Visual backward masking in schizophrenia]

Visual backward masking is used to investigate the function of attention as the initial stage of visual information processing by measuring the shortest stimulus presentation time for accurate cognition. This is achieved by applying a masking stimulus after target stimulus presentation. In this study, 50 controls and 50 schizophrenics (paranoid type) were examined by this method. In the control group, 1) there was a significant decline in correct answers to the target stimulus with age; and 2) there was a significant increase in correct answers with repetition. However, in the schizophrenic group, 1) there was a significantly lower number of correct answers in all age groups compared to that in the controls, along with a greater decline in correct answers with age; and 2) there was no increase in correct answers with repetition; 3) good performers among the schizophrenic patients were young with a short duration of illness and on a low dose of medication. Poor performers showed numerous positive and negative psychotic symptoms, were not on medication, or had positive findings on CTscan; furthermore, 4) longitudinal re-examination of the same subjects showed that even when psychotic symptoms improved and the subjects were able to return to society, their ability to give correct answers remained significantly different compared to that of the controls. These findings seem to reflect the trait-dependence aspect of schizophrenia (paranoid type) on a visual backward masking task. Furthermore, visual backward masking seems to be a convenient and useful measure for this aspect of attention and its trait-dependence in schizophrenia.     

Stability of visual masking performance in recent-onset schizophrenia: an 18-month longitudinal study

Visual masking deficit in schizophrenia has been suggested to be a potential vulnerability marker for schizophrenia. An important characteristic of a vulnerability marker is stability over time, but relatively little is known about the longitudinal course of masking performance of schizophrenia patients. In this study, we examined the stability of visual masking performance in recent-onset schizophrenia patients over an 18-month period. We administered both forward and backward masking trials with multiple stimulus onset asynchronies for four masking conditions at three time points (baseline, 6-month, and 18-month). Recent-onset schizophrenia patients showed stable masking performance for both forward and backward conditions over a period of 18 months. Furthermore, the stable performance was observed across all four masking conditions. The findings of this study provide further support for the view that visual masking deficits reflect a possible vulnerability marker for schizophrenia.     

Visual masking in schizophrenia: overview and theoretical implications

Visual masking provides several key advantages for exploring the earliest stages of visual processing in schizophrenia: it allows for control over timing at the millisecond level, there are several well-supported theories of the underlying neurobiology of visual masking, and it is amenable to examination by electroencephalogram (EEG) and functional magnetic resonance imaging (fMRI). In this paper, we provide an overview of the visual masking impairment schizophrenia, including the relevant theoretical mechanisms for masking impairment. We will discuss its relationship to clinical symptoms, antipsychotic medications, diagnostic specificity, and presence in at-risk populations. As part of this overview, we will cover the neural correlates of visual masking based on recent findings from EEG and fMRI. Finally, we will suggest a possible mechanism that could explain the patterns of masking findings and other visual processing findings in schizophrenia.     

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.     

Modulation of attention during visual masking in schizophrenia

OBJECTIVE: Schizophrenia patients consistently demonstrate performance deficits on visual masking procedures. The present study examined whether attentional manipulation would improve subjects' performance on visual masking. METHOD: A metacontrast task was administered to 105 schizophrenia patients and 52 healthy comparison subjects. Attention was manipulated by associating selected trials of the task with monetary reward. RESULTS: Schizophrenia patients exhibited poorer performance than the comparison subjects across conditions. Patients demonstrated modest, but statistically significant, improvement in performance with the attentional manipulation. This improvement was not significant for the comparison subjects. CONCLUSIONS: These findings suggest that early visual processes in schizophrenia are responsive to attentional manipulation but that the degree of improvement is relatively small, suggesting that these processes are not easily altered.     

