Disease relevance of Endolymphatic Hydrops

• Patients were divided into five aetiologically homogeneous subgroups: (i) those with normal hearing and no identified pathology, (ii) those with sensorineural hearing loss of unknown origin, (iii) those with normal hearing, but complaining of tinnitus related to head injury, (iv) those with endolymphatic hydrops, and (v) those with noise exposure [1].
• Both temporal bones show congenitally hypoplastic endolymphatic sacs and severe endolymphatic hydrops consistent with Meniere's disease [2].
• STUDY DESIGN: Part one of the project involves the surgical induction of endolymphatic hydrops and correlation of long term hearing loss with histological parameters of ELH severity as well as cochlear nerve and eighth cranial nerve diameter measurements [3].
• Possible mechanisms to explain the somewhat paradoxical increase in the resistance to the flow of sound energy through the cochlea following reduction of the endolymphatic hydrops by glycerol dehydration are discussed [4].
• The SP/AP ratio of patients with syphilitic labyrinthitis was not significantly different from that of the patients with Meniere's disease or delayed endolymphatic hydrops, while it was significantly higher than that of the patients with sudden deafness and other types of sensorineural hearing loss [5].

High impact information on Endolymphatic Hydrops

• In cases of endolymphatic hydrops, the diuretics chlorthalidone, hydrochlorothiazide and acetazolamide have been useful [6].
• We speculate that over-expression of AQP2 may be involved in the formation of endolymphatic hydrops [7].
• In experimental endolymphatic hydrops, the expression of Cx26 significantly decreased, whereas there were no obvious changes in the expression of ZO-1 [8].
• Endolymphatic hydrops and CSF pressure [9].
• The present study investigates changes of the ES's epithelia and luminal filling after induction of an acute endolymphatic hydrops [10].

Chemical compound and disease context of Endolymphatic Hydrops

• Distortion-product otoacoustic emissions and glycerol testing in endolymphatic hydrops [11].
• Endolymphatic hydrops induced by chronic administration of vasopressin [12].
• Hearing results of intratympanic steroid treatment of endolymphatic hydrops [13].
• Endolymphatic hydrops was present in all animals from the cisplatin- and the cisplatin + ORG 2766-treated groups [14].
• Glycerol and urea have been widely used as test substances for confirmation of suspected endolymphatic hydrops [15].

Biological context of Endolymphatic Hydrops

• Our findings suggest that oxidative stress is involved in the development of endolymphatic hydrops and may lead to cellular damage which induces apoptosis by activation of cas-3 [16].
• OBJECTIVE: To investigate the localization of Ca(2+)-ATPase (Ca(2+) pump) in the cochlear and its change after endolymphatic hydrops, and to study the relationship between compound action potential (CAP) threshold and the Ca(2+)-ATPase activety [17].
• The increase in the SP (a sensitive indicator of acute endolymphatic hydrops) after perfusion with AVP suggests that this neuropeptide plays a role in the regulation of the ion and fluid balance in the cochlea [18].

Anatomical context of Endolymphatic Hydrops

• Cochleas from animals treated with a daily cisplatin dose of 2.0 mg/kg for 8 consecutive days showed an endolymphatic hydrops [19].
• Animal studies have shown presence of ADH receptors in the inner ear, and chronic vasopressin administration has been shown to induce endolymphatic hydrops [20].
• Although it was not possible to prove a stimulatory effect of nimodipine on the enzyme Na+/K(+)-ATPase cytochemically, the finding of mild endolymphatic hydrops in nimodipine treated control ears suggests (a history of) increased endolymph production [21].
• The aim of this paper was to evaluate the effect of one month of treatment with different dosages of glycerol on experimental endolymphatic hydrops produced by obliteration of endolymphatic sac and duct through an extradural approach [22].
• The change in TEOAE after glycerol administration indicates that the active motile property of outer hair cells may be affected by endolymphatic hydrops [23].

Gene context of Endolymphatic Hydrops

• Endolymphatic hydrops and central nervous system-related dizziness as cofactors with BPPV were associated with the highest recurrence rates [24].
• Endolymphatic hydrops induced by chronic administration of vasopressin [25].
• Endolymphatic hydrops associated with otosclerosis [26].
• In the present study, it was examined whether or not the chronic administration of VP might induce endolymphatic hydrops [25].
• Only 24% had the classic triad of symptoms of endolymphatic hydrops [27].

Analytical, diagnostic and therapeutic context of Endolymphatic Hydrops

• To determine the possible involvement of adenylate cyclase in the formation of endolymphatic hydrops, we measured the endolymphatic K+, Na+, Cl- activities (AK, ANa, ACl) and the endocochlear potential (EP) by means of ion-selective microelectrodes while inner ear adenylate cyclase was activated by perilymphatic perfusion with forskolin [28].
• In order to detect endolymphatic hydrops, we applied three neuro-otologic examination methods, including the furosemide VOR test, the glycerol dehydration test, and electrocochleography in 61 patients with unilateral Menière's disease, 21 patients with delayed endolymphatic hydrops, and 10 patients with syphilitic labyrinthitis [29].
• Vestibular evoked myogenic potentials and distortion-product otoacoustic emissions combined with glycerol testing in endolymphatic hydrops: their value in early diagnosis [30].
• In a previous report it was suggested that intravenous administration of furosemid followed by a comparative caloric test (the furosemid test) could be utilized for detection of endolymphatic hydrops (Kitahara et al., 1973) [31].

References