
Manhattan Eye, Ear and Throat Hospital
Hospital / health systemNew York, New York, United States
Research output, citation impact, and the most-cited recent papers from Manhattan Eye, Ear and Throat Hospital (United States). Aggregated across the NobleBlocks index of 300M+ scholarly works.
Top-cited papers from Manhattan Eye, Ear and Throat Hospital
Purpose: We provide a standardized set of terminology, definitions, and thresholds of myopia and its main ocular complications. Methods: Critical review of current terminology and choice of myopia thresholds was done to ensure that the proposed standards are appropriate for clinical research purposes, relevant to the underlying biology of myopia, acceptable to researchers in the field, and useful for developing health policy. Results: We recommend that the many descriptive terms of myopia be consolidated into the following descriptive categories: myopia, secondary myopia, axial myopia, and refractive myopia. To provide a framework for research into myopia prevention, the condition of "pre-myopia" is defined. As a quantitative trait, we recommend that myopia be divided into myopia (i.e., all myopia), low myopia, and high myopia. The current consensus threshold value for myopia is a spherical equivalent refractive error ≤ -0.50 diopters (D), but this carries significant risks of classification bias. The current consensus threshold value for high myopia is a spherical equivalent refractive error ≤ -6.00 D. "Pathologic myopia" is proposed as the categorical term for the adverse, structural complications of myopia. A clinical classification is proposed to encompass the scope of such structural complications. Conclusions: Standardized definitions and consistent choice of thresholds are essential elements of evidence-based medicine. It is hoped that these proposals, or derivations from them, will facilitate rigorous, evidence-based approaches to the study and management of myopia.
PURPOSE: The purpose of the study was to evaluate the choroidal thickness in patients with central serous chorioretinopathy, a disease attributed to increased choroidal vascular hyperpermeability. METHODS: Patients with central serous chorioretinopathy underwent enhanced depth imaging spectral-domain optical coherence tomography, which was obtained by positioning a spectral-domain optical coherence tomography device close enough to the eye to acquire an inverted image. Seven sections, each comprising 100 averaged scans, were obtained within a 5 degrees x 30 degrees rectangle to encompass the macula. The subfoveal choroidal thickness was measured from the outer border of the retinal pigment epithelium to the inner scleral border. RESULTS: The mean age of subjects undergoing enhanced depth imaging spectral-domain optical coherence tomography was 59.3 years (standard deviation, 15.8 years). Seventeen of 19 patients (89.5%) were men, and 12 (63.2%) patients had bilateral clinical disease. The choroidal thickness measured in 28 eligible eyes of the 19 patients was 505 microm (standard deviation, 124 microm), which was significantly greater than the choroidal thickness in normal eyes (P < or = 0.001). CONCLUSION: Enhanced depth imaging spectral-domain optical coherence tomography demonstrated a very thick choroid in patients with central serous chorioretinopathy. This finding provides additional evidence that central serous chorioretinopathy may be caused by increased hydrostatic pressure in the choroid.
Eleven patients, 40 to 71 years old, had a choroidal vasculopathy that led to hemorrhagic and exudative macular degeneration. The patients had peculiar polypoidal, subretinal, vascular lesions associated with serous and hemorrhagic detachments of the retinal pigment epithelium. This macular disorder, which we have named idiopathic polypoidal choroidal vasculopathy (IPCV), appears to represent a distinct entity that differs clinically and demograph-ically from age-related macular degeneration (AMD) and other macular diseases associated with subretinal neovascularization. Recognition of this condition is important because it may have specific risk factors, natural course, and management considerations that differ from those of age-related macular degeneration
The purpose of this study was to determine whether cyclooxygenase-2 (COX-2) was overexpressed in squamous cell carcinoma of the head and neck (HNSCC). Quantitative reverse transcription-PCR, immunoblotting, and immunohistochemistry were used to assess the expression of COX-2 in head and neck tissue. Mean levels of COX-2 mRNA were increased by nearly 150-fold in HNSCC (n = 24) compared with normal oral mucosa from healthy volunteers (n = 17). Additionally, there was about a 50-fold increase in amounts of COX-2 mRNA in normal-appearing epithelium adjacent to HNSCC (n = 10) compared with normal oral mucosa from healthy volunteers. Immunoblotting demonstrated that COX-2 protein was present in six of six cases of HNSCC but was undetectable in normal oral mucosa from healthy subjects. Immunohistochemical analysis showed that COX-2 was expressed in both HNSCC and adjacent normal-appearing epithelium. Taken together, these results suggest that COX-2 may be a target for the prevention or treatment of HNSCC.
