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The long-standing hypothesis that autism is linked to changes in the visual magnocellular system of the human brain has never been directly examined due to technological constraints. Here, we used a recently developed 7-Tesla functional MRI (fMRI) approach to investigate this hypothesis within the visual sensory thalamus (lateral geniculate nucleus, LGN). The LGN is a crucial component of the primary visual pathway. It is particularly suited to investigate the magnocellular visual system, because within the LGN, the magnocellular (mLGN) uniquely segregates from the parvocellular (pLGN) system. Our results revealed diminished mLGN blood-oxygenation-level-dependent (BOLD) responses in the autism group compared to controls. pLGN responses were comparable across groups. The mLGN alterations were observed specifically for stimuli optimized for mLGN function, i.e., visual displays with low spatial frequency and high temporal flicker frequency. The results confirm the long-standing hypothesis of magnocellular visual system alterations in autism. They substantiate the emerging perspective that sensory processing variations are part of autism symptomatology. [ABSTRACT FROM AUTHOR]

Research on figure-ground perception has consistently found that red images are more likely to be perceived as figure/nearer, yet the mechanisms behind this are not completely clear. The primary theories have pointed to optical chromatic aberrations or cortical mechanisms, such as the antagonistic interactions of the magno-/parvocellular (M/P) systems. Our study explored this color-biased figure-ground perception by examining the duration for which a region was perceived as figure under both binocular and monocular conditions, using all combinations of red, blue, green, and gray. In Experiment 1, we used figure-ground ambiguous Maltese crosses, composed of left- and right-tilting sectors of equal area. In Experiment 2, the crosses were figure-ground biased with size and orientation cues. Here, small sectors of cardinal orientations, likely perceived as figure, were contrasted with larger, obliquely oriented sectors, likely perceived as ground. Under monocular conditions, the results aligned with chromatic aberration predictions: red advanced and blue receded, regardless of size and orientation. However, under binocular conditions, the advancing effect of red continued, but the receding effect of blue was generally not observed. Notably, blue, along with red and green, was more frequently perceived as figure compared to gray. The results under binocular viewing are in line with the expectations of the antagonistic M/P system interactions theory, likely due to the collective input from both eyes, facilitating the anticipated effects. Our findings suggest that color-biased figure-ground perception may arise from the synergistic effect of antagonistic M/P system interactions and other optical and cortical mechanisms, together compensating for chromatic aberrations. [ABSTRACT FROM AUTHOR]

The superior colliculus receives a direct projection from retinal ganglion cells. In primates, it remains unknown if the same ganglion cells also supply the lateral geniculate nucleus. To address this issue, a double-label experiment was performed in two male macaques. The animals fixated a target while injection sites were scouted in the superior colliculus by recording and stimulating with a tetrode. Once suitable sites were identified, cholera toxin subunit B-Alexa Fluor 488 was injected via an adjacent micropipette. In a subsequent acute experiment, cholera toxin subunit B-Alexa Fluor 555 was injected into the lateral geniculate nucleus at matching retinotopic locations. After a brief survival period, ganglion cells were examined in retinal flatmounts. The percentage of double-labeled cells varied locally, depending on the relative efficiency of retrograde transport by each tracer and the precision of retinotopic overlap of injection sites in each target nucleus. In counting boxes with extensive overlap, 76–98% of ganglion cells projecting to the superior colliculus were double labeled. Cells projecting to the superior colliculus constituted 4.0–6.7% of the labeled ganglion cell population. In one particularly large zone, there were 5,746 cells labeled only by CTB-AF555, 561cells double labeled by CTB-AF555 and CTB-AF488, but no cell labeled only by CTB-AF488. These data indicate that retinal input to the macaque superior colliculus arises from a collateral axonal branch supplied by ∼5% of the ganglion cells that project to the lateral geniculate nucleus. Surprisingly, there exist no ganglion cells that project exclusively to the SC. [ABSTRACT FROM AUTHOR]

Individuals at Clinical High Risk (CHR) for psychosis or in their First Episode (FE) of psychosis are in a pivotal time in adolescence or young adulthood when illness can greatly impact their functioning. Finding relevant biomarkers for psychosis in the early stages of illness can contribute to early diagnosis, therapeutic management and prediction of outcome. One such biomarker that has been studied in schizophrenia (SZ) is visual contrast sensitivity (VCS). VCS can be used to differentiate visual information processing function in the magnocellular versus parvocellular visual pathways. Few studies have assessed VCS in early psychosis. Participants included CHR (n = 68), FE psychosis (n = 34) and Healthy Comparison (HC) (n = 63). All were clinically assessed and completed a VCS paradigm that involved near threshold luminance and chromatic stimuli. CHR and FE participants had lower VCS in the luminance condition (F[2166] = 3.42, p < 0.05) compared to HC. There was also a significant sex X group interaction (F[5163] = 4.3, p < 0.001) in the luminance condition (F[5163] = 4.3, p < 0.001) as FE males (p < 0.01) and CHR females (p < 0.01) had the greatest deficits compared to male and female HC participants respectively. VCS deficits in the luminance condition were associated with more thought disorder, slower processing speed, worse executive functioning and poor global functioning (r's 0.25–0.50, p < 0.05). This study supports the hypothesis that there are deficits in visual information processing, particularly in tasks that emphasize the magnocellular pathway, in patients experiencing early psychosis. VCS therefore has the potential to be used as a biomarker in this population. [ABSTRACT FROM AUTHOR]

