Visual processing in schizophrenia: Structural equation modeling of visual masking performance

Schizophrenic patients consistently demonstrate performance deficits on visual masking procedures. In visual masking, the subject's ability to process a target stimulus is reduced by another stimulus (mask) presented either before (forward masking) or after (backward masking) the target. Masking procedures employed in schizophrenia research have used several experimental paradigms. Most early studies have used high-energy masks (i.e., the mask is stronger than the target) and spatially overlapping target and mask. More recently, studies have begun to employ relatively weak (i.e., low-energy) masks, as well as masks that surround, but do not spatially overlap, the target. Data for forward and backward masking components of four masking conditions (target location and identification with a high-energy mask, target identification with a low-energy mask, and target identification with equal energy paracontrast/metacontrast) were collected from 75 patients with schizophrenia. Based on theoretical distinctions among masking procedures, we compared four models of visual masking using structural equation modeling. Although high zero-order correlations were found among the masking parameters, a four-factor model, in which factors were separated on the type of response (target location and identification), the shape of the function (monotonic and non-monotonic), and the overlap of the stimuli (overlapping and non-overlapping), provided the best fit for the data. These findings suggest that the four masking procedures used in this study may tap unique aspects of visual processing and are not redundant. The results also support theories of the different mechanisms underlying performance on these measures.     

How does the hippocampal formation mediate memory for stimuli processed by the magnocellular and parvocellular visual pathways? Evidence from the comparison of schizophrenia and amnestic mild cognitive impairment (aMCI)

Paired associates learning is impaired in both schizophrenia and amnestic mild cognitive impairment (aMCI), which may reflect hippocampal pathology. In addition, schizophrenia is characterized by the dysfunction of the retino-geniculo-striatal magnocellular (M) visual pathway. The purpose of this study was to investigate the interaction between visual perceptual and memory dysfunctions. We administered a modified version of the CANTAB paired associates learning task to patients with schizophrenia (n=20), aMCI (n=20), and two groups of matched healthy controls (n=20 for each patient group). The stimuli in the paired associates learning task biased information processing toward the M pathways (low contrast, low spatial frequency) and parvocellular (P) pathways (high contrast, high spatial frequency). Results revealed that patients with schizophrenia exhibited a more pronounced learning deficit for M-biased relative to P-biased stimuli. In aMCI, there were similar memory deficits for both types of stimuli. Orientation discrimination for M- and P-biased stimuli was intact in both groups of patients. The number of errors in the M-biased memory condition significantly and inversely correlated with the volume of the right hippocampus in schizophrenia. These results suggest an interaction between M-biased perceptual processing and short-term relational memory in schizophrenia, which may be associated with the structural alteration of the right hippocampus.     

Backward masking in unmedicated schizophrenic patients in psychotic remission: possible reflection of aberrant cortical oscillation.

OBJECTIVE: Patients with schizophrenia consistently show performance deficits on measures of visual backward masking, but the nature of these deficits is not well understood. Performance deficits on backward masking tasks may indicate an underlying predisposition instead of the presence of illness, because deficits are present in unaffected first-degree relatives. Performance deficits in remitted patients would constitute converging support for this hypothesis. METHOD: Eleven patients with recent-onset schizophrenia who were in a period of no medication use during remission of psychosis were compared with a matched normal group on three visual masking conditions. These conditions included target identification tasks with a high-energy mask, a low-energy mask, and a blurred target. RESULTS: Patients in psychotic remission showed significant deficits across all conditions. In addition, trend analyses revealed significant group differences in the shape of the masking functions: the comparison group showed an oscillating performance pattern across all masking conditions, whereas the patients did not exhibit this pattern on any condition. CONCLUSIONS: These data from patients in well-documented psychotic remission add converging support for the hypothesis that deficits on backward masking procedures are indicators of vulnerability to schizophrenia. Because visual masking procedures may reflect underlying neural oscillations of 30 to 70 Hz in the visual cortex, the pattern of results is consistent with the theory that visual masking deficits in schizophrenia stem from an underlying failure to establish cortical oscillations.     

