Saccades Flashcards

1
Q

Describe the following saccade metrics: Reaction time, saccade duration, gain, eccentricity, amplitude, peak velocity.

A
  • Reaction time: The time from the onset of a stimulus to the initiation of a saccade. (how fast you react)
  • Saccade duration: The time taken to complete a saccade. (how much time it takes)
  • Gain: The ratio of the saccade amplitude to the target displacement. (how accurate)
  • Eccentricity: The angular distance between the current fixation point and the target. (how far away is the target)
  • Amplitude: The size of the saccade, usually measured in degrees of visual angle. (the distance your eyes move)
    Peak velocity: The highest velocity reached during a saccade. (maximimum speed)
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2
Q

What are antisaccades?

A

Antisaccades require participants to make goal-directed eye movements in the opposite direction of an exogenously presented target, demanding high-level inhibitory control and cognitive flexibility. Essentially, they are eye movements where the participant is instructed to look in the direction opposite to a suddenly appearing target. This requires suppression of the automatic response to look towards the target and instead generating a voluntary saccade in the opposite direction (Dyckman & McDowell, 2005).

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3
Q

What behavioural component do antisaccades measure?

A

Antisaccades measure the ability to inhibit a reflexive saccade towards a stimulus and to instead perform a volitional saccade in the opposite direction. This task assesses cognitive control and executive function, particularly the ability to suppress automatic responses (Dyckman & McDowell, 2005).

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4
Q

Which neural networks and brain regions are antisaccades governed by?

A

Antisaccades are governed by a network involving the V1, V2, V4, frontal eye fields (FEF), supplementary eye fields (SEF), dorsolateral prefrontal cortex (DLPFC), and Substantia Nigra Pars Reticulata (SNPR), and dorsal anterior cingulate cortex (DACC) and pre-supplementary motor areas (Pre-SMA) and cerebellum. These regions are involved in the planning and execution of voluntary eye movements, as well as the inhibition of reflexive saccades (Dyckman & McDowell, 2005; Dafoe et al., 2007).

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5
Q

How often do we perform antisaccades naturally?

A

Naturally occurring antisaccades are rare in everyday life. Most saccadic eye movements are reflexive prosaccades directed towards stimuli of interest. Antisaccades are more commonly studied in controlled experimental settings than performed spontaneously (Dafoe et al., 2007).

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6
Q

What is the average antisaccade reaction time range based on normative data?

A

The average reaction time for antisaccades in healthy adults typically ranges from 250 to 350 milliseconds. This range can vary based on factors such as age, cognitive load, and specific task conditions (Dafoe et al., 2007; Dyckman & McDowell, 2005).

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7
Q

What affects antisaccade reaction times?

A

Antisaccade reaction times are affected by several factors, including age, cognitive load, task difficulty, attentional focus, and the presence of neurological or psychiatric conditions. Training and practice can also improve reaction times by enhancing inhibitory control and saccadic planning (Dafoe et al., 2007; Dyckman & McDowell, 2005).

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8
Q

Which clinical populations show an antisaccade performance deficit?

A

Clinical populations with antisaccade performance deficits include individuals with schizophrenia, ADHD, Parkinson’s disease, Huntington’s disease, and various forms of dementia. These deficits are often characterized by increased reaction times and higher error rates in the antisaccade task (Dyckman & McDowell, 2005; Dafoe et al., 2007).

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9
Q

How are antisaccades typically measured?

A

Antisaccades are typically measured using eye-tracking technology in controlled laboratory settings. Participants are instructed to fixate on a central point and then look in the opposite direction of a suddenly appearing peripheral target. Key metrics include reaction time, accuracy, and the rate of directional errors (Dafoe et al., 2007; Dyckman & McDowell, 2005).

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10
Q

What are prosaccades?

A

Prosaccades are rapid, reflexive eye movements directed towards a visual target. They occur naturally and automatically in response to sudden stimuli in the environment (Dafoe et al., 2007).

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11
Q

What behavioural component do prosaccades measure?

A
  • Prosaccades measure the speed and accuracy of reflexive responses to visual stimuli. They primarily assess sensorimotor integration and the efficiency of the oculomotor system (Dafoe et al., 2007).
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12
Q

Which neural networks and brain regions are prosaccades governed by?

