Visual functions and multimodal imaging of patients with idiopathic focal choroidal excavation.

This study aimed to evaluate visual function and perform multimodal imaging on patients with focal choroidal excavation without any chorioretinal disease (idiopathic focal choroidal excavation [iFCE]). Seventeen eyes of 15 patients with iFCE (8 men, 7 women; mean ± standard deviation age, 56.0 ± 10.8 years) were assessed for visual function including visual acuity, metamorphopsia, aniseikonia, and retinal sensitivity. Multimodal imaging included optical coherence tomography (OCT), fundus autofluorescence (FAF), and OCT angiography. This study found that the maximum width and depth of the excavation were 597 ± 330 (238-1809) µm and 123 ± 45 (66-231) µm, respectively, and that FAF showed normal or hypoautofluorescence corresponding to iFCE. The fundus examination findings were stable during the follow-up period (96 ± 48 months). None of the eyes showed any abnormalities in central retinal sensitivity or aniseikonia. Metamorphopsia was detected using Amsler grid testing and M-CHARTS in two eyes. Therefore, this study is the first to quantitatively and qualitatively study metamorphopsia of patients with iFCE. Our results showed that most patients with iFCE did not have visual impairments, despite the presence of morphological changes in the outer retina and choroid.

Numerous retinal pigment epithelial elevations and drusen associated with unusual dilated choroidal vessels seen at choriocapillaris level in macular area.

PURPOSE: To report the ocular findings in a patient with extensive diffuse elevations of the retinal pigment epithelium (RPE) and drusen associated with dilated choroidal vessels. OBSERVATIONS: The eye of a 72-year-old woman with numerous drusen and dilated choroidal vessels in the macular and surrounding areas of the right eye was studied. Her visual acuity was 20/16 in this eye and she was asymptomatic although the Amsler grid testing showed mild metamorphopsia. Indocyanine green angiography showed dilated choroidal vessels that collected blood from their branches in the macular and surrounding areas and flowed out of the eye at the entry site of a short posterior ciliary artery. A large choroidal vein ran from the nasal quadrants toward the superotemporal quadrant. Optical coherent tomography (OCT) showed two types of RPE elevations over an extensive area: one was a relatively steep dome-shaped RPE elevation, and the other was a flatter placoid-shaped RPE detachment. Detailed examinations including OCT angiography showed that the dome-shaped RPE elevation coincided with the course of the dilated choroidal vessels which were seen at the level of the choriocapillaris. The visual acuity and the ocular findings remained stable during the 2.5-year follow-up period, and this condition did not require any treatments. CONCLUSIONS AND IMPORTANCE: We conclude that the dilated choroidal vessels are most likely parts of the posterior ciliary venous system, and they function as a posterior route of choroidal outflow. Because such eyes might be diagnosed and treated as age-related macular degeneration based on the presence of drusen, RPE detachments, and abnormal vessels beneath the RPE, knowledge of these observations in a functionally normal eye is important to avoid unnecessary treatments.

Changes in expression of aquaporin-4 and aquaporin-9 in optic nerve after crushing in rats.

The purpose of this study was to determine the temporal and spatial changes in the expression of AQP4 and AQP9 in the optic nerve after it is crushed. The left optic nerves of rats were either crushed (crushed group) or sham operated (sham group), and they were excised before, and at 1, 2, 4, 7, and 14 days later. Four optic nerves were pooled for each time point in both groups. The expression of AQP4 and AQP9 was determined by western blot analyses. Immunohistochemistry was used to determine the spatial expression of AQP4, AQP9, and GFAP in the optic nerve. Optic nerve edema was determined by measuring the water content in the optic nerve. The barrier function of the optic nerve vessels was determined by the extravasated Evans blue dye on days 7 and 14. The results showed that the expression of AQP4 was increased on day 1 but the level was significantly lower than that in the sham group on days 4 and 7 (P<0.05). In contrast, the expression of AQP9 gradually increased, and the level was significantly higher than that in the sham group on days 7 and 14 (P<0.05, Tukey-Kramer). The down-regulation of AQP4 was associated with crush-induced optic nerve edema, and the water content of the nerve was significantly increased by 4.3% in the crushed optic nerve from that of the untouched fellow nerve on day 7. The expression of AQP4 and GFAP was reduced at the crushed site where AQP4-negative and AQP9-positive astrocytes were present. The barrier function was impaired at the crushed site on days 7 and 14, restrictedly where AQP4-negative and AQP9-positive astrocytes were present. The presence of AQP9-positive astrocytes at the crushed site may counteract the metabolic damage but this change did not fully compensate for the barrier function defect.

