ABSTRACT
Title
Brain involvement in glaucoma
Authors
C. Nucci
Ophthalmic Unit, Department of Biopathology and Diagnostic Imaging
University of Rome “Tor Vergata”, Rome Italy
Ophthalmic Unit, Department of Biopathology and Diagnostic Imaging
University of Rome “Tor Vergata”, Rome Italy
Abstract
Evidence indicate that glaucoma involvement is not limited to the retinal ganglion cells and their axons, but that it also extends to the central visual pathway. In particular, atrophic degeneration with neuronal cells shrinkage has been described in the lateral geniculate nucleus (LGN) and in the visual cortex of monkeys with experimentally induced ocular hypertension. To address this point in humans, we evaluated the use of diffusion-tensor magnetic resonance imaging (DTI) in patients with glaucoma. Interestingly, we observed that glaucoma stages classified according to the severity of the visual field deficits displayed clear correlation with the diffusion tensor imaging parameters obtained at the level of the optic nerves, thus confirming the strong link between functional impairment of the retina and ultrastructural damage to the optic nerve axons. But the DTI examination also documented glaucomatous involvement of the optic radiations, the fibers that connect the LGN to the visual cortex. So our findings provide the first documented evidence of brain changes in patients with glaucoma.
The pathogenetic mechanisms underlying glaucomatous involvement of central areas are not known. Evidence support the hypothesis that the onset and progression of neuronal damage is linked to increases in intraocular pressure with consequent brain anterograde spread. However, our studies on patients with Alzheimer disease or with vascular perfusion deficits suggest that some cases of glaucoma are manifestations of neurodegenerative processes at the central level or of widespread perfusion deficits, the effects of which are simply aggravated by the additional stress of ocular hypertension.
The pathogenetic mechanisms underlying glaucomatous involvement of central areas are not known. Evidence support the hypothesis that the onset and progression of neuronal damage is linked to increases in intraocular pressure with consequent brain anterograde spread. However, our studies on patients with Alzheimer disease or with vascular perfusion deficits suggest that some cases of glaucoma are manifestations of neurodegenerative processes at the central level or of widespread perfusion deficits, the effects of which are simply aggravated by the additional stress of ocular hypertension.