Diplopia secondary to aniseikonia associated with macular disease

Objective: To provide an explanation for diplopia and the inability to fuse in some patients with macular disease. Methods: We identified 7 patients from our practices who had binocular dipl opia concurrent with epiretinal membranes or vitreomacular traction. A revi ew of the medical records of all patients was performed. In addition to com plete ophthalmologic and orthoptic examinations, evaluation of aniseikonia using the Awaya New Aniseikonia Tests (Handaya Co Ltd, Tokyo,Japan) was per formed on all patients. Results: All patients were referred for troublesome diplopia. Six of the pa tients had epiretinal membranes and 1 had vitreomacular traction. All 7 pat ients had aniseikonia, ranging from 5% to 18%. In 5 of the patients the ima ge in the involved eye was larger, and in the other 2 patients it was small er than in the fellow eye. All patients had concomitant small-angle strabis mus and at least initially did not fuse when the deviation was offset with a prism. Response to optical management and retinal surgery was variable. Conclusions: Aniseikonia caused by separation or compression of photorecept ors can be a contributing factor to the existence of diplopia and the inabi lity to fuse in patients with macular disease. Concomitant small-angle stra bismus and the inability to fuse with prisms may lead the clinician to the incorrect diagnosis of central disruption of fusion. Surgical intervention does not necessarily improve the aniseikonia.