Injury to the primary visual cortex, including lesions and other trauma, leads to the loss of visual experience. However, the residual vision that is left cannot be attributed to V1. According to Schmid et al., "thalamic lateral geniculate nucleus has a causal role in V1-independent processing of visual information". This information was found through experiments using fMRI during activation and inactivation of the LGN and the contribution the LGN has on visual experience in monkeys with a V1 lesion. These researchers concluded that the magnocellular system of the LGN is less affected by the removal of V1, which suggests that it is because of this system in the LGN that 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.