Spatiotemporal visual processing in schizophrenia

Studies examining visual processing in schizophrenia have provided inconsistent results. In this study, the authors measured static and dynamic visual contrast sensitivity (CS) in patients with schizophrenia (n=20) and control subjects (n=15). Extrapyramidal symptoms were evaluated with the Simpson-Angus scale. In the static condition, the patients with schizophrenia showed reduced CS in the spatial frequency range of 2.9-14.4 cycles per degree of visual angle (c/d). In the dynamic condition, CS loss was present over the whole range tested (0.5-14.4 c/d). Higher Simpson-Angus scores and higher doses of antipsychotic medication were associated with more severe CS deficits. These results suggest that the hypodopaminergic state induced by antipsychotic medication may produce parkinsonian visual impairments in schizophrenia patients.     

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 time course of visual backward masking deficits in schizophrenia

Schizophrenia, it has been hypothesized, is linked to a deficiency in the magnocellular portion of the visual system. Abnormal backward masking has been invoked as support for this hypothesis. The rationale for linking backward masking to the magnocellular system is the hypothesis that fast responses in the magnocellular systems catches up with, and then inhibits slower responses in the parvocellular system. However, the latency difference between the magno- and parvocellular systems is at most 20 ms. Magnocellular abnormalities as a result would be expected to manifest themselves only at relatively short stimulus onset asynchronies (SOAs) or interstimulus intervals (ISIs). The present study examines this implication. It is found that a substantial number of investigations have uncovered abnormal masking at SOAs or ISIs of 300 ms or larger, and some even at ISIs as large as 700 ms. It is difficult to reconcile abnormalities at these SOAs and ISIs with magno-parvocellular latency differences of 20 ms or less. It is concluded that the abnormal masking does not support the existence of a magnocellular deficiency in schizophrenia.     

Backward masking, information processing, and schizophrenia

Many researchers have used backward masking to examine information-processing speed in schizophrenic subjects. The validity of this approach rests upon two main assumptions. One is that the mask effectively limits the time a previously presented stimulus is available for processing. The other is that the components of the masking mechanism in schizophrenic subjects are comparable to those in control groups. It is argued that the masking procedures used in these studies fail to meet either assumption. Alternative interpretations of these investigations, however, suggest important hypotheses for further research in our quest to understand information-processing deficits associated with schizophrenia.     

Global-local visual processing in schizophrenia: evidence for an early visual processing deficit.

BACKGROUND: Abnormalities in early-stage visual processing might contribute to observed higher neurocognitive deficits in schizophrenia, but to date no clear link has been established. Schizophrenia has been associated with deficits in the magnocellular visual pathway, suggesting a relative bias for processing elemental (local) as opposed to configural (global) aspects of a hierarchical stimulus; however, global-local paradigm studies in schizophrenia have yielded mixed results. METHODS: In the current study, global-local and event-related potential (ERP) procedures were concomitantly used to assess temporal and spatial characteristics of hierarchical visual stimulus processing abnormalities. RESULTS: Patients (n = 24) had slower and less accurate responses to global stimuli than a healthy comparison group (n = 29). They exhibited a marked decrement in N150 ERP amplitude, which correlated with speed of response to global stimuli. They also failed to show an augmented P300 response to local stimuli. CONCLUSIONS: Behavioral and physiological data are consistent and support a global visual processing deficit in schizophrenia. This is manifest at a relatively early stage of visual processing and might relate to physiological disturbances in areas V3/V3a of the extrastriate cortex.     

