visual representation of schizophrenia

Portrayals of Schizophrenia by Entertainment Media: A Content Analysis of Contemporary Movies

Information & authors, metrics & citations, view options, conclusions:, demographic characteristics., symptoms and stereotypes., conclusions, acknowledgments and disclosures, supplementary material.

View/Download

Information

Published in.

Export Citations

If you have the appropriate software installed, you can download article citation data to the citation manager of your choice. Simply select your manager software from the list below and click Download. For more information or tips please see 'Downloading to a citation manager' in the Help menu .

Format

Citation style
Style

To download the citation to this article, select your reference manager software.

There are no citations for this item

View options

Already a subscriber? Access your subscription through your login credentials or your institution for full access to this article.

Purchase Options

Purchase this article to access the full text.

PPV Articles - Psychiatric Services

Not a subscriber?

Subscribe Now / Learn More

PsychiatryOnline subscription options offer access to the DSM-5-TR ® library, books, journals, CME, and patient resources. This all-in-one virtual library provides psychiatrists and mental health professionals with key resources for diagnosis, treatment, research, and professional development.

Need more help? PsychiatryOnline Customer Service may be reached by emailing [email protected] or by calling 800-368-5777 (in the U.S.) or 703-907-7322 (outside the U.S.).

Share article link

Copying failed.

Next article, request username.

Can't sign in? Forgot your username? Enter your email address below and we will send you your username

If the address matches an existing account you will receive an email with instructions to retrieve your username

Create a new account

Change password, password changed successfully.

Your password has been changed

Reset password

Can't sign in? Forgot your password?

Enter your email address below and we will send you the reset instructions

If the address matches an existing account you will receive an email with instructions to reset your password.

Your Phone has been verified

As described within the American Psychiatric Association (APA)'s Privacy Policy and Terms of Use , this website utilizes cookies, including for the purpose of offering an optimal online experience and services tailored to your preferences. Please read the entire Privacy Policy and Terms of Use. By closing this message, browsing this website, continuing the navigation, or otherwise continuing to use the APA's websites, you confirm that you understand and accept the terms of the Privacy Policy and Terms of Use, including the utilization of cookies.

An official website of the United States government

The .gov means it’s official. Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Publications
Account settings
My Bibliography
Collections
Citation manager

Save citation to file

Email citation, add to collections.

Create a new collection
Add to an existing collection

Add to My Bibliography

Your saved search, create a file for external citation management software, your rss feed.

Search in PubMed
Search in NLM Catalog
Add to Search

The Phenomenology and Neurobiology of Visual Distortions and Hallucinations in Schizophrenia: An Update

Affiliations.

1 Department of Psychiatry, University of Rochester Medical Center, Rochester, NY, United States.
2 Department of Neuroscience, University of Rochester Medical Center, Rochester, NY, United States.
3 Department of Ophthalmology, University of Rochester Medical Center, Rochester, NY, United States.
4 Center for Visual Science, University of Rochester Medical Center, Rochester, NY, United States.
PMID: 34177665
PMCID: PMC8226016
DOI: 10.3389/fpsyt.2021.684720

Schizophrenia is characterized by visual distortions in ~60% of cases, and visual hallucinations (VH) in ~25-50% of cases, depending on the sample. These symptoms have received relatively little attention in the literature, perhaps due to the higher rate of auditory vs. visual hallucinations in psychotic disorders, which is the reverse of what is found in other neuropsychiatric conditions. Given the clinical significance of these perceptual disturbances, our aim is to help address this gap by updating and expanding upon prior reviews. Specifically, we: (1) present findings on the nature and frequency of VH and distortions in schizophrenia; (2) review proposed syndromes of VH in neuro-ophthalmology and neuropsychiatry, and discuss the extent to which these characterize VH in schizophrenia; (3) review potential cortical mechanisms of VH in schizophrenia; (4) review retinal changes that could contribute to VH in schizophrenia; (5) discuss relationships between findings from laboratory measures of visual processing and VH in schizophrenia; and (6) integrate findings across biological and psychological levels to propose an updated model of VH mechanisms, including how their content is determined, and how they may reflect vulnerabilities in the maintenance of a sense of self. In particular, we emphasize the potential role of alterations at multiple points in the visual pathway, including the retina, the roles of multiple neurotransmitters, and the role of a combination of disinhibited default mode network activity and enhanced state-related apical/contextual drive in determining the onset and content of VH. In short, our goal is to cast a fresh light on the under-studied symptoms of VH and visual distortions in schizophrenia for the purposes of informing future work on mechanisms and the development of targeted therapeutic interventions.

Keywords: mechanisms; psychosis; retina; schizophrenia; self; visual distortions; visual hallucinations.

PubMed Disclaimer

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Comparison of pyramidal cell component…

Comparison of pyramidal cell component contributions during waking and dreaming consciousness. The image…

Proposed relative contributions of biological…

Proposed relative contributions of biological factors, and their psychological consequences, involved in different…

Publication types

Search in MeSH

Related information

Linkout - more resources, full text sources.

Europe PubMed Central
Frontiers Media SA
PubMed Central

Miscellaneous

NCI CPTAC Assay Portal

Citation Manager

NCBI Literature Resources

MeSH PMC Bookshelf Disclaimer

The PubMed wordmark and PubMed logo are registered trademarks of the U.S. Department of Health and Human Services (HHS). Unauthorized use of these marks is strictly prohibited.

Visual Perception Disturbances in Schizophrenia: A Unified Model

First Online: 31 May 2016

Cite this chapter

Steven M. Silverstein Ph.D. 4

Part of the book series: Nebraska Symposium on Motivation ((NSM,volume 63))

2658 Accesses

88 Citations

The purpose of this chapter is to demonstrate that the study of visual processing abnormalities in schizophrenia offers a unifying perspective on the etiology, development, pathophysiology, and course of the disorder. This chapter contains six sections. In the first, I provide a brief overview of the importance and promise of studying vision in schizophrenia. In the second, I provide examples of altered visual experience, in multiple aspects of vision, as reported by patients. The third reviews research and controversies related to the most prominent schizophrenia-related visual task deficits, including their psychophysiological and neurobiological aspects. In the fourth, I introduce the construct of contextual modulation and discuss how excesses and reductions in components of this function, in addition to changes in overall level of stimulus sensitivity, can account for many of the visual task deficits associated with schizophrenia. Informed by all of this evidence, I then briefly return to the issue of what the world looks and feels like for people with schizophrenia, and how this may change across illness phases. The paper concludes with a section on future directions for research in the area of vision and schizophrenia.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Subscribe and save.

Get 10 units per month
Download Article/Chapter or eBook
1 Unit = 1 Article or 1 Chapter
Cancel anytime
Available as PDF
Read on any device
Instant download
Own it forever
Available as EPUB and PDF
Compact, lightweight edition
Dispatched in 3 to 5 business days
Free shipping worldwide - see info
Durable hardcover edition

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

A review of abnormalities in the perception of visual illusions in schizophrenia

Early-stage visual perception impairment in schizophrenia, bottom-up and back again

Perceptual Functioning

Paraphrased from a comment at a research conference and a comment from a reviewer at a grant review meeting.

Because contrast sensitivity and spatial frequency processing are typically measured together (e.g., contrast sensitivity is measured across a range of spatial frequencies), there is some overlap in the findings presented in the first two sections.

O’Donnell et al. ( 2006 ) reported no differences between medicated and unmedicated schizophrenia patients. However, these were all chronic patients, and chronic patients withdrawn from medication may differ significantly from untreated high-risk and first episode patients, in terms of illness progression over time, and effects of years of prior medication treatment. Also, in this study, the average time since medication cessation was only 20 days, and this may not be enough time to for changes in dopaminergic tone, that might affect task performance, to occur.

For the purposes of this paper, the term gain refers to the rate at which output strength increases with input strength (e.g., the slope of a psychometric function, as opposed to its offset or threshold). Gain control refers to adjustments made to perceived stimulus intensity to keep it within a range that is useful but also tolerable to the organism. So, for example, in typical systems, weak signals are enhanced to a greater degree than are strong signals. An aspect of gain control is that the activity that implements the modulation would not produce significant output by itself, but can have a large effect given the presence of another signal.

Responses to these criticisms were published by Butler et al. ( 2007 ) and Keri and Benedek ( 2012 ).

Surround suppression in vision refers to the effects on receptive field functioning of stimuli outside of the classical receptive field. It is often operationalized as cases wherein the perception of a central patch is altered based on the nature of a surrounding patch (see Fig. 8 ). For example, a dark patch embedded in a lighter surround will appear darker than when it is perceived alone. However, the same patch would appear to be lighter if surrounded by a darker annulus. Similarly, an inner patch of coherent motion signals will appear to be moving faster if surrounded by a ring of motion signals moving in the opposite direction, but slower if surrounded by cues moving in the same direction. See also discussion of the Ebbinghaus illusion below for an example in the size domain.

With the possible exception of autism. However, in autism it has been argued that performance may be driven by excessive processing of local detail (Dakin & Frith, 2005 ) rather than a reduced ability to group elements into perceptual wholes.

Although human infants are sensitive to the hollow mask illusion (Corrow, Granrud, Mathison, & Yonas, 2011 ), suggesting that this effect is innate, they are not affected by manipulations involving familiarity, such as face inversion (Corrow, Mathison, Granrud, & Yonas, 2014 ), which affect the performance of adults (Papathomas & Bono, 2004 ), and which suggest top-down effects. Therefore, the hollow mask illusion may involve a combination of innate effects to perceive stimuli as convex, and learned effects specific to faces or overlearned stimuli in general. In both cases, however, the issue is that perception has been driven by what has been adaptive in either the past of the individual or the species. For a view of perception heavily based on the view that it is determined largely by what has been adaptive over the course of the evolutionary history of the species, see Lotto and Purves ( 2001 ), Purves, Lotto, Williams, Nundy, and Yang ( 2001 ), and Purves, Wojtach, and Lotto ( 2011 ). In the case of some other illusions, however, learning throughout childhood appears to drive the effect (see below).

Retinal input provides only 5–10 % of input to relay cells in the lateral geniculate nuclei of the thalamus. Most of the remainder are modulatory, and are local and GABAergic, or from cortical and brainstem inputs (Guillery & Sherman, 2002 ; Sherman & Guillery, 2002 ; Van Horn, Erisir, & Sherman, 2000 ; Vitay & Hamker, 2007 ). This demonstrates the massive role of modulatory processes in shaping the visual information that reaches the cortex.

Multiple studies indicate loss of gray and white matter, and/or reduced occipital volume, and/or increased gyrification (suggesting abnormal neurodevelopment) in early visual areas in people with schizophrenia (Dorph-Petersen, Pierri, Wu, Sampson, & Lewis, 2007 ; Schultz et al., 2013 ; Selemon, Rajkowska, & Goldman-Rakic, 1995 ), especially in chronically ill patients with poor functioning (Mitelman & Buchsbaum, 2007 ; Onitsuka et al., 2006 , 2007 ). Note that it is this poor outcome group that typically demonstrates the most severe deficits on mid-level perceptual tasks (Knight, 1984 , 1992 ; Knight & Silverstein, 1998 ; Silverstein & Keane, 2011a ). However, the relationships between occipital structural changes and visual perceptual changes in schizophrenia have yet to be investigated. One hypothesis related to this chapter is that a reduction in occipital neurons leads to reduced gain.

See Phillips (Submitted) for a discussion of the similarities and differences between CM and Bayesian processing views.

