Abnormal Tilt Perception During Centrifugation in Patients with Vestibular Migraine

Abstract

Vestibular migraine (VM), defined as vestibular symptoms caused by migraine mechanisms, is very common but poorly understood. Because dizziness is often provoked in VM patients when the semicircular canals and otolith organs are stimulated concurrently (e.g., tilting the head relative to gravity), we measured tilt perception and eye movements in patients with VM and in migraine and normal control subjects during fixed-radius centrifugation, a paradigm that simultaneously modulates afferent signals from the semicircular canals and otoliths organs. Twenty-four patients (8 in each category) were tested with a motion paradigm that generated an inter-aural centrifugal force of 0.36 G, resulting in a 20° tilt of the gravito-inertial force in the roll plane. We found that percepts of roll tilt developed slower in VM patients than in the two control groups, but that eye movement responses, including the shift in the eye's rotational axis, were equivalent in all three groups. These results demonstrate a change in vestibular perception in VM that is unaccompanied by changes in vestibular-mediated eye movements and suggest that either the brain's integration of canal and otolith signals or the dynamics of otolith responses are aberrant in patients with VM.

Abnormal visuo-vestibular interactions in vestibular migraine: a cross sectional study

“…Vestibular migraine patients exhibited elevated vestibular-ocular and perceptual thresholds during yaw (horizontal plane) rotations. This is in concordance with a previous finding that illustrated elevated thresholds for tilt perception during fixed-radius centrifugation in vestibular migraine patients (Wang and Lewis, 2016). Contrastingly, a separate study revealed that during dynamic roll tilt (frontal plane), vestibular migraine patients’ exhibit decreased perceptual thresholds (i.e.…”

“…Despite the pathophysiology of vestibular migraine remaining largely unknown, recent findings have provided some preliminary insights. These include reports of abnormal vestibular thresholds during tilt (Lewis et al , 2011; Wang and Lewis, 2016) and abnormal cortical interactions between visual and vestibular networks. The evidence for this latter point is provided by a neuroimaging study, which revealed altered metabolic activity in visual and vestibular cortical areas in two patients imaged during an acute episode of vestibular migraine (Shin et al , 2014).…”

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

“…Reorienting the head relative to gravity modulates activity in the semicircular canals, which encode angular head velocity, and otolith organs, which encode gravity and linear acceleration. Based on these observations, we proposed that central integration of canal and otolith signals is abnormal in VM, a hypothesis supported by our recent psychophysical studies (Lewis et al 2011a(Lewis et al , 2011bWang and Lewis 2016).…”

The Intimate Relationship between Vestibular Migraine and Meniere Disease: A Review of Pathogenesis and Presentation

“…Further evidence that VM is a disease of multisensory integration in the central nervous system was seen in a study of tilt perception in VM, migraine, and normal patients. When the 3 groups of patients sat in a centrifuge and an interaural centrifugal force was generated, the development of the perception of tilt in the roll plane was slower in the VM group compared to the other 2, but eye movement responses such as rotational axis shift were the same in all groups [ 46 ]. In other roll-type experiments, VM patients were found to have decreased motion perception thresholds when canal and otolith signals were presented simultaneously, but perception of tilt was slower when the signals were conflicting [ 47 ].…”

“…This may be a potential origin for motion sensitivity in VM patients. The authors believe that these results suggest VM is, at least in part, a result of dysfunctional vestibular signal integration and abnormal sensitization possibly of cerebellar origin [ 46 , 47 ].…”