Ion channels are macromolecular proteins embedded in the cellular membrane. Their main function is to guide the directional flow of ions from inside and outside the cell, through concentration or electrical gradients (Kole et al, 2003). A growing number of diseases are now recognized to be the direct cause of dysfunctional ionic channels, usually through genetic mutation “channelopathies” (Waxman, 2007). Other implicated aetiologies could be autoimmune disorders, ototoxicity (one of the main mechanisms chemical ablation treatment for Meniere’s disease is based on is the interference with calcium channels inside the cochlea), or iatrogenic. Transmission of sound and sharp tuning in the cochlea is largely dependant on ionic concentration of primarily potassium, sodium and calcium ions inside the endolymph. Inner and outer hair cells have distinct K+ channels and express calcium channels too Some kinds of non-syndromic autosomal dominant progressive hearing loss were found to be related to mutations affecting K+ channels expressed in the outer hair cells as well as some syndromic hereditary conditions (Gates, 2005). Other conditions were channelopathies are implicated, like familial ataxia and migraine, have common characteristics with Meniere’s disease Studies looking at the therapeutic effects of some calcium channel blockers in cases of clinical tinnitus (Nimodipine) (Davies et al, 1994) and other neuroprotective drugs (Shulman, 1997) are reviewed. The aim of this presentation is to explore the evidence in literature about possible correlations between the pathological processes implicated in Channelopathies, Meniere’s disease and tinnitus in the literature. New theories regarding the development of endolymphatic hydrops in tinnitus patients and its relation to the generation of hearing loss and tinnitus will also be discussed.
|Translated title of the contribution||The correlation between endolymphatic hydrops, tinnitus and medical channelopathies|
|Title of host publication||BAA annual conference, Liverpool, 2008|
|Publication status||Published - Nov 2008|