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.     

Sensory Contributions to Impaired Emotion Processing in Schizophrenia

Both emotion and visual processing deficits are documented in schizophrenia, and preferential magnocellular visual pathway dysfunction has been reported in several studies. This study examined the contribution to emotion-processing deficits of magnocellular and parvocellular visual pathway function, based on stimulus properties and shape of contrast response functions. Experiment 1 examined the relationship between contrast sensitivity to magnocellular- and parvocellular-biased stimuli and emotion recognition using the Penn Emotion Recognition (ER-40) and Emotion Differentiation (EMODIFF) tests. Experiment 2 altered the contrast levels of the faces themselves to determine whether emotion detection curves would show a pattern characteristic of magnocellular neurons and whether patients would show a deficit in performance related to early sensory processing stages. Results for experiment 1 showed that patients had impaired emotion processing and a preferential magnocellular deficit on the contrast sensitivity task. Greater deficits in ER-40 and EMODIFF performance correlated with impaired contrast sensitivity to the magnocellular-biased condition, which remained significant for the EMODIFF task even when nonspecific correlations due to group were considered in a step-wise regression. Experiment 2 showed contrast response functions indicative of magnocellular processing for both groups, with patients showing impaired performance. Impaired emotion identification on this task was also correlated with magnocellular-biased visual sensory processing dysfunction. These results provide evidence for a contribution of impaired early-stage visual processing in emotion recognition deficits in schizophrenia and suggest that a bottom-up approach to remediation may be effective.     

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.     

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).     

Face recognition in schizophrenia disorder: A comprehensive review of behavioral,neuroimaging and neurophysiological studies

Facial emotion processing has been extensively studied in schizophrenia patients while general face processing has received less attention. The already published reviews do not address the current scientific literature in a complete manner. Therefore, here we tried to answer some questions that remain to be clarified, particularly: are the non-emotional aspects of facial processing in fact impaired in schizophrenia patients? At the behavioral level, our key conclusions are that visual perception deficit in schizophrenia patients: are not specific to faces; are most often present when the cognitive (e.g. attention) and perceptual demands of the tasks are important; and seems to worsen with the illness chronification. Although, currently evidence suggests impaired second order configural processing, more studies are necessary to determine whether or not holistic processing is impaired in schizophrenia patients. Neural and neurophysiological evidence suggests impaired earlier levels of visual processing, which might involve the deficits in interaction of the magnocellular and parvocellular pathways impacting on further processing. These deficits seem to be present even before the disorder out-set. Although evidence suggests that this deficit may be not specific to faces, further evidence on this question is necessary, in particularly more ecological studies including context and body processing.     

Magnocellular contributions to impaired motion processing in schizophrenia

Patients with schizophrenia show impairments in motion processing, along with deficits in lower level processing primarily involving the magnocellular visual pathway. The present study investigates potential magnocellular contributions to impaired motion processing in schizophrenia using a combined neurophysiological and behavioral approach. As compared to prior motion studies in schizophrenia, thresholds were determined for both incoherent and coherent visual motion. In this study, velocity discrimination thresholds were measured for schizophrenia patients (n=14) and age-matched normal control subjects (n=16) using a staircase procedure. Early visual processing was evaluated using steady-state visual evoked potentials (ssVEP), with stimuli biased toward activation of either the magnocellular or parvocellular visual pathways through luminance contrast manipulation. Patients with schizophrenia showed poor velocity discrimination for both incoherent and coherent motion, with no significant group x task interaction. Further, when coherent motion performance was measured at individually determined incoherent motion thresholds, accuracy levels for patients were similar to controls, also indicating similarity of deficit for incoherent vs. coherent motion discrimination. Impairments in velocity discrimination correlated significantly with reduced amplitude of ssVEP elicited by magnocellular -- but not parvocellular -- selective stimuli. This study demonstrates that deficits in motion processing in schizophrenia are significantly related to reduced activation of the magnocellular visual system. Further, this study supports and extends prior reports of impaired motion processing in schizophrenia, and indicates significant bottom-up contributions to higher-order cognitive impairments.     

A new dimension of sensory dysfunction: stereopsis deficits in schizophrenia.

BACKGROUND: Schizophrenia is a neurocognitive disorder with a wide range of cognitive and sensory impairments. Early visual processing has been shown to be especially impaired. This article investigates the integrity of binocular depth perception (stereopsis) in schizophrenia. METHODS: Seventeen schizophrenia patients and 19 healthy control subjects were compared on the Graded Circles Stereo Test. Results of stereoacuity were compared between patients and control subjects using t test. RESULTS: Schizophrenia patients demonstrated significantly (p = .006) reduced stereoacuity (mean = 142 arcseconds) versus control subjects (mean = 55 arcseconds). At the normative level for adults, patients performed below chance. CONCLUSIONS: These findings demonstrate an impairment of binocular depth perception and further confirm deficits of early visual processing in schizophrenia. Findings are discussed in context of magnocellular/dorsal stream processing with implications for visual processing and cognitive deficits.     

