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(1) Background—the magnocellular hypothesis proposes that impaired development of the visual timing systems in the brain that are mediated by magnocellular (M-) neurons is a major cause of dyslexia. Their function can now be assessed quite easily by analysing averaged visually evoked event-related potentials (VERPs) in the electroencephalogram (EEG). Such analysis might provide a useful, objective biomarker for diagnosing developmental dyslexia. (2) Methods—in adult dyslexics and normally reading controls, we recorded steady state VERPs, and their frequency content was computed using the fast Fourier transform. The visual stimulus was a black and white checker board whose checks reversed contrast every 100 ms. M- cells respond to this stimulus mainly at 10 Hz, whereas parvocells (P-) do so at 5 Hz. Left and right visual hemifields were stimulated separately in some subjects to see if there were latency differences between the M- inputs to the right vs. left hemispheres, and these were compared with the subjects’ handedness. (3) Results—Controls demonstrated a larger 10 Hz than 5 Hz fundamental peak in the spectra, whereas the dyslexics showed the reverse pattern. The ratio of subjects’ 10/5 Hz amplitudes predicted their reading ability. The latency of the 10 Hz peak was shorter during left than during right hemifield stimulation, and shorter in controls than in dyslexics. The latter correlated weakly with their handedness. (4) Conclusion—Steady state visual ERPs may conveniently be used to identify developmental dyslexia. However, due to the limited numbers of subjects in each sub-study, these results need confirmation.

The visual system uses parallel pathways to process information. However, an ongoing debate centers on the extent to which the pathways from the retina, via the Lateral Geniculate nucleus to the visual cortex, process distinct aspects of the visual scene and, if they do, can stimuli in the laboratory be used to selectively drive them. These questions are important for a number of reasons, including that some pathologies are thought to be associated with impaired functioning of one of these pathways and certain cognitive functions have been preferentially linked to specific pathways. Here we examine the two main pathways that have been the focus of this debate: the magnocellular and parvocellular pathways. Specifically, we review the results of electrophysiological and lesion studies that have investigated their properties and conclude that while there is substantial overlap in the type of information that they process, it is possible to identify aspects of visual information that are predominantly processed by either the magnocellular or parvocellular pathway. We then discuss the types of visual stimuli that can be used to preferentially drive these pathways.

Knowledge of oscillatory entrainment and its fundamental role in cognitive and behavioral processing has increasingly been applied to research in the field of reading and developmental dyslexia. Growing evidence indicates that oscillatory entrainment to theta frequency spoken language in the auditory domain, along with cross-frequency theta-gamma coupling, support phonological processing (i.e., cognitive encoding of linguistic knowledge gathered from speech) which is required for reading. This theory is called the temporal sampling framework (TSF) and can extend to developmental dyslexia, such that inadequate temporal sampling of speech-sounds in people with dyslexia results in poor theta oscillatory entrainment in the auditory domain, and thus a phonological processing deficit which hinders reading ability. We suggest that inadequate theta oscillations in the visual domain might account for the many magno-dorsal processing, oculomotor control and visual deficits seen in developmental dyslexia. We propose two possible models of a magno-dorsal visual correlate to the auditory TSF: (1) A direct correlate that involves "bottom-up" magnocellular oscillatory entrainment of the visual domain that occurs when magnocellular populations phase lock to theta frequency fixations during reading and (2) an inverse correlate whereby attending to text triggers "top-down" low gamma signals from higher-order visual processing areas, thereby organizing magnocellular populations to synchronize to a theta frequency to drive the temporal control of oculomotor movements and capturing of letter images at a higher frequency.

The magnocellular system has been implicated in the rapid processing of facial emotions, such as fear. Of the various anatomical possibilities, the retino-colliculo-pulvinar route to the amygdala is currently favored. However, it is not clear whether and when amygdala arousal activates the primary visual cortex (V1). Non-linear visual evoked potentials provide a well-accepted technique for examining temporal processing in the magnocellular and parvocellular pathways in the visual cortex. Here, we investigated the relationship between facial emotion processing and the separable magnocellular (K2.1) and parvocellular (K2.2) components of the second-order non-linear multifocal visual evoked potential responses recorded from the occipital scalp (OZ). Stimuli comprised pseudorandom brightening/darkening of fearful, happy, neutral faces (or no face) with surround patches decorrelated from the central face-bearing patch. For the central patch, the spatial contrast of the faces was 30% while the modulation of the per-pixel brightening/darkening was uniformly 10% or 70%. From 14 neurotypical young adults, we found a significant interaction between emotion and contrast in the magnocellularly driven K2.1 peak amplitudes, with greater K2.1 amplitudes for fearful (vs. happy) faces at 70% temporal contrast condition. Taken together, our findings suggest that facial emotional information is present in early V1 processing as conveyed by the M pathway, and more activated for fearful as opposed to happy and neutral faces. An explanation is offered in terms of the contest between feedback and response gain modulation models.

The parallel pathways of the human visual system differ in their tuning to luminance, color, and spatial frequency. These attunements recently have been shown to propagate to differential processing of higher-order stimuli, facial threat cues, in the magnocellular (M) and parvocellular (P) pathways, with greater sensitivity to clear and ambiguous threat, respectively. The role of the third, koniocellular (K) pathway in facial threat processing, however, remains unknown. To address this gap in knowledge, we briefly presented peripheral face stimuli psychophysically biased towards M, P, or K pathways. Observers were instructed to report via a key-press whether the face was angry or neutral while their eye movements and manual responses were recorded. We found that short-latency saccades were made more frequently to faces presented in the K channel than to P or M channels. Saccade latencies were not significantly modulated by expressive and identity cues. In contrast, manual response latencies and accuracy were modulated by both pathway biasing and by interactions of facial expression with facial masculinity, such that angry male faces elicited the fastest, and angry female faces, the least accurate, responses. We conclude that face stimuli can evoke fast saccadic and manual responses when projected to the K pathway.

