THE PATHOGENIC ASPECTS OF TRAUMATIC OPTICAL NEUROPATHY’S NEUROPROTECTIVE THERAPY

The dissertation presents theoretical generalization and new solution of the actual scientific problem, which consists in establishing the features of vegetative humoral regulation in the dynamics of the development of forms of traumatic optical neuropathy in clinical and experimental conditions, as well as the improvement of neuroprotective treatment. The development of inflammatory reactions is one of the major components of the secondary mecha-nisms of damage, which in the initial period is aimed at limiting the primary lesion and cannot be compensated by the appointment of vasodilator therapy, since it pro-motes the spread of inflammatory and toxic mediastinal neurovironirons due to impaired vascular permeability and barrier functions of natural membranes. In connec-tion with the above, the use of high doses of Methylprednisolone, which blocks such reactions, as they stabilize cell membranes (reducing extracellular edema and inflammatory reactions), have antioxidant and neuroprotective effects, whose effectiveness is di-rectly proportional to 300 doses, is justified. However, under these conditions, the toxicity of the drug with possible lethal consequences is increased in patients with severe combined brain damage. Against this background, it is important to improve understanding of the potential benefits and risks of steroids for optical neuropathy in patients with head injuries. This is the reason for the search for alternative treatments to reduce the negative effects of the traditional method. Therefore, a more detailed study of the pathogenetic mechanisms of development and, on their basis, the development of new therapies for the treatment of TON with improvement of recovery processes and reduction of toxic effects remains relevant. Pathogenic mechanisms of development of ul-trastructural changes of the retina under the treatment of traumatic optic neuropathy, which was modeled in 90 rabbits, treated with a 30 mg / kg dose of methylprednisolone and 15 mg / kg in combination with phosphine-electrical stimulation with a force of 800 m, were studied. on the defeat side and 300 mA on the opposite side. According to the results of the experimental re-search, it can be stated that structural changes in the retina occur in two stages: dystrophic-destructive on the 14th day (axonal degeneration of ganglionic neurons and probable thickening of the retinal layers due to disturb-ance of its hemodynamics), and on the 30th - in the 30th - atrophic (hydropic and vacuolar degeneration of gangli-onic neurons and likely reduction in the thickness of the retinal layers). The use of basic treatment contributes to the 14th day to reduce retinal edema. In the ganglionic layer, most neurons are in a state of vacuolar dystrophy and apoptosis, with compensatory-atrophic changes in neu-rons combined with axonal degeneration. After 1 month of treatment, there is a partial restoration of the morpho-logical parameters of the right retina. Compensatory-atrophic changes were observed in ganglionic neurons, and phenomena of axonal degeneration were observed in some nerve fibers. When using the first combination treatment we used, the histological-ultrastructure of the retina and its morphometric parameters approach the intact group of animals.