Key message: The Riddoch syndrome is thought to be caused by damage to the primary visual cortex (V1), usually following a vascular event. This study shows that damage to the anatomical input to V1, i.e., the optic radiations, can result in selective visual deficits that mimic the Riddoch syndrome. The results also highlight the differential susceptibility of the magnocellular and parvocellular visual systems to injury. Overall, this study offers new insights that will improve our understanding of the impact of brain injury and neurosurgery on the visual pathways. The Riddoch syndrome, characterised by the ability to perceive, consciously, moving visual stimuli but not static ones, has been associated with lesions of primary visual cortex (V1). We present here the case of patient YL who, after a tumour resection surgery that spared his V1, nevertheless showed symptoms of the Riddoch syndrome. Based on our testing, we postulated that the magnocellular (M) and parvocellular (P) inputs to his V1 may be differentially affected. In a first experiment, YL was presented with static and moving checkerboards in his blind field while undergoing multimodal magnetic resonance imaging (MRI), including structural, functional, and diffusion, acquired at 3 T. In a second experiment, we assessed YL's neural responses to M and P visual stimuli using psychophysics and high-resolution fMRI acquired at 7 T. YL's optic radiations were partially damaged but not severed. We found extensive activity in his visual cortex for moving, but not static, visual stimuli, while our psychophysical tests revealed that only low-spatial frequency moving checkerboards were perceived. High-resolution fMRI revealed strong responses in YL's V1 to M stimuli and very weak ones to P stimuli, indicating a functional P lesion affecting V1. In addition, YL frequently reported seeing moving stimuli and discriminating their direction of motion in the absence of visual stimulation, suggesting that he was experiencing visual hallucinations. Overall, this study highlights the possibility of a selective loss of P inputs to V1 resulting in the Riddoch syndrome and in hallucinations of visual motion. [ABSTRACT FROM AUTHOR]

Midget and parasol ganglion cells (GCs) represent the major output channels from the primate eye to the brain. On-type midget and parasol GCs exhibit a higher background spike rate and thus can respond more linearly to contrast changes than their Off-type counterparts. Here, we show that a calcium-permeable AMPA receptor (CP-AMPAR) antagonist blocks background spiking and sustained light-evoked firing in On-type GCs while preserving transient light responses. These effects are selective for On-GCs and are occluded by a gap-junction blocker suggesting involvement of AII amacrine cells (AII-ACs). Direct recordings from AII-ACs, cobalt uptake experiments, and analyses of transcriptomic data confirm that CP-AMPARs are expressed by primate AII-ACs. Overall, our data demonstrate that under some background light levels, CP-AMPARs at the rod bipolar to AII-AC synapse drive sustained signaling in On-type GCs and thus contribute to the more linear contrast signaling of the primate On- versus Off-pathway.

Theoretically, the pulsed- and steady-pedestal paradigms are thought to track contrast-increment thresholds (ΔC) as a function of pedestal contrast (C) for the parvocellular (P) and magnocellular (M) systems, respectively, yielding linear ΔC versus C functions for the pulsed- and nonlinear functions for the steady-pedestal paradigm. A recent study utilizing these paradigms to isolate the P and M systems reported no evidence of the M system being suppressed by red light, contrary to previous physiological and psychophysical findings. Curious as to why this may have occurred, we examined how ΔC varies with C for the P and M systems using the pulsed- and steady-pedestal paradigms and stimuli biased towards the P or M systems based on their sensitivity to spatial frequency (SF) and color. We found no effect of color and little influence of SF. To explain this lack of color effects, we used a quantitative model of ΔC (as it changes with C) to obtain Csat and contrast-gain values. The contrast-gain values (i) contradicted the hypothesis that the steady-pedestal paradigm tracks the M-system response, and (ii) our obtained Csat values indicated strongly that both pulsed- and steady-pedestal paradigms track primarily the P-system response. [ABSTRACT FROM AUTHOR]

The pulsed- and steady-pedestal paradigms were designed to track increment thresholds (ΔC) as a function of pedestal contrast (C) for the parvocellular (P) and magnocellular (M) systems, respectively. These paradigms produce contrasting results: linear relationships between ΔC and C are observed in the pulsed-pedestal paradigm, indicative of the P system’s processing, while the steady-pedestal paradigm reveals nonlinear functions, characteristic of the M system’s response. However, we recently found the P model fits better than the M model for both paradigms, using Gabor stimuli biased towards the M or P systems based on their sensitivity to color and spatial frequency. Here, we used two-square pedestals under green vs. red light in the lower-left vs. upper-right visual fields to bias processing towards the M vs. P system, respectively. Based on our previous findings, we predicted the following: (1) steeper ΔC vs. C functions with the pulsed than the steady pedestal due to different task demands; (2) lower ΔCs in the upper-right vs. lower-left quadrant due to its bias towards P-system processing there; (3) no effect of color, since both paradigms track the P-system; and, most importantly (4) contrast gain should not be higher for the steady than for the pulsed pedestal. In general, our predictions were confirmed, replicating our previous findings and providing further evidence questioning the general validity of using the pulsed- and steady-pedestal paradigms to differentiate the P and M systems.

Despite proving its usefulness for over a century, the concept of developmental dyslexia (DD) is currently in severe disarray because of the recent introduction of the phonological theory of its causation. Since mastering the phonological principle is essential for all reading, failure to do so cannot be used to distinguish DD from the many other causes of such failure. To overcome this problem, many new psychological, signal detection, and neurological theories have been introduced recently. All these new theories converge on the idea that DD is fundamentally caused by impaired signalling of the timing of the visual and auditory cues that are essential for reading. These are provided by large 'magnocellular' neurones which respond rapidly to sensory transients. The evidence for this conclusion is overwhelming. Especially convincing are intervention studies that have shown that improving magnocellular function improves dyslexic children's reading, together with cohort studies that have demonstrated that the magnocellular timing deficit is present in infants who later become dyslexic, long before they begin learning to read. The converse of the magnocellular deficit in dyslexics may be that they gain parvocellular abundance. This may often impart the exceptional 'holistic' talents that have been ascribed to them and that society needs to nurture. [ABSTRACT FROM AUTHOR]

Body inversion effects (BIEs) reflect the deployment of the configural processing of body stimuli. BIE modulates the activity of body-selective areas within both the dorsal and the ventral streams, which are tuned to low (LSF) or high spatial frequencies (HSF), respectively. The specific contribution of different bands to the configural processing of bodies along gender and posture dimensions, however, is still unclear. Seventy-two participants performed a delayed matching-to-sample paradigm in which upright and inverted bodies, differing for gender or posture, could be presented in their original intact form or in the LSF- or HSF-filtered version. In the gender discrimination task, participants' performance was enhanced by the presentation of HSF images. Conversely, for the posture discrimination task, a better performance was shown for either HSF or LSF images. Importantly, comparing the amount of BIE across spatial-frequency conditions, we found greater BIEs for HSF than LSF images in both tasks, indicating that configural body processing may be better supported by HSF information, which will bias processing in the ventral stream areas. Finally, the exploitation of HSF information for the configural processing of body postures was lower in individuals with higher autistic traits, likely reflecting a stronger reliance on the local processing of body-part details. [ABSTRACT FROM AUTHOR]

