Fluctuating hearing loss in contralateral delayed endolymphatic hydrops.

Delayed endolymphatic hydrops is a disease entity that can be differentiated from Meniere's disease. Typically it occurs in patients who have sustained a profound hearing loss in one ear, usually from infection or trauma, and then after a prolonged period of time develop either episodic vertigo from the same ear (ipsilateral delayed endolymphatic hydrops) or fluctuating hearing loss, also sometimes with episodic vertigo, in the opposite ear (contralateral delayed endolymphatic hydrops). The ipsilateral form of the disease may be treated by labyrinthectomy but no satisfactory therapy is available for the contralateral form of the disease.

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Delayed Endolymphatic Hydrops: Episodic Vertigo of Delayed Onset after Profound Inner Ear Hearing Loss

Hearing Impairment ◽

10.1007/978-4-431-68397-1_49 ◽

2004 ◽

pp. 256-262

Author(s):

Tamio Kamei ◽

Kenji Watanabe

Keyword(s):

Hearing Loss ◽

Inner Ear ◽

Endolymphatic Hydrops ◽

Delayed Onset ◽

Episodic Vertigo ◽

Delayed Endolymphatic Hydrops

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A Case of Bilateral Profound Hearing loss Caused by Idiopathic Labyrinthitis that Showed a Clinical Course Similar to that of Delayed Endolymphatic Hydrops

Equilibrium Research ◽

10.3757/jser.78.61 ◽

2019 ◽

Vol 78 (2) ◽

pp. 61-68

Author(s):

Keita Tsukada ◽

Hideaki Moteki ◽

Rika Yasukawa ◽

Shin-ichi Usami

Keyword(s):

Hearing Loss ◽

Clinical Course ◽

Endolymphatic Hydrops ◽

Profound Hearing Loss ◽

Delayed Endolymphatic Hydrops

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Delayed Endolymphatic Hydrops: A Case Study

Journal of the American Academy of Audiology ◽

10.3766/jaaa.19.3.3 ◽

2008 ◽

Vol 19 (03) ◽

pp. 204-209 ◽

Cited By ~ 2

Author(s):

Rachel Lazaro ◽

Larry Lundy ◽

David Zapala

Keyword(s):

Hearing Loss ◽

Sensorineural Hearing Loss ◽

Endolymphatic Hydrops ◽

Sensorineural Hearing ◽

Ménière’S Disease ◽

Episodic Vertigo ◽

Delayed Endolymphatic Hydrops ◽

Patient’S History ◽

Estudio De Caso

Delayed endolymphatic hydrops (DEH) is an unusual variation of Ménière's disease characterized by episodic vertigo that develops some time after the onset of a profound, typically unilateral sensorineural hearing loss. This case study describes a 48-year-old male who presented with complaints of episodic vertigo and disequilibrium 15 years following the onset of unilateral sensorineural hearing loss. The patient's history, audiologic findings, and vestibular evaluation led to the diagnosis of DEH. The case highlights the diagnostic and treatment challenges associated with this condition and focuses attention on principles that guide the audiologist in collecting evidence that aids in solving these challenges. El hidrops endolinfático retardado (DEH) es una variante inusual de la Enfermedad de Ménière, caracterizada por vértigo episódico que se desarrolla en el tiempo luego del inicio de una hipoacusia sensorineural unilateral típica. Este estudio de caso describe una varón de 48 años que presentó quejas de vértigo episódico y desequilibrio, 15 años después del inicio de una hipoacusia sensorineural unilateral. La historia del paciente, los hallazgos audiológicos y la evaluación vestibular llevaron al diagnóstico de DEH. El caso destaca los retos diagnósticos y terapéuticos asociados con esta condición y concentra su atención en los principios que guían al audiólogo en la recolección de evidencia que ayude a resolver estos retos.

