Pressure transfer between intracranial and cochlear fluids in patients with Meniere's disease.

OBJECTIVES: To elucidate the pressure transfer between intracranial and labyrinthine fluids in patients with well-defined unilateral Meniere's disease. STUDY DESIGN: Eleven patients previously exposed to hypobaric pressure agreed to be investigated further with the tympanic membrane displacement (TMD) technique. TMD was used to indirectly analyze perilymph pressure changes as the result of changes in body position. METHODS: Repeated measurements for both the diseased and the healthy ears were made with the patients supine and then in a sitting position. The TMD parameters for the maximum inward displacement, the Vi, and the mean volume displacement, the Vm, were calculated and compared. RESULTS: The paired comparison showed statistically significant larger Vi values for both ears in the supine position. A similar tendency was observed for the Vm value. This difference of the Vi was significantly larger for the diseased ear compared with the currently healthy ear. The results were compared to the audiometric and electrocochleographic results previously obtained on the same patients when they were subjected to hypobaric pressure. Patients who experienced the largest differences in hearing level thresholds in the lower frequencies also showed the greatest differences in TMD values as the result of postural changes. CONCLUSIONS: Despite the limited number, the statistically supported results suggest a relation between the efficiency of the routes of pressure transfer and the observed effect of hypobaric exposure. The results also indicate that for the patients tested, the routes of communication are more effective in the diseased ear than in the healthy ear--a condition that may relate to the pathogeneses of Meniere's disease.

Pressure gradients affecting the labyrinth during hypobaric pressure. Experimental study.

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.

Perilymph pressure during hypobaric conditions--cochlear aqueduct obstructed.

Nine cats with the cochlear aqueduct surgically blocked were anaesthetised, put in a pressure chamber, and stepwise exposed to hypobaric pressure, each of the two steps lasting 5 min. The chamber pressure was reduced to -5 and -7 kPa. Concluding the experiment the cats were observed for 5 min after restoration of atmospheric pressure. The perilymph, tympanic cavity, cerebrospinal fluid, central venous, arterial and surrounding chamber pressures were continuously recorded. Reduced chamber pressure caused relative overpressure within the tympanic cavity, thereby inducing pressure gradients between the chamber, the tympanic cavity, the labyrinth and the cerebrospinal fluid and vascular pressures respectively. Our results demonstrate that hypobaric effects on the labyrinth are mediated via pressure changes in the tympanic cavity and not by systemic, vascular or cerebrospinal fluid influence. Substantial perilymph overpressure lasted throughout the hypobaric conditions. The magnitude and the duration of this overpressure were influenced by the patency of the Eustachian tube whereas the rate of the pressure change in the chamber was of little importance. As atmospheric pressure was restored in the chamber the overpressure in the labyrinth was reversed to underpressure--relative to pre-experimental conditions.

Pressure transfer between the perilymph and the cerebrospinal fluid compartments in cats.

This is a review of our studies of the labyrinthine fluid pressure in cats subjected to pressure changes in the middle ear (implosive routes) and the cerebrospinal fluid compartment (explosive routes) as well as to changes in vascular and ambient pressures. The perilymph, cerebrospinal fluid (CSF), middle ear, venous and arterial pressures were measured with the cochlear aqueduct (CA) patent as well as surgically blocked. Experiments on explosive pressure changes revealed that the perilymph pressure was regulated by the CSF in case of CA patency. The CSF influence was dominant enough to obscure any direct effect on the labyrinth from other sources. With the CA obstructed the CSF influence on the labyrinth was apparently mainly via the endolymphatic sac and duct although limited and much delayed. Systemic arterial pressure changes had a pronounced influence on the perilymph pressure, but this effect was revealed only when the CSF influence was reduced by CA obstruction. Experiments on implosive and ambient pressure changes suggested that there was no fundamental difference in the perilymph response to equivalent levels of implosive versus hypobaric pressure. Three factors determined the effect of implosive and hypobaric pressure: the patency of the CA, the rate of the pressure change, and the eustachian tube function.

Transmission of cerebrospinal fluid pressure via the cochlear aqueduct and endolymphatic sac.

The concept of perilymphatic and endolymphatic pressure balance is generally linked to the theory that the endolymphatic sac transmits cerebrospinal fluid (CSF) pressure changes to the endolymph to equalize CSF pressure changes transmitted to the perilymph via the cochlear aqueduct. This theory, and the significance of other mechanisms of CSF pressure influence on the labyrinth, were evaluated experimentally. Continuous measurements of perilymphatic, CSF, venous, and arterial pressures were performed on cats with the cochlear aqueduct patent or obstructed and the inferior cochlear vein intact or occluded. Intracranial pressure changes were induced by subarachnoid infusion of artificial CSF in live and dead animals. With the cochlear aqueduct patent, CSF pressure changes were transmitted to the perilymph without any significant dampening or time lag. With the cochlear aqueduct obstructed, CSF pressure changes induced significantly lower and delayed changes in perilymphatic pressure. Similar results were obtained whether the animals were alive or dead and the cochlear vein intact or blocked. This indicated a passive mechanism not induced by changes in labyrinthine fluid production or blood flow. Long-standing, stable elevation of CSF pressure with the cochlear aqueduct blocked induced a slowly increasing perilymphatic pressure, always stabilizing at a pressure rise significantly less than that of CSF. The results do not suggest any major pressure transfer via perineural or perivascular routes. The endolymphatic sac is postulated to mediate a reduced and delayed transfer of increased intracranial pressure to the labyrinth.