Memory deficits are core features of schizophrenia, and a central aim in biological psychiatry is to identify the etiology of these deficits. Scrutiny is naturally focused on the dorsolateral prefrontal cortex and the hippocampal cortices, given these structures' roles in memory and learning. The fronto-hippocampal framework is valuable but restrictive. Network-based underpinnings of learning and memory are substantially diverse and include interactions between hetero-modal and early sensory networks. Thus, a loss of fidelity in sensory information may impact memorial and cognitive processing in higher-order brain sub-networks, becoming a sensory source for learning and memory deficits. In this overview, we suggest that impairments in magno- and parvo-cellular visual pathways result in degraded inputs to core learning and memory networks. The ascending cascade of aberrant neural events significantly contributes to learning and memory deficits in schizophrenia. We outline the network bases of these effects, and suggest that any network perspectives of dysfunction in schizophrenia must assess the impact of impaired perceptual contributions. Finally, we speculate on how this framework enriches the space of biomarkers and expands intervention strategies to ameliorate this prototypical disconnection syndrome. • The fidelity of unimodal inputs impacts learning and memory. • Schizophrenia is characterized by deficits in magno- and parvocellular pathways. • These deficits will impact frontal-hippocampal network function. • Models of frontal-hippocampal impairment must consider the role of visual pathways. • Thus, dys-connection in schizophrenia is global and not local. [ABSTRACT FROM AUTHOR]

Most of our knowledge about the neural networks mediating reading has derived from studies of developmental dyslexia (DD). For much of the 20th C. this was diagnosed on the basis of finding a discrepancy between children's unexpectedly low reading and spelling scores compared with their normal or high oral and non-verbal reasoning ability. This discrepancy criterion has now been replaced by the claim that the main feature of dyslexia is a phonological deficit, and it is now argued that we should test for this to identify dyslexia. However, grasping the phonological principle is essential for all learning to read; so every poor reader will show a phonological deficit. The phonological theory does not explain why dyslexic people, in particular, fail; so this phonological criterion makes it impossible to distinguish DD from any of the many other causes of reading failure. Currently therefore, there is no agreement about precisely how we should identify it. Yet, if we understood the specific neural pathways that underlie failure to acquire phonological skills specifically in people with dyslexia, we should be able to develop reliable means of identifying it. An important, though not the only, cause in people with dyslexia is impaired development of the brain's rapid visual temporal processing systems; these are required for sequencing the order of the letters in a word accurately. Such temporal, "transient," processing is carried out primarily by a distinct set of "magnocellular" (M-) neurones in the visual system; and the development of these has been found to be impaired in many people with dyslexia. Likewise, auditory sequencing of the sounds in a word is mediated by the auditory temporal processing system whose development is impaired in many dyslexics. Together these two deficits can therefore explain their problems with acquiring the phonological principle. Assessing poor readers' visual and auditory temporal processing skills should enable dyslexia to be reliably distinguished from other causes of reading failure and this will suggest principled ways of helping these children to learn to read, such as sensory training, yellow or blue filters or omega 3 fatty acid supplements. This will enable us to diagnose DD with confidence, and thus to develop educational plans targeted to exploit each individual child's strengths and compensate for his weaknesses. [ABSTRACT FROM AUTHOR]

The lateral geniculate nucleus (LGN) is a key thalamic nucleus in the visual system, which has an important function in relaying retinal visual input to the visual cortex. The human LGN is composed mainly of magnocellular (M) and parvocellular (P) subdivisions, each of which has different stimulus selectivity in neural response properties. Previous studies have discussed the potential relationship between LGN subdivisions and visual disorders based on psychophysical data on specific types of visual stimuli. However, these relationships remain speculative because non-invasive measurements of these subdivisions are difficult due to the small size of the LGN. Here we propose a method to identify these subdivisions by combining two structural MR measures: high-resolution proton-density weighted images and macromolecular tissue volume (MTV) maps. We defined the M and P subdivisions based on MTV fraction data and tested the validity of the definition by (1) comparing the data with that from human histological studies, (2) comparing the data with functional magnetic resonance imaging measurements on stimulus selectivity, and (3) analyzing the test-retest reliability. The findings demonstrated that the spatial organization of the M and P subdivisions was consistent across subjects and in line with LGN subdivisions observed in human histological data. Moreover, the difference in stimulus selectivity between the subdivisions identified using MTV was consistent with previous physiology literature. The definition of the subdivisions based on MTV was shown to be robust over measurements taken on different days. These results suggest that MTV mapping is a promising approach for evaluating the tissue properties of LGN subdivisions in living humans. This method potentially will enable neuroscientific and clinical hypotheses about the human LGN subdivisions to be tested.

Most of our knowledge about the neural networks mediating reading has derived from studies of developmental dyslexia (DD). For much of the 20th C. this was diagnosed on the basis of finding a discrepancy between children’s unexpectedly low reading and spelling scores compared with their normal or high oral and non-verbal reasoning ability. This discrepancy criterion has now been replaced by the claim that the main feature of dyslexia is a phonological deficit, and it is now argued that we should test for this to identify dyslexia. However, grasping the phonological principle is essential for all learning to read; so every poor reader will show a phonological deficit. The phonological theory does not explain why dyslexic people, in particular, fail; so this phonological criterion makes it impossible to distinguish DD from any of the many other causes of reading failure. Currently therefore, there is no agreement about precisely how we should identify it. Yet, if we understood the specific neural pathways that underlie failure to acquire phonological skills specifically in people with dyslexia, we should be able to develop reliable means of identifying it. An important, though not the only, cause in people with dyslexia is impaired development of the brain’s rapid visual temporal processing systems; these are required for sequencing the order of the letters in a word accurately. Such temporal, “transient,” processing is carried out primarily by a distinct set of “magnocellular” (M-) neurones in the visual system; and the development of these has been found to be impaired in many people with dyslexia. Likewise, auditory sequencing of the sounds in a word is mediated by the auditory temporal processing system whose development is impaired in many dyslexics. Together these two deficits can therefore explain their problems with acquiring the phonological principle. Assessing poor readers’ visual and auditory temporal processing skills should enable dyslexia to be reliably distinguished from other causes of reading failure and this will suggest principled ways of helping these children to learn to read, such as sensory training, yellow or blue filters or omega 3 fatty acid supplements. This will enable us to diagnose DD with confidence, and thus to develop educational plans targeted to exploit each individual child’s strengths and compensate for his weaknesses.

