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.     

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.     

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.     

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.     

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.     

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.     

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.     

Differentiation and prediction in schizophrenia using the metacontrast technique

A perceptgenetic, projective test procedure, the metacontrast technique, was performed in a series of 66 young schizophrenics at admission in a psychiatric institution. The test responses to tachistoscopic expositions of stimulus pairs with incongruent or threatening contents are classified in terms of defense strategies representative of neurotic and psychotic states. The sample tested was followed up clinically after 14-17 years. At inception the series of subjects was dichotomized into one nonregressive (latent, pseudoneurotic, n = 42) group and one regressive, with full-blown psychotic symptoms (n = 24). The distribution of response types did not differentiate between the groups; neurotic and psychotic patterns were represented in both. At follow-up, the initial presence of signs of repression was significantly more common in such initially nonregressive patients as had escaped a later psychotic breakdown. A compound expression of test signs, hypothesized to be a predictor of future development, was shown to differentiate also between categories of outcome in terms of clinical picture and working capacity.     

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 .     

Ketamine-induced deficits in auditory and visual context-dependent processing in healthy volunteers: implications for models of cognitive deficits in schizophrenia

BACKGROUND: In patients with schizophrenia, deficient generation of mismatch negativity (MMN)-an event-related potential (ERP) indexing auditory sensory ("echoic") memory-and a selective increase of "context dependent" ("BX") errors in the "A-X" version of the Continuous Performance Test (AX-CPT) indicate an impaired ability to form and use transient memory traces. Animal and human studies implicate deficient N-methyl-D-aspartate receptor (NMDAR) functioning in such abnormalities. In this study, effects of the NMDAR antagonists ketamine on MMN generation and AX-CPT performance were investigated in healthy volunteers to test the hypothesis that NMDARs are critically involved in human MMN generation, and to assess the nature of ketamine-induced deficits in AX-CPT performance. METHODS: In a single-blind placebo-controlled study, 20 healthy volunteers underwent an infusion with subanesthetic doses of ketamine. The MMN-to-pitch and MMN-to-duration deviants were obtained while subjects performed an AX-CPT. RESULTS: Ketamine significantly decreased the peak amplitudes of the MMN-to-pitch and MMN-to-duration deviants by 27% and 21%, respectively. It induced performance deficits in the AX-CPT characterized by decreased hit rates and specific increases of errors (BX errors), reflecting a failure to form and use transient memory traces of task relevant information. CONCLUSIONS: The NMDARs are critically involved in human MMN generation. Deficient MMN in schizophrenia thus suggests deficits in NMDAR-related neurotransmission. N-methyl-D-aspartate receptor dysfunction may also contribute to the impairment of patients with schizophrenia in forming and using transient memory traces in more complex tasks, such as the AX-CPT. Thus, NMDAR-related dysfunction may underlie deficits in transient memory at different levels of information processing in schizophrenia. Arch Gen Psychiatry. 2000;57:1139-1147.     

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.     

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 backward masking: deficits in locating targets are specific to schizophrenia and not related to intellectual decline

Visual backward masking deficits have been postulated as potential vulnerability markers for schizophrenia. This study investigated the diagnostic specificity of a location and an identification variant of the backward masking task for schizophrenia and analyzed masking performance during the course of the tasks. The influence of schizophrenia patients' intellectual decline on masking performance was also examined. Twenty-eight schizophrenia patients were compared to 28 patients with unipolar depression and 28 healthy controls on a letter location task and a letter identification task applying a low spatial frequency mask. Schizophrenia patients made significantly more detection errors on the location task than depressives at an interstimulus interval (ISI) of 50 ms and healthy controls at ISIs of 16.7, 33.3, 50, and 66.7 ms. Thus, the location masking dysfunction of schizophrenia patients was distinctive at a rather long interstimulus interval (50 ms). On the identification task the performance of schizophrenia patients did not differ from that of the two control groups. Identification but not location masking performance improved during the course of the task for all groups. Intellectual deterioration of schizophrenia patients was not correlated with location or identification masking performance. Schizophrenia patients are characterized by specific impairments in spatial visual processing which appear to be independent of intellectual decline. Potential explanations of the location masking deficit found in schizophrenia are discussed.     

Auditory masking experiments in schizophrenia

Twelve schizophrenic subjects with acoustic hallucinations in their case histories were compared with 12 healthy reference subjects and eight subjects with panic disorder in a test of three auditory masking tasks, simultaneous masking (SM), forward masking (FM) and backward masking (BM). The schizophrenic subjects showed no differences from reference subjects on SM but had higher thresholds for the two other conditions (FM and BM). Schizophrenics with very increased thresholds (n=6) had a significantly higher need for residential treatment. Thresholds for SM and BM were not, as for reference subjects, related to age for schizophrenics. No statistically significant differences regarding any masking experiments were found between the panic disorder subjects and the reference subjects. Simultaneous masking, reflecting functions of the basilar membrane and those of elementary brainstem processing, showed no signs of dysfunction in schizophrenic subjects. Schizophrenics showed aberrations in FM and BM, possibly influenced by more central (cortical) processes.     

Affective deficits and social deficits in schizophrenia: what's what?

Affective deficits and social deficits have played an important role in theory and research on schizophrenia, and it has generally been assumed that these are two different types of symptoms. The aim of these comments is to argue that the distinction between these symptoms is not straightforward and that the apparent differences between affective and social deficits virtually disappear when current approaches to their definition and measurement are considered. The implications of this point with regard to theory and research on the etiology and treatment of schizophrenia are discussed, and an approach that has the potential to reveal whether specific schizophrenic symptoms are more closely associated with affective deficits or with social deficits is described.     

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.     

Impaired multisensory processing in schizophrenia: deficits in the visual enhancement of speech comprehension under noisy environmental conditions

BACKGROUND: Viewing a speaker's articulatory movements substantially improves a listener's ability to understand spoken words, especially under noisy environmental conditions. In this study we investigated the ability of patients with schizophrenia to integrate visual and auditory speech. Our objective was to determine to what extent they experience benefit from visual articulation and to detail under what listening conditions they might show the greatest impairments. METHODS: We assessed the ability to recognize auditory and audiovisual speech in different levels of noise in 18 patients with schizophrenia and compared their performance with that of 18 healthy volunteers. We used a large set of monosyllabic words as our stimuli in order to more closely approximate performance in everyday situations. RESULTS: Patients with schizophrenia showed deficits in their ability to derive benefit from visual articulatory motion. This impairment was most pronounced at signal-to-noise levels where multisensory gain is known to be maximal in healthy control subjects. A surprising finding was that despite known early auditory sensory processing deficits and reports of impairments in speech processing in schizophrenia, patients' performance in unisensory auditory speech perception remained fully intact. CONCLUSIONS: Thus, the results showed a specific deficit in multisensory speech processing in the absence of any measurable deficit in unisensory speech processing and suggest that sensory integration dysfunction may be an important and, to date, rather overlooked aspect of schizophrenia.