Visual backward-masking deficits in schizophrenia: relationship to visual pathway function and symptomatology

Patients with schizophrenia have information processing deficits which can be measured using visual backward-masking (VBM) tasks. There are two types of visual pathways: transient and sustained. The former is more sensitive to low spatial frequency (LSF) and the latter to high spatial frequency (HSF) stimuli. It has been hypothesized that the VBM deficit in schizophrenia is due to an overactive transient channel response to the mask. To examine this hypothesis, patients with schizophrenia and comparison volunteers were tested on a traditional backward-masking task as well as on tasks that altered the mask to bias stimulation toward transient (LSF) or sustained (HSF) channels. Medication effects and relationship to symptomatology were also examined. Patients with schizophrenia showed a significant deficit on the traditional backward-masking task and were also significantly impaired on the LSF- and HSF-masking tasks, though a differential deficit was not found on the latter two tasks. A U-shaped function, indicative of masking by interruption, was found on the LSF- and HSF-masking tasks. Masking performance was not altered when the same patients were tested on and off medication, and performance was related to positive and negative symptoms. In conclusion, the finding of a deficit in patients with schizophrenia on tasks producing a U-shaped function suggests that an aberrant transient response to the mask is producing increased interruption of the sustained response to the target.     

Feature similarity and laterality effects in visual masking

Observers attempted to recognize single letters presented to the left or right visual field when preceded or followed by a masking stimulus. When the masking stimulus contained features identical to those of the target letter, there was a left visual field (right hemisphere) advantage for target recognition. When the target and mask contained extremely different features, the opposite visual field advantage was obtained. Implications are discussed for models of hemispheric asymmetry and for interpreting visual laterality studies that use masks to reduce the overall level of performance.     

Dysfunction of early-stage visual processing in schizophrenia.

OBJECTIVE: Schizophrenia is associated with deficits in higher-order processing of visual information. This study evaluated the integrity of early visual processing in order to evaluate the overall pattern of visual dysfunction in schizophrenia. METHOD: Steady-state visual-evoked potential responses were recorded over the occipital cortex in patients with schizophrenia and in age- and sex-matched comparison volunteers. Visual-evoked potentials were obtained for stimuli composed of isolated squares that were modulated sinusoidally in luminance contrast, number of squares, or chromatic contrast in order to emphasize magnocellular or parvocellular visual pathway activity. RESULTS: Responses of patients to magnocellular-biased stimuli were significantly lower than those of comparison volunteers. These lower response levels were observed in conditions using both low luminance contrast and large squares that biased processing toward the magnocellular pathway. In contrast, responses to stimuli that biased processing toward the parvocellular pathway were not significantly different between schizophrenia patients and comparison volunteers. A significant interaction of group and stimulus type was observed in the condition using low luminance contrast. CONCLUSIONS: These findings suggest a dysfunction of lower-level visual pathways, which was more prominent for magnocellular than parvocellular biased stimuli. The magnocellular pathway helps in orienting toward salient stimuli. A magnocellular pathway deficit could contribute to higher-level visual cognitive deficits in schizophrenia.     

New results in the experimental psychopathology of visual dysfunctions in schizophrenia

New theories of schizophrenia put a special emphasis on cognitive deficits, including executive functions, attention, verbal memory, and psychomotor speed. Dysfunctions of low level visual processing are less known. In this paper, the author summarizes recent results from two new tasks and integrates them with the relevant literature of schizophrenia. First, the relationship between the precortical magno (M) and parvocellular (P) pathways was investigated with a new contrast categorization task assessing low level perception, memory, and abstraction. Patients with schizophrenia showed a generalized dysfunction, which suggests contrast-independent memory and abstraction problems. In contrast, siblings were selectively impaired on the task variant that included the 10-15% contrast range, the transition zone between M and P pathway contrast sensitivity. In a second paradigm, the author investigated intrinsic lateral connectivity in the primary visual cortex, the main target of M and P pathways. Using Gabor patches, a reduced facilitation effect of collinear flankers was demonstrated in schizophrenia, which suggests impaired lateral connections in the primary visual cortex. These results are closely related to backward masking and smooth pursuit eye movement abnormalities. As a neurobiological basis of these phenomena, N-methyl-D-aspartate (NMDA) glutamate receptors and integrated synaptic networks may be of special relevance.     