A
  • Prosaccades are governed by neural networks involving V1, V2, V4, the superior colliculus (SC), frontal eye fields (FEF), posterior parietal cortex (PPC), and brainstem oculomotor nuclei, and cerebellum. These regions coordinate the detection of visual targets and the execution of rapid eye movements towards them (Dafoe et al., 2007; Dyckman & McDowell, 2005).
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13
Q

How often do we perform prosaccades naturally?

A

We perform prosaccades frequently in daily life, as they are the primary type of saccade used to quickly redirect gaze towards objects of interest or sudden changes in the visual environment (Dafoe et al., 2007).

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14
Q

What is the average prosaccade reaction time range based on normative data?

A

The average reaction time for prosaccades in healthy adults typically ranges from 150 to 250 milliseconds. This range reflects the rapid, reflexive nature of prosaccadic movements (Dafoe et al., 2007).

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15
Q

What affects prosaccade reaction times?

A

Prosaccade reaction times are affected by factors such as age, attentional state, stimulus properties (e.g., brightness, contrast), and the presence of neurological or psychiatric conditions. Fatigue and cognitive load can also influence reaction times (Dafoe et al., 2007; Dyckman & McDowell, 2005).

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16
Q

Which clinical populations show a prosaccade performance deficit?

A
  • Clinical populations with prosaccade performance deficits include individuals with Parkinson’s disease, Huntington’s disease, multiple sclerosis, and certain psychiatric disorders such as schizophrenia. These deficits are often characterized by delayed reaction times and reduced accuracy (Dafoe et al., 2007).
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17
Q

How are prosaccades typically measured?

A

Prosaccades are typically measured using eye-tracking technology in controlled laboratory settings. Participants are instructed to fixate on a central point and then quickly look at a suddenly appearing peripheral target. Key metrics include reaction time, accuracy, and peak velocity (Dafoe et al., 2007; Dyckman & McDowell, 2005).

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18
Q

What are the strengths and limitations of eyetrackers, specifically EyeLink?

A
  • Strengths:
    ○ High sampling rate (up to 2000 Hz), allowing precise measurement of saccades (Dafoe et al., 2007).
    ○ Real-time data visualization and robust software integration (e.g., MATLAB, Psychophysics Toolbox) (Dafoe et al., 2007).
    ○ Reliable calibration and low drift rate (Dafoe et al., 2007).
  • Limitations:
    ○ Sensitivity to head movements, requiring stabilization with chin rests or head mounts (Dafoe et al., 2007).
    ○ Potential signal loss during blinks or due to poor lighting conditions (Dafoe et al., 2007).
    Cost and complexity of setup and maintenance (Dafoe et al., 2007).
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19
Q

What causes directional errors when performing pro-and-antisaccade tasks?

A

Directional errors in pro- and antisaccade tasks can be caused by failures in inhibitory control, where the automatic reflex to look towards a target is not adequately suppressed in antisaccades. Other factors include attentional lapses, cognitive load, and fatigue (Dafoe et al., 2007; Dyckman & McDowell, 2005).

20
Q

Are directional errors on the antisaccade task common in certain populations or clinical conditions?

A

Yes, directional errors on the antisaccade task are more common in populations with impaired inhibitory control, such as individuals with schizophrenia, ADHD, and frontal lobe damage. These errors are indicative of difficulties in suppressing automatic responses and generating voluntary movements (Dyckman & McDowell, 2005; Dafoe et al., 2007).

21
Q

Can directional errors be improved with practice?

A

Yes, directional errors can be improved with practice. Repeated exposure to antisaccade tasks can enhance inhibitory control and reduce error rates. Training programs and cognitive interventions have been shown to improve antisaccade performance in both healthy individuals and clinical populations (Dyckman & McDowell, 2005).

22
Q

Are antisaccades sensitive to practice effects?

A

Yes, antisaccades are sensitive to practice effects. Repeated practice on antisaccade tasks can lead to significant improvements in performance. Specifically, practice can reduce reaction times and error rates, indicating enhanced inhibitory control and faster saccadic planning (Dyckman & McDowell, 2005).

23
Q

How many training sessions or bouts of practice are required to reduce reaction times?