Early visual processing deficits in schizophrenia: impaired P1 generation revealed by high-density electrical mapping.

Integrity of early visual sensory processing in schizophrenia was assessed using the well characterized P1 and N1 components of the visual evoked potential (VEP) as our dependent measures. VEPs were recorded in response to successively less fragmented line drawings of common objects. P1 amplitudes were significantly reduced across all stimulus conditions for patients versus controls. Further, this decrement was relatively greater at parieto-occipital than occipito-temporal electrode sites. No differences in N1 amplitude were found. The finding of P1 deficits in patients, particularly over dorsal scalp, supports the view that schizophrenia is associated with impairment of early dorsal visual stream processing. On the other hand, the finding of normal N1 amplitudes in patients suggests that early stages of ventral stream processing may be relatively more intact. These results imply that the cognitive impairment seen in schizophrenia is not just due to deficits in higher order aspects of cognition but also encompasses significant deficits in early sensory processing.     

Stereologic analysis of the lateral geniculate nucleus of the thalamus in normal and schizophrenic subjects

Reduction of volume and neuronal number has been found in several association nuclei of the thalamus in schizophrenic subjects. Recent evidence suggests that schizophrenic patients exhibit abnormalities in early visual processing and that many of the observed perceptual deficits are consistent with dysfunction of the magnocellular pathway, i.e. the visual relay from peripheral retinal cells to the two ventrally located magnocellular layers of the lateral geniculate nucleus (LGN). The present study was undertaken to determine whether abnormalities in cell number and volume of the LGN are associated with schizophrenia and whether the structural alterations are restricted to either the magnocellular or parvocellular subdivisions of the LGN. Series of Nissl-stained sections spanning the LGN were obtained from 15 schizophrenic and 15 normal control subjects. The optical disector/fractionator sampling method was used to estimate total neuronal number, total glial number and volume of the magnocellular and parvocellular subdivisions of the LGN. Cell number and volume of the LGN in schizophrenic subjects were not abnormal. Volume of both parvocellular and magnocellular layers of the LGN decreased with age. These findings do not support the hypothesis that early visual processing deficits in schizophrenic subjects are due to reduction of neuronal number in the LGN.     

Abnormal neurological signs, visual contrast sensitivity, and the deficit syndrome of schizophrenia

This study was designed to investigate the relationship between abnormal neurological signs, visual contrast sensitivity, and the deficit syndrome of schizophrenia. Visual contrast sensitivity for counterphase-modulated low spatial frequency gratings was measured in 32 non-deficit and 12 deficit schizophrenia patients and 20 healthy controls subjects. Abnormal neurological signs were evaluated with the Neurological Evaluation Scale (NES). Compared with the controls, patients with schizophrenia displayed impaired visual contrast sensitivity, which was associated with sensory integration deficits, as measured with the NES. The deficit syndrome was predicted by negative symptoms and sensory integration deficits. These results suggest that early-stage perceptual dysfunctions, which may reflect the abnormality of precortical magnocellular visual pathways, are related to a specific group of abnormal neurological signs.     

Impaired visual object recognition and dorsal/ventral stream interaction in schizophrenia

BACKGROUND: Schizophrenia is associated with well-documented deficits in high-order cognitive processes such as attention and executive functioning. The integrity of sensory-level processing, however, has been evaluated only to a limited degree. Our study evaluated the ability of patients with schizophrenia to recognize complete objects based on fragmentary information, a process termed perceptual closure. Perceptual closure processes are indexed by closure negativity (N(cl)), a recently defined event-related potential (ERP) component that is generated within the visual association cortex. This study assessed the neural integrity of perceptual closure processes in schizophrenia by examining N(cl) generation. Generation of the preceding positive (P1) and negative (N1) ERP components was also examined. METHODS: We evaluated 16 patients with chronic schizophrenia and 16 healthy comparison subjects. Successively less fragmented images were presented during high-density ERP recording, which permitted the monitoring of brain activity during perceptual closure processes prior to object recognition. Analyses were performed at parieto-occipital and occipitotemporal sites consistent with dorsal and ventral stream generators of P1, N1, and N(cl). RESULTS: Patients with schizophrenia showed significant impairment in the ability to recognize fragmented objects, along with impaired generation of N(cl). The amplitude of visual P1 was significantly reduced, particularly over dorsal stream sites. In contrast, the generation of visual N1 was intact. CONCLUSIONS: Patients with schizophrenia are profoundly impaired in perceptual closure as indicated by both impaired performance and impaired N(cl) generation. The selective impairment in dorsal stream P1 is consistent with prior reports of impaired magnocellular processing in schizophrenia. By contrast, intact ventral N1 generation suggests that the initial stages of ventral stream processing are relatively preserved and that impaired magnocellular dorsal stream functioning in schizophrenia may lead to secondary dysregulation of ventral stream object recognition processing.     

