Association between sensorineural hearing loss and sleep-disordered breathing: Literature review
- Autori: Ballacchino, A.; Gargano, R.; Martines, F.
- Anno di pubblicazione: 2015
- Tipologia: Capitolo o Saggio (Capitolo o saggio)
- OA Link: http://hdl.handle.net/10447/174075
The cochlea is especially sensitive to circulatory alterations because it is supplied by a single terminal artery and lacks adequate collateral blood supply. To examine the putative association between Sensorineural Hearing Loss (SNHL) and Sleep Disordered Breathing (SDB) through the literature review is very interesting. In fact these medical disorders usually are associated to cerebral circulatory alterations resulting in hypoxia, acute hemodynamic change, and decreased cerebral blood flow, because the Sleep Disorder Breathing (SDB), for example OSAHS (Obstructive Sleep Apnea Hypopnea Syndrome), is characterized by periodic hyposia/reoxygenation. These noxious stimuli can, in turn, activate the sympathetic nervous system, depress parasympathetic activity which results in oxidative stress, endothelial dysfunction, and activation of the inflammatory cascade of different anatomical structure as inner ear. Is reasonable to assume that could cause and/or esacerbate sensorineural hearing loss with/or without tinnitus. Based on these clinical evidences some authors studied the association between SDB and a dysfunction of auditory pathway showing an improved risk of sensorineural hearing loss, a lower transient otoacoustic emissions (TEOAE) reproducibility and an impairment of auditory brainstem responses in OSAHS populatio. In fact it is known that the transduction mechanism of the inner ear and the transmission of nerve impulses along the auditory way are highly dependent upon the oxygen supply. Recent studies evidenced how through oxidative injury due to a hypoxic stress induced apoptosis in spiral ligament and in the cochlear basal turn of the Organ of Corti of obese CD/1 mouses, causes a high frequencies sensorineural hearing loss. Therefore OSAHS may lead to cerebral vascular insufficiency resulting in hypoxia, acute hemodynamic change, and decreased cerebral blood flow during episodes of apnea with consequent ischemic injury to the cochlea.