Top-Down Contributions to Attention Shifting and Disengagement: A Template Model of Visual Attention

Two separate systems are involved in the control of spatial attention; one that is driven by a goal, and the other that is driven by stimuli. While the goal- and stimulus-driven systems follow different general principles, they also interplay with each other. However, the mechanism by which the goal-driven system influences the stimulus-driven system is still debated. The present study examined top-down contributions to two components of attention orienting, shifting and disengagement, with an experimental paradigm in which participants held a visual item in short-term memory and performed a prosaccade task with a manipulation of the gap between fixation offset and target onset. Four experiments showed that the short-term memory content accelerated shifting and impaired disengagement, but the influence on disengagement depended on the utility of short-term memory in guiding attention toward the target. Thus, the use of short-term memory was strategic. Computational models of visual attention were fitted to the experimental data, which suggested that the top-down contributions to shifting was more prominent than those to disengagement. The present study shows that the current modeling framework was particularly useful when examining the contributions of theoretical constructs for the control of visual attention, but it also suggests limitations.

Top-Down Contributions to Attention Shifting and Disengagement: A Template Model of Visual Attention

Two separate systems are involved in the control of spatial attention; one that is driven by a goal, and the other that is driven by stimuli. While the goal- and stimulus-driven systems follow different general principles, they also interplay with each other. However, the mechanism by which the goal-driven system influences the stimulus-driven system is still debated. The present study examined top-down contributions to two components of attention orienting, shifting and disengagement, with an experimental paradigm in which participants held a visual item in short-term memory and performed a prosaccade task with a manipulation of the gap between fixation offset and target onset. Four experiments showed that the short-term memory content accelerated shifting and impaired disengagement, but the influence on disengagement depended on the utility of short-term memory in guiding attention toward the target. Thus, the use of short-term memory was strategic. Computational models of visual attention were fitted to the experimental data, which suggested that the top-down contributions to shifting was more prominent than those to disengagement. The present study indicates that the current modeling framework was particularly useful when examining the contributions of theoretical constructs for the control of visual attention, but it also suggests limitations.

No evidence of atypical attentional disengagement in autism: A study across the spectrum

The ability to disengage attention and reengage elsewhere has been proposed as a fundamental deficit in the autism spectrum, potentially disrupting development of higher cognitive domains. Eye-movements were recorded while 16 autism spectrum children of mixed ability, and 18 typically developing age-matched controls, completed the Gap–Overlap paradigm. A significant difference in latency to fixate target was found between Gap and Overlap conditions. A significant interaction with group was due to autism spectrum participants’ shorter latencies to fixate target in the Gap condition, but similar group responses in the Overlap condition. Considerable within-group variability emerged. We predicted that attentional disengaging would be related to specific features of the phenotype; however, there was no evidence of an association with receptive language, non-verbal IQ, sensory behaviors, or autistic severity in autism spectrum or typically developing groups. In conclusion, while atypical visual attention mechanisms may be a feature of autism spectrum, this is not explained by impaired visual disengaging but is more likely due to increased susceptibility of visual fixation offset cueing. Despite best efforts, nine additional autism spectrum children could not complete testing, and data from a further six were unusable; more work is needed to develop research methods that enable individuals across the spectrum to participate.

Fastigial Oculomotor Region and the Control of Foveation During Fixation

When primates maintain their gaze directed toward a visual target (visual fixation), their eyes display a combination of miniature fast and slow movements. An involvement of the cerebellum in visual fixation is indicated by the severe gaze instabilities observed in patients suffering from cerebellar lesions. Recent studies in non-human primates have identified a cerebellar structure, the fastigial oculomotor region (FOR), as a major cerebellar output nucleus with projections toward oculomotor regions in the brain stem. Unilateral inactivation of the FOR leads to dysmetric visually guided saccades and to an offset in gaze direction when the animal fixates a visual target. However, the nature of this fixation offset is not fully understood. In the present work, we analyze the inactivation-induced effects on fixation. A novel technique is adopted to describe the generation of saccades when a target is being fixated (fixational saccades). We show that the offset is the result of a combination of impaired saccade accuracy and an altered encoding of the foveal target position. Because they are independent, we propose that these two impairments are mediated by the different projections of the FOR to the brain stem, in particular to the deep superior colliculus and the pontomedullary reticular formation. Our study demonstrates that the oculomotor cerebellum, through the activity in the FOR, regulates both the amplitude of fixational saccades and the position toward which the eyes must be directed, suggesting an involvement in the acquisition of visual information from the fovea.

Which Visual Pathways Cause Fixation-Related Inhibition?

Visual stimuli can both inhibit and activate motor mechanisms. In one well-known example, the latency of saccadic eye movements is prolonged in the presence of a fixation stimulus, relative to the case in which the fixation stimulus disappears before the target appears. This automatic sensory-motor effect, known as the gap effect or fixation-offset effect, has been associated with inhibitory connections within the superior colliculus (SC). Visual information is provided to the SC and other oculomotor areas, such as the frontal eye fields (FEF), mainly by the magnocellular geniculostriate pathway, and also by the retinotectal pathway. We tested whether signals in these pathways are necessary to create fixation-related inhibition, by using stimuli invisible to them. We found that such stimuli, visible only to short-wave–sensitive cones (S cones), do produce fixation-related inhibition (including when warning effects were equated). We also demonstrate that this fixation-related inhibition cannot be explained by residual activation of luminance pathways and must be caused by a route separate from that of luminance fixation signals. Thus there are at least two routes that cause fixation-related inhibition, and direct sensory input to the SC or FEF by the magnocellular or retinotectal pathways is not required. We discuss the implications that there may be both cortical and collicular mechanisms.