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Intralabyrinthine schwannoma affecting the low but not high frequency function of the vestibulo-ocular reflex: implications for the clinical diagnosis of chronic peripheral vestibular deficits
  1. B Machner1,
  2. S Gottschalk2,
  3. T Sander3,
  4. C Helmchen3,
  5. H Rambold4
  1. 1Department of Neurology, University Hospitals of Schleswig-Holstein, Campus Luebeck, Germany
  2. 2Department of Neuroradiology, University Hospitals of Schleswig-Holstein, Campus Luebeck, Germany
  3. 3Department of Neurology, University Hospitals of Schleswig-Holstein, Campus Luebeck, Germany
  4. 4National Eye Institute, Bethesda, Maryland, USA
  1. Correspondence to:
 Professor Christoph Helmchen
 Department of Neurology, University Hospitals of Schleswig-Holstein, Campus Luebeck, Ratzeburger Allee 160, D-23538 Lübeck, Germany; christoph.helmchen{at}neuro.uni-luebeck.de

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Peripheral vestibular hypofunction can be identified by asymmetric vestibular responses to caloric irrigation of the horizontal semicircular canal or by the head impulse test.1 Whereas the first test investigates the low frequency function of the vestibulo-ocular reflex (VOR) the latter assesses the high frequency function. The high frequency VOR function is usually more persistently impaired in unilateral vestibular lesions (eg, vestibular neuritis) than the low frequency function and thus the more sensitive parameter to detect chronic peripheral vestibular deficits.2

Contrary to this current vestibular knowledge, we present a patient with a chronic peripheral vestibular deficit showing normal high frequency but impaired low frequency VOR function. This unusual lesion pattern was caused by an intralabyrinthine schwannoma.

Case report

A 47-year-old patient presented with a 3 month history of repetitive episodes of vertigo, nausea and lateropulsion to his right side. The first episode lasted 1.5 h followed by short lasting (seconds to 15 min) episodes once a day. The patient reported a similar episode of vertigo 1 year previously, at that time associated with an acute hearing loss on the right side and persisting tinnitus ever since. Apart from moderate right sided hypacusis, neurological examination was normal in the asymptomatic stages during follow-up examinations over the next 2 years. Particularly, there was no spontaneous or head shaking nystagmus and no gaze evoked nystagmus.

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