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Published on: September 18, 2012
Saccade induced cortical activation in patients with post-stroke visual field defects
Gereon Nelles1, Armin de Greiff, Anja Pscherer
1Neurologische Klinik und Poliklinik, Universitätsklinikum Essen, Essen 45122, Germany. gereon.nelles@uni-essen.de
Journal of Neurology
|August 19, 2007
Summary
Patients with hemianopia, a visual field defect, show altered brain activity during eye movements. Functional MRI reveals changes in the frontoparietal network controlling saccades, suggesting compensatory mechanisms.
Area of Science:
- Neuroscience
- Ophthalmology
- Neurology
Background:
- Hemianopia, resulting from visual field loss, causes significant disability.
- Patients with hemianopia often exhibit impaired saccadic eye movements.
- Saccade training may improve visual search strategies in affected individuals.
Purpose of the Study:
- To investigate the neural representation of saccades in patients with post-stroke hemianopia using functional Magnetic Resonance Imaging (fMRI).
- To compare brain activation patterns during visually guided saccades between patients with hemianopia and healthy controls.
Main Methods:
- Functional MRI (fMRI) was employed to measure brain activation during visually guided saccades.
- Ten patients with pure occipital cortical lesions causing homonymous hemianopia and ten healthy controls participated.
- Statistical Parametric Mapping (SPM'99) was used to analyze differences in brain activation.
Main Results:
- Healthy subjects showed significant activation in bilateral frontal and parietal eye fields and the supplementary eye field.
- These areas were also activated in hemianopia patients, but to a lesser extent.
- Patients exhibited increased activation in the posterior parietal cortex of the unaffected left hemisphere.
Conclusions:
- Post-stroke hemianopia is associated with alterations in the frontoparietal network controlling saccades.
- These findings suggest that visual field defects impact the cortical control of eye movements.
- The posterior parietal cortex may play a compensatory role in hemianopia.
