Focal choroidal excavation: a preliminary interpretation based on clinic and review

AIM: To describe the clinical and imaging characteristics associated with focal choroidal excavation(FCE), analyze the possible complication, and interpret its probable etiopathogenesis.METHODS: Retrospective descriptive case series of 37 eyes of 32 patients with FCE. Findings of spectral-domain optical coherence tomography(SD-OCT),fluorescein angiography, indocyanine green angiography,and clinical features were analyzed. RESULTS: All patients were Chinese. Five patients(15.6%) were bilaterally involved. Patients’ ages ranged from 7 to 66 y. Refractive error ranged between +2.0 D and 11.0 D. Mean best-corrected visual acuity was 0.6(range, 0.1 to 1.2). Fundus examinations exhibited mild-moderate localized pigmentary disturbances in the corresponding area of 17 eyes. Fluorescein angiography performed in 18 patients showed varying degrees of hyperfluorescence and hypofluorescence related to a range of retinal pigment epithelium(RPE) alterations.Indocyanine green angiography performed in 7 patients showed hypofluorescence at the excavation. SD-OCT demonstrated choroidal excavation in all 37 eyes.Twenty-nine eyes showed a single lesion of FCE, and three eyes showed 2-3 separated lesions. Fifteen eyes showed separation between the photoreceptor tips andRPE consistent with nonconforming FCE. Central serous chorioretinopathy(CSC, n =1) and choroidal neovascularization(CNV, n =1) developed during follow-up.CONCLUSION: FCE could be interpreted as congenital focal choroidal dysplasia involving the RPE,choriocapillaris, and photoreceptor associated with the faulty anatomy. The abnormal anatomy of FCE was similar to anatomy at risk of CSC and CNV.

Macular ganglion cell complex injury in different stages of anterior ischemic optic neuropathy

BACKGROUND Anterior ischemic optic neuropathy(AION)is a group of ophthalmic diseases in which the optic nerve is injured causing blindness.However,the pathogenesis,clinical manifestations,and clinical treatments of AION are yet elusive.Only a few related experimental or clinical reports are available on the disease.In this study,spectral domain optical coherence tomography(SD-OCT)was used to examine the morphology of thickness swelling and atrophic changes of macular ganglion cell complex(mGCC)in the different stages of AION that were then compared with the visual fields.Thus,the clinical value of mGCC examination was alleged to be similar to that of the visual field.AIM To explore the mGCC injury at different stages in AION and the clinical significance.METHODS Cases with AION were analyzed in a retrospective study.SD-OCT was used to analyze the correlation between mGCC and peripapillary retinal nerve fiber layer thicknesses at different stages of AION and the changes in the corresponding stages of visual fields.RESULTS A total of 21 cases(28 eyes)presented AION.The onset time of AION was defined as early stage(within 3 wk of onset),middle stage(from 3 wk to 2 mo),and late stage(disease span>2 mo).In the early stage,the mGCC thickness of SD-OCT was within the normal high limit,and the perioptic nerve fibers thickness was more than the normal.The changes in the visual field in early stage were not consistent with the swelling changes in mGCC and peri-disc nerve fibers.In addition,atrophy and thinning appeared in mGCC,and the perioptic nerve fibers were swollen.However,the thickness was lower in the middle period than that in the early stage.The change in visual field was consistent with that of mGCC in this period.In the late stage,mGCC shrank and thinned,and the thickness of the nerve fibers around the optic disc in the corresponding region shrank and thinned.CONCLUSION The changes in mGCC thickness in patients with AION showed early,middle,and late stages of development by SD-OCT.Although the early stage visual field changes of AION were not consistent with the swelling changes of mGCC,the horizontal delimitation or annular atrophy of mGCC was consistent with that in the middle and late stage of the disease.The atrophy of peripheral nerve fibers was later than that of the mGCC atrophy.