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HK Audio Pulsar PL118 Sub a


Third Window Syndrome View all 21 Articles. Over the past two decades, advances in diagnostic techniques have raised the awareness of SCDS and treatment approaches have been refined to improve patient outcomes. However, a number of challenges remain. First, there is currently no standardized clinical testing algorithm for quantifying the effects of superior canal dehiscence SCD.

SCDS mimics a number of common otologic disorders and established metrics such as supranormal bone conduction thresholds and vestibular evoked myogenic potential VEMP measurements; although useful in certain cases, have diagnostic limitations. Second, while high-resolution computed tomography CT is the gold standard for the detection of SCD, a bony defect does not always result in signs and symptoms.

Third, even when SCD repair is indicated, there is a lack of consensus about nomenclature to describe the SCD, ideal surgical approach, specific repair techniques, and type of materials used. Finally, there is no established algorithm in evaluation of SCDS patients who fail primary repair and may be candidates for revision surgery.

Herein, we will discuss both contemporary and emerging diagnostic approaches for patients with SCDS and highlight challenges and controversies in the management of this unique patient cohort. The authors described a series of patients with disequilibrium and sound- and pressure-induced vertigo associated with nystagmus in the plane of the superior semicircular canal SSC. Symptom improvement was observed in patients who underwent surgical plugging of the defect via middle fossa craniotomy.

In subsequent years, auditory symptoms, including autophony, amplification of bodily sounds, pulsatile tinnitus, conductive hearing loss, hyperacusis, and aural fullness as well as vestibular symptoms of chronic disequilibrium and sound- and pressure-induced vertigo and oscillopsia became hallmarks of SCDS 2 — 4. While in most patients symptoms of SCDS can be tolerated and conservative management is reasonable, some individuals suffering from SCDS report decreased quality of life due to challenges in communicating with those around them and completing activities of daily living 5 — 7.

The health utility value HUV , a measure of general health-related quality of life, ranges from poor health 0. For patients with debilitating symptoms, definitive treatment involves surgical repair of the dehiscence. However, the diagnostic evaluation of patients with suspected SCDS can sometimes be difficult to interpret. Established clinical testing that reveals supranormal bone conduction thresholds, low frequency air-bone gap ABG with present acoustic reflexes, low threshold cervical vestibular evoked myogenic potentials cVEMP and increased ocular VEMP oVEMP amplitudes are useful in guiding management options in symptomatic patients with radiologic superior canal dehiscence SCD.

However, some symptomatic patients do not have findings suggesting a classic third window. Furthermore, while clinicians agree that primary and revision surgery is a reasonable option for patients with persistent localizing signs and symptoms, the optimal approach, repair technique and materials are the subject of debate and confusion amongst both providers and patients.

Herein, we will review the pathophysiology and etiology of SCD, present current trends in its diagnosis and management, discuss novel approaches, and finally highlight some of the remaining challenges and controversies. Illustrative cases are provided to complement the literature. In a normal ear, sound is transmitted through the ossicular chain resulting in volume velocity into the cochlea through the oval window and eventually toward the round window bold arrows in Figure 1A.

SCD results in a third mobile window that enables acoustic stimuli at the oval window to dissipate through the vestibular labyrinth, leading to vertigo, and dizziness Figure 1B. Intracranial pressure changes may also inadvertently stimulate vestibular end organs Figure 1C 2 , 3 , 8 , 9. Response to air conduction is reduced resulting in low-frequency hearing loss, and response to bone conduction is increased resulting in hyperacusis, autophony, and amplification of bodily sounds e. Dural pulsations across the dehiscence are the likely cause of pulsatile tinnitus a common auditory symptom in SCDS patients.

The pathophysiology of SCDS remains incompletely understood, especially with regard to the variability in symptomatology among patients, but remains the focus of a number of research studies 8 — 11 , 17 , Figure 1. Schematic representations illustrate inner ear volume velocity with arrows. A Normal anatomy allows volume velocity across the cochlear partition from the oval to the round window two windows.

C Elevated intracranial pressure from Valsalva against closed glottis e. D Enlarged vestibular aqueduct EVA can also act as a third window, shunting volume velocity away from the cochlear partition and toward the widened vestibular aqueduct 2 , 13 — Third window lesions may occur in different anatomic locations including the posterior or horizontal semicircular canals, bony vestibule, or the cochlea.

