Blindsight depends on the lateral geniculate nucleus

Michael C. Schmid (), Sylwia W. Mrowka, Janita Turchi, Richard C. Saunders, Melanie Wilke, Andrew J. Peters, Frank Q. Ye and David A. Leopold
Additional contact information
Michael C. Schmid: Laboratory of Neuropsychology, National Institute of Mental Health (NIMH), 49 Convent Drive, Bethesda, Maryland 20892, USA
Sylwia W. Mrowka: Laboratory of Neuropsychology, National Institute of Mental Health (NIMH), 49 Convent Drive, Bethesda, Maryland 20892, USA
Janita Turchi: Laboratory of Neuropsychology, National Institute of Mental Health (NIMH), 49 Convent Drive, Bethesda, Maryland 20892, USA
Richard C. Saunders: Laboratory of Neuropsychology, National Institute of Mental Health (NIMH), 49 Convent Drive, Bethesda, Maryland 20892, USA
Melanie Wilke: Laboratory of Neuropsychology, National Institute of Mental Health (NIMH), 49 Convent Drive, Bethesda, Maryland 20892, USA
Andrew J. Peters: Laboratory of Neuropsychology, National Institute of Mental Health (NIMH), 49 Convent Drive, Bethesda, Maryland 20892, USA
Frank Q. Ye: Neurophysiology Imaging Facility, NIMH, National Institute of Neurological Disorders and Stroke (NINDS), National Eye Institute (NEI), 49 Convent Drive, Bethesda, Maryland 20892, USA
David A. Leopold: Laboratory of Neuropsychology, National Institute of Mental Health (NIMH), 49 Convent Drive, Bethesda, Maryland 20892, USA

Nature, 2010, vol. 466, issue 7304, 373-377

Abstract: The blindsight pathway 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.

Date: 2010
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DOI: 10.1038/nature09179

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