For example, it has already been demonstrated that visual processing changes in depression lead to patients experiencing the world as more blue and gray than other people (Bubl, Kern, Ebert, Bach, & Tebartz van Elst, 2010 ; Bubl, Tebartz Van Elst, Gondan, Ebert, & Greenlee, 2009 ).

The multiple lines of evidence indicating altered structure and function of the retina in schizophrenia were recently reviewed in Silverstein and Rosen ( 2015 ) and will not be discussed here. This evidence suggests both: (1) excessive retinal signaling related to elevated dopaminergic and glutamatergic drive in early schizophrenia; and (2) loss of structure and function secondary to more chronic illness and to antipsychotic medication use, leading to weakened and noisier retinal signaling over time. The contributions of altered retinal signaling to visual perception disturbances in schizophrenia, and to altered gain and contextual modulation therein, have yet to be explored, however.

Adams, R. A., Stephan, K. E., Brown, H. R., Frith, C. D., & Friston, K. J. (2013). The computational anatomy of psychosis. Frontiers in Psychology, 4 , 47. doi: 10.3389/fpsyt.2013.00047 .

Google Scholar

Adesnik, H., Bruns, W., Taniguchi, H., Huang, Z. J., & Scanziani, M. (2012). A neural circuit for spatial summation in visual cortex. Nature, 490 (7419), 226–231. doi: 10.1038/nature11526 .

Article PubMed PubMed Central Google Scholar

Altmann, C. F., Bulthoff, H. H., & Kourtzi, Z. (2003). Perceptual organization of local elements into global shapes in the human visual cortex. Current Biology, 13 (4), 342–349. doi: S0960982203000526 [pii].

Article PubMed Google Scholar

Anticevic, A., Corlett, P. R., Cole, M. W., Savic, A., Gancsos, M., Tang, Y., … Krystal, J. H. (2015). N-methyl-D-aspartate receptor antagonist effects on prefrontal cortical connectivity better model early than chronic schizophrenia. Biological Psychiatry, 77 (6), 569–580. doi: 10.1016/j.biopsych.2014.07.022 .

Ashby, F. G., Valentin, V. V., & von Meer, S. S. (2015). Differential effects of dopamine-directed treatments on cognition. Neuropsychiatric Disease and Treatment, 11 , 1859–1875.

Atallah, B. V., Bruns, W., Carandini, M., & Scanziani, M. (2012). Parvalbumin-expressing interneurons linearly transform cortical responses to visual stimuli. Neuron, 73 (1), 159–170. doi: 10.1016/j.neuron.2011.12.013 .

Backman, L., Nyberg, L., Lindenberger, U., Li, S. C., & Farde, L. (2006). The correlative triad among aging, dopamine, and cognition: Current status and future prospects. Neuroscience and Biobehavioral Reviews, 30 (6), 791–807. doi: 10.1016/j.neubiorev.2006.06.005 .

Barch, D. M., Carter, C. S., Dakin, S. C., Gold, J., Luck, S. J., Macdonald, A., III, … Strauss, M. E. (2012). The clinical translation of a measure of gain control: The contrast-contrast effect task. Schizophrenia Bulletin, 38 (1), 135–143. doi: 10.1093/schbul/sbr154 .

Bastos, A. M., Vezoli, J., Bosman, C. A., Schoffelen, J. M., Oostenveld, R., Dowdall, J. R., … Fries, P. (2015). Visual areas exert feedforward and feedback influences through distinct frequency channels. Neuron, 85 (2), 390–401. doi: 10.1016/j.neuron.2014.12.018 .

Bayerl, P., & Neumann, H. (2004). Disambiguating visual motion through contextual feedback modulation. Neural Computation, 16 (10), 2041–2066. doi: 10.1162/0899766041732404 .

Behabadi, B. F., Polsky, A., Jadi, M., Schiller, J., & Mel, B. W. (2012). Location-dependent excitatory synaptic interactions in pyramidal neuron dendrites. PLoS Computational Biology, 8 (7), e1002599. doi: 10.1371/journal.pcbi.1002599 .

Bell, A. B. (2006). George Inness: Writings and reflections on art and philosophy . New York, NY: George Braziller.

Black, J. E., Kodish, I. M., Grossman, A. W., Klintsova, A. Y., Orlovskaya, D., Vostrikov, V., … Greenough, W. T. (2004). Pathology of layer V pyramidal neurons in the prefrontal cortex of patients with schizophrenia. American Journal of Psychiatry, 161 (4), 742–744.

Blakemore, S. J., Smith, J., Steel, R., Johnstone, C. E., & Frith, C. D. (2000). The perception of self-produced sensory stimuli in patients with auditory hallucinations and passivity experiences: Evidence for a breakdown in self-monitoring. Psychological Medicine, 30 (5), 1131–1139.

Bodis-Wollner, I. (1990). Visual deficits related to dopamine deficiency in experimental animals and Parkinson’s disease patients. Trends in Neurosciences, 13 (7), 296–302.

Bodis-Wollner, I., & Tzelepi, A. (1998). The push-pull action of dopamine on spatial tuning of the monkey retina: The effects of dopaminergic deficiency and selective D1 and D2 receptor ligands on the pattern electroretinogram. Vision Research, 38 (10), 1479–1487.

Brandies, R., & Yehuda, S. (2008). The possible role of retinal dopaminergic system in visual performance. Neuroscience and Biobehavioral Reviews, 32 (4), 611–656. doi: 10.1016/j.neubiorev.2007.09.004 .

Braun, J. (1999). On the detection of salient contours. Spatial Vision, 12 (2), 211–225.

Brda, D., & Tang, E. C. (2011). Visual hallucinations from retinal detachment misdiagnosed as psychosis. Journal of Psychiatric Practice, 17 (2), 133–136. doi: 10.1097/01.pra.0000396066.79719.c5 .

Brittain, P. J., Surguladze, S., McKendrick, A. M., & Ffytche, D. H. (2010). Backward and forward visual masking in schizophrenia and its relation to global motion and global form perception. Schizophrenia Research, 124 (1–3), 134–141. doi: 10.1016/j.schres.2010.07.008 .

Bubl, E., Kern, E., Ebert, D., Bach, M., & Tebartz van Elst, L. (2010). Seeing gray when feeling blue? Depression can be measured in the eye of the diseased. Biological Psychiatry, 68 (2), 205–208. doi: 10.1016/j.biopsych.2010.02.009 .

Bubl, E., Tebartz Van Elst, L., Gondan, M., Ebert, D., & Greenlee, M. W. (2009). Vision in depressive disorder. World Journal of Biological Psychiatry, 10 (4 Pt 2), 377–384. doi: 10.1080/15622970701513756 .

Bulens, C., Meerwaldt, J. D., van der Wildt, G. J., & Keemink, C. J. (1989). Visual contrast sensitivity in drug-induced Parkinsonism. Journal of Neurology, Neurosurgery, and Psychiatry, 52 (3), 341–345.

Bunney, W. E., Jr., Hetrick, W. P., Bunney, B. G., Patterson, J. V., Jin, Y., Potkin, S. G., & Sandman, C. A. (1999). Structured interview for assessing perceptual anomalies (SIAPA). Schizophrenia Bulletin, 25 (3), 577–592.

Butler, P. D., Abeles, I. Y., Silverstein, S. M., Dias, E. C., Weiskopf, N. G., Calderone, D. J., & Sehatpour, P. (2013). An event-related potential examination of contour integration deficits in schizophrenia. Frontiers in Psychology, 4 , 132. doi: 10.3389/fpsyg.2013.00132 .

Butler, P. D., Abeles, I. Y., Weiskopf, N. G., Tambini, A., Jalbrzikowski, M., Legatt, M. E., … Javitt, D. C. (2009). Sensory contributions to impaired emotion processing in schizophrenia. Schizophrenia Bulletin, 35 (6), 1095–1107. doi: 10.1093/schbul/sbp109 .

Butler, P. D., Chen, Y., Ford, J. M., Geyer, M. A., Silverstein, S. M., & Green, M. F. (2012). Perceptual measurement in schizophrenia: Promising electrophysiology and neuroimaging paradigms from CNTRICS. Schizophrenia Bulletin, 38 (1), 81–91. doi: 10.1093/schbul/sbr106 .

Butler, P. D., Martinez, A., Foxe, J. J., Kim, D., Zemon, V., Silipo, G., … Javitt, D. C. (2007). Subcortical visual dysfunction in schizophrenia drives secondary cortical impairments. Brain, 130 (Pt 2), 417–430. doi: 10.1093/brain/awl233 .

Butler, P. D., Silverstein, S. M., & Dakin, S. C. (2008). Visual perception and its impairment in schizophrenia. Biological Psychiatry, 64 (1), 40–47. doi: 10.1016/j.biopsych.2008.03.023 .

Butler, P. D., Zemon, V., Schechter, I., Saperstein, A. M., Hoptman, M. J., Lim, K. O., … Javitt, D. C. (2005). Early-stage visual processing and cortical amplification deficits in schizophrenia. Archives of General Psychiatry, 62 (5), 495–504. doi: 10.1001/archpsyc.62.5.495 .

Buzsaki, G. (2006). Rhythms of the brain . New York, NY: Oxford University Press.

Book Google Scholar

Cadenhead, K. S., Dobkins, K., McGovern, J., & Shafer, K. (2013). Schizophrenia spectrum participants have reduced visual contrast sensitivity to chromatic (red/green) and luminance (light/dark) stimuli: New insights into information processing, visual channel function, and antipsychotic effects. Frontiers in Psychology, 4 , 535. doi: 10.3389/fpsyg.2013.00535 .

Cadenhead, K. S., Serper, Y., & Braff, D. L. (1998). Transient versus sustained visual channels in the visual backward masking deficits of schizophrenia patients. Biological Psychiatry, 43 (2), 132–138. doi: 10.1016/S0006-3223(97)00316-8 .

Calderone, D. J., Hoptman, M. J., Martinez, A., Nair-Collins, S., Mauro, C. J., Bar, M., … Butler, P. D. (2013). Contributions of low and high spatial frequency processing to impaired object recognition circuitry in schizophrenia. Cerebral Cortex, 23 (8), 1849–1858. doi: 10.1093/cercor/bhs169 .

Calderone, D. J., Martinez, A., Zemon, V., Hoptman, M. J., Hu, G., Watkins, J. E., … Butler, P. D. (2013). Comparison of psychophysical, electrophysiological, and fMRI assessment of visual contrast responses in patients with schizophrenia. Neuroimage, 67 , 153–162. doi: 10.1016/j.neuroimage.2012.11.019 .

Cardin, J. A., Carlen, M., Meletis, K., Knoblich, U., Zhang, F., Deisseroth, K., … Moore, C. I. (2009). Driving fast-spiking cells induces gamma rhythm and controls sensory responses. Nature, 459 (7247), 663–667. doi: 10.1038/nature08002 .

Carr, V., & Wale, J. (1986). Schizophrenia: an information processing model. The Australian and New Zealand Journal of Psychiatry, 20 (2), 136–155.

Castellano, M., Plochl, M., Vicente, R., & Pipa, G. (2014). Neuronal oscillations form parietal/frontal networks during contour integration. Frontiers in Integrative Neuroscience, 8 , 64. doi: 10.3389/fnint.2014.00064 .

Cepeda, C., Andre, V. M., Jocoy, E. L., & Levine, M. S. (2009). NMDA and dopamine: Diverse mechanisms applied to interacting receptor systems. In A. M. Van Dongen (Ed.), Biology of the NMDA receptor . Boca Raton, FL: CRC Press.

