High Tension Glaucoma and Normal Tension Glaucoma in Brain MRI
|Jan Lešták1,2,3*, Jaroslav TintÄra1, Martin KynÄl1, Zuzana Svatá1 and Pavel Rozsíval3|
|1JL Clinic, V HÅ¯rkách 1296/10, Prague, Czech Republic|
|2Czech Technical University in Prague, Faculty of Biomedical Engineering, Czech Republic|
|3Charles University Faculty of Medicine in Hradec Králové, Czech Republic|
|Corresponding Author :||Jan Lestak
Charles University Faculty of Medicine in Hradec Králové
E-mail: [email protected]
|Received May 10, 2013; Accepted August 23, 2013; Published August 30, 2013|
|Citation: Lešták J, TintÄra J, KynÄl M, Svatá Z, Rozsíval P (2013) High Tension Glaucoma and Normal Tension Glaucoma in Brain MRI. J Clin Exp Ophthalmol 4:291. doi:10.4172/2155-9570.1000291|
|Copyright: © 2013 Lešták J, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.|
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Introduction: Functional and structural changes of the central nervous system corresponding to high tension glaucoma (HTG) and normal tension glaucoma (NTG) were studied.
Methods: In four patient groups, 80 eyes in 40 patients were examined. First group of 30 patients had three types of HTG: 10 with primary open angle glaucoma (POAG), 10 with pigmentary glaucoma (PG) and 10 of the monitored patients had pseudoexfoliative glaucoma (PEXG). The last patient group consisted of 10 patients with NTG. Comparison of the visual field, GDx, macular volume, PERG and PVEP was performed with the control group consisting of 40 eyes in 20 healthy subjects of comparable age and refraction.
From the group of patients with HTG and NTG, we further studied functional brain changes using functional magnetic resonance imaging (fMRI). We examined 9 patients with HTG in different stages and 8 NTG patients (stage initial to medium) using fMRI with optical stimulation. Brain activations in both patient groups were compared with group of 8 healthy controls. Moreover, the size of lateral geniculate nucleus in these patients with HTG and different stages of NTG was compared.
Results: Patients with PG had the highest degree of damage of the optic pathway. In the NTG, however, the ganglion cell layer was relatively normal but significant pathological changes were found in the optic pathway. Restriction in visual cortex activation indicates that the progression of high tension glaucoma corresponded to the functional changes in the cerebral cortex. Similar behavior was not observed in patients with NTG. We also proved the reduction of lateral geniculate nucleus (LGN) in both HTG and NTG.
Conclusion: We conclude that in HTG of varied etiology, the damage occurs in the entire optic pathway. Based on our experience as well the medical literature, we think that HTG and NTG are different diseases and therefore their approach should be different.