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S.–F.G. Seidova, O.G. Panteleeva, A.M. Shamshinova; Electroretinographycal Symptoms of Thyroid–Associated Eye Disease (TAED) . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1660.
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© ARVO (1962-2015); The Authors (2016-present)
To develop hypothesis of pathogenesis of neuronal disorders in TAED based on electrophysiological findings in this disease.
60 patients with different stages of TAED aged from 14 to 67 years were studied. Full–field ERG, oscillatory potentials analysis, pattern ERG (PERG), macular ERG, multifocal ERG and ERG with 200–ms long flashes (ON– and OFF–responses) in photopic conditions were recorded.
Changes in all types of ERG responses varied depending on the stage of the disease. The amplitudes of P50, N95 components of the PERG significantly decreased (p<0.05) at subcompecated stage and were almost unreadable at decompensated stage, p<0.05. A–wave amplitude of full–field ERG and flicker ERG were significantly increased at compensated stage (p<0.05). ON– and OFF–ERG responses were normal or supernormal at the compensated stage (p<0.05) and subnormal at decompensated stage.
In TAED the PERG changes appeared to be the earliest which indicates a deterioration at the level of retinal ganglion cell layer. Observed flicker ERG changes indicating cones involvement correlate with a–wave changes of full–field ERG which in its turn indicates both cones and rods involvement. Increased volume of extraocular muscles and retrobulbar tissue due to edema and fibrosis causes both the compressive ischemia of optic nerve and central retinal artery feeding outer retina and the deterioration of the choroidal blood flow feeding the inner retina. These explain our electrophysiological findings displaying damage/cell loss at the level of both retinal photoreceptors and ganglion cells. Supernormal ERG in early TAED may develop due to a complex of reasons: 1) metabolic disorder with excretion of toxic factors; 2) lack of deactivating influence of centrofugal neurofibers due to the optic nerve ischemia; 3) activation, hypertrophy and hyperplasia of Muller cells as a response on hypoxy; 4) affected neuro–humoral regulation of phototransduction. Thus, we propose that along with the optic nerve ischemia, the deteriorations in the retina largely contribute into the pathogenesis of the optic neuropathy in TAED.
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