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Specific marker of neurodegeneration in optic neuritis

Poster Details

First Author: G.Khamraeva UZBEKISTAN

Co Author(s):    H. Kamilov   M. Kasimova           

Abstract Details


To estimate prognostic importance of the neuron-specific enolase (NSE) in the blood serum and tears in diagnosis of the optic neuritis.


Tashkent Institute of Postgraduate Medical Education, Tashkent, Uzbekistan


Standard ophthalmological methods (visometry, tonometry, perymetry for colours, ophthalmoscopy), special methods of investigation: magnetic resonance imaging (MRI) of the brain and orbita with tractography, optic coherent tomography (OCT) (Zeiss, Spectral Domain Technology), examination of the visual evoked potentials (VEP) (Neuron-spectrum 4-VPM), colorimetric analysis of the fundus of eye. The collection of lacrimal fluid (LF) (0.15 ml) was made with the help of canule from the lacrimal lake and inferior conjunctival fornix without touching conjunctiva and cornea. The collection of blood was made from the elbow vein in quantity 5 ml and was centrifuged for the serum isolation. The collected samples of tear and blood serum (BS) were inserted into the test-tube and were sent immediately for testing. The level of NSE in tear and BS were measured by standard technique on the automatic electrochemiluminescent immunoanalyzer Cobas e 411 for chemiluminescent immunoanalysis (Roche Diagnostics, Switzerland).


The analysis of the results of NSE investigation showed significant changes of this parameter depending on the stage of pathological process. The normal NSE parameter was 15.7-17.0 ng/ml. In 19 eyes with hyperemia OND the parameter NSE in the tears accounted for, on the average, 0.92±0.16 ng/ml (p<0.05), in 6 eyes with expressed hyperemia and OND edema the parameter NSE was 8.25±0.20 ng/ml. In the BS the parameter was, on the average, 13.67 ± 1.44 ng/ml, at norm 15.7-17.0 ng/ml. Thus, at the initial stages of ON the parameter of NSE was reduced in comparison with norm 18 times (p<0.05). During progression of disease the parameter NSE raised considerably, but nevertheless, it remained below than norm 2.2 times (p<0.05). Hence, at the stage of hyperemia and swelling of OND the parameter NSE reduced below than norm in the LF, but in the BS it remained within the limits of normal variables, that prove diagnostic value of the used method. In the second group the parameter NSE increased in the LF and accounted for, on the average, 19.86±3.84 ng/ml. Thus, at ischemic and atrophic-gliosis stage of disease this parameter raised considerably in the LF.


The parameter of NSE in LF in the first group was lower than norm 4.29 times (p<0.05). On all probability, it is caused by increase in hypoxia and intensification of the glicolisis process in the neural cells. In the second group in the patients with ON at the stage of transition into atrophy of OND the parameter of NSE increased 1.43 times (p<0.05), probably, it was connected to the beginning destructive processes in the neural tissue with gradual destruction of neurons at neurodegeneration, that results in the output of NSE from the damaged cells into the extracellular space. The level NSE allows finding out depth and intensity of structural and functional disorders of biomembranes in increase of this parameter. The comparative analysis has shown the rather increased level NSE at ON at the stage of transition into atrophia in comparison with the acute form of disease. The analysis of NSE at the patients with ON is the informative diagnostic criterion of the evaluation of neuronal damage of the optic nerve. The definition of NSE in the lacrimal fluid should be included into the complex examination of the patients with ON as additional marker of the inflammatory process available already at the early stages. FINANCIAL INTEREST: NONE

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