In Brief Purpose: To evaluate the validity of commonly used anatomical designations for the four hyperreflective outer retinal bands seen in current-generation optical coherence tomography, a scale model of outer retinal morphology was created using published information for direct comparison with optical coherence tomography scans. Methods: Articles and books concerning histology of the outer retina from 1900 until 2009 were evaluated, and data were used to create a scale model drawing. Boundaries between outer retinal tissue compartments described by the model were compared with intensity variations of representative spectral-domain optical coherence tomography scans using longitudinal reflectance profiles to determine the region of origin of the hyperreflective outer retinal bands. Results: This analysis showed a high likelihood that the spectral-domain optical coherence tomography bands attributed to the external limiting membrane (the first, innermost band) and to the retinal pigment epithelium (the fourth, outermost band) are correctly attributed. Comparative analysis showed that the second band, often attributed to the boundary between inner and outer segments of the photoreceptors, actually aligns with the ellipsoid portion of the inner segments. The third band corresponded to an ensheathment of the cone outer segments by apical processes of the retinal pigment epithelium in a structure known as the contact cylinder. Conclusion: Anatomical attributions and subsequent pathophysiologic assessments pertaining to the second and third outer retinal hyperreflective bands may not be correct. This analysis has identified testable hypotheses for the actual correlates of the second and third bands. Nonretinal pigment epithelium contributions to the fourth band (e.g., Bruch membrane) remain to be determined. Analysis of published outer retinal anatomy, creation of a scale outer retinal model, and comparison of the model with optical coherence tomography images showed that the bands seen in the outer retina appear to correspond to the external limiting membrane, ellipsoid portion of the photoreceptor inner segments, contact cylinders of outer segments, and finally the retinal pigment epithelium.
BACKGROUND: It is known that choroidal neovascularization (CNV) in age-related macular degeneration (ARMD) may erode through the retinal pigment epithelium, infiltrate the neurosensory retina, and communicate with the retinal circulation in what has been referred to as a retinal–choroidal anastomosis (RCA). This is extremely common in the end stage of disciform disease. In recent years, the reverse also seems to be possible, as angiomatous proliferation originates from the retina and extends posteriorly into the subretinal space, eventually communicating in some cases with choroidal new vessels. This form of neovascular ARMD, termed retinal angiomatous proliferation (RAP) in this article, can be confused with CNV. PURPOSE: The purpose of this article is 1) to review the clinical and angiographic characteristics of a series of patients with RAP and 2) to propose a theoretical sequence of events that accounts for the neovascularized process. METHODS: In this retrospective clinical and angiographic analysis, 143 eyes with RAP (108 patients) were reviewed and classified based on their vasogenic nature and course. Clinical biomicroscopic examination, fluorescein angiography, and indocyanine green angiography were used to evaluate patients. RESULTS: The results of this series suggest that angiomatous proliferation within the retina is the first manifestation of the vasogenic process in this form of neovascular ARMD. Dilated retinal vessels and pre-, intra-, and subretinal hemorrhages and exudate evolve, surrounding the angiomatous proliferation as the process extends into the deep retina and subretinal space. One or more dilated compensatory retinal vessels perfuse and drain the neovascularization, sometimes forming a retinal–retinal anastomosis. Fluorescein angiography in these patients usually revealed indistinct staining simulating occult CNV. Indocyanine green angiography was useful to make an accurate diagnosis in most cases. It revealed a focal area of intense hyperfluorescence corresponding to the neovascularization ("hot spot") and other characteristic findings. Based on understanding of the nature and progression of the neovascularized process, patients with RAP were classified into three vasogenic stages. Stage I involved proliferation of intraretinal capillaries originating from the deep retinal complex (intraretinal neovascularization [IRN]). Stage II was determined by growth of the retinal vessels into the subretinal space (subretinal neovascularization [SRN]). Stage III occurred when CNV could clearly be determined clinically or angiographically. A vascularized pigment epithelial detachment and RCA were inconsistent features of this stage. CONCLUSIONS: Retinal angiomatous proliferation appears to be a distinct subgroup of neovascular ARMD. It may present in one of three vasogenic stages: IRN, SRN, or CNV. Whereas ICG angiography is helpful in diagnosing RAP and in documenting the stage of the neovascularized process, it is frequently difficult to determine the precise nature and location of the new vessel formation. It is important for clinicians to recognize the vasogenic potential and the associated manifestations of this peculiar form of neovascular ARMD so that a proper diagnosis can be made, and when possible, an appropriate management administered.
