Neurophysiology and neuroanatomy of reflexive and volitional saccades as revealed by lesion studies with neurological patients and transcranial magnetic stimulation (TMS)

This review discusses the neurophysiology and neuroanatomy of the cortical control of reflexive and volitional saccades in humans. The main focus is on classical lesion studies and studies using the interference method of transcranial magnetic stimulation (TMS). To understand the behavioural function of a region, it is essential to assess oculomotor deficits after a focal lesion using a variety of oculomotor paradigms, and to study the oculomotor consequences of the lesion in the chronic phase. Saccades are controlled by different cortical regions, which could be partially specialised in the triggering of a specific type of saccade. The division of saccades into reflexive visually guided saccades and intentional or volitional saccades corresponds to distinct regions of the neuronal network, which are involved in the control of such saccades.TMS allows to specifically interfere with the functioning of a region within an intact oculomotor network. TMS provides advantages in terms of temporal resolution, allowing to interfere with brain functioning in the order of milliseconds, thereby allowing to define the time course of saccade planning and execution.In the first part of the paper, we present an overview of the cortical structures important for saccade control, and discuss the pro’s and con’s of the different methodological approaches to study the cortical oculomotor network. In the second part, the functional network involved in reflexive and volitional saccades is presented. Finally, studies concerning recovery mechanisms after a lesion of the oculomotor cortex are discussed.     

Neurophysiology and neuroanatomy of reflexive and volitional saccades: Evidence from studies of humans

This review provides a summary of the contributions made by human functional neuroimaging studies to the understanding of neural correlates of saccadic control. The generation of simple visually guided saccades (redirections of gaze to a visual stimulus or pro-saccades) and more complex volitional saccades require similar basic neural circuitry with additional neural regions supporting requisite higher level processes. The saccadic system has been studied extensively in non-human (e.g., single-unit recordings) and human (e.g., lesions and neuroimaging) primates. Considerable knowledge of this system’s functional neuroanatomy makes it useful for investigating models of cognitive control. The network involved in pro-saccade generation (by definition largely exogenously-driven) includes subcortical (striatum, thalamus, superior colliculus, and cerebellar vermis) and cortical (primary visual, extrastriate, and parietal cortices, and frontal and supplementary eye fields) structures. Activation in these regions is also observed during endogenously-driven voluntary saccades (e.g., anti-saccades, ocular motor delayed response or memory saccades, predictive tracking tasks and anticipatory saccades, and saccade sequencing), all of which require complex cognitive processes like inhibition and working memory. These additional requirements are supported by changes in neural activity in basic saccade circuitry and by recruitment of additional neural regions (such as prefrontal and anterior cingulate cortices). Activity in visual cortex is modulated as a function of task demands and may predict the type of saccade to be generated, perhaps via top-down control mechanisms. Neuroimaging studies suggest two foci of activation within FEF - medial and lateral - which may correspond to volitional and reflexive demands, respectively. Future research on saccade control could usefully (i) delineate important anatomical subdivisions that underlie functional differences, (ii) evaluate functional connectivity of anatomical regions supporting saccade generation using methods such as ICA and structural equation modeling, (iii) investigate how context affects behavior and brain activity, and (iv) use multi-modal neuroimaging to maximize spatial and temporal resolution.     

Neurophysiology and neuroanatomy of reflexive and volitional saccades: evidence from studies of humans

This review provides a summary of the contributions made by human functional neuroimaging studies to the understanding of neural correlates of saccadic control. The generation of simple visually guided saccades (redirections of gaze to a visual stimulus or pro-saccades) and more complex volitional saccades require similar basic neural circuitry with additional neural regions supporting requisite higher level processes. The saccadic system has been studied extensively in non-human (e.g., single-unit recordings) and human (e.g., lesions and neuroimaging) primates. Considerable knowledge of this system’s functional neuroanatomy makes it useful for investigating models of cognitive control. The network involved in pro-saccade generation (by definition largely exogenously-driven) includes subcortical (striatum, thalamus, superior colliculus, and cerebellar vermis) and cortical (primary visual, extrastriate, and parietal cortices, and frontal and supplementary eye fields) structures. Activation in these regions is also observed during endogenously-driven voluntary saccades (e.g., anti-saccades, ocular motor delayed response or memory saccades, predictive tracking tasks and anticipatory saccades, and saccade sequencing), all of which require complex cognitive processes like inhibition and working memory. These additional requirements are supported by changes in neural activity in basic saccade circuitry and by recruitment of additional neural regions (such as prefrontal and anterior cingulate cortices). Activity in visual cortex is modulated as a function of task demands and may predict the type of saccade to be generated, perhaps via top-down control mechanisms. Neuroimaging studies suggest two foci of activation within FEF - medial and lateral - which may correspond to volitional and reflexive demands, respectively. Future research on saccade control could usefully (i) delineate important anatomical subdivisions that underlie functional differences, (ii) evaluate functional connectivity of anatomical regions supporting saccade generation using methods such as ICA and structural equation modeling, (iii) investigate how context affects behavior and brain activity, and (iv) use multi-modal neuroimaging to maximize spatial and temporal resolution.     

