Functional Patency of the Cochlear Aqueduct

1982 ◽  
Vol 91 (2) ◽  
pp. 209-215 ◽  
Author(s):  
Björn Carlborg ◽  
Barbara Densert ◽  
Ove Densert
Keyword(s):  
Cerebrospinal Fluid ◽  
Inner Ear ◽  
Middle Ear ◽  
Ambient Pressure ◽  
Ear Canal ◽  
Cochlear Aqueduct ◽  
Pressure Release ◽  
Release Capacity ◽  
Before And After ◽  
Pressure Changes

The perilymphatic (P P) and cerebrospinal fluid (P CSF) pressures were investigated in relation to pressure variations in the ear canal, middle ear and intracranial compartment before and after occlusion of the cochlear aqueduct (CA). Experiments using intracranial infusion showed that the CA was responsible for a perfect hydrodynamic balance between the CSF and the perilymph. There are indications of additional pressure release factors but their capacities were not sufficient to prevent the appearance of a longstanding and substantial pressure gradient following occlusion of the CA. A gradual P P build-up, from zero to its original level after the CA was opened and occluded, indicated perilymph production within the labyrinth. Investigation of pressure transfer from the ear canal and middle ear to the perilymph showed that the CA was the major pressure release route from the cochlea. Occlusion of the CA reduced the compliance of the inner ear and severely reduced the pressure release capacity. In such a situation the inner ear is almost incapable of equilibrating ambient pressure changes.

Pressure Gradients Affecting the Labyrinth during Hypobaric Pressure

1997 ◽  
Vol 106 (6) ◽  
pp. 495-502 ◽  
Author(s):  
Konrád S. Konrádsson ◽  
Björn I. R. Carlborg ◽  
Joseph C. Farmer
Keyword(s):  
Cerebrospinal Fluid ◽  
Eustachian Tube ◽  
Ambient Pressure ◽  
Pressure Gradients ◽  
Cochlear Aqueduct ◽  
Fluid Compartment ◽  
Large Pressure ◽  
Fluid Compartments ◽  
Pressure Changes ◽  
Considerable Pressure

Hypobaric effects on the perilymph pressure were investigated in 18 cats. The perilymph, tympanic cavity, cerebrospinal fluid, and systemic and ambient pressure changes were continuously recorded relative to the atmospheric pressure. The pressure equilibration of the eustachian tube and the cochlear aqueduct was studied, as well as the effects of blocking these channels. During ascent, the physiologic opening of the eustachian tube reduced the pressure gradients across the tympanic membrane. The patent cochlear aqueduct equilibrated perilymph pressure to cerebrospinal fluid compartment levels with a considerable pressure gradient across the oval and round windows. With the aqueduct blocked, the pressure decrease within the labyrinth and tympanic cavities was limited, resulting in large pressure gradients toward the chamber and the cerebrospinal fluid compartments, respectively. We conclude that closed cavities with limited pressure release capacities are the cause of the pressure gradients. The strain exerted by these pressure gradients is potentially harmful to the ear.

Volume receptors in guinea pig labyrinth: relevance with respect to ADH and Na control

1989 ◽  
Vol 257 (3) ◽  
pp. F341-F346 ◽  
Author(s):  
E. Bartoli ◽  
A. Satta ◽  
F. Melis ◽  
M. A. Caria ◽  
W. Masala ◽  
...  
Keyword(s):  
Inner Ear ◽  
Guinea Pigs ◽  
Control Mechanism ◽  
Extracellular Fluid ◽  
Urine Osmolality ◽  
Neural Pathways ◽  
Group Of Seven ◽  
Before And After ◽  
Pressure Changes ◽  
Inner Ear Pressure

