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Updated: Jul 29, 2026

Selective Tracing of Auditory Fibers in the Avian Embryonic Vestibulocochlear Nerve
Published on: March 18, 2013
The pathway for the transmission of external sounds into the fetal inner ear
1Department of Physiology, The Hebrew University-Hadassah Medical School, Jerusalem, Israel. sohmer@md2.huji.ac.il
After at least 20 weeks gestation, the human fetus in utero is able to hear and respond to external and internal (maternal) sounds. The external sounds are attenuated by maternal tissues and fluids - higher frequencies by about 20 dB, and lower frequencies are only slightly reduced. The sounds in the amniotic fluid, which completely envelops the fetus, then reach the fetal inner ear by bone conduction. The sound pressure in the amniotic fluid induces skull vibrations which are transmitted directly into the contents of the cranial cavity (brain and CSF) and from there, presumably by fluid channels connecting them, into the cochlear fluids. A further stage of conductive attenuation is probably involved in this transmission. Since the fetus in utero receives oxygen by placental diffusion (less efficient than pulmonary diffusion), the fetal inner ear is hypoxic compared to that following birth (pulmonary oxygen diffusion). This leads to a reduction in the magnitude of the endocochlear potential, to a depression of cochlear transduction and amplification, and thus to an additional sensorineural component of threshold elevation in the fetus. Upon birth, these conductive and sensorineural attenuations are removed.
After at least 20 weeks gestation, the human fetus in utero is able to hear and respond to external and internal (maternal) sounds. The external sounds are attenuated by maternal tissues and fluids - higher frequencies by about 20 dB, and lower frequencies are only slightly reduced. The sounds in the amniotic fluid, which completely envelops the fetus, then reach the fetal inner ear by bone conduction. The sound pressure in the amniotic fluid induces skull vibrations which are transmitted directly into the contents of the cranial cavity (brain and CSF) and from there, presumably by fluid channels connecting them, into the cochlear fluids. A further stage of conductive attenuation is probably involved in this transmission. Since the fetus in utero receives oxygen by placental diffusion (less efficient than pulmonary diffusion), the fetal inner ear is hypoxic compared to that following birth (pulmonary oxygen diffusion). This leads to a reduction in the magnitude of the endocochlear potential, to a depression of cochlear transduction and amplification, and thus to an additional sensorineural component of threshold elevation in the fetus. Upon birth, these conductive and sensorineural attenuations are removed.
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