Abstract

It has been widely outlined by our group the possibility that a sufferance of the inner ear can take place as a consequence of hemodynamic imbalance which could affect young and healthy people and recognize a merely functional origin. As reported in previous papers, an altered reaction of the autonomic nervous system could actually jeopardize the labyrinthine perfusion even in absence of other damages. From this standpoint, the hypothesis that a hyperactivity of the vagal response to an acute sympathetic drive may result in an inner ear sufferance deserves to be explored. A mechanism which appears to fit to this model is represented by the Bezold-Jarisch reflex (BJR), which is considered to be responsible for vasovagal syncope and is characterized by a dynamic reasonably compatible with our findings. According to these premises, especially considering that the inner ear has a less active protective mechanism against ischemia as compared to brain, in predisposed subjects tinnitus, when considered as an initial symptom of inner ear hypoperfusion, can represent a warning able to prevent the lack of consciousness related to the syncope.