Treatment

In the daily practice it is useful to administer vestibular sedatives such as dimenhydrinate during acute self-limiting attacks [11, 15, 18]. One popular prophylactic treatment regimen tries to reduce the endolymph by low-salt diet or diuretics; another option is to administer betahistine (8–16 mg/day). Higher dosages (up to 3 48 mg) seem to be more effective than lower ones [15], although the efficacy of betahistine has not been proven [18]. No randomized studies on these treatment options have yet been conducted. A retrospective survey of the outcome of 22 patients revealed that intratympanic steroid perfusion was only of short-term benefit [19]. A systematic review of published uncontrolled studies found that gentamicin reduced vestibular function in the treated ear and achieved overall vertigo control (complete or substantial control) in 89% of the patients (range 73–100%); hearing worsened in 26% (0–90%) [20]. A meta-analysis examined the application of gentamicin, which poses the lowest risk of hearing loss [21]. The titration technique with daily or weekly doses until onset of vestibular symptoms, change in vertigo, or hearing loss showed the best rate of vertigo control. Complete ablation of the vestibular function is not typically required for such control [21], as this is also not achieved for a long time with gentamicin instillation [22].

Superior Canal Dehiscence Syndrome

Clinical Aspects

Patients with a so-called superior canal dehiscence syndrome [23, 24] complain of vertigo and oscillopsia, which are induced by intense sound stimuli, a Valsalva maneuver, or in some cases even the heart beat, when nystagmus beats synchronously with the pulse in the plane of the involved vestibular canal [25]. The accompanying jerk nystagmus has vertical and torsional components [23, 24].

Etiology

The superior canal dehiscence syndrome is a special form of inner-ear perilymph fistula [23]. High-resolution computed tomography has shown that the cause is a missing bone coverage between the superior canal and the middle cranial fossa. This results in increased pressure on the superior canal when the intracranial pressure increases. In some patients, the dehiscence may be bilateral [23].

Treatment

Surgical plugging of the canal or resurfacing of the dehiscence can prevent the pressure-induced oscillopsia [23]. Aftereffects are not long lasting.