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What does Neural Plasticity Tell us about Role of Primary Visual Cortex (V1) in Visual Awareness?

Juha Silvanto, Geraint Rees

Frontiers in Psychology January 20, 2011 DOI: 10.3389/fpsyg.2011.00006 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Review Peer reviewed
Topics Neuroplasticity
Keywords Plasticity Transcranial magnetic stimulation Consciousness Blindsight Visual awareness V1 Extrastriate
Key findings Argues that V1 is not necessary for conscious visual perception in all circumstances, citing cases of conscious vision recovery after V1 lesions, hemianopic completion, and stimulation-induced percepts. Proposes that V1's critical role in visual awareness reflects its provision of most extrastriate visual input, rather than any unique functional property, since cat visual recovery involves restored extrastriate tuning rather than V1 emulation.

Abstract

The complete loss of visual awareness resulting from a lesion to the primary visual cortex (V1) suggests that this region is indispensable for conscious visual perception. There are however a number cases of conscious perception in the absence of V1 which appear to challenge this conclusion. These include reports of patients with bilateral V1 lesions sustained at an early age whose conscious vision has spontaneously recovered, as well as stroke patients who have recovered some conscious vision with the help of rehabilitation programs. In addition, the phenomenon of hemianopic completion and percepts induced by brain stimulation suggest that V1 may not be necessary for conscious perception in all circumstances. Furthermore, that the visual abilities in the cat are associated with the recovery of normal extrastriate tuning properties rather than emulation of V1 functions suggests that there is nothing unique about the functional properties of this region in visual awareness. Rather, the dramatic effect of a V1 lesion on visual awareness may be due to its role in providing the majority of extrastriate visual input, the loss of which abolishes normal neural responsiveness throughout the visual cortex.

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