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Pupil diameter, under constant illumination, is known to reflect individuals' internal states, such as surprise about observation and environmental uncertainty. Despite the growing use of pupillometry in cognitive learning studies as an additional measure for examining internal states, few studies have used pupillometry in human motor learning studies. Here, we provide the first detailed characterization of pupil diameter changes in a short-term reach adaptation paradigm. We measured pupil changes in 121 human participants while they adapted to abrupt, gradual, or switching force field conditions. Sudden increases in movement error caused by the introduction/reversal of the force field resulted in strong phasic pupil dilation during movement accompanied by a transient increase in tonic premovement baseline pupil diameter in subsequent trials. In contrast, pupil responses were reduced when the force field was gradually introduced, indicating that large, unexpected errors drove the changes in pupil responses. Interestingly, however, error-induced pupil responses gradually became insensitive after experiencing multiple force field reversals. We also found an association between baseline pupil diameter and incidental knowledge of the gradually introduced perturbation. Finally, in all experiments, we found a strong co-occurrence of larger baseline pupil diameter with slower reaction and movement times after each rest break. Collectively, these results suggest that tonic baseline pupil diameter reflects one's belief about environmental uncertainty, whereas phasic pupil dilation during movement reflects surprise about a sensory outcome (i.e., movement error), and both effects are modulated by novelty. Our results provide a new approach for nonverbally assessing participants' internal states during motor learning.

How is the primary motor cortex (M1) organized to control fine finger movements? We investigated the population activity in M1 for single finger flexion and extension, using 7T functional magnetic resonance imaging (fMRI) in female and male human participants, and compared these results to the neural spiking patterns recorded in two male monkeys performing the identical task. fMRI activity patterns were distinct for movements of different fingers, but quite similar for flexion and extension of the same finger. In contrast, spiking patterns in monkeys were quite distinct for both fingers and directions, similar to what was found for muscular activity patterns. The discrepancy between fMRI and electrophysiological measurements can be explained by two (non-mutually exclusive) characteristics of the organization of finger flexion and extension movements. Given that fMRI reflects predominantly input and recurrent activity, the results can be explained by an architecture in which neural populations that control flexion or extension of the same finger produce distinct outputs, but interact tightly with each other and receive similar inputs. Additionally, neurons tuned to different movement directions for the same finger (or combination of fingers) may cluster closely together, while neurons that control different finger combinations may be more spatially separated. When measuring this organization with fMRI at a coarse spatial scale, the activity patterns for flexion and extension of the same finger would appear very similar. Overall, we suggest that the discrepancy between fMRI and electrophysiological measurements provides new insights into the general organization of fine finger movements in M1.Significance statementThe primary motor cortex (M1) is important for producing individuated finger movements. Recent evidence shows that movements that commonly co-occur are associated with more similar activity patterns in M1. Flexion and extension of the same finger, which never co-occur, should therefore be associated with distinct representations. However, using carefully controlled experiments and multivariate analyses, we demonstrate that human fMRI activity patterns for flexion or extension of the same finger are highly similar. In contrast, spiking patterns measured in monkey M1 are clearly distinct. This suggests that populations controlling opposite movements of the same finger, while producing distinct outputs, may cluster together and share inputs and local processing. These results provide testable hypotheses about the organization of hand control in M1.

© 2019, The Author(s), under exclusive licence to Springer Nature America, Inc. Motor behaviour is most efficiently controlled by correcting only disturbances that influence task success. It is currently thought that such control is computed within a transcortical feedback pathway. Here we show that, for postural hand control, even the fastest spinal feedback pathway can produce efficient corrective responses, forcing a re-evaluation of how the nervous system derives the control laws that support motor behavior.

Motor behaviour is most efficiently controlled by correcting only disturbances that influence task success. It is currently thought that such control is computed within a transcortical feedback pathway. Here we show that, for postural hand control, even the fastest spinal feedback pathway can produce efficient corrective responses, forcing a re-evaluation of how the nervous system derives the control laws that support motor behavior.