Submitted manuscript version. Published version available in Tracking changes in spatial frequency sensitivity during natural image processing in school-age: an event-related potential study (2018) 166, s. 664-678. Several studies have shown that behavioral and electrophysiological correlates of processing visual images containing low or high spatial frequency (LSF or HSF) information undergo development after early childhood. However, the maturation of spatial frequency sensitivity in school-age has been investigated using abstract stimuli only. The aim of the current study was to assess how LSF and HSF features affect the processing of everyday photographs at the behavioral and electrophysiological levels in children aged 7-15 years and adults. We presented grayscale images containing either animals or vehicles and their luminance-matched modified versions filtered at low or high spatial frequencies. Modulations of classification accuracy, reaction time and visual event-related potentials (posterior P1 and N1 components) were compared across five developmental groups and three image types. We found disproportionately worse response accuracies for LSF stimuli relative to HSF images in children aged 7-8 years, an effect that was accompanied by smaller LSF-evoked P1 amplitudes in this age period. At 7-8 years of age, P1 and N1 amplitudes were modulated by HSF and LSF stimuli (P1: HSF>LSF; N1: LSF>HSF), with a gradual shift towards the opposite pattern (P1: LSF>HSF; N1: HSF>LSF) with increasing age. Our results indicate that early cortical processing of both spatial frequency ranges undergo substantial development in school-age, with a relative delay of LSF analysis, and underline the utility of our paradigm in tracking the maturation of LSF vs. HSF sensitivity in this age group.

Perception consists of the brain's single best interpretation of the sensory world at a given moment in time. Multiple channels of visual input - be they from the two eyes or from the many parallel visual pathways that originate as early as the retina - must be reconciled to arrive at a unified percept. The fact that this must occur in roughly real time as the visual scene changes poses special challenges and constraints. I investigated two classes of visual processes relevant for the perception of time-varying visual stimuli: prediction, with a probable neural substrate in early visual cortical areas, and parallel processing in the magnocellular (M) and parvocellular (P) pathways. In Chapters 2 and 3, I asked how prediction and parallel pathways, respectively, contribute to perceptual selection using dynamic binocular rivalry stimuli. In binocular rivalry, incompatible images presented to the two eyes result in just one of the images being selected for awareness at any given time. This bistability makes rivalry a useful tool for the study of perceptual selection. In Chapter 2, we found that predictive context in the form of an unambiguous rotating grating biased perceptual selection during subsequent rivalry towards the expected next grating in the rotation sequence, compared to an orthogonal grating. This provided evidence that a prediction-like process influences perceptual selection during rivalry between gratings, which other work has shown is likely resolved at early stages of visual processing. In Chapter 3, we studied spatial, temporal, luminance, and chromatic factors influencing perceptual selection during interocular switch rivalry. In this type of rivalry, flickering orthogonal gratings are periodically exchanged between the two eyes, resulting in either the perception of a fast, regular alternation between orthogonally oriented gratings (similar to the display presented to a single eye) or a slow, irregular alternation, a percept that requires integration across the two eyes over time. We found that stimuli biased toward the M pathway increased the prevalence of fast, regular alternations, while stimuli biased toward the P pathway increased the prevalence of slow, irregular alternations. This finding suggested that the M and P pathways can make distinct contributions to perception during binocular rivalry and led us to propose a new framework for understanding perceptual selection during interocular switch rivalry.Physiological measurement of activity in the M and P pathways can lead to greater understanding of how these pathways contribute to perceptual experience, but methods for measuring functional signals from the M and P pathways of humans have been lacking. Therefore, in Chapter 4, we developed a procedure for functionally mapping the M and P subdivisions of human LGN, the site where these pathways are most clearly segregated, using functional magnetic resonance imaging (fMRI). We observed a gradient of more M-like to more P-like responses across the LGN. Importantly, this gradient had a spatial layout consistent with known LGN anatomical organization. This new method for localizing the M and P subdivisions of the LGN provides a way forward for investigating the function of these pathways in human visual perception, in both healthy and clinical populations.In summary, prediction and parallel processing are two classes of mechanisms that contribute to perception of dynamic visual stimuli. Here we have shown how such mechanisms operating at low levels of the visual system can help resolve competition between percepts, thereby affecting the contents of visual awareness. In addition, we developed a method for the physiological study of the M and P LGN subdivisions in the human brain, which is a promising technique for the future investigation of the roles of the M and P pathways in human visual perception, among other applications.

Although primarily conceptualized as a disorder of phonological awareness, developmental dyslexia is often associated with broader problems perceiving and attending to transient or rapidly-moving visual stimuli. However, the extent to which such visual deficits represent the cause or the consequence of dyslexia remains contentious, and very little research has examined the relative contributions of phonological, visual, and other variables to reading performance more broadly. We measured visual sensitivity to global motion (GM) and global form (GF), performance on various language and other cognitive tasks believed to be compromised in dyslexia (phonological awareness, processing speed, and working memory), together with a range of social and demographic variables often omitted in previous research, such as age, gender, non-verbal intelligence, and socio-economic status in an unselected sample (n = 132) of children aged 6–11.5 yrs from two different primary schools in Edinburgh, UK. We found that: (i) Mean GM sensitivity (but not GF) was significantly lower in poor readers (medium effect size); (ii) GM sensitivity accounted for only 3% of the variance in reading scores; (iii) GM sensitivity deficits were observed in only 16% of poor readers; (iv) the best predictors of reading performance were phonological awareness, non-verbal intelligence, and socio-economic status, suggesting the importance of controlling for these in future studies of vision and reading. These findings suggest that developmental dyslexia is unlikely to represent a single category of neurodevelopmental disorder underpinned by lower-level deficits in visual motion processing.

Human faces evolved to signal emotions, with their meaning contextualized by eye gaze. For instance, a fearful expression paired with averted gaze clearly signals both presence of threat and its probable location. Conversely, direct gaze paired with facial fear leaves the source of the fear-evoking threat ambiguous. Given that visual perception occurs in parallel streams with different processing emphases, our goal was to test a recently developed hypothesis that clear and ambiguous threat cues would differentially engage the magnocellular (M) and parvocellular (P) pathways, respectively. We employed two-tone face images to characterize the neurodynamics evoked by stimuli that were biased toward M or P pathways. Human observers (N = 57) had to identify the expression of fearful or neutral faces with direct or averted gaze while their magnetoencephalogram was recorded. Phase locking between the amygdaloid complex, orbitofrontal cortex (OFC) and fusiform gyrus increased early (0–300 ms) for M-biased clear threat cues (averted-gaze fear) in the β-band (13–30 Hz) while P-biased ambiguous threat cues (direct-gaze fear) evoked increased θ (4–8 Hz) phase locking in connections with OFC of the right hemisphere. We show that M and P pathways are relatively more sensitive toward clear and ambiguous threat processing, respectively, and characterize the neurodynamics underlying emotional face processing in the M and P pathways.

