Neuropsychologia 47 (2009) 77–82 Contents lists available at ScienceDirect Neuropsychologia journal homepage: www.elsevier.com/locate/neuropsychologia Perisaccadic mislocalization in dyslexia Elizabeth Liddle ∗ , Yu Ju Chou 1 , Stephen Jackson University of Nottingham, United Kingdom a r t i c l e i n f o Article history: Received 5 January 2008 Received in revised form 30 April 2008 Accepted 15 August 2008 Available online 22 August 2008 Keywords: Perisaccadic spatial compression Spatial constancy Saccade Visual deficits a b s t r a c t Evidence from experiments designed to elicit the phenomenon of perisaccadic mislocalization of briefly presented probe stimuli suggests that mechanisms implicated in the planning of a saccade are also implicated in the means by which spatial constancy is maintained across saccades. We postulated that impairments of visual attention observed in dyslexic readers may arise from impairment of mechanisms that also subserve the maintenance of spatial constancy, leading to visual confusion during reading. To test this hypothesis, we compared the performance of adults with dyslexia with that of non-impaired control participants on a task designed to elicit perisaccadic mislocalization. Typically in such tasks, when probes are presented close to saccade onset, mislocalization of all probes, including those presented beyond the saccade target, are mislocalized in the direction of the saccade target, a phenomenon known as perisaccadic spatial compression. In addition, a second tendency, in which all probes are mislocalized in the direction of the saccade itself is referred to as shift. Dyslexic participants showed attenuated perisaccadic compression effects relative to those found in control participants, while the degree to which the reported positions of the probes were shifted in the direction of the saccade did not differ significantly between groups. We propose that compression errors are likely to arise from predictive mechanisms that normally maintain spatial constancy across saccades. Our finding was therefore interpreted as support for the hypothesis that predictive spatial constancy mechanisms may be disrupted in dyslexia. © 2008 Elsevier Ltd. All rights reserved. 1. Introduction A growing body of evidence suggests that dyslexia may be associated with deficits in visual attention. These deficits may be manifest overtly by atypical performance in tasks requiring saccadic eye movements (Biscaldi, Fischer, & Hartnegg, 2000; Biscaldi, Gezeck, & Stuhr, 1998; Crawford & Higham, 2001; Eden, Stein, Wood, & Wood, 1994; Moores, Frisby, Buckley, Reynolds, & Fawcett, 1998), or indirectly by atypical performance on tasks designed to tap the efficiency of magnocellular dorsal stream pathways specialized for the transmission of rapid sensory information (Greatrex & Drasdo, 1995; Keen & Lovegrove, 2000; Livingstone, Rosen, Drislane, & Galaburda, 1991; Lovegrove, 1996; Slaghuis & Ryan, 1999; Stein & Walsh, 1997). Dyslexic participants have been found to have lower fusion or higher gap detection thresholds with both auditory and visual stimuli (Farmer & Klein, 1995), leading to the theory that impairments in the rapid processing of sensory infor- ∗ Corresponding author at: Developmental Psychiatry, E Floor, South Block, Queen’s Medical Centre, Nottingham, NG7 2UH, United Kingdom. Tel.: +44 115 8230272; fax: +44 115 8230256. E-mail address: Elizabeth.Liddle@nottingham.ac.uk (E. Liddle). 1 Now at: Department of Clinical and Counseling Psychology, National Dong Hwa University. 0028-3932/$ – see front matter © 2008 Elsevier Ltd. All rights reserved. doi:10.1016/j.neuropsychologia.2008.08.013 mation arising from anomalies in magnocellular development in any sensory domain may underlie the phenomenon of developmental dyslexia (Stein, 2003; Stein & Walsh, 1997). If this is the case, the question arises as to whether the postulated magnocellular deficit affects reading solely via the auditory modality, by disrupting the development of phonemic awareness and thus the acquisition of the phonological decoding skills that facilitate successful reading. If so, associated visual anomalies could be accounted for as epiphenomena associated with reading disorder merely aetiologically. Alternatively, or additionally, dorsal stream pathway deficits might directly impair reading by disrupting the fluent shifting of covert and/or overt visual attention across the written text (Vidyasagar, 1999). Eden and colleagues (Eden et al., 1994; Eden, Stein, Wood, & Wood, 1995) investigated eye movements in children with dyslexia and found that dyslexic children were significantly impaired as compared with non-disabled controls in fixation and vergence control. Biscaldi et al. (1998) found that saccadic reaction times (saccade latencies) were more variable in dyslexic participants, who made more late saccades (>700 ms) and more express saccades. They speculate that their findings may be accounted for by deficits in attentional selection processes that result in dyslexic readers failing to utilize peripheral or parafoveal cues to direct their attention across the visual field while reading. Crawford and Higham (2001) investigated saccade trajectories to single and dou- 78 