Motor behaviour is most efficiently controlled by only correcting disturbances or deviations that influence task success. It is currently thought that such sophisticated control is computed within a transcortical feedback pathway. Here we show that even the fastest spinal feedback pathway can produce corrective responses that adhere to this control scheme. We first applied small mechanical perturbations that flexed the elbow joint – stretching the triceps muscle – and simultaneously flexed or extended the wrist joint, displacing the hand various distances away from a central target. We then changed the arm’s orientation and applied the same joint perturbations, which reversed the mapping between joint motion and hand displacement. In all cases, we found that the triceps’ spinal stretch reflex was tuned to the hand’s displacement relative to the target, and not how the triceps muscle was stretched. Our findings reveal that the fastest spinal feedback pathway is capable of integrating and modulating feedback from multiple muscles to produce efficient corrective responses, forcing a re-evaluation of the how the nervous system derives the sophisticated control laws that support natural motor behaviour.

The completion of an antisaccade delays the reaction time (RT) of a subsequent prosaccade; however, the converse switch does not influence RT. In accounting for this result, the task-set inertia hypothesis contends that antisaccades engender a persistent nonstandard task-set that delays the planning of a subsequent prosaccade. In contrast, the coordinate system transformation hypothesis asserts that the transformation required to construct a mirror-symmetrical target representation persistently inhibits prosaccade planning. The authors tested the latter hypothesis by examining switch-costs for pro- and antisaccades directed to visual (i.e., the stimuli used in previous work) and auditory targets. Notably, auditory cues are specified in a head-centered frame of reference prior to their conversion into the retinocentric coordinates necessary for saccade output. Thus, if the coordinate system transformation hypothesis is correct then auditory pro- and antisaccades should elicit a bidirectional switch-cost because each requires a coordinate transformation. RTs for visual and auditory modalities showed a reliable--and equivalent magnitude--prosaccade switch-cost. Moreover, performance (e.g., movement time) and kinematic (e.g., velocity) variables indicated the switch-cost was restricted to response planning. As such, results are incompatible with the coordinate system transformation hypothesis and therefore provide convergent evidence that a task-set inertia contributes to the prosaccade switch-cost.

A transcortical pathway helps support goal-directed reaching by processing somatosensory information to produce rapid feedback responses across multiple joints and muscles. Here we tested whether such feedback responses can account for changes in arm configuration and for arbitrary visuomotor transformations – two manipulations that alter how muscles at the elbow and wrist need to be coordinated to achieve task success. Participants used a planar three degree-of-freedom exoskeleton robot to move a cursor to a target following a mechanical perturbation that flexed the elbow. In our first experiment, the cursor was mapped to the veridical position of the robot handle, but participants grasped the handle with two different hand orientations (thumb pointing upward or thumb point downward). We found that large rapid feedback responses were evoked in wrist extensor muscles when wrist extension helped move the cursor to the target (i.e., thumb upward), and in wrist flexor muscles when wrist flexion helped move the cursor to the target (i.e., thumb downward). In our second experiment, participants grasped the robot handle with their thumb pointing upward, but the cursor’s movement was either veridical, or was mirrored such that flexing the wrist moved the cursor as if the participant extended their wrist, and vice versa. After extensive practice, we found that rapid feedback responses were appropriately tuned to the wrist muscles that supported moving the cursor to the target when the cursor was mapped to the mirrored movement of the wrist, but were not tuned to the appropriate wrist muscles when the cursor was remapped to the wrist’s veridical movement.New and NoteworthyWe show that rapid feedback responses were evoked in different wrist muscles depending on the arm’s orientation, and this muscle activity was appropriate to generate the wrist motion that supported a reaching action. Notably, we also show that these rapid feedback responses can be evoked in wrist muscles that are detrimental to a reaching action if a non-veridical mapping between wrist and hand motion is extensively learned.

The completion of an antisaccade (i.e., a nonstandard task) lengthens the reaction time (RT) of a subsequent prosaccade: a behavioral phenomenon termed the unidirectional prosaccade switch-cost. One explanation for the unidirectional prosaccade switch-cost is suppressing a stimulus-driven prosaccade during the preceding antisaccade trial engenders a residual inhibition of the oculomotor networks that support prosaccade planning (i.e., the oculomotor inhibition hypothesis). Alternatively, the unidirectional prosaccade switch-cost may reflect the persistent activation of the antisaccade's nonstandard task rules (i.e., task set), which delays the planning of the next prosaccade (i.e., task-set inertia hypothesis). To determine which hypothesis provides the most parsimonious account for the unidirectional prosaccade switch-cost, participants alternated between pro- and antisaccades wherein task instructions (i.e., pro- and antisaccade) were provided before (i.e., classic cuing) or concurrent (i.e., delayed cuing) with response cuing. Importantly, pro- and antisaccades elicited via the delayed cuing condition required the suppression of a stimulus-driven prosaccade at response cuing (i.e., response suppression) to discern the appropriate to-be-performed task. Results showed that classic and delayed antisaccades, but not delayed prosaccades, lengthened the RT of subsequent prosaccades. That delayed prosaccades, which require response suppression for their successful execution, did not lengthen the RT of subsequent prosaccades indicates that the oculomotor inhibition hypothesis does not account for the unidirectional prosaccade switch-cost. Instead, the current findings are in line with the assertion that the task set associated with a nonstandard antisaccade persists inertially and delays the planning of a subsequent prosaccade (i.e., task-set inertia hypothesis).

