Kétoldali akut látásromlással járó PRES- (posterior reversible encephalopathy) szindróma

Az alábbiakban egy preeclampsiával szövődött terhességet követően fellépő poszterior reverzibilis encephalopathia-szindróma (PRES) esetét mutatjuk be. Az akut császármetszést követő posztoperatív időszakban hirtelen fellépő, kétoldali fájdalmatlan látásvesztést panaszoló, romló tudatállapotban lévő kismamához kértek szemészeti konzíliumot. Az ágy melletti szemészeti vizsgálat során ép bulbust, ép pupillareflexeket írtunk le, amely alapján magasabb szintű agyi érintettséget valószínűsítettünk, és sürgős MRI-vizsgálatot indikáltunk. A PRES-szindrómára jellemző, hogy a hirtelen vérnyomásváltozás hatására elsősorban a parietalis és occipitalis lebenyt érintő kérgi és subcorticalis léziók alakulnak ki, amelyek látáspanaszt okozhatnak és a bemutatott esetben is a látásromlás hátterében állhattak. A korai felismerés, és az időben alkalmazott antihipertenzív kezelés hatására a beteg neurológiai és szemészeti tünetei rövid időn belül reverzibilisnek bizonyultak. A bemutatott esetben a szemész, mint konziliárus szerepelt, a szemészeti tünetek alapján merült fel központi idegrendszeri érintettség, és vezetett a diagnózishoz. Ismert, hogy a PRES csak korai kezelés mellett reverzibilis, így a kórkép ismerete a szemészetet gyakorló klinikusok számára is elengedhetetlen

Immunocytochemical analysis of misplaced rhodopsin-positive cells in the developing rodent retina.

During the first postnatal weeks of the developing rodent retina, rhodopsin can be detected in a number of neuron-like cells in the inner retina. In the present study, we aim to characterize the morphology, number and staining characteristics of this peculiar population. Misplaced rhodopsin-positive cells (MRCs) were analyzed on retinas of four rodent species, labeled with various rhodopsin-specific antibodies. To investigate their possible relation with non-photoreceptor cells, sections were double-stained against distinct retinal cell types and proteins of the phototransduction cascade. The possibility of synapse formation and apoptosis were also investigated. In all species studied, misplaced cells comprised a few percent of all rhodopsin-positive elements. This ratio declined from the end of the second week and MRCs disappeared nearly completely from the retina by P24. MRCs resembled resident neurons of the inner retina, while outer segment-like processes were seen only rarely. MRCs expressed no other photopigment types and showed no colocalization with any of the bipolar, horizontal, amacrine and ganglion cell markers used. While all MRCs colabeled for arrestin and recoverin, other proteins of the phototransduction cascade were only detectable in a minority of the population. Only a few MRCs were shown to form synaptic-like endings. Our results showed that, during development, some rhodopsin- expressing cells are displaced to the inner retinal layers. Although most MRCs lack morphological features of photoreceptors, they contain some but not all, elements of the phototransduction cascade, indicating that they are most probably misplaced rods that failed to complete differentiation and integrate into the photoreceptor mosaic

Novel features of neurodegeneration in the inner retina of early diabetic rats

The literature indicates that in diabetes retinal dysfunctions related to neural retinal alterations exist prior to clinically detectable vasculopathy. In a previous report, a detailed description about the alteration of the outer retina was given, where diabetic degeneration preceded apoptotic loss of cells (Enzsöly et al., 2014). Here, we investigated the histopathology of the inner retina in early diabetes using the same specimens. We examined rat retinas with immunohistochemistry and Western blotting, 12 weeks after streptozotocin induction of diabetes. Glial reactivity was observed in all diabetic retinal specimens; however, it was not detectable all over the retina, but appeared in randomly arranged patches, with little or no glia activation in between. Similarly, immunoreactivity of parvalbumin (staining mostly AII amacrine cells) was also decreased only in some regions. We propose that these focal changes appear prior to affecting the whole retina and overt loss of cells. In contrast to these, most other markers used (calretinin, recoverin, tyrosin hydroxylase anti-Brn-3a and also calbindin in the optic part of the retina) did not show any major alterations in the intensity of immunoreactivity or in the number of stained elements. Interestingly, under diabetic conditions, the labeling pattern of PKC-α and calbindin in the ciliary retina showed a clear resemblance to the pattern described during development. This observation is in line with our previous study, reporting an increase in the number of dual cones, coexpressing two photopigments, which is another common feature with developing retinas. These data may indicate a previously uninvestigated regenerative capacity in diabetic retin

Pathologic alterations of the outer retina in streptozotocin-induced diabetes.

PURPOSE: Neurodegeneration as an early event of diabetic retinopathy preceding clinically detectable vascular alterations is a widely proven issue today. While there is evidence for the impairment of color vision and contrast sensitivity in early diabetes, suggesting deteriorated photoreceptor function, the underlying neuropathology of these functional alterations is still unknown. The aim of the present study was to investigate the effects of early diabetes on the outer retinal cells. METHODS: The retinal pigment epithelium, photopigment expression, and density and morphology of photoreceptors were studied using immunocytochemistry in streptozotocin-induced diabetes in two rat strains. The fine structure of photoreceptors and pigment epithelium was also investigated with transmission electron microscopy. RESULTS: Here we found that retinal thickness was unchanged in diabetic animals and that no significant increase in the number of apoptotic cells was present. Although the density of cones expressing middle (M)- and shortwave (S)-sensitive opsins was similar in diabetic and control retinas, we detected remarkable morphologic signs of degeneration in the outer segments of diabetic rods, most M-cones, and some S-cones. A decrease in thickness and RPE65 protein immunoreactivity of the pigment epithelium were evident. Furthermore, an increased number of dual cones, coexpressing both M- and S-opsins, was detected at the peripheral retina of diabetic rats. CONCLUSIONS: Degenerative changes of photoreceptors and pigment epithelium shown here prior to apoptotic loss of photoreceptors may contribute to functional alterations reported in diabetic human patients and different animal models, thus may serve as a potential model for testing the efficacy of neuroprotective agents in diabetes

Stratified organization and disorganization of inner plexiform layer revealed by TNAP activity in healthy and diabetic rat retina.

Tissue non-specific alkaline phosphatase (TNAP), an abundant ectophosphatase, is present in various organs including the brain and retina of several vertebrate species. Evidence is emerging that TNAP influences neural functions in multiple ways. In rat, strong TNAP activity has been found in retinal vessels, photoreceptors, and both synaptic layers. In the present study, we identified eleven strata of the inner plexiform layer (IPL) by using TNAP histochemistry alone. The TNAP strata corresponded exactly to the strata seen after combined immunohistochemistry with four canonical IPL markers (TH-ChAT-CR-PKCalpha). Therefore, as described in other mammalian species, our data support the existence of multiple morphologically and functionally discernible IPL strata in rats. Remarkably, the stratification pattern of the IPL was severely disrupted in a diabetic rat model, even before changes in the canonical IPL markers were detectable. These findings indicate that TNAP histochemistry offers a more straightforward, but also more sensitive, method for investigating retinal strata and their diabetes-induced degeneration