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Abstract
Background: Electrical vestibular stimulation is believed to directly activate the vestibular afferents to mediate an electrically evoked vestibulo-ocular reflex (eVOR). Gentamicin, an aminoglycoside antibiotic, induces vestibulotoxicity by hair cell damage and death.
Objective: To determine if human eVOR is impaired by hair cell damage and death in systemic gentamicin vestibulotoxicity (GV).
Methods: Three-dimensional binocular eye movements evoked by bilateral, bipolar, 100 msec direct current-step at intensities of 0.9, 2.5, 5.0, 7.5, and 10.0 mA were recorded with dual-search coils in 12 GV patients, and the results were compared to 13 healthy subjects.
Results: Normal eVOR was predominantly torsional, comprising phasic eVOR initiation and cessation acceleration pulses at 9 msec latency after current onset and offset, with a tonic eVOR velocity-step during the 100 msec intervening period of maintained current. Normal phasic eVOR increased, while tonic eVOR scaled linearly, with current intensity. GV impaired phasic eVOR more severely than tonic eVOR, and prolonged the latency to 12–13 msec. In patients without mechanical response to vestibular tests, phasic eVOR was reduced to one-fifth of normal amplitude, doubled in duration, had reduced ability to vary with current intensity, and threshold was increased. Tonic eVOR was reduced to one-third of normal, but still scaled linearly with current intensity. Patients, who retained partial mechanical responses to vestibular tests, had phasic eVOR impairment without tonic eVOR abnormality.
Conclusion: Impairment of evoked vestibulo-ocular reflex (eVOR) in gentamicin vestibulotoxicity (GV) suggests that vestibular hair cells, activated by electrical stimulation, mediate the eVOR. Abnormalities of the eVOR, especially the phasic component, might be a marker of vestibular injury in GV.
GLOSSARY: eVOR = electrically evoked vestibulo-ocular reflex; EVS = electrical (galvanic) vestibular stimulation; GV = gentamicin vestibulotoxicity.
Footnotes
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Supplemental data at www.neurology.org
Supported by National Health and Medical Research Council Australia, University of Sydney, The Garnett Passe and Rodney Williams Memorial Foundation, The Clive and Vera Ramaciotti Foundations, Neurology Trustees Royal Prince Alfred Hospital, and Brain Foundation.
Disclosure: The authors report no conflicts of disclosures.
Received April 13, 2008. Accepted in final form August 26, 2008.
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