Systemic simvastatin rescues retinal ganglion cells from optic nerve injury possibly through suppression of astroglial NF-κB activation.

Neuroinflammation is involved in the death of retinal ganglion cells (RGCs) after optic nerve injury. The purpose of this study was to determine whether systemic simvastatin can suppress neuroinflammation in the optic nerve and rescue RGCs after the optic nerve is crushed. Simvastatin or its vehicle was given through an osmotic minipump beginning one week prior to the crushing. Immunohistochemistry and real-time PCR were used to determine the degree of neuroinflammation on day 3 after the crushing. The density of RGCs was determined in Tuj-1 stained retinal flat mounts on day 7. The effect of simvastain on the TNF-α-induced NF-κB activation was determined in cultured optic nerve astrocytes. On day 3, CD68-positive cells, most likely microglia/macrophages, were accumulated at the crushed site. Phosphorylated NF-κB was detected in some astrocytes at the border of the lesion where the immunoreactivity to MCP-1 was intensified. There was an increase in the mRNA levels of the CD68 (11.4-fold), MCP-1 (22.6-fold), ET-1 (2.3-fold), GFAP (1.6-fold), TNF-α (7.0-fold), and iNOS (14.8-fold) genes on day 3. Systemic simvastatin significantly reduced these changes. The mean ± SD number of RGCs was 1816.3±232.6/mm(2) (n = 6) in the sham controls which was significantly reduced to 831.4±202.5/mm(2) (n = 9) on day 7 after the optic nerve was crushed. This reduction was significantly suppressed to 1169.2±201.3/mm(2) (P = 0.01, Scheffe; n = 9) after systemic simvastatin. Simvastatin (1.0 µM) significantly reduced the TNF-α-induced NF-κB activation in cultured optic nerve astrocytes. We conclude that systemic simvastatin can reduce the death of RGCs induced by crushing the optic nerve possibly by suppressing astroglial NF-κB activation.

Choroidal venous pulsations at an arterio-venous crossing in polypoidal choroidal vasculopathy.

It has been reported that pulsations in abnormal vessels are observed on indocyanine green (ICG) angiography in half of patients with polypoidal choroidal vasculopathy (PCV), although the mechanism of the pulsation is unknown. In this study, we report a case of PCV showing venous pulsations at an arterio-venous (A-V) crossing, and discuss a possible mechanism of polypoidal vessel formation and pulsations in PCV. A 66-year-old female presented with a reddish-orange elevated lesion and serous retinal detachment in the macula of her left eye, and was diagnosed as PCV. She was treated with photodynamic therapy (PDT), and followed-up through routine examinations, including ICG angiography. ICG angiography at presentation showed a branching vascular network and choroidal venules with dye leakage (polypoidal vessels) in the left eye. Pulsations, supposedly of venous origin, were observed at an A-V crossing in the abnormal vessels. Within 3 months after PDT, the polypoidal vessel ceased to leak and the pulsations vanished. The reddish-orange lesion gradually decreased in size with complete disappearance of retinal detachment. This study suggests that an unusual compression at an A-V crossing may make a venule polypoidal, and fluctuations of blood flow and pressure in the venule may cause pulsatile movements of the vessel wall.

Early structural changes during spontaneous closure of idiopathic full-thickness macular hole determined by optical coherence tomography: a case report.

BACKGROUND: Spontaneous closure of an idiopathic full-thickness macular hole has been reported to occasionally occur. However, the cells involved in plugging the macular hole have not been determined conclusively. We aimed to report the early structural changes that occur during a spontaneous closure of an idiopathic full-thickness macular hole determined by spectral-domain optical coherence tomography. CASE PRESENTATION: A 71-year-old Japanese man with an idiopathic full-thickness macular hole and subclinical posterior vitreous detachment in the left eye was followed. Three weeks after the identification of the macular hole, optical coherence tomography showed tissue that protruded from the interior wall of the macular hole at the level of the external limiting membrane toward the center of the macular hole. Five months after the first examination, he returned with improvements of his visual symptoms, and the macular hole was closed by a thin retinal tissue which included the restored external limiting membrane that bridged across the macular hole. However, the inner segment/outer segment junction line was not intact and the fovea was detached. Two months later, optical coherence tomography showed an almost normal foveal configuration with an essentially restored inner segment/outer segment junction line and foveal reattachment. CONCLUSION: Our results suggest that Müller cells proliferate and/or extend at the level of the end of the external limiting membrane to form a tissue bridge across the macular hole associated with the external limiting membrane restoration first of all. This leads to the adhesion of other retinal layers and resolution of the foveal detachment.

