To define themain clinical mechanisms involved in the pathogenesis of macular holes MH in patients affect Retinitis Pigmentosa Vitreoretinal interface Vitreous C GIUSTI R FORTE EM VINGO ID: 939579
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Pale ÒwaxyÓ optic disc pallor, attenuation of . To define themain clinical mechanisms involved in the patho-genesis of macular holes (MH) in patients affect- Retinitis Pigmentosa, Vitreoretinal interface, Vitreous. C. GIUSTI, R. FORTE, E.M. VINGOLOInstitute of Ophthalmology, ÒLa SapienzaÓ University Ð Rome (Italy) 46 forms (i.e., Usher or Laurence-Moon-Bardet-rettes daily), pregnancy, aphakia or�mmHg, refractive error ±4 D, history ofvitreoretinal surgery, previous retinal occlu-. In particular, vitrealstatic and dynamic biomicroscopy was per-formed on fully dilated pupils (one drop oflenses (Super Field and +78D Volk Lenses).The examination angle ranged from 14¡to20¡and the slit-lamp beam amplitude mea-sured 12 mm. Vitreal alterations were care-ed and, inside this area, all angiograms weregraded by one examiner only (E.M.V.) ac-cor
ding to the previously published FishmanÕsThe prevalence of posterior vitreous de-VRIA, CME, BEM and MH Ð was reported.(Apple Macintosh, StatView II program).Among a total amount of 472 eyes, only455 of them were statistically consideredin greater detail, in Table I. Normal macula(26.81% of the cases), BEM (21.54%), CME(9.45%), VRIA (26.15%) and mixed formsthy (178 eyes; Table I: E+G+H+I).A total number of 25 eyes (5.5%) were af-ular, in 9 of these cases (40.9%) MH was cor-were present separately. MH was identifiedas isolated vitreoretinal pathology in 3 casestively, the total number of eyes or only thoseMoreover, among a total number of 57eyes presenting both VRIA and CME (TableI: H+I), MH was diagnosed in 9 of them(15.79%) compared to 11 (20.37%) of 54 eyes(Table I: D+F) and 2 (1.65%) of 121 eyes(Table I: E+G) presenting CME or VRIAsepara
tely. phane maculopathy, BEM and CME areC. Giusti, R. Forte, E.M. Vingolo commonly associated with RP and seem to. In 1977, Fishman et al.,presented a BEM, 20% a CME and/or VRIApaper, even though performed on 31 subjectsonly, where the following percentages were. Thereafter,RP eyes: 42% BEM; 14% CME; 20% VRIA;Regarding MH, both Fishman et al. andPruett found a partial or full thickness MH inassociated with cystic degeneration of theMoreover, according to a very recent paper Figure 1.la; BEM = ÒbullÕs eyeÓ maculopathy; CME = cystoid macular edema; VRIA = vitreoretinal interface alterations; MH able I.Different associations found in the examined eyes between retinal and vitreal alterations (+ = presence; Ð =absence). MacularCystoid macularBullÕs eyeÓ VitreoretinalEyesholeedemaÒmaculopathyinterface alterations3 (0.66%)A122 (26.81%)B98 (21.54%)
C11 (2.42%)D2 (0.44%)E43 (9.45%)F119 (26.15%)G48 (10.55%)H9 (1.98%)I 48 generation of the vitreous body may repre-However, this difference may probably betients (38.5 ±14.9 years) but also to the moreIn summary, our investigation may not besmall number of patients enrolled and theiryoung mean age. However, even though furtherReferencesLBERTophthalmology. Philadelphia: Saunders, 1994.P, SCHUBERT. Retina and vitreous. Textbook ofOphthalmology, vol. 9. London: Mosby, 1994.TP, BFriedenwald Lecture. Invest Ophthalmol Vis Sci1995; 36: 1197-1200.M, MGA, Mtions and correlations. Trans Am Ophthalmol SocORTEment of cystoid macular edema in patients affect-ed by Retinitis Pigmentosa. A pilot study. Eur Rev8)MMF, AG, AG, BORTE. Vitreal al-ETINOPATHYof diabetic retinopathy. Invest Ophthalmol Vis Sci11)ILBERTMEMIYAAKAWAG, BC. Giusti, R. Forte, E.M. Vingo