An antisaccade is the execution of a saccade to the mirror-symmetrical location (i.e., same amplitude but opposite visual field) of a single and exogenously presented visual target. Such a response requires top-down decoupling of the normally direct spatial relations between stimulus and response and results in increased planning times and directional errors compared to their spatially compatible prosaccade counterparts. Moreover, antisaccades are associated with diffuse changes in cortical and subcortical saccade networks: a finding that has, in part, been attributed to pre-setting the oculomotor system to withhold a stimulus-driven prosaccade. Moreover, recent work has shown that a corollary cost of oculomotor pre-setting is that the planning time for a to-be-completed prosaccade is longer when preceded by an antisaccade (i.e., the unidirectional prosaccade switch-cost). Notably, this result has been attributed to antisaccades imparting a residual inhibition of the oculomotor networks that support the planning of stimulus-driven prosaccades. In the current investigation, we sought to determine if the number of antisaccades preceding a prosaccade increases this residual inhibition and thus influences the magnitude of the unidirectional prosaccade switch-cost. To that end, participants alternated between pro- and antisaccades after every second (i.e., AABB schedule) and every fourth (i.e., AAAABBBB schedule) trial. In addition, participants completed pro- and antisaccades in separate blocks of trials. Results demonstrated that task-switch prosaccades produced longer reaction times than their task-repetition and blocked condition counterparts, whereas antisaccade reaction times did not vary across task-repetition, task-switch and blocked condition trials. Most notably, the magnitude of the unidirectional prosaccade switch-cost was not modulated across the different task-switching schedules. Thus, we propose that the top-down requirements of the antisaccade task do not produce additive inhibition of stimulus-driven saccade networks.

Persons with an objective cognitive impairment (OCI) are at increased risk for progression to Alzheimer's disease and related dementias. The present pilot project sought to examine whether participation in a long-term exercise program involving cognitive-motor (CM) dual-task gait training and aerobic exercise training improves executive function in persons with an OCI. To accomplish our objective, individuals with an OCI (n = 12) as determined by a Montreal Cognitive Assessment (MoCA) score of less than 26 and older adults (n = 11) deemed to be cognitively healthy (i.e., control group: MoCA score ≥26) completed a six-month moderate-to-high intensity (65-85% maximum heart rate) treadmill-based CM and aerobic exercise training program wherein pre- and post-intervention executive control was examined via the antisaccade task. Notably, antisaccades require a goal-directed eye-movement mirror-symmetrical to a target and represent an ideal tool for the study of executive deficits because of its hands- and language-free nature. As well, the cortical networks mediating antisaccades represent regions associated with neuropathology in cognitive decline and dementia (e.g., dorsolateral prefrontal cortex). Results showed that antisaccade reaction times for the OCI group reliably decreased by 30 ms from pre- to post-intervention, whereas the control group did not produce a reliable pre- to post-intervention change in reaction time (i.e., 6 ms). Thus, we propose that in persons with OCI long-term CM and aerobic training improves the efficiency and effectiveness of the executive mechanisms mediating high-level oculomotor control.

