New neurological deficit behind lazy eye identified

WASHINGTON - Scientists have apparently identified a new neurological deficit behind amblyopia, or ‘lazy eye’.

Their findings shed additional light on how amblyopia results from disrupted links between the brain and normal visual processing.

Previous research on amblyopia has largely focused on one aspect of visual processing-that in the primary visual cortex, or V1.

Researchers at New York University’s Center for Neural Science studied a brain area called MT, which has a well-established role in processing information about moving visual objects.

To do this, the researchers studied the visual processing of macaque monkeys, examining those who had normal vision and those whose vision was impaired by amblyopia.

The researchers recorded both the monkeys’ ability to detect motion and how MT’s neurons functioned in this process.

Their results showed striking changes in neuron activity in MT. In monkeys with normal vision, the MT neurons responded through both eyes.

However, in those with amblyopia, the MT neurons showed stronger response in one eye-usually the one not affected by the disorder.

Normal visual motion perception relies on neurons that integrate information about the position of moving objects as they cross the visual image.

The NYU researchers found that this ability to integrate motion information was defective in neurons driven through the affected eye, which might explain the animal’s deficits in motion perception.

The findings appeared in the Journal of Neuroscience. (ANI)