Despite much current research into the visual processing style of individuals with Autism Spectrum Disorder (ASD), understanding of the neural mechanisms is lagging, especially with respect to the contributions of the overlapping dichotomies of magnocellular/parvocellular (afferent neural pathways), global/local (perception) and dorsal/ventral (cortical streams). Here, we addressed this deficiency by measuring inspection times (ITs) for novel global/local stimuli as well as recording nonlinear visually evoked potentials (VEPs), in particular, magnocellular and parvocellular temporal efficiencies. The study was conducted on a group of male ASD children and a typically developing (TD) group matched for mean age and mean non-verbal intelligence, as measured by the Raven’s Progressive Matrices. The IT results did not differ between groups, however a negative correlation between global IT and Raven’s score was found in the ASD group, that was not evident in the TD group. Nonlinear VEP showed the ASD group had smaller amplitude parvocellular-generated second order responses compared to the TD group. This is a sign of improved temporal responsiveness in ASD vs. TD groups. Principal Component Analysis linked global IT, non-verbal intelligence scores and VEP parvocellular efficiency in a single factor for the ASD but not the TD group. The results are suggestive of a constraint on pathways available for cognitive response in the ASD group, with temporal processing for those with ASD becoming more reliant on the parvocellular pathway.

In healthy humans, passage reading depends upon a critical organizing role played by the magnocellular/dorsal visual pathway. In a recent study, we found a significant correlation between orthographic reading deficits in schizophrenia and deficits in contrast sensitivity to low spatial frequency stimuli, suggesting an underlying magnocellular processing abnormality. The interrelationship between magnocellular dysfunction and passage reading impairments in schizophrenia was investigated in 21 patients with schizophrenia and 17 healthy control volunteers using behavioral and functional MRI (fMRI) based measures. fMRI activation patterns during passage- and single-word reading were evaluated in relation to cortical areas with differential sensitivity to low versus high spatial frequency cortical regions indentified using a phase-encoded fMRI paradigm.On average, patients with schizophrenia read at the 6th grade level, despite completion of more than 12years of education and estimated normal pre-morbid IQ. Schizophrenia patients also showed significantly impaired contrast sensitivity to low spatial frequencies and abnormal neural activity in response to stimulation with low spatial frequencies, consistent with dysfunction of magnocellular processing. Further, these magnocellular deficits were predictive of poor performance on a standardized psychoeducational test of passage reading. These findings suggest that reading is an important index of cognitive dysfunction in schizophrenia and highlight the contribution of magnocellular dysfunction to overall cognitive impairments in schizophrenia.

Purpose As well as obtaining confirmation of the magnocellular system involvement in developmental dyslexia (DD); the aim was primarily to search for a possible involvement of the parvocellular system; and, furthermore, to complete the assessment of the visual chromatic axis by also analysing the koniocellular system. Methods Visual evoked potentials (VEPs) in response to achromatic stimuli with low luminance contrast and low spatial frequency, and isoluminant red/green and blue/yellow stimuli with high spatial frequency were recorded in 10 dyslexic children and 10 age- and sex-matched, healthy subjects. Results Dyslexic children showed delayed VEPs to both achromatic stimuli (magnocellular-dorsal stream) and isoluminant red/green and blue/yellow stimuli (parvocellular-ventral and koniocellular streams). To our knowledge, this is the first time that a dysfunction of colour vision has been brought to light in an objective way (i.e., by means of electrophysiological methods) in children with DD. Conclusion These results give rise to speculation concerning the need for a putative approach for promoting both learning how to read and/or improving existing reading skills of children with or at risk of DD. The working hypothesis would be to combine two integrated interventions in a single programme aimed at fostering the function of both the magnocellular and the parvocellular streams.

The arginine-vasopressin (AVP)-containing hypothalamic magnocellular neurosecretory neurons (VPMNNs) are known for their role in hydro-electrolytic balance control via their projections to neurohypophysis. Recently, projections from these same neurons to hippocampus, habenula, and other brain regions, in which vasopressin infusion modulates contingent social and emotionally-affected behaviors, have been reported. Here, we present evidence that VPMNN collaterals also project to the amygdaloid complex, and establish synaptic connections with neurons in central amygdala (CeA). The density of AVP innervation in amygdala was substantially increased in adult rats that had experienced neonatal maternal separation (MS), consistent with our previous observations that MS enhances VPMNN number in the paraventricular (PVN) and supraoptic (SON) nuclei of the hypothalamus. In the CeA, V1a AVP receptor mRNA was only observed in GABAergic neurons, demonstrated by complete co-localization of V1a transcripts in neurons expressing Gad1 and Gad2 transcripts in CeA using the RNAscope method. V1b and V2 receptors mRNA were not detected, using the same method. Water-deprivation for 24 hrs, which increased the metabolic activity of VPMNNs, also increased anxiety-like behavior measured using the elevated plus maze test, and this effect was mimicked by bilateral microinfusion of VP into the CeA. Anxious behavior induced by either water deprivation or VP infusion was reversed by CeA infusion of V1a antagonist. VPMNNs are thus a newly discovered source of central amygdala inhibitory circuit modulation, through which both early-life and adult stress coping signals are conveyed from the hypothalamus to the amygdala.

Foveated stimuli receive visual processing that is quantitatively and qualitatively different from nonfoveated stimuli. At normal interpersonal distances, people move their eyes around another's face so that certain features receive foveal processing; on any given fixation, other features therefore project extrafoveally. Yet little is known about the processing of extrafoveally presented facial features, how informative those extrafoveally presented features are for face perception (e.g., for assessing another's emotion), or what processes extract task-relevant (e.g., emotion-related) cues from facial features that first appear outside the fovea, and how these processes are implemented in the brain. © The Author(s) 2013.

It is well known that pattern reversal visual evoked potentials (VEPs) are age-sensitive. Through the use of this technique, it is possible to assess both of the major visual pathways (i.e., the magnocellular and parvocellular ones) in terms of function and development. What developmental path these pathways follow, and if they develop/age in parallel across the human lifespan is a matter of ongoing debate, yet, only a few VEP studies have dealt with this issue. This cross-sectional study examined a sample of 115 healthy volunteers aged 5 to 84 years. Beyond the standard checkerboard pattern reversal stimulation at 97% contrast, we recorded pattern-reversal VEPs at 6% contrast to selectively stimulate the M pathway and isoluminant red and green checkerboard stimulation was also used to selectively stimulate the P pathway. Our results do not support the developmental advantage of any of the pathways. The development of both pathways appear to take a remarkably long time (well into the 30s), and the signs of aging become marked over 50 years of age, especially in the case of the magnocellular pathway.