Paracontrast and metacontrast in schizophrenia: clarifying the mechanism for visual masking deficits

Schizophrenic patients consistently demonstrate performance deficits on visual masking procedures. Visual masking can occur through two distinctly different mechanisms: interruption and integration. One highly effective way to limit the masking mechanism to interruption is to use a mask that surrounds, but does not spatially overlap, the target. These procedures are called paracontrast and metacontrast (for forward and backward masking, respectively). Despite their clear advantages for interpretation, paracontrast and metacontrast have not been used previously in schizophrenia. In the present study, we examined the reliability of the paracontrast and metacontrast procedures by administering these tasks to 103 schizophrenic patients and 49 normal control subjects. In addition, we compared the results to those from a low-energy masking condition, which is an alternative way to limit masking to interruption. Patients showed deficits on both the paracontrast and metacontrast procedures. The deficits in paracontrast and metacontrast were comparable to those seen previously with low-energy masking. These results suggest that the paracontrast/metacontrast procedure and the procedure using a low-energy mask are roughly equally sensitive to deficits in early visual processing among schizophrenic patients. These results bolster previous conclusions that schizophrenic patients show deficits on visual masking tasks even when masking on those tasks occurs entirely through the interruption mechanism.     

Visual information decoding deficits in schizophrenia.

Schizophrenic and control subjects were tested on two-flash fusion (TFF) and visual backward masking (VBM) tasks in a repeated measures design. Each subject was tested in a single session. Both tasks used the same equipment and stimuli. There was no difference between the groups in their ability to detect the presence of two separate stimuli in the TFF task. Schizophrenic subjects did require longer interstimulus intervals (ISI) than control subjects to accurately report one of the two targets in the VBM task. Analysis of individual targets reveals that the VBM deficit is a function of the similarity of the target and mask. The more feature detail discrimination necessary, the longer an ISI is required in VBM. The data are interpreted as supporting the conclusion that since the groups did not differ in their performance of the TFF task, which would also have been affected by a sensory abnormality, the deficit in VBM must be explained by reference to a higher level of information processing. The VBM deficit is a failure to decode the target stimulus, and is not simply a function of abnormalities due to an overactive transient channel system.     

Impairments in generation of early-stage transient visual evoked potentials to magno- and parvocellular-selective stimuli in schizophrenia.

OBJECTIVE: Patients with schizophrenia demonstrate significant impairments of early visual processing, potentially implicating dysfunction of the magnocellular visual pathway. The present study evaluates transient visual evoked potential (tVEP) responses to stimuli biased toward the magnocellular (M) or parvocellular (P) systems in patients with schizophrenia vs. normal volunteers first to evaluate relative contributions of M and P systems to specific tVEP components in schizophrenia and, second, to evaluate integrity of early M and P processing in schizophrenia. METHODS: Seventy-four patients with schizophrenia and schizoaffective disorder were compared with 59 control subjects using separate stimuli to assess the tVEP response to M, P and mixed M/P conditions. Stimuli were biased toward M vs. P processing by manipulation of chromatic and achromatic contrast. C1, P1, N1 and P2 components were compared between patients and controls. All subjects showed 20/32 vision or better. RESULTS: Waveforms were obtained to low contrast (M), chromatic contrast (P) and high contrast (mixed M/P) stimuli in both patients and controls. C1 was present to P and mixed M/P stimuli. Patients showed a significant reduction in amplitude and an increase in latency of the C1 component. P1 was elicited primarily by M and mixed M/P stimuli, whereas N1 was elicited primarily by P and mixed M/P stimuli. Patients showed reductions in both P1 and N1 amplitudes across conditions. However, only reductions in P1 amplitude survived covariation for between group differences in visual acuity. Further, P1 amplitude reductions in the M condition correlated with a proxy measure of global outcome. CONCLUSIONS: M- and P-selective stimuli elicit differential components of the tVEP. Patients with schizophrenia show significant reductions in response even to simple visual stimuli. Deficits, particularly within the M system, may correlate significantly with global outcome and level of community functioning. SIGNIFICANCE: Whereas deficits in high-order cognitive processing have been extensively documented in schizophrenia, integrity of early-stage sensory processing has been studied to a lesser degree. The present findings suggest that deficits in early-stage visual processing are significantly related to overall clinical outcome in schizophrenia. Further, between-group differences in visual acuity may influence VEP results, even for subjects with 'normal' vision (20/32 or better).     