Validation of a Behavioral Approach for Measuring Saccades in Parkinson's Disease

Speed and control of saccades are related to disease progression and cognitive functioning in Parkinson's disease (PD). Traditional eye-tracking complexities encumber application for individual evaluations and clinical trials. The authors examined psychometric properties of standalone tasks for reflexive prosaccade latency, volitional saccade initiation, and saccade inhibition (antisaccade) in a heterogeneous sample of 65 PD patients. Demographics had minimal impact on task performance. Thirty-day test–retest reliability estimates for behavioral tasks were acceptable and similar to traditional eye tracking. Behavioral tasks demonstrated concurrent validity with traditional eye-tracking measures; discriminant validity was less clear. Saccade initiation and inhibition discriminated PD patients with cognitive impairment. The present findings support further development and use of the behavioral tasks for assessing latency and control of saccades in PD.     

Strategic control over saccadic eye movements: studies of the fixation offset effect

We studied the strategic (presumably cortical) control of ocular fixation in experiments that measured the fixation offset effect (FOE) while manipulating readiness to make reflexive or voluntary eye movements. The visual grasp reflex, which generates reflexive saccades to peripheral visual signals, reflects an opponent process in the superior colliculus (SC) between fixation cells at the rostral pole, whose activity helps maintain ocular position and increases when a stimulus is present at fixation, and movement cells, which generate saccades and are inhibited by rostral fixation neurons. Voluntary eye movements are controlled by movement and fixation cells in the frontal eye field (FEF). The FOE--a decrease in saccade latency when the fixation stimulus is extinguished--has been shown to reflect activity in the collicular eye movement circuitry and also to have an activity correlate in the FEF. Our manipulation of preparatory set to make reflexive or voluntary eye movements showed that when reflexive saccades were frequent and voluntary saccades were infrequent, the FOE was attenuated only for reflexive saccades. When voluntary saccades were frequent and reflexive saccades were infrequent, the FOE was attenuated only for voluntary saccades. We conclude that cortical processes related to task strategy are able to decrease fixation neuron activity even in the presence of a fixation stimulus, resulting in a smaller FOE. The dissociation in the effects of a fixation stimulus on reflexive and voluntary saccade latencies under the same strategic set suggests that the FOEs for these two types of eye movements may reflect a change in cellular activity in different neural structures, perhaps in the SC for reflexive saccades and in the FEF for voluntary saccades.     

Cluster analysis reveals distinct patterns of saccade impairment and their relation to cognitive profiles in Parkinson's disease

Saccade performance has been reported to be altered in Parkinson's disease (PD), however, with a large variability between studies as both motor and cognitive impairment interfere with oculomotor control. The aim of this study was to identify different patterns in saccade alterations in PD using a data-driven approach and to explore their relationship with cognitive phenotypes. Sixty-one participants with PD and 25 controls performed eye-tracking (horizontal and vertical prosaccades, antisaccades) and neuropsychological testing. Hierarchical cluster analysis was applied to the eye-tracking data to subsequently compare the clusters based on demographical, clinical and cognitive characteristics. The three identified clusters of saccade alterations differed in cognitive profiles from healthy controls, but not in PD-related motor symptoms or demographics. The rate of directive errors in the antisaccade task was increased in clusters 1 and 2. Further, cluster 1 was defined by a general disinhibition of reflexive saccades and executive dysfunction in the neuropsychological evaluation. In cluster 2, prolonged saccade latencies and hypometria were accompanied by multidomain cognitive impairment. The cluster 3 showed increased antisaccade latency and vertical hypometria despite lack of evidence for cognitive impairment. Our results suggest that there may be at least two opposing patterns of saccade alterations associated with cognitive impairment in PD, which may explain some of the contradictory results of previous studies.     