A

According to Dyckman and McDowell (2005), significant improvements in antisaccade performance can be observed after just one week of daily practice. In their study, participants trained on antisaccade tasks for four days a week over a two-week period, with substantial improvements noted as early as after the first week. Participants showed a decrease in antisaccade errors by 6.3% after one week of practice while maintaining their reaction times, indicating that the accuracy did not improve at the expense of speed (Dyckman & McDowell, 2005). Therefore, it is suggested that at least one week of consistent daily practice is effective in reducing reaction times and improving accuracy in antisaccade tasks.

24
Q

Does exercise improve directional error rates on the antisaccade task?

A

Some studies suggest that acute exercise can improve cognitive function and inhibitory control, potentially leading to reduced directional error rates on the antisaccade task. Exercise-induced improvements in attention and executive function are thought to contribute to better performance (Dyckman & McDowell, 2005).

25
Q

What is the average reaction time on antisaccades and prosaccades for people with SRC and how does this compare to a healthy population?

A

People with sports-related concussions (SRC) tend to have longer reaction times on both antisaccades and prosaccades compared to healthy individuals. For example, while healthy adults may have antisaccade reaction times around 250-350 ms and prosaccade reaction times around 150-250 ms, individuals with SRC often show delays beyond these ranges. For example, The magnitude of the between-group antisaccade RT difference is approximately 40-50 ms as reported by Johnson et al. (2015b; <7 days post-injury) and Ayala and Heath (2020; <12 days post-injury), respectively, and no difference to 15 ms difference for prosaccades (Johnson et al. 2015, Web et al)

26
Q

Is there a speed-accuracy trade-off when it comes to post-exercise improvements in antisaccade reaction times and if not, why?

A

There is not always a speed-accuracy trade-off in post-exercise improvements in antisaccade reaction times. Exercise can enhance cognitive function, leading to both faster and more accurate responses. Improved neurochemical and physiological states post-exercise contribute to better overall performance without necessarily compromising accuracy (Dyckman & McDowell, 2005).

27
Q

Do individuals with an SRC have a higher frequency of antisaccade directional errors? If so, why?

A
  • Yes, individuals with SRC often have a higher frequency of antisaccade directional errors. This is likely due to impairments in the neural circuits involved in inhibitory control and executive function, which are commonly affected by concussions. These impairments lead to difficulties in suppressing reflexive responses and generating accurate voluntary movements (Dyckman & McDowell, 2005).
28
Q

Can you explain how pupillometry is used to measure cognitive and neural processing during saccade preparation?

A
  • Pupillometry measures pupil size, which is modulated by saccade preparation demands and reflects neural activity in regions such as the superior colliculus (SC) and frontal eye fields.
  • During saccade preparation, the pupil undergoes a sharp constriction in response to fixation onset, known as the pupillary light response, followed by a dilation (TEPD).
  • This dilation represents cognitive and neural processing related to saccade preparation, particularly in the locus coeruleus, SC, and frontal eye fields.
  • Studies have shown that antisaccades elicit a greater pupil dilation compared to prosaccades, reflecting increased executive control.
29
Q

What did Ayala and Heath (2020) find regarding TEPD differences between SRC and control groups during antisaccades and prosaccades?

A
  • Ayala and Heath (2020) found larger TEPDs for antisaccades compared to prosaccades in both SRC and control groups, with significantly larger TEPDs in the SRC group.
  • This suggests greater executive demands during saccade preparation for individuals with SRC while the intact pupillary light reflex suggests preserved basic oculomotor function.
  • These results align with studies showing hyperactivity in frontal and posterior brain regions during antisaccades in acute SRC recovery, indicating executive-related oculomotor dysfunction.
  • Persistently larger TEPDs in the SRC group at follow-up also suggest a prolonged recovery period for executive functions compared to other cognitive domains.
30
Q

Why did you not include pupillometry measures in your oculomotor task? How can you be sure that physiological arousal wasn’t the cause of the reduced postexercise antisaccade reaction times?

A
  • We controlled for arousal levels in our experimental design by providing sufficient rest periods before the task, which was confirmed by postexercise HR and BP measurements.
  • The antisaccade task is a robust measure of executive function that is less susceptible to general arousal effects. Previous research, such as Ayala and Heath (2020), has shown that task-evoked pupillary dilation (TEPD) correlates with saccade preparation and executive control rather than just physiological arousal.
    Although we did not include pupillometry measures, the existing evidence supports our interpretation that the reduced postexercise antisaccade reaction times can be attributed to improvements in executive function rather than merely an increase in physiological arousal.
31
Q

Armstrong & Munoz (2003)

A

Adults with ADHD show impaired inhibitory control in oculomotor countermanding tasks compared to controls.
Different types of stop signals (central visual, peripheral visual, and non-localized sound) affect performance, with the central visual stop signal yielding the best performance.
This study highlights the utility of oculomotor countermanding tasks in quantifying impulsive dysfunction in ADHD, emphasizing the importance of stop signal modality (Armstrong & Munoz, 2003).

