| Description |
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Because there are no elastic fibers in the atrophic or dimeric portion of the tympanic membrane, the pars tensa has no rebound. Once the pulsion pocket has been displaced laterally by positive intratympanic pressure, it will remain in this displaced or herniated position as long as the intratympanic pressure remains either positive or equal to the ambient atmospheric pressure.
There seems to be more than one reason for the development of positive middle ear pressure. A common phenomenon in some patients appears to be a laxity in the incudostapedial joint, usually caused by a partial resorption of the lenticular process of the incus. This phenomenon is characterized clinically by a fluctuating conductive hearing loss in which the transmission of sound through the middle ear improves when the ossicular chain is placed under tension by the forced inflation of the middle ear. Since these individuals hear better with positive intratympanic pressure, any attempt to equalize this pressure by myringotomy or with pressure-equalization tubes will generally result in an extremely unhappy patient.
Patients with pulsion hernias all have well-ventilated middle ears and patent Eustachian tubes.
Tympanometry in these patients will reveal the presence of an increased tympanic membrane mobility due to the defect in the fibrous middle layer of the pars tensa and a normal or positive intratympanic pressure. |