Rationale: Visuo-perceptive deficits in severe alcohol use disorder (SAUD) remain little understood, notably regarding the respective involvement of the two main human visual streams, i.e., magnocellular (MC) and parvocellular (PC) pathways, in these deficits. Besides, in healthy populations, low-level visual perception can adapt depending on the nature of visual cues, among which emotional features, but this MC and PC pathway adaptation to emotional content is unexplored in SAUD. Objectives: To assess MC and PC functioning as well as their emotional modulations in SAUD. Methods: We used sensitivity indices (d′) and repeated-measures analyses of variance to compare orientation judgments of Gabor patches sampled at various MC- and PC-related spatial frequencies in 35 individuals with SAUD and 38 matched healthy controls. We then explored how emotional content modulated performances by introducing neutral or fearful face cues immediately before the Gabor patches and added the type of cue in the analyses. Results: SAUD patients showed a general reduction in sensitivity across all spatial frequencies, indicating impoverished processing of both coarse and fine-scale visual content. However, we observed selective impairments depending on facial cues: individuals with SAUD processed intermediate spatial frequencies less efficiently than healthy controls following neutral faces, whereas group differences emerged for the highest spatial frequencies following fearful faces. Altogether, SAUD was associated with mixed MC and PC deficits that may vary according to emotional content, in line with a flexible but suboptimal use of low-level visual content. Such subtle alterations could have implications for everyday life's complex visual judgments. [ABSTRACT FROM AUTHOR]

Visuospatial impairments have long been reported in Severe Alcohol Use Disorder but remain poorly understood, notably regarding the involvement of magnocellular (MC) and parvocellular (PC) pathways. This empirical gap hampers the understanding of the implications of these visual changes, especially since the MC and PC pathways are thought to sustain central bottom-up and top-down processes during cognitive processing. They thus influence our ability to efficiently monitor our environment and make the most effective decisions. To overcome this limitation, we measured PC-inferred spatial and MC-inferred temporal resolution in 35 individuals with SAUD and 30 healthy controls. We used Landolt circles displaying small apertures outside the sensitivity range of MC cells or flickering at a temporal frequency exceeding PC sensitivity. We found evidence of preserved PC spatial resolution combined with impaired MC temporal resolution in SAUD. We also measured how spatial and temporal sensitivity is influenced by the prior presentation of fearful faces – as emotional content could favor MC processing over PC one – but found no evidence of emotional modulation in either group. This spatio-temporal dissociation implies that individuals with SAUD may process visual details efficiently but perceive rapidly updating visual information at a slower pace. This deficit has implications for the tracking of rapidly changing stimuli in experimental tasks, but also for the decoding of crucial everyday visual incentives such as faces, whose micro-expressions vary continuously. Future studies should further specify the visual profile of individuals with SAUD to incorporate disparate findings within a theoretically grounded model of vision. • Severe Alcohol Use Disorder is related to long-term changes in visual abilities. • We measured their spatial and temporal nature through psychophysical paradigms. • Patients showed a specific deficit for rapid flickers but not small details. • They present a dissociation between impaired temporal/preserved spatial resolution. [ABSTRACT FROM AUTHOR]

Dyslexic individuals have been reported to have reduced global motion sensitivity, which could be attributed to various causes including atypical magnocellular or dorsal stream function, impaired spatial integration, increased internal noise and/or reduced external noise exclusion. Here, we applied an equivalent noise experimental paradigm alongside a traditional motion-coherence task to determine what limits global motion processing in dyslexia. We also presented static analogues of the motion tasks (orientation tasks) to investigate whether perceptual differences in dyslexia were restricted to motion processing. We compared the performance of 48 dyslexic and 48 typically developing children aged 8 to 14 years in these tasks and used equivalent noise modelling to estimate levels of internal noise (the precision associated with estimating each element's direction/orientation) and sampling (the effective number of samples integrated to judge the overall direction/orientation). While group differences were subtle, dyslexic children had significantly higher internal noise estimates for motion discrimination, and higher orientation-coherence thresholds, than typical children. Thus, while perceptual differences in dyslexia do not appear to be restricted to motion tasks, motion and orientation processing seem to be affected differently. The pattern of results also differs from that previously reported in autistic children, suggesting perceptual processing differences are condition-specific.

Keywords: Grasping; perception and action; spatial frameworks; parvocellular; magnocellular EN Grasping perception and action spatial frameworks parvocellular magnocellular 109 112 4 09/16/22 20220201 NES 220201 Davida's striking pattern of visual deficits and spared visual abilities presents us with a real challenge of interpretation (Vannuscorps et al., [8]). Others simply move their finger and thumb directly to edges of the object, a strategy that Davida appears to adopt when showing how she would grasp the line (see movie S6 in supplementary movies). In the absence of haptic feedback, Davida would have had to rely more heavily on I visual i feedback about the position of her fingers with respect to the ends of the target line to compute an error signal for updating her subsequent grasps. [Extracted from the article]

Abstract Aim Fear conditioning tests are intended to elucidate a subject's ability to associate a conditioned stimulus with an aversive, unconditioned stimulus, such as footshock. Among these tests, a paradigm related to precise cortical functions would be increasingly important in drug screening for disorders such as schizophrenia and dementia. Therefore, we established a new fear conditioning paradigm using a visual cue in mice. In addition, the validity of the test was evaluated using a genetically engineered mouse, heterozygous deficient in Mdga1 (Mdga1+/‐), which is related to schizophrenia. Results Mice were given footshocks associated with a visual cue of moving gratings at training in 25‐minute sessions. The mice showed the conditioned response of freezing behavior to the visual stimulus at testing 24 hours after the footshocks. In the test for validation, the Mdga1+/‐ deficient mice showed significantly less freezing than wild‐type mice. Conclusion The visually cued fear conditioning paradigm with moving gratings has been established, which is experimentally useful to evaluate animal cortical functions. The validity of the test was confirmed for Mdga1‐deficient mice with possible deficiency in cortical functions.

