Choroidal circulation hemodynamics in eyes with ocular blunt trauma has not been quantitatively examined yet. We quantitatively examined changes in choroidal blood flow velocity and thickness at the lesion site using laser speckle flowgraphy (LSFG) and enhanced depth imaging optical coherence tomography (EDI-OCT) in a patient with chorioretinopathy associated with ocular blunt trauma. A 13-year-old boy developed a chorioretinal lesion with pigmentation extending from the optic disc to the superotemporal side in the right eye after ocular blunt trauma. The patient’s best-corrected visual acuity (BCVA) was 0.2 in the right eye. Indocyanine green angiography showed hypofluorescence from the initial phase, with a decrease of mean blur rate (MBR) on LSFG color map, which corresponded to the chorioretinal lesion. The BCVA and foveal outer retinal morphologic abnormality spontaneously improved during follow-up. MBR and choroidal thickness increased by 23–31% and 13–17 μm at the lesion site and by 11–22% and 33–42 μm at the fovea, respectively, during the 6-month follow-up period after baseline measurements in the affected eye. In contrast, these parameters showed little or no changes at the normal retinal site in the affected eye and the fovea in the fellow eye. Current data revealed that both blood flow velocity and thickness in the choroid at the lesion site decreased in the acute stage and subsequently increased together with improvements in visual function and outer retinal morphology. These results suggest that LSFG and EDI-OCT may be useful indices that can noninvasively evaluate activity of choroidal involvement in ocular blunt trauma-associated chorioretinopathy.

Placental growth factor (PlGF) belongs to the vascular endothelial growth factor (VEGF) family of proteins that participate in angiogenesis and vasculogenesis. Anti-VEGF therapy has become the standard treatment for ocular angiogenic disorders in ophthalmological practice. However, there is emerging evidence that anti-VEGF treatment may increase the risk of atrophy of the retinal pigment epithelium (RPE), which is important for the homeostasis of retinal tissue. Whereas the cytoprotective role of VEGF family molecules, particularly that of VEGF A (VEGFA) through its receptor VEGF receptor-2 (VEGFR-2), has been recognized, the physiological role of PlGF in the retina is still unknown. In this study, we explored the role of PlGF in the RPE using PlGF-knockdown RPE cells generated by retrovirus-based PlGF-shRNA transduction. We show that VEGFA reduced apoptosis induced by serum starvation in RPE cells, whereas the antiapoptotic effect of VEGFA was abrogated by VEGFR-2 knockdown. Furthermore, PlGF knockdown increased serum starvation–induced cell apoptosis and unexpectedly reduced the protein level of VEGFR-2 in the RPE. The antiapoptotic effect of VEGFA was also diminished in PlGF-knockdown RPE cells. In addition, we found that glycogen synthase kinase 3 activity was involved in proteasomal degradation of VEGFR-2 in RPE cells and inactivated by PlGF via AKT phosphorylation. Overall, the present data demonstrate that PlGF is crucial for RPE cell viability and that PlGF supports VEGFA/VEGFR-2 signaling by stabilizing the VEGFR-2 protein levels through glycogen synthase kinase 3 inactivation.

A highly invasive intracranial malignant schwannoma containing several masses was detected in a 28-week-old male Crl:CD(SD) rat. Macroscopically, 3 masses were noted in the cranial cavity; one was present at the bottom of the cranial cavity and involved the trigeminal nerve, and the other two were in the parietal bone. Histologically, each mass consisted of fusiform cells with interlacing fascicular, wavy and nuclear pseudopalisading arrangements and round cells with cystic lesions. The tumor cells invaded not only the brain but also the parietal bone. In the brain, the tumor cells infiltrated diffusely into the leptomeningeal and perivascular spaces and parenchyma, in which the tumor cell morphology and invasive pattern closely resembled those of malignant astrocytoma and malignant reticulosis. Immunohistochemically, the tumor cells in the masses showed positive reactions for both S-100 protein and GFAP, while those in the cerebral invasion sites were negative for GFAP and less positive for S-100 protein. Electron microscopically, a single basal lamina layer and short intricate cell processes were confirmed in the tumor cells. From these results, the present tumor was diagnosed as a malignant schwannoma arising in the cranial cavity, probably originating from the trigeminal nerve. The present tumor is considered to be a relatively unique malignant schwannoma based on its growth and invasion patterns.

