Costimulation of the Horizontal Semicircular Canal during Skull Vibrations in Superior Canal Dehiscence Syndrome

Park, Joo Hyun; Kim, Hyo Jung; Kim, Ji-Soo; Koo, Ja-Won

doi:10.1159/000358002

Cited by 17 publications

(19 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This result is consistent with the BC facilitation inherent in this third window pathology (65–69). These results correspond to the acoumetry (Weber test) and the side of the conductive hearing loss as described by our group (7) and confirmed by Park et al (25). …”

Section: Svin In Various Patient Conditionssupporting

confidence: 92%

“…This is opposite to the usual direction after UVL in which the unaffected ear shows the greater response. The observation of a SVIN horizontal component beating toward the lesion side is probably correlated with the concomitant stimulation of the ipsilateral horizontal SCC and/or utricle (25, 35) (Figure 6). The vertical most often up-beating SVIN suggests a more global stimulation than the sole anterior SCC (7).…”

Section: Svin In Various Patient Conditionsmentioning

confidence: 92%

“…Vibration-induced nystagmus has been described in various inner ear diseases (Table 1); most publications address cranial BCV stimulations (2–7, 9–25, 27–29, 41–43, 45) but others deal with cervical and cranial vibrations (26, 30, 31) and a few with cervical stimulations only (32–34, 40, 44). This review is only mainly restricted to BCV with cranium stimulations which are now more clearly documented by physiology (35–39).…”

Section: Introduction—historical Backgroundmentioning

confidence: 99%

See 2 more Smart Citations

The Skull Vibration-Induced Nystagmus Test of Vestibular Function—A Review

et al. 2017

View full text Add to dashboard Cite

A 100-Hz bone-conducted vibration applied to either mastoid induces instantaneously a predominantly horizontal nystagmus, with quick phases beating away from the affected side in patients with a unilateral vestibular loss (UVL). The same stimulus in healthy asymptomatic subjects has little or no effect. This is skull vibration-induced nystagmus (SVIN), and it is a useful, simple, non-invasive, robust indicator of asymmetry of vestibular function and the side of the vestibular loss. The nystagmus is precisely stimulus-locked: it starts with stimulation onset and stops at stimulation offset, with no post-stimulation reversal. It is sustained during long stimulus durations; it is reproducible; it beats in the same direction irrespective of which mastoid is stimulated; it shows little or no habituation; and it is permanent—even well-compensated UVL patients show SVIN. A SVIN is observed under Frenzel goggles or videonystagmoscopy and recorded under videonystagmography in absence of visual-fixation and strong sedative drugs. Stimulus frequency, location, and intensity modify the results, and a large variability in skull morphology between people can modify the stimulus. SVIN to 100 Hz mastoid stimulation is a robust response. We describe the optimum method of stimulation on the basis of the literature data and testing more than 18,500 patients. Recent neural evidence clarifies which vestibular receptors are stimulated, how they cause the nystagmus, and why the same vibration in patients with semicircular canal dehiscence (SCD) causes a nystagmus beating toward the affected ear. This review focuses not only on the optimal parameters of the stimulus and response of UVL and SCD patients but also shows how other vestibular dysfunctions affect SVIN. We conclude that the presence of SVIN is a useful indicator of the asymmetry of vestibular function between the two ears, but in order to identify which is the affected ear, other information and careful clinical judgment are needed.

show abstract

Section: Svin In Various Patient Conditionssupporting

confidence: 92%

Section: Svin In Various Patient Conditionsmentioning

confidence: 92%

Section: Introduction—historical Backgroundmentioning

confidence: 99%

See 1 more Smart Citation

The Skull Vibration-Induced Nystagmus Test of Vestibular Function—A Review

et al. 2017

View full text Add to dashboard Cite

show abstract

“…Patients with SCD syndrome present with auditory and vestibular symptoms, including autophony, hyperacusis, oscillopsia and vertigo induced by loud sounds or pressure [Aw et al, 2006;Brantberg et al, 2006;Minor et al, 1998]. Not only the radiological demonstration of the bony dehiscence but also the functional demonstration of cochleovestibular hyperresponsiveness is important in the diagnosis of SCD [Cloutier et al, 2008;Crane et al, 2008;Hirvonen et al, 2003;Park et al, 2014].…”

Section: Introductionmentioning

confidence: 99%

Thickness of the Bony Otic Capsule: Etiopathogenetic Perspectives on Superior Canal Dehiscence Syndrome

et al. 2015

Self Cite

View full text Add to dashboard Cite

The etiology of superior canal dehiscence (SCD) is controversial. An embryological perspective suggests that SCD may occur through the failure of postnatal bone formation over the superior semicircular canal (SC), whereas an acquired theory suggests that trauma or pressure from the overlying temporal lobe could break or gradually thin the SC. We infer the etiology of SCD by comparing the thickness of the bony otic capsule of the unaffected side of SCD patients with that of non-SCD participants. Twelve SCD patients (13 SCD ears and 11 normal ears) and 34 age-matched controls (68 ears) were included. The control group was subdivided into an aerated group (49 ears) and a nonaerated group (19 ears), as defined by the presence of air cells above the SC. A high-resolution temporal bone CT was performed in all participants. The thicknesses of the SC, horizontal canal (HC) and posterior canal (PC) of the unaffected ears of SCD patients were compared with those of the controls. The SC of the unaffected side in the SCD group (n = 11, 0.41 ± 0.23 mm) was significantly thinner than the one in the control group (n = 68, 0.64 ± 0.21 mm, p = 0.002). The HC and PC were also thinner in the SCD group (n = 24, 0.58 ± 0.11 and 1.39 ± 0.31 mm, respectively) than in the controls (0.70 ± 0.08 and 1.61 ± 0.32 mm; p < 0.0001 and p = 0.005, respectively). The SC, HC and PC thicknesses were also compared between the aerated and nonaerated ears within the control group. The SC was significantly thicker in the aerated group (0.73 ± 0.14 mm) than in the nonaerated group (0.60 ± 0.23 mm; p = 0.046); however, no significant difference was observed for the HC and PC thickness (aerated group, n = 49, 0.72 ± 0.07 and 1.67 ± 0.34 mm; nonaerated group, n = 19, 0.70 ± 0.09 and 1.59 ± 0.34 mm; p = 0.350 and p = 0.428, respectively). The bony otic capsule was significantly thinner in the SCD patients than in the controls. However, even within unaffected individuals, SCs lacking overlying air cells were also thinner than those with overlying air cells. These results suggest that both embryological and acquired factors affect the occurrence of SCD.

show abstract

“…SCD may be suspected in patients presenting with typical symptoms and signs and can be confirmed by visible dehiscence on high resolution temporal bone computed tomography (HR-TBCT). It is important to demonstrate not only anatomical SCD by HR-TBCT, but also to obtain physiologic confirmation of cochleovestibular hyper-responsiveness using certain laboratory tests, because of the possibilities of asymptomatic radiographically apparent dehiscences or false positive radiologic findings (Carey et al, 2007;Park et al, 2014).…”

Section: Introductionmentioning

confidence: 99%