[Age-dependent idiopathic macular foramen. Current concepts of the pathogenesis, diagnosis, and treatment]

Senile macular hole usually affects only one eye. It is caused by tangential contraction of the premacular vitreous cortex, particularly that in the foveolar area. Its early stages produce characteristic biomicroscopic findings. In approximately 50% of cases, spontaneous vitreofoveal separation and recovery of vision occurs. Differentiation between a stage 1 impending hole and a stage 2 hole may be difficult. A stage 2 hole may begin as either a central foveolar dehiscence or as a foveolar tear. In both cases, the holes may be accompanied by a similar appearing prehole opacity (pseudo-operculum in the former, and an operculum in the latter cases) in 75 to 80% of the cases. The visual prognosis is probably better in patients whose hole begin in the center. Histopathological examination of the prehole opacity for evidence of retinal tissue at the time of surgery should provide us with important information concerning the relative frequency of the two types of hole development. Meanwhile, there is accumulating circumstantial evidence to suggest that the majority of macular holes begin as a central dehiscence with little loss of retinal tissue and enlarge as a result of centrifugal displacement and concentration of the retinal receptors around the hole, and that visual improvement following surgery occurs not only because of reattachment of the retina, but also centripetal movement of the retinal receptors. Results of a small randomized study of treatment of stage 1 impending holes, while inconclusive, suggest that surgery is of little benefit. Although uncontrolled pilot studies of surgical treatment of full-thickness holes are encouraging, we must await results of the randomized trials to know its value.