Item

Abstract

Cortical damage of the visual pathway as a result of stroke typically leads to a loss of conscious vision in the affected region of the contralateral visual hemifield (scotoma). The most common visual injury involves the primary visual cortex (V1), the major relay of visual information to the rest of the cortex. However, in spite of this, several higher visual areas have been shown to be modulated by visual stimuli presented inside the scotoma. This suggests that there are alternate pathways to transmit information from the retina to the cortex that bypass V1 and transmit information directly to extrastriate visual areas. A much debated issue is whether adult visual cortex is able to reorganize after injury, and if so, what is the extent and the mechanism of the observed reorganization. The purpose of this study is to map visual cortex organization after injury, gathering information about the role that specific networks of brain areas play in cortical reorganization and recovery. To this end, we use functional
magnetic resonance imaging (fMRI) methods to study several subjects with quadrandanopia and hemianopia and compare them to a group of normal controls. FMRI measurements were
obtained during the presentation of a moving bar stimulus, which traverses the visual field while the subjects are fixating. These measurements are used to estimate voxel based population receptive field centers and radii using a direct isotropic Gaussian method introduced by Dumoulin and Wandell (1). In select controls an area of the stimulus is obscured (“artificial scotoma”) to simulate as much as possible the real scotoma of each patient. Preliminary results suggest that receptive field measurements obtained both in patients and in subjects examined under the artificial scotoma condition differ from measurements obtained in controls. In general, there appear to be no significant retinotopic map alterations in the borders of early visual areas of patients suffering from cortical lesions. However, there are some differences in the organization of higher visual areas such as hV5/MT+ compared to those of normal subjects. This may in part reflect the fact that some of the input to hV5/MT+ receptive fields has been lost with the V1+ lesion, but there are also suggestions that V1 bypassing pathways contribute.
In addition, population receptive field size of some of the patients’ spared visual areas show deviations from the normal range of population receptive field sizes derived from the control subjects with and without the artificial scotoma condition.