Apical Lesions of the Cochlea in Idiopathic Endolymphatic Hydrops and other Disorders: Pathophysiological Implications

Schuknecht, Harold F.; Richter, E.

doi:10.1159/000275478

Cited by 20 publications

(8 citation statements)

References 17 publications

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“…low-frequency hearing loss), primarily manifest in the cochlear apex. These pathological abnormalities were attributed to chronic alterations in the local fluid environment of the cochlear apex [ 82 ]. Ménière's disease-specific abnormalities in the cochlear apex that explain these morphological and functional impairments have not yet been described at the molecular level.…”

Section: Discussionmentioning

confidence: 99%

Water permeability of the mammalian cochlea: functional features of an aquaporin-facilitated water shunt at the perilymph–endolymph barrier

Eckhard

Müller

Salt

et al. 2014

Pflugers Arch - Eur J Physiol

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The cochlear duct epithelium (CDE) constitutes a tight barrier that effectively separates the inner ear fluids, endolymph and perilymph, thereby maintaining distinct ionic and osmotic gradients that are essential for auditory function. However, in vivo experiments have demonstrated that the CDE allows for rapid water exchange between fluid compartments. The molecular mechanism governing water permeation across the CDE remains elusive. We computationally determined the diffusional (PD) and osmotic (Pf) water permeability coefficients for the mammalian CDE based on in silico simulations of cochlear water dynamics integrating previously derived in vivo experimental data on fluid flow with expression sites of molecular water channels (aquaporins, AQPs). The PD of the entire CDE (PD = 8.18 × 10−5 cm s−1) and its individual partitions including Reissner's membrane (PD = 12.06 × 10−5 cm s−1) and the organ of Corti (PD = 10.2 × 10−5 cm s−1) were similar to other epithelia with AQP-facilitated water permeation. The Pf of the CDE (Pf = 6.15 × 10−4 cm s−1) was also in the range of other epithelia while an exceptionally high Pf was determined for an epithelial subdomain of outer sulcus cells in the cochlear apex co-expressing AQP4 and AQP5 (OSCs; Pf = 156.90 × 10−3 cm s−1). The Pf/PD ratios of the CDE (Pf/PD = 7.52) and OSCs (Pf/PD = 242.02) indicate an aqueous pore-facilitated water exchange and reveal a high-transfer region or “water shunt” in the cochlear apex. This “water shunt” explains experimentally determined phenomena of endolymphatic longitudinal flow towards the cochlear apex. The water permeability coefficients of the CDE emphasise the physiological and pathophysiological relevance of water dynamics in the cochlea in particular for endolymphatic hydrops and Ménière's disease.

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Section: Discussionmentioning

confidence: 99%

Water permeability of the mammalian cochlea: functional features of an aquaporin-facilitated water shunt at the perilymph–endolymph barrier

Eckhard

Müller

Salt

et al. 2014

Pflugers Arch - Eur J Physiol

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“…Hyperosmolar fluid reflux theory: A somewhat similar theory to the electrolyte imbalance theory, Schucknecht77 along with Levenson17 and Okamoto74 theorize that the endolymphatic sac fluid, which is known to contain hyperosmolar fluid, can reflux more easily through the enlarged endolymphatic sac and duct and enter the inner ear resulting in damage to the inner ear structures. Arguing against this theory is an MRI study that found endolymphatic sac volume and intensity vary dynamically and independently of hearing in cases of enlarged vestibular aqueduct.…”

Section: Discussionmentioning

confidence: 99%

Enlarged vestibular aqueduct: Review of controversial aspects

et al. 2011

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“…Repeated toxic insults could account for fluctuations in threshold and word discrimination, eventually producing ganglion cell loss in the apical tum. 64 Continued viral release may eventually extend down the scala tympani to affect more basal segments of the SG, producing an even threshold elevation for all frequencies in advanced MD.…”

Section: Discussionmentioning

confidence: 99%

The Three Faces of Vestibular Ganglionitis

Gacek

2002

Ann Otol Rhinol Laryngol

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We present temporal bone and clinical evidence that common syndromes of recurrent vertigo are caused by a viral infection of the vestibular ganglion. In the present series, histopathologic and radiologic changes in the vestibular ganglion and meatal ganglion were consistent with a viral inflammation of ganglion cells in cases of Meniere's disease, benign paroxysmal positional vertigo, and vestibular neuronitis. Clinical observations of multiple neuropathies involving cranial nerves V, VII, and VIII on the same side in patients with recurrent vertigo are best explained by a cranial polyganglionitis caused by a neurotrophic virus, which is reactivated by a stressful event later in life. The reactivation of the latent virus may manifest as one of the above vertigo syndromes, depending on the part of the vestibular ganglion that is inflamed, the type and strain of the virus, and host resistance.

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Apical Lesions of the Cochlea in Idiopathic Endolymphatic Hydrops and other Disorders: Pathophysiological Implications

Cited by 20 publications

References 17 publications

Water permeability of the mammalian cochlea: functional features of an aquaporin-facilitated water shunt at the perilymph–endolymph barrier

Water permeability of the mammalian cochlea: functional features of an aquaporin-facilitated water shunt at the perilymph–endolymph barrier

Enlarged vestibular aqueduct: Review of controversial aspects

The Three Faces of Vestibular Ganglionitis

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