Fundoscopy in GA typically shows a well-circumscribed oval or round area of pigment epithelium atrophy, usually sparing the fovea until late stages (Fig. 2).

All precursor lesions of this final appearance can also be present: large drusen (>125 microns), focal pigmentation changes and refractile deposits^(3,23).

On fluorescein angiography, GA appears as a sharply delineated window defect due to atrophy of overlying layers of RPE (Fig. 3).

A prolonged choroid filling phase has been described as a clinical marker for changes in Bruch’s membrane, and as a risk factor for development of geographic atrophy⁽²⁴⁾.

Despite these aspects in GA, fluorescein angiography may be indicated only in atypical cases, in order to allow the correct diagnosis⁽³⁸⁾.

OCT scan shows thinning of hyperreflective external band, corresponding to attenuation of RPE/Bruch’s complex, and deeper hyperreflectivity because of loss of outer layers including photoreceptors (Fig. 4)^(39,40).

In high resolution OCT the atrophic area shows hyperreflective clumps at different levels, segmented plaques of the outer band and elevations with variable reflectivity⁽⁴¹⁾.

In the perilesional area there are elevations of the outer retinal layers, as well as thickening of outer hyperreflective band.

At the junction area the outer band shows different degrees of loss⁽⁴¹⁾.

Fundus spectrophotometric studies in vivo by Delori and co-workers, have shown that FAF represents an accumulation of lipofuscin in the lysossomes of RPE cells, mainly derived from photoreceptors outer segments degradation.

The compound is found as micrometer-sized spherical particles and is characterized by yellow autofluorescence when exposed to blue light^(42,43,44).

It has been shown with confocal scanning laser ophthalmoscopy (cSLO) that FAF response is very low or extinguished in areas of atrophy.

The lack of RPE cells or its low number and therefore of lipofuscin, (the dominant fluorophore) explain this reduction⁽⁴⁵⁾.

Increased FAF precedes development of GA^(46,47).

FAF is increased in junctional zone around areas of atrophy, and intensity seems to correlate with extension of the atrophic area, and also with reduction of retinal sensitivity detected by fundus perimetry^(48,49).

Despite the works of Holz and Valkenberg, the prognostic value of FAF remains controverse.

In a recent study, FAF was not a strong risk factor for development or extension of GA⁽⁵⁰⁾.