Classically, hypothalamic neuroendocrine cells that synthesise oxytocin and vasopressin were categorised in two major cell types: the magnocellular and parvocellular neurones. It was assumed that magnocellular neurones project exclusively to the pituitary gland where they release oxytocin and vasopressin into the systemic circulation. The parvocellular neurones, on the other hand, project within the brain to regulate discrete brain circuitries and behaviours. Within the last few years, it has become evident that the classical view of these projections is outdated. It is now clear that oxytocin and vasopressin in the brain are released extrasynaptically from dendrites and from varicosities in distant axons. The peptides act principally to modulate information transfer through conventional synapses (such as glutamate synapses) by actions at respective receptors that may be preferentially localised to synaptic regions (on either side of the synapse) to alter the 'gain' of conventional synapses. [ABSTRACT FROM AUTHOR]

Summary: How abnormal visual experiences early in life influence human subcortical pathways is poorly understood. Using high-resolution fMRI and pathway-selective visual stimuli, we investigate the influence of amblyopia on response properties and the effective connectivity of subcortical visual pathways of the adult human brain. Compared to the normal and fellow eyes, stimuli presented to the amblyopic eye show selectively reduced response in the parvocellular layers of the lateral geniculate nucleus and weaker effective connectivity to V1. Compared to the normal eye, the response of the amblyopic eye to chromatic stimulus decreases in the superficial layers of the superior colliculus, while response of the fellow eye robustly increases in the deep SC with stronger connectivity from the visual cortex. Therefore, amblyopia leads to selective parvocellular alterations of the geniculostriate and corticotectal pathways. These findings provide the neural basis for amblyopic deficits in visual acuity, ocular motor control, and attention.

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. [ABSTRACT FROM AUTHOR]

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.

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.

Michael F Wesner,1 James Brazeau2 1Psychology Department, Lakehead University, Thunder Bay, Ontario P7B 5E1, Canada; 2Center for Pediatric Excellence, Ottawa, ON K2G 1W2, CanadaCorrespondence: Michael F WesnerPsychology Department, Lakehead University, 955 Oliver Road, Thunder Bay, Ontario P7B 5E1, CanadaTel +1-807-768-0564Email michael.wesner@lakeheadu.caIntroduction: Although conscious, image-forming illusions have been noted in migraine, few studies have specifically sought to collectively evaluate the role of all three parallel visual processing streams in the retinogeniculostriate pathway involved with image-forming vision and their implications in the development of migraine symptoms.Methods: We psychophysically assessed the functionality of the inferred magnocellular (MC), parvocellular (PC), and koniocellular (KC) streams at different hierarchical loci across three clinical groups: individuals who experience migraine with aura (MA; n=13), experience migraine without aura (MWO; n=14), and Controls (n=15). Participants completed four experiments: Experiment 1 designed to assess retinal short-wavelength-sensitive (S-) cone sensitivities; Experiment 2 intended to measure postretinal temporal and spatiochromatic contrast sensitivities; Experiment 3 intended to assess postretinal spatiotemporal achromatic contrast sensitivities; and Experiment 4 designed to measure thalamocortical color discriminations along the three cone-excitation axes.Results: S-cone deficits were revealed with greater retinal areas being affected in MA compared to MWO participants. Findings across the four experiments suggest a prominent retinal locus of dysfunction in MA (lesser in MWO) with potential feedforward compensations occurring within the KC visual stream.Conclusion: Complex, integrative network compensations need to be factored in when considering the dysregulating influences of migraine along the visual pathway.Keywords: migraine, S-cones, koniocellular, parvocellular, magnocellular, spatiochromatic

Objectives As we age, the functional field of view (FFOV) declines and these declines predict falls and motor vehicle accidents in older adults (Owsley, C. (2013). Visual processing speed. Vision Research , 90, 52–56. doi:10.1016/j.visres.2012.11.014). To increase understanding of possible causes of this decline, the current study explored whether the FFOV in older adults is associated with the sensitivity of the magnocellular and parvocellular sub-cortical pathways. Method Forty-four younger (M = 27.18, SD = 5.40 years) and 44 older (M = 72.18, SD = 5.82 years) adults completed an FFOV test and the steady- and pulsed-pedestal paradigms of Pokorny and Smith (Pokorny, J. & Smith, V. C. (1997). Psychophysical signatures associated with magnocellular and parvocellular pathway contrast gain. Journal of the Optical Society of America. A, Optics, Image Science, and Vision , 14, 2477–2486. doi:10.1364/josaa.14.002477) as measures of magnocellular and parvocellular pathways, respectively. Results Older adults made more FFOV errors and had higher contrast discrimination thresholds in both the steady- and pulsed-pedestal paradigms, than younger adults. FFOV errors in the younger group were not related to contrast discrimination thresholds. In multiple regression, older group FFOV errors showed a strong unique association with contrast discrimination thresholds mediated via the magnocellular, but not the parvocellular pathway. Discussion We infer that reduced magnocellular pathway contrast sensitivity may contribute to reduced functional vision in older adults. [ABSTRACT FROM AUTHOR]

Background: Severe alcohol use disorder (SAUD) is associated with widespread cognitive impairments, including low‐level visual processing deficits that persist after prolonged abstinence. However, the extent and characteristics of these visual deficits remain largely undetermined, impeding the identification of their underlying mechanisms and influence on higher‐order processing. In particular, little work has been conducted to assess the integrity of the magnocellular (MC) and parvocellular (PC) visual pathways, namely the 2 main visual streams that convey information from the retina up to striate, extrastriate, and dorsal/ventral cerebral regions. Methods: We investigated achromatic luminance contrast processing mediated by inferred MC and PC pathways in 33 patients with SAUD and 32 matched healthy controls using 2 psychophysical pedestal contrast discrimination tasks that promote responses of inferred MC or PC pathways. We relied on a staircase procedure to assess participants' ability to detect small changes in luminance within an array of 4 gray squares that were either continuously presented (steady pedestal, MC‐biased) or briefly flashed (pulsed pedestal, PC‐biased). Results: We replicated the expected pattern of MC and PC contrast responses in healthy controls. We found preserved dissociation of MC and PC contrast signatures in SAUD but higher MC‐mediated mean contrast discrimination thresholds combined with a steeper PC‐mediated contrast discrimination slope compared with healthy controls. Conclusion: These findings indicate altered MC‐mediated contrast sensitivity and PC‐mediated contrast gain, confirming the presence of early sensory disturbances in individuals with SAUD. Such low‐level deficits, while usually overlooked, might influence higher‐order abilities (e.g., memory, executive functions) in SAUD by disturbing the "coarse‐to‐fine" tuning of the visual system, which relies on the distinct functional properties of MC and PC pathways and ensures proper and efficient monitoring of the environment. [ABSTRACT FROM AUTHOR]