32
Q

Dafoe et al. (2007)

A

○ The study focuses on various aspects of oculomotor performance, including reaction time, saccade duration, gain, and peak velocity.
○ Detailed analyses of eye movements provide insights into the underlying neural mechanisms and the effects of different conditions on saccadic behavior.
Emphasis on the methodological approaches used in eye-tracking research, including calibration techniques and data processing methods (Dafoe et al., 2007).

33
Q

Dyckman et al. (2005)

A

○ Daily practice of antisaccades significantly decreases error rates without increasing reaction times (RTs), indicating improved accuracy without a speed-accuracy trade-off.
○ Participants who practiced prosaccades made more errors in antisaccade tasks, while those who practiced fixation tasks showed no change in antisaccade performance.
○ Significant improvements in antisaccade performance were observed within the first week of practice.
Behavioral plasticity is evident in the oculomotor system, demonstrating that antisaccade performance can be enhanced with deliberate practice (Dyckman & McDowell, 2005).

34
Q

Edelman et al. (2006)

A

○ The research investigates the neural correlates of saccadic eye movements and the role of different brain regions in controlling saccades.
○ It examines how various factors, such as attention and cognitive load, influence saccadic performance.
The study provides a comprehensive analysis of the relationship between brain activity and eye movement metrics, contributing to our understanding of the neural basis of saccadic control (Edelman et al., 2006).

35
Q

Everling & Johnston (2006)

A

○ This study explores the mechanisms of inhibitory control in antisaccade tasks and the role of the prefrontal cortex.
○ It highlights the differences in brain activation patterns between prosaccades and antisaccades, emphasizing the cognitive demands of inhibiting reflexive saccades.
The findings underscore the importance of the prefrontal cortex in successful antisaccade performance and its implications for disorders involving executive function deficits (Everling & Johnston, 2006).

36
Q

Fischer & Weber (1992)

A

○ The research examines the developmental trajectory of saccadic eye movements, focusing on the differences between children and adults.
○ It provides evidence for the maturation of the oculomotor system and the improvement of antisaccade performance with age.
The study discusses the implications of these developmental changes for understanding cognitive and neural development (Fischer & Weber, 1992).

37
Q

Fitts (1992)

A

○ Fitts’ Law: Larger targets that are closer require less time to saccade to compared to smaller targets that are farther away.
The larger the target and/or the shorter the distance, the faster the saccade can be made.

Explored in the context of saccadic eye movements, analyzing the trade-off between speed and accuracy in saccade tasks.
○ The research demonstrates how saccadic performance conforms to Fitts’ Law, with implications for understanding the constraints on motor control.
The study provides a theoretical framework for examining the dynamics of eye movements and their relationship to motor performance (Fitts, 1992).

38
Q

Gillen & Heath (2014)

A

○ This study investigates the effects of cognitive load on antisaccade performance, demonstrating that increased cognitive demands impair saccadic control.
○ It highlights the role of executive function in maintaining antisaccade accuracy under challenging conditions.
○ The findings have implications for understanding the interaction between cognitive processes and oculomotor control (Gillen & Heath, 2014).

39
Q

Hallet (1997)

A

○ The research focuses on the neural mechanisms underlying saccadic eye movements, particularly the role of the frontal eye fields (FEF) and supplementary eye fields (SEF).
○ It examines the coordination between different brain regions in generating and inhibiting saccades.
The study contributes to our knowledge of the neural circuitry involved in eye movement control and its relevance to various neurological conditions (Hallet, 1997).

40
Q

Kaufman et al. (2011)

A

○ Patients with mild Alzheimer’s disease (AD) made more antisaccade errors and corrected fewer errors than age-matched controls.
○ Antisaccade impairments suggest clinically detectable dorsolateral prefrontal cortex (DLPFC) pathology may be present earlier than previously thought.
Antisaccade tasks can effectively reveal executive function deficits in mild AD (Kaufman et al., 2011).