The pulsed-pedestal paradigm consists of the simultaneous brief presentation of a test stimulus and luminance pedestals. Processing with this paradigm is thought to be mediated by the parvocellular pathway. The steady-pedestal paradigm consists of the brief presentation of a test stimulus against a continuously presented luminance pedestals. Processing with this paradigm is thought to be mediated by the magnocellular pathway. To test the prediction that transient attention should have a differential effect on performance with these two paradigms, we added to their typical procedures peripheral precues that trigger transient attention. As expected, we have found that the attraction of transient attention to the target location improved performance with the pulsed-pedestal paradigm, but had no reliable effect on performance with the steady-pedestal paradigm. These findings support the hypothesis that transient attention favors parvocellular over magnocellular processing.

To evaluate whether luminance contrast discrimination losses in amblyopia on putative magnocellular (MC) and parvocellular (PC) pathway tasks reflect deficits at retinogeniculate or cortical sites. Fifteen amblyopes including six anisometropes, seven strabismics, two mixed and 12 age-matched controls were investigated. Contrast discrimination was measured using established psychophysical procedures that differentiate MC and PC processing. Data were described with a model of the contrast response of primate retinal ganglion cells. All amblyopes and controls displayed the same contrast signatures on the MC and PC tasks, with three strabismics having reduced sensitivity. Amblyopic PC contrast gain was similar to electrophysiological estimates from visually normal, non-human primates. Sensitivity losses evident in a subset of the amblyopes reflect cortical summation deficits, with no change in retinogeniculate contrast responses. The data do not support the proposal that amblyopic contrast sensitivity losses on MC and PC tasks reflect retinogeniculate deficits, but rather are due to anomalous post-retinogeniculate cortical processing of retinal signals.

Visual processing deficits in dyslexic readers are argued to evolve as a consequence of reading failure. This study examines dorsal stream functioning of children before they commence formal reading instruction to determine whether visual deficits precede reading difficulties. Coherent motion and visual frequency doubling detection were measured in children at familial risk for dyslexia and in children unselected for family reading history. Here we show that children who are at family risk for dyslexia demonstrate dorsal stream deficits before they learn to read, whilst demonstrating no corresponding deficits in coherent form and static grating control tasks. Results indicate that the dorsal visual deficits observed in dyslexic readers are unlikely to be the result of reading failure.

Much work in the cognitive neuroscience of schizophrenia has focused on attention, memory, and executive functioning. To date, less work has focused on perceptual processing. However, perceptual functions are frequently disrupted in schizophrenia, and thus this domain has been included in the CNTRICS (Cognitive Neuroscience Treatment Research to Improve Cognition in Schizophrenia) project. In this article, we describe the basic science presentation and the breakout group discussion on the topic of perception from the first CNTRICS meeting, held in Bethesda, Maryland on February 26 and 27, 2007. The importance of perceptual dysfunction in schizophrenia, the nature of perceptual abnormalities in this disorder, and the critical need to develop perceptual tests appropriate for future clinical trials were discussed. Although deficits are also seen in auditory, olfactory, and somatosensory processing in schizophrenia, the first CNTRICS meeting focused on visual processing deficits. Key concepts of gain control and integration in visual perception were introduced. Definitions and examples of these concepts are provided in this article. Use of visual gain control and integration fit a number of the criteria suggested by the CNTRICS committee, provide fundamental constructs for understanding the visual system in schizophrenia, and are inclusive of both lower-level and higher-level perceptual deficits.

It is well established that sensitivity is not necessarily equivalent at isoeccentric locations across the visual field. The focus of this study was a psychophysical examination of the spatial sensitivity differences between the upper and lower visual hemifields under conditions biased toward the presumed magnocellular or parvocellular visual pathway. Experiment 1 showed higher contrast sensitivity in the lower visual field when visual sensitivity was biased toward the parvocellular pathway; no visual field anisotropy was found when sensitivity was biased toward the magnocellular pathway. Experiment 2 showed that the magnitude of the contrast sensitivity anisotropy within the presumed parvocellular pathway increased when test targets of higher spatial frequency were used. The results of this study have relevance for the design both of psychophysical paradigms and clinical training programs for patients with heterogeneous visual field loss.

Saccadic suppression—the reduction of visual sensitivity during rapid eye movements—has previously been proposed to reflect a specific suppression of the magnocellular visual system, with the initial neural site of that suppression at or prior to afferent visual information reaching striate cortex. Dysfunction in the magnocellular visual pathway has also been associated with perceptual and physiological anomalies in individuals with autism spectrum disorder or high autistic tendency, leading us to question whether saccadic suppression is altered in the broader autism phenotype. Here we show that individuals with high autistic tendency show greater saccadic suppression of low versus high spatial frequency gratings while those with low autistic tendency do not. In addition, those with high but not low autism spectrum quotient (AQ) demonstrated pre-cortical (35–45 ms) evoked potential differences (saccade versus fixation) to a large, low contrast, pseudo-randomly flashing bar. Both AQ groups showed similar differential visual evoked potential effects in later epochs (80–160 ms) at high contrast. Thus, the magnocellular theory of saccadic suppression appears untenable as a general description for the typically developing population. Our results also suggest that the bias towards local perceptual style reported in autism may be due to selective suppression of low spatial frequency information accompanying every saccadic eye movement.

Paying attention to visual stimuli is typically accompanied by event-related desynchronizations (ERD) of ongoing alpha (7-14 Hz) activity in visual cortex. The present study used time-frequency based analyses to investigate the role of impaired alpha ERD in visual processing deficits in schizophrenia (Sz). Subjects viewed sinusoidal gratings of high (HSF) and low (LSF) spatial frequency designed to test functioning of the parvo- versus magnocellular pathways, respectively. Patients with Sz and healthy controls paid attention selectively to either the LSF or HSF gratings which were presented in random order. Event-related brain potentials (ERPs) were recorded to all stimuli. As in our previous study, it was found that Sz patients were selectively impaired at detecting LSF target stimuli and that ERP amplitudes to LSF stimuli were diminished, both for the early sensory-evoked components and for the attend minus unattend difference component (the Selection Negativity), which is generally regarded as a specific index of feature-selective attention. In the time-frequency domain, the differential ERP deficits to LSF stimuli were echoed in a virtually absent theta-band phase locked response to both unattended and attended LSF stimuli (along with relatively intact theta-band activity for HSF stimuli). In contrast to the theta-band evoked responses which were tightly stimulus locked, stimulus-induced desynchronizations of ongoing alpha activity were not tightly stimulus locked and were apparent only in induced power analyses. Sz patients were significantly impaired in the attention-related modulation of ongoing alpha activity for both HSF and LSF stimuli. These deficits correlated with patients’ behavioral deficits in visual information processing as well as with visually based neurocognitive deficits. These findings suggest an additional, pathway-independent, mechanism by which deficits in early visual processing contribute to overall cognitive impairment in Sz.

