Definition

During visual tracking, the main objective of the observer is to keep the image of the fixated item on the fovea, the area of the retina where visual resolution is best. Normally, the observer tracks moving targets using a combination of smooth pursuit movements and small saccades. Smooth pursuit movements allow the observer to track a moving object, while saccades (derived from the French word for jerk or to pull) allow the observer to quickly redirect their gaze to the object of interest. During smooth pursuit, eye velocities are generated that approximate the velocity of the moving target object. When the eyes and target are in synch, the velocity of the target’s retinal image is reduced to zero. If the eyes fall short of, or overshoot the target, saccades are generated to reposition the image of the target object back on to the region of the fovea. During visual tracking, the vestibulo-ocular reflex and optokinetic movements permit the observer to compensate for head movements, which helps to stabilize the visual image on the retina.

Eye tracking methodologies are commonly used to monitor and quantify eye movements in the laboratory setting. Eye tracking can be used to study eye movements in response to both moving and stationary images. Because saccadic eye movements are thought to be closely linked to attention, they have received significant examination in studies of attentional and perceptual processes using eye tracking techniques (see Fig. 1). More advanced research approaches combine eye tracking with multimodal neuroimaging techniques, permitting additional methods of examining the underlying neural correlates of visual tracking. In the clinic setting, visual tracking and oculomotor scanning abilities are assessed using tests of visual attention and perception, such as the line bisection test and cancellation tests. Saccadic and smooth pursuit movements can also be assessed in the clinic by asking the patient to look back and forth between two widely spaced targets (e.g., the examiner’s left and right index fingers) and by asking the patient to follow a moving target, as is done during a neurologic examination.

Visual Tracking, Fig. 1
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The images depict examples of oculomotor scanning patterns captured over an 8-s viewing period using eye tracking. The scan patterns shown were made by a healthy adult during a task in which the viewer was asked to examine the image and identify the type of scene viewed. Yellow circles represent fixations; yellow lines depict saccades. The size of the circles indicates length of fixation duration, with larger circles corresponding to longer duration times

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Current Knowledge

Smooth pursuit movements are significantly slower than saccades and typically occur at velocities of around 100° per second. This speed permits feedback from the vestibular and visual systems, which help to regulate the speed and duration of the movements. Generation of smooth pursuit movements involves a complex network of neural structures, including the cerebellum, vestibular nuclei, and cortical regions. Extrastriate regions sensitive to visual motion are implicated in the origination of smooth pursuit commands. Information from these regions is integrated with signals from the brainstem and the frontal eye fields during smooth pursuit movements. Functional imaging studies have been used to explore neural regions associated with smooth pursuit; however, interpretation of findings is sometimes complicated by the fact that visual tracking involves a combination of both smooth pursuit movements and saccades. Activation related to smooth pursuit has been reported in the frontal eye fields, lateral occipito-temporal cortex, lingual gyrus, dorsomedial cuneus, and dorsal occipito-parietal cortex.

In patients with unilateral cerebral lesions, ipsidirectional smooth pursuit defects are noted. That is to say, smooth pursuit movements are impaired when tracking targets moving in the direction toward the side of the lesion. In general, cerebral pursuit defects are asymptomatic but can often be observed clinically or in the laboratory setting. Patients with parietal and occipito-temporal lesions can show ipsidirectional pursuit defects, as can patients with lesions of the frontal eye fields, supplementary eye fields, or prefrontal cortex. Ipsidirectional defects in pursuit can also be observed following lesions of the posterior limb of the internal capsule, which affect descending cortical connections with brainstem nuclei.

Saccadic eye movements are extremely rapid; they can reach velocities of up to 700° per second. They are important in visual tracking behaviors and play a primary role in visual exploration. They allow the observer to sample several bits of visual information from the environment, such as during scene viewing or reading. The neural circuitry that supports saccadic eye movements has been studied extensively and is quite intricate; it involves regions in the brainstem, subcortical structures, and several areas in the cerebral cortex. Primary cortical regions include the frontal eye fields, posterior parietal cortex, prefrontal cortex, and supplemental eye fields. The contribution of subcortical regions (i.e., the basal ganglia) to saccade generation and control is also well documented (see below). The frontal eye fields are involved in the generation of saccades made under volitional control, while posterior parietal regions are thought to be involved in the generation of automatic or reflexive saccades, which are saccades made to stimuli that occur suddenly in the environment (e.g., a person walking by or a load noise in the periphery). The prefrontal cortex supports saccades made based on spatial memory, as well as the suppression of reflexive saccades. The supplemental eye fields are noted to play a role in the temporal organization of saccades.

Bilateral cerebral lesions can cause significant disturbances in saccadic eye movements. For example, bilateral injury to the parietal lobes, such as in Balint’s syndrome, can result in marked impairments in voluntary saccade generation. Most unilateral cerebral lesions do not result in saccadic dysfunction; however, unilateral frontal eye field lesions can cause delayed latencies when making voluntary saccades to the contralateral side (especially when the anterior limb of the internal capsule or white matter near the frontal horns are affected), while vertical saccades remain intact. Patients with unilateral frontal eye field lesions spend less time scanning complex scenes on the side of the image that is contralateral to the lesion. Some consider the behaviors resulting from unilateral frontal eye field lesions to represent an exploratory or intentional type of hemineglect. Notably, some patients with unilateral frontal eye field lesions demonstrate mild signs of neglect on neuropsychological measures (e.g., line bisection and cancellation tests). Unilateral lesions of the posterior parietal cortex are associated with abnormalities in reflexive saccades characterized by prolonged activation latencies. Typically this abnormality is only seen in reflexive saccades made to the contralateral side, but in some patients, the abnormality can be observed in both directions horizontally.

The basal ganglia are also implicated in saccade generation and control. They are noted to play a role in the temporal organization of saccades. Individuals with disorders affecting the basal ganglia (e.g., Parkinson’s disease, Huntington’s disease) often exhibit eye movement abnormalities. In individuals with Parkinson’s disease, saccades can be small, jerky, and slow. Huntington’s disease and Parkinson’s disease patients also demonstrate deficits in generating memory-guided saccades.

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