blindsight occurs. furthermore, once the lgn was inactivated, virtually all of the extrastriate areas of the brain no longer showed a response on the fmri. the information leads to a qualitative assessment that included "scotoma stimulation, with the lgn intact had fmri activation of ~20% of that under normal conditions". this finding agrees with the information obtained from, and fmri images of, patients with blindsight. the same study also supported the conclusion that the lgn plays a substantial role in blindsight. specifically, while injury to v1 does create a loss of vision, the lgn is less affected and may result in the residual vision that remains, causing the "sight" in blindsight. functional magnetic resonance imaging has launched has also been employed to conduct brain scans in normal, healthy human volunteers to attempt to demonstrate that visual motion can bypass v1, through a connection from the lgn to the human middle temporal complex. their findings concluded that there was an indeed a connection of visual motion information that went directly from the lgn to the v5/hmt+ bypassing v1 completely. evidence also suggests that, following a traumatic injury to v1, there is still a direct pathway from the retina through the lgn to the extrastriate visual areas. the extrastriate visual areas include parts of the occipital lobe that surround v1. in non-human primates, these often include v2, v3, and v4. in a study conducted in primates, after partial ablation of area v1, areas v2 and v3 were still excited by visual stimulus. other evidence suggests that "the lgn projections that survive v1 removal are relatively sparse in density, but are nevertheless widespread and probably encompass all extrastriate visual areas," including v2, v4, v5 and the inferotemporal cortex region.