Postnatal functional changes in the activity of the ear and auditory pathway in neonatal guinea pigs [from day of birth (postnatal day, PND = 0), PNDs 1–4, 7 and then weekly up to 7 weeks] were studied as a model of maturation of hearing in human neonates. On the day of birth there were signs of a conductive hearing loss: negative middle ear pressure, auditory nerve brainstem evoked response (ABR) threshold elevation, ABR wave 1 latency prolongation and low amplitude otoacoustic emissions. The conductive hearing loss is probably a result of the (amniotic) fluid found in the neonatal middle-ear cavity. Over the next PNDs, this conductive hearing loss was resolved. In order to confirm this neonatal conductive hearing loss and its resolution, saline was instilled into the middle ear of guinea pigs. This induced signs of a conductive hearing loss similar to those seen in the neonatal guinea pigs which disappeared with clearance of this fluid. Therefore it may be concluded that most of the changes in auditory function seen over the first PNDs are due to absorption of amniotic fluid from the middle-ear cavity.

The human fetus in utero is able to respond to sounds in the amniotic fluid enveloping the fetus after about 20 weeks gestation. The pathway by which sound reaches and activates the fetal inner ear is not entirely known. It has been suggested that in this total fluid environment, the tympanic membrane and the round window membrane become ‘transparent’ to the sound field, enabling the sounds to reach the inner ear directly through the tympanic membrane and the round window membrane. It is also possible that sounds reach the inner ear by means of tympanic membrane – ossicular chain – stapes footplate conduction (as in normal air conduction). There is also evidence that sounds reach the fetal inner ear by bone conduction. Several animal and human models of the fetus in utero were studied here in order to investigate the pathway enabling sounds to reach and activate the fetal inner ear. This included studying the auditory responses to sound stimuli of animals and humans under water. It was clearly shown in all the models that the dominant mechanism was bone conduction, with little if any contribution from the external and middle ears. Based on earlier experiments on the mechanism and pathway of bone conduction, the results of this study lead to the suggestion that the skull bone vibrations induced by the sound field in the amniotic fluid enveloping the fetus probably give rise to a sound field within the fetal cranial cavity (brain and CSF) which reaches the fetal inner ear through fluid communication channels connecting the cranial cavity and the inner ear.

This study demonstrates the feasibility in general of using short-latency evoked potentials to evaluate functional cochleotoxicity and vestibulotoxicity of ototoxic drugs and to differentiate between them.

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Taking into consideration that this is an animal study, the results suggest that clearance of amniotic fluid from the newborn middle ear takes longer than has been generally thought. In addition, an animal model for assessing the clearance of fluid from the middle ear has been developed.