The long-latency stretch response (muscle activity 50–100 ms after a mechanical perturbation) can be coordinated across multiple joints to support goal-directed actions. Here we assessed the flexibility of such coordination and whether it serves to counteract intersegmental dynamics and exploit kinematic redundancy. In three experiments, participants made planar reaches to visual targets after elbow perturbations and we assessed the coordination of long-latency stretch responses across shoulder, elbow, and wrist muscles. Importantly, targets were placed such that elbow and wrist (but not shoulder) rotations could help transport the hand to the target—a simple form of kinematic redundancy. In experiment 1 we applied perturbations of different magnitudes to the elbow and found that long-latency stretch responses in shoulder, elbow, and wrist muscles scaled with perturbation magnitude. In experiment 2 we examined the trial-by-trial relationship between long-latency stretch responses at adjacent joints and found that the magnitudes of the responses in shoulder and elbow muscles, as well as elbow and wrist muscles, were positively correlated. In experiment 3 we explicitly instructed participants how to use their wrist to move their hand to the target after the perturbation. We found that long-latency stretch responses in wrist muscles were not sensitive to our instructions, despite the fact that participants incorporated these instructions into their voluntary behavior. Taken together, our results indicate that, during reaching, the coordination of long-latency stretch responses across multiple joints counteracts intersegmental dynamics but may not be able to exploit kinematic redundancy.

The antisaccade task requires the suppression of a reflexive prosaccade (i.e., response suppression) and the remapping of a target location to mirror-symmetrical space (i.e., vector inversion). Moreover, antisaccades are associated with increased activation of cortical oculomotor networks: a finding attributed to the top-down requirements of response suppression and vector inversion. The goal of the present study was to determine if the increased cortical activity associated with antisaccades elicits a residual inhibition of oculomotor planning networks. To that end, each trial in this investigation entailed the onset of a single and exogenously presented target (i.e., archetypical antisaccade task) and participants were instructed to alternate between pro- and antisaccades in blocked and random task-switching schedules. In the blocked schedule, the saccade tasks (i.e., pro- and antisaccades) alternated on every second trial (AABB paradigm) whereas in the random schedule the saccade tasks were pseudo-randomly interleaved on a trial-by-trial basis. Reaction times for task-switch prosaccades were longer and more variable than their task-repetition counterparts, whereas antisaccades did not vary as a function of task-switch and task-repetition trials: a finding that was consistent across blocked and random presentation schedules. In other words, results demonstrate a unidirectional switch-cost for prosaccades. As such, we propose that the top-down processes required to complete an antisaccade results in residual inhibition of oculomotor networks supporting a subsequent prosaccade.

The authors examined whether the diminished online control of antisaccades is related to a trade-off between movement planning and control or the remapping of target properties to a mirror-symmetrical location (i.e., vector inversion). Pro- and antisaccades were examined in a standard no-delay schedule wherein target onset served as the movement imperative and a delay cuing schedule wherein responses were initiated 2,000 ms following target onset. Importantly, the delay cuing schedule was employed to equate pro- and antisaccade reaction times. Online control was evaluated by indexing the strength of trajectory amendments at normalized increments of movement time. Antisaccades exhibited fewer online corrections than prosaccades, and this result was consistent across cuing schedules. Thus, the diminished online control of antisaccades cannot be tied to a trade-off between movement planning and control. Rather, the authors propose that the intentional nature of dissociating stimulus and response (i.e., vector inversion) engenders a slow mode of cognitive control that is not optimized for fast oculomotor corrections.

Many studies have demonstrated that muscle activity 50–100 ms after a mechanical perturbation (i.e., the long-latency stretch response) can be modulated in a manner that reflects voluntary motor control. These previous studies typically assessed modulation of the long-latency stretch response from individual muscles rather than how this response is concurrently modulated across multiple muscles. Here we investigated such concurrent modulation by having participants execute goal-directed reaches to visual targets after mechanical perturbations of the shoulder, elbow, or wrist while measuring activity from six muscles that articulate these joints. We found that shoulder, elbow, and wrist muscles displayed goal-dependent modulation of the long-latency stretch response, that the relative magnitude of participants' goal-dependent activity was similar across muscles, that the temporal onset of goal-dependent muscle activity was not reliably different across the three joints, and that shoulder muscles displayed goal-dependent activity appropriate for counteracting intersegmental dynamics. We also observed that the long-latency stretch response of wrist muscles displayed goal-dependent modulation after elbow perturbations and that the long-latency stretch response of elbow muscles displayed goal-dependent modulation after wrist perturbations. This pattern likely arises because motion at either joint could bring the hand to the visual target and suggests that the nervous system rapidly exploits such simple kinematic redundancy when processing sensory feedback to support goal-directed actions.

