Abstract
When the primary visual cortex (V1) is damaged, the principal visual pathway is lost, causing a loss of vision in the opposite visual field. While conscious vision is impaired, patients can still respond to certain images; this is known as ‘blindsight’. Recently, a direct anatomical connection between the lateral geniculate nucleus (LGN) and human motion area hMT+ has been implicated in blindsight. However, a functional connection between these structures has not been demonstrated. We quantified functional MRI responses to motion in 14 patients with unilateral V1 damage (with and without blindsight). Patients with blindsight showed significant activity and a preserved sensitivity to speed in motion area hMT+, which was absent in patients without blindsight. We then compared functional connectivity between motion area hMT+ and a number of structures implicated in blindsight, including the ventral pulvinar. Only patients with blindsight showed an intact functional connection with the LGN but not the other structures, supporting a specific functional role for the LGN in blindsight.
Highlights
Damage to the primary visual cortex (V1) that may occur following a stroke causes visual loss in the corresponding part of the visual field
Neither a specific role for the lateral geniculate nucleus (LGN) nor a functional connection to hMT+ has been shown in human blindsight and would significantly advance our understanding of how patients respond to visual images in the absence of V1
At the most basic level, we have shown that human motion area hMT+ does not require V1 to demonstrate a normal functional MRI (fMRI) response to speed
Summary
Damage to the primary visual cortex (V1) that may occur following a stroke causes visual loss in the corresponding part of the visual field (homonymous hemianopia, [1]). Extensive research has shown that some patients retain an ability to respond to images inside their scotoma, even though they may not consciously see them [2]. This phenomenon is called blindsight, and recent work applied diffusion MRI and tractography in patients with V1 damage to try to uncover which pathways may underlie this residual visual function [3]. Neither a specific role for the LGN nor a functional connection to hMT+ has been shown in human blindsight and would significantly advance our understanding of how patients respond to visual images in the absence of V1
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