Macular Degeneration and Brain Plasticity

A new study from MIT in the March 4 issue of the Journal of Neuroscience explains some of the neural mechanism involved in the brain remapping seen in macular degeneration. Macular degeneration affects just 1.75 million people in the United States.

Macular degeneration is the most prevalent form of adult blindness. Patients lose vision progressively in the center of their visual field, thus depriving the equivalent part in the visual cortex of input. Previous research has shown that the deprived neurons start responding to visual input from another spot on the retina; this is evidence of plasticity in the adult cortex Until now it was unknown just how such neuroplasticity occurred.

“This study shows us one way that the brain changes when its inputs change. Neurons seem to ‘want’ to receive input: when their usual input disappears, they start responding to the next best thing,” says Nancy Kanwisher of MIT, senior author of the study.

“Our study shows that the changes we see in neural response in people with MD are probably driven by the lack of input to a population of neurons, not by a change in visual information processing strategy,” said Kanwisher.

Loss of Vision and Brain Plasticity

Loss of vision commences in the fovea of the retina, the central area which provides the high acuity vision we use for reading and other visually challenging tasks. Patients normally compensate by using an adjacent patch of undamaged retina. This Preferred Retinal Locus (PRL) is often below the blind region in the visual field, thus causing patients to roll their eyes upward to look at someone’s face, for instance.

The visual cortex includes a map of the visual field on the retina. In macular degeneration, the neurons which map to the fovea no longer receive an input. Numerous labs, including Kanwisher’s, previously discovered that the neurons in the visual cortex that once responded just to input from central vision begin responding to stimuli at the PRL. In essence, the visual map has reorganized.

“We wanted to know if the chronic, prior use of the PRL causes the cortical change that we had observed in the past, according to what we call the use-dependent hypothesis,” said first author Daniel D. Dilks. “Or, do the deprived neurons respond to stimulation at any peripheral location, regardless of prior visual behavior, according to the use-independent hypothesis?”

Preferred Retinal Locus

Prior studies did not solve this mystery since they had only tested patients’ PRL. But the MIT study tests both the PRL and another peripheral location, by means of functional magnetic resonance imaging (fMRI), scanning two macular degeneration patients who had no central vision, and therefore had a deprived central visual cortex.

Due to the fact that patients habitually use the PRL like a new fovea, it is feasible that the deprived cortex might respond preferentially to this location. However, that is not what the researchers found. Rather, the deprived region responded in the same way to stimuli at both the preferred and nonpreferred locations. This suggests that the long-term change in visual behavior is not driving the brain’s remapping, but that brain changes are a relatively passive response to visual deprivation.

“Macular degeneration is a great opportunity to learn more about plasticity in the adult cortex.” Kanwisher says. Should scientists one day develop technologies to substitute for the lost light-sensitive cells in the fovea, macular degeneration patients might be able to regain central vision, since the neurons there are still alive and functioning.

Daniel D. Dilks, Chris I. Baker, Eli Peli, and Nancy Kanwisher
Reorganization of Visual Processing in Macular Degeneration Is Not Specific to the “Preferred Retinal Locus”
J. Neurosci. 2009 29: 2768-2773; doi:10.1523/JNEUROSCI.5258-08.2009