Previous studies showed that the lateral masking of a fast-moving low spatial frequency (SF) target was strong when exerted by static flankers of lower or equal to the target SF and absent when flankers' SF was higher than the target's one. These masking and unmasking effects have been interpreted as due to Magnocellular-Magnocellular (M-M) inhibition and Parvocellular-on-Magnocellular (P-M) disinhibitory coactivation, respectively. Based on the hypothesis that the balance between the two systems is perturbed in Developmental Dyslexia (DD), we asked whether dyslexic children (DDs) behaved differently than Typically Developing children (TDs) in conditions of lateral masking. DDs and TDs performed a motion discrimination task, of a .5c/deg Gabor target moving at 16 deg/sec, either isolated or flanked by static Gabors with a SF of .125, .5 or 2 c/deg (Experiment 1). As a control, they also performed a contrast detection task of a static target, either isolated or flanked (Experiment 2). DDs did not perform any different from TDs with either a static target or an isolated moving target of low spatial frequency, thus suggesting efficient feedforward Magnocellular (M) and Parvocellular (P) processing. Also, DDs showed similar contrast thresholds to TDs in the M-M inhibition condition. Conversely, DDs did not recover from lateral masking in the M-P coactivation condition. In addition, their performance in this condition negatively correlated with non-words accuracy, supporting the suggestion that an inefficient Magno-Parvo coactivation may possibly be associated to both higher visual suppression and reduced perceptual stability during reading. [ABSTRACT FROM AUTHOR]

BackgroundIndividuals 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 the M channel, while VCS for near threshold chromatic (red/green) stimuli is governed by the P channel.MethodsVCS 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 off antipsychotic medication), 22 individuals diagnosed with schizotypal personality disorder and 53 healthy comparison subjects.ResultsSchizophrenia 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.ConclusionsThese 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.

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.

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.

Several neurodevelopmental disorders (NDDs) including Developmental Dyslexia (DD), Autism Spectrum Disorder (ASD), but not Attention Deficit Hyperactive Disorder (ADHD), are reported to show deficits in global motion processing. Such behavioral deficits have been linked to a temporal processing deficiency. However, to date, there have been few studies assessing the temporal processing efficiency of the Magnocellular M pathways through temporal modulation. Hence, we measured achromatic flicker fusion thresholds at high and low contrast in nonselective samples of NDDs and neurotypicals (mean age 10, range 7–12 years, n = 71) individually, and group matched, for both chronological age and nonverbal intelligence. Autistic tendencies were also measured using the Autism-Spectrum Quotient questionnaire as high AQ scores have previously been associated with the greater physiological amplitude of M-generated nonlinearities. The NDD participants presented with singular or comorbid combinations of DD, ASD, and ADHD. The results showed that ASD and DD, including those with comorbid ADHD, demonstrated significantly lower flicker fusion thresholds (FFTs) than their matched controls. Participants with a singular diagnosis of ADHD did not differ from controls in the FFTs. Overall, the entire NDD plus control populations showed a significant negative correlation between FFT and AQ scores (r = −0.269, p < 0.02 n = 71). In conclusion, this study presents evidence showing that a temporally inefficient M pathway could be the unifying network at fault across the NDDs and particularly in ASD and DD diagnoses, but not in singular diagnosis of ADHD.

Schizophrenia (Sz) is associated with deficits in fluent reading ability that compromise functional outcomes. Here, we utilize a combined eye-tracking, neurophysiological, and computational modeling approach to analyze underlying visual and oculomotor processes. Subjects included 26 Sz patients (SzP) and 26 healthy controls. Eye-tracking and electroencephalography data were acquired continuously during the reading of passages from the Gray Oral Reading Tests reading battery, permitting between-group evaluation of both oculomotor activity and fixation-related potentials (FRP). Schizophrenia patients showed a marked increase in time required per word (d = 1.3, P <.0001), reflecting both a moderate increase in fixation duration (d =.7, P =.026) and a large increase in the total saccade number (d = 1.6, P <.0001). Simulation models that incorporated alterations in both lower-level visual and oculomotor function as well as higher-level lexical processing performed better than models that assumed either deficit-type alone. In neurophysiological analyses, amplitude of the fixation-related P1 potential (P1f) was significantly reduced in SzP (d =.66, P =.013), reflecting reduced phase reset of ongoing theta-alpha band activity (d =.74, P =.019). In turn, P1f deficits significantly predicted increased saccade number both across groups (P =.017) and within SzP alone (P =.042). Computational and neurophysiological methods provide increasingly important approaches for investigating sensory contributions to impaired cognition during naturalistic processing in Sz. Here, we demonstrate deficits in reading rate that reflect both sensory/oculomotor- and semantic-level impairments and that manifest, respectively, as alterations in saccade number and fixation duration. Impaired P1f generation reflects impaired fixation-related reset of ongoing brain rhythms and suggests inefficient information processing within the early visual system as a basis for oculomotor dyscontrol during fluent reading in Sz. [ABSTRACT FROM AUTHOR]

Aim: Fear conditioning tests are intended to elucidate a subject's ability to associate a conditioned stimulus with an aversive, unconditioned stimulus, such as footshock. Among these tests, a paradigm related to precise cortical functions would be increasingly important in drug screening for disorders such as schizophrenia and dementia. Therefore, we established a new fear conditioning paradigm using a visual cue in mice. In addition, the validity of the test was evaluated using a genetically engineered mouse, heterozygous deficient in Mdga1 (Mdga1+/‐), which is related to schizophrenia. Results: Mice were given footshocks associated with a visual cue of moving gratings at training in 25‐minute sessions. The mice showed the conditioned response of freezing behavior to the visual stimulus at testing 24 hours after the footshocks. In the test for validation, the Mdga1+/‐ deficient mice showed significantly less freezing than wild‐type mice. Conclusion: The visually cued fear conditioning paradigm with moving gratings has been established, which is experimentally useful to evaluate animal cortical functions. The validity of the test was confirmed for Mdga1‐deficient mice with possible deficiency in cortical functions. [ABSTRACT FROM AUTHOR]

