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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 This discrepancy criterion has now been replaced by the claim that the main feature of dyslexia is a phonological deficit, and it is now argued that we should test for this to identify dyslexia.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]

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 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.

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]

As the visual system ages, flicker sensitivity decreases and the latencies of cortical visual evoked potentials (VEP) increase. However, the extent to which these effects reflect age-related changes in the magnocellular (M) and or parvocellular (P) pathways remain unclear. Here, we investigated the relation between flicker fusion frequencies and VEP non-linearities induced by rapid stimulation, as a function of age over 6 decades. The approach, using Wiener kernel analysis of multifocal flash (mf)VEP, allows the extraction of signatures of both M and P processing and hence establishing a neural basis of the known decline in flicker fusion threshold. We predicted that, in a sample of 86 participants, age would be associated with a latency increase in early mfVEP response components and that flicker fusion thresholds, for both low and high contrast stimuli, would relate to the temporal efficiency of the M-generated VEP component amplitudes. As expected, flicker fusion frequency reduced with age, while latencies of early second order peaks of the mfVEP increased with age, but M temporal efficiency (amplitude ratio of first to second order peaks) was not strongly age-related. The steepest increases in latency were associated with the M dominated K2.1 (second order first slice) N70 components recorded at low and high contrast (6.7 and 5.9 ms/decade, respectively). Interestingly, significant age-related latency shifts were not observed in the first order responses. Significant decreases in amplitude were found in multiple first and second order components up to 30 years of age, after which they remained relatively constant. Thus, aging and decline in visual function appears to be most closely related to the response latencies of non-linearities generated by the M pathway.

The rapidity with which the visual system can recover from stimulation in order to respond again has important implications for efficiently processing environmental stimuli in real time. To date, there has been little integration of the human psychophysical and physiological research underlying the neural mechanisms contributing to temporal limits on human visual perception. Hence, we investigated the relationship between achromatic flicker fusion frequency and temporal analysis of the magnocellular (M) and parvocellular (P) contributions to the achromatic non-linear multifocal Visual Evoked Potential (mfVEP) responses recorded from occipital scalp (Oz). It was hypothesized, on the basis of higher temporal cut-off frequencies reported for primate M vs. P neurons, that sinusoidal flicker fusion frequencies would negatively correlate with the amplitude of M- but not P-generated non-linearities of the mfVEP. This hypothesis was borne out in 72 typically developing young adults using a four-way forced choice sinusoidal flicker fusion task: amplitudes of all non-linearities that demonstrated a clear M-generated component correlated negatively with flicker thresholds. The strongest of these correlations were demonstrated by the main M non-linearity component (K2.1N70−P100) for both high contrast (r = −0.415, n = 64, p < 0.0005) and low contrast (r = −0.345 n = 63, p < 0.002) conditions, indicating that higher achromatic flicker fusion threshold is linked to a more efficient (smaller second order kernels) M system. None of the peaks related to P activity showed significant correlations. These results establish flicker thresholds as a functional correlate of M-pathway function as can be observed in the non-linear analysis of mfVEP.

As the visual system ages, flicker sensitivity decreases and the latencies of cortical visual evoked potentials (VEP) increase. However, the extent to which these effects reflect age-related changes in the magnocellular (M) and or parvocellular (P) pathways remain unclear. Here, we investigated the relation between flicker fusion frequencies and VEP non-linearities induced by rapid stimulation, as a function of age over 6 decades. The approach, using Wiener kernel analysis of multifocal flash (mf)VEP, allows the extraction of signatures of both M and P processing and hence establishing a neural basis of the known decline in flicker fusion threshold. We predicted that, in a sample of 86 participants, age would be associated with a latency increase in early mfVEP response components and that flicker fusion thresholds, for both low and high contrast stimuli, would relate to the temporal efficiency of the M-generated VEP component amplitudes. As expected, flicker fusion frequency reduced with age, while latencies of early second order peaks of the mfVEP increased with age, but M temporal efficiency (amplitude ratio of first to second order peaks) was not strongly age-related. The steepest increases in latency were associated with the M dominated K2.1 (second order first slice) N70 components recorded at low and high contrast (6.7 and 5.9 ms/decade, respectively). Interestingly, significant age-related latency shifts were not observed in the first order responses. Significant decreases in amplitude were found in multiple first and second order components up to 30 years of age, after which they remained relatively constant. Thus, aging and decline in visual function appears to be most closely related to the response latencies of non-linearities generated by the M pathway. [ABSTRACT FROM AUTHOR]

The rapidity with which the visual system can recover from stimulation in order to respond again has important implications for efficiently processing environmental stimuli in real time. To date, there has been little integration of the human psychophysical and physiological research underlying the neural mechanisms contributing to temporal limits on human visual perception. Hence, we investigated the relationship between achromatic flicker fusion frequency and temporal analysis of the magnocellular (M) and parvocellular (P) contributions to the achromatic non-linear multifocal Visual Evoked Potential (mfVEP) responses recorded from occipital scalp (Oz). It was hypothesized, on the basis of higher temporal cut-off frequencies reported for primate M vs. P neurons, that sinusoidal flicker fusion frequencies would negatively correlate with the amplitude of M- but not P-generated non-linearities of the mfVEP. This hypothesis was borne out in 72 typically developing young adults using a four-way forced choice sinusoidal flicker fusion task: amplitudes of all non-linearities that demonstrated a clear M-generated component correlated negatively with flicker thresholds. The strongest of these correlations were demonstrated by the main M non-linearity component (K2.1N70-P100) for both high contrast (r = -0.415, n = 64, p < 0.0005) and low contrast (r = -0.345 n = 63, p < 0.002) conditions, indicating that higher achromatic flicker fusion threshold is linked to a more efficient (smaller second order kernels) M system. None of the peaks related to P activity showed significant correlations. These results establish flicker thresholds as a functional correlate of M-pathway function as can be observed in the non-linear analysis of mfVEP. [ABSTRACT FROM AUTHOR]

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.

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. [ABSTRACT FROM AUTHOR]

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.

The arginine-vasopressin (AVP)-containing hypothalamic magnocellular neurosecretory neurons (VPMNNs) are known for their role in hydro-electrolytic balance control via their projections to the 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 receptor mRNAs were not detected, using the same method. Water-deprivation (WD) for 24 h, which increased the metabolic activity of VPMNNs, also increased anxiety-like behavior measured using the elevated plus maze (EPM) test, and this effect was mimicked by bilateral microinfusion of AVP into the CeA. Anxious behavior induced by either WD or AVP infusion was reversed by CeA infusion of V1a antagonist. VPMNNs are thus a newly discovered source of CeA inhibitory circuit modulation, through which both early-life and adult stress coping signals are conveyed from the hypothalamus to the amygdala. [ABSTRACT FROM AUTHOR]

In addition to its core social deficits, autism is characterised by altered visual perception, with a preference for local percept in those high in autistic tendency. Here, the balance of global versus 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, or to differences in the deployment of attention between the two groups.

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 (SF) designed to test functioning of the parvo- vs. 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. [ABSTRACT FROM AUTHOR]

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) versus 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. Methods: VCS for luminance and chromatic stimuli (counterphase-reversing sinusoidal gratings, 1.22 c/deg, 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. 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.

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 towards 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, fifteen patients with schizophrenia and eleven 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.

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.