The development of middle-ear structures in the mouse was examined in nine groups of pups between 1 and 45 days of age. The area of the tympanic membrane (pars tensa and pars flaccida), the length of the lever arms of the malleus and incus, the surface area of the oval window, and the volume of the bulla all showed systematic changes during neonatal life. The area of the oval window reached maturity first and the lever arms achieved 90% of their adult size on day 11. The tympanic membrane achieved the same criterion on day 18. These data help us further to understand the processes that contribute to the functional ontogeny of the middle ear.

There are few clinical neuro‐otologic investigations of acute head injury. We obtained impedance and auditory brain stem response measures for 25 acute head‐injured patients, usually within 76 hours following injury. All patients were comatose at the time of assessment. Impedance abnormalities were found for over three‐fourths of the patients. Generally, they were associated with transient, reversible dysfunction, such as high negative middle ear pressure. The acoustic stapedius reflex, however, was seldom observed, even in patients with apparently normal middle ear function. Auditory brain stem response measures showed evidence of CNS dysfunction in 80% of the patients. Abnormalities ranged from prolonged latency and reduced amplitude of the wave V auditory brain stem response component to total absence of brain stem auditory activity. There was a relationship between auditory brain stem response findings and neurologic outcome at 1 month post assessment. Electrophysiologic auditory measures are clinically valuable in neuro‐otologic diagnosis and neurologic prognosis of acute, severe head injury.

Three case studies are presented to illustrate the clinical usefulness of serial electrophysiologic and behavioral audiologic assessments in describing CNS function in severe head injury. There was an association among acute auditory brain stem and middle-latency evoked response findings, computed tomography of brain abnormality and neurologic status, and rate of recovery. Auditory evoked response findings 4 days after injury were also correlated with long-term outcome of diagnostic speech audiometry.

Changes in endocochlear DC potential (EP) and potassium ion concentrations in endolymph were measured simultaneously during anoxia or during perfusion of the perilymphatic space with furosemide, 10(-2)M, in normal and kanamycin-deafened guinea pigs. The potassium ion conductance (Gk) through the cochlear partitions was calculated. Thirty minutes after the onset of anoxia, the Gk is 22.1 microM/min/mV in normal guinea pigs and 4.8 microM/min/mV in kanamycin-deafened guinea pigs. At that time the EP is -29.5 mV in normal guinea pigs and 1.4 mV in kanamycin-deafened guinea pigs. In the early stage of anoxia the rate of potassium ion concentration decrease in the endolymph per unit time is greater in normal guinea pigs than in kanamycin-deafened guinea pigs. These results suggest a rapid increase in the permeability of potassium ions in the organ of Corti in the early stage of anoxia might produce a large negative potassium ion diffusion potential or negative EP in normal guinea pigs and the failure to develop the negative EP in kanamycin-deafened guinea pigs might be due to the lack of such a rapid increase in the permeability because of the loss of the hair cells.