A high jugular bulb and poor development of perivestibular aqueductal air cells are not the cause of endolymphatic hydrops in patients with Ménière's disease. Issue 4 (August 2018) - Oya, Ryohei
Abstract: Objective: The presence of endolymphatic hydrops in the inner ear, which can be detected with gadolinium-enhanced magnetic resonance imaging (Gd-MRI), is widely recognized as the main pathological cause of Ménière's disease (MD). However, the precise mechanisms underlying the development of endolymphatic hydrops remains unclear. One hypothesis proposes a relationship between the presence of a high jugular bulb (HJB) and MD, which disrupts the vestibular aqueduct leading to the development of endolymphatic hydrops. This study sought to identify anatomical features in MD patients using computed tomography (CT) images of the temporal bone. Methods: Fifty-nine MD patients meeting the AAO-HNS diagnostic criteria and exhibiting endolymphatic hydrops in Gd-MRI were enrolled between July 2009 and December 2015. We only included MD patients who showed unilateral endolymphatic hydrops in Gd-MRI. Sixty-six patients with otosclerosis or facial palsy were also enrolled as control participants. In both groups, patients with other pathologies (e.g., chronic otitis media or cholesteatoma) and patients <16 years old were excluded. HJB was defined as a JB that was observable in the axial CT image at the level where the round window could be visualized. JB surface area was measured on the axial image at the level where the foramen spinosum could be visualized. Finally, to investigate the relationship between the pneumatization of perivestibular aqueductal air cells and the existence of endolymphatic hydrops, the development of the air cells was rated using a three-grade evaluation system and the distance between the posterior semicircular canal (PSCC) and the posterior fossa dura was measured. Results: The presence of HJB was observed in 22 of 59 affected sides of MD patients and in 17 healthy sides. The likelihood that HJB was detected on an affected side (22/39) was not significantly above chance (50%). The HJB detection rate did not significantly differ between the three groups (MD affected side, MD healthy side, and control patients). Furthermore, there were no significant group differences in JB surface area, distance between the PSCC and posterior fossa dura, or the development of perivestibular aqueductal air cells. Conclusion: We did not find any relationship between the anatomy of the temporal bones and the existence of endolymphatic hydrops. Moreover, we found no evidence suggesting that HJB or poor development of perivestibular aqueductal air cells were the cause of endolymphatic hydrops in MD patients.