PECULIARITIES OF LAMINA CRIBROSA THICKNESS IN PATIENTS WITH DIABETIC OPTIC NEUROPATHY
Lamina cribrosa morphology is ever changing in health and disease, and its changes might cause primary optic nerve damage and secondary damage due to the decrease of blood supply and axoplasmic transport. There is no information in literature about the peculiarities of lamina cribrosa thickness in patients with diabetic optic neuropathy (DON) in vivo.
The objective was to study the morphometric changes of the lamina cribrosa and changes of its scleral canal in patients with diabetes mellitus (DM) depending on the type and stage of the diabetic optic neuropathy, and to establish the clinicopathogenetic role of lamina cribrosa morphometric changes in the development of DON.
Materials and methods. 575 patients (1150 eyes) with type II DM were examined. In addition to standard ophthalmologic methods optical coherent tomography (OCT) of the retina and optic nerve was performed. Lamina cribrosa thickness was measured with the help of SD OCT using LC_Thickness_programm.m and main_low_ noise_fi lters_programm.m, based on the adaptive compensation algorithm for eliminating a high-level noise in the deep layers of the optic nerve and improving the visualization of the posterior border of the lamina cribrosa, as well as for processing B-scan with a set of 3 digital fi lters: Butterworth Low-pass Filter inverion image, Wavelet Low-pass Filter Analysis Daubechies original and inversion image. The area of lamina cribrosa scleral canal was measured with the help of SD OCT using the LC_cut_position_programm.m for choosing the depth of measurement and LC_diameter_calculation_programm.m for improvement of the selected image by the main digital fi lters.
Results. Analyzing the results of examination, the correlation between the type and stage of DON and scleral lamina cribrosa thickness in patients with DM was revealed. An average index of lamina cribrosa thickness in patients with DM without diabetic optic neuropathy was 1.4 times higher than that of the control group; in subclinical stage of axial DON – 1.9 times higher, in initial stage – 2.1 times higher, in severe stage of axial DON and diabetic papillopathy – 2.6 times higher, in anterior ischemic DON – 2.7 times higher, in dystrophic stage – 3.1 times higher than that of the control group (303±56 μm) (р<0,001).
Conclusions. As a result of the study a thickening of scleral lamina cribrosa in average 1.9 times greater as compared to healthy persons of an appropriate age was found. In 78.9 % of eyes of the patients with DM a mild thickening of scleral lamina cribrosa (<700 μm) was observed; in 16.6 % of eyes a moderate thickening (700–900 μm), and in 3.8 % of eyes – a signifi cant thickening (<900 μm) was observed. The scientifi c data about the mechanisms of diabetic optic neuropathy were amplifi ed. A thickening of scleral lamina cribrosa was found to play an essential role in the pathogenesis of diabetic optic neuropathy.
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