Early-Stage Visual Processing and Cortical Amplification Deficits in Schizophrenia

Butler, Pamela D.; Zemon, Vance; Schechter, Isaac; Saperstein, Alice M.; Hoptman, Matthew J.; Lim, Kelvin O.; Revheim, Nadine; Silipo, Gail; Javitt, Daniel C.

doi:10.1001/archpsyc.62.5.495

Cited by 345 publications

(351 citation statements)

References 81 publications

(118 reference statements)

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“…Deficits in M pathway processing, in particular, correlated significantly with global outcome. These deficits, which may be related to both structural and functional abnormalities within the early visual pathway in schizophrenia (Butler et al, 2005), are deserving of further study. A. Graph showing the group average waveforms for the high contrast (mixed M/P) condition over time for controls and patients with running t-test.…”

Section: Discussionmentioning

confidence: 99%

“…In the visual system, deficits have been shown to include increased visual thresholds (Cadenhead et al, 1997;Schechter et al, 2003), greater sensitivity to backward masking (Braff et al, 1991;Butler et al, 1996;Green and Nuechterlein, 1999a;Schechter et al, 2003), and decreased contrast sensitivity (Butler et al, 2005;Keri et al, 2002;Slaghuis and Curran, 1999), as well as motion perception (Chen et al, 1999;Li, 2002;Schwartz et al, 1999) and eye tracking deficits (Holzman et al, 1974;Levy et al, 1993;Trillenberg et al, 2004). Further, it has been suggested that these impairments may contribute to 'upstream' cognitive and social impairments (Brenner et al, 2002;Bruder et al, 1998;Kee et al, 1998;Ohno et al, 2000;Perry and Braff, 1994;Sergi and Green, 2003) and overall functional outcome of patients (Green et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

“…In contrast, more recent models subdivide into distinct magnocellular (M) vs. parvocellular (P) pathways defined based on neuroanatomy and response properties of underlying neurons with schizophrenia associated with M system underactivity on the basis of contrast sensitivity (Butler et al, 2005;Keri et al, 2002Keri et al, ,1998Slaghuis, 1998) and steady state VEPs (Butler et al, 2001(Butler et al, , 2005. Properties of M neurons correspond closely to those of the 'transient' pathway, whereas properties of the P neurons correspond to those of the sustained pathway.…”

Section: Introductionmentioning

confidence: 99%

“…Although behavioral (Butler et al, 2005;Keri et al, 2002Keri et al, , 2004O'Donnell et al, 1996O'Donnell et al, , 2002Slaghuis, 1998Slaghuis, , 2004 and steady state VEP (Butler et al, 2001(Butler et al, , 2005 studies suggest deficits in early-stage visual processing in schizophrenia particularly involving underactivity of the M system, previous studies of transient VEP (tVEP) in schizophrenia have been conflicting. Initial, as well as current, studies of the tVEP (Shagass et al, 1977;Straumanis et al, 1982;van der Stelt et al, 2004) have found no impairment in the early components of the waveform, reporting a deficit only at 200 ms (Shagass, 1980) or later (van der Stelt et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

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

Schechter

Butler

Zemon

et al. 2005

Clinical Neurophysiology

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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

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

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

Schechter

Butler

Zemon

et al. 2005

Clinical Neurophysiology

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137

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“…Patients with schizophrenia show deficits in early sensory information processing in the visual as well as the auditory modality (Butler et al, 2005;Javitt et al, 2000b). These impairments can be measured in behavioral paradigms (eg tone matching tasks, habituation, and prepulse inhibition of the startle response (PPI)), or EEG paradigms (mismatch negativity, P300, paired tone paradigm, peak recovery paradigm).…”

Section: Introductionmentioning

confidence: 99%

Early Auditory Sensory Processing Deficits in Mouse Mutants with Reduced NMDA Receptor Function

Bickel

Lipp

Umbricht

2007

Neuropsychopharmacol

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Cognitive deficits in schizophrenia include impairments at automatic, preattentive stages of sensory information processing. These deficits are evident in the prepulse inhibition-(PPI) and habituation of the auditory startle response paradigm, the paired tone paradigm in the EEG, and the peak recovery function of auditory evoked potentials (AEP). Administration of NMDA receptor antagonists reliably disrupts PPI and habituation of the startle, but not gating of AEPs in rodents. In the peak recovery paradigm, patients with schizophrenia and primates treated with NMDA receptor antagonists show reduced maximal response at long interstimulus intervals (ISI), but normal responses at short ISIs. Thus reduced NMDA receptor signalling may underlie alterations in these paradigms observed in schizophrenia. We tested the paradigms mentioned in mouse mutants with reduced expression of the NR1 subunit of the NMDA receptor (N ¼ 15) and their wild-type littermates (N ¼ 16). The NR1 mutant mice showed impaired habituation and PPI of the auditory startle response, as well as impaired gating in the paired tone paradigm. Deficits between the two gating measures did not correlate, corroborating previous evidence that these paradigms measure distinct processes. In the peak recovery paradigm, the NR1 mutants showed increased responses of the AEPs P1 and N1 at short ISIs but no difference between groups were observed at long ISIs. In conclusion, the NR1 hypomorphic mice modelled sensory and sensorimotor gating and startle habituation deficits observed in schizophrenia, but failed to model alterations in the peak recovery function.

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Functional Neuroanatomy of Visual Masking Deficits in Schizophrenia

Green¹,

Lee²,

Cohen³

et al. 2009

Arch Gen Psychiatry

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Context Visual masking procedures assess the earliest stages of visual processing. Patients with schizophrenia reliably show deficits on visual masking, and these procedures have been used to explore vulnerability to schizophrenia, probe underlying neural circuits, and help to explain functional outcome. Objective The goal of the current study was to identify and compare regional brain activity associated with one form of visual masking (i.e. backward masking) in schizophrenia patients and healthy controls. Design, Setting, and Participants Nineteen patients with schizophrenia and 19 healthy control subjects were recruited from the VA Greater Los Angles Healthcare System and local communities. Subjects received functional magnetic resonance imaging (fMRI) scans. While in the scanner, subjects performed a backward masking task, and were given three functional localizer activation scans to identify early visual processing regions of interest (ROIs). Main Outcome Measures The main outcome measure was the magnitude of the fMRI signal during backward masking. Results Two ROIs (lateral occipital complex (LO), and motion sensitive area, hMT+) showed sensitivity to the effects of masking, meaning that signal in these areas increased as the target became more visible. Patients had lower activation than controls in LO across all levels of visibility, but did not differ in other visual processing ROIs. Using whole brain analyses, we also identified areas outside the ROIs that were sensitive to masking effects (including bilateral inferior parietal lobe and thalamus), but groups did not differ in signal magnitude in these areas. Conclusions The study results support a key role in LO for visual masking, consistent with previous studies in healthy controls. The current results indicate that patients fail to activate LO to the same extent as controls during visual processing regardless of stimulus visibility, suggesting a neural basis for the visual masking deficit, and possibly other visual integration deficits, in schizophrenia.

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Early-Stage Visual Processing and Cortical Amplification Deficits in Schizophrenia

Cited by 345 publications

References 81 publications

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

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

Early Auditory Sensory Processing Deficits in Mouse Mutants with Reduced NMDA Receptor Function

Functional Neuroanatomy of Visual Masking Deficits in Schizophrenia

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