Dissecting the cellular contributions to early visual sensory processing deficits in schizophrenia using the VESPA evoked response

Electrophysiological research has shown clear dysfunction of early visual processing mechanisms in patients with schizophrenia. In particular, the P1 component of the visual evoked potential (VEP) is substantially reduced in amplitude in patients. A novel visual evoked response known as the VESPA (Visual Evoked Spread Spectrum Analysis) was recently described. This response has a notably different scalp topography from that of the traditional VEP, suggesting preferential activation of a distinct subpopulation of cells. As such, this method constitutes a potentially useful candidate for investigating cellular contributions to early visual processing deficits. In this paper we compare the VEP and VESPA responses between a group of healthy control subjects and a group of schizophrenia patients. We also introduce an extension of the VESPA method to incorporate nonlinear processing in the visual system. A significantly reduced P1 component was found in patients using the VEP (with a large effect size; Cohen's d=1.6), while there was no difference whatsoever in amplitude between groups for either the linear or nonlinear VESPA. This pattern of results points to a highly specific cellular substrate of early visual processing deficits in schizophrenia, suggesting that these deficits are based on dysfunction of magnocellular pathways with parvocellular processing remaining largely intact.     

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.     

A few remarks on attention and magnocellular deficits in schizophrenia

In connection with schizophrenia, it has been proposed that the magnocellular system is specifically linked to the guiding of covert visual attention. The argument is that the magnocellular pathway provides input to the dorsal cortical stream which then projects back to area V1. We review problems with this model. (1) It requires that responses in the magnocellular system have a lead time over responses in the parvocellular system. However, measurements indicate that the actual response time difference between the two systems is small or negligible when entering the visual cortex. (2) Attention can be modified by stimuli that do not activate the magnocellular system. And, (3) lesions to area MT in the dorsal stream impair smooth pursuit eye movements, but not saccadic eye movements which are associated with shifts in attention. For these reasons, it is difficult to link attention defects in schizophrenia to potential magnocellular deficits.     

Auditory processing in schizophrenia during the middle latency period (10-50 ms): high-density electrical mapping and source analysis reveal subcortical antecedents to early cortical deficits

INTRODUCTION: Auditory sensory processing dysfunction is a core component of schizophrenia, with deficits occurring at 50 ms post-stimulus firmly established in the literature. Given that the initial afference of primary auditory cortex occurs at least 35 ms earlier, however, an essential question remains: how early in sensory processing do such deficits arise, and do they occur during initial cortical afference or earlier, which would implicate subcortical auditory dysfunction. OBJECTIVE: To establish the onset of the earliest deficits in auditory processing, we examined the time window demarcating the transition from subcortical to cortical processing: 10 ms to 50 ms during the so-called middle latency responses (MLRs). These remain to be adequately characterized in patients with schizophrenia. METHODS: We recorded auditory evoked potentials (AEPs) to simple tone-pips from 15 control subjects and 21 medicated patients with longer-term schizophrenia or schizoaffective disorder (illness duration 16 yr, standard deviation [SD] 9.4 yr), using high-density electrical scalp recordings. Between-group analyses assessed the integrity of the MLRs across groups. In addition, 2 source-localization models were conducted to address whether a distinction between subcortical and cortical generators of the MLRs can be made and whether evidence for differential dorsal and ventral pathway contributions to auditory processing deficits can be established. RESULTS: Robust auditory processing deficits were found for patients as early as 15 ms. Evidence for subcortical generators of the earliest MLR component (P20) was provided by source analysis. Topographical mapping and source localization also pointed to greater decrements in processing in the dorsal auditory pathway of patients, providing support for a theory of pervasive deficits that are organized along the lines of a dorsal-ventral distinction. CONCLUSIONS: Auditory sensory dysfunction in schizophrenia begins extremely early in processing, is evident during initial cortical afference and is also seen at earlier subcortical processing stages in the thalamus. The implication is that well-established sensory processing deficits in schizophrenia may be secondary to earlier subcortical dysfunction. Our findings do not preclude the possibility of even earlier deficits in auditory sensory processing during the auditory brainstem responses.     