Antisaccades require the top-down suppression of a stimulus-driven prosaccade (i.e., response suppression) and the inversion of a target's spatial location to mirror-symmetrical space (i.e., vector inversion). Moreover, recent work has shown that antisaccade amplitudes are characterized by a statistical summary representation (SSR) of the target eccentricities included in a stimulus-set--a result suggesting that antisaccades are supported via the same relative visual information as perceptions. The present investigation sought to determine whether response suppression and the disruption of real-time control or vector inversion contribute to a SSR in oculomotor control. Participants completed pro- and antisaccades (target eccentricities of 10.5°, 15.5°, and 20.5°) in blocks of trials that differed with regard to the frequency that individual target eccentricities were presented. The manipulation of target eccentricity frequency was used to determine whether the most frequently presented target within a stimulus-set (i.e., the SSR) influences saccade amplitudes. Moreover, we disrupted the real-time control of prosaccades by requiring participants to suppress their response for a brief visual delay (i.e., 2000 ms: so-called delay prosaccade). As expected, antisaccades and delay prosaccades produced equivalent reaction times. In turn, amplitudes for delay prosaccades were refractory to the manipulation of target eccentricity frequency, whereas antisaccades were biased in the direction of the most frequently presented target within a stimulus-set. Accordingly, we propose that vector inversion contributes to the mediation of target eccentricities via a SSR and that such a phenomenon provides convergent evidence that a relative visual percept mediates antisaccades.

The execution of an antisaccade selectively increases the reaction time (RT) of a subsequent prosaccade (the unidirectional prosaccade switch-cost). To explain this finding, the task-set inertia hypothesis asserts that an antisaccade requires a cognitively mediated non-standard task-set that persists inertially and delays the planning of a subsequent prosaccade. The present study sought to directly test the theoretical tenets of the task-set inertia hypothesis by examining the concurrent behavioural and the event-related brain potential (ERP) data associated with the unidirectional prosaccade switch-cost. Participants pseudo-randomly alternated between pro- and antisaccades while electroencephalography (EEG) data were recorded. As expected, the completion of an antisaccade selectively increased the RT of a subsequent prosaccade, whereas the converse switch did not influence RTs. Thus, the behavioural results demonstrated the unidirectional prosaccade switch-cost. In terms of the ERP findings, we observed a reliable change in the amplitude of the P3 - time-locked to task-instructions - when trials were switched from a prosaccade to an antisaccade; however, no reliable change was observed when switching from an antisaccade to a prosaccade. This is a salient finding because extensive work has shown that the P3 provides a neural index of the task-set required to execute a to-be-completed response. As such, results showing that prosaccades completed after antisaccades exhibited increased RTs in combination with a P3 amplitude comparable to antisaccades provides convergent evidence that the unidirectional prosaccade switch-cost is attributed to the persistent activation of a non-standard antisaccade task-set.

The latency of a prosaccade is increased when completed following an antisaccade (the prior-antisaccade effect). This finding has been attributed to the inhibition of the oculomotor networks necessary for an antisaccade engendering a persistent response set that delays a to-be-executed prosaccade. The goal of the present investigation was to determine whether the prior-antisaccade effect influences not only the planning but also the control of an unfolding prosaccade trajectory. To accomplish that objective, we employed a task-switching paradigm wherein participants alternated between pro- and antisaccades on every second trial (i.e., AABB paradigm). Importantly, trajectory control was evaluated by computing the proportion of variance (R 2 values) explained by the spatial position of the eye at decile increments of movement time relative to the response’s ultimate movement endpoint: small R 2 values indicate a response that unfolds with error-reducing trajectory amendments (i.e., online control), whereas larger R 2 values reflect a response that unfolds with few—if any—online corrections. As expected, results showed a prior-antisaccade effect for response planning; that is, prosaccade latencies were increased when completed after an antisaccade. Moreover, prosaccades completed after an antisaccade elicited larger R 2 values and less accurate endpoints than trials wherein a prosaccade was completed after another prosaccade. These results provide first evidence of a prior-antisaccade effect for trajectory control and indicate that the persistent and inhibitory response set arising from an antisaccade diminishes the online corrections, and thus endpoint accuracy, of a subsequent prosaccade.

