Noise-induced hearing loss and tinn

Noise-induced hearing loss and tinnitus

Abstract
Excessive sound exposure is a significant cause of temporary and permanent hearing loss and tinnitus. This presentation reviews the nature of the pathology of NIHL, the pathogenesis injury and, briefly, considers how this relates to tinnitus generation.
Classically, injury is localised to sensory cells and primary afferent neurones
innervating inner hair cells (IHC). There is increasing evidence of changes to lateral
wall tissues, particularly loss of spiral ligament fibrocytes and stria vascularis atrophy,
which may be a more generalised pathology than previously indicated. Changes to
sensory and neural structures are correlated to loss of sensitivity and tuning, however,the consequences of the lateral wall alterations are not established but may be a deficit in potassium homeostasis and the endocochlear potential (driving potential to sensory cells).
Mechanisms of cell death include oxidative stress, glutamate excitotoxicity and
initiation of apoptosis. Chronic noise generates a cochlear inflammatory response
which may exacerbate injury and the relevance to tinnitus of chronic inflammation
and irritation of cochlear structures, needs to be considered. Clearly many noise
effects are pathological but we need to consider that many may also reflect
physiological adaptations to excessive stimulation. For example, noise activation of
efferent pathways is known to influence hair cell sensitivity; the ear can be conditioned to excessive sound; and there are molecular mechanisms that regulate the sensitivity of the cochlea in noise. That these mechanisms are “protective” around
high level physiological sound is important and the possibility that sensitivity to
NIHL may relate to the individual efficacy of these adaptive processes needs to be
considered.
In terms of tinnitus, these pathological and physiological changes to the cochlea in
response to loud sound temporarily and permanently alter the pattern and nature of
input to the central nervous system which are manifest in changes in the Cochlear
Nucleus, Inferior Colliculus and Cortex.