An enlarged vestibular aqueduct EVA can cause a third window phenomenon in children and adults. A pathologically widened vestibular aqueduct produces a communication between the bony vestibule and intracranial cavity that can result in an ABG and mechanical characteristics similar to that observed in patients with SCDS Figure 1D Patients with EVA present with normal hearing thresholds, conductive hearing loss, mixed hearing loss, or sensorineural hearing loss SNHL 13 — Third window-like symptoms have also been described in cases of post-traumatic membranous or hypermobile stapes footplate The etiology of SCD is unknown, but two theories have been proposed in the literature: congenital and acquired.

The congenital theory of SCD proposes that failure of fetal and postnatal bone development of the temporal bone predisposes to and causes SCD. Proponents of the congenital theory cite temporal bone histopathology studies that show thinning or dehiscence over the superior canal without evidence of bony remodeling Additionally, there is a high prevalence of radiologic SCD in infants, although these findings usually resolve in the first decade of life with the final postnatal bone development 24 — Some patients with SCD have generalized thin bone throughout the lateral skull base, multiple tegmen defects, and develop SCDs bilaterally, which may further support the congenital theory 24 , 28 , It has been hypothesized that congenital thin bone of the lateral skull base predisposes a patient to develop SCD due to a second event later in life.

For example, head trauma could disrupt the seal over the endosteum or membraneous labyrinth created by the dura, thus resulting in symptomatic SCDS 4 , 24 , 28 , Concomitant tegmen defects are important to recognize as they may alter the findings of audiometric and vestibular testing Figure 2.

Figure 2. Concomitant tegmen tympani defect with dural herniation. There have been reports of a high prevalence of SCD in patients with a variant of Usher syndrome and overrepresentation of SCD in some families, suggesting that there may be genetic correlates that have not been completely identified 4 , 30 — The acquired theory of SCD proposes that increased intracranial hypertension and repeated pulsations could degrade the bone overlying the SSC over time.

Of note, however, a clear association between intracranial hypertension and SCDS has not been established 33 — Furthermore, there is not a tendency of obesity among patients who undergo SCD repair Causes of acquired SCD also include: neoplasms such as meningioma 38 , vascular malformations 39 , chronic osteomyelitis 40 , fibrous dysplasia 41 , and head trauma with temporal bone fractures Diagnosing SCDS can be challenging as symptoms vary greatly and may mimic other otologic and neurotologic conditions.

The mechanism by which SCD produces such a wide range in symptoms among individuals remains poorly understood 9 , 43 , 48 , CT findings of a bony dehiscence over the SSC are diagnostic; however, it is important to recognize that not all individuals with radiologic evidence of dehiscence have relevant symptoms and suffer from SCDS 24 , In this section, we will 1 discuss the advantages and disadvantages of each of these established testing modalities to narrow the differential diagnosis, and 2 review emerging modalities including wideband acoustic immittance and electrocochleography for evaluating patients with third-window symptoms.

In the office, bone conduction testing with a Hz tuning fork often lateralizes to the affected or worse ear, further supporting the theory that SCD generates a pseudo-conductive hearing loss. Low-frequency ABG due to SCD are caused by the combined effects of two separate mechanisms verified by consistency of clinical, temporal bone, and computational modeling data. The low-frequency decrease in air conduction hearing higher air conduction thresholds is due to volume velocity shunting via the SCD Figure 1B 9 , The low-frequency increase in bone conduction hearing lower bone conduction thresholds is due to altered inner-ear volume velocities and pressures in response to vibration of the skull and altered mass of the inner ear fluid as determined recently in Guan et al.

The presence of low-frequency conductive hearing loss and other SCDS-related symptoms such as autophony and aural fullness are also seen in patients with otosclerosis, Eustachian tube dysfunction, patulous Eustachian tube, and other middle ear pathologies Acoustic reflex testing and tympanometry are essential to rule out middle-ear pathology or Eustachian tube dysfunction 50 , Of note, SCD effects on audiometric, immittance, and VEMP testing may be masked by concomitant middle ear abnormalities or tegmen tympani defects with dural herniation into the middle ear because these conditions affect sound transmission Figure 2.

