AbstractGlaucoma is a leading cause of irreversible vision loss. The study of structural and neurophysiological processes of the upper divisions of the visual analyzer in patients with primary glaucoma helps in detecting primary structural lesions in this pathology. The investigation of brain evoked potentials provides the most important information about the processes in the visual cortex of the brain, and the study of visual evoked potentials (VEP) provides us with the most valuable information. When performing a comparative evaluation of VEP responses for each eye good correlation between the obtained VEP parameters and the results of Humphrey perimetry is observed. It is well known that in clinical practice there are no specific neurophysiological tests for diagnosing glaucoma. However, neurophysiological examinations detect the changes which are asymptomatic for a remarkably long period of time until the occurrence of clinical manifestations quite often being especially important for early diagnosis of any glaucomatous process.The objective of the research was to study the appropriateness of using neurophysiological methods for early detection of primary open-angle glaucoma.Materials and methods. Complex clinical and neurophysiological study of both eyes of 186 patients (358 eyes) with primary open-angle glaucoma (POAG) and those whose diagnosis was still not clarified was performed at the Filatov Institute of Eye Diseases and Tissue Therapy of National Academy of Medical Sciences of Ukraine. The main group included 81 (51.92%) females and 75 (48.08%) males with different stages of the glaucomatous process. The average age of patients was 56.8±4.26 years. Neurophysiological methods - VEPs (both flash and checkerboard type) - were used to diagnose the pathological condition. The study of VEPs was performed using a RETI-scan multifocal ERG system (Roland Consult, Wiesbaden, Germany). Results. In patients with suspected glaucoma latency values of the N75 and P100 remained within the normal range in 96.1% (р<0.05) and 86.2% (р<0.05) of cases, respectively. When examining the N75-P100 and P100-N135 peaks an increase in the amplitude above the normal range (according to the standards of the equipment and the laboratory where the research was conducted) was observed in 78.6% (р<0.05) and 65.5% (р<0.05) of cases, respectively. The threshold for electrically induced phosphenes was within normal limits (65.61±7.32 Hz); the lability of the visual analyzer (phosphene electrical stimulation) increased by 13.63%, р<0.05 compared to the control group. In patient with mild glaucoma latency values of the N75 and P100 remained within the normal range in 86.4% (р<0.05) і 81.2% (р<0.05) of cases, respectively. When examining the N75-P100 and P100-N135 peaks an increase in the amplitude above the normal range was observed in 65.15% (р<0.05) and 58.14% (р<0.05) of cases, respectively. The threshold for electrically induced phosphenes was within normal limits (71.69±9.08 Hz); the lability of the visual analyzer (phosphene electrical stimulation) reduced by 9.63%, р<0.05 compared to the control group. In 78.4% of patients with suspected glaucoma the diagnosis of primary open-angle glaucoma was confirmed by clinical investigations 6 months and 1 year after the examination. Additional neurophysiological methods revealed more pronounced changes in the glaucomatous process in 34.80% of patients with mild glaucoma. They were included to the group of patients with advanced glaucoma. Optimal treatment tactics was applied.
Moiseenko RA, Golubchikov MV, Slabkiy GO, Rykov SA, et al. Ophthalmological care in Ukraine in 2006-2011. Kyiv. 2012;183.
Rykov SA, Vitovskaya OP, Shargorodskaya IV, et al. Unified clinical protocol of medical care. Primary open-angle glaucoma. Primary and secondary care. Clinical guidelines. Order of Ministry of Health of Ukraine No 816, (November 24, 2011). Kyiv. 2011;37.
Quigley HA, Broman A. The number of people with glaucoma worldwide in 2010 and 202o. Br.J. Ophthalmol 2006;90(3):262-267. Available from: http://bjo.bmj.com/cgi/doi/10.1136/bjo.2005.081224 PubMed PMID: 16527231. doi: 10.1136/bjo.2005.081224.
Liesegang TJ. Glaucoma: changing concepts and future directions. May. Clin. Prac 1996;71(7):689-694. Available from: http://www.diseaseinfosearch.org/result/3065 PubMed PMID: 8656711. doi: 10.1016/S0025-6196(11)63007-3.
Alekseev V, Gаzizova I. Meaning of neurodegeneration in the pathogenesis of glaucoma.11th EGS Congress. Nice. 2014;60.
Shamshynova AM, Andreeva TM. Clinical physiology of vision. Moscow. 2006; 956.
Stotska LM, Stotska LS. Peculiarities of activity of chromatic visual channels in different stages of primary glaucoma. Oftalmol. Zhurn. 2013;6:22-25.
Zavgorodnyaya NV, Pasechnikova NV. Primary glaucoma. New look at an old problem. Zaporizhzhia. 2010;192.
Valladares AM, Amoros NP, Cortes AC, Morollon JP, Moreno IF. Validity of ganglion cell-inner plexiform layer thickness measurement in the diagnosis of preperimetric glaucoma: correlation with retinal nerve fiber layer thickness. Glaucoma Unit of Albacete. Albacete. Spain.11th EGS Congress. Nice. 2014;133.
Kachan TV, Marchenko LN, Birich TA, Dalidovich AA, Mushtina TA, Verenich AM. Comparative evaluation of optical coherence tomography and scanning laser polarimetry in the diagnosis and monitoring of optic neuropathy in patients with glaucoma. Oftalmologiya. Vostochn. Yevropa. 2014;4(23):186-190.
Wu De Zheng, Liu Yan. Atlas of testing and clinical application for Roland Electrophysiological Instrument. Beigind science and technology. Press. China. 2006;5-19.
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.