Rehabilitating homonymous visual field deficits: white matter markers of recovery-stage 1 registered report

Damage to the primary visual cortex (V1) or its afferent white matter tracts results in loss of vision in the contralateral visual field that can present as homonymous visual field deficits. Recent evidence suggests that visual training in the blind field can partially reverse blindness at trained locations. However, the efficacy of visual training to improve vision is highly variable across subjects, and the reasons for this are poorly understood. It is likely that variance in residual functional or structural neural circuitry following the insult may underlie the variation among patients. Many patients with visual field deficits retain residual visual processing in their blind field, termed 'blindsight', despite a lack of awareness. Previous research indicates that an intact structural and functional connection between the dorsal lateral geniculate nucleus (dLGN) and the human extrastriate visual motion-processing area (hMT+) is necessary for blindsight to occur. We therefore predict that changes in this white matter pathway will underlie improvements in motion discrimination training. Twenty stroke survivors with unilateral, homonymous field defects from retro-geniculate brain lesions will complete 6 months of motion discrimination training at home. Visual training will involve performing two daily sessions of a motion discrimination task, at two non-overlapping locations in the blind field, at least 5 days per week. Motion discrimination and integration thresholds, Humphrey perimetry and structural and diffusion-weighted MRI will be collected pre- and post-training. Changes in fractional anisotropy will be analysed in two visual tracts: (i) between the ipsilesional dLGN and hMT+ and (ii) between the ipsilesional dLGN and V1. The (non-visual) tract between the ventral posterior lateral nucleus of the thalamus (VPL) and the primary somatosensory cortex (S1) will be analysed as a control. Tractographic changes will be compared to improvements in motion discrimination and Humphrey perimetry-derived metrics. We predict that (i) improved motion discrimination performance will be directly related to increased fractional anisotropy in the pathway between ipsilesional dLGN and hMT+ and (ii) improvements in Humphrey perimetry will be related to increased fractional anisotropy in the dLGN-V1 pathway. There should be no relationship between behavioural measures and changes in fractional anisotropy in the VPL-S1 pathway. This study has the potential to lead to greater understanding of the white matter microstructure of pathways underlying the behavioural outcomes resulting from visual training in retro-geniculate strokes. Understanding the neural mechanisms that underlie visual rehabilitation is fundamental to the development of more targeted and thus effective treatments for this underserved patient population.