We tested the hypothesis that changes in extracellular fluid volume are reflected by pressure changes within structures of the inner ear and that through neural pathways, a control mechanism exerts an influence on antidiuretic hormone (ADH) release and Na excretion. The study was performed on 35 guinea pigs. In protocol 1, 13 animals were studied before and after decompression of the inner ear by bilateral fluid withdrawal in an experimental setting of sustained isotonic expansion that kept the osmoreceptor partially activated and the intrathoracic volume receptors suppressed. A group of six sham-operated animals served as control. In protocol 2, nine animals were studied before and after a unilateral rise in their inner ear pressure during slightly hypertonic low-rate infusions that kept the osmoreceptor and thoracic volume receptors stimulated. A group of seven sham-operated guinea pigs served as controls. Decompression of the inner ear was attended by a rise in plasma ADH from 11.9 +/- 2.4 to 29.1 +/- 6.9 pg/ml, in urine osmolality (Uosmol) from 470 +/- 48 to 712 +/- 46 mosmol/kg (P less than 0.001), and a fall in urine flow rate (V) from 184 +/- 47 to 71 +/- 11 microliters/min (P less than 0.01), whereas plasma Na (PNa) and osmolality (Posmol) did not change. During inner ear hypertension, plasma ADH fell from 25.6 +/- 3.9 to 18.4 +/- 3.1, Uosmol from 829 +/- 58 to 627 +/- 43 (P less than 0.001), and V rose from 51 +/- 11 to 130 +/- 23 (P less than 0.001), whereas glomerular filtration rate, PNa, and Posmol did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Rupture of the round Window Membrane

1976 ◽  
Vol 85 (1) ◽  
pp. 105-110 ◽  
Author(s):  
P. H. Taylor ◽  
P. G. Bicknell
Keyword(s):  
Middle Ear ◽  
Surgical Intervention ◽  
Round Window ◽  
Oval Window ◽  
Round Window Membrane ◽  
Physical Effort ◽  
Cochlear Aqueduct ◽  
Definite Improvement ◽  
History Of ◽  
Pressure Changes

A case of sudden deafness due to rupture of the round window membrane is presented. Nineteen similar cases have previously been reported in the literature. In a review of these twenty patients, it is noted that a history of concurrent physical effort or barotrauma was present in eighteen. This supports the view that the injury is produced by pressure changes acting either along the cochlear aqueduct (the explosive route) or, directly on the middle ear structures (the implosive route). At operation, the rupture may be difficult to see, and a separate leak from the oval window may be present. The timing of any surgical intervention is important. The authors recommend that this should be deferred for one week after the onset of symptoms, as the fistula may heal spontaneously. If no definite improvement has occurred at the end of this time, then tympanotomy should be undertaken during the next week.

Lymphocytic Streaming as an Indicator of Inner Ear Compartmentalization

1981 ◽  
Vol 89 (5) ◽  
pp. 836-840
Author(s):  
George Roffman ◽  
Richard W. Babin
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Inner Ear ◽  
Lymphoblastic Leukemia ◽  
Cochlear Aqueduct ◽  
Fluid Channel ◽  
Temporal Bones ◽  
Perilymphatic Space ◽  
Physiologic Data

Despite a great deal of anatomic and physiologic data in animals, controversy still exists over whether or not the perilymphatic space in man is directly connected to the intracranial space via a patent cochlear aqueduct or other fluid channel. Human physiologic data are limited, indirect, and conflicting. Anatomic and pathologic data have heretofor been inadequate for answering the question convincingly. The temporal bones of a 19-year-old woman with central nervous system lymphoblastic leukemia are discussed. The passive-appearing movement of lymphoblasts between cerebrospinal fluid and perilymphatic spaces suggests both a functionally patent cochlear aqueduct and alternate pathways.

Contraindications to the Small Hole Stapedectomy

1981 ◽  
Vol 90 (6) ◽  
pp. 636-639 ◽  
Author(s):  
Brown Farrior
Keyword(s):  
Inner Ear ◽  
Tympanic Membrane ◽  
Middle Ear ◽  
Fluid Pressure ◽  
Internal Auditory Canal ◽  
Air Pressure ◽  
Small Hole ◽  
Excessive Pressure ◽  
Pressure Changes

A small hole stapedectomy with an unprotected piston is contraindicated in an ear subjected to excessive pressure changes whether these are excessive fluid pressure changes which occur in the inner ear or excessive air pressure changes in the middle ear. Excessive fluid pressure changes in the inner ear may be the result of an overly patent aqueduct of the cochlea or a permeable internal auditory canal. These excessive fluid pressure changes may produce fistulas or a dilated blister around the piston called a tented piston. Excessive air pressure changes in the middle ear will produce excessive excursions of the tympanic membrane which may result in vertigo or a dislocated piston.