BACKGROUND: It is known that choroidal neovascularization (CNV) in age-related macular degeneration (ARMD) may erode through the retinal pigment epithelium, infiltrate the neurosensory retina, and communicate with the retinal circulation in what has been referred to as a retinal-choroidal anastomosis (RCA). This is extremely common in the end stage of disciform disease. In recent years, the reverse also seems to be possible, as angiomatous proliferation originates from the retina and extends posteriorly into the subretinal space, eventually communicating in some cases with choroidal new vessels. This form of neovascular ARMD, termed retinal angiomatous proliferation (RAP) in this article, can be confused with CNV. PURPOSE: The purpose of this article is 1) to review the clinical and angiographic characteristics of a series of patients with RAP and 2) to propose a theoretical sequence of events that accounts for the neovascularized process. METHODS: In this retrospective clinical and angiographic analysis, 143 eyes with RAP (108 patients) were reviewed and classified based on their vasogenic nature and course. Clinical biomicroscopic examination, fluorescein angiography, and indocyanine green angiography were used to evaluate patients. RESULTS: The results of this series suggest that angiomatous proliferation within the retina is the first manifestation of the vasogenic process in this form of neovascular ARMD. Dilated retinal vessels and pre-, intra-, and subretinal hemorrhages and exudate evolve, surrounding the angiomatous proliferation as the process extends into the deep retina and subretinal space. One or more dilated compensatory retinal vessels perfuse and drain the neovascularization, sometimes forming a retinal-retinal anastomosis. Fluorescein angiography in these patients usually revealed indistinct staining simulating occult CNV. Indocyanine green angiography was useful to make an accurate diagnosis in most cases. It revealed a focal area of intense hyperfluorescence corresponding to the neovascularization ("hot spot") and other characteristic findings. Based on understanding of the nature and progression of the neovascularized process, patients with RAP were classified into three vasogenic stages. Stage I involved proliferation of intraretinal capillaries originating from the deep retinal complex (intraretinal neovascularization [IRN]). Stage II was determined by growth of the retinal vessels into the subretinal space (subretinal neovascularization [SRN]). Stage III occurred when CNV could clearly be determined clinically or angiographically. A vascularized pigment epithelial detachment and RCA were inconsistent features of this stage. CONCLUSIONS: Retinal angiomatous proliferation appears to be a distinct subgroup of neovascular ARMD. It may present in one of three vasogenic stages: IRN, SRN, or CNV. Whereas ICG angiography is helpful in diagnosing RAP and in documenting the stage of the neovascularized process, it is frequently difficult to determine the precise nature and location of the new vessel formation. It is important for clinicians to recognize the vasogenic potential and the associated manifestations of this peculiar form of neovascular ARMD so that a proper diagnosis can be made, and when possible, an appropriate management administered.
BACKGROUND: The pathogenesis of central serous chorioretinopathy (CSC) is poorly understood. Abnormalities in the choroidal circulation have been hypothesized to be causative factors. Fluorescein angiography has not been particularly useful in identifying specific choroidal defects in CSC, largely because of inherent limitations in imaging with this technique. Recent technologic advances in digital indocyanine green videoangiography allow enhanced imaging of the choroid and other subretinal structures in comparison with fluorescein angiography. METHODS: We performed digital indocyanine green videoangiography in 29 consecutive eyes with CSC and compared our results with clinical and fluorescein angiographic findings. RESULTS: Several newly recognized subretinal abnormalities in CSC were noted with digital indocyanine green videoangiography, including (1) presumed hyperpermeability of the choroidal circulation surrounding active retinal pigment epithelial leaks, (2) additional focal and multifocal areas of presumed choroidal hyperpermeability not associated with abnormalities detectable by fluorescein angiography or clinical examination, and (3) multiple presumed "occult" serous retinal pigment epithelial detachments with a characteristic indocyanine green videoangiographic pattern. CONCLUSION: We suggest that the pathogenesis of CSC may be due to a choroidal vascular hyperpermeability with and without associated active pigment epithelial leaks and multiple presumed "occult" serous retinal pigment epithelial detachments. Based on these findings, a hypothetical model can be constructed related to the pathogenesis of CSC, beginning with choroidal abnormalities that secondarily affect the retinal pigment epithelium and neurosensory retina.