Chandna, A., Pennefather, P. M., Kovacs, I., & Norcia, A. M. (2001). Contour integration deficits in anisometropic amblyopia. Investigative Ophthalmology & Visual Science, 42 (3), 875–878.

Chapman, J. (1966). The early symptoms of schizophrenia. British Journal of Psychiatry, 112 (484), 225–251.

Chawla, D., Lumer, E. D., & Friston, K. J. (1999). The relationship between synchronization among neuronal populations and their mean activity levels. Neural Computation, 11 (6), 1389–1411.

Chechile, R. A., Anderson, J. E., Krafczek, S. A., & Coley, S. L. (1996). A syntactic complexity effect with visual patterns: Evidence for the syntactic nature of the memory representation. Journal of Experimental Psychology: Learning, Memory, and Cognition, 22 (3), 654–669.

PubMed Google Scholar

Chen, Y. (2011). Abnormal visual motion processing in schizophrenia: A review of research progress. Schizophrenia Bulletin, 37 (4), 709–715. doi: 10.1093/schbul/sbr020 .

Chen, Y., Levy, D. L., Sheremata, S., & Holzman, P. S. (2004). Compromised late-stage motion processing in schizophrenia. Biological Psychiatry, 55 (8), 834–841. doi: 10.1016/j.biopsych.2003.12.024 .

Chen, Y., Levy, D. L., Sheremata, S., Nakayama, K., Matthysse, S., & Holzman, P. S. (2003). Effects of typical, atypical, and no antipsychotic drugs on visual contrast detection in schizophrenia. The American Journal of Psychiatry, 160 (10), 1795–1801.

Chen, Y., McBain, R., Norton, D., & Ongur, D. (2011). Schizophrenia patients show augmented spatial frame illusion for visual and visuomotor tasks. Neuroscience, 172 , 419–426. doi: 10.1016/j.neuroscience.2010.10.039 .

Chen, Y., Nakayama, K., Levy, D., Matthysse, S., & Holzman, P. (2003). Processing of global, but not local, motion direction is deficient in schizophrenia. Schizophrenia Research, 61 (2–3), 215–227.

Chen, Y., Norton, D., & Ongur, D. (2008). Altered center-surround motion inhibition in schizophrenia. Biological Psychiatry, 64 (1), 74–77. doi: 10.1016/j.biopsych.2007.11.017 .

Chen, M., Yan, Y., Gong, X., Gilbert, C. D., Liang, H., & Li, W. (2014). Incremental integration of global contours through interplay between visual cortical areas. Neuron, 82 (3), 682–694. doi: 10.1016/j.neuron.2014.03.023 .

Chey, J., & Holzman, P. S. (1997). Perceptual organization in schizophrenia: Utilization of the Gestalt principles. Journal of Abnormal Psychology, 106 (4), 530–538.

Ciaramelli, E., Leo, F., Del Viva, M. M., Burr, D. C., & Ladavas, E. (2007). The contribution of prefrontal cortex to global perception. Experimental Brain Research, 181 (3), 427–434. doi: 10.1007/s00221-007-0939-7 .

Clark, A. (2013). Whatever next? Predictive brains, situated agents, and the future of cognitive science. Behavioral and Brain Sciences, 36 (3), 181–204.

Cohen, J. D., & Servan-Schreiber, D. (1992). Context, cortex, and dopamine: A connectionist approach to behavior and biology in schizophrenia. Psychological Review, 99 (1), 45–77.

Cohen, J. D., & Servan-Schreiber, D. (1993). A theory of dopamine function and its role in cognitive deficits in schizophrenia. Schizophrenia Bulletin, 19 (1), 85–104.

Conrad, K. (1958). Die beginnende Schizophrenie. Versuch einer Gestaltanalyse des Wahns (3rd ed.). Stuttgart, Germany: Thieme.

Corlett, P. R., Frith, C. D., & Fletcher, P. C. (2009). From drugs to deprivation: A Bayesian framework for understanding models of psychosis. Psychopharmacology, 206 (4), 515–530. doi: 10.1007/s00213-009-1561-0 .

Corlett, P. R., Honey, G. D., Krystal, J. H., & Fletcher, P. C. (2011). Glutamatergic model psychoses: Prediction error, learning, and inference. Neuropsychopharmacology, 36 (1), 294–315. doi: 10.1038/npp.2010.163 .

Corrow, S., Granrud, C. E., Mathison, J., & Yonas, A. (2011). Six-month-old infants perceive the hollow-face illusion. Perception, 40 (11), 1376–1383.

Corrow, S. L., Mathison, J., Granrud, C. E., & Yonas, A. (2014). Six-month-old infants’ perception of the hollow face illusion: Evidence for a general convexity bias. Perception, 43 (11), 1177–1190.

Cox, M. D., & Leventhal, D. B. (1978). A multivariate analysis and modification of a preattentive, perceptual dysfunction in schizophrenia. Journal of Nervous and Mental Disease, 166 (10), 709–718.

Cromwell, R. (1984). Pre-emptive thinking and schizophrenia research. In W. D. Spaulding & J. K. Cole (Eds.), Theories of schizophrenia and psychosis (pp. 1–46). Lincoln, NE: University of Nebraska Press.

Cuthbert, B. N., & Insel, T. R. (2010). Toward new approaches to psychotic disorders: The NIMH Research Domain Criteria project. Schizophrenia Bulletin, 36 (6), 1061–1062. doi: 10.1093/schbul/sbq108 .

Cutting, J., & Dunne, F. (1986). The nature of the abnormal perceptual experiences at the onset of schizophrenia. Psychopathology, 19 (6), 347–352.

Dakin, S., Carlin, P., & Hemsley, D. (2005). Weak suppression of visual context in chronic schizophrenia. Current Biology, 15 (20), R822–R824. doi: 10.1016/j.cub.2005.10.015 .

Dakin, S., & Frith, U. (2005). Vagaries of visual perception in autism. Neuron, 48 (3), 497–507. doi: 10.1016/j.neuron.2005.10.018 .

Davis, R. A., Bockbrader, M. A., Murphy, R. R., Hetrick, W. P., & O’Donnell, B. F. (2006). Subjective perceptual distortions and visual dysfunction in children with autism. Journal of Autism and Developmental Disorders, 36 (2), 199–210. doi: 10.1007/s10803-005-0055-0 .

Davis, K. L., Kahn, R. S., Ko, G., & Davidson, M. (1991). Dopamine in schizophrenia: A review and reconceptualization. The American Journal of Psychiatry, 148 (11), 1474–1486.

de Souza, C. F., Kalloniatis, M., Polkinghorne, P. J., McGhee, C. N., & Acosta, M. L. (2012). Functional activation of glutamate ionotropic receptors in the human peripheral retina. Experimental Eye Research, 94 (1), 71–84. doi: 10.1016/j.exer.2011.11.008 .

DeLue, R. A. (2004). George Inness and the science of landscape . Chicago, IL: The University of Chicago Press.

Diefendorf, A., & Dodge, R. (1908). An experimental study of the ocular reactions of the insane from photographic records. Brain, 31 , 451–489.

Article Google Scholar

Dima, D., Dietrich, D. E., Dillo, W., & Emrich, H. M. (2010). Impaired top-down processes in schizophrenia: A DCM study of ERPs. NeuroImage, 52 (3), 824–832. doi: 10.1016/j.neuroimage.2009.12.086 .

Dima, D., Dillo, W., Bonnemann, C., Emrich, H. M., & Dietrich, D. E. (2011). Reduced P300 and P600 amplitude in the hollow-mask illusion in patients with schizophrenia. Psychiatry Research, 191 (2), 145–151. doi: 10.1016/j.pscychresns.2010.09.015 .

Dima, D., Roiser, J. P., Dietrich, D. E., Bonnemann, C., Lanfermann, H., Emrich, H. M., & Dillo, W. (2009). Understanding why patients with schizophrenia do not perceive the hollow-mask illusion using dynamic causal modelling. Neuroimage, 46 (4), 1180–1186. doi: 10.1016/j.neuroimage.2009.03.033 .

Doherty, M. J., Campbell, N. M., Tsuji, H., & Phillips, W. A. (2010). The Ebbinghaus illusion deceives adults but not children. Developmental Science, 13 (5), 714–721.

Doniger, G. M., Foxe, J. J., Murray, M. M., Higgins, B. A., & Javitt, D. C. (2002). Impaired visual object recognition and dorsal/ventral stream interaction in schizophrenia. Archives of General Psychiatry, 59 (11), 1011–1020. doi: 10.1001/archpsyc.59.11.1011 .

Doniger, G. M., Foxe, J. J., Murray, M. M., Higgins, B. A., Snodgrass, J. G., Schroeder, C. E., & Javitt, D. C. (2000). Activation timecourse of ventral visual stream object-recognition areas: High density electrical mapping of perceptual closure processes. Journal of Cognitive Neuroscience, 12 (4), 615–621.

Dorph-Petersen, K. A., Pierri, J. N., Wu, Q., Sampson, A. R., & Lewis, D. A. (2007). Primary visual cortex volume and total neuron number are reduced in schizophrenia. Journal of Comparative Neurology, 501 (2), 290–301. doi: 10.1002/cne.21243 .

Eaton, W. W., Hayward, C., & Ram, R. (1992). Schizophrenia and rheumatoid arthritis: A review. Schizophrenia Research, 6 (3), 181–192.

Ebel, H., Gross, G., Klosterkotter, J., & Huber, G. (1989). Basic symptoms in schizophrenic and affective psychoses. Psychopathology, 22 (4), 224–232.

Elkashef, A. M., Doudet, D., Bryant, T., Cohen, R. M., Li, S. H., & Wyatt, R. J. (2000). 6-(18)F-DOPA PET study in patients with schizophrenia. Positron emission tomography. Psychiatry Research, 100 (1), 1–11.

Elliott, D. B. (1987). Contrast sensitivity decline with ageing: A neural or optical phenomenon? Ophthalmic and Physiological Optics, 7 (4), 415–419.

Emrich, H. M. (1989). A three-component-system hypothesis of psychosis. Impairment of binocular depth inversion as an indicator of a functional dysequilibrium. British Journal of Psychiatry, 155 (Suppl 5), 37–39.

Emrich, H. M., Leweke, F. M., & Schneider, U. (1997). Towards a cannabinoid hypothesis of schizophrenia: Cognitive impairments due to dysregulation of the endogenous cannabinoid system. Pharmacology, Biochemistry, and Behavior, 56 (4), 803–807.

Engel, A. K., Fries, P., & Singer, W. (2001). Dynamic predictions: Oscillations and synchrony in top-down processing. Nature Reviews Neuroscience, 2 (10), 704–716. doi: 10.1038/35094565 .

Everson, R. M., Prashanth, A. K., Gabbay, M., Knight, B. W., Sirovich, L., & Kaplan, E. (1998). Representation of spatial frequency and orientation in the visual cortex. Proceedings of the National Academy of Sciences of the United States of America, 95 (14), 8334–8338.

Feigenson, K. A., Keane, B. P., Roche, M. W., & Silverstein, S. M. (2014). Contour integration impairment in schizophrenia and first episode psychosis: State or trait? Schizophrenia Research, 159 (2–3), 515–520. doi: 10.1016/j.schres.2014.09.028 .

Ffytche, D. H. (2007). Visual hallucinatory syndromes: Past, present, and future. Dialogues in Clinical Neuroscience, 9 (2), 173–189.