This would obscure SCD-related findings Figure 2. During impedance measurements such as Hz tympanometry, pulse-synchronous waves have been observed in some SCD patients 56 — VEMP testing assesses the function of the otolith organs of the vestibular periphery by measuring surface electromyography responses to acoustic stimulation.

In cVEMP testing, the saccule is stimulated leading to an inhibitory response in the ipsilateral sternocleidomastoid muscle modulated by the inferior vestibular nerve. In oVEMP testing, the utricle is stimulated leading to activation of the contralateral eye muscles.

Another initiative to improve the diagnostic accuracy of cVEMP was the use 2, Hz stimulus instead of the commonly used Hz tone burst. Figure 3. Example of an adult patient with symptoms of left-sided SCDS. Bone-conducted VEMP testing is an alternative approach in cases of concurrent middle ear pathology. Despite these diagnostic advancements, there are limitations to the clinical utility of VEMP testing in the evaluation of a patient with suspected SCD.

First, VEMP responses assume normal sound transmission through the middle ear, inner ear, otolith organs, and vestibular nerves. Patients with vestibular hypofunction may not demonstrate lowered thresholds or increased amplitudes on VEMP testing of the affected side 70 — 72 , and thus the test may not be used with a high degree of accuracy in this patient population.

As vestibular deficits have been observed in some patients following surgical repair of SCD, VEMP testing after surgery can be difficult to interpret.

For example, evaluation of patients for revision surgery can be difficult because the thresholds can be elevated for various reasons. VEMP responses are dependent on normal sound transmission to the oval window, which may not be the case if there is middle ear pathology, obscuring the SCD-related changes Figures 2 , 4. Second, VEMP responses decrease with age, although the SCD effect seems to dominate the age effect 60 , and conversely, stronger sternocleidomastoid muscle contraction is correlated with larger cVEMP amplitude Third, there is no known association between cVEMP thresholds and severity of auditory or vestibular symptoms Finally, due to lack of standardization in measurement conditions, comparisons of VEMP data across institutions remains challenging and no standard cutoff values for threshold and amplitude exist 60 , 70 , Figure 4.

Concomitant SCD and malleus fixation. A year-old woman presented with the sole complaint of hearing loss in the right ear. E Large low-frequency air-bone gap on the right. F Normal tympanometry bilaterally. G Absent acoustic reflexes in right ear. Vestibular function testing, including calorics and vestibular ocular reflexes VOR e. For example, patients with contralateral vestibular hypofunction based on calorics and VEMPs are at risk for prolonged recovery following surgical repair Vestibular testing is critical in the evaluation of patients for revision SCD surgery.

For example, caloric testing will assay the residual function of the superior vestibular nerve cVEMPs measure inferior vestibular nerve function in the operated ear and provides baseline data on the function of the contralateral ear. In patients with bilateral SCD, evaluation of residual vestibular function of the operated ear is useful prior to consideration for surgery in the second ear Indeed not all patients have sound- and pressure-induced vertigo or nystagmus, and even in patients with subjective vertigo to sound and pressure stimuli, a nystagmus may not be detected of note, there is limited literature on the prevalence of this finding in SCDS patients 1 , 78 , In some patients with a large dehiscence, the VOR response to e.

WAI is a non-invasive measure of the mechano-acoustic impedance of the middle and inner ear. While standard tympanometry uses a single frequency acoustic stimulus, WAI measures function across a range of acoustic frequencies. Wideband tympanometry is WAI measured at different static pressures. One of the most commonly computed metric of WAI is absorbance , a measure of the power ratio of reflected sound from the eardrum and the forward sound stimulus presented at the ear canal Figure 5A Figure 5.


HK Audio COSMO CF118 pasivni line array subwoofer

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Setting Up A Cf 118 Array - HK Audio COSMO Series Instructions For Use Manual

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U osnovi je to subwoofer CS s dodanim utorima. Da bi ste ostavili recenziju morate biti prijavljeni. It is essentially a CS subwoofer with added rigging points. Engineered for maximum efficiency and exceedingly high power handling, its unusually expansive dynamic headroom extends down to the lowest frequencies.

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