Effect of Semicircular Canal Dehiscence on Contralateral Canal Bone Thickness

Gracia-Tello, Borja; Cisneros, Ana; Crovetto, Rafael; Martínez, Claudio; Rodríguez, Olivia; Lecumberri, Iñigo; Crovetto, Miguel Ángel

doi:10.1016/j.otoeng.2013.04.004

Cited by 11 publications

(17 citation statements)

References 15 publications

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“…These results are consistent with previous studies on cadavers [Carey et al, 2000] and with TBCT-based studies [Gracia-Tello et al, 2013;Hirvonen et al, 2003] and provide further evidence that thinning occurs bilaterally, regardless of whether SCD is congenital or acquired. The HC and PC thickness was also significantly thinner in the SCD patients than in the healthy controls, which leads us to infer that the thinning of the otic capsular bone in SCD patients is congenital.…”

Section: Discussionsupporting

confidence: 92%

“…The HC and PC thickness was also significantly thinner in the SCD patients than in the healthy controls, which leads us to infer that the thinning of the otic capsular bone in SCD patients is congenital. A recent study [Gracia-Tello et al, 2013] that analyzed the thickness of the SC and PC in SCD patients demonstrated that the contralateral SC of the patients was also significantly thinner than that of the controls, but the mean thickness of the PC of the patients was not different from that of the controls. They measured the distance between the PC and the posterior fossa in the axial sections of the CT scan and concluded that the thickness of the PC was not different in the SCD patients.…”

Section: Discussionmentioning

confidence: 87%

“…2 c). We did not consider the distance from the PC to the posterior fossa in the axial sections as the thickness of the PC [Gracia-Tello et al, 2013] since the thickness of the PC is quite variable depending on the status of the aeration between the PC and the posterior fossa, and we wanted to see if the actual otic capsule thickness of the PC is different in SCD ( fig. 3 ).…”

Section: Measurement Of Sc Hc and Pc Thicknessmentioning

confidence: 99%

“…There have been a few studies to explore the etiopathogenic cause of SCD through temporal bone CT (TBCT) analysis [Gracia-Tello et al, 2013;Hirvonen et al, 2003]. Hirvonen et al [2003] evaluated the thickness of bone overlying the SC and reported that SCD patients had a thinner bony thickness on the intact side than that noted in the controls, and the thickness of the bone overlying the SC on one side correlated with that on the other side in the controls.…”

Section: Introductionmentioning

confidence: 99%

“…They suggest that a developmental anomaly affecting the formation of the bone overlying the SC underlies the SCD syndrome. Similarly, other authors analyzed the thickness of the posterior canal (PC) in addition to the SC on the unaffected side of the patients and reported that SCD is associated with bone thinning in the SC on the opposite side, but not with the PC [Gracia-Tello et al, 2013]. Recently, some authors have suggested that the mastoid pneumatization is closely related to the generation of SCD [Cho et al, 2014;Shim et al, 2012].…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 87%

Section: Measurement Of Sc Hc and Pc Thicknessmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

et al. 2015

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Idiopathic intracranial hypertension: Contemporary review and implications for the otolaryngologist

et al. 2017

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Objectives: 1) Review controversies pertaining to the pathophysiology, diagnosis, and treatment of idiopathic intracranial hypertension. 2) Discuss the evolving role of otolaryngologists in managing this disease and related disorders.Data Sources: Primary literature review, Centers for Disease Control and Prevention website, International Classification of Headache Disorders, Second Edition.Methods: A comprehensive review of the primary literature was performed from 1990 to 2016 utilizing keywords idiopathic intracranial hypertension, pseudotumor cerebri, benign intracranial hypertension, spontaneous cerebrospinal fluid leak, and encephalocele. Articles were included at the discretion of the authors based on novel and/or historical contributions to the literature.Results: The incidence of idiopathic intracranial hypertension is increasing along with the obesity epidemic. Undiagnosed patients may present to otolaryngologists with pulsatile tinnitus, dizziness, sleep apnea, and spontaneous cerebrospinal fluid leaks. Although diagnosis is predicated upon imaging findings and lumbar puncture, radiographic signs including empty sella, optic nerve dilation, and globe flattening may suggest the diagnosis. The most effective intervention is weight loss combined with acetazolamide. Surgery is reserved for severe or refractory symptoms and can be highly morbid. Otolaryngologists are increasingly responsible for managing a number of secondary disorders including cerebrospinal fluid rhinorrhea and otorrhea. Failure to manage intracranial hypertension may lead to adverse surgical outcomes.Conclusions: The knowledge base for idiopathic intracranial hypertension has greatly expanded over the past 25 years. This disease is associated with a number of conditions directly relevant to otolaryngologists. A keen understanding of this disorder and its management may optimize outcomes in a growing number of patients.

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Dehiscence of the superior semicircular canal: a review of the literature on its possible pathogenic explanations

Brandolini

Modugno

Pirodda

2013

Eur Arch Otorhinolaryngol

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The dehiscence of superior semicircular canal is a well-known affection which is able to explain some cases of hearing loss, tinnitus and/or vertigo unexpectedly presenting in adults without previous otologic affections. Although a diagnostic algorithm has been assessed and a surgical therapy has been indicated, the review of the literature shows that a completely satisfactory explanation for the reason why symptoms of a supposed congenital condition only occur in adulthood is still lacking. A pathogenic hypothesis based on the slow metabolism of the bony labyrinth, which could in time result in a prevalence of bone re-absorption on new bone formation leading to a dehiscence, despite some controversial findings could represent a the most reliable explanation for the question.

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Effect of Semicircular Canal Dehiscence on Contralateral Canal Bone Thickness

Cited by 11 publications

References 15 publications

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

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

Idiopathic intracranial hypertension: Contemporary review and implications for the otolaryngologist

Dehiscence of the superior semicircular canal: a review of the literature on its possible pathogenic explanations

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