Abstract
Superior semicircular canal dehiscence syndrome was first reported by Lloyd Minor and colleagues in 1998. Patients with a dehiscence in the bone overlying the superior semicircular canal experience symptoms of pressure or sound-induced vertigo, bone conduction hyperacusis, and pulsatile tinnitus. The initial series of patients were diagnosed based on common symptoms, a physical examination finding of eye movements in the plane of the superior semicircular canal when ear canal pressure or loud tones were applied to the ear, and high-resolution computed tomography imaging demonstrating a dehiscence in the bone over the superior semicircular canal. Research productivity directed at understanding better methods for diagnosing and treating this condition has substantially increased over the last two decades. We now have a sound understanding of the pathophysiology of third mobile window syndromes, higher resolution imaging protocols, and several sensitive and specific diagnostic tests. Furthermore, we have a treatment (surgical occlusion of the superior semicircular canal) that has demonstrated efficacy. This review will highlight some of the fundamental insights gained in SCDS, propose diagnostic criteria, and discuss future research directions.
Highlights
In 1998, Minor et al described a series of patients with symptoms of chronic disequilibrium and sound- or pressure-induced vertigo and nystagmus in the plane of the superior semicircular canal [1]
A key insight that led to the discovery of superior canal dehiscence syndrome (SCDS) was observing that when patients were exposed to pressure changes or loud sounds they had eye movements in the plane of the ipsilateral superior semicircular canal, linking their symptoms to anatomy
We have suggested that focal thinning— perhaps accompanied by pinpoint dehiscences—of otic capsule bone can in some cases transmit pressure and cause symptoms of SCDS [61], and others have suggested that a more global thinning in some conditions such as Paget’s disease [60, 62] can lead to similar phenomena
Summary
In 1998, Minor et al described a series of patients with symptoms of chronic disequilibrium and sound- or pressure-induced vertigo and nystagmus in the plane of the superior semicircular canal [1]. Superior Semicircular Canal Dehiscence Syndrome sound to access the perilymph of the inner ear via the labyrinth, and the free communication of the perilymph with the cochlea results in hearing bone-conducted sounds better than normal. This “bony hyperacusis” manifests as symptoms of autophony (hearing one’s own voice as loud or distorted); pulsatile tinnitus; and audible eye movements, footsteps, chewing, bowel movements, etc. Pressure gradients between the oval window and dehiscence cause flow of endolymph in the superior canal ampulla, causing vertigo and nystagmus corresponding to either excitation or inhibition of the superior canal These pressure gradients can be generated in the ampullofugal (excitatory) direction by loud sound, positive pressure applied to the external auditory canal, or Valsalva against pinched nostrils. This review will highlight some of the fundamental insights gained in SCDS, propose diag nostic criteria, and discuss future research directions
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