Purpose-To investigate the relationship between drusen extent and foveolar choroidal blood flow in non-exudative AMD.Methods-Total drusen area, average druse area, and total drusen number were determined using a computer program developed to quantify the extent of manually outlined drusen from fundus photographs of 157 patients (239 eyes) with non-exudative AMD. Laser Doppler flowmetry was used to assess relative choroidal blood velocity (ChB Vel ), volume (ChB Vol ), and flow (ChB Flow ) in the center of the fovea.Results-We found a significant inverse relationship between total drusen area and ChB Vol or ChB Flow . For every 1 mm 2 increase in total drusen area, ChB Vol decreased by 0.0061 arbitrary units (AU; p=0.03) and ChB Flow decreased by 0.23 AU (p=0.049). Average druse area was also significantly inversely related to ChB Vol and ChB Flow . For every 0.01 mm 2 increase in average druse area, the ChB Vol decreased by 0.0149 AU (p=0.001) and the ChB Flow decreased by 0.4951 AU (p=0.003). Adjustment for age weakened the significance, though it remained strong for average druse area versus ChB Flow (p=0.017) and ChB Vol (p=0.004). The computer-aided quantification of drusen used in this study showed high intra-and inter-grader agreement.Conclusion-In patients with non-exudative AMD, there is an association between increased drusen extent and decreased ChB Vol and ChB Flow . This suggests the presence of ischemia and possibly the reason why patients with high risk drusen are prone to advanced disease.

amplification with a normal CDH11 copy number (Figure 2). MYCN amplification may account for the aggressiveness of the ovarian tumor, as it does for highly fatal neuroblastomas. 7 The evidence indicates that the ovarian tumor was an independent retinoblastoma rather than a metastasis. While our analysis did not attempt to reveal the cell of origin that underwent malignant transformation, marker analysis revealed that it was not of ovarian origin. Instead, we speculate that it may have been a retinal cell displaced into the ovary by an unknown mechanism. Alternatively, a primitive pluripotent cell persisting in the ovary may have acquired the second RB1 and subsequent other mutations allowing the malignant transformation.