CoChat
Sign Up
Cited by 362Schizophrenia research and treatmentVisual perception and processing mechanismsHallucinations in medical conditions

Early-stage visual processing and cortical amplification deficits in schizophrenia

Open access
Butler, Pamela D., Zemon, Vance, Schechter, Isaac, Saperstein, Alice M., Hoptman, Matthew J., Lim, Kelvin O., Revheim, Nadine, Silipo, Gail +1 more·2005·Archives of General Psychiatry
DOI 10.1001/archpsyc.62.5.495PMC PMC1298183
Open this paper in CoChat — free account

Abstract

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.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1001/archpsyc.62.5.495

Cites

79 of 79 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • The reduced amplitude responses to simple visual stimuli indicate deficits in contrast gain control within the early visual system.

    “Second, patients show reduced amplitude responses to simple visual stimuli with steady-state or transient electrophysiological techniques (21,22), indicating deficits in contrast gain control within the early visual system.”

    From Visual perception and its impairment in schizophrenia (2008) · cites this paper as [22]

  • Patients show reduced amplitude responses to simple visual stimuli with steady-state or transient electrophysiological techniques.

    “Second, patients show reduced amplitude responses to simple visual stimuli with steady-state or transient electrophysiological techniques (21,22), indicating deficits in contrast gain control within the early visual system.”

    From Visual perception and its impairment in schizophrenia (2008) · cites this paper as [22]

  • In steady-state evoked potential studies, differential M- versus P-pathway biased responses have been observed.

    “In steady-state evoked potential studies, stimuli have been biased toward M- versus P-pathways with different standing levels of luminance contrast (“pedestals”). Under such conditions, differential M- versus P-pathway biased responses have been observed (22) (Figure 3B and 3C).”

    From Visual perception and its impairment in schizophrenia (2008) · cites this paper as [22]

  • In one study in which thresholds were higher (e.g., >16% contrast), relative preservation at high spatial frequencies was observed.

    “In one study in which thresholds were higher (e.g., > 16% contrast), relative preservation at high spatial frequencies was observed (22).”

    From Visual perception and its impairment in schizophrenia (2008) · cites this paper as [22]

  • Patients with schizophrenia show preferential M-pathway dysfunction, although deficits have also been observed in parvocellular processing.

    “Patients with schizophrenia show preferential M-pathway dysfunction (21,22,28,35–38), although deficits have also been observed in parvocellular processing (19,20).”

    From Visual perception and its impairment in schizophrenia (2008) · cites this paper as [22]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Research works printed but not linked: 6

  1. [2]Goldberg TE, Gold JM. Neurocognitive functioning in patients with schizophrenia: an overview. In: Bloom FE, Kupfer DJ, eds. Psychopharmacology, the Fourth Generation of Progress New York, NY: Raven Press Ltd; 1995:1245–1257.
  2. [6]Braff DL, Saccuzzo DP, Geyer MA. Information processing dysfunctions in schizophrenia: studies of visual backward masking, sensorimotor gating, and habituation. In: Steinhauer SR, Gruzelier JH, Zubin J, eds. Handbook of Schizophrenia Vol 5. New York, NY: Elsevier; 1991:303–334.
  3. [25]Casagrande VA, Xu X. Parallel visual pathways: a comparative perspective. In: Chalupa LM, Werner JS, eds. The Visual Neurosciences Vol 1. Cambridge, Mass: MIT Press; 2003.
  4. [35]Kaplan E. The receptive field structure of retinal ganglion cells in cat and monkey. In: Leventhal AG, ed. Vision and Visual Dysfunction Boston, Mass: CRC Press; 1991:10–40.
  5. [42]Cornblatt BA, Malhotra AK. Impaired attention as an endophenotype for molecular genetic studies of schizophrenia. . Am J Med Genet. 2001;105:11–15. [PubMed] [Google Scholar]
  6. [44]First MB, Spitzer RL, Gibbon M, Williams JBW. Structured Clinical Interview for DSM-IV Axis I Disorders–Patient Edition New York: New York State Psychiatric Institute; 1997.

Cited by

Sorted by citations

Related

Authors
Butler, P. D., Zemon, V., Schechter, I., Saperstein, A. M., Hoptman, M. J., Lim, K. O., Revheim, N., Silipo, G., & Javitt, D. C.
Affiliations
  • Nathan Kline Institute for Psychiatric Research (US)
  • Yeshiva University (US)
ORCID
Venue
Archives of General Psychiatry
Publisher
American Medical Association (AMA)
Published
2005-05-01
Volume
62
Issue
5
Pages
495
ISSN
0003-990X (ISSN-L)
DOI
10.1001/archpsyc.62.5.495
PMC
PMC1298183
OpenAlex
W1968584106
Cited by
362
References
79
Citations by year
2026: 10 · 2025: 5 · 2024: 19 · 2023: 11 · 2022: 15 · 2021: 11 · 2020: 21 · 2019: 18 · 2018: 13 · 2017: 16 · 2016: 8 · 2015: 16 · 2014: 18 · 2013: 24 · 2012: 19
FWCI
14.24
Type
journal article
Language
en
Open access
Locations
  • Archives of General Psychiatry (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institute of Mental Health (R37MH049334, R01 MH60662, R37MH49334, R01MH066374, K02-MH-01439, R01 MH66374, R01MH060662, R01MH064783, K02MH001439, R01-MH-64783)
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Visual perception and processing mechanisms
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Hallucinations in medical conditions
Keywords
schizophrenia, contrast sensitivity, visual evoked potentials, white matter integrity, optic radiation, glutamatergic dysfunction, NMDA receptor, community functioning, thalamocortical circuits
MeSH terms
Adult, Agnosia, Ambulatory Care, Evoked Potentials, Visual, Female, Glutamates, Hospitalization, Hospitals, Psychiatric, Humans, Male, Neuropsychological Tests, Psychiatric Status Rating Scales, Psychotic Disorders, Schizophrenia, Schizophrenic Psychology, Thalamus, Visual Cortex, Visual Pathways, Visual Perception, Contrast Sensitivity, Receptors, N-Methyl-D-Aspartate

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review