Abstract
Macular degeneration causes loss of central vision while leaving peripheral vision unaffected. People use central vision for many important tasks such as reading and most daily tasks that require attention. Loss of central vision is a drastic change in experience, due to decreased inputs to central vision and the requirement to use peripheral vision for attention-demanding tasks like reading and recognizing faces (Kwon, Nandy, and Tjan, 2013). Central vision loss may lead to changes in cortical properties. This plasticity is thought to be different at different ages and could result in disparate cortical changes depending on when the disease presents. In this experiment, cortical thickness in visual cortex was analyzed in a database of people with juvenile onset macular degeneration (JMD) and adult onset macular degeneration (AMD) and compared between these two groups. A new brain parcellation was used to mark boundaries of V1, V2, and V3 in the left hemisphere of 24 JMD subjects, 33 healthy young controls (HCY), 24 AMD subjects, and 20 healthy older controls (HCO). Each of these areas were divided into separate ROIs based on eccentricity measured using a retinotopic atlas. The data show a clear difference in cortical thickness between participants with central vision loss due to AMD and JMD and their respective controls. ROIs corresponding to central vision show decreased cortical thickness in both AMD and JMD groups. Thinner representations of central vision in both JMD and AMD groups are consistent with decreased activity due to lack of visual input in those regions. Some patterns of cortical thickness differed between AMD and JMD groups, however: AMD had thicker cortex in more peripheral regions corresponding to visual areas of increased use, while the JMD group had similar or thinner cortex. This indicates that the pattern of cortical plasticity differs between JMD and AMD.
Meeting abstract presented at VSS 2017