This study examined the extent to which letter optotypes and grating stimuli provide equivalent measures of contrast sensitivity under conditions designed to favor the magnocellular (MC) and parvocellular (PC) pathways. The contrast sensitivity functions (CSFs) of three visually normal observers were measured for Sloan letters and Gabor patches, using steady- and pulsed-pedestal paradigms to bias processing toward MC and PC pathways, respectively. CSFs for Gabor patches were low-pass for the steady-pedestal paradigm and band-pass for the pulsed-pedestal paradigm, in agreement with previous reports. However, CSFs for letters were low-pass for both testing paradigms. CSFs for letters restricted in frequency content by spatial filtering were equivalent to those for Gabor patches for both testing paradigms. Results indicate that conventional letter optotypes can provide a misleading measure of contrast sensitivity, especially under conditions emphasizing the PC pathway. The use of spatially band-pass filtered letters can provide a more appropriate evaluation of spatial contrast sensitivity while maintaining some of the potential advantages of letters.

We measured contrast thresholds for perception of the Hermann grid illusion, using different contrast polarities and mean luminances, in dyslexics and non-dyslexics. Both groups of subjects gave significantly lower thresholds with grids having dark squares and light paths, but there was no significant threshold difference between groups. Perceived strength of illusion was also measured in grids at suprathreshold contrast levels. Dyslexics perceived the illusion to be significantly stronger than non-dyslexics when the grid had light paths and low luminance.

The effects of transient spatial attention on temporal resolution were recently studied and compared with attentional effects on spatial resolution. It was found that in contrast to the attentional enhancement of spatial resolution, transient attention impairs temporal resolution. To account for these findings a novel attentional mechanism was suggested. This attentional mechanism facilitates parvocellular neurons at the attended location, which in turn inhibit the activity of magnocellular neurons at the same location [Yeshurun & Levy, Psychol. Sci. 14 (3) (2003a) 225]. The goal of the present study was to replicate the attentional decrement in temporal resolution (Experiment 1), and perform direct tests of this `parvo facilitation––magno inhibition' hypothesis. The employment of isoluminant stimuli (Experiments 2a and 2b) or a red background (Experiment 3) ensured that the parvo system was the main system mediating performance. Consequently, any parvo–magno inhibitory processes elicited by the attentional mechanism should only have a minor effect on performance. As predicted, these manipulations either significantly attenuated or completely eliminated the attentional decrement in temporal resolution. These findings provide direct support to the hypothesis that attention favors parvocellular over magnocellular neurons.

Dyslexia is a specific impairment in reading that affects 1 in 10 people. Previous studies have failed to isolate a single cause of the disorder, but several candidate genes have been reported. We measured motion perception in two groups of dyslexics, with and without a deletion within theDCDC2gene, a risk gene for dyslexia. We found impairment for motion particularly strong at high spatial frequencies in the population carrying the deletion. The data suggest that deficits in motion processing occur in a specific genotype, rather than the entire dyslexia population, contributing to the large variability in impairment of motion thresholds in dyslexia reported in the literature.

The magnocellular (M) and parvocellular (P) subdivisions of primate LGN are known to process complementary types of visual stimulus information, but a method for noninvasively defining these subdivisions in humans has proven elusive. As a result, the functional roles of these subdivisions in humans have not been investigated physiologically. To functionally map the M and P subdivisions of human LGN, we used high-resolution fMRI at high field (7. T and 3. T) together with a combination of spatial, temporal, luminance, and chromatic stimulus manipulations. We found that stimulus factors that differentially drive magnocellular and parvocellular neurons in primate LGN also elicit differential BOLD fMRI responses in human LGN and that these responses exhibit a spatial organization consistent with the known anatomical organization of the M and P subdivisions. In test-retest studies, the relative responses of individual voxels to M-type and P-type stimuli were reliable across scanning sessions on separate days and across sessions at different field strengths. The ability to functionally identify magnocellular and parvocellular regions of human LGN with fMRI opens possibilities for investigating the functions of these subdivisions in human visual perception, in patient populations with suspected abnormalities in one of these subdivisions, and in visual cortical processing streams arising from parallel thalamocortical pathways. © 2014 Elsevier Inc.