Faces are special,but facial expressions aren’t: Insights from an oculomotor capture paradigm

We compared the ability of angry and neutral faces to drive oculomotor behaviour as a test of the widespread claim that emotional information is automatically prioritized when competing for attention. Participants were required to make a saccade to a colour singleton; photos of angry or neutral faces appeared amongst other objects within the array, and were completely irrelevant for the task. Eye-tracking measures indicate that faces drive oculomotor behaviour in a bottom-up fashion; however, angry faces are no more likely to capture the eyes than neutral faces are. Saccade latencies suggest that capture occurrs via reflexive saccades and that the outcome of competition between salient items (colour singletons and faces) may be subject to fluctuations in attentional control. Indeed, although angry and neutral faces captured the eyes reflexively on a portion of trials, participants successfully maintained goal-relevant oculomotor behaviour on a majority of trials. We outline potential cognitive and brain mechanisms underlying oculomotor capture by faces.     

Positive affect increases cognitive control in the antisaccade task

To delineate the modulatory effects of induced positive affect on cognitive control, the current study investigated whether positive affect increases the ability to suppress a reflexive saccade in the antisaccade task. Results of the antisaccade task showed that participants made fewer erroneous prosaccades in the condition in which a positive mood was induced compared to the neutral condition (i.e. in which no emotional mood was induced). This improvement of oculomotor inhibition was restricted to saccades with an express latency. These results are in line with the idea that enhanced performance in the positive affect condition could be caused by increased dopaminergic neurotransmission the brain.     

Pharmacological treatment effects on eye movement control

The increasing use of eye movement paradigms to assess the functional integrity of brain systems involved in sensorimotor and cognitive processing in clinical disorders requires greater attention to effects of pharmacological treatments on these systems. This is needed to better differentiate disease and medication effects in clinical samples, to learn about neurochemical systems relevant for identified disturbances, and to facilitate identification of oculomotor biomarkers of pharmacological effects. In this review, studies of pharmacologic treatment effects on eye movements in healthy individuals are summarized and the sensitivity of eye movements to a variety of pharmacological manipulations is established. Primary findings from these studies of healthy individuals involving mainly acute effects indicate that: (i) the most consistent finding across several classes of drugs, including benzodiazepines, first- and second- generation antipsychotics, anticholinergic agents, and anticonvulsant/mood stabilizing medications is a decrease in saccade and smooth pursuit velocity (or increase in saccades during pursuit); (ii) these oculomotor effects largely reflect the general sedating effects of these medications on central nervous system functioning and are often dose-dependent; (iii) in many cases changes in oculomotor functioning are more sensitive indicators of pharmacological effects than other measures; and (iv) other agents, including the antidepressant class of serotonergic reuptake inhibitors, direct serotonergic agonists, and stimulants including amphetamine and nicotine, do not appear to adversely impact oculomotor functions in healthy individuals and may well enhance aspects of saccade and pursuit performance. Pharmacological treatment effects on eye movements across several clinical disorders including schizophrenia, affective disorders, attention deficit hyperactivity disorder, Parkinson’s disease, and Huntington’s disease are also reviewed. While greater recognition and investigation into pharmacological treatment effects in these disorders is needed, both beneficial and adverse drug effects are identified. This raises the important caveat for oculomotor studies of neuropsychiatric disorders that performance differences from healthy individuals cannot be attributed to illness effects alone. In final sections of this review, studies are presented that illustrate the utility of eye movements for use as potential biomarkers in pharmacodynamic and pharmacogenetic studies. While more systematic studies are needed, we conclude that eye movement measurements hold significant promise as tools to investigate treatment effects on cognitive and sensorimotor processes in clinical populations and that their use may be helpful in speeding the drug development pathway for drugs targeting specific neural systems and in individualizing pharmacological treatments.     

