A seven-year-old boy in Australia who has lost most of his visual cortex in infancy but has somehow retained normal vision mystifies scientists.
How can a boy with an injury to his primary visual cortex still be able to see?
The boy, referred only as “BI”, developed a rare condition called medium-chain acyl-Co-A dehydrogenase deficiency as an infant, leading him to lose most of his brain’s visual cortex as a result. The visual cortex, in a nutshell, is what enables us to see. Our primary visual cortex contains neurons that are sensitive to things like the direction of moving objects and a contour’s orientation. People missing these neurons, like BI, usually suffer from cortical blindness, resulting in a partial or total loss of sight.
However, BI still has normal vision, and his biggest issue is just that he’s short-sighted. The boy can still recognize faces, and is even able to play soccer. What, therefore, has enabled BI to keep his sight despite missing neurons in his primary visual cortex?
BI is able to play soccer even with an injury in his visual cortex.
Being able to have normal albeit short-sighted vision is unheard of in people with injury to the visual parts of their brain. BI’s case, therefore, was certainly a fascinating one for researchers. According to a study on BI’s condition, which was presented in the 37th Annual Scientific Meeting of the Australasian Neuroscience Society, medium-chain acyl-Co-A dehydrogenase deficiency is an illness that prevents the conversion of certain fats into energy. This led to a lesion in BI’s primary visual cortex. At the very least, this lesion should have made it difficult for BI to form coherent visual images.
However, that’s not the case. "Despite the extensive bilateral occipital cortical damage, BI has extensive conscious visual abilities, is not blind, and can use vision to navigate his environment," the researchers say. Iñaki-Carril Mundiñano, one of the researchers, reports that BI is able to see colors and identify whether certain facial expressions are happy or neutral.
Why, then, is BI still able to see all these things despite the injury in his brain? It’s possible that the lesion occurred when BI was still young enough to have his brain simply reroute information from his retina to other units in his visual cortex. If this is the case, how can researchers confirm if it’s in fact true or not?
BI may have been lucky to have suffered the injury as a baby.
The researchers used a magnetic resonance imaging (MRI) machine to create a map of BI’s neuralpathways. A special area of interest was pathway that connected the inferior pulvinar and a part of the visual cortex called the middle temporal visual area, a region that helps us recognize motion. Both the inferior pulvinar and the middle temporal visual area are close to the visual cortex.
According to the results of the MRI scans, the pathway appeared larger than usual. This may indicate that the inferior pulvinar did a lot of the primary visual cortex’s work early on in BI’s development. In other words, other parts of the brain compensated for the primary visual cortex and picked up a lot of the slack.
This may have happened because of the brain plasticity of babies and children. If BI suffered the same injury in his brain as an adult, his vision would not be as good as it is now.
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