Responsiveness of eyes with polypoidal choroidal vasculopathy with choroidal hyperpermeability to intravitreal ranibizumab.

BACKGROUND: To determine the role played by vascular endothelial growth factor (VEGF) in polypoidal choroidal vasculopathy (PCV) based on an interventional immunology theory. METHODS: Eyes with PCV were divided in a masked fashion into those with choroidal hyperpermeability (HP group) and those with normal choroidal permeability (NP group) based on the indocyanine green angiograms. The inter-rater agreement rate was evaluated using Fleiss' kappa. Patients were treated by intravitreal ranibizumab (IVB). The central choroidal thickness and central foveal thickness (CFT) at the baseline and 7 days after the treatment were measured by optical coherence tomography. RESULTS: Among the 57 consecutive eyes diagnosed with PCV, 42 eyes of 42 patients met the inclusion criteria (21 eyes/HP group vs 21 eyes /NP group). Central choroidal thickness in HP group was significantly thicker than that in the NP group (P < .001, Mann-Whitney U test). The inter-rater agreement was high with a Fleiss' kappa = 0.95, P < .0001. The percentage reduction in the CFT in HP group (14.0%) was significantly less than that in NP group (20.4%; P = .013, Mann-Whitney U test). CONCLUSIONS: Eyes with PCV that are associated with choroidal hyper-permeability may not be strongly associated with VEGF-related pathology, and may not respond favorably to anti-VEGF monotherapy.

Hyperreflective dots surrounding the central retinal artery and vein in optic disc melanocytoma revealed by spectral domain optical coherence tomography.

PURPOSE: To report findings of optic disc melanocytoma (ODM) obtained using spectral domain optical coherence tomography (SD OCT), with special reference to the central retinal artery and vein surrounded by hyperreflective dots. METHODS: Retrospective review of five eyes of five patients with ODM. Demographic information, ophthalmic examination including best-corrected visual acuity, dilated funduscopic examination, and SD OCT images were evaluated. RESULTS: Dome-shaped, darkly pigmented tumors were seen ophthalmoscopically in the optic discs of all eyes. On OCT, the first branches of the central retinal artery and/or vein were well defined as oblique sections of tubular structures with a perivascular distribution of hyperreflective dots in the elevated retina (nerve fiber layer) over the tumor. The portions where these vessels turn toward the retina were displaced more anteriorly than those of eyes without ODM. Hyperreflective dots of various sizes were also observed in elevated retinas over the tumors, which shadowed and obscured the subjacent tissue in all eyes. CONCLUSIONS: SD OCT provides higher definition images of ODM relating to the branches of the central retinal artery/vein, revealing anterior displacement of vessels and perivascular distribution of hyperreflective dots that suggest melanophages and/or tumor cells or proteins and/or lipid deposits.

Predictable signs of benign course of polypoidal choroidal vasculopathy: based upon the long-term observation of non-treated eyes.

PURPOSE: To find predictable signs of benign polypoidal choroidal vasculopathy (PCV). METHODS: Medical records of 13 eyes from 12 patients who were followed up for 5 years or longer without treatment among 258 consecutive patients with PCV were reviewed retrospectively. The main outcomes measured were best corrected visual acuity (BCVA) and fundus findings during the follow-up period. RESULTS: The average age at presentation was 68 years, and the average follow-up period after diagnosis was 80 months (range, 62-119 months). The initial mean logarithmic value of the minimal angle of resolution (logMAR) BCVA was 0.28 +/- 0.26, and the final mean logMAR BCVA was 0.62 +/- 0.72. The difference in the logMAR BCVA values between the two points was not statistically significant (p > 0.05). The trend of change from baseline at 2-year follow-up was consistent with those at 5-year follow-up in nine eyes. Fundus findings at the initial examination were classified into two patterns: (i) reddish-orange nodules and detachment of the retinal pigment epithelium with/without detachment of the neurosensory retina (nine eyes); (ii) reddish-orange nodules alone, or nodules and small subretinal haemorrhage (four eyes). In the eyes with the first pattern, clinical course and visual prognosis were variable. An absence of hard exudates could be a sign to maintain a benign clinical course or stable vision with this pattern. The eyes with the second pattern took a benign clinical course with stable vision. CONCLUSIONS: There is certainly a group of PCV eyes with a benign prognosis. Considering the huge cost and risk of current therapies, the initial ocular findings could be deciding factors that determine the necessity for further treatment.

