Contribution of intravestibular sensory conflict to motion sickness and dizziness in migraine disorders

Abstract

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 postrotational tilt paradigm generated a conflict between canal cues (which indicate the head is rotating) and 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 vestibuloocular reflex and shifting of the rotational axis of the vestibuloocular reflex toward 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 intravestibular 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.

Temporal Patterns of Vertigo and Migraine in Vestibular Migraine

“…Other factors that should be considered were the contributions of motion sickness history and anxiety, which were more common in VM patients with concurrent vertigo and migraine. Anxiety was associated with significantly increased recurrence of VM (Formeister et al, 2018) and motion sickness could enhance motion intolerance (Wang and Lewis, 2016).…”

Purkinje cells of vestibulocerebellum play an important role in acute vestibular migraine

“…VM is closely related to motion sickness, with vestibular symptoms being the main clinical manifestation. Possible mechanisms include: (i) Abnormal integration of semicircular canal and otolith system activity in patients with vestibular migraine; (ii) Symptoms such as nausea, dizziness, and headache of VM and motion sickness may share the same brainstem neural circuit; (iii) There are extensive connections between the caudal part of the trigeminal spinal tract nucleus and the vestibular nuclei (Cuomo-Granston and Drummond, 2010;Diagne et al, 2006;Lewis et al, 2011;Wang and Lewis, 2016).…”

Cybersickness: a Multisensory Integration Perspective

“…While the underlying basis for sensory conflict-based models remains debated, empirical evidence for the involvement of sensory conflicts in motion sickness induced by physical movement (i.e., sea-sickness, car-sickness) highlights their contribution to the development of sickness symptoms (Kato and Kitazaki 2008;Wang and Lewis 2016;Wada and Yoshida 2016). The specific evidence for visuo-vestibular conflicts in cybersickness is growing, suggesting that the strength of the sensory conflict between visual and vestibular cues can lead to increased sickness (Bonato et al 2009;Nishiike et al 2013).…”