Saccadic eye movements as indicators of cognitive function in older adults

Older adults appear to have greater difficulty ignoring distractions during day-to-day activities than younger adults. To assess these effects of age, the ability of adults aged between 50 and 80 years to ignore distracting stimuli was measured using the antisaccade and oculomotor capture tasks. In the antisaccade task, observers are instructed to look away from a visual cue, whereas in the oculomotor capture task, observers are instructed to look toward a colored singleton in the presence of a concurrent onset distractor. Index scores of the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) were compared with capture errors, and with prosaccade errors on the antisaccade task. A higher percentage of capture errors were made on the oculomotor capture tasks by the older members of the cohort compared to the younger members. There was a weak relationship between the attention index and capture errors, but the visuospatial/constructional index was the strongest predictor of prosaccade error rate in the antisaccade task. The saccade reaction times (SRTs) of correct initial saccades in the oculomotor capture task were poorly correlated with age, and with the neurospsychological tests, but prosaccade SRTs in both tasks moderately correlated with antisaccade error rate. These results were interpreted in terms of a competitive integration (or race) model. Any variable that reduces the strength of the top-down neural signal to produce a voluntary saccade, or that increases saccade speed, will enhance the likelihood that a reflexive saccade to a stimulus with an abrupt onset will occur.     

Saccades elicit obligatory allocation of visual working memory

In daily life, visual working memory (VWM) typically works in contexts in which people make frequent saccades. Here, we investigated whether people can effectively control the allocation of VWM when making a saccade. Subjects were required to make an intervening saccade in the process of a memory task. The saccade target was either a to-be-remembered item or an extra, not-to-be-remembered item. The results showed that memory performance was poorer when a saccade was made to the extra, not-to-be-remembered item, regardless of its similarity to the memory item(s). In contrast, when memorizing the items while remaining fixated, subjects had similar memory performance whether an extra, not-to-be-remembered item was present or not. Taken together, these results demonstrated that volitional control over VWM allocation is greatly impaired when a saccade is made, indicating that VWM contains an automatic part that cooperates with eye movements and is allocated to a saccade target obligatorily.     

Deficits in volitional oculomotor control align with language status in autism spectrum disorders

Eye‐tracking paradigms are increasingly used to investigate higher‐level social and cognitive processing in autism spectrum disorder (ASD). However, the integrity of the oculomotor system within ASD is unclear, with contradictory reports of aberrant eye‐movements on basic oculomotor tasks. The purpose of the current study was to determine whether reducing population heterogeneity and distinguishing neurocognitive phenotypes can clarify discrepancies in oculomotor behaviour evident in previous reports. Reflexive and volitional eye‐movement control was assessed in 73 children aged 8–14 years from four distinct groups: Autism Language Normal (ALN), Autism Language Impaired (ALI), non‐autistic Language Impaired (LI) and Typically Developing (TD). Eye‐movement control was measured using pro‐ and antisaccade tasks and a novel ‘search distracter’ task to measure distractibility. Reflexive eye‐movements were equivalent across groups, but deficits in volitional eye‐movement control were found that aligned with language status, and were not specific to ASD. More than 80% of ALI and LI children presented error rates at least 1.5 SDs below the TD mean in an antisaccade task. In the search distracter task, 35.29% of ALI children and 43.75% of LI children had error rates greater than 1.5 SDs compared with 17.64% of ALN children. A significant proportion of children with neurodevelopmental disorders involving language function have pronounced difficulties suppressing reflexive saccades and maintaining fixations in the presence of competing stimuli. We extend the putative link between ALI and LI populations to non‐language tasks, and highlight the need to account for co‐morbidity in understanding the ontogenesis of ASD.     

Aging and the strategic control of the fixation offset effect

A study was conducted to examine potential age-related differences in the strategic control of exogenous and endogenous saccades within the context of the fixation offset effect (FOE; i.e., faster saccades when a fixation point is removed than when it is left on throughout a trial). Subjects were instructed to make rapid saccades either on the basis of a suddenly appearing peripheral visual stimulus (exogenous saccade) or in response to a tone (endogenous saccade). On half of the trials the fixation point was removed simultaneously with the occurrence of the cue stimulus. Subjects' preparatory set was varied by manipulating the proportion of saccades generated to a visual and auditory stimulus within a trial block. Young and old adults both produced FOEs, and the FOEs were strategically modulated by preparatory set. The data are discussed in terms of aging and oculomotor control.     