PubMed PubMed Central Google Scholar

Field, D. J., Hayes, A., & Hess, R. F. (1993). Contour integration by the human visual system: Evidence for a local “association field”. Vision Research, 33 (2), 173–193.

Firestone, C., & Scholl, B. (in press). Cognition does not affect perception: Evaluating the evidence for ‘top-down’ effects. Behavioral and Brain Sciences .

Flevaris, A. V., Martinez, A., & Hillyard, S. A. (2013). Neural substrates of perceptual integration during bistable object perception. Journal of Vision, 13 (13), 17. doi: 10.1167/13.13.17 .

Foxe, J. J., Doniger, G. M., & Javitt, D. C. (2001). Early visual processing deficits in schizophrenia: Impaired P1 generation revealed by high-density electrical mapping. Neuroreport, 12 (17), 3815–3820.

Fries, P., Neuenschwander, S., Engel, A. K., Goebel, R., & Singer, W. (2001). Rapid feature selective neuronal synchronization through correlated latency shifting. Nature Neuroscience, 4 (2), 194–200. doi: 10.1038/84032 .

Friston, K. (2010). The free-energy principle: A unified brain theory? Nature Reviews Neuroscience, 11 (2), 127–138. doi: 10.1038/nrn2787 .

Frith, C. D., Stevens, M., Johnstone, E. C., Owens, D. G., & Crow, T. J. (1983). Integration of schematic faces and other complex objects in schizophrenia. Journal of Nervous and Mental Disease, 171 (1), 34–39.

Fuster, J. M. (2005). Cortex and mind: Unifying cognition . New York, NY: Oxford University Press.

Gilbert, C. D., & Sigman, M. (2007). Brain states: Top-down influences in sensory processing. Neuron, 54 (5), 677–696. doi: 10.1016/j.neuron.2007.05.019 .

Glantz, L. A., & Lewis, D. A. (2000). Decreased dendritic spine density on prefrontal cortical pyramidal neurons in schizophrenia. Archives of General Psychiatry, 57 (1), 65–73.

Glezer, V. D. (1989). Vision and mind: Modeling mental functions . New York, NY: Elsevier.

Glezer, V. D., & Tsoukkerman, I. I. (1961). Information and vision . Leningrad: Izdatelstwo Akademii Nau SSSR.

Gonzalez-Burgos, G., Cho, R. Y., & Lewis, D. A. (2015). Alterations in cortical network oscillations and parvalbumin neurons in schizophrenia. Biological Psychiatry, 77 (12), 1031–1040. doi: 10.1016/j.biopsych.2015.03.010 .

Gorwood, P., Pouchot, J., Vinceneux, P., Puechal, X., Flipo, R. M., De Bandt, M., … Club Rhumatisme et, Inflammation. (2004). Rheumatoid arthritis and schizophrenia: A negative association at a dimensional level. Schizophrenia Research, 66 (1), 21–29.

Gottlob, I., & Stangler-Zuschrott, E. (1990). Effect of levodopa on contrast sensitivity and scotomas in human amblyopia. Investigative Ophthalmology & Visual Science, 31 (4), 776–780.

Grano, N., Salmijarvi, L., Karjalainen, M., Kallionpaa, S., Roine, M., & Taylor, P. (2015). Early signs of worry: Psychosis risk symptom visual distortions are independently associated with suicidal ideation. Psychiatry Research, 225 (3), 263–267. doi: 10.1016/j.psychres.2014.12.031 .

Green, M. F., Hellemann, G., Horan, W. P., Lee, J., & Wynn, J. K. (2012). From perception to functional outcome in schizophrenia: Modeling the role of ability and motivation. Archives of General Psychiatry, 69 (12), 1216–1224. doi: 10.1001/archgenpsychiatry.2012.652 .

Green, M. F., Lee, J., Wynn, J. K., & Mathis, K. I. (2011). Visual masking in schizophrenia: Overview and theoretical implications. Schizophrenia Bulletin, 37 (4), 700–708. doi: 10.1093/schbul/sbr051 .

Green, M. F., Mintz, J., Salveson, D., Nuechterlein, K. H., Breitmeyer, B., Light, G. A., & Braff, D. L. (2003). Visual masking as a probe for abnormal gamma range activity in schizophrenia. Biological Psychiatry, 53 (12), 1113–1119. doi: 10.1016/S0006-3223(02)01813-9 .

Gregory, R. L. (1970). The intelligent eye (pp. 126–131). New York, NY: McGraw-Hill.

Grutzner, C., Wibral, M., Sun, L., Rivolta, D., Singer, W., Maurer, K., & Uhlhaas, P. J. (2013). Deficits in high- (>60 Hz) gamma-band oscillations during visual processing in schizophrenia. Frontiers in Human Neuroscience, 7 , 88. doi: 10.3389/fnhum.2013.00088 .

Guillery, R. W., & Sherman, S. M. (2002). Thalamic relay functions and their role in corticocortical communication: Generalizations from the visual system. Neuron, 33 (2), 163–175.

Haenschel, C., Bittner, R. A., Haertling, F., Rotarska-Jagiela, A., Maurer, K., Singer, W., & Linden, D. E. (2007). Contribution of impaired early-stage visual processing to working memory dysfunction in adolescents with schizophrenia: A study with event-related potentials and functional magnetic resonance imaging. Archives of General Psychiatry, 64 (11), 1229–1240. doi: 10.1001/archpsyc.64.11.1229 .

Haider, B., & McCormick, D. A. (2009). Rapid neocortical dynamics: Cellular and network mechanisms. Neuron, 62 (2), 171–189. doi: 10.1016/j.neuron.2009.04.008 .

Hanslmayr, S., Volberg, G., Wimber, M., Dalal, S. S., & Greenlee, M. W. (2013). Prestimulus oscillatory phase at 7 Hz gates cortical information flow and visual perception. Current Biology, 23 (22), 2273–2278. doi: 10.1016/j.cub.2013.09.020 .

Harris, J. P., Calvert, J. E., Leendertz, J. A., & Phillipson, O. T. (1990). The influence of dopamine on spatial vision. Eye (London, England), 4 (Pt 6), 806–812. doi: 10.1038/eye.1990.127 .

Harvey, P. O., Lee, J., Cohen, M. S., Engel, S. A., Glahn, D. C., Nuechterlein, K. H., … Green, M. F. (2011). Altered dynamic coupling of lateral occipital complex during visual perception in schizophrenia. Neuroimage, 55 (3), 1219–1226. doi: 10.1016/j.neuroimage.2010.12.045 .

Hebert, M., Gagne, A. M., Paradis, M. E., Jomphe, V., Roy, M. A., Merette, C., & Maziade, M. (2010). Retinal response to light in young nonaffected offspring at high genetic risk of neuropsychiatric brain disorders. Biological Psychiatry, 67 (3), 270–274. doi: 10.1016/j.biopsych.2009.08.016 .

Heeger, D. J. (1992). Normalization of cell responses in cat striate cortex. Visual Neuroscience, 9 (2), 181–197.

Herzog, M. H., & Brand, A. (2015). Visual masking and schizophrenia. Schizophrenia Research: Cognition, 2 (2), 64–71.

Herzog, M. H., Roinishvili, M., Chkonia, E., & Brand, A. (2013). Schizophrenia and visual backward masking: A general deficit of target enhancement. Frontiers in Psychology, 4 , 254. doi: 10.3389/fpsyg.2013.00254 .

Hesse, H. (1971). Autobiographical Writings (D. Lindley, Trans. T. Ziolkowski Ed.). New York: Farrar, Straus, and Giroux

Homayoun, H., & Moghaddam, B. (2006). Bursting of prefrontal cortex neurons in awake rats is regulated by metabotropic glutamate 5 (mGlu5) receptors: Rate-dependent influence and interaction with NMDA receptors. Cerebral Cortex, 16 (1), 93–105. doi: 10.1093/cercor/bhi087 .

Horton, H. K., & Silverstein, S. M. (2011). Visual context processing deficits in schizophrenia: Effects of deafness and disorganization. Schizophrenia Bulletin, 37 (4), 716–726. doi: 10.1093/schbul/sbr055 .

Howes, O. D., & Kapur, S. (2009). The dopamine hypothesis of schizophrenia: Version III—The final common pathway. Schizophrenia Bulletin, 35 (3), 549–562. doi: 10.1093/schbul/sbp006 .

Huang, P. C., Hess, R. F., & Dakin, S. C. (2006). Flank facilitation and contour integration: Different sites. Vision Research, 46 (21), 3699–3706. doi: 10.1016/j.visres.2006.04.025 .

Huber, G., & Gross, G. (1989). The concept of basic symptoms in schizophrenic and schizoaffective psychoses. Recenti Progressi in Medicina, 80 (12), 646–652.

Insel, T. R. (2010). Rethinking schizophrenia. Nature, 468 (7321), 187–193. doi: 10.1038/nature09552 .

Issa, N. P., Trepel, C., & Stryker, M. P. (2000). Spatial frequency maps in cat visual cortex. Journal of Neuroscience, 20 (22), 8504–8514.

Joseph, J., Bae, G., & Silverstein, S. M. (2013). Sex, symptom, and premorbid social functioning associated with perceptual organization dysfunction in schizophrenia. Frontiers in Psychology, 4 , 547. doi: 10.3389/fpsyg.2013.00547 .

Jung, C. G. (1958). Schizophrenia (R. F. C. Hull, Trans.). In H. Read, M. Fordham & G. Adler (Eds.), The psychogenesis of mental disease (Vol. 3). Princeton, NJ: Princeton University Press.

Jung, C.G. (1960). The psychology of dementia praecox (R. F. C. Hull, Trans. Vol. 3). Princeton, NJ: Princeton University Press. (Original work published 1907)

Kantrowitz, J. T., Butler, P. D., Schecter, I., Silipo, G., & javitt, D. C. (2009). Seeing the world dimly: The impact of early visual deficits on visual experience in schizophrenia. Schizophrenia Bulletin, 35 (6), 1085–1094. doi: 10.1093/schbul/sbp100 .

Kapadia, M. K., Ito, M., Gilbert, C. D., & Westheimer, G. (1995). Improvement in visual sensitivity by changes in local context: Parallel studies in human observers and in V1 of alert monkeys. Neuron, 15 (4), 843–856. doi: 10.1016/0896-6273(95)90175-2 .

Kavsek, M., & Granrud, C. E. (2012). Children’s and adults’ size estimates at near and far distances: A test of the perceptual learning theory of size constancy development. Iperception, 3 (7), 459–466. doi: 10.1068/i0530 .

Kay, J. W., & Phillips, W. A. (2010). Coherent Infomax as a computational goal for neural systems. Bulletin of Mathematical Biology, 73 (2), 344–372. doi: 10.1007/s11538-010-9564-x .

Keane, B. P., Erlikhman, G., Kastner, S., Paterno, D., & Silverstein, S. M. (2014). Multiple forms of contour grouping deficits in schizophrenia: What is the role of spatial frequency? Neuropsychologia, 65 , 221–233. doi: 10.1016/j.neuropsychologia.2014.10.031 .

Keane, B. P., Kastner, S., Paterno, D., & Silverstein, S. M. (2015). Is 20/20 vision good enough? Visual acuity differences within the normal range predict contour element detection and integration. Psychonomic Bulletin and Review, 22 (1), 121–127. doi: 10.3758/s13423-014-0647-9 .

Keane, B. P., Paterno, D., & Silverstein, S. M. (Submitted). A more sensitive contour integration test validates visual integration dysfunction as a biomarker in schizophrenia.

