RESUMO
A consolidated therapy for "idiopathic" acute disorders of the inner ear, including Meniere's Disease (MD), does not exist despite the long-lasting and widespread attempts: this lack is strictly linked to pathogenic uncertainties. According to the theoretical model that our group developed and tested over the years, a possible cause of labyrinthine damage could be identified in systemic hemodynamic changes followed by an abnormal peripheral vasoconstriction: the latter could be responsible for a more or less prolonged ischemia able to threaten a highly energy-requiring and complicated organ as the inner ear. A possible way to treat MD attacks - as well as other inner ear disorders that possibly share the same origin - according to our model should be addressed to modulate the peripheral circulation and to maintain the balance of ion exchange, acting both on systemic hemodynamics and on cell and organelle membranes. Despite the absence of such a proposal in the English literature, a reliable solution could derive from the supplementation of the intake of a nutritional principle as Omega-3 (omega-3) polyunsaturated fatty acids (PUFAs) that seem to theoretically fulfil all the requirements necessary to achieve a homeostasis of the inner ear.
Assuntos
Ácidos Graxos Ômega-3/uso terapêutico , Doenças do Labirinto/tratamento farmacológico , Doença de Meniere/tratamento farmacológico , Hemodinâmica/efeitos dos fármacos , Homeostase , Humanos , Doenças do Labirinto/etiologia , Doenças do Labirinto/fisiopatologia , Doença de Meniere/etiologia , Doença de Meniere/fisiopatologia , Modelos BiológicosRESUMO
Increasingly more detailed imaging techniques have recently highlighted the frequent occurrence of bony labyrinthine dehiscence. Among them, superior canal dehiscence (SCD) has been described in a number of cases presenting different features. Here, we report a series of 13 cases, in which the detection of vestibular evoked myogenic potentials (VEMPs) in response to stimuli of abnormally low intensity as compared to normal responses led us to suspect the presence of a 'third window effect'. An accurate HRCT investigation allowed the diagnosis of SCD. Anamnestic and symptomatologic differences seem difficult to explain, although in our opinion a dural rupture could be at the basis of the onset of pathologic manifestations after many years of silence of a probably malformative condition.