PURPOSE: To identify the precise choroidal abnormalities associated with idiopathic polypoidal choroidal vasculopathy (IPCV), patients with IPCV were examined with indocyanine green (ICG) videoangiography. METHODS: Twelve patients with IPCV were examined using standard clinical, fluorescein, and ICG videoangiographic techniques. RESULTS: Indocyanine green videoangiography showed two basic choroidal vascular changes: a branching network of vessels in the inner choroid, and vascular dilations at the border of the network of vessels. The vascular dilations appeared to be associated with the exudative and hemorrhagic manifestations of IPCV. CONCLUSION: The choroidal vasculopathy seen in IPCV is distinct from the changes seen in other choroidal abnormalities. Recognition of these changes aids in diagnosis and patient management, since the clinical implications of IPCV differ from those of other similar entities.
In the search for injectable subcutaneous fillers, fat harvested, transferred, and placed in the manner previously described has most of the characteristics of an ideal filler. It is biocompatible, versatile, stable, long-lasting, and natural-appearing. The key to successful fat grafting lies in the technique. Harvesting, refinement, and transfer of subcutaneous tissue to provide pure, intact parcels of fat are essential for successful fat grafting. The surgeon also must infiltrate the refined fat parcels into the recipient site so that they survive predictably and uniformly, become integrated into the host tissues, and accomplish the desired structural alteration. The key to attaining these goals is the placement of minuscule amounts of fatty tissue with each withdrawal of the infiltrating cannula. This maneuver maximizes the surface area of contact between the newly transplanted tissues and the recipient tissues. Applying this technique to enact structural volume alteration of the face can result in subtle or striking improvements in the appearance of patients. The ideal substance for soft-tissue augmentation still eludes physicians, but fat grafting through a blunt cannula seems to be the safest of all of the fillers used; in the hands of an experienced surgeon, it can provide long-lasting, natural-appearing structural changes.
PURPOSE: To describe the short-term anatomical and visual acuity responses after intravitreal injection of bevacizumab (Avastin, Genentech) in patients with choroidal neovascularization (CNV) secondary to age-related macular degeneration (AMD). METHODS: We conducted a retrospective study of patients with CNV secondary to AMD who were treated with intravitreal injection of bevacizumab (1.25 mg) during a 3-month period. Patients underwent best-corrected Snellen visual acuity testing, optical coherence tomography, and ophthalmoscopic examination at baseline and follow-up visits. RESULTS: There were 266 consecutive eyes of 266 patients who received injections, and follow-up information was available for 251 (94.4%). The mean age of the patients was 80.3 years, the mean baseline visual acuity was 20/184, and 175 (69.7%) had inadequate response to alternate methods of treatment. At the 1-month follow-up (data available for 244 patients), the mean visual acuity was 20/137 (P < 0.001 as compared with baseline), and 74 (30.3%) of patients had improvement in visual acuity as defined by a halving of the visual angle. At the 2-month follow-up (data available for 222 patients), the mean visual acuity was 20/122 (P < 0.001), and 78 (31.1%) of patients had visual improvement. At the 3-month follow-up (data available for 141 patients), the mean visual acuity was 20/109 (P < 0.001), and 54 (38.3%) of patients had visual acuity improvement. The mean central macular thickness at baseline was 340 mum and decreased to a mean of 247 microm at month 1 (P < 0.001) and 213 microm at month 3 (P < 0.001). At 1 month, two patients had mild vitritis, as did one patient at 2 months, who had a history of recurrent uveitis. No endophthalmitis, increased intraocular pressure, retinal tear, or retinal detachment occurred. The risk for thromboembolic disorders did not seem to be different than reported previously in studies concerning macular degeneration. CONCLUSION: There were no apparent short-term safety concerns for intravitreal bevacizumab injection for CNV. Treated eyes had a significant decrease in macular thickness and improvement in visual acuity. The follow-up was too short to make any specific treatment recommendations, but the favorable short-term results suggest further study is needed.