E. Liddle et al. / Neuropsychologia 47 (2009) 77–82 Fig. 1. Global effect and spatial compression. The upper panel (a) shows Godijn and Theeuwes’ (2002) model of the centre-of-gravity effect. The neural activity elicited by each stimulus is represented by a distribution of activation, peaking at the location of the stimulus (broken lines). The tails of the distribution drop below a baseline, reflecting inhibition at those locations. When the summed activation at any point in the map reaches a threshold, a saccade is triggered. The two close salient locations (distractor and target) produce a single peak at a location between the two, resulting in a saccade that terminates between target and distractor. The lower panel (b) shows a typical pattern of mislocalization when a probe is presented close to the onset of a left-to-right saccade. The veridical positions of the probes are shown as solid white lines, while the reported positions are shown as broken white lines. Fixation is −5◦ from centre (0◦ ) and the saccade target is +5◦ from centre. Probes are presented at −10◦ , 0◦ , and +10◦ , giving a true mean position 0◦ and a true standard deviation of 10◦ . Reported positions are at −7◦ , +2◦ and +8◦ , giving an apparent mean position of +1◦ , and an apparent standard deviation of +7.5◦ . The degree to which the apparent mean is more positive than the true mean indexes shift, while the degree to which the apparent standard deviation is smaller than the true standard deviation, indexes compression. ble stimuli in dyslexic and non-dyslexic participants. When more than one saccade target is presented, a global or centre-of-gravity effect is sometimes observed, whereby, if the two targets are relatively close, saccades tend to terminate midway between the two targets (Walker, Deubel, Schneider, & Findlay, 1997). Crawford and Higham (2001) found that dyslexic participants and non-dyslexic control participants were equally accurate on a task requiring a saccade to be made to a single stimulus presented at one of two eccentricities. However, when stimuli were presented at both locations simultaneously, the control participants showed the expected centre-of-gravity effect, while in the dyslexic participants this effect was attenuated, the endpoints of the saccades of the dyslexic participants being closer to the nearer stimulus. A model proposed by Godijn and Theeuwes (2002) can account neatly for the centre-of-gravity effect. Their model postulates that neural representations on a saccade map of nearby salient locations have mutual lateral excitatory effects while remote locations exert mutual lateral inhibitory effects, and that a saccade is triggered when activation at a new location reaches a threshold level. Stimuli presented spatially close together will therefore elicit a single wide distribution of activation, its peak representing a saccade target somewhere between the two stimuli, while two remote stimuli will result in mutual inhibition, increasing saccade latencies to the target, but leaving its endpoint unaffected (Fig. 1a). Interpreted in the light of Godijn and Theeuwes’s model, Crawford and Higham’s (2001) finding of attenuated centre-ofgravity effects in dyslexic participants could indicate reduced lateral excitation from neural representations of salient peripheral stimuli, possibly from noise in the system by which potential saccade vectors are represented on a neural visual–spatial map. Should this be the case, perisaccadic processes by which spatial constancy is maintained across saccades may also be compromised, thus potentially accounting for visual confusion during reading, and thus to disruption to the processes by which text is recognized. When we make a saccade, the world appears to stay still, even though the images of objects in the visual field have been displaced on the retina. The fact that spatial constancy is maintained across saccades implies that with each saccade, the spatiotopic representation of a visual stimulus is translated from a coordinate system with the initial fixation point as origin, to one with the upcoming fixation point as origin. Evidence that this remapping process is at least partially predictive is provided by single neuron recordings from lateral intra-parietal (LIP) neurons in macaques indicating that the receptive field properties of these neurons show anticipatory shifts in their receptive fields immediately prior to a saccadic eye movement (Duhamel, Colby, & Goldberg, 1992; Kusunoki & Goldberg, 2003). If saccades are poorly specified in dyslexia, one consequence may be that this predictive remapping process fails. As predictive remapping is thought to be necessary to enable the perceptual system to distinguish between retinal displacement that is due to an eye movement from retinal displacement that is due to the movement of the object itself, failure of this system might be expected to lead to illusory movement of elements in the visual field during a task such as reading. Poorly specified saccades might therefore account for the visual anomalies reported by some dyslexic readers, such as letters and words appearing to change position on the page (Stein, 2003). E. Liddle et al. / Neuropsychologia 47 (2009) 