Early visual information processing in schizophrenia compared to recurrent depression

Patients with schizophrenia have repeatedly shown deficits in early visual processing using backward masking (VBM) tasks. Whether this represents a specific dysfunction in schizophrenia is an unsolved question. Patients with recurrent unipolar depression represent an interesting comparison group to examine the question of specificity, but have never previously been assessed on VBM. In addition to comparing VBM performance in patients with schizophrenia and patients with depression, we wanted to examine the relations between VBM and clinical symptoms. Fifty-one patients with schizophrenia were compared to 49 patients with recurrent unipolar depression and 47 healthy controls. All subjects were administered a two-digit identification task in a no-masking and four masking conditions. Patients with schizophrenia performed significantly worse than normal controls on four of the five conditions. No significant difference was found between depression patients and normal controls. The effect of masking stimuli had no differential effects on the three groups. VBM correlated strongly with positive symptoms in the schizophrenia group.     

Exploring the short term visual store in schizophrenia using the attentional blink

Schizophrenia patients exhibit numerous deficits on visual processing tasks, ranging from very early stages of visual processing (e.g., backward masking) to the later working memory stages (e.g., delayed match-to-sample, N-back). However, little is known about deficits in an intermediate stage of visual information processing, namely short term visual memory (STVM). The attentional blink (AB) paradigm is considered to be a valid way to assess the STVM, and recent studies have reported AB deficits in schizophrenia. However, it is not clear whether the reported AB deficit in schizophrenia patients is due to their increased susceptibility to backward masking or increased vulnerability in the STVM. In this study we first found poorer performance in the AB task in 37 schizophrenia patients compared to 26 normal controls. To examine the effects of increasing and decreasing mask strength on AB performance in patients and controls, we next systematically varied the masking effect by varying the length of the distracters immediately following the targets. The manipulation had relatively little effect on the patient--control differences and patients continued to show an enhanced AB effect across conditions. The findings suggest that the enhanced AB effect in schizophrenia reflects an abnormality in their short term visual memory, as opposed to their enhanced susceptibility to visual masking.     

Dichoptic visual masking reveals that early binocular neurons exhibit weak interocular suppression: implications for binocular vision and visual awareness

Visual masking effects are illusions in which a target is rendered invisible by a mask, which can either overlap or not overlap the target spatially and/or temporally. These illusions provide a powerful tool to study visibility and consciousness, object grouping, brightness perception, and much more. As such, the physiological mechanisms underlying the perception of masking are critically important to our understanding of visibility. Several models that require cortical circuits have been proposed previously to explain the mysterious spatial and timing effects associated with visual masking. Here we describe single-unit physiological experiments from the awake monkey that show that visual masking occurs in at least two separate and independent circuits, one that is binocular and one that is monocular (possibly even subcortical), without feedback from higher-level visual brain areas. These and other results together fail to support models of masking that require circuits found only in the cortex, but support our proposed model that suggests that simple ubiquitous lateral inhibition may itself be the fundamental mechanism that explains visual masking across multiple levels in the brain. We also show that area V1 neurons are dichoptic in terms of excitation, but monoptic in terms of inhibition. That is, responses within area V1 binocular neurons reveal that excitation to monocular targets is inhibited strongly only by masks presented to the same eye, and not by masks presented to the opposite eye. These results lead us to redefine the model for the first stage of binocular processing in the visual system, and may be crucial to interpreting the effects of other similar binocular and dichoptic stimulation paradigms, such as the binocular rivalry family of illusions.     

Early-stage visual processing and cortical amplification deficits in schizophrenia