Eleven patients, 40 to 71 years old, had a choroidal vasculopathy that led to hemorrhagic and exudative macular degeneration. The patients had peculiar polypoidal, subretinal, vascular lesions associated with serious and hemorrhagic detachments of the retinal pigment epithelium. This macular disorder, which we have named idiopathic polypoidal choroidal vasculopathy (IPCV), appears to represent a distinct entity that differs clinically and demographically from age-related macular degeneration (AMD) and other macular diseases associated with subretinal neovascularization. Recognition of this condition is important because it may have specific risk factors, natural course, and management considerations that differ from those of age-related macular degeneration.
To report nine cases of pachychoroid pigment epitheliopathy.An observational case series of nine patients who underwent comprehensive ophthalmic examination, fundus photography, fundus autofluorescence, spectral-domain optical coherence tomography, and enhanced depth imaging optical coherence tomography.Eighteen eyes of 9 patients, aged 27 years to 89 years, were diagnosed with pachychoroid pigment epitheliopathy based on the characteristic funduscopic appearance of reduced fundus tessellation with overlying retinal pigment epithelial changes in one or both eyes, fundus autofluorescence abnormalities, and increased subfoveal choroidal thickness confirmed by enhanced depth imaging optical coherence tomography (mean, 460.2 μm). The five older patients had been previously diagnosed with age-related macular degeneration, while the four younger subjects were referred for possible inflammatory chorioretinitis, pattern dystrophy, or nonspecific drusen. No subjects had a history of or subsequently developed subretinal fluid.Pachychoroid pigment epitheliopathy falls within a spectrum of diseases associated with choroidal thickening that includes central serous chorioretinopathy and polypoidal choroidal vasculopathy, and it should be suspected in eyes with a characteristic fundus appearance related to choroidal thickening and associated retinal pigment epithelial abnormalities but no history of subretinal fluid. Enhanced depth imaging optical coherence tomography confirming an abnormally thick choroid and characteristic retinal pigment epithelial changes on fundus autofluorescence support the diagnosis. Because these patients are frequently misdiagnosed, the recognition of pachychoroid pigment epitheliopathy may avoid unnecessary diagnostic testing and interventions.
A consecutive series of newly-diagnosed patients with central serous chorioretinopathy (CSC) was compared to two independent control groups chosen from the same patient population for the presence of a Type A behavioral pattern based on the Jenkins Activity Survey. The patients selected as matched controls had painless, reduced central vision and other chorioretinal diseases (Group I), or non-chorioretinal ocular conditions (Group II). The Type A behavior was significantly more frequent in study patients than in either Control Group I(X2 =6.1 and P<0.025) or Control Group II patients (X2=17.7 and P<0.001). When both control groups were combined for comparison to the CSP patients, there was also a highly significant difference with regard to Type A behavior (X2=14.1 and P<0.001). A comparison of Control Group I with Control Group II revealed no significant difference in Type A behavior. Subfactor analysis of the Type A behavior pattern was also studied. The results of this clinical study were used in conjunction with experimental evidence linking catecholamines with CSP in developing a multifactorial etiologic hypothesis. The hypothesis suggests that the eyes as an organ system, and the macula as an ultimate target area, can be intermittently or continuously stimulated adversely by Type A behavior and its physiological consequences, most notably a sympathetic discharge. The multifactorial concept alludes to other potential risk factors such as age, race, sex, refractive state, or unknown tissue susceptabilities. The pathogenesis implies an inter-relationship between finely balanced components of a complex biopsychological system involving an individual's genetic endowment, his environment, and his behavioral pattern. The concept also offers new possible lines of investigation for the treatment of CSP, utilizing pharmacological regulators and for its prevention through early identification of CSP-prone individuals. A review of the pertinent cardiovasculature literature linking the Type A behavior with coronary artery disease and the significant papers in the ophthalmic literature on central serous pigment epitheliopathy are included in the discussion.
