Abstract

PurposeTo estimate and compare cerebral cortex thickness in patients with unilateral end-stage glaucoma with that of age-matched individuals with unaffected vision.Methods14 patients with unilateral end-stage primary open angle glaucoma (POAG) and 12 age-matched control individuals with no problems with vision were selected for the study based on detailed ophthalmic examination. For each participant 3D high-resolution structural brain T1-weighted magnetization prepared MR images were acquired on a 3.0 T scanner. Brain cortex thickness was estimated using the FreeSurfer image analysis environment. After warping of subjects' cortical surfaces to FreeSurfer common space, differences between POAG and control groups were inferred at the group analysis level with the General Linear Model.ResultsThe analysis performed revealed local thinning in the visual cortex areas in the POAG group. Statistically significant differences form 600 mm2 clusters located in the Brodmann area BA19 in the left and right hemisphere.ConclusionUnilateral vision loss due to end-stage neuropathy from POAG is associated with significant thinning of cortical areas employed in vision.

Highlights

  • According to the current definition the term glaucoma describes a group of diseases that involve optic neuropathy determined by characteristic structural change and functional deficit related to the loss of retinal ganglion cells (RGC) which originate in axons that exit the eye and form the optic nerve

  • In the retina glaucoma selectively affects the layer of RGC, post-mortem histology has revealed that signs of neurodegeneration and associated metabolic changes are not restricted to RGC and the optic nerve, but encompass upstream parts of the central visual pathway including visual cortex

  • Gupta et al [5] reported in the brain of a patient with advanced glaucoma and 50% visual field loss the evidence of degenerative changes in the brain involving the intracranial optic nerve, lateral geniculate nucleus, and visual cortex

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Summary

Introduction

According to the current definition the term glaucoma describes a group of diseases that involve optic neuropathy determined by characteristic structural change and functional deficit related to the loss of retinal ganglion cells (RGC) which originate in axons that exit the eye and form the optic nerve. The most prevalent type is primary open-angle glaucoma (POAG), distinguished by late onset (typically after the age of 60) and slow progression over months to years. This type of disease is frequently unilateral, and even in the absence of treatment only a minority of patients develop bilateral blindness [1]. Gupta et al [5] reported in the brain of a patient with advanced glaucoma and 50% visual field loss the evidence of degenerative changes in the brain involving the intracranial optic nerve, lateral geniculate nucleus, and visual cortex. Application of various neuroimaging methods (such as T2weighted imaging, diffusion tensor imaging, functional magnetic resonance and magnetic resonance spectroscopy) to studies of glaucoma patients brains provided further confirmation for involvement of the entire visual pathway in patients suffering of glaucoma, in particular in the advanced stage (see [6,7,8,9,10] and reviews [11,12])

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