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Dissociated temporal and spatial impairments of microsaccade dynamics in homonymous hemianopia following ischemic
Ying Gao1,2,3, Huiguang He1,4,5, Bernhard A Sabel2,6
1NeuBCI Lab, State Key Laboratory of Brain Cognition and Brain-inspired Intelligence Technology, Institute of Automation, Chinese Academy of Sciences, Beijing, China.
This study examines the temporal and spatial components of microsaccade dynamics in homonymous hemianopia (HH) after ischemic stroke, and their association with patients' visual impairments. The eye position data were recorded during visual field testing in 15 patients with HH and 15 controls. Microsaccade rate (temporal) and direction (spatial) dynamics in HH were analyzed across visual field sectors with varying defect depth and compared with controls. Support vector machines were trained to characterize the visual field defects in HH based on microsaccade dynamics. Patients exhibited stronger microsaccadic inhibition in the sighted areas, postponed and stronger microsaccadic inhibition in areas of residual vision (ARVs) compared to controls. Meanwhile, a rebound was evident in the sighted areas but absent in the ARVs and blind areas. Microsaccades surviving the inhibition were more attracted toward the stimulus, whereas microsaccades after the inhibition were directed away from the stimulus in controls. Such pattern was not observed in HH. Dissociated temporal and spatial impairments of microsaccade dynamics suggest multi-fold impairments of the visual and oculomotor networks in HH. Based on the microsaccadic phase signature underlying microsaccade rate dynamics, we characterized patients' visual field defects and discovered regions with residual function inside both the blind and sighted hemifields. These findings suggest that monitoring microsaccade dynamics may provide valuable supplementary information beyond that captured by behavioral responses.
This study examines the temporal and spatial components of microsaccade dynamics in homonymous hemianopia (HH) after ischemic stroke, and their association with patients' visual impairments. The eye position data were recorded during visual field testing in 15 patients with HH and 15 controls. Microsaccade rate (temporal) and direction (spatial) dynamics in HH were analyzed across visual field sectors with varying defect depth and compared with controls. Support vector machines were trained to characterize the visual field defects in HH based on microsaccade dynamics. Patients exhibited stronger microsaccadic inhibition in the sighted areas, postponed and stronger microsaccadic inhibition in areas of residual vision (ARVs) compared to controls. Meanwhile, a rebound was evident in the sighted areas but absent in the ARVs and blind areas. Microsaccades surviving the inhibition were more attracted toward the stimulus, whereas microsaccades after the inhibition were directed away from the stimulus in controls. Such pattern was not observed in HH. Dissociated temporal and spatial impairments of microsaccade dynamics suggest multi-fold impairments of the visual and oculomotor networks in HH. Based on the microsaccadic phase signature underlying microsaccade rate dynamics, we characterized patients' visual field defects and discovered regions with residual function inside both the blind and sighted hemifields. These findings suggest that monitoring microsaccade dynamics may provide valuable supplementary information beyond that captured by behavioral responses.
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