BACKGROUND: Patients with schizophrenia show deficits in early-stage visual processing, potentially reflecting dysfunction of the magnocellular visual pathway. The magnocellular system operates normally in a nonlinear amplification mode mediated by glutamatergic (N-methyl-D-aspartate) receptors. Investigating magnocellular dysfunction in schizophrenia therefore permits evaluation of underlying etiologic hypotheses. OBJECTIVES: To evaluate magnocellular dysfunction in schizophrenia, relative to known neurochemical and neuroanatomical substrates, and to examine relationships between electrophysiological and behavioral measures of visual pathway dysfunction and relationships with higher cognitive deficits. DESIGN, SETTING, AND PARTICIPANTS: Between-group study at an inpatient state psychiatric hospital and outpatient county psychiatric facilities. Thirty-three patients met DSM-IV criteria for schizophrenia or schizoaffective disorder, and 21 nonpsychiatric volunteers of similar ages composed the control group. MAIN OUTCOME MEASURES: (1) Magnocellular and parvocellular evoked potentials, analyzed using nonlinear (Michaelis-Menten) and linear contrast gain approaches; (2) behavioral contrast sensitivity measures; (3) white matter integrity; (4) visual and nonvisual neuropsychological measures, and (5) clinical symptom and community functioning measures. RESULTS: Patients generated evoked potentials that were significantly reduced in response to magnocellular-biased, but not parvocellular-biased, stimuli (P = .001). Michaelis-Menten analyses demonstrated reduced contrast gain of the magnocellular system (P = .001). Patients showed decreased contrast sensitivity to magnocellular-biased stimuli (P<.001). Evoked potential deficits were significantly related to decreased white matter integrity in the optic radiations (P<.03). Evoked potential deficits predicted impaired contrast sensitivity (P = .002), which was in turn related to deficits in complex visual processing (P< or =.04). Both evoked potential (P< or =.04) and contrast sensitivity (P = .01) measures significantly predicted community functioning. CONCLUSIONS: These findings confirm the existence of early-stage visual processing dysfunction in schizophrenia and provide the first evidence that such deficits are due to decreased nonlinear signal amplification, consistent with glutamatergic theories. Neuroimaging studies support the hypothesis of dysfunction within low-level visual pathways involving thalamocortical radiations. Deficits in early-stage visual processing significantly predict higher cognitive deficits.     

Neural substrates of visual masking by object substitution in schizophrenia

Despite a well‐known behavioral finding of visual backward masking impairment in schizophrenia, its underlying neural mechanism remains obscure. This study examined neural correlates of a distinct type of visual backward masking, object substitution masking (OSM), in schizophrenia. Twenty schizophrenia patients and 26 healthy controls completed a 4‐Dot OSM task and three functional localizer tasks for the lateral occipital (LO), human motion‐sensitive (hMT+), and retinotopic areas in the scanner. In 4‐dot masking, subjects detected a target that was followed by a mask consisting of 4 dots that surrounded a target. Stimulus‐onset asynchrony (SOA) between target and mask was varied to examine the modulation of masking: (1) within three visual processing areas regions of interest (ROI) (i.e., ROI analysis) and (2) in brain regions outside the three visual processing areas (i.e., whole brain analysis). In the ROI analyses, LO and retinotopic areas showed increased peak amplitude when SOA become longer in both patients and controls. There was also an effect of ROI in that both groups showed higher activation in LO and hMT+ compared with the retinotopic areas. The whole brain analyses revealed a significantly activated area for longer SOAs vs. a short SOA in the occipital cortex in controls only, but the group contrast was not significant. Overall, this study did not find strong evidence for neural abnormalities of OSM in schizophrenia, suggesting that neural substrates of OSM in schizophrenia are not as compromised as those involved in the more common masking methods that rely on disruption of object formation. Hum Brain Mapp 35:4654–4662, 2014. © 2014 Wiley Periodicals, Inc .     

The magnocellular visual system and schizophrenia: what can the color red tell us?

Previous research has suggested that genetic loading for schizophrenia is related to a dysfunctional magnocellular (M) subcortical visual pathway-responsible for processing movement and location. However, data substantiating this mechanism remains inconclusive. The present study used a novel technique to selectively suppress the M system in order to investigate the impact of genetic loading for schizophrenia on its functioning. A visual backward masking task was administered to 28 healthy first-degree relatives of persons with schizophrenia and 31 healthy controls. The task was administered on both a red and neutral background, as diffuse red light has been shown to selectively suppress the M system in basic vision research. On a location condition of backward masking, controls demonstrated reduced accuracy on the red compared to the neutral background. In contrast, relatives did not display differential performance between the two backgrounds. The differential effect on the two groups appears to be attributable to a difference in activity of the M pathway. Performance in the relatives was consistent with the notion of a hyperactive M pathway.     

