Altered Processing of Visual Stimuli in Vestibular Migraine Patients Between Attacks: A Combined VEP and sLORETA Study

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.

Dissociation between Caloric and Video Head Impulse Tests in Dizziness Clinics

“…To date, there is extensive variability on test findings that may result from ictal/interictal testing, and duration of the condition [ 31 , 55 , 56 , 57 , 58 ]. It appears that Cal is more commonly abnormal in VM vs vHIT [ 30 , 31 , 36 , 59 , 60 , 61 , 62 ], and that patients with abnormal gains on VHIT frequently have hypofunction on Cal, which is more common than the other way around [ 60 ]. Moreover, it is not unusual to observe corrective saccades with normal gains on vHIT [ 63 ].…”

Subjective and objective responses to caloric stimulation help separate vestibular migraine from other vestibular disorders

“…Clinicians and researchers have long described symptoms of sensory sensitivity (e.g., photophobia and phonophobia), in migraine headache patients [ 5 , 29 , 33 – 35 ] and evidence suggests migraineurs show sensory dysmodulation with diminished sensory thresholds [ 36 – 39 ]. Abnormal visual processing and interictal habituation deficit have been reported on visual-evoked potential studies of migraine headache patients [ 40 – 44 ], also in VM patients [ 45 ]. Motion hypersensitivity and motion sickness is well reported in VM [ 46 – 51 ] and reduced vestibular perceptual thresholds in VM have been demonstrated with head movements [ 52 ] and using chair rotation [ 53 ].…”

What visuospatial perception has taught us about the pathophysiology of vestibular migraine

“…Regardless of the source of the central sensitization, altered activity in vestibular system can impact various perceptual functions because of the strong and extensive multimodal sensory convergence of vestibular inputs. The structural and functional changes within TPJ in VM patients provide evidence towards the involvement of these higher order neural mechanisms– in particular those that contribute to sensory integration for visuospatial functions [32,33,34 ▪▪ ]. VM patients were also found to have higher thalamic activity in response to caloric irrigation in comparison with migraine patients without aura or healthy controls [35].…”