77–82 One paradigm designed to tap the efficiency of the mechanisms involved in maintaining spatial constancy across saccades, is, paradoxically, a paradigm designed to elicit perisaccadic mislocalization—the mislocalization of stimuli presented briefly within a small time window in which a saccadic eye movement occurs. A typical paradigm used to elicit perisaccadic spatial mislocalization is that developed by Ross, Morrone, and Burr (1997). In this paradigm, a brief probe stimulus is presented around the time of a saccade, and participants are asked to report the position of the probe. The saccade is made between two stimuli, positioned several degrees of visual angle apart. Participants are asked to fixate the first stimulus, and to make a saccade to the second stimulus when it appears. At a variable stimulus onset asynchrony (SOA) from the onset of the saccade cue, a probe stimulus is briefly presented in one of three categories of position: contralateral to the saccade target; beyond the saccade target; and at a position midway between the initial fixation point and the saccade target. On completion of the saccade, participants are asked to indicate the location at which the probe appeared. Typically, participants make relatively accurate judgments about the position of the probe as long as it appears substantially before, or substantially after, the onset of the saccade (Lappe, Awater, & Krekelberg, 2000; Ross et al., 1997; Ross, Morrone, Goldberg, & Burr, 2001). However, if the probe appears within 50 ms of saccade onset, it tends to be mislocalized. Two mislocalization tendencies are observed. One is the tendency of all probes, including those presented beyond the saccade target, to be mislocalized in the direction of the saccade target. This tendency is referred to as shift, and can be quantified as the degree to which the mean reported probe positions deviate from the mean of their veridical positions. The tendency is more marked when no visual landmarks are available post-saccade (Lappe et al., 2000), suggesting that uncorrected anticipatory eye position error may be a causal factor. However, as long as visual references are available post-saccade, a second tendency is also manifest, in which all probes tend to be mislocalized in the direction of the saccade target itself, probes presented beyond the saccade target tending to be mislocalized against the direction of the saccade. Thus the space between all probes is effectively compressed, and the pattern of mislocalization is referred to as spatial compression (Fig. 1b). This tendency can be quantified as the root mean square of the deviation of the reported probe positions from the mean of all the reported positions (i.e. the standard deviation of all the reported probe positions). The smaller the standard deviation of the reported positions relative to the standard deviation of the veridical positions of the probes, the greater the degree of compression. This pattern of mislocalization is difficult to explain in terms of anticipatory eye position error, and suggests rather that it may arise when errors in predictive encoding of space at the time of probe onset (Awater & Lappe, 2006; Liddle, 2006) are remapped to stable visual landmarks. Perisaccadic mislocalization of briefly presented, abrupt onset stimuli, is therefore a phenomenon found in unimpaired participants, and likely to reflect processes subserving normal vision, such as the maintenance of spatial constancy across saccades. A predictive process is likely to prove advantageous for the visual system, as a working model of the way the world will look on completion of a saccade that is made before or during a saccade will require only minimal confirmatory re-calibration on saccade completion (Deubel, 2004; Deubel, Bridgeman, & Schneider, 1998; Findlay & Gilchrist, 2003). However, the efficiency of such a predictive process must partially depend on the efficiency of the saccade programming process itself, and thus likely to be reflected to the phenomenon of spatial compression (Liddle, 2006). 79 Crawford and Higham’s (2001) finding of an attenuated centreof-gravity effect in dyslexic participants may therefore indicate that dyslexic participants may suffer from deficits in predictive mechanisms that subserve spatial constancy. If so, this should be manifest in dyslexic participants as attenuated perisaccadic compression of space. We tested this hypothesis in an experiment in which the performance of dyslexic adults was compared that of non-dyslexic adults on a task designed to elicit perisaccadic spatial compression. 