In a nutshell: Children with injury to the brain’s visual cortex often regain near normal vision; the same injuries in adults damages sight permanently. New research suggests infant brains can compensate by using an alternative pathway to send visual information through the brain.

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The big picture:

According to the textbooks, information from the eye is transmitted for processing across the brain’s visual cortex through a part of the brain called the lateral geniculate nucleus or LGN for short.

Recently a second route was discovered through the pulvinar. Both these regions sit in the thalamus, site of some of the brain’s major highways.

Here, a team led by James Bourne and his colleagues at ARMI and CIBF show that the infant brain uses the secondary route through the pulvinar to compensate for brain damage that affects the main one.

Bourne and his team did this using a novel combination of brain imaging techniques, including one called diffusion MRI, which allowed them to map the connections between brain cells, and watch how they changed following injury.

The ability to switch to the secondary pathway could be one explanation for why certain types of brain damage cause permanent blind spots in adults, but not in children.

“We’re a long way off but this opens up a whole new line of inquiry to see if we can develop regenerative techniques to restore vision loss,” said Claire Warner, a PhD student in the Bourne lab.

The Bourne team also found that as the brain matures, the preferred pathway through the LGN becomes hardwired for the transmission of visual information that is used for conscious vision. The secondary pathway becomes hardwired for subconscious motion perception.

And the ability to switch between pathways is largely lost.

Next steps:
Understanding how the brain develops and refines the visual pathways during infancy may help recovery from brain injuries in adults.

Warner, C. E., Kwan, W. C., Wright, D., Johnston, L. A., Egan, G. F., & Bourne, J. A. (2015). Preservation of vision by the pulvinar following early-life primary visual cortex lesions. Current Biology, 25(4), 424-434.

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