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While otic capsule bone differs from the rest of the skeleton in having low bone turnover, the otic capsule is thought to develop for several years after birth.

Many groups have observed that the prevalence of a dehiscence on CT is high in infants but decreases during the first decade of life 29 — 32providing some support for the congenital theory. Although there are a few cases of familial SCDS 3435 and a new report that indicates a high prevalence of canal dehiscence in patients with CDH23 variants Usher syndrome type 1D 36strong genetic correlates have not been identified.

In as many as one quarter of cases, however, another inciting injury such as a traumatic head injury or Valsalva initiates symptoms Many surgeons have noticed that patients with SCDS often have numerous tegmen defects 238 — 40 as well as a dehiscent geniculate ganglion 4142with some groups arguing that this supports a congenital etiology, and a few to speculate that over many years the slow pulsations of the brain and cerebrospinal fluid that surrounds it may lead to the development of both SCDS and tegmen defects Supporting the acquired theory is the observation on CT imaging of increasing thinning of the bone over the superior semicircular canal with advanced age 4546 and a few cases in which radiographic progression has been observed Unusual cases of abnormalities of the middle and posterior cranial fossae have been identified as causing cases of SCDS 48 — 51but these are exceptional.

Aside from dehiscence of the superior semicircular canal, several other sources of labyrinthine dehiscence can lead to symptoms similar to those in SCDS, including that of the posterior semicircular canal 5253lateral semicircular canal 1754vestibular aqueduct 55facial nerve 56internal auditory canal 57and the carotid canal 58 Merchant and Rosowski synthesized many of these reports and broadly proposed that any dehiscence of the inner ear can lead to an inner ear conductive hearing loss from a third mobile window Nakajima and colleagues have emphasized that any perte de poids daurélie secret story officiel, even pinpoint ones, can sufficiently alter the impedance of the otic capsule to cause a functional third mobile window 12 The most common symptoms of SCDS include bone conduction hyperacusis, autophony, pulsatile tinnitus, and sound- or pressure-induced vertigo 2 Some of the internal noises that patients report as being particularly disturbing include hearing their eyeballs move, hearing their footfalls loudly, chewing, belching, or borborygmi.

Patients also experience aural fullness. Patulous Eustachian tube dysfunction can also present with autophony, voice distortion, and pulsatile tinnitus Many patients with SCDS also have migraine, but this may represent the high prevalence of migraine in the general population and that SCDS is an effective migraine trigger. Some unusual symptoms have included a patient with tinnitus with head movements in the plane of the affected semicircular canal 67as well as vertical head movements when hearing a loud sound.

The vestibular system influences reflexes that control the neck musculature, as evidenced by the early vestibular physiology studies performed in pigeons and referenced above. It is therefore particularly interesting that a few patients can develop involuntary head movements in response to loud sounds, and that these movements occur in the plane of the superior semicircular canal 6. Vestibular contributions to the muscles controlling head movements may explain the neck muscular strain reported by some patients with SCDS.

Whether SCDS is progressive is unclear. It appears that the hearing loss does not significantly change over time There have been reported cases of worsening conductive hearing loss over time and cases have been reported in which soin visage paris avis progressed over many years 354769while at least one case developed rapid mixed hearing loss If SCDS is related to a congenital predisposition, patients may develop worsening symptoms as the dehiscence becomes larger with increasing age.

As a result, pediatric patients may present differently than adults Despite the high prevalence of an anatomic dehiscence noted on CT in young children described aboveonly a few cases of pediatric SCDS has been reported 71even fewer of whom underwent surgical repair Computed tomography imaging demonstrating a dehiscence is an important diagnostic feature of SCDS, but it is not sufficient for diagnosis and may mislead the ordering physician.

On review of 1, temporal bones, the prevalence of a dehiscent superior semicircular canal is 0. Higher resolution studies can improve diagnostic accuracy. Due to volume averaging and other factors, however, CT imaging can still overcall a dehiscence Furthermore, many patients with CT evidence of a dehiscence are asymptomatic, perhaps reflecting the protective role of inelastic dura in preventing pressure transmission through some bony dehiscences.

In addition to a dehiscence of CT imaging, therefore, patients must also have both symptoms consistent with the syndrome and physiological evidence of a third mobile window.

Magnetic resonance imaging MRI has been explored as a possible alternative to CT for diagnosis 7576 ; and some centers routinely perform MRI in addition to CT to better evaluate the skull base for vascular malformations, masses, or encephaloceles prior to surgery. It has been our preference to reserve MRI only for cases of persistent symptoms after an initial attempt at surgery.

If an MRI is performed, the best sequences for viewing the semicircular canals are heavily T2 weighted and have a variety of names depending on the MRI manufacturer e. In these sequences, semicircular canal fluid signal is bright; loss of this signal can be useful for assessing adequacy of prior surgical plugging Fortunately, for diagnostic purposes a variety of abnormal physiologic findings have been observed in SCDS that can provide evidence of a third mobile window.

In many of the first patients described by Minor et al.

