Abstract
BackgroundVestibular patients occasionally report aggravation or triggering of their symptoms by visual stimuli, which is called visually induced dizziness (VID). These patients therefore experience dizziness, discomfort, disorientation and postural unsteadiness. The underlying pathophysiology of VID is still poorly understood.ObjectiveThe aim of the current explorative study was to gain a first insight in the underlying neural aspects of VID.MethodsWe included 10 VID patients and 10 healthy matched controls, all of which underwent a resting state fMRI scan session. Changes in functional connectivity were explored by means of the intrinsic connectivity contrast (ICC). Seed-based analysis was subsequently performed in visual and vestibular seeds.ResultsWe found a decreased functional connectivity in the right central operculum (superior temporal gyrus), as well as increased functional connectivity in the occipital pole in VID patients as compared to controls in a hypothesis-free analysis. A weaker functional connectivity between the thalamus and most of the right putamen was measured in VID patients in comparison to controls in a seed-based analysis. Furthermore, also by means of a seed-based analysis, a decreased functional connectivity between the visual associative area and the left parahippocampal gyrus was found in VID patients. Additionally, we found increased functional connectivity between thalamus and occipital and cerebellar areas in the VID patients, as well as between the associative visual cortex and both middle frontal gyrus and precuneus.ConclusionsWe found alterations in the visual and vestibular cortical network in VID patients that could underlie the typical VID symptoms such as a worsening of their vestibular symptoms when being exposed to challenging visual stimuli. These preliminary findings provide the first insights into the underlying functional brain connectivity in VID patients. Future studies should extend these findings by employing larger sample sizes, by investigating specific task-based paradigms in these patients and by exploring the implications for treatment.
Highlights
A fundamental characteristic of mammals and humans is the ability to maintain gaze stabilization and postural control in normal⁎ Corresponding author at: Antwerp University Research Centre for Equilibrium and Aerospace (AUREA), Department of Biomedical Physics, University of Antwerp, Groenenborgerlaan 171, 2020 Antwerpen, Belgium.A
Chronic vestibular symptoms triggered by an acute vestibular disorder can manifest as chronic subjective dizziness (CSD) (Staab et al, 2004; Staab and Ruckenstein, 2005) or phobic postural vertigo (PPV) (Brandt, 1996; Kapfhammer et al, 1997), of which the former is characterized by increased sensitivity to visual motion (Staab and Ruckenstein, 2005)
The results showed decreased functional connectivity in the right central operculum in visually induced dizziness (VID) patients, while an increased functional connectivity was found in the occipital pole (Table 2; Fig. 1)
Summary
Vestibular patients occasionally report aggravation or triggering of their symptoms by visual stimuli, which is called visually induced dizziness (VID). These patients experience dizziness, discomfort, disorientation and postural unsteadiness. By means of a seed-based analysis, a decreased functional connectivity between the visual associative area and the left parahippocampal gyrus was found in VID patients. Conclusions: We found alterations in the visual and vestibular cortical network in VID patients that could underlie the typical VID symptoms such as a worsening of their vestibular symptoms when being exposed to challenging visual stimuli These preliminary findings provide the first insights into the underlying functional brain connectivity in VID patients. Future studies should extend these findings by employing larger sample sizes, by investigating specific task-based paradigms in these patients and by exploring the implications for treatment
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