Ординатура / Офтальмология / Английские материалы / Visual Fields Examination and Interpretation_Walsh_2011
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Figure 7-5. Pathologic myopia. (A) and (B) Goldmann visual field of right and left eye show central scotoma. (C) and (D) Fundus photo, right and left eye.
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Visual Field Defects in Chorioretinal Disorders |
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Figure 7-5. (Continued)
7-5 INFLAMMATORY/INFECTIOUS DISEASES
Inflammatory diseases can cause visual field changes due to structural sequelae of the underlying inflammation, such as vitritis, macular edema, or optic disc edema. Lesions in the choroid and retina will also cause visual field defects.
Several of the “white dot syndromes” are associated with classic visual field findings that help distinguish one from another. Multiple evanescent white dot syndrome (MEWDS) and acute zonal occult outer retinopathy (AZOOR) may present with an enlarged blind spot without evidence of optic disc edema.3,4 MEWDS is a unilateral acute-onset syndrome, often associated with a viral prodrome that presents with multiple white spots. Fluorescein angiography often demonstrates early punctate hyperfluorescence with a “wreathlike” configuration that stains late. Symptoms usually resolve within 2 months. AZOOR, in contrast, may have few initial fundus findings but is characterized with an insidious, progressive loss of outer retinal function and irreversible ERG changes. Large visual field defects may develop and correlate with late fundus findings of loss of RPE and attenuated vessels.5
Ocular histoplasmosis has a field defect that is correlated with fundus histo lesions (Figure 7-12). Serpiginous choroidopathy often presents with subretinal lesions that begin in the peripapillary region and spread in a centrifugal fashion. The resulting “serpentine” lesions block early and stain late on fluorescein angiography. Active lesions will present with absolute scotomas, which can involve central fixation if the fovea is involved.
Birdshot chorioretinopathy (BSCR) is a chronic uveitic condition that is characterized by bilateral yellowish ovoid spots in the mid periphery associated with a mild vitritis. Visual loss from BSCR often results from recurrent cystoid macular edema or progressive retinal dysfunction with constriction of the peripheral visual
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Figure 7-6. Diabetic macular edema. (A) HVF 24-2 of both eyes show nonspecific changes. (B) Fundus photo, right eye. (C) Fluorescein angiogram, left eye. Late phase shows diffuse leakage in macula with multiple microaneurysms and macular ischemia. (D) Stratus OCT shows retinal thickening with associated cystic spaces.
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Figure 7-6. (Continued)
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Figure 7-7. Central retinal vein occlusion (CRVO). (A) HVF 24-2, right eye, with inferior central depression. (B) Fundus photo, right eye. Note diffuse intraretinal hemorrhages and macular edema. (C) Fluorescein angiogram, right eye. Late phase shows enlarged foveal avascular zone with macular and perivascular leakage. (D) Stratus OCT shows cystoid macular edema.
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Figure 7-7. (Continued)
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Figure 7-8. Branch retinal vein occlusion (BRVO). (A) Branch retinal vein occlusion (BRVO). HVF 24-2, left eye, with superior depression. (B) Fundus photo, left eye. Intraretinal hemorrhages and exudates in inferior macula. (C) Stratus OCT. Note diffuse retinal thickening.
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Figure 7-8. (Continued)
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Figure 7-9. Choroideremia. (A) HVF 10-2, both eyes, with bilateral dense defects and relative central sparing. (B) and (C) Goldmann visual field, right and left eye. (D) and (E) Fundus photo, right and left eye. Choroideremia is characterized by diffuse atrophy of the choriocapillaris, choroid, and retinal pigment epithelium.
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Figure 7-9. (Continued)
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