The Effect of Impulse Noise on Cochlear Vessels

Abstract

and long-term changes in the cochlear vasculature and long-term changes in the sensorineuroepithelium were studied in guinea pigs after they were exposed to impulse noise. Vessel histology and cochlear hair cell loss were assessed, using a surface-preparation technique, and the results showed considerable variability. Hair cell loss and radial tears in the organ of Corti were a common finding in the animals killed four weeks after impulse-noise exposure. Impulse-noise exposure resulted in few cochlear vascular changes in the acutely and chronically affected groups. Compared with the results of our previous studies using continuous-noise exposure of different characteristics and in different mammals, this impulse-noise experiment resulted in a nonsignificant damaging effect on the cochlear vasculature. (Arch Otolaryngol 1984;110:111-115) Extensive speculations have been made concerning the traumatic mechanisms of noise on the cochlea. Among different theories to explain the sensorineural hearing loss at low¬ er sound intensities (ie, 85 to 120 dB measured on the A scale [dBA]), one proposal has been that deficient function of cochlear vessels leads to sensory cell loss. The concept is that sensory cells during increased need for oxygen and energy do not receive a sufficient supply from the cochlear vessels, possibly due to a vessel con¬ striction created by the noise itself. Most experimenters agree that me¬ chanical factors are responsible for damage to the sensorineuroep¬ ithelium at high sound intensities (ie, > 120 dBA). It is assumed that impulse-noise exposure results in tears of the cochlear membranes and other kinds of mechanical damage, eg, holes in the reticular lamina. Howev¬ er, there is little information avail¬ able concerning the specific shortterm persistent effects of impulse noise on cochlear vessels. In rats, ves¬ sel constriction in response to sound bursts can occur at intensities as low as at hearing threshold.1 Such vessel constriction in the periphery (ie, cochlea) could theoretically restrict the oxygen and energy supply and induce permanent sensory cell dam¬ age on a vascular basis. After expo¬ sure to gunshots, Kellerhals2 observed the packing of RBCs in the stria vascularis of experimental guinea pigs, which was not limited to the area of greatest hair cell damage. Stria vascularis capillaries were tightly packed with an abnormal homogenous mass of RBCs, but similar packing was absent in other vessels.These changes were present imme¬ diately and up to several days after exposure. Occlusion of lumina, col¬ lapse of vessels in the external wall of the cochlea, and degeneration of capil¬ laries with intravascular strands have been demonstrated with impulsenoise exposure.3 In animals exposed to sonic booms, hemorrhages were found in the scala tympani localized to the lower middle or basal turn of the cochlea." The mechanism was sup¬ posed to be a stretching of blood ves¬ sels on the tympanic surface of the basilar membrane, and the hemor¬ rhage was interpreted as a sign of mechanical dam...

Acoustic Trauma Caused by the Telephone

“…Such intensities are known to have a damaging effect on the inner ear. Most ex perimenters agree that mechanical factors are responsible for damage to the sensorineuroepithelium at sound intensities higher than 120 dBA [5], It is likely that other physicians have seen one or more isolated cases but have not picked up on the midfrequency hearing loss, or paid any particular attention to them and therefore have not reported the cases. These accidents may easily be misdiagnosed as be ginning Meniere's disease or sudden deaf ness due to viral infection.…”