41
Q

Munoz & Everling (2004)

A

○ This comprehensive review synthesizes research on the neural basis of antisaccades, covering the roles of the FEF, SEF, DLPFC, and PPC.
○ It discusses the implications of antisaccade performance for understanding executive function and cognitive control.
The review highlights the clinical relevance of antisaccade tasks in diagnosing and monitoring neurological and psychiatric disorders (Munoz & Everling, 2004).

42
Q

Peltsch et al. (2013)

A

○ Both amnestic mild cognitive impairment (aMCI) and mild AD patients exhibited similar impairments in antisaccade tasks, including increased latencies and higher error rates compared to controls.
○ Antisaccade tasks are effective in detecting executive dysfunction in aMCI and AD, making them useful for early diagnosis and tracking disease progression.
Saccade tasks can assess executive function deficits when neuropsychological tests are impractical (Peltsch et al., 2013).

43
Q

What is gain variability and what does it tell you?

A
  • Gain variability refers to the within-participant standard deviation of saccade amplitude divided by the veridical (true) target location. It provides information about the variability in saccade amplitude relative to the actual target location.
  • Specifically, gain variability tells you the consistency of saccade accuracy within a participant:
  • Lower gain variability suggests the participant can generate more precise, consistent saccades to the target.
  • Higher gain variability suggests the participant has less precise, more variable saccadic eye movements.
  • Lower gain variability indicates the saccadic system is operating more efficiently, with less noise and variability.
    Higher gain variability suggests less efficient saccadic control mechanisms.
44
Q

Why are antisaccades usually overshot or undershot?

A
  • It is due to the perceptual averaging hypothesis (Gillen & Heath, 2014)
  • Antisaccades use a general, averaged sense of target location rather than precise information.
  • This “perceptual averaging” provides a simpler basis for the oculomotor system to generate the appropriate eye movements.
    The oculomotor system can rely on this relative, non-veridical (not exact) visual information to specify the sensorimotor transformations needed for antisaccades.
45
Q

Describe what happens in the brain during pro and antisaccades

A

Prosaccades:

Visual input: The visual stimulus is processed in the visual cortex and relayed to higher-order visual areas.
Saccade planning: The posterior parietal cortex (PPC), particularly the lateral intraparietal area (LIP), represents the target and generates the saccadic command. The frontal eye fields (FEF) and superior colliculus (SC) integrate the visual and cognitive information to plan the saccade.
Saccade execution: The FEF and SC project to the brainstem oculomotor nuclei, which generate the motor command to move the eyes towards the target. The cerebellum fine-tunes the saccadic movement.
Antisaccades:

Visual input and inhibition: As in prosaccades, the visual stimulus is processed, but the dorsolateral prefrontal cortex (DLPFC) inhibits the automatic saccade towards the target.
Saccade planning and execution: The DLPFC activates the voluntary saccade-related circuits in the FEF and SC to generate a saccade in the opposite direction. The SNpr (Substantia Nigra Pars Retuculata) provides tonic inhibition of SC to help suppress prosaccades. The brainstem and cerebellum execute the voluntary saccade.
Cognitive control and monitoring: The dorsal anterior cingulate cortex (dACC) and pre-supplementary motor area (pre-SMA) detect the conflict between the automatic and voluntary saccades, engaging the DLPFC for top-down control.

46
Q

Describe the key elements in Ayala & Heath’s saccade figure

A

Here are the key elements of the saccadic eye movement graph:

Saccade onset: The point where the green and red lines start to deviate from the baseline, around the 200 ms mark.

Reaction time: The time between the stimulus onset (not shown in the graph) and the saccade onset, which is approximately 200 ms in this case.

Saccade offset: The point where the green and red lines reach their maximum amplitude and flatten out, around the 400 ms mark.

Saccade duration: The time between saccade onset and saccade offset, which is roughly 200 ms (from 200 ms to 400 ms on the time axis).

Peak velocity: The highest point of the red line, which represents the maximum velocity reached during the saccade.

Amplitude: The maximum vertical distance between the baseline and the green line, which indicates the size of the saccadic eye movement.

Gain: The ratio of the actual saccade amplitude to the desired saccade amplitude (not directly shown in the graph, as the desired amplitude is not provided).

47
Q
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