Keane, B. P., Silverstein, S. M., Barch, D. M., Carter, C. S., Gold, J. M., Kovacs, I., …. Strauss, M. E. (2012). The spatial range of contour integration deficits in schizophrenia. Experimental Brain Research, 220 (3–4), 251–259. doi: 10.1007/s00221-012-3134-4 .

Keane, B. P., Silverstein, S. M., Wang, Y., & Papathomas, T. V. (2013). Reduced depth inversion illusions in schizophrenia are state-specific and occur for multiple object types and viewing conditions. Journal of Abnormal Psychology, 122 (2), 506–512. doi: 10.1037/a0032110 .

Kegeles, L. S., Abi-Dargham, A., Frankle, W. G., Gil, R., Cooper, T. B., Slifstein, M., … Laruelle, M. (2010). Increased synaptic dopamine function in associative regions of the striatum in schizophrenia. Archives of General Psychiatry, 67 (3), 231–239. doi: 10.1001/archgenpsychiatry.2010.10 .

Kelemen, O., Kiss, I., Benedek, G., & Keri, S. (2013). Perceptual and cognitive effects of antipsychotics in first-episode schizophrenia: The potential impact of GABA concentration in the visual cortex. Progress in Neuropsychopharmacology and Biological Psychiatry, 47 , 13–19. doi: 10.1016/j.pnpbp.2013.07.024 .

Keri, S., Antal, A., Szekeres, G., Benedek, G., & Janka, Z. (2002). Spatiotemporal visual processing in schizophrenia. Journal of Neuropsychiatry and Clinical Neurosciences, 14 (2), 190–196.

Keri, S., & Benedek, G. (2007). Visual contrast sensitivity alterations in inferred magnocellular pathways and anomalous perceptual experiences in people at high-risk for psychosis. Visual Neuroscience, 24 (2), 183–189. doi: 10.1017/S0952523807070253 .

Keri, S., & Benedek, G. (2012). Why is vision impaired in fragile X premutation carriers? The role of fragile X mental retardation protein and potential FMR1 mRNA toxicity. Neuroscience, 206 , 183–189. doi: 10.1016/j.neuroscience.2012.01.005 .

Keri, S., Kelemen, O., Benedek, G., & Janka, Z. (2004). Vernier threshold in patients with schizophrenia and in their unaffected siblings. Neuropsychology, 18 (3), 537–542. doi: 10.1037/0894-4105.18.3.5372004-16644-014 .

Keri, S., Kelemen, O., Benedek, G., & Janka, Z. (2005). Lateral interactions in the visual cortex of patients with schizophrenia and bipolar disorder. Psychological Medicine, 35 (7), 1043–1051.

Keri, S., Kiss, I., Kelemen, O., Benedek, G., & Janka, Z. (2005). Anomalous visual experiences, negative symptoms, perceptual organization and the magnocellular pathway in schizophrenia: A shared construct? Psychological Medicine, 35 (10), 1445–1455. doi: 10.1017/S0033291705005398 .

Kim, D. W., Shim, M., Song, M. J., Im, C. H., & Lee, S. H. (2015). Early visual processing deficits in patients with schizophrenia during spatial frequency-dependent facial affect processing. Schizophrenia Research, 161 (2-3), 314–321. doi: 10.1016/j.schres.2014.12.020 .

Kim, H. S., Shin, N. Y., Choi, J. S., Jung, M. H., Jang, J. H., Kang, D. H., & Kwon, J. S. (2010). Processing of facial configuration in individuals at ultra-high risk for schizophrenia. Schizophrenia Research, 118 (1–3), 81–87. doi: 10.1016/j.schres.2010.01.003 .

Kim, D., Wylie, G., Pasternak, R., Butler, P. D., & Javitt, D. C. (2006). Magnocellular contributions to impaired motion processing in schizophrenia. Schizophrenia Research, 82 (1), 1–8. doi: 10.1016/j.schres.2005.10.008 .

Kiss, I., Fabian, A., Benedek, G., & Keri, S. (2010). When doors of perception open: Visual contrast sensitivity in never-medicated, first-episode schizophrenia. Journal of Abnormal Psychology, 119 (3), 586–593. doi: 10.1037/a0019610 .

Kiss, I., Janka, Z., Benedek, G., & Keri, S. (2006). Spatial frequency processing in schizophrenia: Trait or state marker? Journal of Abnormal Psychology, 115 (3), 636–638. doi: 10.1037/0021-843X.115.3.636 .

Klosterkotter, J., Hellmich, M., Steinmeyer, E. M., & Schultze-Lutter, F. (2001). Diagnosing schizophrenia in the initial prodromal phase. Archives of General Psychiatry, 58 (2), 158–164.

Knight, R. A. (1984). Converging models of cognitive deficits in schizophrenia. In Spaulding, W. & J. Coles (Eds.), Nebraska Symposium on Motivation: Theories of Schizophrenia and Psychosis (Vol. 31, pp. 93–156). Lincoln, NE: University of Nebraska Press.

Knight, R. A. (1992). Specifying cognitive deficiencies in poor premorbid schizophrenics. In E. F. Walker, R. Dworkin, & B. Cornblatt (Eds.), Progress in experimental psychology & psychopathology research (Vol. 15, pp. 252–289). New York, NY: Springer.

Knight, R. A., Elliott, D. S., & Freedman, E. G. (1985). Short-term visual memory in schizophrenics. Journal of Abnormal Psychology, 94 (4), 427–442.

Knight, R. A., Manoach, D. S., Elliott, D. S., & Hershenson, M. (2000). Perceptual organization in schizophrenia: The processing of symmetrical configurations. Journal of Abnormal Psychology, 109 (4), 575–587.

Knight, R. A., & Silverstein, S. M. (1998). The role of cognitive psychology in guiding research on cognitive deficits in schizophrenia. In M. Lenzenweger & R. H. Dworkin (Eds.), Origins and development of schizophrenia: Advances in experimental psychopathology (pp. 247–295). Washington, DC: APA Press.

Chapter Google Scholar

Knight, R. A., & Silverstein, S. M. (2001). A process-oriented approach for averting confounds resulting from general performance deficiencies in schizophrenia. Journal of Abnormal Psychology, 110 (1), 15–30.

Koethe, D., Kranaster, L., Hoyer, C., Gross, S., Neatby, M. A., Schultze-Lutter, F., … Leweke, F. M. (2009). Binocular depth inversion as a paradigm of reduced visual information processing in prodromal state, antipsychotic-naive and treated schizophrenia. European Archives of Psychiatry and Clinical Neuroscience, 259 (4), 195–202. doi: 10.1007/s00406-008-0851-6 .

Kourtzi, Z., Tolias, A. S., Altmann, C. F., Augath, M., & Logothetis, N. K. (2003). Integration of local features into global shapes: Monkey and human FMRI studies. Neuron, 37 (2), 333–346. doi: 10.1016/S0896-6273(02)01174-1 .

Kovacs, I. (2000). Human development of perceptual organization. Vision Research, 40 (10–12), 1301–1310. doi: 10.1016/s0042-6989(00)00055-9 .

Kovacs, I., & Julesz, B. (1993). A closed curve is much more than an incomplete one: Effect of closure in figure-ground segmentation. Proceedings of the National Academy of Sciences of the United States of America, 90 (16), 7495–7497.

Kovacs, I., Polat, U., Pennefather, P. M., Chandna, A., & Norcia, A. M. (2000). A new test of contour integration deficits in patients with a history of disrupted binocular experience during visual development. Vision Research, 40 (13), 1775–1783.

Kozma-Weibe, P., Silverstein, S. M., Feher, A., Kovacs, I., Uhlhaas, P., & Wilkniss, S. (2006). Development of a World-Wide-Web based contour integration test: Reliability and validity. Computers in Human Behavior, 22 , 971–980.

Kraepelin, E. (1903). Lehrbuch der Psychiatrie (7th ed.). Leipzig, Germany: Barth.

Kressel, N. J. (1990). Systemic barriers to progress in academic social psychology. The Journal of Social Psychology, 130 (1), 5–27.

Landgraf, S., & Osterheider, M. (2013). “To see or not to see: That is the question.” The “Protection-Against-Schizophrenia” (PaSZ) model: Evidence from congenital blindness and visuo-cognitive aberrations. Frontiers in Psychology, 4 , 352. doi: 10.3389/fpsyg.2013.00352 .

Laprevote, V., Oliva, A., Delerue, C., Thomas, P., & Boucart, M. (2010). Patients with schizophrenia are biased toward low spatial frequency to decode facial expression at a glance. Neuropsychologia, 48 (14), 4164–4168. doi: 10.1016/j.neuropsychologia.2010.10.017 .

Larkum, M. (2013). A cellular mechanism for cortical associations: An organizing principle for the cerebral cortex. Trends in Neurosciences, 36 (3), 141–151. doi: 10.1016/j.tins.2012.11.006 .

Larkum, M. E., Nevian, T., Sandler, M., Polsky, A., & Schiller, J. (2009). Synaptic integration in tuft dendrites of layer 5 pyramidal neurons: A new unifying principle. Science, 325 (5941), 756–760. doi: 10.1126/science.1171958 .

Larkum, M. E., & Phillips, W. A. (in press). Are apical amplification and disamplification enhanced by arousal-induced NE release? Behavioral and Brain Sciences.

Larkum, M. E., Zhu, J. J., & Sakmann, B. (1999). A new cellular mechanism for coupling inputs arriving at different cortical layers. Nature, 398 (6725), 338–341. doi: 10.1038/18686 .

Laruelle, M., Abi-Dargham, A., Gil, R., Kegeles, L., & Innis, R. (1999). Increased dopamine transmission in schizophrenia: Relationship to illness phases. Biological Psychiatry, 46 (1), 56–72.

Lee, M. S., & Fern, A. I. (2004). Fluphenazine and its toxic maculopathy. Ophthalmic Research, 36 (4), 237–239. doi: 10.1159/000078784 .

Lee, J., Gosselin, F., Wynn, J. K., & Green, M. F. (2011). How do schizophrenia patients use visual information to decode facial emotion? Schizophrenia Bulletin, 37 (5), 1001–1008. doi: 10.1093/schbul/sbq006 .

Lee, S. H., Kwan, A. C., Zhang, S., Phoumthipphavong, V., Flannery, J. G., Masmanidis, S. C., … Dan, Y. (2012). Activation of specific interneurons improves V1 feature selectivity and visual perception. Nature, 488 (7411), 379–383. doi: 10.1038/nature11312 .

Lee, C. C., & Sherman, S. M. (2010). Drivers and modulators in the central auditory pathways. Frontiers in Neuroscience, 4 , 79. doi: 10.3389/neuro.01.014.2010 .

Leivada, E., & Boeckx, C. (2014). Schizophrenia and cortical blindness: Protective effects and implications for language. Frontiers in Human Neuroscience, 8 , 940. doi: 10.3389/fnhum.2014.00940 .

Lencer, R., Nagel, M., Sprenger, A., Heide, W., & Binkofski, F. (2005). Reduced neuronal activity in the V5 complex underlies smooth-pursuit deficit in schizophrenia: Evidence from an fMRI study. NeuroImage, 24 (4), 1256–1259. doi: 10.1016/j.neuroimage.2004.11.013 .

Lenzenweger, M. F. (2011). Schizotypy and schizophrenia: The view from experimental psychopathology . New York, NY: Guilford Press.