Enhanced saccadic control in young people with Tourette syndrome despite slowed pro‐saccades

Tourette syndrome (TS) is a neurodevelopmental disorder characterized by motor and vocal tics. Tics are repetitive and uncontrolled behaviours that have been associated with basal ganglia dysfunction. We investigated saccadic eye movements in a group of young people with TS but without co‐morbid ADHD. Participants performed two tasks. One required them to perform only pro‐saccade responses (pure pro‐saccade task). The other involved shifting, unpredictably, between executing pro‐ and anti‐saccades (mixed saccade task). We show that in the mixing saccade task, the TS group makes significantly fewer errors than an age‐matched control group, while responding equally fast. By contrast, on the pure pro‐saccade task, the TS group were shown to be significantly slower to initiate and to complete the saccades (longer movement duration and decreased peak velocity) than controls, while movement amplitude and direction accuracy were not different. These findings demonstrate enhanced shifting ability despite slower reflexive responding in TS and are discussed with respect to a disorder‐related adaptation for increased cognitive regulation of behaviour.     

Differential roles of the frontal and parietal cortices in the control of saccades

Although externally as well as internally-guided eye movements allow us to flexibly explore the visual environment, their differential neural mechanisms remain elusive. A better understanding of these neural mechanisms will help us to understand the control of action and to elucidate the nature of cognitive deficits in certain psychiatric populations (e.g. schizophrenia) that show increased latencies in volitional but not visually-guided saccades. Both the superior precentral sulcus (sPCS) and the intraparietal sulcus (IPS) are implicated in the control of eye movements. However, it remains unknown what differential contributions the two areas make to the programming of visually-guided and internally-guided saccades. In this study we tested the hypotheses that sPCS and IPS distinctly encode internally-guided saccades and visually-guided saccades. We scanned subjects with fMRI while they generated visually-guided and internally-guided delayed saccades. We used multi-voxel pattern analysis to test whether patterns of cue related, preparatory and saccade related activation could be used to predict the direction of the planned eye movement. Results indicate that patterns in the human sPCS predicted internally-guided saccades but not visually-guided saccades in all trial periods and patterns in the IPS predicted internally-guided saccades and visually-guided saccades equally well. The results support the hypothesis that the human sPCS and IPS make distinct contributions to the control of volitional eye movements.     

Long-lasting modifications of saccadic eye movements following adaptation induced in the double-step target paradigm

The adaptation of saccadic eye movements to environmental changes occurring throughout life is a good model of motor learning and motor memory. Numerous studies have analyzed the behavioral properties and neural substrate of oculomotor learning in short-term saccadic adaptation protocols, but to our knowledge, none have tested the persistence of the oculomotor memory. In the present study, the double-step target protocol was used in five human subjects to adaptively decrease the amplitude of reactive saccades triggered by a horizontally-stepping visual target. We tested the amplitude of visually guided saccades just before and at different times (up to 19 days) after the adaptation session. The results revealed that immediately after the adaptation session, saccade amplitude was significantly reduced by 22% on average. Although progressively recovering over days, this change in saccade gain was still statistically significant on days 1 and 5, with an average retention rate of 36% and 19%, respectively. On day 11, saccade amplitude no longer differed from the pre-adaptation value. Adaptation was more effective and more resistant to recovery for leftward saccades than for rightward ones. Lastly, modifications of saccade gain related to adaptation were accompanied by a decrease of both saccade duration and peak velocity. A control experiment indicated that all these findings were specifically related to the adaptation protocol, and further revealed that no change in the main sequence relationships could be specifically related to adaptation. We conclude that in humans, the modifications of saccade amplitude that quickly develop during a double-step target adaptation protocol can remain in memory for a much longer period of time, reflecting enduring plastic changes in the brain.     