Subjective Perceptual Distortions and Visual Dysfunction in Children with Autism

Case reports and sensory inventories suggest that autism involves sensory processing anomalies. Behavioral tests indicate impaired motion and normal form perception in autism. The present study used first-person accounts to investigate perceptual anomalies and related subjective to psychophysical measures. Nine high-functioning children with autism and nine typically-developing children were given a questionnaire to assess the frequency of sensory anomalies, as well as psychophysical tests of visual perception. Results indicated that children with autism experience increased perceptual anomalies, deficits in trajectory discrimination consistent with dysfunction in the cortical dorsal pathway or in cerebellar midsagittal vermis, and high spatial frequency contrast impairments consistent with dysfunctional parvocellular processing. Subjective visual hypersensitivity was significantly related to greater deficits across vision tests.     

Magnocellular and parvocellular contributions to responses in the middle temporal visual area (MT) of the macaque monkey

Many lines of evidence suggest that the visual signals relayed through the magnocellular and parvocellular subdivisions of the primate dorsal LGN remain largely segregated through several levels of cortical processing. It has been suggested that this segregation persists through to the highest stages of the visual cortex, and that the pronounced differences between the neuronal response properties in the parietal cortex and inferotemporal cortex may be attributed to differential contributions from magnocellular and parvocellular signals. We have examined this hypothesis directly by recording the responses of cortical neurons while selectively blocking responses in the magnocellular or parvocellular layers of the LGN. Responses were recorded from single units or multiunit clusters in the middle temporal visual area (MT), which is part of the pathway leading to parietal cortex and thought to receive primarily magnocellular inputs. Responses in the MT were consistently reduced when the magnocellular subdivision of the LGN was inactivated. The reduction was almost always pronounced and often complete. In contrast, parvocellular block rarely produced striking changes in MT responses and typically had very little effect. Nevertheless, unequivocal parvocellular contributions could be demonstrated for a minority of MT responses. At a few MT sites, responses were recorded while magnocellular and parvocellular blocks were made simultaneously. Responses were essentially eliminated for all these paired blocks. These results provide direct evidence for segregation of magnocellular and parvocellular contributions in the extrastriate visual cortex and support the suggestion that these signals remain largely segregated through the highest levels of cortical processing.     

Visuoperceptual impairment in MS patients: nature and possible neural origins.

Failures on visuoperceptual neuropsychological tasks (on neuropsychological tests of visuo-spatial perception or on tests concerning semantic properties of visual objects), may indicate focal deficits of visuoperceptual function, or could be the result of (an)other (peripheral) visual deficit(s), or be the effect of a more general cognitive decline. In multiple sclerosis (MS) patients exhibiting sufficient visual acuity and not showing severe cognitive deterioration, impairment on a comprehensive set of 31 visuoperceptual neuropsychological tasks was compared with spatial resolution deficits (SRD), temporal resolution deficits (TRD) for visual stimuli, abnormal pattern shift visual evoked potential (PSVEP) responses, and failing scores on neuropsychological tasks other than visuoperceptual tasks. Impairment on the visuoperceptual neuropsychological tasks was highly independent from the other abnormal visual and cognitive neurological impairments examined, suggesting that it mostly represented focal deficits. Only TRD in both eyes related to this impairment and this relationship was rather weak. Thus in some MS patients a slowed visual information processing may be one of the combined deficits underlying visuoperceptual neuropsychological task impairment. Given that SRD and TRD were not related to another stage of MS and reflect disturbances of a P (parvocellular channel and ventral stream projections) and M (magnocellular channel and dorsal stream projections) visual-system function respectively, demyelination of a certain M pathway may become a co-determinant of visuoperceptual neuropsychological task impairment more rapidly than damage to a certain P pathway.     

Hyperactivation balances sensory processing deficits during mood induction in schizophrenia

While impairments in emotion recognition are consistently reported in schizophrenia, there is some debate on the experience of emotion. Only few studies investigated neural correlates of emotional experience in schizophrenia. The present functional magnetic resonance imaging study compared a standard visual mood induction paradigm with an audiovisual method aimed at eliciting emotions more automatically. To investigate the interplay of sensory, cognitive and emotional mechanisms during emotion experience, we examined connectivity patterns between brain areas. Sixteen schizophrenia patients and sixteen healthy subjects participated in two different mood inductions (visual and audiovisual) that were administered for different emotions (happiness, sadness and neutral). Confirming the dissociation of behavioral and neural correlates of emotion experience, patients rated their mood similarly to healthy subjects but showed differences in neural activations. Sensory brain areas were activated less, increased activity emerged in higher cortical areas, particularly during audiovisual stimulation. Connectivity was increased between primary and secondary sensory processing areas in schizophrenia. These findings support the hypothesis of a deficit in filtering and processing sensory information alongside increased higher-order cognitive effort compensating for perception deficits in the affective domain. This may suffice to recover emotion experience in ratings of clinically stable patients but may fail during acute psychosis.     

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.