DYNAMICS OF THE COURSE OF RETINITIS PIGMENTOSA IN A CHILD WITH MACULAR INVOLVEMENT OVER 6 YEARS.

Purpose: The purpose of this work was to describe retinitispigmentosa involving themaculain a child with a follow-upof6years.Methods: Casereport.Results: Over 6 years, the child exhibited an expansion of thelesionareaofthecentralretina.Onopticalcoherencetomography (OCT), there is a sharp thinning of the centralregion of the retina with pathology of the photoreceptorandpigmentlayers.Conclusion: In some cases of retinitis pigmentosa, there arechangesinthemacula,characteristicofthedryformofmaculardegeneration; in other cases, there are cysts associatedwith cystoid macular oedema; and in other cases, there is amacularhole.Inourcase,therewasanatrophiclesionofthemacula,characteristicofthedryformofage-relatedmaculardegeneration. Apparently, such involvement of the macula inthe process is typical for children with early progression of thedisease.

MACULAR DETACHMENT IN MORNING GLORY SYNDROME

Purpose:Thepurposeofthisstudyistoreportauniquecaseofmorning glorysyndrome.Methods: This study included ophthalmologic examination, opticalcoherencetomography and areviewoftherelevantliterature.Result: A 7-year-old girl with a history of morning glory syndromewas periodicallyexamined in ourclinic for5 years. Suddenly,shepresentedwiththecomplaintofdecreasedvision.Examinationsrevealed macular detachment. The visual field of the affected eye wassignificantly narrowed. OCT also revealed the presence of a fibrouscord in the centreof the optic nerve, which protruded into the vitreousbody.Discussion:Morningglorysyndromeis anuncommoncongenitaldisordercharacterizedbyawidelyenlargedpapillathatispink-orangeincolour,witha small glial tuft in thecentre. The retinalvessels are arranged radially in relation to the papilla. A pigmentedring surrounds the excavation. The incidence is not well known. Theeffectisgenerallyunilateral.Thissyndromemanifestsasopticatrophy. However, the atrophy does not progress. Visual impairmentsometimes occurs when maculardetachmentarises,as occurred inourpatient.After5yearsofobservation,ourpatient’svisiondramatically worsened as a result of macular detachment. There arevarious theories for the development of macular detachment in MGS:exudative, tractionand rhegmatogenous8.Nobreakwasfound inourpatient,sothecauseofthedetachmentwasmostlikelytheinflammatoryprocess

CLINICAL CASE OF SEVERE INTENSIFICATION OF BLOOD FLOW IN THE CONJUNCTIVA OF THE EYEBALL ONE DAY PRIOR TO THE ONSET OF INTERMEDIATE UVEITIS

Purpose: A clinical case is presented of posterior uveitis inapatientwhoreceivedasubconjunctivalinjectionofKenalog. This finding was revealed during the course of adailyassessmentofconjunctivalmicrovascularhemodynamics.Methods:Slitlampbiomicroscopyoftheconjunctivalmicrovasculaturewasperformedbeforeandaftertheemergenceofintermediateuveitisina28-year-oldman.Result: A case of acute vision loss and the occurrence ofintermediate uveitis of the right eye is described in a patientwhopreviouslyreceivedKenalogadministeredsubconjunctivally to treat mild anterior uveitis, which waswithoutvisualimpairment.Dailymonitoringoftheconjunctival microvasculature revealed that the blood flowrate of the right eye considerably increased after Kenalogadministrationthedaybeforepatientvisiondeterioratedand posterioruveitiswithopacityofthevitreousbodyoccurred.The extent of the pronounced intensification ofblood flow wassurprising.Conclusion:The emergence ofacute intermediate uveitisfollowing Kenalog administration was preceded by a severeincrease in bloodcirculation in theconjunctivalvesselsofthe eye, which decreased one day after a severe decrease invisualacuity. It is suggested that this increase in blood flowprecedingpathologymaybeacharacteristicofanyinflammatoryprocessthatoccursinthehumanbody

A TYPICAL FEATURES IN IRVAN SYNDROME DEMONSTRATED ON MULTIMODAL IMAGING

Purpose:Thepurposeofthis workwastodescribeidiopathicretinalvasculitis,aneurysms,andneuroretinitis(IRVAN)syndrome ina32-year-oldmale.Methods: Casereport.Case report: A 32-year-old male presented with acute visualdisturbance. Multimodal imaging revealed retinal vasculitis,aneurysmsandneuroretinitisinadditiontovitreousinflammation,retinalischemiaandepiretinalmembrane.Opticalcoherencetomographyangiography(OCTA)demonstratedmultiplemicroaneurysm inbotheyes.Conclusion: Multimodal imaging was helpful in diagnosinganddifferentiatingIRVANsyndromefromothersimilar-lookingclinicalentities.Retinalaneurysmsandretinalischaemiaweredetectablebyfundusfluoresceinangiography(FFA). However, OCTA showed multiple microaneurysmsthatwerenotclearlydifferentiablebyFFAbecauseofvitreousinflammationandvascularleakage.MicroaneurysmsinIRVAN syndrome area previously unreportedobservation.OCTAmayhelpdetectthesechangeswithaccuratedetails

AGING OF SOMATIC CELLS AS AN EXAMPLE OF STRUCTURAL CHANGE IN THE VITREOUS BODY WITH AGE

Purpose:Based on the literature review and previous data, an analogy is drawn between the structure of the vitreous body and somatic cells. A comparison is made between changes in the vitreous body with age and the aging of somatic cells. Methods: A review of the literature and hypotheses. Results(Hypothesis): With age, the amount of hyaluronic acid and microfibrils decreases and the volume of “empty space” increases, leading to the collapse of the vitreous body and a complete detachment. Let us imagine the vitreous body as a giant cell with a central nucleus. The cytoskeleton permeates the entire cell. The cytoskeleton provides a structural framework for the cell, serving as a framework that determines cell shape and the general organization of the cytoplasm. Importantly, the cytoskeleton is much less rigid and permanent than its name implies. We see the same thing in the microfibrils of the vitreous body.Conclusion:With age, the density of the fibrillarstructure of the vitreous body decreases. This structure is apparently, is an evolutionary intracellular formation that formed as a result of the apoptosis of the mesenchymal cells that form the primary vitreous body. An analogy is drawn between the loss of the density of fibrils of the vitreous body and the density of the cytoskeleton of asomatic cell. The loss of the cytoskeleton of a cell is a fatal process that cannot be stopped. The cytoskeleton cannot hold the nucleus in the center of the cell, whichis why the nucleiof theoldercells are not in the center, but are shifted to the periphery.