In his opinion paper, Breitmeyer (2014) sought to identify the contributions from the magno- and parvocellular systems to conscious and unconscious vision. One approach employed in this attempt was to study the effect of contrast. This was based on the well established finding that magno- and parvocellular cells differ in their contrast-response functions (Kaplan and Shapley, 1986): Magnocellular responses increase rapidly with contrast at low contrast levels but saturate at medium contrasts. Parvocellular responses, on the other hand, increase with contrast at a relatively constant rate. In his Figure 5, Breitmeyer makes the suggestion based on the effect of contrast, that visible priming reflects magnocellular activity whereas invisible priming reflects parvocellular responses. In Figure ​Figure11 is shown (solid line) the function: Figure 1 The contrast-response curve from Breitmeyer (2014) (solid line) generated form Equation 1 which was by Breitmeyer attributed to magnocellular responses. Also shown are contrast-response curves for magnocellular cells (dotted line) and for cells in cortical ... r=(66.5 c2.9)/(0.0762.9+c2.9) (1) where c denotes contrast, which was assumed by Breitmeyer to reflect the contrast-response relationship of magnocellular neurons. Sclar et al. (1990) found that contrast-response data from visual neurons can be described by the equation: r=rmax cn/(cn+c50n) (2) where c denotes contrast and the constants rmax, c50, and n differ for the different types of neurons. For magnocellular cells these values were 52.7, 0.11, and 1.2, respectively (Sclar et al., 1990). By using these values in Equation 2 the dotted curve in Figure ​Figure11 was generated. The functions in the figure have been normalized so as to give a response of 1.0 for a contrast of 1.0. This is the only adjustment made. As can be seen, the function for the magnocellular cells from Sclar et al. does not provide a particularly close fit to the function of Breitmeyer. This prompts the question: Would functions for other types of cells provide a better fit? Sclar et al. (1990) found that c50 (in Equation 2) for MT cells increases with decreasing stimulus size and that for very small stimuli it is comparable to that for magnocellular neurons. However, the exponent, n, was was found to be unchanged and the maximum response, rmax, underwent only minor changes. The latter, however, is irrelevant in the present context since the responses are normalized. Using Equation 2 MT cell responses have been calculated for large and small stimuli. For large stimuli the constants rmax, c50, and n were set to 36, 0.07, and 3.0 (from Sclar et al., 1990). In the case of small stimuli the value 0.11 (i.e., the value for magnocellular cells from Sclar et al.) was used for c50. As can be seen, the curves for MT cells (marked MT-L and MT-S for large and small stimuli, respectively) provide closer fits to the curve of Breitmeyer than does the function for magnocellular responses and the function of Breitmeyer falls between the two curves for MT cells. Area MT is part of the dorsal cortical stream. The ventral and dorsal cortical streams represent two sets of cortical areas (Merigan and Maunsell, 1993). Many authors (e.g., Breitmeyer, 2014) have conflated the magno- and parvocellular systems with, respectively, the dorsal and ventral streams. This, however, faces some difficulties. In the case of the dorsal stream, although it clearly receives a substantial portion of its input from the magnocellular system it also receives sizable inputs from the koniocellular (Sincich et al., 2004) and parvocellular systems (Nassi et al., 2006). In the case of the ventral stream, as exemplified by Area V4, lesion studies have indicated that it receives about equally strong inputs from the magno- and parvocellular systems (Ferrera et al., 1994). Also, lesions placed in the dorsal and ventral streams have quite different effects from those placed in the magno- and parvocellular systems (Merigan and Maunsell, 1993). Figure ​Figure11 emphasizes that the magnocellular system and the dorsal stream (exemplified here by Area MT) also differ in regard to contrast-response functions.

In addition to its core social deficits, autism is characterized by altered visual perception, with a preference for local percept in those high in autistic tendency. Here, the balance of global vs. local percepts for the perceptually rivalrous diamond illusion was assessed between groups scoring high and low on the Autism Spectrum Quotient (AQ). The global percept of a diamond shape oscillating horizontally behind three occluders can as easily be interpreted as the local percept of four line elements, each moving vertically. Increasing the luminance contrast of the occluders with respect to background resulted in an increase of initial global percept in both groups, with no difference in sensitivity between groups. Presenting the target further into the periphery resulted in a marked increase in the percentage of global perception with visual field eccentricity. However, while the performance for centrally presented diamond targets was not different between AQ groups, the peripheral global performance of the High AQ group was significantly reduced compared with the Low AQ group. On the basis of other imaging studies, this peripheral but not foveal global perceptual neglect may indicate an abnormal interaction between striate cortex and the Lateral Occipital Complex (LOC), or to differences in the deployment of attention between the two groups.

Research on schizophrenia has provided evidence of both impaired attentional control and dysfunctional magnocellular sensory processing. The present study tested the hypothesis that these impairments may be related, such that people with schizophrenia would be differentially distracted by stimuli that strongly activate the magnocellular pathway. To accomplish this, we used a visual attention paradigm from the basic cognitive neuroscience literature designed to assess the capture of attention by salient but irrelevant stimuli. Participants searched for a target shape in an array of non-target shapes. On some trials, a salient distractor was presented that either selectively activated the parvocellular system (parvo-biased distractors) or activated both the magnocellular and parvocellular systems (magno+parvo distractors). For both manual reaction times and eye movement measures, the magno+parvo distractors captured attention more strongly than the parvo-biased distractors in people with schizophrenia, but the opposite pattern was observed in matched healthy control participants. These results indicate that attentional control deficits in schizophrenia may arise, at least in part, by means of an interaction with magnocellular sensory dysfunction.

The goal of this study was to establish the spatial summation properties associated with inferred PC- and MC-pathway mediated psychophysical contrast discrimination. Previous work has established two paradigms that reveal characteristic signatures of these pathways. In the pulse paradigm, a four-square array was pulsed briefly, on a constant background. In the steady-pedestal paradigm, the stimulus array was presented continuously as a steady-pedestal within a constant surround. In both paradigms, one square differed from the others, giving the observer a forced choice spatial discrimination task. Area summation functions derived for the pulse paradigm decreased with area, with a slope of −0.25 on a log–log axis. Area summation functions derived for the steady-pedestal paradigm decreased as a power function of area, approaching an asymptote above one square degree. The latter are consistent with the classical data of threshold spatial summation.

Displacement thresholds with incremental chromatic and luminance edges were measured on different backgrounds. Above 3% luminance contrast, thresholds were always similar. At luminance contrasts below 3%, luminance edges could not be detected, but chromatic edges were still visible. At these low contrasts displacement thresholds for chromatic edges increased to a high level. We interpret these data in terms of multiple mechanisms; above 3% contrast a luminance mechanism determines thresholds, but when, at lower contrasts, chromatic mechanisms support detection, they also support the spatial task. Physiological data were consistent with the different mechanisms originating at the retinal ganglion cell level.

Foveal pathway visual function was assessed in 11 patients having tumours extending into the suprasellar region but without evidence of visual impairment as assessed by visual acuity and Bjerrum screen campimetry. Psychophysical and routine visual evoked potential (VEP) measurements were obtained from the eye ipsilateral to the maximal suprasellar extension. The sensitivity of luminance and chromatic pathways was assessed psychophysically by measuring increment thresholds for white and red flashes of light presented on a white adapting field. Temporal sensitivity was assessed psychophysically by measuring threshold modulation sensitivity for sinusoidally modulating stimuli (de Lange attenuation characteristic). The patient group showed approximately equal significant psychophysical losses in chromatic, luminance and temporal sensitivities relative to normal controls. Midline VEP P100 latencies of the patient group did not significantly differ from those of the normal control group. It is concluded that tumours extending into the suprasellar region can cause foveal pathway dysfunction affecting both magno- and parvo-cellular pathways, even in the presence of normal visual acuity and fields suggesting a more widespread and insidious abnormality of the visual pathways in this condition than previously thought.

