Blindsight depends on the lateral geniculate nucleus

Top Cited Papers
Open Access
Publisher Website
Google Scholar
Abstract
The primary visual cortex (V1) is crucial for vision, but nearly 40 years ago it was noted that, intriguingly, human patients with V1 injuries can still point to or avoid visual stimuli despite having no conscious perception of them. It has long been thought that this 'blindsight' relies on visual pathways that bypass the usual route from the lateral geniculate nucleus (LGN) to the V1. Using a combination of permanent and reversible lesions, along with behavioural testing and functional magnetic resonance imaging (fMRI) of multiple visual areas in macaques, Schmid et al. show that the LGN itself is a vital link in the 'alternate pathway'. In V1-lesioned animals, LGN inactivation abolishes both visual detection and fMRI activation in higher visual areas, implicating direct LGN projections not only in blindsight, but also as a viable secondary pathway for fast detection during normal vision. The primary visual cortex (V1) is crucial for vision, yet people with V1 injuries might still point to or avoid visual stimuli, despite having no conscious perception of them. It has been thought that this 'blindsight' relies on visual pathways that bypass the usual route from lateral geniculate nucleus (LGN) to V1. But it is shown here — using a combination of permanent and reversible lesions, behavioural testing and functional magnetic resonance imaging (fMRI) mapping — that a critical link in the alternative pathway is in fact the LGN. Injury to the primary visual cortex (V1) leads to the loss of visual experience. Nonetheless, careful testing shows that certain visually guided behaviours can persist even in the absence of visual awareness1,2,3,4. The neural circuits supporting this phenomenon, which is often termed blindsight, remain uncertain4. Here we demonstrate that the thalamic lateral geniculate nucleus (LGN) has a causal role in V1-independent processing of visual information. By comparing functional magnetic resonance imaging (fMRI) and behavioural measures with and without temporary LGN inactivation, we assessed the contribution of the LGN to visual functions of macaque monkeys (Macaca mulatta) with chronic V1 lesions. Before LGN inactivation, high-contrast stimuli presented to the lesion-affected visual field (scotoma) produced significant V1-independent fMRI activation in the extrastriate cortical areas V2, V3, V4, V5/middle temporal (MT), fundus of the superior temporal sulcus (FST) and lateral intraparietal area (LIP) and the animals correctly located the stimuli in a detection task. However, following reversible inactivation of the LGN in the V1-lesioned hemisphere, fMRI responses and behavioural detection were abolished. These results demonstrate that direct LGN projections to the extrastriate cortex have a critical functional contribution to blindsight. They suggest a viable pathway to mediate fast detection during normal vision.