Migraine is associated with enhanced motion sickness susceptibility and can cause episodic vertigo (vestibular migraine, VM), but the mechanisms relating migraine to these vestibular symptoms remain uncertain. We tested the hypothesis that the central integration of rotational cues (from the semicircular canals) and gravitational cues (from the otolith organs) is abnormal in migraine patients. A post-rotational tilt paradigm generated a conflict between the canal cues (which indicate the head is rotating) and the otolith cues (which indicate the head is tilted and stationary), and eye movements were measured to quantify two behaviors that are thought to minimize this conflict - suppression and reorientation of the central angular velocity signal, evidenced by attenuation ("dumping") of the vestibulo-ocular reflex (VOR) and shifting of the VOR's rotational axis towards the earth-vertical. We found that normal and migraine subjects, but not VM patients, displayed an inverse correlation between the extent of dumping and the size of the axis shift such that the net "conflict resolution" mediated through these two mechanisms approached an optimal value, and that the residual sensory conflict in VM patients (but not migraine or normal subjects) correlated with motion sickness susceptibility. Our findings suggest that: the brain normally controls the dynamic and spatial characteristics of central vestibular signals to minimize intra-vestibular sensory conflict; and that this process is disrupted in VM, which may be responsible for the enhance motion intolerance and episodic vertigo that characterize this disorder.
- motion sickness
- eye movements
- Copyright © 2016, Journal of Neurophysiology