Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
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Voxel-based morphometry of the visual-related cortex in primary open angle glaucoma.

Current Eye Research 2012 September
PURPOSE: To study changes in the morphometric characteristics of the whole brain visual-related cortex in various stages of primary open angle glaucoma (POAG) in vivo.

MATERIALS AND METHODS: Thirty POAG patients (nine early stage cases and 21 advanced-late stage cases) and 30 gender-, education-, and age-matched healthy controls were enrolled in the study. Image data were obtained with a T1 weighted three-dimensional magnetization prepared rapid acquisition gradient echo sequence (T1WI 3D MP RAGE). Voxel-based morphometry (VBM) analysis was used to assess regional differences in gray matter (GM) densities on T1WI 3D MP RAGE scans of patients versus controls.

RESULTS: Compared with controls, brain regions with GM density changes were not found in the early stage of POAG patients but were found in the advanced-late stage of POAG patients. These changes with GM density reduction were mainly located in the bilateral primary visual cortex (BA17 and BA18), bilateral paracentral lobule (BA5), right precentral gyrus (BA6), right middle frontal gyrus (BA9), right inferior temporal gyrus (BA20), right angular gyrus (BA39), left praecuneus (BA7), left middle temporal gyrus (BA21), and superior temporal gyrus (BA22). Conversely, patients showed increased GM density in BA39 near the most damaged regions. In addition, in the advanced-late stage of POAG, some reduced GM density areas were related to binocular mean defect (MD) and disease duration (ranging from r = -0.761 to r = -0.458).

CONCLUSIONS: Our results suggest that there are different types of pathogenesis at different stages of POAG. Atrophy and degeneration of the visual-related cortex existed in the dorsal and ventral visual pathways in the advanced-late stage of POAG but were not found in the early stage of POAG using VBM. Such GM density changes are likely associated with the pathogenesis of POAG.

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