2. Method 2.1. Participants A total of 49 students at the University of Nottingham (mean age = 22.2, S.D. = 3.7 years) participated in the experiment. The study was approved by the Ethics Committee of the School of Psychology, University of Nottingham, and all participants gave written consent before participating in the experiment. Participants were recruited in two batches. In the first batch, 23 participants were recruited, 11 by means of an advertisement requesting participants who had been diagnosed with dyslexia, and 12 were recruited by a general advertisement. In the second batch, a further 26 participants were recruited, 12 by means of an advertisement requesting participants who had been diagnosed with dyslexia, and 14 by a general advertisement. The first batch undertook a version of the spatial compression paradigm in which they were required to make a saccade from left to right. The second batch performed the same task, except that they were required to make a saccade from right to left. All participants were screened for dyslexia using 10 items of the 11 items in the dyslexia adult screening test (DAST, Fawcett & Nicolson, 1998). The postural stability was omitted, and the at risk quotient (ARQ) pro-rated to take account of the omitted item. A cut off ARQ score of .07 was used to confirm whether participants were, or were not, likely to suffer from developmental dyslexia, and any control participant scoring .07 or greater was excluded from the study. In addition, participants were asked to read 30 single non-words, and were scored for accuracy. The Wechsler Abbreviated Scale of Intelligence was used to estimate full scale IQ (FSIQ), performance IQ (PIQ) and verbal IQ (VIQ). 2.2. Stimuli The experimental stimuli were programmed in E prime software (E Prime 1.1.4.1, Psychology Software Tools, Inc. Pittsburgh, PA), and presented on a 14 in. computer monitor with a screen refresh rate of 16.6 ms. Stimuli were presented on a grey ground. Each trial began with a fixation point (a black circle subtending 1◦ ) located either 5◦ to the left (for the left-to-right version) or to the right (for the right-to-left version) of the vertical midline of the screen. After 1104 ms, this fixation point offset, and was replaced by a second identical target stimulus 5◦ to the right (for the leftto-right version) or to the left (for the right-to-left version) of the vertical midline of the screen. At a varied stimulus onset asynchrony (SOA), selected randomly from a quasi-Gaussian distribution (mean = 174 ms; standard deviation = 66 ms), a bright green vertical bar extending from top to bottom of the screen and subtending 1◦ horizontal visual angle appeared centred on the following three positions: 10◦ to the left of the midline; at the midline; and 10◦ to the right of the midline. This bar remained on screen for 17 ms (one screen refresh rate), and was immediately replaced by a horizontal ruler, marked in multiples of 5◦ . The midline position was marked “0”, positions to the left being marked as negative (−5◦ , −10◦ and −15◦ ) and positions to the right were marked as positive (5◦ , 10◦ and 15◦ ). The three probe locations were randomized. Participants were asked to fixate on the first fixation point, and to make a saccade to the target as soon as it appeared. They were requested to try not to fixate the bar, but to note its position, and, when the ruler appeared, to give an estimate of the probe’s position relative to the ruler. The experimenter notated their verbal responses, and the next trial was initiated by the participant, using the spacebar of the computer keyboard. Each participant performed 262 trials. A schematic representation of the experimental stimuli is given in Fig. 2. Eye movements were recorded using electro-oculography (EOG) eye tracking equipment. Two electrodes were taped to the skin of the temples, over the lateral rectus muscles (which produce lateral movement of the eye), and a ground electrode was taped above the nose. Voltage differences between the electrodes were sampled at 200 Hz, and data were acquired using Acqknowledge (Biopac Systems, Inc.) Separate EOG recordings lasting 3.5 s each were made of each trial, and were triggered at the onset of the first fixation point. 3. Analysis and results 3.1. Analysis An independent samples t test was used to check that FSIQ did not differ between the two groups. To compare the two groups 80 E. Liddle et al. / Neuropsychologia 47 (2009) 77–82 Fig. 2. Stimuli for spatial compression task. In each trial, a fixation stimulus of 1104 ms duration is presented, after which a saccade target (second frame) is presented. The participant is asked to make a saccade to the target. After a varying SOA, a brief green probe stimulus (third frame) is presented for 17 ms, immediately followed by a ruler stimulus. Participants are asked to report the observed position of the probe relative to the ruler (fourth frame). The ruler remains on screen until the participant’s response is recorded by the experimenter. The participant then initiates the next trial with a by pressing the space bar of the computer keyboard. on the subtests of the DAST (Fawcett & Nicolson, 1998), participants who scored in the third stanine or below (23rd percentile), according to the population norms supplied by the DAST, were coded as having an impairment on that subtest. For each subtest, chi square tests were then used to determine whether the proportion of participants with a substantial impairment was significantly greater in the dyslexic group than in the non-dyslexic group. Ranked scores on the test of non-word reading were compared using a non-parametric test. Saccade detection was partially automated using an algorithm written in LabView 7.1.1 (National Instruments Corporation). The algorithm took a moving window of eight consecutive voltage samples, and