Tinnitus is substantially associate

Tinnitus is substantially associated with noise exposure and noise-induced hearing
loss and thus the noise-induced cochlear injury is likely a significant pathology
associated with the generation of tinnitus. This brief review describes the pathology
and mechanisms of cochlear injury in noise-induced hearing loss, drawing
predominately on animal studies.
The predominant site of injury to the auditory system from excessive noise exposure
is the cochlea of the inner ear (Figure 1). The cochlea houses the auditory sensory
organ, the organ of Corti containing the auditory sensory cells (inner and outer hair
cells) and their primary afferent neurons (the type I and II spiral ganglion neurons,
respectively). Adjacent to the organ of Corti, on the lateral wall of the cochlea, is the
spiral ligament and the stria vascularis, two structures that collectively are important
for the maintenance of the cochlear fluids which bathe the sensory cells and neurons
and provide the correct electrochemical environment for sensory cell function. Most important is production and regulation of the endolymph, a unique extracellular fluid
with a high potassium content (approximately 150mM) and large positive voltage (80-
100mV compared with perilymph), which covers the apical surface of the organ of
Corti.3 This high voltage is essential for sensory cell function as it provides the
driving force for ion (potassium) flow through the hair cell transduction channels.
Figure 1: Cross-section of the mouse cochlea showing the fluid spaces, scala vestibuli (SV) and scala tympani (ST) containing perilymph and scala media (SM) containing endolymph, the sensory organ the organ of Corti (OC) and the lateral wall with the spiral ligament (SL) and stria vascularis (*). Marker 1mm.
Pathology—Cochlear injury from noise exposure has been well identified and
characterised with respect to the parameters of noise exposure and also the hearing
loss. Damage or loss of sensory cells, particularly the outer hair cells (OHC) are
now well established as the characteristic injury from noise exposure. Injured
sensory cells may survive but with permanently distorted or fused stereocilia (sensory
hairs), although loss of stereocilia appears to herald the eventual loss of the sensory
cell. The vulnerability of these cells to noise injury is seen across species and the hair
cell pathology is also observed in human cochleae. The primary afferent neurons, or
more specifically the boutons of the type I neurons innervating inner hair cells (IHC),
are also targets in noise-induced hearing loss.
Swelling and degeneration of these nerve terminals is observed after noise exposure,
but no direct effect of noise exposure has been observed on the type II neurons
innervating the OHC. More recently Kujawa and Liberman8 have described more
extensive neuronal degeneration with little other cochlear injury indicating that the
neural consequences of noise exposure may be more extensive. Direct injury of the
supporting cells of the organ of Corti appears to be a consequence of very intense,
impulse or long duration noise exposures. Often when there is injury to the supporting
structures there is complete loss of the integrity of the organ of Corti.