Leventhal, A. G., Wang, Y., Pu, M., Zhou, Y., & Ma, Y. (2003). GABA and its agonists improved visual cortical function in senescent monkeys. Science, 300 (5620), 812–815. doi: 10.1126/science.1082874 .

Levy, D. L., Holzman, P. S., Matthysse, S., & Mendell, N. R. (1993). Eye tracking dysfunction and schizophrenia: A critical perspective. Schizophrenia Bulletin, 19 (3), 461–536.

Li, W., Piech, V., & Gilbert, C. D. (2006). Contour saliency in primary visual cortex. Neuron, 50 (6), 951–962. doi: 10.1016/j.neuron.2006.04.035 .

Li, W., Piech, V., & Gilbert, C. D. (2008). Learning to link visual contours. Neuron, 57 (3), 442–451. doi: 10.1016/j.neuron.2007.12.011 .

Logan, G. D., & Zbrodoff, N. J. (1999). Selection for cognition: Cognitive constraints on visual spatial attention. Visual Cognition, 6 (1), 51–81.

Lotto, R. B., & Purves, D. (2001). An empirical explanation of the Chubb illusion. Journal Cognitive Neuroscience, 13 (5), 547–555. doi: 10.1162/089892901750363154 .

Lykken, D. (1991). What’s wrong with psychology, anyway? In D. Cicchetti & W. M. Grove (Eds.), Matters of public interest . Minneapolis, MN: University of Minnesota Press.

Major, G., Larkum, M. E., & Schiller, J. (2013). Active properties of neocortical pyramidal neuron dendrites. Annual Review of Neuroscience, 36 , 1–24. doi: 10.1146/annurev-neuro-062111-150343 .

Marcus, D. S., & Van Essen, D. C. (2002). Scene segmentation and attention in primate cortical areas V1 and V2. Journal of Neurophysiology, 88 (5), 2648–2658. doi: 10.1152/jn.00916.2001 .

Martinez, A., Hillyard, S. A., Bickel, S., Dias, E. C., Butler, P. D., & Javitt, D. C. (2012). Consequences of magnocellular dysfunction on processing attended information in schizophrenia. Cerebral Cortex, 22 (6), 1282–1293. doi: 10.1093/cercor/bhr195 .

Martinez, A., Revheim, N., Butler, P. D., Guilfoyle, D. N., Dias, E. C., & Javitt, D. C. (2012). Impaired magnocellular/dorsal stream activation predicts impaired reading ability in schizophrenia. NeuroImage: Clinical, 2 , 8–16. doi: 10.1016/j.nicl.2012.09.006 .

Mather, M., Clewett, D., Sakaki, M., & Harley, C. W. (In press). Norepinephrine ignites local hot spots of neuronal excitation: How arousal amplifies selectivity in perception and memory. Behavioral and Brain Sciences .

Matussek, P. (1952). Untersuchungen über die Wahnwahrnehmung. 1. Mitteilung. Veränderungen der Wahrnehmungswelt bei beginnendem, primären Wahn. Archiv für Psychiatrie und Zeitschrift für die gesammte Neurologie, 189 , 279–319.

Matussek, P. (1953). Untersuchungen über die Wahnwahrnehmung. 2. Mitteilung: Die auf einem abnormen Vorrang von Wesenseigenschaftenberuhenden Eigentümlichkeiten derWahnwahrnehmung Schweizer Archiv für Neurologie und Psychiatrie, 71 , 189–210.

Matussek, P. (1987). Studies in delusional perception. Translated and condensed. In M. S. J. Cutting (Ed.), Clinical roots of the schizophrenia concept. Translations of seminal European contributions on schizophrenia . Cambridge, England: Cambridge University Press.

McBain, R., Norton, D., & Chen, Y. (2010). Differential roles of low and high spatial frequency content in abnormal facial emotion perception in schizophrenia. Schizophrenia Research, 122 (1–3), 151–155. doi: 10.1016/j.schres.2010.03.034 .

McCarty, C. A., Wood, C. A., Fu, C. L., Livingston, P. M., Mackersey, S., Stanislavsky, Y., & Taylor, H. R. (1999). Schizophrenia, psychotropic medication, and cataract. Ophthalmology, 106 (4), 683–687. doi: 10.1016/S0161-6420(99)90151-3 .

Mitelman, S. A., & Buchsbaum, M. S. (2007). Very poor outcome schizophrenia: Clinical and neuroimaging aspects. International Review of Psychiatry, 19 (4), 345–357. doi: 10.1080/09540260701486563 .

Mittal, V. A., Gupta, T., Keane, B. P., & Silverstein, S. M. (2015). Visual context processing dysfunctions in youth at high risk for psychosis: Resistance to the Ebbinghaus illusion and its symptom and social and role functioning correlates. Journal of Abnormal Psychology, 124 (4), 953–960.

Mizobe, K., Polat, U., Pettet, M. W., & Kasamatsu, T. (2001). Facilitation and suppression of single striate-cell activity by spatially discrete pattern stimuli presented beyond the receptive field. Visual Neuroscience, 18 (3), 377–391.

Moghaddam, B., & Javitt, D. (2012). From revolution to evolution: The glutamate hypothesis of schizophrenia and its implication for treatment. Neuropsychopharmacology, 37 (1), 4–15. doi: 10.1038/npp.2011.181 .

Monte-Silva, K., Liebetanz, D., Grundey, J., Paulus, W., & Nitsche, M. A. (2010). Dosage-dependent non-linear effect of L-dopa on human motor cortex plasticity. Journal of Physiology, 588 (Pt 18), 3415–3424. doi: 10.1113/jphysiol.2010.190181 .

Mors, O., Mortensen, P. B., & Ewald, H. (1999). A population-based register study of the association between schizophrenia and rheumatoid arthritis. Schizophrenia Research, 40 (1), 67–74.

Nagel, M., Sprenger, A., Nitschke, M., Zapf, S., Heide, W., Binkofski, F., & Lencer, R. (2007). Different extraretinal neuronal mechanisms of smooth pursuit eye movements in schizophrenia: An fMRI study. Neuroimage, 34 (1), 300–309. doi: 10.1016/j.neuroimage.2006.08.025 .

Nakajima, S., Caravaggio, F., Mamo, D. C., Mulsant, B. H., Chung, J. K., Plitman, E., … Graff-Guerrero, A. (2015). Dopamine D(2)/(3) receptor availability in the striatum of antipsychotic-free older patients with schizophrenia-A [(1)(1)C]-raclopride PET study. Schizophrenia Research, 164 (1–3), 263–267. doi: 10.1016/j.schres.2015.02.020 .

Neill, E., Joshua, N., Morgan, C., & Rossell, S. L. (2015). The effect of ketamine on configural facial processing. Journal of Clinical Psychopharmacology, 35 (2), 188–191. doi: 10.1097/JCP.0000000000000278 .

Nemati, F. (2009). Size and direction of distortion in geometric-optical illusions: Conciliation between the Muller-Lyer and Titchener configurations. Perception, 38 (11), 1585–1600.

Nevian, T., Larkum, M. E., Polsky, A., & Schiller, J. (2007). Properties of basal dendrites of layer 5 pyramidal neurons: A direct patch-clamp recording study. Nature Neuroscience, 10 (2), 206–214. doi: 10.1038/nn1826 .

Nitsche, M. A., Monte-Silva, K., Kuo, M. F., & Paulus, W. (2010). Dopaminergic impact on cortical excitability in humans. Reviews in the Neurosciences, 21 (4), 289–298.

Norton, D., McBain, R., Holt, D. J., Ongur, D., & Chen, Y. (2009). Association of impaired facial affect recognition with basic facial and visual processing deficits in schizophrenia. Biological Psychiatry, 65 (12), 1094–1098. doi: 10.1016/j.biopsych.2009.01.026 .

O’Donnell, B. F., Bismark, A., Hetrick, W. P., Bodkins, M., Vohs, J. L., & Shekhar, A. (2006). Early stage vision in schizophrenia and schizotypal personality disorder. Schizophrenia Research, 86 (1–3), 89–98. doi: 10.1016/j.schres.2006.05.016 .

O’Donnell, B. F., Potts, G. F., Nestor, P. G., Stylianopoulos, K. C., Shenton, M. E., & McCarley, R. W. (2002). Spatial frequency discrimination in schizophrenia. Journal of Abnormal Psychology, 111 (4), 620–625.

O’Donohue, W., Ferguson, K. E., & Naugle, A. E. (2003). The structure of the cognitive revolution: An examination from the philosophy of science. Behavior Analyst, 26 (1), 85–110.

Okamoto, M., Naito, T., Sadakane, O., Osaki, H., & Sato, H. (2009). Surround suppression sharpens orientation tuning in the cat primary visual cortex. European Journal of Neuroscience, 29 (5), 1035–1046. doi: 10.1111/j.1460-9568.2009.06645.x .

Oken, R. J., & Schulzer, M. (1999). At issue: Schizophrenia and rheumatoid arthritis: The negative association revisited. Schizophrenia Bulletin, 25 (4), 625–638.

Olney, J. W., & Farber, N. B. (1995). Glutamate receptor dysfunction and schizophrenia. Archives of General Psychiatry, 52 (12), 998–1007.

Olypher, A. V., Klement, D., & Fenton, A. A. (2006). Cognitive disorganization in hippocampus: A physiological model of the disorganization in psychosis. Journal of Neuroscience, 26 (1), 158–168. doi: 10.1523/JNEUROSCI.2064-05.2006 .

Onitsuka, T., McCarley, R. W., Kuroki, N., Dickey, C. C., Kubicki, M., Demeo, S. S., … Shenton, M. E. (2007). Occipital lobe gray matter volume in male patients with chronic schizophrenia: A quantitative MRI study. Schizophrenia Research, 92 (1–3), 197–206. doi: 10.1016/j.schres.2007.01.027 .

Onitsuka, T., Niznikiewicz, M. A., Spencer, K. M., Frumin, M., Kuroki, N., Lucia, L. C., … McCarley, R. W. (2006). Functional and structural deficits in brain regions subserving face perception in schizophrenia. American Journal of Psychiatry, 163 (3), 455–462. doi: 10.1176/appi.ajp.163.3.455 .

Palaniyappan, L., Simmonite, M., White, T. P., Liddle, E. B., & Liddle, P. F. (2013). Neural primacy of the salience processing system in schizophrenia. Neuron, 79 (4), 814–828. doi: 10.1016/j.neuron.2013.06.027 .

Palmer, S. E. (1999). Vision science: Photons to phenomenology . Cambridge, MA: MIT Press.

Papathomas, T. V., & Bono, L. M. (2004). Experiments with a hollow mask and a reverspective: Top-down influences in the inversion effect for 3-D stimuli. Perception, 33 (9), 1129–1138.

Parnas, J., Vianin, P., Saebye, D., Jansson, L., Volmer-Larsen, A., & Bovet, P. (2001). Visual binding abilities in the initial and advanced stages of schizophrenia. Acta Psychiatrica Scandinavica, 103 (3), 171–180.

Patterson, T., Spohn, H. E., & Hayes, K. (1987). Topographic evoked potentials during backward masking in schizophrenics, patient controls and normal controls. Progress in Neuropsychopharmacology and Biological Psychiatry, 11 (6), 709–728.

Phillips, W. A. (Submitted). Cognitive functions of intracellular mechanisms for contextual amplification.

Phillips, W. A., Clark, A., & Silverstein, S. M. (2015). On the functions, mechanisms, and malfunctions of intracortical contextual modulation. Neuroscience and Biobehavioral Reviews, 52 , 1–20. doi: 10.1016/j.neubiorev.2015.02.010 .