Background/Objectives: The aim of this study was to determine artificial intelligence-based macular fluid (MF) parameters in diabetic macular edema (DME) with optical coherence tomography (OCT) and examine stage-by-stage differences in MF parameters and their relationship with best-corrected visual acuity (BCVA). Methods: This study enrolled 104 eyes with treatment-naïve DME. Intraretinal fluid (IRF) and subretinal fluid (SRF) were detected in horizontal OCT images based on the “Hokkaido University MF segmentation model” when DME was first observed together with BCVA testing. The MF area, the mean brightness, and the variance of brightness were compared between mild or moderate non-proliferative diabetic retinopathy (mNPDR, n = 33), severe NPDR (sNPDR, n = 52), and PDR eyes (n = 19). Correlations between logMAR BCVA and MF parameters were also examined. Results: All the MF parameters tended to increase with DR stages. Especially, the mean brightness of IRF was significantly greater in PDR than in mNPDR. The variance of brightness of IRF increased in sNPDR compared to mNPDR, whereas that of SRF increased in PDR compared to sNPDR. LogMAR BCVA showed positive correlations with MF areas and the variance of brightness of SRF. Conclusions: The qualitative and quantitative MF parameters may be useful for better understanding DME pathogenesis according to DR progression.

Acute posterior multifocal placoid pigment epitheliopathy (APMPPE) is a disease characterized by multiple yellowish-white placoid lesions. Although most lesions resolve spontaneously, some turn into scars and lead to permanent visual dysfunction. In this report, we found suggestive findings in fundus autofluorescence (FAF) that may be useful for distinguishing severe lesions requiring treatment in APMPPE. Case 1: A 29-year-old woman was referred to our hospital with multiple yellowish-white placoid lesions on the fundi of both eyes (OU). FAF showed hyperautofluorescence in some of these placoid lesions. Based on the findings of fluorescein angiography, a diagnosis of APMPPE was established, and oral prednisolone (PSL) was initiated, given that some lesions were located in the macula. One week later, exacerbation occurred with the newly developed hyperautofluorescent lesions. Some lesions in the right eye (OD) that were hyperautofluorescent at the first visit became hypoautofluorescent. Afterward, although all hypoautofluorescent lesions persisted, most of the hyperautofluorescent lesions disappeared, so oral PSL could be stopped. Two months later, however, the recurrence occurred along with multiple new placoid lesions. Some lesions located at the macula were hyperautofluorescent on FAF OU, indicating the possibility of becoming scar lesions with hypoautofluorescence. Accordingly, oral PSL was given again. A 47-year-old woman noticed decreased vision OD, and she was referred to us. Multiple yellowish-white placoid lesions were seen in the fundi OU. FAF showed hyperautofluorescence both with and without corresponding hypoautofluorescence in the placoid lesions OU. A diagnosis of APMPPE was established, and oral PSL was initiated. Four months later, some lesions that were hyperautofluorescent at the first visit had turned isoautofluorescent, and some lesions OU became hypoautofluorescent. However, all hypoautofluorescent lesions remained hypoautofluorescent OU. Only some hyperautofluorescent lesions recovered to isoautofluorescence without scars. In APMPPE, lesions showing hyperautofluorescence on FAF may change into hypoautofluorescence indicating scar formation. Therefore, the presence of hyperautofluorescent lesions in the macula may be a good indicator of the need for intensive corticosteroid treatments to avoid leaving hypoautofluorescent scars that are related to irreversible visual dysfunction.