Relationship of extinction to perceptual thresholds for single stimuli

OBJECTIVE: To demonstrate the effects of target stimulus intensity on extinction to double simultaneous stimuli. BACKGROUND: Attentional deficits contribute to extinction in patients with brain lesions, but extinction (i.e., masking) can also be produced in healthy subjects. The relationship of extinction to perceptual thresholds for single stimuli remains uncertain. METHODS: Brief electrical pulses were applied simultaneously to the left and right index fingers of 16 healthy volunteers (8 young and 8 elderly adults) and 4 patients with right brain stroke (RBS). The stimulus to be perceived (i.e., target stimulus) was given at the lowest perceptual threshold to perceive any single stimulus (i.e., Minimal) and at the threshold to perceive 100% of single stimuli. The mask stimulus (i.e., stimulus given to block the target) was applied to the contralateral hand at intensities just below discomfort. RESULTS: Extinction was less for target stimuli at 100% than Minimal threshold for healthy subjects. Extinction of left targets was greater in patients with RBS than elderly control subjects. Left targets were extinguished less than right in healthy subjects. In contrast, the majority of left targets were extinguished in patients with RBS even when right mask intensity was reduced below right 100% threshold for single stimuli. RBS patients had less extinction for right targets despite having greater left mask - threshold difference than control subjects. In patients with RBS, right "targets" at 100% threshold extinguished left "masks" (20%) almost as frequently as left masks extinguished right targets (32%). CONCLUSIONS: Subtle changes in target intensity affect extinction in healthy adults. Asymmetries in mask and target intensities (relative to single-stimulus perceptual thresholds) affect extinction in RBS patients less for left targets but more for right targets as compared with control subjects.     

Development of a computerized assessment for visual masking

Visual masking provides a highly informative means of assessing the earliest stages of visual processing. This procedure is frequently used in psychopathology research, most commonly in the study of schizophrenia. Deficits in visual masking tasks appear to reflect vulnerability factors in schizophrenia, as opposed to the symptoms of the illness. Visual masking procedures are typically conducted on a tachistoscope, which limits standardization across sites, as well as the number of variables that can be examined in a testing session. Although visual masking can be administered on a computer, most methods used so far have had poor temporal resolution and yielded a limited range of variables. We describe the development of a computerized visual masking battery. This battery includes a staircase procedure to establish an individual's threshold for target detection, and a relatively dense sampling of masking intervals. It includes both forward and backward masking trials for three different masking conditions that have been used previously in experimental psychopathology (target location, target identification with high-energy mask, and target identification with low-energy mask).     

The visual backward masking deficit in schizophrenia

1. Subjects with schizophrenia have an impairment very early in visual information processing, requiring a longer minimal stimulus duration than normal controls to identify a target stimulus. Subjects with schizophrenia have a deficit in visual backward masking, identifying fewer target stimuli than normal controls when the target is briefly obscured by a second visual stimulus When interstimulus interval is increased parametrically, subjects with schizophrenia have trouble identifying target stimuli at intervals that do not affect the performance of normal controls. 2. The visual backward masking deficit: is trait-related; is associated with negative symptoms but has also been associated with measures of thought disorder; may or may not be related to treatment with neuroleptic medication or other neurocognitive deficits of schizophrenia; is of unclear etiology, though researchers have speculated that it involves magnocellular channels and/or the cortical dorsal visual processing stream; has been shown to be heritable in one study. 3. If visual information processing deficits are observed in the unaffected siblings of schizophrenic patients, it may be a candidate intermediate phenotype.     

Development of visual perception and attention,assessed by backward masking and application in children with epilepsy

Visual masking assesses visual perception and attention; it occurs when a visual stimulus (mask) interferes with the perception of a stimulus that the participant is trying to identify (target). A backward masking study (target presented before mask) was performed on 662 children without disabilities (338 females), aged between 6 and 17 years, in order to evaluate if performance varies with age. In the masking procedure 10 letters were presented through a tachistoscope as target stimuli. Fragments of letters oriented at random ('noise') represented the mask. A slight improvement of visual performance from the beginning of school age to 9-12 years of age was found. This paper gives normative data for the most important parameters which can be used as a standardized reference for the procedure employed. We also studied 113 children with epilepsy (56 females), aged between 5 and 19 years, who attended a mainstream school and had been seizure free for at least 2 years. Children were tested just before starting antiepileptic drug withdrawal and re-tested 1 year later; they were drug free for 3 months before the second test. These children showed, during and after treatment, only slightly worse results when compared with healthy children of the same age; after therapy withdrawal, their visual performance slightly improved but this was not statistically significant.