Force and contraction velocity of the middle ear muscles in the cat and the rabbit.
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The respective effects of pentobarbital-sodium, enibumal-sodium, urethane, urethane-chloralose and lidocaine on the function of the acoustic middle ear reflex in the rabbit were studied. The response of the middle ear muscles was measured by recording changes in both ears' acoustic impedance when the reflex was elicited by applying pure tone stimuli (2,000 Hz) to the two ears one at a time. In that way both the crossed and the uncrossed reflexes were studied. All the drugs were found to depress the reflex in such a way that a higher sound intensity was required after administration to achieve the same impedance change as before. The effect of the anesthetics was roughly proportional to their known anesthetic power. Lidocaine produced only a slight depression of the reflex. The crossed reflex showed a greater susceptibility to the general anesthetics than did the uncrossed reflex which suggests a greater complexity of the crossed reflex. Because the method of recording the reflex response does not require any surgery and is equally well applicable in unrestrained rabbits and in humans, it is suggested as a way of testing the effect of drugs on the central nervous system.
In the adult male rat the precise volumes of the middle ear cavity, the lateral attic compartment and a maximally retracted pars flaccida were calculated to 550 microliter, 21 microliter and 3 microliter respectively, using Woods metal. Small intratympanal pressure or volume changes caused the pars flaccida to move in a medial-lateral direction. As the volume of a maximally retracted or bulging pars flaccida only amounted to about 0.5% of the total middle ear volume and the pars flaccida reacted even at volume changes of 0.1% of the middle ear, it would seem that the pressure equilibrating capacity of the elastic pars flaccida is negligible. On the other hand the pars flaccida is extremely sensitive to pressure and volume changes in the middle ear and may take part in the pressure equilibrating system as a detector for minute pressure and/or volume changes in the middle ear.
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The primate nasopharynx-eustachian tube-middle ear complex is being used to model both the normal and pathologic functions of the human eustachian tube by several researchers. An extensive search of the literature has indicated little detailed information on the primate eustachian tube/middle ear system. This study was undertaken to define the anatomical characteristic of the system in the Rhesus monkey (Macaca mulatta) and to determine the limits on the use of the monkey as a model of human eustachian tube function. Although the direct application of morphologic data to explain the function of a system is tenuous, the data on the Rhesus monkey eustachian tube appears to be consistent with that published for other mammals. The tensor veli palatni muscle appears to be the only muscle to act directly on the tube and effect tubal dilation. The muscle is attached to the lateral membranous tubal wall along its extrabullar extension. The muscle has an inferior attachment to the posterior hard palate and thus possesses a vector directed inferolaterally; contraction would appear to pull the membranous wall inferiorly and laterally, resulting in the tubal dilation. The eustachian tube relationships of the salpingopharyngeus, levator veli palatini, and internal pterygoid muscles are described. Their possible role in primate tubal function is minimal at best.
It has been our hypothesis that different types of middle ear effusions and the clinical manifestations with which they are associated represent the typical inflammatory response. Employing an animal model under controlled conditions, we present statistical evidence that change in the mucosa of the middle ear in otitis media can occur along a continuum, with early forms regressing to more chronic stages of the disease. We also demonstrate an increase in the thickness and a decrease in the permeability of the round window membrane in a longitudinal study of otitis media in the same animal model. Histopathologic changes in human temporal bones with otitis media with effusion or chronic otitis media are similar to the changes in the animal models. These results support a concept that all categories of otitis media (serous, purulent, mucoid, and chronic) represent different stages in a continuum of events.
Two temporal bones are discussed that contain ectopic striated muscle in the horizontal fallopian canal. In one instance, this muscle was clearly innervated by a branch from the geniculate ganglion. This is an unusual histologic finding and the innervation to such a muscle has been rarely identified. The facial nerve surgeon should be aware that a mass encountered during decompression may be developmental rather than neoplastic.
Many species of echolocating bats emit intense orientation sounds. If such intense sounds directly stimulated their ears, detection of faint echoes would be impaired. Therefore, possible mechanisms for the attenuation of self-stimulation were studied with Myotis lucifugus. The acoustic middle-ear-muscle reflex could perfectly and transiently regulate the amplitude of an incoming signal only at its beginning. However, its shortest latency in terms of electromyograms and of the attenuation of the cochlear microphonic was 3-4 and 4-8 msec, respectively, so that these muscles failed to attenuate orientation signals by the reflex. The muscles, however, received a message from the vocalization system when the bat vocalized, and contracted synchronously with vocalization. The duration of the contraction-relaxation was so short that the self-stimulation was attenuated, but the echoes were not. The tetanus-fusion frequency of tha stapedium muscle ranged between 260 and 320/sec. Unlike the efferent fibres in the lateral-line and vestibular systems, the olivo-cochlear bundle showed no sign of attenuation of self-stimulation.
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Two cases demonstrating the effects of myogenic artifact on the electrical auditory brainstem response (EABR) when using a promontory stimulation site are presented. Intensity-response functions were obtained in the unparalyzed condition, then repeated after infusion of a neuromuscular paralyzing agent. In both cases, the myogenic response was observed at lower stimulus intensities than the EABR components. As intensity increased, the myogenic responses grew at extremely rapid rates and made any subsequent identification of auditory responses virtually impossible. To alleviate the adverse influence of myogenic components, general anesthesia and a paralyzing agent must be incorporated into the test protocol when acquiring the EABR using a promontory site of stimulation.