Moyseyenko N. Neurovegetative dysfunction in mechanisms of traumatic optical neuropathy development and pathogenic background of their correction (clinical-experimental study)

The thesis is devoted to the establishing of the neurovegetative dysfunction role in development of functional, dystrophic degenerative and neuroprotective processes in the retina and optical nerve and effectiveness of corticosteroids and phosphine electrical stimulation of hypothalamus in their remodeling for traumatic optical neuropathy Our clinical-experimental researches established the mechanisms of secondary damage development of the optic nerve in traumatic optical neuropathy. It was determined that dominance of the sympathetic tonus lead to optic nerve ischemia, decrease of the liquids’ perfusion and minute volume of the intraocular fluid for two weeks after injury. Secondary pathological reactions develop for the later period (after 3 months) as its consequence The minute volume of the intraocular fluid was increased in three times (p<0,05) and contributed to the reperfusion lesions. The parasympathetic system’s predominance leaded to inflammatory reactions and swelling, ischemia and pathological for one month after the injury. These mechanisms conduced to optic nerve irreversible atrophy. Neuroprotective therapy including phosphine electrical stimulation and Methylprednisolone activated hypothalamus, balanced autonomy regulation, blocked inflammatory responses and potentiated the secretion of the neuroprotective factor, as result contributed formation of compensatory-regenerative processes. The results of our research promote more profound understanding of the traumatic optical neuropathy pathogenesis. This determines the state of vegetative and humoral dysfunction, and to optimal use of corticosteroids and phosphine electrical stimulation combination in neuroprotective treatment.