Ear Malformation and Hearing Loss in Patients with Treacher Collins Syndrome

1993 ◽  
Vol 30 (1) ◽  
pp. 97-103 ◽  
Author(s):  
Gaylene Pron ◽  
Cheryl Galloway ◽  
Derek Armstrong ◽  
Jeffrey Posnick
Keyword(s):  
Hearing Loss ◽  
Inner Ear ◽  
Middle Ear ◽  
Conductive Hearing Loss ◽  
Treacher Collins Syndrome ◽  
External Ear ◽  
Ear Canal ◽  
Ear Malformations ◽  
Asymmetric Hearing Loss ◽  
Conductive Hearing

Although the hearing loss of patients with Treacher Collins syndrome is well documented, few studies have reported jointly on their hearing loss and ear pathology. This paper reports on the hearing loss and computerized tomography (CT) assessments of ear malformations in a large pediatric series of patients with Treacher Collins. Of the 29 subjects assessed by the Craniofacial Program between 1986 and 1990, paired audiologic and complete CT assessments were available for 23 subjects. The external ear canal abnormalities were largely symmetric, either bilaterally stenotic or atretic. In most cases, the middle ear cavity was bilaterally hypoplastic and dysmorphic, and ossicles were symmetrically dysmorphic or missing. Inner ear structures were normal in all patients. The majority of patients had a unilateral or bilateral moderate or greater degree of hearing loss and almost half had an asymmetric hearing loss. The hearing loss of all subjects was conductive, except for three whose loss was bilateral mixed. Two types of bilaterally symmetric hearing loss configurations, flat and reverse sloping, were noted. Conductive hearing loss in patients with Treacher Collins is mainly attributable to their middle ear malformations, which are similar for those of patients with malformed or missing ossicles.

Barotrauma Vis-a-Vis the “Chronic Otitis Media Syndrome”: Two Conditions with Middle Ear Gas Deficiency

2003 ◽  
Vol 112 (3) ◽  
pp. 230-235 ◽  
Author(s):  
Jacob Sadé ◽  
Amos Ar ◽  
Camil Fuchs
Keyword(s):  
Otitis Media ◽  
Middle Ear ◽  
Ambient Pressure ◽  
Chronic Otitis Media ◽  
Mastoid Pneumatization ◽  
Large Pressure ◽  
Pass Through ◽  
Pressure Changes ◽  
Gas Volume ◽  
Normal Controls

We compared 17 patients (29 ears) with barotrauma with 171 patients suffering from “chronic ears” (secretory otitis media, atelectasis, or previously operated cholesteatoma). The patients with “chronic ears” were followed up prospectively, and none were found to suffer from barotrauma after flying on a commercial airplane. The mastoid pneumatization (seen on lateral mastoid radiographs) was significantly larger in ears with barotrauma, averaging 16.85 cm2, versus 12.9 cm2 in normal controls, whereas in “chronic ears” it was only 3.6 cm2. During flight on a commercial airplane, the middle ear has to equalize about 20% of its gas volume with the ambient pressure. This equalization must happen within 15 to 20 minutes of ascent and descent in order to avoid barotrauma. This 20% is a fivefold greater task for ears with a large mastoid pneumatization than for ears with an undeveloped pneumatization; “chronic ears” usually have an undeveloped mastoid pneumatization. The smaller the middle ear (mastoid) volume, the smaller the volume of gas needed to pass through the eustachian tube in order to equalize pressure changes during flying. This factor may explain why “chronic ears” rarely suffer from barotrauma. It also implies that eustachian tubes of secretory otitis, atelectatic, and cholesteatomatous ears have little problem in equalizing large pressure differences (over 2,000 mm H2O) within 15 to 20 minutes of landing, in contrast to what has been traditionally believed. Individuals with “chronic ears” can be advised that they can fly safely.

Sign in / Sign up

Export Citation Format

Share Document