Intraocular expression and release of high-mobility group box 1 protein in retinal detachment.

High-mobility group box 1 (HMGB1) protein is a multifunctional protein, which is mainly present in the nucleus and is released extracellularly by dying cells and/or activated immune cells. Although extracellular HMGB1 is thought to be a typical danger signal of tissue damage and is implicated in diverse diseases, its relevance to ocular diseases is mostly unknown. To determine whether HMGB1 contributes to the pathogenesis of retinal detachment (RD), which involves photoreceptor degeneration, we investigated the expression and release of HMGB1 both in a retinal cell death induced by excessive oxidative stress in vitro and in a rat model of RD-induced photoreceptor degeneration in vivo. In addition, we assessed the vitreous concentrations of HMGB1 and monocyte chemoattractant protein 1 (MCP-1) in human eyes with RD. We also explored the chemotactic activity of recombinant HMGB1 in a human retinal pigment epithelial (RPE) cell line. The results show that the nuclear HMGB1 in the retinal cell is augmented by death stress and upregulation appears to be required for cell survival, whereas extracellular release of HMGB1 is evident not only in retinal cell death in vitro but also in the rat model of RD in vivo. Furthermore, the vitreous level of HMGB1 is significantly increased and is correlated with that of MCP-1 in human eyes with RD. Recombinant HMGB1 induced RPE cell migration through an extracellular signal-regulated kinase-dependent mechanism in vitro. Our findings suggest that HMGB1 is a crucial nuclear protein and is released as a danger signal of retinal tissue damage. Extracellular HMGB1 might be an important mediator in RD, potentially acting as a chemotactic factor for RPE cell migration that would lead to an ocular pathological wound-healing response.

Nasal and independent polypoidal lesions in polypoidal choroidal vasculopathy.

BACKGROUND: Polypoidal vessels in polypoidal choroidal vasculopathy (PCV) are known to occur frequently in the macular and peripapillary regions. The aim of this study is to describe patients with polypoidal vessels that are nasal to the optic disc, being independent of macular polypoidal lesions. METHODS: A 75-year-old man and a 65-year-old man with polypoidal vessels in the macula of both eyes were followed up through routine examinations including indocyanine green angiography and optical coherence tomography. RESULTS: A polypoidal vessel located 1.5 disc diameters to the nasal margin of the disc was found in the right eye during the first examination in one case, and in the other case it developed during the follow-up period, after successful treatment using photodynamic therapy for the polypoidal lesion in the macula of the left eye. Indocyanine green angiography disclosed no continuity between the polypoidal vessels nasal to the disc and the polypoidal vessels in the macula region in either case. The nasal polypoidal vessels were not associated with exudative changes in either case, and the vessel in one case disappeared spontaneously without any treatment. CONCLUSIONS: The findings of this study demonstrate that PCV could involve regions outside the macula and occur in multiple areas independently. The results also indicate the dynamic nature and transitory appearance of polypoidal vessels. Polypoidal vessels nasal to the disc might be overlooked, especially in cases that are not associated with exudative changes, and careful examination might disclose more subclinical nasal polypoidal vessels. Further detailed examination would be helpful to gain a better understanding of the pathogenesis of PCV.

Clinical features of early and late stage polypoidal choroidal vasculopathy characterized by lesion size and disease duration.