The classic theorem of Fitts (1954) asserts that the combined effects of movement amplitude and target width (index of difficulty: ID) define movement times (MTs) for goal-directed reaches. Moreover, Fitts' theorem states that reaches yielding the same ID produce equivalent MTs regardless of the response's amplitude and width combination. However, most work providing direct support for Fitts' theorem has employed short movement amplitudes and small target widths. Thus, no direct evidence supports the unitary nature of MT/ID relations across a range of amplitudes and widths used in contemporary studies of goal-directed reaching. To that end, we contrasted MT/ID relations for discrete reaches equated for movement ID but differing with respect to their amplitude (15.5, 19, 25.5, and 38 cm) and width (2, 3, 4, and 5 cm) requirements. Results show that amplitude and width manipulations yielded robust linear MT/ID relations; however, the slope of the MT/ID function was markedly steeper in the former (amplitude = 92 ms; width = 13 ms). Such findings indicate that the constituent elements of movement ID are dissociable and that the fixed parameter nature of Fitts' theorem cannot be applied to a continuous range of veridical movement amplitudes and target widths. Keywords: action, Fitts, index of difficulty, reaching, visually guided The seminal work of Paul Fitts described the information processing demands associated with reciprocal (Fitts, 1954) and discrete (Fitts & Peterson, 1964) goal-directed reaching movements. According to Fitts, the demands of a reaching response are determined by the task's index of difficulty (ID: in bits of information) that is reflected by the equation log2(2A/W): where A represents movement amplitude and W the width associated with the goaldefined target object. Notably, Fitts observed that increasing ID gave rise to a linear increase in movement time (MT) and further noted that MTs for any two movements were equivalent given a constant ratio between 2A/W. The importance of Fitts'1 research is undoubtedly recognised by the myriad of studies that have cited his work. Moreover, the fact that Fitts' equation generalizes across a range of tasks (for a comprehensive list see Plamondon & Alimi, 1997) has lead many movement scientists to adopt his findings as a law-based index of human performance (so-called Fitts Law). It is important to recognise that much of the subsequent work applying Fitts' equation has not examined MTAD relations across fully factorial combinations of amplitude and width. Moreover, contemporary research has largely limited the exploration of MT/ID relations to singular manipulations of amplitude or width; that is, a change in ID is accomplished by manipulating amplitude while maintaining a constant width (or vice versa). To demonstrate the first point, we outline a frequently cited study by Langolf, Chaffin, and Foulke (1976).2 In their study, small amplitude (As = 0.25 and 1.27 cm) movements requiring the reciprocal transfer of a peg (Ws = 0.0076 and 0.107 cm) were completed under visualfield magnification (e.g., IDs ranging from 2.22 to 8.38 bits). Additionally, the same group of participants completed a standard tapping task involving similar movement amplitudes (As = 5.08, 10.2, 20.3, and 30.5 cm) and target widths (Ws = 0.64, 1.27, 2.54, and 5.08 cm) employed by Fitts (1954), for example, IDs ranging from 2.00 to 6.58 bits.3 What is frequently recorded from this work is that MT/ID relations for both magnified and nonmagnified tasks elicited robust linear fits (R2 values: 0.98-1.00): a finding providing an archetypal demonstration of the generalizability of Fitts' equation. It is, however, important to recognise that inspection of Langolf et al. 's Figure 6 indicates that neither the magnified nor nonmagnified tasks included factorial arrangements of amplitude and width. For example, Figure 6 shows that only 11 of the 16 possible arrangements of amplitude and width were evaluated in the standard (i. …

The completion of an antisaccade selectively increases the reaction tiME (RT) of a subsequent prosaccade: a result that has been interpreted to reflect the residual inhibition of stimulus-driven saccade networks [1], [2]. In the present investigation we sought to determine whether the increase in prosaccade RT is contingent on the constituent antisaccade planning processes of response suppression and vector inversion or is limited to response suppression. To that end, in one block participants alternated between pro- and antisaccades after every second trial (task-switching block), and in another block participants completed a series of prosaccades that were randomly (and infrequently) interspersed with no-go catch-trials (go/no-go block). Notably, such a design provides a framework for disentangling whether response suppression and/or vector inversion delays the planning of subsequent prosaccades. As expected, results for the task-switching block showed that antisaccades selectively increased the RTs of subsequent prosaccades. In turn, results for the go/no-go block showed that prosaccade RTs were increased when preceded by a no-go catch-trial. Moreover, the magnitude of the RT 'cost' was equivalent across the task-switching and go/no-go blocks. That prosaccades preceded by an antisaccade or a no-go catch-trial produced equivalent RT costs indicates that the conjoint processes of response suppression and vector inversion do not drive the inhibition of saccade planning mechanisms. Rather, the present findings indicate that a general consequence of response suppression is a residual inhibition of stimulus-driven saccade networks.