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Anatomy and Physiology of Balance
Published in R James A England, Eamon Shamil, Rajeev Mathew, Manohar Bance, Pavol Surda, Jemy Jose, Omar Hilmi, Adam J Donne, Scott-Brown's Essential Otorhinolaryngology, 2022
Nishchay Mehta, Andrew Forge, Jonathan Gale
The endolymphatic duct is formed from smaller ducts leading off the medial surfaces of the utricle and saccule and travels in the vestibular aqueduct. It courses behind the arcs of the posterior semicircular canal and narrows at its isthmus before it leads to the endolymphatic sac, which is a highly complex structure of interconnecting tubules, cisterns, and crypts. The distal, extraosseous portion of the sac rests on the posterior wall of the petrous bone, between layers of dura.
Ear, Nose, and Paranasal Sinus
Published in Swati Goyal, Neuroradiology, 2020
The external auditory canal (EAC), with lateral one-third cartilaginous and medial two-thirds bony composition, extends from the auricle to the tympanic membrane. The middle ear cavity is within the petrous portion of the temporal bone and consists of the tympanic cavity (containing the ossicles, namely the malleus, incus, and stapes) and the antrum. The mastoid antrum communicates with the epitympanum via aditus ad antrum. The middle ear also contains muscles (tensor tympani and stapedius), the round and oval windows, and the chorda tympani nerve. The inner ear consists of the osseous labyrinth (cochlea, vestibule, and the three semicircular canals, namely the superior, posterior, and lateral canals) and the membranous labyrinth (the cochlear duct, utricle, saccule, semicircular ducts, endolymphatic duct, and endolymphatic sac). The membranous labyrinth contains endolymph, surrounded by perilymph, and is enclosed within the bony labyrinth. The internal auditory canal (IAC) is located in the petrous bone and transmits facial and vestibulocochlear nerves along with the labyrinthine artery. The pars flaccida is the upper delicate part that is associated with Eustachian tube dysfunction and cholesteatoma. The pars tensa is larger and more robust, and associated with perforations.
Nonconventional Clinical Applications of Otoacoustic Emissions: From Middle Ear Transfer to Cochlear Homeostasis to Access to Cerebrospinal Fluid Pressure
Published in Stavros Hatzopoulos, Andrea Ciorba, Mark Krumm, Advances in Audiology and Hearing Science, 2020
Blandine Lourenço, Fabrice Giraudet, Thierry Mom, Paul Avan
The first issue is that ICP monitoring through the ear rests on the hypothetical presence of connections between intralabyrinthine fluids and CSF. Several anatomical pathways have been identified that possibly transmit pressure between these two spaces: The cochlear aqueduct, the endolymphatic duct and sac, and the venous system (Fig. 8.2). The cochlear aqueduct seems to provide a straightforward pressure communication with the cochlea; however, its very small diameter and the fact that normally when the cochlea is opened during surgery no gusher is observed suggest that a normal cochlear aqueduct is not patent to CSF flow. Anatomical data suggesting that the cochlear aqueduct gets gradually blocked with increasing age (Wlodyka, 1978) have been later challenged (Gopen et al., 1997). It has been shown that normal variations in ICP such as those induced by heartbeats and breathing are filtered by the pathways connecting CSF and cochlea in humans (Traboulsi and Avan, 2007), such that transmission of pressure waves from the skull to labyrinth undergoes a delay of the order of 10 seconds. Anyway, all that the in-ear monitoring of ICP requires is that there exist canal(s) between CSF and endocochlear fluid spaces that are patent to hydrostatic pressure even if they are not patent to fluid flow.