PURPOSE: To report 3 cases of pachychoroid neovasculopathy, a form of Type 1 (sub-retinal pigment epithelium) neovascularization, occurring over areas of increased choroidal thickness and dilated choroidal vessels. METHODS: A retrospective observational case series of three patients who underwent comprehensive ophthalmic examination and multimodal imaging with fundus photography, fundus autofluorescence, spectral domain optical coherence tomography, enhanced depth imaging optical coherence tomography, fluorescein angiography, and indocyanine green angiography. RESULTS: In all 3 eyes of 3 patients, aged 55 years to 63 years, there was Type 1 neovascularization overlying a localized area of choroidal thickening and dilated choroidal vessels seen with enhanced depth imaging optical coherence tomography. With indocyanine green angiography, there were large choroidal veins and choroidal hyperpermeability seen beneath the area of the neovascular tissue in all three eyes. No eyes had evidence of submacular exudative detachment or autofluorescence changes to suggest antecedent acute or chronic central serous chorioretinopathy. No eyes had drusen or degenerative changes to suggest age-related macular degeneration or other degenerative diseases. In one patient, the fellow unaffected eye demonstrated retinal pigment epithelium abnormalities, best seen with fundus autofluorescence, overlying focal dilated choroidal vessels seen with enhanced depth imaging optical coherence tomography and associated choroidal hyperpermeability seen with indocyanine green angiography, consistent with the diagnosis of pachychoroid pigment epitheliopathy. All three eyes showed the appearance of polypoidal structures within the neovascular tissue. CONCLUSION: Pachychoroid neovasculopathy falls within a spectrum of diseases associated with choroidal thickening that includes pachychoroid pigment epitheliopathy, central serous chorioretinopathy, and polypoidal choroidal vasculopathy and should be considered as a possible diagnosis in eyes with features of Type 1 neovascularization and choroidal thickening in the absence of characteristic age-related macular degeneration or degenerative changes. Pachychoroid neovasculopathy may occur as a focal abnormality within the macula, even in myopic eyes with normal subfoveal choroidal thickness. Pachychoroid neovasculopathy can ultimately progress to the development of polypoidal choroidal vasculopathy.
Central serous chorioretinopathy (CSC) is a common cause of central vision loss, primarily affecting men 20-60 years of age. To date, no consensus has been reached regarding the classification of CSC, and a wide variety of interventions have been proposed, reflecting the controversy associated with treating this disease. The recent publication of appropriately powered randomised controlled trials such as the PLACE trial, as well as large retrospective, non-randomised treatment studies regarding the treatment of CSC suggest the feasibility of a more evidence-based approach when considering treatment options. The aim of this review is to provide a comprehensive overview of the current rationale and evidence with respect to the variety of interventions available for treating CSC, including pharmacology, laser treatment, and photodynamic therapy. In addition, we describe the complexity of CSC, the challenges associated with treating CSC, and currently ongoing studies. Many treatment strategies such as photodynamic therapy using verteporfin, oral mineralocorticoid antagonists, and micropulse laser treatment have been reported as being effective. Currently, however, the available evidence suggests that half-dose (or half-fluence) photodynamic therapy should be the treatment of choice in chronic CSC, whereas observation may be the preferred approach in acute CSC. Nevertheless, exceptions can be considered based upon patient-specific characteristics.
OBJECTIVES: To review the frequency and nature of idiopathic macular telangiectasia and to classify the disorders based on new clinical and imaging observations. METHODS: A combined retrospective and prospective analysis of newly diagnosed patients seen over a period of 3 years. Patients were identified based on the Gass-Blodi classification and were studied with biomicroscopy, fluorescein angiography, and optical coherence tomography. RESULTS: Ten patients associated with aneurysmal telangiectasia (Gass-Blodi group 1) and 26 patients with perifoveal telangiectasia (Gass-Blodi group 2) were recruited. None with occlusive telangiectasia (Gass-Blodi group 3) were identified. New observations based on clinical, fluorescein angiographic, and optical coherence tomographic findings were made. CONCLUSIONS: Our series was similar to that in the Gass-Blodi study in terms of frequency. New observations in groups 1 and 2 have expanded our knowledge of the clinical spectrum of these disorders. A simplified classification termed idiopathic macular telangiectasia with 2 distinct types (type I, or aneurysmal telangiectasia, and type II, or perifoveal telangiectasia) was proposed to produce a better understanding of the entities and to enhance teaching and research. The third type, occlusive telangiectasia, has been omitted from our classification based on its rarity and presence of capillary nonperfusion rather than macular telangiectasia as the primary abnormality.
