Vortical flow in the utricle and the ampulla: a computational study on the fluid dynamics of the vestibular system
ABSTRACT We present a computational study of the fluid dynamics in healthy semicircular canals (SCCs) and the utricle. The SCCs are the primary sensors for angular velocity and are located in the vestibular part of the inner ear. The SCCs are connected to the utricle that hosts the utricular macula, a sensor for linear acceleration. The transduction of angular motion is triggered by the motion of a fluid called endolymph and by the interaction of this fluid with the sensory structures of the SCC. In our computations, we observe a vortical flow in the utricle and in the ampulla (the enlarged terminal part of the SCCs) which can lead to flow velocities in the utricle that are even higher than those in the SCCs. This is a fundamentally new result which is in contrast to the common belief that the fluid velocities in the utricle are negligible from a physiological point of view. Moreover, we show that the wall shear stresses in the utricle and the ampulla are maximized at the positions of the sensory epithelia. Possible physiological and clinical implications are discussed.
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ABSTRACT: In patients with Ménière's disease (MD), caloric testing can show, depending on the stage and activity of the disease, a variety of results. Between attacks, many, or perhaps even most, patients with unilateral early or mild MD have normal caloric tests; late MD can show abnormalities ranging from mild to severe unilateral canal paresis with or without directional preponderance. The explanation of canal paresis in MD is not clear. The most obvious explanation, severe loss of lateral canal hair cells, is not likely to be correct because hair cell loss will not explain the fluctuating canal paresis to caloric stimulation. In contrast, the published evidence is that rotational testing of semicircular canal function in MD patients typically shows little reduction in function and even enhancement of vestibulo-ocular reflex gain, at least in the early stages of the disease. Here, we offer a novel explanation for this dissociation. We propose that hydropic expansion of the lateral canal membranous labyrinth permits convective recirculation within the duct that allows dissipation of the hydrostatic force that would normally cause cupular displacement and nystagmus in the caloric test. © 2015 New York Academy of Sciences.Annals of the New York Academy of Sciences 02/2015; DOI:10.1111/nyas.12687 · 4.31 Impact Factor
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ABSTRACT: In this paper, we study the Posterior Semicircular Canal of the Peripheral Vestibular system containing moving Otoconia (Calcium Carbonate crystals) which leads to the condition of Benign Paroxysmal Positional Vertigo (BPPV). Using the governing equations of the affected semicircular canal we develop a novel MEMS device to mimic the pathophysiological condition wherein the kinocilia structure is modeled using PZT-2 micro-cantilever placed at various positions in the device to sense the position of the otoconia. The deflection produces a voltage of 0.416 mV indicating the proximity of the particles. Using this information we describe a functional block of this device that aids in treating BPPV via an audio assisted Canalith Repositioning Procedure (CRP).2013 8th IEEE International Conference on Nano/Micro Engineered and Molecular Systems (NEMS); 04/2013
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ABSTRACT: In our daily life, small flows in the semicircular canals (SCCs) of the inner ear displace a sensory structure called the cupula which mediates the transduction of head angular velocities to afferent signals. We consider a dysfunction of the SCCs known as canalithiasis. Under this condition, small debris particles disturb the flow in the SCCs and can cause benign paroxysmal positional vertigo (BPPV), arguably the most common form of vertigo in humans. The diagnosis of BPPV is mainly based on the analysis of typical eye movements (positional nystagmus) following provocative head maneuvers that are known to lead to vertigo in BPPV patients. These eye movements are triggered by the vestibulo-ocular reflex, and their velocity provides an indirect measurement of the cupula displacement. An attenuation of the vertigo and the nystagmus is often observed when the provocative maneuver is repeated. This attenuation is known as BPPV fatigue. It was not quantitatively described so far, and the mechanisms causing it remain unknown. We quantify fatigue by eye velocity measurements and propose a fluid dynamic interpretation of our results based on a computational model for the fluid-particle dynamics of a SCC with canalithiasis. Our model suggests that the particles may not go back to their initial position after a first head maneuver such that a second head maneuver leads to different particle trajectories causing smaller cupula displacements.Journal of Biomechanics 03/2014; 47(8). DOI:10.1016/j.jbiomech.2014.03.019 · 2.50 Impact Factor