Magnetic resonance imaging of the endolymphatic space in patients with benign paroxysmal positional vertigo: volume ratio and distribution rate of the endolymphatic space
Published in Acta Oto-Laryngologica, 2022
Hiroshi Inui, Tsuyoshi Sakamoto, Taeko Ito, Tadashi Kitahara
In 1938, Hallpike and Cairns [12] reported that endolymphatic fluid is produced in the cochlea and absorbed in the endolymphatic duct by longitudinal flow. Schuknecht frequently observed ruptures of Reissner’s membrane, and the rupture and potassium intoxication theory has been the predominant theory of Meniere’s vertigo attacks since the 1960s [13]. On the contrary, Brown et al. [14] rejected this theory and considered the alternative theory of raised endolymphatic pressure. Some researchers have described that the relationship between BPPV and the ELH. They observed otoconial debris floats freely within the endolymphatic fluid in patients with BPPV and they concluded that endolymphatic debris may cause either or both positional vertigo and hydrops [6,15]. In the present study, we reported significant differences in the TFS volume of the cochlea, vestibule, and SCCs and in the ELS volume of the SCCs between the CS and BPPV groups. We previously found age-related difference in the TFS volume in the inner ear, sex-related difference in the TFS volume in the cochlea, and left-right-related difference in the TFS volume in the vestibule in healthy controls [16]. Therefore, we analysed the ELS/TFS volume ratios (%). The differences in the ELS/TFS volume ratio between the BPPV and CS groups were not significant. Extended ELS did not exist in patients with BPPV.
Magnetic resonance imaging of endolymphatic hydrops in patients with unilateral Meniere’s disease: volume ratio and distribution rate of the endolymphatic space
Published in Acta Oto-Laryngologica, 2021
Hiroshi Inui, Tsuyoshi Sakamoto, Taeko Ito, Tadashi Kitahara
The ELS exists in the cochlear duct, reuniens, sacculus, utriculus, saccular and utricular duct, ampulla of three SCCs, endolymphatic duct, and endolymphatic sac [11]. The endolymph is presumed to be produced in the apex of the cochlea and is absorbed in the endolymphatic sac [12]. Several factors have been proposed to lead to the development of ELH, including the loss of sensory or neural structures within the inner ear, such as hair cells, neuronal cells, stria vascularis, and dark cells [13]. Nonetheless, ELH is the result of blockage of longitudinal flow of the endolymphatic fluid and/or the malabsorption of endolymph from the cochlea to the endolymphatic sac [14] as well as obstruction of the utriculo-endolymphatic valve and ductus reuniens. When ELH is observed in the inner ear of patients with uMD, the total endolymph increased owing to the dysfunction in the sensory system for hydrostatic pressure, which may have been further obstructed in the endolymphatic duct or sac. The pathophysiological considerations for endolymphatic flow include the longitudinal and radial flow theories. Radial flow may play a more important role in early (compensated) MD, while longitudinal flow may dominate in late (decompensated) MD [15]; However, MD, a chronic disease, has been known to occur months or years after the initiation of the factors; in the present study, the mean duration from first onset of MD to MRI examination was 75.0 months.
Significance of high signal intensity in the endolymphatic duct on magnetic resonance imaging in ears with otological disorders
Published in Acta Oto-Laryngologica, 2020
Kyoko Morimoto, Tadao Yoshida, Masumi Kobayashi, Satofumi Sugimoto, Naoki Nishio, Masaaki Teranishi, Shinji Naganawa, Michihiko Sone
The endolymphatic duct (ED) is an insensitive component of the closed membranous labyrinth that drains endolymph. The utricular and saccular ducts join within the vestibule to form the ED, which drains into the endolymphatic sac (ES) and vestibular aqueduct (VA), passes through the distal VA and the external aperture of the aqueduct, and terminates in the epidural space of the posterior cranial fossa [1]. The ED is a short (2 mm) single-lumen tubule [2] that is part of a much larger and more complex structure of connecting tubules, cisterns, and crypts. Although the ED and ES contain small amounts of endolymph, the stomas of the ED and ES are more voluminous than are their endolymph-filled lumens [2]. According to longitudinal flow theory, endolymph produced by the stria vascularis flows through the ED to the ES, where it is absorbed by epithelial cells [3]. The flow is characterized as low, to the degree that solute movement is by diffusion and volume flow. A microchemistry study in humans reported a high protein concentration (1000–3000 mg/dL, 10–30 g/L) in the ES, and greater hyperosmolarity of fluid in the ES than in the remainder of the membranous labyrinth [4]. In healthy subjects and in patients with Meniere’s disease (MD), the ED and ES are small structures that are not usually visible on thin-slice MRI [5].