEASURES: Both patients underwent imaging studies to detect and evaluate inner ear anomalies. Longitudinal audiometric analysis of the hearing threshold data over the previous 23 years was performed. Caloric tests were performed at various ages. RESULTS: The son had a short, wide internal acoustic canal, a hypoplastic cochlea, a plump vestibule, and a wide vestibular aqueduct on both sides; the semicircular canals and endolymphatic sac were of normal size. He showed progressive fluctuant sensorineural hearing loss. Caloric tests disclosed hyporeflexia on the left side. The father had a plump internal acoustic canal and hypoplastic cochlea on both sides. The left vestibule was hypoplastic, and the left vestibular aqueduct was marginally enlarged. He showed severe hearing impairment, without substantial progression or fluctuation, and caloric areflexia on the left side. CONCLUSION: These findings suggest a correlation between progressive fluctuant sensorineural hearing loss with caloric hypofunction and the presence of an enlarged vestibular aqueduct in the BOR syndrome. Additional longitudinal case studies are needed to further evaluate such a correlation.

Adult↗

PubMed1989

Mean intracranial pressure monitoring by a non-invasive audiological technique: a pilot study.

Intracranial pressure is normally transmitted to the perilymph of the cochlea via the cochlear aqueduct. The relationship between perilymphatic pressure, indirectly measured by tympanic membrane displacement, and mean intracranial pressure defined either clinically or by direct measurement has been examined in 58 patients (aged 5-77 years), with hydrocephalus, benign intracranial hypertension, intracranial tumours, subarachnoid haemorrhage and head injuries. The most consistent results were obtained in young patients with hydrocephalus and benign intracranial hypertension. However, the technique was not suitable when the stapedial reflex was absent as a result of middle ear/brainstem dysfunction and did not reflect intracranial pressure when the cochlear aqueduct was not patent. This pilot study suggests that the tympanic membrane displacement technique may provide a useful non-invasive method for serial monitoring of intracranial pressure in young patients with hydrocephalus or benign intracranial hypertension.

Acoustic Impedance Tests↗

PubMed2005

Perilymph sampling from the cochlear apex: a reliable method to obtain higher purity perilymph samples from scala tympani.

Measurements of drug levels in the fluids of the inner ear are required to establish kinetic parameters and to determine the influence of specific local delivery protocols. For most substances, this requires cochlear fluids samples to be obtained for analysis. When auditory function is of primary interest, the drug level in the perilymph of scala tympani (ST) is most relevant, since drug in this scala has ready access to the auditory sensory cells. In many prior studies, ST perilymph samples have been obtained from the basal turn, either by aspiration through the round window membrane (RWM) or through an opening in the bony wall. A number of studies have demonstrated that such samples are likely to be contaminated with cerebrospinal fluid (CSF). CSF enters the basal turn of ST through the cochlear aqueduct when the bony capsule is perforated or when fluid is aspirated. The degree of sample contamination has, however, not been widely appreciated. Recent studies have shown that perilymph samples taken through the round window membrane are highly contaminated with CSF, with samples greater than 2microL in volume containing more CSF than perilymph. In spite of this knowledge, many groups continue to sample from the base of the cochlea, as it is a well-established method. We have developed an alternative, technically simple method to increase the proportion of ST perilymph in a fluid sample. The sample is taken from the apex of the cochlea, a site that is distant from the cochlear aqueduct. A previous problem with sampling through a perforation in the bone was that the native perilymph rapidly leaked out driven by CSF pressure and was lost to the middle ear space. We therefore developed a procedure to collect all the fluid that emerged from the perforated apex after perforation. We evaluated the method using a marker ion trimethylphenylammonium (TMPA). TMPA was applied to the perilymph of guinea pigs either by RW irrigation or by microinjection into the apical turn. The TMPA concentration of the fluid sample was compared with that measured in perilymph prior to taking the sample using a TMPA-selective microelectrode sealed into ST. Data were interpreted with a finite element model of the cochlear fluids that was used to simulate each aspect of the experiment. The correction of sample concentration back to the perilymph concentration prior to sampling can be performed based on the known ST volume (4.7microL in the guinea pig) and the sample volume. A more precise correction requires some knowledge of the profile of drug distribution along the cochlear prior to sampling. This method of sampling from the apex is technically simple and provides a larger sample volume with a greater proportion of perilymph compared to sampling through the RW.

Animals↗

PubMed1987

The effect of round window membrane rupture on endolymphatic and perilymphatic pressures.

We used a guinea pig model to investigate the effect of round window membrane rupture on endolymphatic and perilymphatic pressures under conditions known to increase these pressures: anoxia, hypercapnia, increased intracranial pressure, and occlusion of the vein of the cochlear aqueduct. When the round window membrane was not ruptured, increases in endolymphatic pressure paralleled the perilymphatic pressure following exposure to each of the experimental conditions. After the round window membrane had been ruptured, however, no increases in perilymphatic pressure or endolymphatic pressure were seen. These results suggest that endolymphatic pressure is dependent on perilymphatic pressure, even when the round window membrane is ruptured.

Animals↗

PubMed2004

Hearing impairment associated with spinal anesthesia.

