Meniere’s attack – a volume or pressure phenomenon?

Meniere’s disease (MD) still raises since its discovery in 1860 pathophysiological and etiopathogenical issues. The main pathophysiological feature that has emerged for decades is an anatomic one, the endolymphatic hydrops (EH), defined by the inflation of the endolymphatic part of the membranous labyrinth. However, the causal relationship between EH and MD has not been proven. Several attempts have been achieved in animals to induce EH. The best known is the blockage of the vestibular duct, which causes a chronic volume inflation of the endolymphatic part. This model is characterized by the discrepancy between electrophysiological findings and scala media inflation. Pressure measurements vary among studies. The endolymphatic infusion model, which attempts to model the acute clinical picture of MD consistently shows pressure equilibration between the endolymphatic and perilymphatic compartments, and rapid recovery of the electrophysiological finding once the injection is stopped.

Delayed Hearing Loss after Surgery for Acoustic Neurinomas: Clinical and Electrophysiological Observations

In a series of 26 patients with medium-sized and large acoustic neurinomas and documented hearing before surgery, 7 patients had preservation of hearing initially after the procedure but then developed delayed hearing loss. The most prominent intraoperative electrophysiological finding in these cases was a gradual deterioration of brain stem auditory evoked potentials (BAEP);, especially of Wave V. Four additional patients with a similar gradual intraoperative loss of BAEP and severe postoperative hearing deterioration received vasoactive treatment after surgery (low-molecular weight dextran);. In all 4 patients, including 1 patient with documented total deafness after surgery, hearing was preserved. Initial preservation of cochlear nerve function after the removal of an acoustic neurinoma does not guarantee postoperative hearing. Intraoperative BAEP help to identify patients at risk for delayed postoperative hearing loss. The pathophysiological mechanism can be attributed to disturbances of the microcirculation in endoneurial vasa nervorum caused by the mechanical manipulation of the cochlear nerve.