Phillips, W. A., & Silverstein, S. M. (2003). Convergence of biological and psychological perspectives on cognitive coordination in schizophrenia. Behavioral and Brain Sciences, 26 (1), 65–82. discussion 82–137.

Phillips, W. A., & Silverstein, S. M. (2013). The coherent organization of mental life depends on mechanisms for context-sensitive gain-control that are impaired in schizophrenia. Frontiers in Psychology, 4 , 307. doi: 10.3389/fpsyg.2013.00307 .

Phillips, W. A., & Singer, W. (1997). In search of common foundations for cortical computation. Behavioral and Brain Sciences, 20 (4), 657–683. discussion 683–722.

Phillipson, O. T., & Harris, J. P. (1985). Perceptual changes in schizophrenia: A questionnaire survey. Psychological Medicine, 15 (4), 859–866.

Polat, U., & Sagi, D. (1993). Lateral interactions between spatial channels: Suppression and facilitation revealed by lateral masking experiments. Vision Research, 33 (7), 993–999.

Purves, D., Lotto, R. B., Williams, S. M., Nundy, S., & Yang, Z. (2001). Why we see things the way we do: Evidence for a wholly empirical strategy of vision. Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences, 356 (1407), 285–297. doi: 10.1098/rstb.2000.0772 .

Purves, D., Wojtach, W. T., & Lotto, R. B. (2011). Understanding vision in wholly empirical terms. Proceedings of the National Academy of Sciences of the United States of America, 108 (Suppl 3), 15588–15595. doi: 10.1073/pnas.1012178108 .

Rabinowicz, E. F., Opler, L. A., Owen, D. R., & Knight, R. A. (1996). Dot Enumeration Perceptual Organization Task (DEPOT): Evidence for a short-term visual memory deficit in schizophrenia. Journal of Abnormal Psychology, 105 (3), 336–348.

Rassovsky, Y., Green, M. F., Nuechterlein, K. H., Breitmeyer, B. G., & Mintz, J. (2005). Visual processing in schizophrenia: Structural equation modeling of visual masking performance. Schizophrenia Research, 78 (2–3), 251–260. doi: 10.1016/j.schres.2005.05.011 .

Rassovsky, Y., Horan, W. P., Lee, J., Sergi, M. J., & Green, M. F. (2011). Pathways between early visual processing and functional outcome in schizophrenia. Psychological Medicine, 41 (3), 487–497. doi: 10.1017/S0033291710001054 .

Revheim, N., Corcoran, C. M., Dias, E., Hellmann, E., Martinez, A., Butler, P. D., … Javitt, D. C. (2014). Reading deficits in schizophrenia and individuals at high clinical risk: Relationship to sensory function, course of illness, and psychosocial outcome. American Journal of Psychiatry, 171 (9), 949–959. doi: 10.1176/appi.ajp.2014.13091196 .

Rivolta, D., Castellanos, N. P., Stawowsky, C., Helbling, S., Wibral, M., Grutzner, C., … Uhlhaas, P. J. (2014). Source-reconstruction of event-related fields reveals hyperfunction and hypofunction of cortical circuits in antipsychotic-naive, first-episode schizophrenia patients during Mooney face processing. Journal of Neuroscience, 34 (17), 5909–5917. doi: 10.1523/JNEUROSCI.3752-13.2014 .

Robol, V., Tibber, M. S., Anderson, E. J., Bobin, T., Carlin, P., Shergill, S. S., & Dakin, S. C. (2013). Reduced crowding and poor contour detection in schizophrenia are consistent with weak surround inhibition. PLoS One, 8 (4), e60951. doi: 10.1371/journal.pone.0060951 .

Rokem, A., Yoon, J. H., Ooms, R. E., Maddock, R. J., Minzenberg, M. J., & Silver, M. A. (2011). Broader visual orientation tuning in patients with schizophrenia. Frontiers in Human Neuroscience, 5 , 127. doi: 10.3389/fnhum.2011.00127 .

Saccuzzo, D. P., Hirt, M., & Spencer, T. J. (1974). Backward masking as a measure of attention in schizophrenia. Journal of Abnormal Psychology, 83 (5), 512–522.

Saccuzzo, D. P., & Schubert, D. L. (1981). Backward masking as a measure of slow processing in schizophrenia spectrum disorders. Journal of Abnormal Psychology, 90 (4), 305–312.

Saks, E. (2008). The center cannot hold: My journey through madness . New York, NY: Hachette Books.

Salinas, E., & Sejnowski, T. J. (2001). Gain modulation in the central nervous system: Where behavior, neurophysiology, and computation meet. The Neuroscientist, 7 (5), 430–440.

Schallmo, M. P., Sponheim, S. R., & Olman, C. A. (2013a). Abnormal contextual modulation of visual contour detection in patients with schizophrenia. PLoS One, 8 (6), e68090. doi: 10.1371/journal.pone.0068090 .

Schallmo, M. P., Sponheim, S. R., & Olman, C. A. (2013b). Correction: Abnormal contextual modulation of visual contour detection in patients with schizophrenia. PLoS One, 8 (10). doi: 10.1371/annotation/f082ec4d-419c-43ce-ae50-e05107539bf3 .

Schechter, I., Butler, P. D., Silipo, G., Zemon, V., & Javitt, D. C. (2003). Magnocellular and parvocellular contributions to backward masking dysfunction in schizophrenia. Schizophrenia Research, 64 (2–3), 91–101.

Schenkel, L. S., Spaulding, W. D., DiLillo, D., & Silverstein, S. M. (2005). Histories of childhood maltreatment in schizophrenia: Relationships with premorbid functioning, symptomatology, and cognitive deficits. Schizophrenia Research, 76 (2-3), 273–286. doi: 10.1016/j.schres.2005.03.003 .

Schenkel, L. S., Spaulding, W. D., & Silverstein, S. M. (2005). Poor premorbid social functioning and theory of mind deficit in schizophrenia: Evidence of reduced context processing? Journal of Psychiatric Research, 39 (5), 499–508. doi: 10.1016/j.jpsychires.2005.01.001 .

Schiffman, J., Maeda, J. A., Hayashi, K., Michelsen, N., Sorensen, H. J., Ekstrom, M., … Mednick, S. A. (2006). Premorbid childhood ocular alignment abnormalities and adult schizophrenia-spectrum disorder. Schizophrenia Research, 81 (2–3), 253–260. doi: 10.1016/j.schres.2005.08.008 .

Schneider, U., Borsutzky, M., Seifert, J., Leweke, F. M., Huber, T. J., Rollnik, J. D., & Emrich, H. M. (2002). Reduced binocular depth inversion in schizophrenic patients. Schizophrenia Research, 53 (1–2), 101–108. doi: 10.1016/S0920-9964(00)00172-9 .

Schobel, S. A., Chaudhury, N. H., Khan, U. A., Paniagua, B., Styner, M. A., Asllani, I., … Small, S. A. (2013). Imaging patients with psychosis and a mouse model establishes a spreading pattern of hippocampal dysfunction and implicates glutamate as a driver. Neuron, 78 (1), 81–93. doi: 10.1016/j.neuron.2013.02.011 .

Schubert, E. W., Henriksson, K. M., & McNeil, T. F. (2005). A prospective study of offspring of women with psychosis: Visual dysfunction in early childhood predicts schizophrenia-spectrum disorders in adulthood. Acta Psychiatrica Scandinavica, 112 (5), 385–393. doi: 10.1111/j.1600-0447.2005.00584.x .

Schultz, C. C., Wagner, G., Koch, K., Gaser, C., Roebel, M., Schachtzabel, C., … Schlosser, R. G. (2013). The visual cortex in schizophrenia: Alterations of gyrification rather than cortical thickness—A combined cortical shape analysis. Brain Structure and Function, 218 (1), 51–58. doi: 10.1007/s00429-011-0374-1 .

Schummers, J., Marino, J., & Sur, M. (2002). Synaptic integration by V1 neurons depends on location within the orientation map. Neuron, 36 (5), 969–978.

Seeman, P., Schwarz, J., Chen, J. F., Szechtman, H., Perreault, M., McKnight, G. S., … Sumiyoshi, T. (2006). Psychosis pathways converge via D2high dopamine receptors. Synapse, 60 (4), 319–346. doi: 10.1002/syn.20303 .

Sehatpour, P., Dias, E. C., Butler, P. D., Revheim, N., Guilfoyle, D. N., Foxe, J. J., & Javitt, D. C. (2010). Impaired visual object processing across an occipital-frontal-hippocampal brain network in schizophrenia: An integrated neuroimaging study. Archives of General Psychiatry, 67 (8), 772–782. doi: 10.1001/archgenpsychiatry.2010.85 .

Sehatpour, P., Molholm, S., Javitt, D. C., & Foxe, J. J. (2006). Spatiotemporal dynamics of human object recognition processing: An integrated high-density electrical mapping and functional imaging study of “closure” processes. NeuroImage, 29 (2), 605–618. doi: 10.1016/j.neuroimage.2005.07.049 .

Selemon, L. D., Rajkowska, G., & Goldman-Rakic, P. S. (1995). Abnormally high neuronal density in the schizophrenic cortex. A morphometric analysis of prefrontal area 9 and occipital area 17. Archives of General Psychiatry, 52 (10), 805–818. Discussion 819–820.

Self, M. W., Kooijmans, R. N., Super, H., Lamme, V. A., & Roelfsema, P. R. (2012). Different glutamate receptors convey feedforward and recurrent processing in macaque V1. Proceedings of the National Academy of Sciences of the United States of America, 109 (27), 11031–11036. doi: 10.1073/pnas.1119527109 .

Sesack, S. R., Hawrylak, V. A., Melchitzky, D. S., & Lewis, D. A. (1998). Dopamine innervation of a subclass of local circuit neurons in monkey prefrontal cortex: Ultrastructural analysis of tyrosine hydroxylase and parvalbumin immunoreactive structures. Cerebral Cortex, 8 (7), 614–622.

Sheremata, S., & Chen, Y. (2004). Co-administration of atypical antipsychotics and antidepressants disturbs contrast detection in schizophrenia. Schizophrenia Research, 70 (1), 81–89. doi: 10.1016/j.schres.2003.09.005 .

Sherman, S. M., & Guillery, R. W. (2002). The role of the thalamus in the flow of information to the cortex. Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences, 357 (1428), 1695–1708. doi: 10.1098/rstb.2002.1161 .

Shoshina, I. I., & Shelepin Iu, E. (2013). The contrast sensitivity in schizophrenia with different durations disease. Rossiĭskii Fiziologicheskiĭ Zhurnal Imeni I.M. Sechenova, 99 (8), 928–936.

Silverstein, S. M. (2008). Measuring specific, rather than generalized, cognitive deficits and maximizing between-group effect size in studies of cognition and cognitive change. Schizophrenia Bulletin, 34 (4), 645–655. doi: 10.1093/schbul/sbn032 .

Silverstein, S. M., All, S. D., Kasi, R., Berten, S., Essex, B., Lathrop, K. L., & Little, D. M. (2010). Increased fusiform area activation in schizophrenia during processing of spatial frequency-degraded faces, as revealed by fMRI. Psychological Medicine, 40 (7), 1159–1169. doi: 10.1017/S0033291709991735 .

Silverstein, S. M., All, S. D., Thompson, J. L., Williams, L. M., Whitford, T. J., Nagy, M., … Gordon, E. (2012). Absolute level of gamma synchrony is increased in first episode schizophrenia during face processing. Journal of Experimental Psychopathology, 3 , 702–723.