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This finding is not observed in all patients 2and when observed is not always in the plane of the superior semicircular canal. When the Tullio phenomenon elicits eye movements not in the plane of the superior semicircular canal, however, clinicians should consider alternative diagnoses due to the rarity of this finding. As a result, many early cases were suspected of having otosclerosis; it is important to perform acoustic reflexes, as these are commonly normal in SCDS.

There have been a few cases reported in which patients have both otosclerosis and SCDS, but these cases are atypical 78 — Increased dehiscence length has been shown to correlate with larger air-bone gaps 6381and this is predicted on modeling of a dehiscence as well In many patients, the bone conduction threshold at these frequencies is negative or better than normal. Sometimes, the tuning fork can be heard in the affected ear when placed on the medial malleolus or other distant bony prominences Vestibular-evoked myogenic potentials are electromyographic potential reflex tests that in the non-dehiscent ear are thought to reflect function of the saccule cervical VEMP or utricle ocular VEMP The cervical VEMP involves an inhibitory neural reflex pathway from the saccule to the ipsilateral sternocleidomastoid muscle.

The ocular VEMP involves an excitatory pathway from the utricle to the contralateral inferior oblique muscle. In SCDS, these tests are frequently abnormal, as the affected ear is especially sensitive to the auditory or vibratory stimuli used to evoke these myogenic potentials. Ocular VEMP amplitudes in particular have been found to be highly sensitive and specific for the diagnosis of an intraoperative confirmed dehiscence 84 Arts et al.

These findings have subsequently been observed by us and others 88 While the results have not yet correlated with postoperative hearing outcomes, changes such as rapid rises in the SP are often observed during surgery and likely reflect changes in inner ear biomechanics during vestibular surgery.

The clinical utility of this test for diagnosis and intraoperative use is still under investigation; nevertheless, ECoG appears to reflect the presence of a third mobile window, similar to the other diagnostic testing described above. High-resolution computed tomography imaging with 0.

He elected to proceed with surgery via middle cranial fossa approach. The middle cranial fossa was resurfaced with hydroxyapatite cement.

Autophony improved after surgery, hearing was preserved, and vestibular dysfunction was limited to the superior semicircular canal as determined by clinical head impulse testing in all semicircular canal planes. Proposed diagnostic criteria for superior canal dehiscence syndrome SCDS.

Bone conduction hyperacusis in the form of autophony, audible eye movements, audible footsteps, etc. Pressure-induced vertigo via nasal or glottic Valsalva or pressure applied to the external auditory canal. Elevated summating potential to action potential ratio on electrocochleography in the absence of a sensorineural hearing loss. There are no known effective medical treatments for SCDS. While some patients with SCDS are content to have an explanation for their symptoms, some about half in our experience pursue surgery.

We offer surgery to patients when we can relate their symptoms to SCDS and when the patient can tell themselves that their symptoms are debilitating. The goal of surgery is elimination of the third mobile window pathophysiology. A few of the original patients that underwent resurfacing alone without plugging experienced recurrence of symptoms after surgery Since this report, it has been our practice to plug the affected canal in order to obtain a watertight seal with a combination of fascia, bone dust, and bone chips.

The middle cranial fossa is then resurfaced with fascia and hydroxyapatite cement. Resurfacing material also varies and can include cartilage, fascia, bone dust, fibrin glue, and hydroxyapatite cement. The transmastoid approach to plugging the canal has also been used in many cases with excellent results 3890 — Prior to pursuing bcm minceur efficace, however, control of migraine is critical to avoid exacerbation of migraine after surgery and to distinguish treatable symptoms that are unlikely to be helped by repairing a dehiscence.

Jung et al. The middle cranial fossa approach is familiar to neurotologists and allows the advantages of directly observing the dehiscent canal and providing assurance that the canal is adequately plugged on either side of the dehiscence. In some cases in which the dehiscence is located adjacent to the superior petrosal sinus or the more posterior aspect of the canal near the common crus, the transmastoid approach is preferred.

Alternatively, an angled endoscope may extend visualization for plugging via middle cranial fossa approach Furthermore, in some cases the transmastoid approach is not feasible due to a contracted mastoid with a low-hanging tegmen.

We feel a significant disadvantage of the transmastoid approach is the lack of directly seeing the dehiscence, thereby risking inadequate plugging on either side of the dehiscence. Some have suggested this can be circumvented by elevating dura over the dehiscence via the mastoid and using a mirror to ensure the canal is adequately plugged Patients generally do well after surgery to plug the affected semicircular canal, with improvements in autophony 9dizziness handicap 8and overall health-related quality of life This corresponds with elimination of the third mobile window, as has been demonstrated by the normalization of cervical VEMP thresholds 96the ocular VEMP amplitudes 96the elevated SP to AP ratio 8689and the low-frequency air-bone gap After surgical plugging, patients have expected reduction in the function of the superior semicircular canal 7 Perhaps surprisingly in the history of otology, exposing and manipulating the membranous labyrinth at surgery only rarely results in a significant loss of hearing, even in patients undergoing revision surgery 97— In our experience, the recurrence rate from plugging and resurfacing of the canal is quite low Furthermore, patients who undergo revision surgery for SCDS tend to do well, but the success rates are lower than in primary surgery.

