Self-motion perception is sensitized in vestibular migraine: pathophysiologic and clinical implications

• Published in: Scientific reports Vol. 9; no. 1; pp. 14323 - 12
• Main Authors: King, Susan, Priesol, Adrian J., Davidi, Shmuel E., Merfeld, Daniel M., Ehtemam, Farzad, Lewis, Richard F.
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 04.10.2019; Nature Publishing Group
• Subjects: 631/378/3917; 692/617/375/1654; Adult; Brain stem; Cerebellum; Female; Headache; Humanities and Social Sciences; Humans; Integration; Male; Migraine; Migraine Disorders - complications; Migraine Disorders - diagnosis; Migraine Disorders - physiopathology; Motion detection; Motion Perception - physiology; Movement - physiology; multidisciplinary; Otolithic Membrane - physiology; Patients; Science; Science (multidisciplinary); Semicircular canals; Semicircular Canals - physiology; Vertigo; Vertigo - diagnosis; Vertigo - etiology; Vertigo - physiopathology; Vestibular Function Tests; Vestibular nuclei; Vestibular Nuclei - physiopathology; Vestibular system; Vestibulo-ocular reflex
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-019-50803-y

Vestibular migraine (VM) is the most common cause of spontaneous vertigo but remains poorly understood. We investigated the hypothesis that central vestibular pathways are sensitized in VM by measuring self-motion perceptual thresholds in patients and control subjects and by characterizing the vestibulo-ocular reflex (VOR) and vestibular and headache symptom severity. VM patients were abnormally sensitive to roll tilt, which co-modulates semicircular canal and otolith organ activity, but not to motions that activate the canals or otolith organs in isolation, implying sensitization of canal-otolith integration. When tilt thresholds were considered together with vestibular symptom severity or VOR dynamics, VM patients segregated into two clusters. Thresholds in one cluster correlated positively with symptoms and with the VOR time constant; thresholds in the second cluster were uniformly low and independent of symptoms and the time constant. The VM threshold abnormality showed a frequency-dependence that paralleled the brain stem velocity storage mechanism. These results support a pathogenic model where vestibular symptoms emanate from the vestibular nuclei, which are sensitized by migraine-related brainstem regions and simultaneously suppressed by inhibitory feedback from the cerebellar nodulus and uvula, the site of canal-otolith integration. This conceptual framework elucidates VM pathophysiology and could potentially facilitate its diagnosis and treatment.