Mechanisms of visual attention revealed by saccadic eye movements

Fischer, Burkhart; Breitmeyer, Bruno G.

doi:10.1016/0028-3932(87)90044-3

Cited by 353 publications

(200 citation statements)

References 23 publications

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“…Since a period of fixation is an event that is common to both the Visual Scan and Steady Gaze tasks, the fact that the target onset lag effect is equally strong in both tasks is to be expected. This explanation of the target onset lag effect therefore supports those hypotheses of express saccade production for which disinhibition of saccadic mechanisms with continued fixation is a major component, such as the "disengagement" of attention hypothesis (Fischer & Breitmeyer, 1987) and the "visuomotor" physiological idea (Rohrer & Sparks,1986) that is revived below. This third explanation is less compatible with other hypotheses, such as those which propose that express saccades are generated by triggering a buffered "motor program" (reviewed by Kowler, 1990); such hypotheses rely on the presence of partial saccade preparation before target onset and an anticipation that the target is about to appear, i.e.…”

Section: Target Onset Lag Effectsupporting

confidence: 79%

Express saccades elicited during visual scan in the monkey

Sommer

1994

Vision Research

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Monkeys trained to saccade to visual targets can develop separate "express" and "regular" modes in their distribution of saccadic latencies. The purpose of this study was to determine whether this occurs under more natural viewing conditions, when targets are suddenly presented in a structured visual field during visual scan. It was found that scanning saccades stopped appearing 60 msec after a target's onset, and subsequent saccades, which were directed toward the suddenly appearing target, had a bimodal distribution of latencies. Express saccades were more likely to occur as the target was presented later in a fixation. Regular mode saccades were more likely to occur with longer target durations. Scanning saccades made to stimuli of the structured visual field always had unimodal inter-saccadic interval distributions. All these effects were apparent after only 2-3 days of training. These findings, taken together with recent physiological results, suggest that the visuomotor cells of the superior collculus mediate latency bimodality.

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Section: Target Onset Lag Effectsupporting

confidence: 79%

Express saccades elicited during visual scan in the monkey

Sommer

1994

Vision Research

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“…Confirming previous studies using tasks evaluating global alertness (Robertson, 1989), the attentional blink (Husain et al, 1997), global attentional processing capacity (Duncan et al, 1999) or speed of visual processing (Battelli et al, 2003) this central bias shows that neglect patients have severe spatially unspecific processing deficits. An influential hypothesis explains the increase of saccade latency by a fixated distracter in terms of impaired disengagement of attention from fixation (Fischer and Breitmeyer, 1987). Since attentional disengagement is an important component of spatial neglect (e.g.…”

Section: Discussionmentioning

confidence: 99%

A non-spatial bias favouring fixated stimuli revealed in patients with spatial neglect

Ptak

Schnider

Golay

et al. 2007

Brain

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The cardinal feature of spatial neglect is severely impaired exploration of the contralesional space, a failure resulting in unawareness of many contralesional stimuli. This deficit is exacerbated by a reflexive attentional bias toward ipsilesional items. Here we show that, in addition to these spatially lateralized failures, neglect patients also exhibit a severe bias favouring stimuli presented at fixation. We tested neglect patients and matched healthy and right-hemisphere damaged patients without neglect in a task requiring saccade execution to targets in the left or right hemifield. Targets were presented alone or simultaneously with a distracter that appeared in the same hemifield, in the opposite hemifield, or at fixation. We found two fundamental biases in saccade initiation of neglect patients: irrelevant distracters presented in the preserved hemifield tended to capture gaze reflexively, resulting in a large number of saccades erroneously directed toward the distracter. Additionally, distracters presented at fixation severely disrupted saccade initiation irrespective of saccade direction, leading to disproportionately increased latencies of left and right saccades. This latency increase was specific to oculomotor responses of neglect patients and was not observed when a manual response was required. These results show that, in addition to their failure to inhibit reflexive glances toward ipsilesional items neglect patients exhibit a strong oculomotor bias favouring fixated stimuli. We conclude that impaired initiation of saccades in any direction contributes to the deficits of spatial exploration that characterize spatial neglect.

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“…Covert attention shifts may in fact be used to direct a gaze shift (Posner and Cohen, 1984;Fischer and Breitmeyer, 1987). Single cell recordings in alert monkeys have demonstrated that activity in parietal cortex precedes an intended eye movement to predict the location of expected visual input (Duchamel et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

Spatial Attention Deficits in Patients with Acquired or Developmental Cerebellar Abnormality

et al. 1999

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Recent imaging and clinical studies have challenged the concept that the functional role of the cerebellum is exclusively in the motor domain. We present evidence of slowed covert orienting of visuospatial attention in patients with developmental cerebellar abnormality (patients with autism, a disorder in which at least 90% of all postmortem cases reported to date have Purkinje neuron loss), and in patients with cerebellar damage acquired from tumor or stroke. In spatial cuing tasks, normal control subjects across a wide age range were able to orient attention within 100 msec of an attention-directing cue. Patients with cerebellar damage showed little evidence of having oriented attention after 100 msec but did show the effects of attention orienting after 800-1200 msec. These effects were demonstrated in a task in which results were independent of the motor response. In this task, smaller cerebellar vermal lobules VI-VII (from magnetic resonance imaging) were associated with greater attention-orienting deficits.Although eye movements may also be disrupted in patients with cerebellar damage, abnormal gaze shifting cannot explain the timing and nature of the attention-orienting deficits reported here. These data may be consistent with evidence from animal models that suggest damage to the cerebellum disrupts both the spatial encoding of a location for an attentional shift and the subsequent gaze shift. These data are also consistent with a model of cerebellar function in which the cerebellum supports a broad spectrum of brain systems involved in both nonmotor and motor function.

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Mechanisms of visual attention revealed by saccadic eye movements

Cited by 353 publications

References 23 publications

Express saccades elicited during visual scan in the monkey

Express saccades elicited during visual scan in the monkey

A non-spatial bias favouring fixated stimuli revealed in patients with spatial neglect

Spatial Attention Deficits in Patients with Acquired or Developmental Cerebellar Abnormality

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