Lateralization of visuospatial attention

Background: Lateralization of visuospatial attention, referred as pseudoneglect manifests as a mostly leftward attentional bias in healthy people, and is stablished by the lateralized activation of attentional network. Due MS, the forming lesions in white matter and the atrophy affecting the gray matter alters patient’s cognitive ability. Objectives: In this thesis, we aim to demonstrate how invariant the visuospatial attention in healthy people is, and how the brain laterization on microstructural level contributes to the behavioral manifestation. Furthermore, we set out to reveal how visuospatial attention differs in MS patients, and what structural brain alterations can be identified in association with the behavior. Methods: In Study 1, tract-based spatial statistics was used to investigate how lateralization of white matter microstructure, characterized by fractional anisotropy, associated with visuospatial attentional bias in 20 healthy controls. Structural connectivity of white matter tracts associated with the extent and lateralization of visuospatial attentional bias was also investigated. In addition, healthy subjects performed Landmark task on three consecutive days in order to measure the reproducibility of pseudoneglect. In Study 2, Fierro scores of 35 multiple sclerosis patients and 20 healthy controls were compared. Using voxel-based morphometry and lesion-symptom mapping, we aimed to identify the structural background of the altered attentional bias in MS patients. Association between visuospatial attention and clinical or cognitive scores of MS patients were also analyzed. Results: In Study 1, the integrity of white matter microstructure in parietal lobe significantly correlated (p<0.05) with the visuospatial attentional bias in healthy controls. The more the parietal white matter was integrated in one hemisphere, the more lateralized and extended the visuospatial attention to the contralateral side was. The significant parietal clusters showed connectivity towards the dorsal and ventral nodes of the attentional network. Furthermore, our results revealed good-excellent reproducibility of the attentional bias in healthy patients (ICC=0.74). In our second study, we found that the variability of visuospatial attention differed in MS patients compared to healthy controls (F(34,25)=2.18, p=0.04). Our lesion-symptom mapping analysis showed that lesion probability in the superior longitudinal fascicle in the left hemisphere is associated with the leftward shift of visuospatial attention (p<0.05). There was no significant correlation between gray matter atrophy nor the clinical as well as cognitive scores and the visuospatial attentional bias. Conclusions: Our work revealed that visuospatial attentional bias in healthy people is highly consistent over time. Due this consistency we hypothesed that the microstructural correlates of visuospatial attention can be identified. The positive correlation found in the parietal white matter between the individual bias and the microstructural integrity supported our hypothesis. In our second study we set up to reveal whether visuospatial attentional bias alters due the damaged white matter integrity in MS patients. We found that the variability of attentional bias is higher in MS patients compared to healthy controls, and this increased variability is associated with the presence of lesions located in the superior longitudinal fascicle. Our results might be substantial in order to understand how visuospatial attention functions, and how alterations in healthy brain structure and lateralization affect visuospatial attention.