Rapid hearing threshold assessment with modified auditory brainstem response protocols in dogs

This study examines auditory brainstem responses (ABR) elicited by rising frequency chirps. The time course of frequency change for the chirp theoretically produces simultaneous displacement maxima by compensating for travel-time differences along the cochlear partition. This broadband chirp was derived on the basis of a linear cochlea model [de Boer, "Auditory physics. Physical principles in hearing theory I," Phys. Rep. 62, 87-174 (1980)]. Responses elicited by the broadband chirp show a larger wave-V amplitude than do click-evoked responses for most stimulation levels tested. This result is in contrast to the general hypothesis that the ABR is an electrophysiological event most effectively evoked by the onset or offset of an acoustic stimulus, and unaffected by further stimulation. The use of this rising frequency chirp enables the inclusion of activity from lower frequency regions, whereas with a click, synchrony is decreased in accordance with decreasing traveling velocity in the apical region. The use of a temporally reversed (falling) chirp leads to a further decrease in synchrony as reflected in ABR responses that are smaller than those from a click. These results are compatible with earlier experimental results from recordings of compound action potentials (CAP) [Shore and Nuttall, "High synchrony compound action potentials evoked by rising frequency-swept tonebursts," J. Acoust. Soc. Am. 78, 1286-1295 (1985)] reflecting activity at the level of the auditory nerve. Since the ABR components considered here presumably reflect neural response from the brainstem, the effect of an optimized synchronization at the peripheral level can also be observed at the brainstem level. The rising chirp may therefore be of clinical use in assessing the integrity of the entire peripheral organ and not just its basal end.

Peripheral deafness may be inherited or acquired, congenital or later-onset, and sensorineural or conductive. The most commonly observed forms are inherited congenital sensorineural, acquired later-onset sensorineural (ototoxicity, presbycusis) and acquired later-onset conductive (chronic otitis externa/media). In most dog and cat breeds inherited congenital sensorineural deafness results from perinatal degeneration of the stria vascularis, the vascular bed of the outer wall of the cochlear duct, which leads to hair cell degeneration. The strial degeneration appears to result from the absence of melanocytes, but their function in this structure is unknown. Ototoxicity may result from any of a large number of drugs and chemicals that directly or indirectly destroy cochlear hair cells. The effects are dose-dependent and in rare cases reversible. The most commonly recognized ototoxic drugs are the aminoglycoside antibiotics. Presbycusis, the ageing-related progressive hearing loss unattributable to other causes, is sensorineural but may also include mechanical changes in the tympanum and ossicles. Hearing aids may be accepted by some dogs as long as some residual function remains. Breeds reported to have been affected by congenital sensorineural deafness are listed and those with the highest prevalence are noted. Methods for diagnosis of deafness are described.