Superior semicircular canal dehiscence syndrome by the superior petrosal sinus

Koo, Ja-Won; Hong, Sung Kwang; Kim, Dong Kyu; Kim, Ji Soo

doi:10.1136/jnnp.2008.155564

Cited by 41 publications

(28 citation statements)

References 11 publications

(11 reference statements)

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“…• Increased bone conduction with increased perception of sounds produced by the body itself (somatosounds) such as bloodflow sounds, autophony, eye movement sounds, and acoustic perception of the patient's own footsteps (32,33). Treatment for semicircular canal dehiscence is surgery to cover the affected semicircular canal or obliteration of it.…”

Section: Tinnitus Arising In the Veinsmentioning

confidence: 98%

Pulsatile Tinnitus

Hofmann¹,

Behr²,

Neumann‐Haefelin³

et al. 2013

Deutsches Ärzteblatt International

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Section: Tinnitus Arising In the Veinsmentioning

confidence: 98%

Pulsatile Tinnitus

Hofmann¹,

Behr²,

Neumann‐Haefelin³

et al. 2013

Deutsches Ärzteblatt International

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“…This resulted from costimulation of the PC in addition to the SC, considering that the location of the dehiscence by the superior petrous sinus was closer to the common crus than to the superior canal ampulla in this patient. Simultaneous stimulation of the left SC and PC would generate rather pure torsional eye movements because the vertical components would cancel each other out [Koo et al, 2010]. One case with a 4.7-mm SCD (case No.…”

Section: Discussionmentioning

confidence: 99%

“…Mastoid vibration, on the other hand, using a commercially available hand-held vibrator, induced substantial horizontal VOR that were in the excitatory direction and had a smaller vertical component. In our previous case report, describing a symptomatic case of SCD with superior petrosal sinus, tone-burst stimulation to the left, affected ear evoked mainly clockwise torsional nystagmus with little vertical eye movement, while mastoid vibration induced considerable left-beating nystagmus with a counterclockwise torsional component [Koo et al, 2010]. We suggested that the cause of atypical induced VOR by tone-burst stimulation in that patient was the location of the SCD, which was closer to the common crus rather than at the top of the SC, facing the middle fossa dura.…”

Section: Introductionmentioning

confidence: 99%

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

Park¹,

Kim²,

Kim³

et al. 2014

Audiol Neurotol

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A sound- and pressure-induced vestibuloocular reflex (VOR) has been described as vertical and torsional in superior canal dehiscence (SCD), and the rotational axes of induced VOR have been assumed to fit with the axis of the affected superior semicircular canal (SC). However, it has been difficult to characterize the pattern of vibration-induced VOR (ViVOR). We aimed to characterize the pattern of ViVOR by comparing the intensity and the axis of ViVOR with several clinical parameters of SCD. Ten symptomatic SCD patients were recruited. SCD size and location were measured on a reformatted image in the plane of the SC. Unilateral vibratory stimulation (100 Hz) was applied to the mastoid surface. ViVOR were recorded using 3D videooculography. The median 3D velocity of ViVOR was measured and the 3D vector trajectory plotted for reference against the axes of the human semicircular canals. A correlation between the magnitude of ViVOR and the size of SCD was evaluated. We also compared the location of SCD with the vertical-to-torsional component ratio of the ViVOR. ViVOR were present in 7 patients; 6 patients showed a substantial horizontal component in the excitatory direction in addition to strong torsional and weak vertical components. The computed rotational axes of ViVOR were located mostly between the axes of the ipsilateral SC and horizontal canal (HC) with a variable deviation to the axis of the ipsilateral posterior canal (PC). The magnitude of ViVOR was not related to the size of the SCD. The vertical-to-torsional component ratio of ViVOR tended to decline as the dehiscence was closer to the common crus. In SCD, mastoid vibration may stimulate the affected-side HC and PC as well as the SC. SCD can be suspected when excitatory horizontal torsional ViVOR direct to the side of the auditory symptoms.

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“…SCD is located most frequently on the arcuate eminence facing the middle fossa dura and also occurs at the superior petrosal sinus [Carey et al, 2000;Koo et al, 2010]. However, the etiology of SCD still remains controversial.…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2015

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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.

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Superior semicircular canal dehiscence syndrome by the superior petrosal sinus

Cited by 41 publications

References 11 publications

Pulsatile Tinnitus

Pulsatile Tinnitus

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

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

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