Injuries to the Immature Optic Radiation Show Correlated Thinning of the Macular Ganglion Cell Layer.

Finn Lennartsson,Maria Nilsson,Olof Flodmark,Jonas Larsson,Lena Jacobson

doi:10.3389/fneur.2018.00321

Abstract

Injuries to the immature optic radiation (OR) are associated with thinning of the retinal nerve fiber layer and corresponding visual field (VF) defects. The aim of the current study was to seek evidence for causal retrograde trans-synaptic degeneration by exploring the correspondence between the localization and extension of the injury to the OR and the structure of the macular ganglion cell complex, and the relation to VF function. Seven adults (age range 18–35) with visual dysfunction secondary to white-matter damage of immaturity and six healthy adults (age range 22–33) underwent magnetic resonance imaging (MRI). Fiber tractography was used to generate the geniculate projections to the dorsal and ventral striate cortex, delineated by retinotopic functional MRI mapping. The structure of the macular ganglion cell complex was measured with optical coherence tomography. The tractography showed overlaps between the dorsal and ventral geniculo-striate projections. However, in four patients with inferior VF defects, the dorsal projections were to a large extent traversing the space normally solely occupied by ventral projections. This is consistent with structural changes to the OR and suggests of re-organization upon injury. Diffusion parameters were significantly different between patients and controls, and most pronounced in the dorsal geniculo-striate projections, with a pattern indicating primary injury. The macular ganglion cell complex was significantly thinner in the patients and most pronounced in the superior sectors; a pattern particularly evident in the four patients with inferior VF defects. The ratio of the mean thickness of the macular ganglion cell complex in the superior and inferior sectors significantly correlated with the axial and mean diffusivities in the contra- and ipsilateral dorsal striate projections. The results suggest a causal link between injuries to the superior portion of the immature OR and secondary thinning in the macular ganglion cell complex, resulting in inferior VF defects.

Highlights

Injury to the brain has become the most common cause of visual impairment in children in high-income countries [1]
Brain lesions acquired during the early third trimester, 24–34 gestational weeks, can be referred to as white-matter damage of immaturity (WMDI) [3], as they either occur in the preterm newborn or in utero and most frequently affect to the periventricular white matter [4]
WMDI is best detected with magnetic resonance imaging (MRI) [6], subtle lesions may only be detected on diffusion-weighted MRI [7, 8]

Summary

Introduction

Injury to the brain has become the most common cause of visual impairment in children in high-income countries [1]. Mitry et al [2] highlighted a more than twofold increase in the number of new blind and partial-sighted children registered in England between 1982 and 2011 This is as a result of the improved survival rates of critically ill newborns, those born preterm. The inferior VF is commonly affected as bilateral quadrantdysopias/ anopias [13], indicating bilateral injuries to the superior portions of the ORs. The severity of MRI changes of WMDI correlates with the degree of cerebral visual impairment [10]. Alterations to diffusion parameters along the OR indicate progressive maturation up until term [18] and are related to early visual function [18,19,20] as well as to the level of white-matter injury [21]

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Results

Conclusion