Abstract

Objective: Vestibular migraine (VM) is one of the most common causes of recurrent vertigo, but the neural mechanisms that mediate such symptoms remain unknown. Since visual symptoms and photophobia are common clinical features of VM patients, we hypothesized that VM patients have abnormally sensitive low-level visual processing capabilities. This study aimed to investigate cortex abnormalities in VM patients using visual evoked potential (VEP) and standardized low-resolution brain electromagnetic tomography (sLORETA) analysis.Methods: We employed visual stimuli consisting of reversing displays of circular checkerboard patterns to examine “low-level” visual processes. Thirty-three females with VM and 20 healthy control (HC) females underwent VEP testing. VEP components and sLORETA were analyzed.Results: Patients with VM showed significantly lower amplitude and decreased latency of P1 activation compared with HC subjects. Further topographic mapping analysis revealed a group difference in the occipital area around P1 latency. sLORETA analysis was performed in the time frame of the P1 component and showed significantly less activity (deactivation) in VM patients in the frontal, parietal, temporal, limbic, and occipital lobes, as well as sub-lobar regions. The maximum current density difference was in the postcentral gyrus of the parietal lobe. P1 source density differences between HC subjects and VM patients overlapped with the vestibular cortical fields.Conclusion: The significantly abnormal response to visual stimuli indicates altered processing in VM patients. These findings suggest that abnormalities in vestibular cortical fields might be a pathophysiological mechanism of VM.

Highlights

  • Vestibular migraine (VM) is one of the most common conditions contributing to recurrent vertigo and afflicts up to 1% of the whole population with female predominance (Russo et al, 2014)

  • The mechanisms underlying abnormal visual evoked potentials (VEPs) responses to visual stimulation in patients with VM are currently unknown, but we know that the P1 source density differences between healthy control (HC) subjects and VM patients overlapped with the vestibular cortical fields (Figures 3, 4)

  • We found that the P1 source density differences between HC subjects and VM patients overlapped with the vestibular cortical fields

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Summary

Introduction

Vestibular migraine (VM) is one of the most common conditions contributing to recurrent vertigo and afflicts up to 1% of the whole population with female predominance (Russo et al, 2014). Typical signs of VM include a heightened sensitivity to head motion or visual stimuli, spatial misperceptions, and/or sudden feelings of lopsidedness or tilt. These symptoms often severely limit daily functioning in VM patients. Different from typically brief migraine auras, VM symptoms can last from hours to several days (Beh, 2019). Despite well-defined diagnostic criteria, like those proposed by the Bárány Society and the Migraine Classification Subcommittee of the International Headache Society (Lempert et al, 2012), VM pathophysiology is still unclear and remains controversial. While it is agreed that genetic, epigenetic, and environmental factors are probably involved in VM progression, there is an ongoing dispute concerning whether its primary origin is central or peripheral (Espinosa-Sanchez and Lopez-Escamez, 2015)

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