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Since we analyze complex visual scenes in chunks by saccading from one location to another, information about saccades must be used to break the constant stream of data coming from the eyes into chunks belonging to different locations in the visual field.

By contrasting performance in a condition in which their test subjects actually made saccades to that in a condition when only the image in front of their eyes was exchanged, Paradiso et al. showed that explicit information about saccades --- not just the change of visual input itself --- is responsible for resetting visual processing.

While the signal indicating a saccade could be proprioceptive, the timing in Paradiso et al.'s experiments hints at corollary discharge.

O'Regan and Noë speak of the geometric laws that govern the relationship between moving the eyes and body and the change of an image in the retina.

The geometry of the changes—straight lines becoming curves on the retina when an object moves in front of the eyes—are not accessible to the visual system, initially, because nothing tells the brain about the spatial relations between photoreceptors in the retina.

FEF stimulation elicits saccadic eye movements.

Presaccadic activity is not measured in FEF for spontaneous saccades but for purposive saccades.

The motor map is not monotonic across the entire FEF, but sites that are close to each other have similar characteristic saccades.

Certain neurons in the deep SC emit bursts of activity before making a saccade.

It has long been known that stimulating the SC can elicit eye movements.

Onset times of visually guided saccades have a bimodal distribution. The faster type of saccades are termed `express saccades'. Ablation of the SC but not of the FEF makes express saccades disappear.

Brainstem premotor neurons producing the commands for eye movements are located in pons, medulla (horizontal movements), and the rostral midbrain (vertical movements).

There are neurons in the supplementary eye field which are related to

  • eye movements,
  • arm movements,
  • ear movements,
  • spatial attention.

Eye movements are important for visual consciousness.

In the Sprague effect, removing (or deactivating) one visual cortex eliminates visually induced orienting behavior to stimuli in the contralateral hemifield.

Lesioning (or deactivating) the contralateral SC restores the orienting behavior.

``The heminanopia that follows unilateral removal of the cortex that mediates visual behavior cannot be explained simply in classical terms of interruption of the visual behavior cannot be explained simply in classical terms of interruption of the visual radiations that serve cortical function.
Explanation fo the deficit requires a broader point of view, namely, that visual attention and perception are mediated at both forebrain and midbrain levels, which interact in their control of visually guided behavior.''

(Sprague, 1966)

The SC is multisensory: it reacts to visual, auditory, and somatosensory stimuli. It does not only initiate gaze shifts, but also other motor behaviour.

The deeper layers of the SC project strongly to brainstem, spinal cord, especially to those regions involved in moving eyes, ears, head and limbs, and to sensory and motor areas of thalamus.

According to King, the principal function of the SC is initiating gaze shifts.

Before a saccade is made, the region that will be the target of that saccade is perceived with higher contrast and visual contrast.

People fixate on different parts of an image depending on the questions they are asked or task they are trying to accomplish.

People look where they point and point where they look.

Reasons why pointing and gazing are so closely connected may be

  • that gaze guides pointing,
  • that gazing and pointing use the same information,
  • or that a common motor command guides both.

Brouwer et al found that their subjects looked more at the contact position of the index finger when they were told to grasp an object than when they were just to look at it.

In the first experiment by Brouwer et al, people fixated different parts of a shape depending on whether the task was just to look at it or grasp it.

The subject's initial saccade, however, was not influenced by the task.

Looking behavior in newborns may be dominated by non-cortical processes.

Tadpoles make eye movements which compensate for swimming movements independent of visual or vestibular input. Their rhythmic swimming motor commands are generated by spinal central pattern generators (CGPs). Efference copies of these motor commands appear to be what induces the eye movements.

The SC is also involved in eye, head, whole-body, ear, whisker and other body movements.

LIP is retinotopic and involved in gaze shifts.

The medial intraparietal area (MIP) is retinotopic and involved in reaching.

Correct pro-saccades are executed earlier than correct anti-saccades.

In saccade/anti-saccade experiments, direction errors are confined to the anti-saccade condition.

In anti-saccade experiments, incorrect saccades (those in the direction of the visual stimulus) occur earlier after target onset than do correct anti-saccades.

The timing of correct pro-saccades has a bi-modal distribution. One class of pro-saccades happens very fast (express saccades), the others take a little longer.

Express saccades are thought of as reflex behavior. The reflex behind them is referred to as the 'visual grasp reflex'.

They are believed to be the result of a direct translation of a visual stimulus into a motor command.

In anti-saccade conditions, the `visual grasp reflex' must be suppressed.

One family of models for saccades and anti-saccades are the `accumulator models'.

These models pose that activation of saccade and saccade suppression neurons race each other. The one first to reach a threshold wins.

Activation of FEF and SC neurons is higher before direction error saccades in anti-saccade tasks than before correct anti-saccades.

Munoz and Everling assume that there are distinct populations of fixation and saccade neurons in the SC and FEF.

In a more recent paper, Casteau and Vitu state that there is some debate about that. However, they, too argue for distinct fixation neurons. On the other hand, they also state that fixation neurons probably are not located in the SC itself, which is in contrast of what Munoz and Everling write.