Research Projects

Visual Plasticity After Brain Damage

Damage to the primary visual cortex (V1) causes a loss of conscious vision over the same part of the visual field through both eyes. Clinically, his increasingly common cause of permanent disability is still considered intractable. However, the existence of blindsight (a largely unconscious ability to sense moving and flickering stimuli) suggests partial preservation of visual processing in cortically blind fields. The now, well-documented existence of visual pathways that bypass V1 and convey information from the eyes to higher-level visual cortical areas, begs the question: can they be recruited to restore vision in cortical blindness?

Our team recently discovered that visual training can recover normal threshold levels of discrimination and awareness for both simple and complex motion in the trained regions of cortically blind fields. However, the extent of recovery possible and the mechanisms underlying it are unknown.

Vision restoration in occipital stroke patients

• Visual perceptual training: manipulating visual attention and low-level features to enhance recovery (collaboration with Marisa Carrasco, Duje Tadin)
• Changes in visual computations that accompany training-induced visual recovery (collaboration with Duje Tadin and Michael Melnick)
• Natural history of perimetric visual defects after stroke (collaboration with Elizabeth Saionz, Geoffrey Aguirre and Brent Johnson)
• Critical or sensitive periods for recovery:
  • Differences in visual processing in sub-acute versus chronic stroke patients
  • Differences in efficacy and properties of visual training in sub-acute versus chronic stroke patients

Retrograde degeneration of early visual pathways

• Time course of structural changes and predictive power for recovery potential (collaboration with Holly Bridge and Sara Ajina)
• Training alters the progression of retinal degeneration after V1 damage (collaboration with Steven Feldon)

Visual system circuit plasticity after V1 damage

• Consequences of V1 damage and training on electrophysiological response properties in the dLGN and extrastriate cortex (collaboration with Farran Briggs and Kristina Nielsen)
• Changes in human fMRI responses after V1 damage and visual training (collaboration with David Heeger and Elisha Merriam)
• Tractography and neurochemistry of the residual visual circuitry after V1 damage (collaboration with Holly Bridge)
• Mechanisms underlying persistence of orientation and direction selectivity in the residual visual circuitry after V1 damage (collaboration with Elisha Merriam, Robbe Goris and James Bourne)

Effects of V1 damage on visually-guided actions

• Effect of cortical damage on microsaccades and fixational eye movements (collaboration with Martina Poletti and Ashley Clark)
• Effect of cortical damage on pre-processing of motion information at peripheral saccade targets (collaboration with Jude Mitchell and Sunwoo Kwon)
• Steering and driving in virtual reality: processing of optic flow after V1 damage (collaboration with Gabriel Diaz, Duje Tadin and Brett Fajen)

Quality of life after occipital Stroke

• Natural progression
• Effect of visual training on quality of life after stroke

Relearning to see with a damaged V1