Two main subcortical pathways serving conscious visual perception are the midget-parvocellular (P), and the parasol-magnocellular (M) pathways. It is generally accepted that the P pathway serves red-green color vision, but the relative contribution of P and M pathways to spatial vision is a long-standing and unresolved issue. Here, we mapped the spatial sampling properties of P and M pathways across the human retina. Data were obtained from immunolabeled vertical sections of six postmortem male and female human donor retinas and imaged using high-resolution microscopy. Cone photoreceptors, OFF-midget bipolar cells (P pathway), OFF-diffuse bipolar (DB) types DB3a and DB3b (M pathway), and ganglion cells were counted along the temporal horizontal meridian, taking foveal spatial distortions (postreceptoral displacements) into account. We found that the density of OFF-midget bipolar and OFF-midget ganglion cells can support one-to-one connections to 1.05-mm (3.6°) eccentricity. One-to-one connections of cones to OFF-midget bipolar cells are present to at least 10-mm (35°) eccentricity. The OFF-midget ganglion cell array acuity is well-matched to photopic spatial acuity measures throughout the central 35°, but the OFF-parasol array acuity is well below photopic spatial acuity, supporting the view that the P pathway underlies high-acuity spatial vision. Outside the fovea, array acuity of both OFF-midget and OFF-DB cells exceeds psychophysical measures of photopic spatial acuity. We conclude that parasol and midget pathway bipolar cells deliver high-acuity spatial signals to the inner plexiform layer, but outside the fovea, this spatial resolution is lost at the level of ganglion cells. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Several neurodevelopmental disorders (NDDs) including Developmental Dyslexia (DD), Autism Spectrum Disorder (ASD), but not Attention Deficit Hyperactive Disorder (ADHD), are reported to show deficits in global motion processing. Such behavioral deficits have been linked to a temporal processing deficiency. However, to date, there have been few studies assessing the temporal processing efficiency of the Magnocellular M pathways through temporal modulation. Hence, we measured achromatic flicker fusion thresholds at high and low contrast in nonselective samples of NDDs and neurotypicals (mean age 10, range 7–12 years, n = 71) individually, and group matched, for both chronological age and nonverbal intelligence. Autistic tendencies were also measured using the Autism-Spectrum Quotient questionnaire as high AQ scores have previously been associated with the greater physiological amplitude of M-generated nonlinearities. The NDD participants presented with singular or comorbid combinations of DD, ASD, and ADHD. The results showed that ASD and DD, including those with comorbid ADHD, demonstrated significantly lower flicker fusion thresholds (FFTs) than their matched controls. Participants with a singular diagnosis of ADHD did not differ from controls in the FFTs. Overall, the entire NDD plus control populations showed a significant negative correlation between FFT and AQ scores (r = −0.269, p < 0.02 n = 71). In conclusion, this study presents evidence showing that a temporally inefficient M pathway could be the unifying network at fault across the NDDs and particularly in ASD and DD diagnoses, but not in singular diagnosis of ADHD. [ABSTRACT FROM AUTHOR]

Visual object recognition appears to be effortless and virtually instantaneous for humans. A number of previous investigations have suggested that visual perception follows a coarse‐to‐fine processing sequence in which low‐spatial‐frequency (LSF) information provides a coarse representation of an object for an initial guess and guides the fine processing of the object based on high‐spatial‐frequency (HSF) information. A category‐level visual search of real‐world scenes shares many aspects of processing mechanisms with object recognition. However, a key difference between them is the target template in visual search that is generally known in advance. In the present study, we investigated the role of spatial frequency information in the category‐level visual search of real‐world scenes with three behavioral experiments. In Experiment 1, we showed that the representation of the target template, which is held in short‐term memory, had biased attention more towards LSF information than HSF information in the probe trials. In Experiments 2 and 3, we further demonstrated that the near‐threshold LSF information could implicitly facilitate object recognition compared with HSF information, thereby providing supporting evidence that the LSF information of the target template implicitly facilitates target recognition and search performance. These findings support the role of the coarse‐to‐fine principle in rapid visual search performance of real‐world scenes. [ABSTRACT FROM AUTHOR]

Evidence suggests a link between deficits in visuo-spatial attention, and subsequent reading ability. However, all the research in the area thus far has been conducted using traditional, lab-based psychophysics, with very tightly controlled visual parameters. In order to take this research further, such as using visuo-spatial tasks for remediation purposes, it must be established that such tasks can be taken out of the laboratory, 'gamified', and still predict reading ability. This study aimed to determine if subtle visual deficits in poor readers could be detected outside a traditional laboratory, in relatively uncontrolled settings using portable game-like technology. Classic visual search and change detection programs, thought to rely on the visual dorsal stream, were modified to a game-like format. They were administered on a portable computer tablet within the participants' school setting. Whilst IQ predicted reading rate, visuo-spatial tasks such as visual search speed, and change detection, each accounted for unique variance in reading rate over and above IQ, age and phonological ability. These results are consistent with the visuo–spatial attention deficit hypothesis, and provide support for the development of portable computerised games that may assess and potentially target this deficit in poor readers. • Magnocellular-dorsal tasks were converted to child-friendly games. • These 'games' predicted reading ability in an unselected sample of children. • Games accounted for unique variance in reading, over IQ, age and phonological ability. • Results strongly support the use of games for assessing dorsal/magnocellular deficits in dyslexia. [ABSTRACT FROM AUTHOR]