Some otologic surgeons have recently begun offering a procedure to reinforce the round window by a variety of methods as an attempt to dampen SCDS symptoms This procedure is proposed as a minimally invasive approach that might provide relief from SCDS symptoms. The proponents argue that stiffening the round window partially dampens one of the three inner ear windows, leaving the oval window and the dehiscence as the primary remaining inner ear windows.

Lempert and other proponents of horizontal semicircular canal fenestration invoked a similar philosophy in the early treatment of otosclerosisbypassing the fixed oval window and using instead the round window and a new semicircular canal fenestration to restore compression and rarefaction of inner ear fluids. There have been significant advancements in the understanding of inner ear biomechanics that would suggest that these approaches should induce vertigo, by shunting acoustic energy preferentially across vestibular sensory epithelia.

This in fact appears to be the case with complete round window occlusion in two patients with SCDS who subsequently had the process reversed Furthermore, occlusion of the round window is thought to induce a hearing loss In the series by Silverstein et al.

Among patients who have had this procedure performed elsewhere, we have observed that if successful, round window reinforcement has provided only temporary relief for SCDS and that some have reported hearing loss and new tinnitus. Whether this transient relief is caused by a reduction in hearing or some other mechanism remains to be determined, and thus far there has not been a proposed model to explain how this alteration in physiology can improve symptoms.

We believe this surgery requires additional study before it is recommended to patients. There are many interesting remaining questions in SCDS. As described above, the etiology of SCDS remains unknown, in particular an explanation is needed for why patients tend to present later in life if this is primarily a congenital phenomenon.

In some cases, symptoms occur after a traumatic incident or sudden increase in intracranial pressure leading to symptom onset. However, many patients do not report an inciting event. It may therefore be some combination of congenital and acquired pathology Identifying the etiology is important for purposes of treatment, for if the etiology can be identified, research toward medical management may become feasible.

Comparative outcomes among surgical approaches are lacking, in part due to a lack of a well-designed disease-specific outcome measure in SCDS to assess for symptom improvement. A validated outcome measure would be a significant step forward in assessing post-intervention outcomes.

We believe plugging the canal by middle cranial fossa approach currently is the gold standard for treatment based on the available data.

This procedure reduces function of the superior semicircular canal and poses additional risk to the inner ear.

While the outcome from canal plugging is supported by reductions in symptoms, improvements in quality of life, and a low risk of recurrence, methods of effectively addressing the pathology without producing impaired inner ear function would be desirable.

Perhaps, individually fabricated 3D-printed reconstructions could prevent the third mobile window phenomena without risks of disease recurrence or persistence that have been observed with resurfacing alone While we know from temporal bone studies and surveys of CT imaging the approximate prevalence of an anatomic dehiscence, we still do not know the prevalence or incidence of SCDS or whether there are modifiable risk factors. For diagnosis, there are many available tests that appear to represent the abnormal pressure transmission associated with a third mobile window ocular and cervical VEMPs, pure tone audiometry, and ECoGnevertheless, improved CT imaging techniques such as cone beam or flat panel CT may improve diagnostic accuracy.

A recent study observed that some patients with SCDS may also have endolymphatic hydrops as determined by MRI with intratympanic gadolinium This observation needs to be confirmed in a larger, well-defined population, for if confirmed, it may have implications for etiology. Finally, we have identified some patients with thin, but not frankly dehiscent bone over the superior semicircular canal i. These patients often have symptoms of SCDS, physiologic evidence of a third mobile window, and in some cases are noted to have compliance of the thin bone at the time of surgery.

On obesite definition larousse traduction other hand, these patients tended not to fair as well after surgical repair.

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It remains to be determined whether patients with thin bone over the superior semicircular canal have poorer outcomes, and plat dietetique poulet data are needed. Although there are still unanswered questions, superior semicircular canal dehiscence syndrome has become one of the most well-described vestibular disorders.

This has been the result of a combination of several developments including our collective understanding of novel methods of vestibular testing, development of high-resolution imaging, and pioneering surgeries demonstrating the safety and efficacy of semicircular canal plugging. Consistent diagnostic criteria and a disease-specific outcome measure would allow improved ability to compare treatment outcomes in developing even safer and more enduring therapies. BW reviewed literature and wrote the initial draft.

JC and LM performed critical analysis of the initial draft and revisions. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The reviewer, ES, and handling Editor declared their shared affiliation, and the handling Editor states that the process nevertheless met the standards of a fair and objective review. National Center for Biotechnology InformationU.

Journal List Front Neurol v. Front Neurol. Published online Apr Bryan K. Carey1 and Lloyd B. Minor 2. John P. Lloyd B. Author information Article notes Copyright and License information Disclaimer.

Ward, ude.

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Specialty section: This article was submitted to Neuro-otology, a section of the journal Frontiers in Neurology. Received Jan 25; Accepted Apr The use, distribution or reproduction in other forums is permitted, provided the original author s or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice.

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