Early-stage visual processing deficits in schizophrenia

PURPOSE OF REVIEW: While cognitive dysfunction including memory and attentional deficits are well known in schizophrenia, recent work has also shown basic sensory processing deficits. Deficits are particularly prominent in the visual system and may be related to cognitive deficits and outcome. This article reviews studies of early-stage visual processing in schizophrenia published during the past year. These studies reflect the growing interest and importance of sensory processing deficits in schizophrenia. RECENT FINDINGS: The visual system is divided into magnocellular and parvocellular pathways which project to dorsal and ventral visual areas. Recent electrophysiological and behavioral investigations have found preferential magnocellular/dorsal stream dysfunction, with some deficits in parvocellular function as well. These early-stage deficits appear to be related to higher level cognitive, social, and community function. Structural studies of occipital cortex and particularly optic radiations provide anatomical support for early visual processing dysfunction. SUMMARY: These findings highlight the importance of sensory processing deficits, in addition to higher cognitive dysfunction, for understanding the pathophysiology of schizophrenia. Understanding the nature of sensory processing deficits may provide insight into mechanisms of pathology in schizophrenia, such as N-methyl-D-aspartate dysfunction or impaired signal amplification, and could lead to treatment strategies including sensory processing rehabilitation that may improve outcome.     

Revisiting the backward masking deficit in schizophrenia: individual differences in performance and modeling with transcranial magnetic stimulation.

BACKGROUND: Deficits in backward masking have been variably reported in schizophrenia patients, but individual differences in the expression of these deficits have not been explicitly investigated. In addition, increased knowledge of the visual system has opened the door for new techniques such as transcranial magnetic stimulation (TMS) to explore these deficits physiologically. METHODS: Patients with schizophrenia and healthy controls were tested using a backward masking paradigm. In order to examine the functionality of visual pathways involved in backward masking, subjects were retested on a backward masking paradigm using single pulse TMS applied to occipital cortex in lieu of the masking stimuli. RESULTS: Compared with controls, patients had significantly delayed recovery from visual backward masking. However, 23.5% of patients (compared to 5% of controls) never recovered to levels approaching unmasked performance. When these subjects were segregated from the analysis, group differences vanished. In addition, stimulus masking with occipital TMS followed the same pattern in both patients and controls. CONCLUSIONS: Observations of individual differences in visual masking performance may identify a subgroup of schizophrenia patients. The TMS data suggest that this deficit may not localize to the occipital cortex. However, TMS can be a useful tool for localizing processing deficits in schizophrenia.     

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.     

Dysfunction of early-stage visual processing in schizophrenia: harmonic analysis

Schizophrenia is associated with severe neurocognitive deficits that constitute a core feature of the disorder. Deficits have been most extensively studied in relationship to higher-order processes. This study evaluated the integrity of early visual processing in order to evaluate the overall pattern of visual dysfunction in schizophrenia. Steady-state visual-evoked potentials (ssVEPs) were recorded over the occipital cortex (Oz) in patients with schizophrenia and schizoaffective disorder (N=26) and in age-matched comparison volunteers (N=22). Two stimuli were used: windmill-dartboard and partial-windmill, which are contrast-reversing ( approximately 4 Hz), radial patterns with dominant low spatial-frequency content. Each stimulus was presented for 1 min. Fourier analysis was performed on the ssVEP data to extract the relevant temporal frequency (i.e., harmonic) components. Magnitude-squared coherence (MSC) was computed to estimate the relative signal level for each frequency component. The patients showed reduced amplitude and coherence of second harmonic responses in both conditions, but intact first harmonic responses in the windmill-dartboard condition. This finding of a differential deficit may indicate a significant loss in the magnocellular pathway, which contributes to the generation of the second harmonic component under these conditions. Early sensory deficits may lead to impairments in subsequent stages of processing.     

Thalamic-insular dysconnectivity in schizophrenia: evidence from structural equation modeling

Structural and functional studies have shown that schizophrenia is often associated with frontolimbic abnormalities in the prefrontal and mediotemporal regions. It is still unclear, however, if such dysfunctional interaction extends as well to relay regions such as the thalamus and the anterior insula. Here, we measured gray matter volumes of five right-hemisphere regions in 68 patients with schizophrenia and 77 matched healthy subjects. The regions were amygdala, thalamus, and entorhinal cortex (identified as anomalous by prior studies on the same population) and dorsolateral prefrontal cortex and anterior insula (isolated by voxel-based morphometry analysis). We used structural equation modeling and found altered path coefficients connecting the thalamus to the anterior insula, the amygdala to the DLPFC, and the entorhinal cortex to the DLPFC. In particular, patients exhibited a stronger thalamus-insular connection than healthy controls. Instead, controls showed positive entorhinal-DLPFC and negative amygdalar-DLPFC connections, both of which were absent in the clinical population. Our data provide evidence that schizophrenia is characterized by an impaired right-hemisphere network, in which intrahemispheric communication involving relay structures may play a major role in sustaining the pathophysiology of the disease.     