Pharmacological treatment effects on eye movement control

The increasing use of eye movement paradigms to assess the functional integrity of brain systems involved in sensorimotor and cognitive processing in clinical disorders requires greater attention to effects of pharmacological treatments on these systems. This is needed to better differentiate disease and medication effects in clinical samples, to learn about neurochemical systems relevant for identified disturbances, and to facilitate identification of oculomotor biomarkers of pharmacological effects. In this review, studies of pharmacologic treatment effects on eye movements in healthy individuals are summarized and the sensitivity of eye movements to a variety of pharmacological manipulations is established. Primary findings from these studies of healthy individuals involving mainly acute effects indicate that: (i) the most consistent finding across several classes of drugs, including benzodiazepines, first- and second- generation antipsychotics, anticholinergic agents, and anticonvulsant/mood stabilizing medications is a decrease in saccade and smooth pursuit velocity (or increase in saccades during pursuit); (ii) these oculomotor effects largely reflect the general sedating effects of these medications on central nervous system functioning and are often dose-dependent; (iii) in many cases changes in oculomotor functioning are more sensitive indicators of pharmacological effects than other measures; and (iv) other agents, including the antidepressant class of serotonergic reuptake inhibitors, direct serotonergic agonists, and stimulants including amphetamine and nicotine, do not appear to adversely impact oculomotor functions in healthy individuals and may well enhance aspects of saccade and pursuit performance. Pharmacological treatment effects on eye movements across several clinical disorders including schizophrenia, affective disorders, attention deficit hyperactivity disorder, Parkinson’s disease, and Huntington’s disease are also reviewed. While greater recognition and investigation into pharmacological treatment effects in these disorders is needed, both beneficial and adverse drug effects are identified. This raises the important caveat for oculomotor studies of neuropsychiatric disorders that performance differences from healthy individuals cannot be attributed to illness effects alone. In final sections of this review, studies are presented that illustrate the utility of eye movements for use as potential biomarkers in pharmacodynamic and pharmacogenetic studies. While more systematic studies are needed, we conclude that eye movement measurements hold significant promise as tools to investigate treatment effects on cognitive and sensorimotor processes in clinical populations and that their use may be helpful in speeding the drug development pathway for drugs targeting specific neural systems and in individualizing pharmacological treatments.     

Endogenous saccades are preceded by shifts of visual attention: evidence from cross-saccadic priming effects

The present study examines whether endogenous saccades are preceded by shifts of attention. Three experiments are reported in which participants were required to execute a saccadic eye movement to a certain location and to subsequently identify the orientation of a target triangle. Prior to the execution of the saccade a prime was presented, which was compatible or incompatible with the target. A priming effect (faster responses in the compatible condition than in the incompatible condition) occurred only when the prime was presented at the saccade destination, and this effect was larger when the prime was presented during oculomotor programming than when it was presented prior to oculomotor programming. The results indicate that an endogenous shift of attention precedes endogenous saccades, providing further support for theories of visual selection that assume a tight coupling between attention and saccades.     

酒精对视觉加工和眼动行为控制的影响(中文)

Although moderate alcohol consumption is known to degrade performance in a variety of tasks, the exact nature and extent of such impairments is not well understood. We examined alcohol effects on different levels of visual processing and oculomotor control. On the lowest level(automatic), reflexive responses were tested using the prosaccade task. The‘automated’level, incorporating routine behavior based on implicit learning, was studied using the double step paradigm, while the highest level, representing voluntary control, was examined with antisaccade and memory guided tasks. In addition, sentence reading was included as a prototypical complex task with high ecological validity. Participant′s baseline performance was compared to alcohol conditions with intoxication levels around 70mg% of breath alcohol concentration. Functioning on the automatic level was intact, except for a substantial slowing in saccade latencies. On the automated level, deficits in the ability to adaptively reprogram saccades on the basis of new information were found. Impairments in voluntary control were apparent in hypermetric saccade amplitudes whenever a reprogramming of the initial saccade target was necessary. There was also a small but significant detrimental effect on visuospatial short term memory. Somewhat surprisingly, no alcohol related deficits emerged with regard to inhibitory functions. ‘Reading under the influence’resulted in substantially prolonged fixation durations with only a modest increase in total viewing time per word. A trade-off between increased duration and decreased number of fixations pointed to the possibility that the extra time available under alcohol can be used for linguistic processing, which in itself did not appear to be impaired. This idea is supported by the fact that there was no interaction between alcohol and word frequency. Contrary to expectation, the processing of parafoveal information during reading was not impeded. Overall, results provide a largely coherent pattern of selective effects that begin to form a comprehensive picture of alcohol related deficits.     

Inhibitory inefficiency and failures of intention activation: age-related decline in the control of saccadic eye movements

Young and older adults' control of saccadic eye movements was compared using an antisaccade task, which requires the inhibition of a reflexive saccade toward a peripheral onset cue followed by an intentional saccade in the opposite direction. In 2 experiments, an age-related decline was found in the suppression of reflexive eye movements, as indicated by an increased proportion of saccades toward the cue, and a longer time needed to initiate correct antisaccades. The results from Experiment 2 suggested that older adults' slower antisaccades may be explained partly in terms of increased failures to maintain the cue-action representation at a sufficient activation level. The results suggest that the notion of selective preservation with age of the ability to inhibit spatial responses does not apply to the active inhibition of prepotent spatial responses.