The presence of focal lesions in primary visual cortex (V1) provides an opportunity to study the role of extra-geniculo-striate pathways for activating extra-striate areas. Single unit measurements reported inactivation of more than 95% of V2 and V3 neurons following reversible cooling of V1 (Girard and Bullier, 1989; Girard et al., 1991a; Schiller et al., 1974). Here we used fMRI in anesthetized monkeys (Logothetis et al., 1999) to study the organization and activation levels of areas V2 and V3 from one month up to 681 days following a focal V1 aspiration lesion. We find that the strength of stimulus driven BOLD activation inside the area V2, V3 lesion projection zones (LPZ) drops by ~70 % compared to baseline and shows no systematic change between the first month post-lesioning and the maximum time studied. Interestingly, the retinotopic organization of the area V2, V3 LPZs remains similar to pre-lesion maps. Restricting the stimulus to the non-lesioned visual field is not effective in activating the ipsi-lesional LPZ ruling out the possibility that callosal input mediates the observed pattern of responses. We conclude that residual activity in V2 and V3 devoid of V1 input is likely due to parallel subcortical pathways possibly contributing to the behavioral phenomenon of blindsight. Figure Caption: Eccentricity map of the right visual cortex of a rhesus macaque 681 days post-V1 lesioning. Visual stimulation was performed using a rotating checkerboard ring stimulus (gray inset) expanding in time and space which resulted in a phase shift of the BOLD response (retinotopic mapping). Voxels with similar phase values are color-coded (colored inset) and superimposed on the anatomical flat map. The lesion in V1 extends from ~2.3 to 7°, and from the external calcarine to the lunat