compared the mean of the first four samples with the mean of the second. When the difference between the two means exceeded a threshold value, a possible saccade onset was identified; visual inspection of the plot was then used to distinguish between saccades and artefacts. Thresholds were set for each subject by trial and error, using visual inspection of a few sample plots. All trials in which no saccade could be discerned were discarded, as were trials in which no response was made. The time interval in milliseconds between probe onset and saccade onset was computed for each trial. The apparent positions of each probe were coded relative to the direction of the saccade. Pro-saccadic mislocalizations of the probe (in the direction of the saccade) were coded with a positive value, and contra-saccadic mislocalizations (against the direction of the saccade) were coded with a negative value. Thus, a probe perceived to be to the left of its veridical position was coded with a negative value for left-to-right saccades and with a positive value for right-to-left saccades, while a probe perceived to be to the right of its veridical position was coded with a positive value for left-to-right saccades and with a negative value for right-to-left saccades. For each participant, valid trials (those in which a response was made and a saccade was detected) were allocated to one of two time bins. The first bin consisted of trials in which the saccade was initiated within 50 ms of the onset of the probe; these were des- ignated perisaccadic trials. The second consisted of trials in which the saccade was made 200 ms before or after probe onset; these were designated fixation trials. For each subject, the mean reported position of the probe was computed for each real position (central; 10◦ to the right of the midline; or 10◦ to the left of the midline) for each trial type (perisaccadic and fixation). Then, for each trial type, indices of shift and compression were computed. Indices of shift and compression were derived for each participant for each time bin from as the means and standard deviations of the reported positions of the probe, respectively. As the mean of the veridical positions was coded as zero, a shift index of zero indicates an absence of shift. A positive value indicates shift in the direction of the saccade and a negative value shift against the direction of the saccade. As the three probes were presented at −10◦ , 0 and 10◦ respectively, the standard deviation (root mean square of the deviation from the mean of zero) of the veridical probe positions was 10◦ . A value of the compression index (standard deviation of the reported positions, i.e. the root mean square of the deviation of the reported positions from the mean of all the reported positions) that is equal or greater than 10◦ therefore indicates absence of compression, while a value less than 10◦ indicates compression. A 2 × 2 × 2 repeated-measures ANOVA was then conducted on both the shift and the compression measures, with two betweensubjects factors and one within-subjects factor. Time-bin was the within-subjects factor, with two levels, perisaccadic trials and fixation trials. Between-subjects factors were diagnostic group (two levels: dyslexic and non-dyslexic) and direction group (two levels: left-to-right and right-to-left). 4. Results In the case of two participants, no responses were recorded for any trial in which their saccade was initiated more than 200 before or after the onset of the probe, for at least one trial type. Both had performed the right-to-left paradigm; one was from the dyslexic group and one was from the non-dyslexic group. These participants were therefore deleted from further analysis, leaving 11 dyslexic participants in each condition, 12 non-dyslexic participants in the left-to-right group, and 13 non-dyslexic participants in the rightto-left group. There was no significant difference in mean FSIQ between the two diagnostic groups of participants, t(45) = 1.206 (dyslexic: M = 121, S.D. = 13; non-dyslexic: M = 124, S.D. = 8), nor in mean performance IQ, t(45) = 0.524 (dyslexic: M = 119, S.D. = 13; nondyslexic: M = 121, S.D. = 10) or verbal IQ, t(45) = 0.524 (dyslexic: M = 120, S.D. = 15; non-dyslexic: M = 124, S.D. = 10). However, of the DAST sub-tests, a significantly greater proportion of the dyslexic group than of the control group showed an impairment (third stanine or below) on: rapid naming (z = 3.3350, p < .001); 1-min reading (z = 4.106, p < .001); 2-min spelling (z = 4.737, p < .001); backward digit span (z = 2.664, p < .01); nonsense passage reading (z = 4.848, p < .001); 1-min writing (z = 3.572, p < .001) and verbal fluency (z = 2.352, p < .05). A greater proportion of the dyslexic group were also impaired on phonemic segmentation than of the non-dyslexic group, but this did not reach statistical significance (z = 1.900, p = .057). The proportions of each groups showing an impairment on semantic fluency were not significantly different. On the test of single non-word reading, the dyslexic group were significantly less accurate than the control group (z = 3.577, p < .001). For the dependent variable compression, the interaction between diagnostic group and