Graefe's Arch Clin Exp Ophthalmol (1987)225:315-320 Graefe's Archive for Clinical and Experimental Ophthalmology © Springer-Verlag 1987 Nd-YAG laser treatment in preretinal macular fibrosis*' ** M.J. Tassignon, M. Brihaye, and N. Stempels Akademisch Ziekenhuis V.U.B., Department of Ophthalmology, Laarbeeklaan 101, B-J090 Brussels, Belgium Abstract. Three eyes with preretinal macular fibrosis (PMF) were treated with the Q-switched Nd-YAG laser. The PMF was idiopathic in two eyes and associated with a vitreous hemorrhage, due to ocular trauma, in the third eye. The three eyes had in common a partial posterior vitreous de- tachment with vitreous traction on the macula. The Nd- YAG laser beam was focused on the detached posterior hyaloid in front of the macular region. Some holes were made in this membrane or in the adjacent collapsed vitreous cortex. Treatment increased the visual acuity in the three eyes; the vitreous remained partially detached in the two eyes with idiopathic PMF and detached completely in the eye with the secondary PMF. The disentanglement of the fovelar area was revealed by the unfolded appearance of the retinal vessels on fluoangiography. Introduction Preretinal macular fibrosis (PMF) is the term most cur- rently used to designate the shrinkage of the internal retinal surface. Other terms used in the literature are: the Jaffe syndrome, primary retinal folds, silent central vein obstruc- tion, wrinkling of the internal retinal surface, preretinal membrane, macular pucker, and cellophane maculopathy. The role of the vitreous in the anatomical and functional changes accompanying idiopathic preretinalfibrosis has not yet been fully established. Clinical descriptions of vitreo- retinal adhesion in PMF have been given by Schepens (1954) and Jaffe (1967a) and recently stressed by Sebag and Balazs (1984). Based on the principle of vitreoretinal adhesion, Jaffe (1967a) distinguished between a traction and a contraction phase in the clinical appearance of idio- pathic preretinal fibrosis. The traction phase is characterized by the presence of a whitish-grey membrane, covering and adhering to the macula. In the contraction phase, the termi- nal branches of the perimacular vessels become tortuous. The contraction capacity of these membranes has been stressed by Allen and Gass (1976). The pseudomacular hole presented in his case report was caused by the spontaneous contraction of an idiopathic epiretinal membrane surround- ing the macular area. * Presented at the XVth Meeting of the Club Jules Gonin, Copen- hagen, 10-15 August 1986 ** This work was supported by the Belgian National Foundation for Scientific Research Offprint requests to: M.J. Tassignon Idiopathic and secondary preretinal macular fibrosis can be considered, from a histological point of view, two differ- ent entities. In idiopathic preretinal macular fibrosis, the proliferation of glial cells of retinal origin through a defect in the internal limiting membrane was postulated by Roth and Foos (1971) and Foos (1974) and then subsequently demonstrated by Bellhorn et al. (1975). The proliferative capacity of the glial cells in these preretinal membranes was experimentally confirmed by Yamashita et al. (1985 a). A subclassification of idiopathic PMF was made by Foos (1974, 1980) and Kampik et al. (1980): "simple and complex nonvascular proliferative extraretinopathy." The morphologically differentiating features between these sub- groups are the presence and predominance of fibrocytelike and macrophagelike cells in the complex group, in addition to the glial cells found in the simple group. Secondary prere- final macular fibrosis, investigated by Machemer and La- qua (1975), Clarkson et al. (1977) and Kampik et al. (1981), is formed by various combinations of four morphologically distinct basic cell types: glial cells, fibrocytes, macrophages, and retinal pigment epithelial cells. The presence of micro- filaments in these cell types, as demonstrated by Yamashita et al. (1985b), can be the explanation of the contractile ca- pacity of these membranes. Stern et al. (1982) and Barry et al. (1985) suggested that the pathogenesis of secondary epiretinal membranes after total vitrectomy is primarily cell-mediated. To date, studies of the cellular origin of these preretinal membranes have been inconclusive. Fig. 1. Schematic illustration of the impacts focused on the de- tached posterior hyaloid in front of the macular area