In previous times diagnosis of a macular hole appeared to be easily done by biomicroscopy or just by ophthalmoscopy. It was a comparatively rare diagnosis without therapeutic relevance. It is only 10 years ago that specific diagnostic criteria were set to consider surgical intervention.1 Further studies have established the usefulness of vitreoretinal surgery for macular holes. Macular hole is now a common diagnosis, affecting almost 3% of the elderly population. However, diagnostic and therapeutic details remain an enigma.

Today, two types of surgical intervention are used to treat macular holes. One is to perform vitrectomy, remove the vitreous cortex, apply some sort of biological chorioretinal glue2 over the macula, and finally to fill the vitreous cavity with a long lasting gas bubble, tamponading the macular hole with the patient in a prone position. The “biological glue” in use may be transforming growth factor β, autologous serum or plasma, platelet concentrates, thrombin, and others. Another surgical approach is to omit the biological glue and instead remove the internal limiting membrane of the retina including the adhering fibrocellular proliferations.3 4 Both modifications of surgery for macular holes have a very high rate of success in closing the macular hole; the results with regard to functional outcome are not yet comparable in a randomised fashion.

So far, it is not clear whether there are different forms or specific types of macular holes which warrant one or the other type of operation. Also, it is unclear why differing surgical approaches are leading to similar good results. It would therefore be of great interest to have predictive diagnostic criteria to obtain more insight into the pathogenesis of macular hole formation. In short, it is of interest to know whether changes at the vitreoretinal interface or changes at the metabolic level of the retina and/or the retinal pigment epithelium (RPE) are responsible for the formation of a macular hole, thus determining the mode of therapeutic action. Diagnostic tools to answer these questions are most desirable.

It not surprising, therefore, that all available diagnostic tools are used to achieve the most precise diagnostic evaluation. So far fluorescein angiography, optical coherence tomography (OCT) and, most recently, the retinal thickness analyser (RTA) have been used. In this issue (p 346) confocal laser scanning ophthalmoscopy (cLSO) is discussed as a potential alternative in the assessment and differential diagnosis of full thickness macular holes. However, measurement of increased fundus autofluorescence in the area of a macular hole may accurately detect a defect in the shadowing effect of xanthophyll. It may permit an unhindered view of the lipofuscin laden RPE, but this measurement of autofluorescence does not give a clue to any specific pathogenic mechanisms. Thus, cLSO might help to differentiate between true full thickness macular holes and pseudoholes, but does not help to answer the puzzling questions mentioned above. Despite its elegant help in confirming a definite diagnosis, cLSO so far does not have a prognostic value similar to fluorescein angiography.

In order to elucidate major pathogenic factors of macular hole formation and, subsequently, the appropriate treatment comparative evaluation of morphological and functional tests will be necessary. Analysis of any removed tissue5 and possibly more insight into the cell biology of glial cell proliferation and posterior vitreous separation are needed to answer the enigma of the macular hole and its therapy.