Cortical thickness in human V1 associated with central vision loss.

Wesley K Burge,Kristina M Visscher,Dawn K Decarlo,Rodolphe Nenert,Lawrence W Ver Hoef,Abdurahman Elkhetali,Lesley A Ross,Joseph C Griffis

doi:10.1038/srep23268

Abstract

Better understanding of the extent and scope of visual cortex plasticity following central vision loss is essential both for clarifying the mechanisms of brain plasticity and for future development of interventions to retain or restore visual function. This study investigated structural differences in primary visual cortex between normally-sighted controls and participants with central vision loss due to macular degeneration (MD). Ten participants with MD and ten age-, gender-, and education-matched controls with normal vision were included. The thickness of primary visual cortex was assessed using T1-weighted anatomical scans, and central and peripheral cortical regions were carefully compared between well-characterized participants with MD and controls. Results suggest that, compared to controls, participants with MD had significantly thinner cortex in typically centrally-responsive primary visual cortex – the region of cortex that normally receives visual input from the damaged area of the retina. Conversely, peripherally-responsive primary visual cortex demonstrated significantly increased cortical thickness relative to controls. These results suggest that central vision loss may give rise to cortical thinning, while in the same group of people, compensatory recruitment of spared peripheral vision may give rise to cortical thickening. This work furthers our understanding of neural plasticity in the context of adult vision loss.

Highlights

Better understanding of the extent and scope of visual cortex plasticity following central vision loss is essential both for clarifying the mechanisms of brain plasticity and for future development of interventions to retain or restore visual function
Macular degeneration (MD) causes central retinal lesions, resulting in a loss of central vision essential for everyday activities that require high visual acuity, for example reading or recognizing faces[2]. This central vision loss can be devastating for MD patients, many learn to rely on their spared peripheral vision to compensate for central vision loss to perform everyday activities[3]
We first present the results from the Bar regions of interest (ROIs) that represent the upper, middle, and lower visual fields for a given eccentricity. Following this we present the results from the additional “circle” ROIs that are specific to a location along the gyrus or sulcus, to control for differences in sulcus/gyrus surface area ratios between groups in a particular ROI

Summary

Introduction

Better understanding of the extent and scope of visual cortex plasticity following central vision loss is essential both for clarifying the mechanisms of brain plasticity and for future development of interventions to retain or restore visual function. Patients with MD have decreased grey matter volume and density in the lesion projection zone – the region of primary visual cortex that receives input from the damaged macula[13,14,15].This suggests cortical atrophy resulting from loss of visual input. Interpretation of this finding is difficult because it is not known what aspects of cortical anatomy are reflected by measurements of grey matter www.nature.com/scientificreports/. We hypothesized that participants with MD, as compared to the matched controls, would (a) have thinner cortex in centrally responsive parts of V1 (e.g. lesion projection zone) following the reduced use of central vision, and (b) thicker cortex in peripherally responsive parts of V1 following the increased use of peripheral vision as a compensatory strategy for central vision loss

Methods

Results

Conclusion