PURPOSE: The authors studied the indocyanine green (ICG) videoangiography findings of central serous chorioretinopathy (CSC) in older adults. BACKGROUND: Central serous chorioretinopathy in older adults may be confused with the exudative forms of age-related macular degeneration (AMD) because the two entities may have similar ophthalmoscopic and fluorescein angiographic findings. Because of its enhanced ability to image the choroidal circulation, ICG videoangiography has been used to describe certain choroidal vascular abnormalities in young adults with CSC, as well as older patients with choroidal neovascularization (CNV). The ICG videoangiography findings in CSC in older adults is largely unknown. METHODS: The authors performed ICG videoangiography on 36 patients aged 50 years or older with CSC to characterize their findings. RESULTS: The ICG videoangiography findings of the patients were consistent, revealing choroidal vascular hyperpermeability manifested by areas of hyperfluorescence that were first seen in the midphase of the angiogram. In the later phases of the angiogram, there were dispersion of the hyperfluorescence and a distinctive silhouetting of the larger choroidal vessels. CONCLUSIONS: Older patients with CSC have a unique temporal and topographic pattern of hyperpermeability that can help establish the proper diagnosis.
OBJECTIVE: To expand the clinical spectrum of idiopathic polypoidal choroidal vasculopathy based on historical cases and newly recognized observations. METHODS: A review of the previously reported 45 cases was carried out. An additional 20 cases were retrospectively reviewed to examine the clinical nature and course of idiopathic polypoidal choroidal vasculopathy. RESULTS: New observations on the clinical spectrum of idiopathic polypoidal choroidal vasculopathy were noted for demographic features, the nature and course of the vascular lesion, the possible association with intraocular inflammation, and the indocyanine green angiographic characteristics. CONCLUSIONS: Idiopathic polypoidal choroidal vasculopathy seems to be a distinct clinical entity that has a predilection for individuals of pigmented races. The disorder should be differentiated from typical choroidal neovascularization and other known choroidal degenerative, inflammatory, and ischemic disorders because of differences in clinical course and treatment.
PURPOSE: To correlate clinical manifestations with choroidal morphology in pachychoroid disorders, including central serous chorioretinopathy, pachychoroid pigment epitheliopathy, pachychoroid neovasculopathy, and polypoidal choroidal vasculopathy, using en face swept-source optical coherence tomography (OCT). METHODS: Patients with pachychoroid spectrum diagnoses were identified nonconsecutively through a review of charts and multimodal imaging. Each eye was categorized as uncomplicated pachychoroid, pachychoroid pigment epitheliopathy, central serous chorioretinopathy, pachychoroid neovasculopathy, or polypoidal choroidal vasculopathy. All patients included in this series then underwent bilateral swept-source OCT. RESULTS: Sixty-six eyes of 33 patients were included. Numbers assigned to diagnostic categories were 8 uncomplicated pachychoroid, 13 pachychoroid pigment epitheliopathy, 27 central serous chorioretinopathy, 15 pachychoroid neovasculopathy, and 3 polypoidal choroidal vasculopathy. One eye was classified as normal. Swept-source OCT choroidal thickness maps confirmed increased thickness under the areas of pachychoroid pigment epitheliopathy, central serous chorioretinopathy, type 1 NV (pachychoroid neovasculopathy), or polyps (polypoidal choroidal vasculopathy). En face swept-source OCT showed dilated outer choroidal vessels in all eyes. In several eyes with a chronic disease, focal choriocapillaris atrophy with inward displacement of deep choroidal vessels was noted. CONCLUSION: Although clinical manifestations of pachychoroid spectrum disorders vary considerably, these entities share morphologic findings in the choroid, including increased thickness and dilated outer choroidal vessels. En face swept-source OCT localizes these changes to disease foci and shows additional findings that may unify our understanding of disease pathogenesis.