How the visual capabilities of those with schizophrenia differ from those of individuals without schizophrenia is a topic of active research. Of special interest is the question of whether or not they might have a magnocellular deficiency. It has been concluded that contrast sensitivity in schizophrenic subjects is characterized by a general reduction in sensitivity, and so does not indicate a magnocellular deficiency (Skottun and Skoyles, 2007). Likewise, many of the reported cases of abnormal visual masking linked to schizophrenia can be described by a general reduction (see, e.g., Rassovsky et al., 2004). Also this is hard to reconcile with a magnocellular deficit since, according to the theory, such a deficit would have been expected to cause a reduction that was related specifically to the U-shaped Type-B masking function (Skottun and Skoyles, 2009). These observations prompt the question of whether or not other differences between schizophrenic subjects and controls that have been attributed to magnocellular deficiencies can also be accounted by a general reduction in sensitivity or response. Differences between schizophrenic subjects and nonschizophrenic controls attributed to magnocellular deficiencies have been found using visually evoked potentials (VEP). Butler et al. (2009) obtained VEP data for schizophrenic subjects and controls under two conditions. One condition aimed at predominantly stimulating the magnocellular system, the other the parvocellular system. Butler et al. (2009) found statistically significant reduction in the responses from the schizophrenic subjects, relative to those of controls, under the condition favoring the magnocellular system but not under the parvocellular condition. The authors interpreted this as evidence for a magnocellular deficiency linked to schizophrenia. The present report examines the possibility that these results could reflect instead a general response reduction. The data of Butler et al. (2009) have been re-plotted in Figure ​Figure1.1. The open and filled symbols give the results for the schizophrenic subjects and controls, respectively, while panels A and B give the data obtained under the magno- and parvocellular conditions. A general response reduction was modeled by a simple linear scaling of the response from the control group. The scaling factor was determined by the best fit to the data of the schizophrenic subjects by calculating the smallest sum of squared deviations. Analyses of both magno- and parvocellular data conditions were included, giving a single scaling value of 0.756. (The scaling factors for the magno- and parvocellular data sets computed separately were 0.737 and 0.797, respectively). The scaled data are indicated by the dashed lines in Figure ​Figure1.1. Even though the data for the schizophrenic subjects in the magnocellular condition in some instances are slightly below the dashed line and the data in the parvocellular condition in some cases are slightly above the dashed line, the overall finding is that the scaled data give close fits to the data for the schizophrenic subjects for both conditions. This suggests that Butler et al.'s (2009) data for schizophrenic subjects in both the magnocellular and the parvocellular conditions are consistent with scaling by the same factor. This is consistent with a general reduction in the response rather than a difference (as suggested by Butler et al., 2009) between the magnocellular and parvocellular systems. No reason therefore exists to account for these data with a deficiency linked specifically to the magnocellular system. Figure 1 Data re-plotted from Figure 4 of Butler et al. (2009). Open and filled symbols give data for schizophrenic subjects (N = 20) and controls (N = 17), respectively. (A,B) Give results obtained under conditions aimed at stimulating predominately the magno- ... One explanation for the differences between controls and schizophrenic subjects being significant in the magnocellular condition but not in the parvocellular one could be that the response differences were larger in the magnocellular condition. The fact that the responses were larger in this condition would have made the difference between the groups (as a result of scaling by a constant) larger under this condition, and so more likely to result in a statistically significant difference. Further, it is an invalid inference to conclude that a magnocellular deficiency exists solely based on the finding that a magnocellular condition gives statistically significant differences whereas a parvocellular condition does not. To do so would require making an interpretation of the non-significant data—but a statistically non-significant result does not allow any conclusions to be inferred (Gill, 1999). The finding that the difference is statistically significant under the magnocellular condition and not under the parvocellular condition, moreover, is not itself strictly pertinent. What might have been somewhat more relevant would have been if the difference between the data obtained under the two conditions were statistically significant. (It should in this connection be kept in mind that the difference between a statistically significant result and a non-significant result need not itself be statistically significant. Gelman and Stern, 2006). However, it is not clear that even this would have solved the problem since it may be possible for a single factor to have effects that are different under different conditions (as shown in Figure ​Figure1).1). The difference between these effects may, or may not, be statistically significant.

Background: Individuals with schizophrenia spectrum diagnoses have deficient visual information processing as assessed by a variety of paradigms including visual backward masking, motion perception and visual contrast sensitivity (VCS). In the present study, the VCS paradigm was used to investigate potential differences in magnocellular (M) vs. parvocellular (P) channel function that might account for the observed information processing deficits of schizophrenia spectrum patients. Specifically, VCS for near threshold luminance (black/white) stimuli is known to be governed primarily by theM channel, while VCS for near threshold chromatic (red/green) stimuli is governed by the P channel. Methods: VCS for luminance and chromatic stimuli (counterphase-reversing sinusoidal gratings, 1.22 c/degree, 8.3 Hz) was assessed in 53 patients with schizophrenia (including 5 offantipsychotic medication), 22 individuals diagnosed with schizotypal personality disorder and 53 healthy comparison subjects. Results: Schizophrenia spectrum groups demonstrated reduced VCS in both conditions relative to normals, and there was no significant group by condition interaction effect. Post-hoc analyses suggest that it was the patients with schizophrenia on antipsychotic medication as well as SPD participants who accounted for the deficits in the luminance condition. Conclusions: These results demonstrate visual information processing deficits in schizophrenia spectrum populations but do not support the notion of selective abnormalities in the function of subcortical channels as suggested by previous studies. Further work is needed in a longitudinal design to further assess VCS as a vulnerability marker for psychosis as well as the effect of antipsychotic agents on performance in schizophrenia spectrum populations. © 2013 Cadenhead, Dobkins, McGovern and Shafer.

Studies have shown that patients with schizophrenia exhibit visual processing impairments, particularly regarding the processing of spatial frequencies. In a previous work, we found that, compared to healthy volunteers, patients were biased toward low spatial frequencies (LSF) to identify facial expression at a glance. Given the ubiquity of faces in visual perception, it remains an open question whether the LSF bias is face specific or also occurs with other visual objects. Here, 15 patients with schizophrenia and 11 healthy control adults performed a categorization task with hybrid stimuli. These stimuli were single images consisting of two different objects, a fruit and an animal, each in a specific spatial frequency range, either low (LSF) or high (HSF). Observers were asked to report if they saw an animal or a fruit. The reported category demonstrated which spatial scale was preferentially perceived in each trial. In a control experiment, participants performed the same task but with images of only a single object, either a LSF or HSF filtered animal or fruit, to verify that participants could perceive both HSF or LSF when presented in isolation. The results on the categorization task showed that patients chose more frequently LSF with hybrid stimuli compared to healthy controls. However, both populations performed equally well with HSF and LSF filtered pictures in the control experiment, demonstrating that the LSF preference found with hybrid stimuli in patients was not due to an inability to perceive HSF. The LSF preference found in schizophrenia confirms our previous study conducted with faces, and shows that this LSF bias generalizes to other categories of objects. When a broad range of spatial frequencies are present in the image, as in normal conditions of viewing, patients preferentially rely on coarse visual information contained in LSF. This result may be interpreted as a dysfunction of the guidance of HSF processing by LSF processing.

