Disrupted topological organization of white matter structural networks in high myopia patients revealed by diffusion kurtosis imaging and tractography.

INTRODUCTION

High myopia (HM) is a public health issue that can lead to severe visual impairment. Previous studies have exhibited widespread white matter (WM) integrity damage in HM patients. However, how these WM damages are topologically related, and the network-level structural disruptions underlying HM has not been fully defined. We aimed to assess the alterations of brain WM structural networks in HM patients using diffusion kurtosis imaging (DKI) and tractography in the present study.

METHODS

Individual whole-brain and ROI-level WM networks were constructed using DKI tractography in 30 HM patients and 33 healthy controls. Graph theory analysis was then applied to explore the altered global and regional network topological properties. Pearson correlations between regional properties and disease duration in the HM group were also assessed.

RESULTS

For global topology, although both groups showed a small-world network organization, HM patients exhibited significant decreased local efficiency and clustering coefficient compared with controls. For regional topology, HM patients and controls showed highly similar hub distributions, except for three additional hub regions in HM patients including left insula, anterior cingulate and paracingulate gyri (ACG), and median cingulate and paracingulate gyri (DCG). In addition, HM patients showed significantly altered nodal betweenness centrality (BC) mainly in the bilateral inferior occipital gyrus (IOG), left superior occipital gyrus (SOG), caudate nucleus, rolandic operculum and right putamen, pallidum, and gyrus rectus compared with controls. Intriguingly, the nodal BC of left IOG was negatively correlated with disease duration in HM patients.

DISCUSSION

Our findings suggest that HM exhibited alterations in WM structural networks as indicated by decreased local specialization. This study may advance the current understanding of the pathophysiological mechanisms underlying HM.