Some people doubt that the concept of developmental dyslexia (DD) is useful at all because the phonological weaknesses seen in DD cannot be distinguished from those found in every person with poor reading skills, whatever their cause. Here I argue that true DD is characterised by poor temporal processing, hence impaired visual and auditory sequencing, that is caused by impaired development of transient/magnocellular (M-) systems throughout the brain. These deficits can be measured in order to distinguish the causes of the phonological weaknesses in DD from those causing similar deficits in other types of poor reading. Importantly this knowledge can be exploited to develop effective improvements in treatment. The evidence for impaired visual magnocellular function in many, if not all, people with dyslexia is now overwhelming; it is supported not only by psychophysical tests of M- function, but also by electrophysiological, eye movement, attentional, imaging, interventional and genetic findings. Analogously, auditory temporal processing is mediated by auditory transient, 'magnocellular', processing systems, and evidence is accumulating persuasively that this system is also impaired in dyslexics. I briefly introduce the idea that 'motor magnocellular systems' may also be impaired in dyslexia, then consider genetic, immunological and nutritional factors that interact to cause the impaired magnocellular phenotype. I then discuss why the dyslexic phenotype is so common by speculating about what strengths it might confer that would maintain the responsible genes in the human genome. • The phonological deficit in developmental dyslexia is due to poor visual sequencing of the letters and poor auditory sequencing of the letter sounds in words. • These deficiencies result from impaired development of CNS timing systems which are mediated by large 'magnocellular' neurones throughout the brain. • The evidence is now overwhelming that people with dyslexia have impaired development of magnocellular neurons. • This abnormality has a genetic, immunological and nutritional basis. • This new understanding is enabling greatly improved diagnosis and remediation. [ABSTRACT FROM AUTHOR]

Electroretinograms (ERGs) elicited by high temporal frequency (26-95 Hz) L- and M-cone isolating sine-wave stimuli were investigated in human observers for full-field (FF) and different spatially restricted stimulus sizes (70°, 50°, 30°, and 10° diameter). Responses to L- and M-cone isolating FF stimuli were maximal around 48 Hz and decreased gradually with increasing temporal frequency up to 95 Hz. The response maximum was shifted to about 30-32 Hz for both L- and M-cone driven responses obtained with spatially restricted stimuli. The M-cone driven responses could only be measured up to 54 Hz with 70° stimuli. The response amplitudes for L- and M-cones and L-/M-cone amplitude ratios decreased with decreasing stimulus size. The ERG response phases to L- and M-cone isolating stimuli decreased with increasing temporal frequency and were about -160° apart for all stimulus sizes up to 34 Hz. Further increase in the temporal frequency displayed a positive correlation between stimulus size and L-M phase difference. The ERG data indicate that the responses evoked by high temporal frequency cone isolating stimuli reflect two mechanisms, one that is more centrally located and displays a maximum at about 30-32 Hz and a peripheral mechanism that is sensitive to higher temporal modulations. We propose that the peripheral mechanism (FF ERGs) reflects magnocellular activity, whereas the central mechanism (ERGs with spatially restricted stimuli) is based on a parvocellular activity up to about 30 Hz. [ABSTRACT FROM AUTHOR]

The magnocellular deficit theory of dyslexia suggests a selective impairment in contrast detection of stimuli involving pure magnocellular response (e.g. Gabor patches of 0.5 c/deg, 30 Hz, low contrast). An alternative hypothesis is that, dyslexia may be associated with a reduction of typical facilitation that normal readers present for stimuli relying on low-level magno-parvo co-activation, relative to stimuli eliciting pure magno activation. According to this hypothesis, any advantage in contrast sensitivity, produced by either decreasing stimuli temporal frequency (from 30 to 10 Hz, Experiment 1) or using static stimuli of increasing spatial frequency (from 0.5 to 4 c/deg, Experiment 2), would be ascribed to the coexisting responses of the magnocellular and parvocellular systems. In the control group, this advantage in contrast sensitivity was found for a 0.5 c/deg Gabor (either static or flickering at 10 Hz) and for a static Gabor of 4 c/deg. In contrast to magnocellular deficit theory predictions, dyslexic individuals showed no deficit in the unmixed magnocellular response. However, they showed no advantage when the relative weight between magnocellular and parvocellular inputs was thrown off balance in favor of the latter. These results suggest that in order to interpret low-level visual deficits in dyslexia, it is worth considering that fast, feedforward low-frequency representations of spatial structures may result from the coexisting responses of two systems. Our results suggest that in dyslexia, the relative contribution of these two systems in visual processing is perturbed, and that this may have detrimental consequences in word processing, both within the parafovea and the fovea during fixation. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Abstract Patients with schizophrenia often show impairments in visual information processing that have been linked to abnormal magnocellular or dorsal stream functioning. However, such deficits are not consistently reported, possibly due to the broad symptomology inherent to schizophrenia, and/or medication effects. To avoid these latter issues this study employed visual perceptual tasks targeting magnocellular (flicker-defined form contrast threshold), dorsal stream (motion coherence, change detection) and ventral stream (form coherence) processing, and compared performance of groups of high and low sub-clinical schizotypy traits from a neurotypical population (n = 20 per group). Significantly worse performance of high compared with low schizotypy participants was only demonstrated on the change detection task that requires rapid attention acquisition and encoding of the first visual array into short term memory prior to a comparison of a second array presentation. No group differences on the other tasks were established. Given this potentially important effect is apparent in a non-clinical population, there are likely to be implications for understanding visual and attentional abnormalities in the schizophrenia spectrum more broadly. Highlights • The schizophrenia spectrum has been associated with visual processing impairments. • Clinical research can be confounded by heterogeneity and medication effects. • We investigated visual processing in neurotypical adults with high or low schizoptypy traits. • Visual change detection task performance was worse in a neurotypical sample with higher schizotypy traits. [ABSTRACT FROM AUTHOR]

Some individuals with dyslexia demonstrate deficits in reading, visual attention, and visual processing which can be attributed to a functional failure of the magnocells in the visual system or in the dorsal visual pathway. The study examines the role of magno/dorsal function in dyslexic adults compared with normal, illiterate, and semi-literate readers. Coherent motion and coherent form were used in Experiment 1, and the frequency doubling illusion and static-gratings were used in Experiment 2. If a magno/dorsal deficit is demonstrated for dyslexic readers but not illiterate, semi-literate, and normal reading adults, then the deficit cannot be attributed to reading experience. Illiterate adults performed the same as normal and semi-literate readers in coherent motion and frequency doubling tasks, and all three groups performed better than the dyslexic readers. There was no difference between any of the groups in the coherent form or static grating tasks. Together, these studies show that illiterate and semi-literate adults do not demonstrate a magno/dorsal deficit that is a characteristic of some sufferers of dyslexia. Therefore, magno/dorsal deficits in dyslexia are unlikely to be a consequence of failing to learn to read but rather provides evidence to suggest a causal role for reduced visual magno/dorsal processing. [ABSTRACT FROM AUTHOR]