BACKGROUND: The pathogenesis of polypoidal choroidal vasculopathy (PCV), and even its clinical features, are controversial. Previous histopathological studies have identified different features; either dilated choroidal vessels or intra-Bruch's neovascularization. These differences might be partly attributable to the influence of the disease stage. We therefore evaluated the clinical features of early and late stage PCV. METHODS: The medical records of 110 eyes of 97 PCV patients were retrospectively reviewed. The time between the subjective onset of visual abnormality and examination at our clinic and the greatest linear dimension of the total lesion at the first examination were investigated. The period of disturbed vision and lesion size data were placed in ascending order to determine the first quartile point. Eyes with both values at or below the first quartile point were classified as 'small-short' (early stage). Eyes with both values equal to at least the third quartile point were classified as 'large-long' (late stage). Fundus photography, indocyanine green and fluorescein angiography, visual acuity, and clinical course were compared. RESULTS: Twelve eyes from 12 patients were small-short cases (period of disturbed vision of 1 month or less, lesion size 2.0 disc diameters or less). Eleven eyes from ten patients were large-long cases (period of disturbed vision 36 months or more, lesion size at least 5.0 disc diameters). The large-long eyes were characterized by occult choroidal neovascular membrane or scar tissue secondary to exudative age-related macular degeneration. Noticeable in the small-short eyes were atrophic changes in the retinal pigment epithelium, choroidal vessel hyperpermeability and pulsation. The visual prognosis and clinical course were different between the groups. CONCLUSIONS: The difference of clinical features between the groups might reflect different disease stages, although not all of the features observed in the small-short group appeared to represent the early stages of those recorded in the large-long group. Thus, the variation in histopathologic features among previous reports might be partly attributable to differences in disease stage.

Intravitreal triamcinolone acetonide for exudative age-related macular degeneration among Japanese patients.

AIM: To study the results of intravitreal triamcinolone acetonide (TA) for exudative age-related macular degeneration (AMD) among Japanese patients. METHODS: 13 eyes of 12 Japanese patients (9 males and 3 females) with subfoveal choroidal neovascularization (CNV) of exudative AMD received intravitreal TA (8 mg). Visual acuity, size of CNV and serous retinal detachment, and complications related to treatment were evaluated for 6 months or longer. RESULTS: Postoperative maximum visual acuity significantly improved (p < 0.05). Postoperative eyes had a greater probability of a reduced size of CNV and/or retinal detachment compared to preoperative eyes. Seven eyes showed increased intraocular pressure (21 mm Hg or over), which was controlled well by medication. Cataract development and advancement were observed in 90% of phakic eyes. No other serious complications were found. CONCLUSIONS: Intravitreal TA might be an effective treatment for subfoveal CNV of exudative AMD among Japanese as well as Caucasian patients for a comparatively short period.

Gene transfer to corneal epithelium and keratocytes mediated by ultrasound with microbubbles.

PURPOSE: The cornea is an ideal organ for evaluating gene transfer because it can be treated noninvasively and monitored easily. The present study was performed to investigate the practical efficacy and safety of ultrasound (US) plus microbubble (MB)-mediated gene transfer to cornea. METHODS: Cultured rabbit corneal epithelial (RC-1) cells were incubated in 24-well dishes with plasmid DNA having a green fluorescent protein (GFP) gene under a cytomegalovirus promoter. The cells were exposed to US under different intensities (1 MHz; power, 0.5 approximately 2 W/cm2; duration, 15-120 seconds; duty cycle, 20%-100%). The effect of simultaneous stimulation with MBs was also examined. Gene transfer was quantified by counting the number of GFP-positive cells under microscopy. Furthermore, in vivo gene transfer was examined by GFP plasmid injection into rabbit cornea and US exposure with MBs. RESULTS: In the in vitro study, DNA exposure alone could not transfer gene into cultured RC-1 cells; US enhanced gene transfer slightly. Coexposure with MBs significantly increased gene transfer efficiency. In the in vivo study, DNA injection alone could transfer the gene to a limited degree, but plasmid injection plus US with MBs strongly increased gene transfer efficiency without apparent tissue damage, and gene transfer was achieved two dimensionally. CONCLUSIONS: US with MBs greatly increases gene transfer to in vivo and in vitro corneal cells. This noninvasive gene transfer method may be a useful tool for clinical gene therapy.

Reduced N-acetylaspartate levels in mice lacking aralar, a brain- and muscle-type mitochondrial aspartate-glutamate carrier.

