BACKGROUND: 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.
METHODS: 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.
RESULTS: 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).
CONCLUSIONS: 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.

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.

CONCLUSIONS: 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.

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.

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.

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.

When two sufficiently different stimuli are presented to each eye, perception alternates between them. This binocular rivalry is conceived as a competition for representation in the single stream of visual consciousness. The magnocellular (M) and parvocellular (P) pathways, originating in the retina, encode disparate information, but their potentially different contributions to binocular rivalry have not been determined. Here, we used functional magnetic resonance imaging to measure the human lateral geniculate nucleus (LGN), where the M and P neurons are segregated into layers receiving input from a single eye. We had three participants (one male, two females) and used achromatic stimuli to avoid contributions from color opponent neurons that may have confounded previous studies. We observed activity in the eye-specific regions of LGN correlated with perception, with similar magnitudes during rivalry or physical stimuli alternations, also similar in the M and P regions. These results suggest that LGN activity reflects our perceptions during binocular rivalry and is not simply an artifact of color opponency. Further, perception appears to be a global phenomenon in the LGN, not just limited to a single information channel.

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.

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.

Parasol-magnocellular pathway ganglion cells form an important output stream of the primate retina and make a major contribution to visual motion detection. They are known to comprise ON and OFF type response polarities but the relative numbers of ON and OFF parasol cells, and the overall contribution of parasol cells to high-acuity foveal vision are not well understood. Here we use antibodies against carbonic anhydrase 8 (CA8) and intracellular injections of the liphilic dye DiI to show that CA8 selectively labels OFF parasol cells in macaque retina. By combined labeling with CA8 antibodies and a previously-described marker for parasol cells (GABAA receptor antibodies), we show that ON and OFF parasol cells each comprise ∼ 6% of all ganglion cells in central retina (each peak density ∼ 3000 cells/mm2 at 5 deg.), and each population comprises ∼ 10% of all ganglion cells in peripheral temporal retina. Thus, the spatial density of parasol cells in central retina is greater than reported by previous anatomical studies, and the central-peripheral gradient in parasol cell density is shallower than previously reported. The data nevertheless predict decline in spatial acuity with visual field eccentricity for both midget-parvocellular pathway and parasol-magnocellular pathway mediated visual functions. The spatial resolving power of the OFF parasol array (peak ∼ 7 cpd) falls short of macaque behavioral grating acuity by at least a factor of three throughout the retina.