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.     

Attentional modulation of early-stage visual processing in schizophrenia

This study shows that paying attention to the color of a visual stimulus is manifested by an early endogenous scalp-positive event-related brain potential (ERP) component, referred to as "selection positivity", that emerges within the first 100 ms after stimulus onset in healthy observers. In contrast, recently ill and chronically ill schizophrenia patients as well as patients at high risk for schizophrenia all failed to show this early ERP component while attending to color. These results suggest that a relatively early stage of visual-selective processing in posterior extrastriate cortex is disrupted in schizophrenia.     

Social perception and early visual processing in schizophrenia

Persons with schizophrenia experience deficits in social cognition-the cognitive processes involved in how people perceive and interpret information about themselves, others, and social situations. These deficits may be related to the neurocognitive impairments often experienced by persons with schizophrenia. Our primary objective was to examine associations between social perception and early visual processing in schizophrenia. Our secondary objective was to examine whether outpatients with schizophrenia and healthy persons differ in social perception. Forty outpatients with schizophrenia and 30 healthy persons completed a measure of social perception (the Half-Profile of Nonverbal Sensitivity), visual masking procedures, and ratings of positive and negative symptoms. Within patients, performance on visual masking procedures was related to performance on the Half-Profile of Nonverbal Sensitivity. Patients with schizophrenia and the healthy persons differed significantly in their performance on the Half-Profile of Nonverbal Sensitivity, but this difference became nonsignificant when education was a covariate. These findings suggest that social perception in schizophrenia is related to very early aspects of visual processing.     

精神分裂症视觉加工障碍的研究进展

视觉损伤是精神分裂症的重要特征之一,几乎所有视觉处理领域都存在缺陷,研究最多的包括对比敏感度、空间频率处理、视觉掩蔽、运动知觉及知觉组织等.这些视觉加工障碍具有潜在的临床意义,早期视觉处理的缺陷会导致更高层次的认知障碍.目前对精神分裂症视觉加工障碍的研究相对较少.现将对精神分裂症视觉加工相关的心理、物理学和神经影像学研...     

Reading impairment and visual processing deficits in schizophrenia

Individuals with schizophrenia show magnocellular visual pathway abnormalities similar to those described in dyslexia, predicting that reading disturbance should be a common concomitant of schizophrenia. To date, however, reading deficits have not been well established, and, in fact, reading is often thought to be normal in schizophrenia based upon results of tests such as the WRAT, which evaluate single word reading. This study evaluated "real world" reading ability in schizophrenia, relative to functioning of the magnocellular visual pathway. Standardized psychoeducational reading tests and contrast sensitivity measures were administered to 19 patients and 10 controls. Analyses of between group differences were further refined by classification of participants into reading vs. non-reading impaired groups using a priori and derived theoretical models. Patients with schizophrenia, as a group, showed highly significant impairments in reading (p<0.04-p<0.001), with particular deficits on tests of rate, comprehension and phonological awareness. Between 21% and 63% of patients met criteria for dyslexia depending upon diagnostic model vs. 0-20% of the controls. The degree of deficit correlated significantly with independent measures of magnocellular dysfunction. Reading impairment in schizophrenia reaches the level of dyslexia and is associated with compromised magnocellular processing as hypothesized. Findings related to symptoms, functioning and recommendations for reading ability assessment are discussed.