Aralar is a mitochondrial calcium-regulated aspartate-glutamate carrier mainly distributed in brain and skeletal muscle, involved in the transport of aspartate from mitochondria to cytosol, and in the transfer of cytosolic reducing equivalents into mitochondria as a member of the malate-aspartate NADH shuttle. In the present study, we describe the characteristics of aralar-deficient (Aralar-/-) mice, generated by a gene-trap method, showing no aralar mRNA and protein, and no detectable malate-aspartate shuttle activity in skeletal muscle and brain mitochondria. Aralar-/- mice were growth-retarded, exhibited generalized tremoring, and had pronounced motor coordination defects along with an impaired myelination in the central nervous system. Analysis of lipid components showed a marked decrease in the myelin lipid galactosyl cerebroside. The content of the myelin lipid precursor, N-acetylaspartate, and that of aspartate are drastically decreased in the brain of Aralar-/- mice. The defect in N-acetylaspartate production was also observed in cell extracts from primary neuronal cultures derived from Aralar-/- mouse embryos. These results show that aralar plays an important role in myelin formation by providing aspartate for the synthesis of N-acetylaspartate in neuronal cells.

Pulsatile blood flow in the polypoidal choroidal vasculopathy.

OBJECTIVE: To describe patients with pulsatile polypoidal vessels in polypoidal choroidal vasculopathy (PCV). DESIGN: Retrospective, observational case series. PARTICIPANTS: Eighty-four eyes of 74 patients with PCV. METHODS: The medical records of patients diagnosed with PCV between 1998 and 2004 at Kagoshima University Hospital were reviewed. MAIN OUTCOME MEASURES: A pulsatile polypoidal vessel (PV) on indocyanine green angiography (ICGA). RESULTS: Seven of 74 patients (9.5%) had PVs in the macula. Four eyes revealed pulsatile PVs on the day the diagnosis of PCV was first made, and PVs in the other 3 eyes showed pulsatile movement during the follow-up period. Two patterns of pulsatile movement were observed on ICGA: (1) a rhythmic variation in the caliber of a choroidal vessel (caliber variation pattern) and (2) a pulsatile blood flow in a tortuous and relatively narrow choroidal vessel (pulsatile blood flow pattern). Both patterns of pulsatile PVs appeared in the early frames of the ICGA, and some of them were observable even during the first 15 minutes after the ICG dye injection. The pulsatile movement disappeared spontaneously without treatment in some patients, and the period in which pulsatile PVs was detectable on ICGA was limited in each patient. CONCLUSIONS: We report the features of pulsatile PV in PCV. It is a unique and important characteristic that has not been reported with any other chorioretinal diseases and may provide a clue to understanding the pathogenesis of PCV.

Visual improvement following trans-Tenon's retrobulbar triamcinolone acetonide infusion for polypoidal choroidal vasculopathy.

PURPOSE: To report a case of polypoidal choroidal vasculopathy (PCV) that was successfully treated by sub-Tenon's infusion of triamcinolone acetonide (TA). METHODS: A 56-year-old Japanese man had PCV in his left eye with vision of 20/32. Fluorescein angiography demonstrated a hyper-fluorescent spot, and indocyanine green angiography showed marked leakage of dye from the polypoidal vessel. Optical coherence tomography showed anterior protrusion of highly reflective layers and subretinal fluid. RESULTS: The patient underwent trans-Tenon's retrobulbar infusion of 12 mg TA. Subsequently, the reddish-orange lesion decreased in size and elevation with complete resolution of the serous retinal detachment, and visual acuity improved to 20/20. Visual acuity remained good through a 15-month follow-up during which the patient was free of endophthalmitis and elevated intraocular pressure. CONCLUSIONS: Trans-Tenon's retrobulbar TA infusion is potentially effective in treating PCV.

Plasticity of polypoidal lesions in polypoidal choroidal vasculopathy.

PURPOSE: The aim of this study was to describe the clinical course in a patient with polypoidal choroidal vasculopathy (PCV). METHODS: A 68-year-old man with PCV in the left eye was followed up by means of routine examinations including fluorescein angiography and indocyanine green angiography for over 60 months. RESULTS: Throughout the follow-up period, the patient experienced repeated lesions in the macula, such as serosanguineous detachment of the retinal pigment epithelium and neurosensory retina, but retained good visual acuity. Indocyanine green angiography disclosed spontaneous regression of polypoidal vessels followed by significant changes in the choroidal circulation: a group of polypoidal structures disappeared, and after several months a small choroidal vessel became apparent that was distant from the previously observed polypoidal structure rather than representing an extension of the original lesion. CONCLUSION: The clinical observation suggests that in some cases of PCV the choroidal vasculature may be altered with time, in that some vessels in the inner choroid and even the choriocapillaris may close and collateral vessels and/or new vessels may develop to form complex such as that described here.