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Quantitative Study of Scarpa's Ganglion and Vestibular Sense Organs in Endolymphatic Hydrops

Annals of Otology Rhinology & Laryngology ◽

10.1177/000348948109000205 ◽

1981 ◽

Vol 90 (2) ◽

pp. 121-125 ◽

Cited By ~ 7

Author(s):

Ernst Richter

Keyword(s):

Hearing Loss ◽

Ganglion Cell ◽

Endolymphatic Hydrops ◽

Sense Organs ◽

Episodic Vertigo ◽

Cell Counts ◽

Scarpa's Ganglion ◽

Caloric Response ◽

Temporal Bones ◽

Fluctuating Hearing Loss

The density of vestibular hair cells and the number of neurons in Scarpa's ganglion were estimated for 11 temporal bones with endolymphatic hydrops. The ten subjects from which these bones were taken all exhibited decreased caloric response (when tested), fluctuating hearing loss, and episodic vertigo. The degeneration of vestibular sense organs was found within the “normal” range for all except one case, which showed total degeneration of the posterior crista ampullaris. Ganglion cell counts in all cases were low. In three of the ten subjects, counts fell below the lowest values seen in a sample of “normal” ears. These three subjects exhibited fluctuating hearing loss and episodic vertigo for more than six years prior to death. In cases of unilateral endolymphatic hydrops there was no significant difference between counts in the affected and unaffected ear. Thus, the apparent ganglion cell degeneration may be due to ear disease other than endolymphatic hydrops.

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Recovery of Otoacoustic Emission Function in Luetic Endolymphatic Hydrops: A Possible Measure of Improvement in Cochlear Function

International Journal of Otolaryngology ◽

10.1155/2009/942096 ◽

2009 ◽

Vol 2009 ◽

pp. 1-3 ◽

Cited By ~ 4

Author(s):

Robert H. Chun ◽

Jayant M. Pinto ◽

Rebecca Blankenhorn ◽

Vijay S. Dayal

Keyword(s):

Hearing Loss ◽

Otoacoustic Emissions ◽

Endolymphatic Hydrops ◽

Treponema Pallidum ◽

Low Frequency ◽

Otoacoustic Emission ◽

Speech Discrimination ◽

Cochlear Function ◽

Fluctuating Hearing Loss ◽

Emission Function

Syphilis is a preventable and curable multi-organ disease caused byTreponema pallidumthat may also affect the inner ear. First reported in 1887 by Adam Politzer, luetic endolymphatic hydrops (LEH) is a treatable complication of syphilis which causes a potentially reversible sensorineural hearing loss. Symptoms of LEH include fluctuating hearing loss (often low frequency), tinnitus, and vertigo. Though audiometric parameters have been examined in patients with otosyphilis, few studies have examined the use of otoacoustic emissions (OAEs) as a tool to measure improvement in cochlear function. Here we report an improvement in hearing loss, speech discrimination, and OAEs following treatment of LEH.

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Long-term efficacy of triple semicircular canal plugging in the treatment of patients with ipsilateral delayed endolymphatic hydrops

Scientific Reports ◽

10.1038/s41598-021-82683-6 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Daogong Zhang ◽

Yafeng Lv ◽

Xiaofei Li ◽

Yawei Li ◽

Yongdong Song ◽

...

Keyword(s):

Hearing Loss ◽

Semicircular Canal ◽

Endolymphatic Hydrops ◽

Complete Control ◽

Term Efficacy ◽

Delayed Endolymphatic Hydrops ◽

Intratympanic Gentamicin ◽

Substantial Control

AbstractThis study aims to explore the long-term efficacy of triple semicircular canal plugging (TSCP) in the treatment of intractable ipsilateral delayed endolymphatic hydrops (DEH), so as to provide an alternative therapy for this disease. Forty-eight patients diagnosed with ipsilateral DEH referred to vertigo clinic of our hospital between Dec. 2010 and Dec. 2017, were included in this study for retrospective analysis. All patients were followed up for 2 years. Vertigo control and auditory functions were measured and analyzed. Pure tone audiometry, caloric test, and vestibular evoked myogenic potential (VEMP) were performed in two-year follow-up. Forty-five patients who accepted intratympanic gentamicin (26.7 mg/mL) twice given one week apart were selected as a control group. The total control rate of vertigo in TSCP group was 97.9% (47/48) in the two-year follow-up, with complete control rate of 83.3% (40/48) and substantial control rate of 14.6% (7/48). The rate of hearing loss was 22.9% (11/48). The total control rate of vertigo in intratympanic gentamicin group was 80.0% (36/45), with complete control rate of 57.8% (26/45) and substantial control rate of 22.2% (10/45), and the rate of hearing loss was 20.0% (9/45). The vertigo control rate of TSCP was significantly higher than that of intratympanic gentamicin (χ2 = 6.01, p < 0.05). There was no significant difference of hearing loss rate between two groups. (χ2 = 0.12, p > 0.05). TSCP, which can reduce vertiginous symptoms in patients with intractable ipsilateral DEH, represents an effective therapy for this disorder.

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