A comparison of reading, in people with simulated and actual central vision loss, with static text, horizontally scrolling text, and rapid serial visual presentation.

Reading with central vision loss (CVL), as caused by macular disease, may be enhanced by presenting text using dynamic formats such as horizontally scrolling text or rapid serial visual presentation (RSVP). The rationale for these dynamic text formats is that they can be read while holding gaze away from the text, potentially supporting reading while using the eccentric viewing strategy. This study was designed to evaluate the practice of reading with CVL, with passages of text presented as static sentences, with horizontal scrolling sentences, or as single-word RSVP. In separate studies, normally sighted participants with a simulated (artificial) central scotoma, controlled by an eye-tracker, or participants with CVL resulting from macular degeneration read passages of text using the eccentric viewing technique. Comprehension was better overall with scrolling text when reading with a simulated CVL, whereas RSVP produced lower overall comprehension and high error rates. Analysis of eye movement behavior showed that participants consistently adopted a strategy of making multiple horizontal saccades on the text itself. Adherence to using eccentric viewing was better with RSVP, but this did not translate into better reading performance. Participants with macular degeneration and an actual CVL also showed the highest comprehension and lowest error rates with scrolling text and the lowest comprehension and highest errors with RSVP. We conclude that scrolling text can support effective reading in people with CVL and has potential as a reading aid.

Following the Status of Visual Cortex Over Time in Patients With Macular Degeneration Reveals Atrophy of Visually Deprived Brain Regions.

Purpose: Previous research has shown atrophy of visual cortex can occur in retinotopic representations of retinal lesions resulting from eye disease. However, the time course of atrophy cannot be established from these cross-sectional studies, which included patients with longstanding disease of varying severity. Our aim, therefore, was to measure visual cortical structure over time in participants after onset of unilateral visual loss resulting from AMD. Methods: Inclusion criteria were onset of acute unilateral neovascular AMD with bilateral dry AMD based on clinical examination. Therefore, substantial loss of unilateral visual input to cortex was relatively well-defined in time. Changes in cortical anatomy were assessed in the occipital lobe as a whole, and in cortical representations of the lesion and intact retina, the lesion and intact projection zones, respectively. Whole brain, T1-weighted magnetic resonance imaging was taken at diagnosis (before antiangiogenic treatment to stabilize the retina), during the 3- to 4-month initial treatment period, with a long-term follow-up approximately 5 (range 3.8-6.1 years) years later. Results: Significant cortical atrophy was detected at long-term follow-up only, with a reduction in mean cortical volume across the whole occipital lobe. Importantly, this reduction was explained by cortical thinning of the lesion projection zone, which suggests additional changes to those associated with normal aging. Over the period of study, antiangiogenic treatment stabilized visual acuity and central retinal thickness, suggesting that the atrophy detected was most likely governed by long-term decreased visual input. Conclusions: Our results indicate that consequences of eye disease on visual cortex are atrophic and retinotopic. Our work also raises the potential to follow the status of visual cortex in individuals over time to inform on how best to treat patients, particularly with restorative techniques.