time bin was significant, F(1,43) = 4.500,p < 0.05, indicating that the non-dyslexic participants displayed a greater increase in compression in the perisaccadic trials as compared with their compression in the E. Liddle et al. / Neuropsychologia 47 (2009) 77–82 Fig. 3. Spatial compression in dyslexic and non-dyslexic participants. Compression is indexed by the standard deviation of the three apparent positions (the root mean square of the deviation from the mean of all reported positions), which is shown on the vertical axis. The smaller the standard deviation the greater the degree of apparent spatial compression. While both groups of subjects showed significantly greater compression (smaller standard deviation) on perisaccadic than on fixation trials (lower compression index value), the increase in compression was significantly greater in the non-dyslexic group than the dyslexic group. (Error bars = standard error.) fixation trials than the non-dyslexic participants (Fig. 3). A simple effects analysis was therefore carried out on the two diagnostic groups separately in order to ascertain whether a main effect of time bin was found in either group. Both groups showed a significant main effect of time bin, indicating that both the dyslexic, F(1,20) = 22,892, p < 0.001, and the non-dyslexic F(1,23) = 46.832, p < 0.001 participants showed significantly more compression on perisaccadic than on fixation trials. In neither diagnostic group was saccade direction a significant predictor of compression, nor did it interact significantly with time bin. For the dependent variable shift, the interaction between direction group and time bin was significant, F(1,43) = 13.101, p < 0.001, and indicated a greater increase in shift on perisaccadic trials in the right-to-left condition than in the left-to-right condition. There was no interaction or main effect of diagnostic group. A simple effects analysis conducted on each direction group indicated that for the left-to-right group, shift was not significantly greater in the perisaccadic condition than in the fixation condition, whereas in the right-to-left group, a significant main effect of time bin indicated that participants showed greater mean shift on perisaccadic than on fixation trials, F(1,22) = 21.919, p < 0.001. Again, there was no main effect of diagnostic group, nor interaction between diagnostic group and any other group. 5. Discussion Although both dyslexic and non-dyslexic participants showed significantly greater spatial compression on perisaccadic trials as compared with fixation trials, the dyslexic participants, as predicted, showed significantly less increase in compression on perisaccadic trials, relative to fixation trials, than did the nondyslexic participants. Interpreted in terms of the proposed model of perisaccadic compression, this is consistent with the finding of Crawford and Higham (2001) of attenuated centre-of-gravity effects in dyslexic participants, and is also consistent with the hypothesis that peripheral stimuli are less clearly specified in terms of potential saccade targets in dyslexic than in non-dyslexic partic- 81 ipants, resulting in reduced distortion by probes presented during the perisaccadic period to the estimate of the planned saccade. There was no difference between diagnostic groups in terms of the degree of shift observed. This suggests that the dyslexic participants did not differ from the non-dyslexic participants as to the degree to which they made anticipatory eye position errors at time of coding, or, alternatively, in the degree to which they made saccade-wise re-calibration errors post-saccade. However, participants who participated in the right-to-left version of the paradigm, whether dyslexic or non-dyslexic, showed both greater perisaccadic shift of probe locations in the direction of the saccade than those who undertook the left-to-right version of the paradigm. As this was a between-subjects comparison, interpretation needs to be made with caution; however, one possible explanation of this effect may be that as readers of English, all participants in the experiment were more practiced at making left-to-right than rightto-left saccades. It is possible, therefore, that the visual system may be less well tuned to right-to-left saccades, resulting in greater saccade-wise eye position errors and/or spatiotopic recalibration errors when saccades are made in this direction. We postulate that perisaccadic spatial compression arises when probes are both abrupt in onset, and brief in duration, and reflects the operation of a mechanism in the visual system postulated to make a model of the way the world will look after a saccade is completed that requires only minimal recalibration post-saccade (Findlay & Gilchrist, 2003). While the mechanism is postulated to result in the mislocalization of a kind of stimulus that is rare in the natural world (brief, salient, abrupt onset stimuli), this would be a small price to pay for a system that facilitates the maintenance of spatial constancy across saccades. However, the rapid transmission of retinal information is likely to be critical for the efficiency of such a system. 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