OBJECTIVES: Hearing loss after spinal anesthesia has been reported to be related to the transmission of a reduced subarachnoid pressure to the inner ear via the cochlear aqueduct due to loss of spinal fluid. However, there are also some controversies related to this phenomenon, which require systematic investigation. MATERIAL AND METHODS: The effect of spinal needle diameter on hearing loss was investigated using audiometric tests in a prospective comparative study of 30 patients who were scheduled for surgery with spinal anesthesia. The bony structure of the cochlear and vestibular aqueducts was determined from temporal bone CT scans. RESULTS: Four out of 15 patients (26.67%) treated with a 22 G spinal needle demonstrated hearing loss the day after surgery, which recovered within 2-5 weeks. However, none of the patients treated with a 27 G spinal needle had statistically significant hearing loss in either ear at any frequency. Three out of four patients with hearing loss had an acute-onset balance problem. There was no difference between the two groups in terms of the widths of the vestibular and cochlear aqueducts. CONCLUSIONS: It has been shown audiometrically that the diameter of the spinal needle used to induce spinal anesthesia seems to have an effect on subsequent hearing loss. The patency of the bony canal determines the transmission of pressure changes to the inner ear. However, the individual risk of this complication is not predictable as there is no radiological abnormality of the canal.

Acoustic Impedance Tests↗

PubMed1993

Vascular patterns of the saccule of the rat: a microcorrosion cast study.

A scanning electron microscope study of corrosion cast preparations of the vessels of the saccule was carried out in adult rats. This method shows the microvasculature of the saccule in the three-dimensional model. As a result of this technique we have been able to demonstrate a particular microvasculature of the saccule in the rat's inner ear. The main blood supply of the saccule consists of the arterioles coming from the vestibulocochlear artery entering the anterior margin of the macula sacculi. A few branches of the anterior vestibular artery enter the macula sacculi from the superior margin. The saccular vein drains the venous blood from a dense capillary area underneath the striola to the posterior vestibular vein which eventually ends in the vein of the cochlear aqueduct.

Animals↗

PubMed1978

Fetal respiratory distress causing CNS and inner ear hemorrhage.

Fifty-two consecutive temporal bones of infants who died neonatally, or in utero of natural causes, were studied. Complete autopsies were performed. Twenty-eight infants had a variety of pulmonary disorders which resulted in severe respiratory distress prior to their death. Of these, the majority had bleeding intracranially and into the inner ear. There were five major pathways of central nervous system and subarachnoid hemorrhage involvement of the inner ear: 1) the modiolus, 2) cochlear aqueduct, 3) retrograde via the cochlear vein, 4) episodes of spontaneous bleeding into various compartments of the inner ear, and 4) hemorrhage via the otic capsule. The remaining 24 infants died of other natural causes. Two had CNS bleeding with no extension to the inner ear. We propose that there is a syndrome which consists of 1) neonatal respiratory distress, 2) intracranial hemorrhage, and 3) bleeding into the inner ear--an extension of a subarachnoid or subependymal matrix bleeding diathesis.

Cerebral Hemorrhage↗

PubMedDate not supplied

Experimental viral infections of the inner ear. II. Simian virus 40 induced tumors of the temporal bone.

Pathological and virological studies were performed on temporal bones of 23 hamsters which developed tumors subsequent to neonatal inoculation of simian virus 40 (SV40). Four to five months after viral inoculation, 22 hamsters developed undifferentiated sarcomas in the subcutaneous space adjacent to the temporal bone. Nine tumors invaded the temporal bone, occassionally extending to the subarachnoid space but not to the inner ear. Choroid plexus papillomas developed in four animals, with one tumor demonstrating invasion of the cochlear aqueduct, internal auditory canal, and cochlear modiolus. Cells grown from a sarcoma and a choroid plexus papilloma contained tumor antigen and established that the tumors were SV40 virus induced.

Animals↗

PubMed1995

[Clinical analysis of 102 patients with congenital inner ear malformation].

Hearing loss and CT findings of 200 ears from 102 cases with congenital malformation of inner ear were included in our study. Hearing loss was typically bilateral severe, or total deafness. 75 percent of them were found deaf within one-year-old. In addition, 47 patients' (46%) mothers were noted to have caught a cold in first trimester of pregnancy. Temporal bone abnormalties were described as five types: 1. Michel malformation, 2. Mondini malformation, 3. enlargement of the vestibular aqueducts, 4. developmental deformity of cochlear aqueduct, 5. developmental deformity of internal acoustic meatus. Most cases showed malformations of vestibule or vestibular aqueducts.

Child↗

PubMed2001

[Inner ear and subarachnoid spaces: relations and diseases].

The purpose of this article is to describe, with 5 clinical cases, the physiological communications between the inner ear and the subarachnoid spaces (SAS) and present the imaging features with regard to. Therefore we briefly illustrate abnormal communications between SAS and perilymphatic fluids in certain cochlear and internal acoustic meatus (IAM) malformations and their consequences. Imaging features may depict diffusion pathway of bacterial meningitis to membranous labyrinth via the cochlear aqueduct or via the IAM. Rarely, in some patients referred for cochleovestibular symptoms, imaging features may display skull base tumors involving the area of cochlear or vestibular aqueduct aperture. Therefore, in patients referred for cochleovestibular symptoms, MR and CT study should carefully scrutinise not only the IAM but also the aperture of the cochlear and the vestibular aqueducts and the cerebellopontine meninges.

Adult↗

PubMed2004

An overview of congenital/developmental sensorineural hearing loss with emphasis on the vestibular aqueduct syndrome.

The evaluation of children with congenital/developmental hearing loss has undergone substantial transformation in recent years. This communication focuses on the most common cause of this type of hearing loss for which there are imaging findings: the vestibular aqueduct syndrome. The normal anatomy of the vestibular aqueduct is discussed in detail. The cochlear aqueduct with which it is commonly confused is also discussed. An overview of other congenital defects and abnormal middle/inner ear communications is also included. A brief discussion of cochlear implants is also included for completeness.

Cochlear Implants↗