Delayed Endolymphatic Hydrops as a Clinical Disease Entity.

Kamei, Tamio

doi:10.2974/kmj.51.1

Cited by 26 publications

(49 citation statements)

References 22 publications

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“…Schuknecht [1] proposed to call these conditions DEH and elaborated on its etiology: a labyrinthine insult of sufficient magnitude to cause total deafness but preservation of vestibular function, and delayed atrophy or fibrous obliteration of the endolymphatic resorptive system. The concept of DEH is still controversial, but it is a clinical entity distinct from Ménière's disease [17] . Schuknecht [5] subdivided this disease entity into ipsi-and contralateral types.…”

Section: Discussionmentioning

confidence: 99%

Indication of the Side of Delayed Endolymphatic Hydrops by Vestibular Evoked Myogenic Potential and Caloric Test

Egami

Ushio

Yamasoba

et al. 2010

ORL

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Objective: Delayed endolymphatic hydrops (DEH) can be clinically classified into ipsi- and contralateral types. This study aims to investigate the relationship between the results of vestibular evoked myogenic potential (VEMP) and caloric testing and the clinical type of DEH. Methods: The data of 33 patients with DEH who underwent both VEMPs and caloric testing were retrospectively examined. The type of DEH was judged from its clinical and audiological course. Theasymmetry ratios of the VEMPs and canal paresis on the caloric test were measured. Results: The results of VEMP and the caloric testing were consistent with the type of DEH in 61 and 76% of DEH patients, respectively. Combined use of VEMP and caloric testing correctly identified the type of DEH in 82% of patients. Conclusions: The combined use of VEMP and caloric testing can indicate the type of DEH at a reasonably high rate, but inconclusively.

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Section: Discussionmentioning

confidence: 99%

Indication of the Side of Delayed Endolymphatic Hydrops by Vestibular Evoked Myogenic Potential and Caloric Test

Egami

Ushio

Yamasoba

et al. 2010

ORL

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“…This association was first described by Kamei et al [1971], and further characterized by others [Nadol et al, 1975;Wolfson and Leiberman, 1975;Schuknecht, 1978;Kamei, 2004]. The previously existing deafness is generally a profound unilateral loss, beginning in childhood, although cases following bilateral deafness have also been described [Karmody, 1982;Fina et al, 2003;Kamei, 2004]. The etiology of the initial unilateral deafness can be quite variable including bacterial and viral labyrinthitis, acoustic and head trauma, otosclerosis, sudden deafness without known cause, congenital cytomegalovirus (CMV), and migraine [Nadol et al, 1975;Wolfson and Leiberman, 1975;Schuknecht, 1978;LeLiever and Barber, 1980;Paparella and Mancini, 1983;Schuknecht and Gulya, 1983;Kemink and Graham, 1985;Lambert, 1985;Hicks and Wright, 1988;Ylikoski, 1988;Schuknecht et al, 1990;Langman and Lindeman, 1995;Huygen and Admiraal, 1996;Lee et al, 2000].…”

Section: Introductionmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 92%

“…Symptoms of contralateral DEH typically include fluctuating hearing loss, tinnitus, aural fullness, and at times episodic vertigo in the setting of long standing deafness in the opposite ear. The age of onset of symptoms is typically in later childhood and adolescence (ages 11-20) or between 40 and 60 years of age [Takeda et al, 1998;Kamei, 2004] with a latency ranging from 1 to 74 years, which appears to be shorter with acoustic trauma [Nadol et al, 1975;Lambert, 1985;Ylikoski, 1988;Schuknecht et al, 1990;Langman and Lindeman, 1995].…”

Section: Introductionmentioning

confidence: 99%

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Familial unilateral deafness and delayed endolymphatic hydrops

Dodson

Kamei

Sismanis

et al. 2007

American J of Med Genetics Pt A

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Delayed endolymphatic hydrops (DEH) is a unique disorder characterized by fluctuating otologic symptoms in the setting of preexisting unilateral deafness. The symptoms include aural fullness, fluctuating hearing, and/or episodes of vertigo similar to those observed in Meniere disease and may occur ipsilateral or contralateral to the previously deafened ear. In most reported cases, the unilateral deafness has been a profound sensorineural hearing loss with a sudden onset that has been variously attributed to bacterial or viral labyrinthitis, acoustic or cranial trauma, otosclerosis, and congenital CMV infection. Familial occurrence of the syndrome has not previously been reported in the literature. In this report, we describe two possible familial instances of delayed DEH. These patients raise the possibility that genetic factors may sometimes be the cause of this unusual syndrome.

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“…They were diagnosed with definite Meniere's disease (MD) [10] in 58 (left 32, right 26), vestibular neuritis [11] in 18 (left 10, right 8), recurrent vestibulopathy [12] in 10 (left 6, right 4), the vertigo accompanying sudden deaf [13] in 13 (left 6, right 7), vestibular involved inner ear malformation [14] in 5 (left dominant 3, right dominant 7), acoustic neuromas [15] before surgery in 2 (both right), labyrinth involved temporal bone fracture [16] in 2 (both right), delayed endolymphatic hydrops [17] in 2 (both right), idiopathic loss of inner ear function [18] in 2 (both right). The patients with spontaneous nystagmus, eardrum perforation and cervical spondylosis were excluded from the present study.…”

Section: Patients Groupmentioning

confidence: 99%

Vibration-Induced Nystagmus in Patients with Unilateral Peripheral Vestibular Disorders

Xie

Guo

Wu³

et al. 2013

Indian J Otolaryngol Head Neck Surg

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This study was done to clarify the clinical significance of vibration-induced nystagmus (VIN) and to calculate the sensitivity and the specificity of the vibration test. One hundred and twelve patients with unilateral peripheral vestibular disorders and thirty normal subjects were enrolled into this study. However, patients with spontaneous nystagmus were excluded. Vibration stimuli (approximately 100 Hz) were presented to the mastoids and the forehead. Patients and normal subjects also underwent head shaking nystagmus (HSN) test and caloric testing. Among the 112 patients, 91(81 %) showed VIN which were mainly horizontal. VIN was more frequently elicited on the mastoids than on the forehead. In the majority of patients (76 cases), the direction of VIN was toward the healthy side, whereas patients with Meniere's disease (15 cases), showed nystagmus toward the affected side. None of 30 normal subjects showed VIN. Whereas HSN was found in 70 (63 %) patients and 9 (30 %) in normal subjects. Among 112 patients, 10 showed a canal paresis (CP) value of caloric testing less than 25 %, while 32 with a CP value between 25 and 40 %, 48 with a CP value between 40 and 70 %, and 22 with a CP value no less than 70 %. It is notable that with increasing CP value on caloric testing, VIN was more likely to be elicited. So VIN test is a simple, non-invasive and well-tolerated clinical test that indicates unilateral peripheral vestibular dysfunction. VIN test had greater sensitivity and specificity than HSN test in the diagnosis of unilateral peripheral vestibular disorders.

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Delayed Endolymphatic Hydrops as a Clinical Disease Entity.

Cited by 26 publications

References 22 publications

Indication of the Side of Delayed Endolymphatic Hydrops by Vestibular Evoked Myogenic Potential and Caloric Test

Indication of the Side of Delayed Endolymphatic Hydrops by Vestibular Evoked Myogenic Potential and Caloric Test

Familial unilateral deafness and delayed endolymphatic hydrops

Vibration-Induced Nystagmus in Patients with Unilateral Peripheral Vestibular Disorders

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