Affiliations: [a] Departments of Otology and Laryngology, Harvard Medical School, Boston MA, USA | [b] Departments of Otology and Neurology, Harvard Medical School, Boston MA, USA | [c] Jenks Vestibular Physiology Laboratory, Massachusetts Eye and Ear Infirmary, Boston MA, USA | [d] Department of Clinical Neurosciences, Service of Otorhinolaryngology, Head and Neck Surgery, University Hospitals of Geneva, Geneva, Switzerland
Correspondence:
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Corresponding author: Dr. Richard Lewis, Massachusetts Eye and Ear Infirmary, 243 Charles Street, Boston MA 02114, USA. Tel.: +1 617 573 3501; Fax: +1 617 573 4154; E-mail: richard_lewis@meei.harvard.edu
Abstract: Vestibular symptoms caused by migraine, referred to as vestibular migraine, are a frequently diagnosed but poorly understood entity. Based on recent evidence that normal subjects generate vestibular-mediated percepts of head motion and reflexive eye movements using different mechanisms, we hypothesized that percepts of head motion may be abnormal in vestibular migraine. We therefore measured motion detection thresholds in patients with vestibular migraine, migraine patients with no history of vestibular symptoms, and normal subjects using the following paradigms: roll rotation while supine (dynamically activating the semicircular canals); quasi-static roll tilt (statically activating the otolith organs); and dynamic roll tilt (dynamically activating the canals and otoliths). Thresholds were determined while patients were asymptomatic using a staircase paradigm, whereby the peak acceleration of the motion was decreased or increased based on correct or incorrect reports of movement direction. We found a dramatic reduction in motion thresholds in vestibular migraine compared to normal and migraine subjects in the dynamic roll tilt paradigm, but normal thresholds in the roll rotation and quasi-static roll tilt paradigms. These results suggest that patients with vestibular migraine may have enhanced perceptual sensitivity (e.g. increased signal-to-noise ratio) for head motions that dynamically modulate canal and otolith inputs together.