Previous studies have identified a magnocellular pathway defect in approximately 75 % of dyslexics. Since these experiments have not classified dyslexia into subtypes, the purpose of this experiment was to determine if adult dyseidetic dyslexics or dysphoneidetic dyslexics suffer from a defect in the magnocellular pathway. Nine dyseidetic dyslexics, eight dysphoneidetic dyslexics, and nine normal readers participated in the experiment. Contrast sensitivity functions (CSF) were determined with vertically oriented sine wave gratings (0.5, 1.0, 2.0, 4.0, 8.0, 12.0 c/deg drifting at 1 and 10 Hz) by employing a two-alternative, forced-choice technique. The results of the experiment indicated that dysphoneidetic dyslexics had reduced sensitivity to low spatial frequencies at 10 Hz, whereas dyseidetic dyslexics did not have reduced sensitivity at either 1 or 10 Hz. These results suggest that the type of dyslexia influences whether losses in perception are found which are consistent with a magnocellular deficit.

Developmental dyslexics perform differently from controls on a number of low level visual tasks. We carried out three experiments to explore some of these differences. Dyslexics have been found to have reduced luminance contrast sensitivity at mesopic luminance levels. We failed to replicate this finding at photopic luminance levels. We also compared the (photopic) coherent motion detection thresholds of groups of child and adult dyslexics with those of age matched controls. Dyslexics were significantly less sensitive to motion. The results are discussed in relation to a recent suggestion that developmental dyslexia may be associated with a magnocellular visual deficit.

Both theoretical and experimental evidence suggests that duration perception is mediated preferentially by the colour-blind but high temporally sensitive luminance pathway. In this experiment we tested whether colour modulated stimuli and high spatial frequency luminance modulated stimuli, which are known to be relayed mostly by the slow parvocellular system, are able to elicit reliable sense of duration. We show that ramped colour modulated stimuli seem to last less than luminance modulated stimuli matched for visibility. The effect is large, about 200 ms and is constant at all durations tested (range 500 - 1100 ms). However high spatial frequency luminance stimuli obtain duration matches similar to those of low spatial frequency luminance modulated stimuli. The results at various levels of contrast and temporal smoothing indicate that equiluminant stimuli have higher contrast thresholds to activate the mechanisms which time visual stimuli. Overall the results imply that both the magnocellular and the parvocellular systems access reliably the timing mechanisms with a difference only in the way these are engaged.

Although developmental dyslexia (DD) is frequently associate to a linguistic deficit, the underlying neurobiological cause remains unclear. One prominent vision science hypothesis suggests a specific deficit in magnocellular (M) pathway in DD. However, a recent hypothesis proposes that M-deficits contribute to the etiology of phonological decoding ability (i.e., new word and nonword reading), impairing selectively the attentional orienting process onto letter string. Thus, a specific M-pathway impairment in association with an attentional orienting disorder in DD children with phonological decoding deficit was specifically predicted by this neurobiological hypothesis. In the present study we investigated the M-pathway and attentional orienting in 18 dyslexic (10 with phonological decoding deficit) and in 29 chronological age and IQ matched normally reading children by measuring dynamic stimuli sensibility (i.e., spatial frequency doubling illusion) and the time-course of automatic covert attention (i.e., target detection effect at different SOAs of a non-predictive and peripheral spatial cue), respectively. The results showed a specific deficit of the M-pathway task in dyslexic with phonological decoding deficit. More importantly, the same group of dyslexics with M-deficit presented a sluggish attentional orienting: attentional facilitation was present at longer cue-target SOAs compared with normal readers. These results highlight that a M-deficit linked to a parietal-attentional dysfunction might impair the phonological decoding mechanisms that are critical for reading acquisition.

Recently developed psychophysical techniques permit the biasing of the processing of the stimulus by early visual channels so that responses reflect characteristics of either magno- or parvocellular pathways (Pokorny & Smith, 1997). We used such techniques to test psychophysically whether the global magnocellular dysfunction reported in schizophrenia also affects early processes. Seven schizophrenic patients and 19 normal controls participated. The task was a four-alternative forced-choice luminance discrimination, using a 2 × 2 configuration of four 1-deg squares. Target luminance threshold was determined in three conditions: the stimulus, including the target, was pulsed for 17 ms (pulse paradigm); the target was presented on a steady background of four squares (steady paradigm), or the target was presented alone (no background paradigm). We replicated previous results demonstrating magnocellular and parvocellular signatures in control participants. No evidence for an early magnocellular deficit could be detected as the thresholds of all schizophrenic observers were higher both in the steady paradigm (presumed magnocellular mediation) and in the pulse paradigm (presumed parvocellular mediation). Magnocellular dysfunction, if present in schizophrenia, must concern more integrated processes, possibly at levels at which parvocellular and magnocellular paths interact.

Developmental dyslexia is a language-based learning disability with frequently associated non-linguistic sensory deficits that have been the basis of various perception-based theories. It remains an open question whether the underlying deficit in dyslexia is a low level impairment that causes speech and orthographic perception deficits that in turn impedes higher phonological and reading processes, or a high level impairment that affects both perceptual and reading related skills.We investigated by means of contrast detection thresholds two low-level theories of developmental dyslexia, the magnocellular and the fast temporal processing hypotheses, as well as a more recent suggestion that dyslexics have difficulties in sequential comparison tasks that can be attributed to a higher-order deficit. It was found that dyslexics had significantly higher thresholds only on a sequential, but not a spatial, detection task, and that this impairment was found to be independent of the inter-stimulus interval. We also found that the poor performance of dyslexics on the temporal task was dependent on the size of the required memory trace of the image rather than on the number of images. Our findings do not support the magnocellular theory and challenge the fast temporal deficit hypothesis. We suggest that dyslexics may have a higher order, dual mechanism impairment. We also discuss the clinical implications of our findings.