Abstract
PurposeTo analyze the correlation between structural characteristics of intraorbital optic nerve (ION) and lateral geniculate nucleus (LGN) measured by 3-Tesla magnetic resonance imaging (3T MRI), and the severity of glaucomatous damage.MethodsIn this cross-sectional study, 41 glaucoma patients and 12 age- and sex-matched controls underwent standard automated perimetry (SAP) and frequency doubling technology (FDT) as functional evaluation; optic disc stereophotograph, spectral-domain optical coherence tomography (OCT) and confocal scanning laser tomography as ocular structural evaluation; and 3T MRI. Structure-structure and structure-function correlation were performed using bootstrap resampling method for clustered data.ResultsThe ION mean diameter and cross-sectional area were different between glaucoma and control groups at 5mm and 10mm (all, p≤0.011) from the globe, but not at 15mm (both, p≥0.067). LGN height was significantly lower in glaucoma group (p = 0.005). OCT rim area and functional parameters (SAP and FDT) correlated significantly with all ION segments, showing stronger correlations at 10 and 15 mm. ION parameters at 10 and 15 mm presented mild-to-moderate correlation with OCT peripapillary nerve fiber layer thickness, and ION at 15mm had mild association with the neuroretinal rim area on stereophotographs. Although LGN height was significantly smaller in glaucoma group (p = 0.005), LGN parameters were not associated with any ocular structural or functional parameter.ConclusionAssessment of central and peripheral nervous systems using 3T MRI confirmed that glaucoma patients had smaller ION dimensions and LGN height compared to the control group. In general, ION dimensions presented mild to moderate correlations with functional and ocular structural parameters. Although ION had significant correlations at any distance from the eye, the ION distal locations correlated better with OCT results and functional parameters. However, LGN parameters were not associated with functional or ocular structural parameters.
Highlights
lateral geniculate nucleus (LGN) height was significantly smaller in glaucoma group (p = 0.005), LGN parameters were not associated with any ocular structural or functional parameter
Assessment of central and peripheral nervous systems using 3-Tesla magnetic resonance imaging (3T Magnetic resonance imaging (MRI)) confirmed that glaucoma patients had smaller intraorbital optic nerve (ION) dimensions and LGN height compared to the control group
Results from 3T MRI showed that the mean diameter and cross-sectional area of the ION were significantly different between glaucoma and control groups at 5 mm and 10 mm behind the globe, but not at 15 mm
Summary
Glaucoma is a degenerative optic neuropathy characterized by progressive loss of retinal ganglion cells and their axons, resulting in characteristic changes at the optic nerve head (ONH) and correspondent visual field loss.[1, 2] Previous research in experimental and human glaucoma demonstrated degeneration of structures from the anterior visual pathway, including the optic nerve and the lateral geniculate nucleus (LGN).[3,4,5,6,7,8,9,10,11]In the anterior visual pathway, there are different types of retinal ganglion cells that comprise separate paths and are named according to their targets in the LGN. Glaucoma is a degenerative optic neuropathy characterized by progressive loss of retinal ganglion cells and their axons, resulting in characteristic changes at the optic nerve head (ONH) and correspondent visual field loss.[1, 2] Previous research in experimental and human glaucoma demonstrated degeneration of structures from the anterior visual pathway, including the optic nerve and the lateral geniculate nucleus (LGN).[3,4,5,6,7,8,9,10,11]. Glaucoma leads cells from both magnocellular and parvocellular visual pathways to atrophy, some investigators suggested a preferential damage of larger axons in the optic nerve in experimental glaucoma, [5, 6] and a more prominent cell loss was reported on magnocellular than on parvocellular layers of the LGN.[9, 10] such alterations at the LGN were not confirmed by other researchers,[13] whether one of those pathways is preferentially affected in living human glaucoma still remains controversial
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