Pathogenesis of cystoid macular edema: An anatomic consideration of vitreoretinal adhesions

https://doi.org/10.1016/0039-6257(84)90231-5Get rights and content

Abstract

Although it had been widely accepted that vitreous traction plays a key role in the pathogenesis of aphakic cystoid macular edema, vitreoretinal traction is not observable in many patients and other hypotheses have also been investigated. The authors review the present knowledge of the anatomy of the vitreoretinal interface and the pathologic findings in cystoid macular edema. A new hypothesis combining the effects of both traction and inflammation is proposed.

References (31)

  • EA Balazs

    The Vitreous. Int Ophthalmol Clin

    (1973)
  • M Boniuk

    Cystic macular edema secondary to vitreoretinal traction

    Surv Ophthalmol

    (1968)
  • G Eisner

    Biomicroscopy of the peripheral fundus

    Surv Ophthalmol

    (1972)
  • G Eisner

    Clinical examination of the vitreous

    Trans Ophthalmol Soc UK

    (1975)
  • BS Fine et al.
  • Cited by (121)

    • Correlation of collagen fibril properties and inner limiting membrane thickness with vitreoretinal adhesion in human eyes

      2022, Experimental Eye Research
      Citation Excerpt :

      Collagen fibrils in the vitreous cortex have been shown to penetrate the inner limiting membrane of the retina at the vitreous base (Wang et al., 2003; Gloor and Daicker, 1975) and are thought to superficially intersect the retina at the macula in the posterior pole (Foos, 1975; Sebag and Balazs, 1984, 1989). Between these anterior–posterior regions, collagen is thought to run parallel and attach to the retina with a type of extracellular matrix ‘glue’ (Foos, 1972b; Sebag and Balazs, 1984; Matsumoto et al., 1984). Collagen fibril penetration in the posterior pole may explain the disrupted ILM found by the peel tests in Creveling et al. and fibers running parallel to the equator may explain the lack of ILM disruption in the equator.

    • The effect of pars plana vitrectomy with internal limiting membrane peeling on the durability of the intravitreal dexamethasone implant in the treatment of diabetic macular edema

      2022, American Journal of Ophthalmology Case Reports
      Citation Excerpt :

      A slow-release intravitreal implant of 0.7 mg Dexamethasone (DEX-I) (Ozurdex, Allergan, Dublin, Republic of Ireland) is a proven therapy for DME, improving Best Corrected Visual Acuity (BCVA) and reducing Central Foveal Thickness (CFT) for up to six months,2 although in some eyes the first signs of recurrence are found after three or four months.3–5 The vitreous body, together with the posterior hyaloid and the internal limiting membrane (ILM), may be involved in the pathogenesis of DME,6–8 and pars plana vitrectomy (PPV) may have a positive functional effect especially when macular traction is evident. Nevertheless, before the advent of intravitreal therapy, many case series reported positive effects of PPV also in eyes with non-tractional DME.9–12

    • Coincident PAMM and AMN and Insights Into a Common Pathophysiology

      2022, American Journal of Ophthalmology
      Citation Excerpt :

      Fine and Brucker39 studied three patients with pre-enucleated FA that demonstrated cystoid macular edema, whereas the postenucleated histopathology showed that the Müller cell cytoplasm was swollen without enlargement of intercellular spaces, thus supporting the concept of intracellular/cytotoxic Müller cell edema secondary to vascular abnormalities. The swelling of Müller cells preceded extracellular edema formation.39,40 Main limitations of the current study include the retrospective nature of the cases review and the limited number of eyes included.

    • Numerical investigation of partially liquefied vitreous dynamics as two-phase viscoelastic-Newtonian fluid flow in a planar cavity due to oscillatory motion

      2020, International Journal of Multiphase Flow
      Citation Excerpt :

      Two types of the PVL configurations with liquid parts located inside a circular cavity with Ro equal to 12.5 mm (the radius of human vitreous chamber) are illustrated in Fig. 1. These two configurations are selected based on previous researches and clinical observations which have shown that vitreous liquefaction usually originates from the central and the posterior portions of the vitreous (Eisner, 1975; Tolentino et al., 1975; Sebag and Balazs, 1984; Sebag, 1987; Kishi and Shimizu, 1990). As depicted, the PVL contains two regions: one liquefied vitreous assumed as a Newtonian fluid (purely viscous fluid), and the other vitreous gel with viscoelastic properties occupying the rest of the domain.

    View all citing articles on Scopus
    View full text