Silverstein, S. M., Bakshi, S., Chapman, R. M., & Nowlis, G. (1998). Perceptual organization of configural and nonconfigural visual patterns in schizophrenia: Effects of repeated exposure. Cognitive Neuropsychiatry, 3 , 209–223.

Silverstein, S. M., Bakshi, S., Nuernberger, S., Carpinello, K., & Wilkniss, S. (2005). Effects of stimulus structure and target-distracter similarity on the development of visual memory representations in schizophrenia. Cognitive Neuropsychiatry, 10 (3), 215–229. doi: 10.1080/13546800444000029 .

Silverstein, S. M., Berten, S., Essex, B., Kovacs, I., Susmaras, T., & Little, D. M. (2009). An fMRI examination of visual integration in schizophrenia. Journal of Integrative Neuroscience, 8 (2), 175–202.

Silverstein, S. M., Harms, M. P., Carter, C. S., Gold, J. M., Keane, B. P., MacDonald, A., III, … Barch, D. M. (2015). Cortical contributions to impaired contour integration in schizophrenia. Neuropsychologia, 75 , 469–480. doi: 10.1016/j.neuropsychologia.2015.07.003 .

Silverstein, S. M., Hatashita-Wong, M., Schenkel, L. S., Wilkniss, S., Kovacs, I., Feher, A., … Savitz, A. (2006). Reduced top-down influences in contour detection in schizophrenia. Cognitive Neuropsychiatry, 11 (2), 112–132. doi: 10.1080/13546800444000209 .

Silverstein, S. M., & Keane, B. P. (2009). Perceptual organization in schizophrenia: Plasticity and state-related change. Learning and Perception, 1 , 229–261.

Silverstein, S. M., & Keane, B. P. (2011a). Perceptual organization impairment in schizophrenia and associated brain mechanisms: Review of research from 2005 to 2010. Schizophrenia Bulletin, 37 (4), 690–699. doi: 10.1093/schbul/sbr052 .

Silverstein, S. M., & Keane, B. P. (2011b). Vision science and schizophrenia research: Toward a re-view of the disorder editors’ introduction to special section. Schizophrenia Bulletin, 37 (4), 681–689. doi: 10.1093/schbul/sbr053 .

Silverstein, S. M., Keane, B. P., Barch, D. M., Carter, C. S., Gold, J. M., Kovacs, I., … Strauss, M. E. (2012). Optimization and validation of a visual integration test for schizophrenia research. Schizophrenia Bulletin, 38 (1), 125–134. doi: 10.1093/schbul/sbr141 .

Silverstein, S. M., Keane, B. P., Papathomas, T. V., Lathrop, K. L., Kourtev, H., Feigenson, K., … Paterno, D. (2014). Processing of spatial-frequency altered faces in schizophrenia: Effects of illness phase and duration. PLoS One, 9 (12), e114642. doi: 10.1371/journal.pone.0114642 .

Silverstein, S. M., Keane, B. P., Wang, Y., Mikkilineni, D., Paterno, D., Papathomas, T. V., & Feigenson, K. (2013). Effects of short-term inpatient treatment on sensitivity to a size contrast illusion in first-episode psychosis and multiple-episode schizophrenia. Frontiers in Psychology, 4 , 466. doi: 10.3389/fpsyg.2013.00466 .

Silverstein, S. M., Knight, R. A., Schwarzkopf, S. B., West, L. L., Osborn, L. M., & Kamin, D. (1996). Stimulus configuration and context effects in perceptual organization in schizophrenia. Journal of Abnormal Psychology, 105 (3), 410–420.

Silverstein, S. M., Kovacs, I., Corry, R., & Valone, C. (2000). Perceptual organization, the disorganization syndrome, and context processing in chronic schizophrenia. Schizophrenia Research, 43 (1), 11–20. doi: 10.1016/S0920-9964(99)00180-2 .

Silverstein, S. M., Moghaddam, B., & Wykes, T. (Eds.). (2013). Schizophrenia: Evolution and synthesis (Vol. 13). Cambridge, MA: MIT Press.

Silverstein, S. M., & Rosen, R. (2015). Schizophrenia and the eye. Schizophrenia Research: Cognition, 2 (2), 46–55.

Silverstein, S. M., Schenkel, L. S., Valone, C., & Nuernberger, S. W. (1998). Cognitive deficits and psychiatric rehabilitation outcomes in schizophrenia. Psychiatric Quarterly, 69 (3), 169–191.

Silverstein, S. M., Wang, Y., & Keane, B. P. (2012). Cognitive and neuroplasticity mechanisms by which congenital or early blindness may confer a protective effect against schizophrenia. Frontiers in Psychology, 3 , 624. doi: 10.3389/fpsyg.2012.00624 .

Silverstein, S. M., Wang, Y., & Roche, M. W. (2013). Base rates, blindness, and schizophrenia. Frontiers in Psychology, 4 , 157. doi: 10.3389/fpsyg.2013.00157 .

Siris, S. G. (2000). Depression in schizophrenia: Perspective in the era of “Atypical” antipsychotic agents. The American Journal of Psychiatry, 157 (9), 1379–1389.

Skottun, B. C., & Skoyles, J. R. (2007). Contrast sensitivity and magnocellular functioning in schizophrenia. Vision Research, 47 (23), 2923–2933. doi: 10.1016/j.visres.2007.07.016 .

Skottun, B. C., & Skoyles, J. R. (2009). Are masking abnormalities in schizophrenia specific to type-B masking? World Journal of Biological Psychiatry, 10 (4 Pt 3), 798–808. doi: 10.1080/15622970903051944 .

Skottun, B. C., & Skoyles, J. (2013). Is vision in schizophrenia characterized by a generalized reduction? Frontiers in Psychology, 4 , 999. doi: 10.3389/fpsyg.2013.00999 .

Slaghuis, W. L. (1998). Contrast sensitivity for stationary and drifting spatial frequency gratings in positive- and negative-symptom schizophrenia. Journal of Abnormal Psychology, 107 (1), 49–62.

Slaghuis, W. L., Holthouse, T., Hawkes, A., & Bruno, R. (2007). Eye movement and visual motion perception in schizophrenia II: Global coherent motion as a function of target velocity and stimulus density. Experimental Brain Research, 182 (3), 415–426. doi: 10.1007/s00221-007-1003-3 .

Slifstein, M., van de Giessen, E., Van Snellenberg, J., Thompson, J. L., Narendran, R., Gil, R., … Abi-Dargham, A. (2015). Deficits in prefrontal cortical and extrastriatal dopamine release in schizophrenia: A positron emission tomographic functional magnetic resonance imaging study. JAMA Psychiatry, 72 (4), 316–324. doi: 10.1001/jamapsychiatry.2014.2414 .

Snyder, S., Rosenthal, D., & Taylor, A. (1961). Perceptual closure in schizophrenics. Journal of Abnormal and Social Psychology, 63 , 131–136.

Sohal, V. S., Zhang, F., Yizhar, O., & Deisseroth, K. (2009). Parvalbumin neurons and gamma rhythms enhance cortical circuit performance. Nature, 459 (7247), 698–702. doi: 10.1038/nature07991 .

Spencer, K. M., Nestor, P. G., Niznikiewicz, M. A., Salisbury, D. F., Shenton, M., & McCarley, R. (2003). Abnormal neural synchrony in schizophrenia. The Journal of Neuroscience, 23 , 7407–7411.

Spencer, K. M., Nestor, P. G., Perlmutter, R., Niznikiewicz, M. A., Klump, M. C., Frumin, M., …. McCarley, R. (2004). Neural synchrony indexes disordered perception and cognition in schizophrenia. Proceedings of the National Academy of Sciences of the United States of America, 101 , 17288–17293.

Sun, L., Castellanos, N., Grutzner, C., Koethe, D., Rivolta, D., Wibral, M., … Uhlhaas, P. J. (2013). Evidence for dysregulated high-frequency oscillations during sensory processing in medication-naive, first episode schizophrenia. Schizophrenia Research, 150 (2–3), 519–525. doi: 10.1016/j.schres.2013.08.023 .

Sun, L., Grutzner, C., Bolte, S., Wibral, M., Tozman, T., Schlitt, S., … Uhlhaas, P. J. (2012). Impaired gamma-band activity during perceptual organization in adults with autism spectrum disorders: Evidence for dysfunctional network activity in frontal-posterior cortices. Journal of Neuroscience, 32 (28), 9563–9573. doi: 10.1523/JNEUROSCI.1073-12.2012 .

Sun, J., Tang, Y., Lim, K. O., Wang, J., Tong, S., Li, H., & He, B. (2014). Abnormal dynamics of EEG oscillations in schizophrenia patients on multiple time scales. IEEE Transactions on Biomedical Engineering, 61 (6), 1756–1764. doi: 10.1109/TBME.2014.2306424 .

Tadin, D., Kim, J., Doop, M. L., Gibson, C., Lappin, J. S., Blake, R., & Park, S. (2006). Weakened center-surround interactions in visual motion processing in schizophrenia. Journal of Neuroscience, 26 (44), 11403–11412. doi: 10.1523/JNEUROSCI.2592-06.2006 .

Tibber, M. S., Anderson, E. J., Bobin, T., Antonova, E., Seabright, A., Wright, B., … Dakin, S. C. (2013). Visual surround suppression in schizophrenia. Frontiers in Psychology, 4 , 88. doi: 10.3389/fpsyg.2013.00088 .

Tibber, M. S., Anderson, E. J., Bobin, T., Carlin, P., Shergill, S. S., & Dakin, S. C. (2015). Local and global limits on visual processing in schizophrenia. PLoS One, 10 (2), e0117951. doi: 10.1371/journal.pone.0117951 .

Tost, H., Alam, T., & Meyer-Lindenberg, A. (2010). Dopamine and psychosis: Theory, pathomechanisms and intermediate phenotypes. Neuroscience and Biobehavioral Reviews, 34 (5), 689–700. doi: 10.1016/j.neubiorev.2009.06.005 .

Turetsky, B. I., Kohler, C. G., Indersmitten, T., Bhati, M. T., Charbonnier, D., & Gur, R. C. (2007). Facial emotion recognition in schizophrenia: When and why does it go awry? Schizophrenia Research, 94 (1-3), 253–263. doi: 10.1016/j.schres.2007.05.001 .

Uhlhaas, P. J., Linden, D. E., Singer, W., Haenschel, C., Lindner, M., Maurer, K., & Rodriguez, E. (2006). Dysfunctional long-range coordination of neural activity during Gestalt perception in schizophrenia. Journal of Neuroscience, 26 (31), 8168–8175. doi: 10.1523/JNEUROSCI.2002-06.2006 .

Uhlhaas, P. J., Millard, I., Muetzelfeldt, L., Curran, H. V., & Morgan, C. J. (2007). Perceptual organization in ketamine users: Preliminary evidence of deficits on night of drug use but not 3 days later. Journal of Psychopharmacology, 21 (3), 347–352. doi: 10.1177/0269881107077739 .

Uhlhaas, P. J., & Mishara, A. L. (2007). Perceptual anomalies in schizophrenia: Integrating phenomenology and cognitive neuroscience. Schizophrenia Bulletin, 33 (1), 142–156. doi: 10.1093/schbul/sbl047 .

Uhlhaas, P. J., Phillips, W. A., Mitchell, G., & Silverstein, S. M. (2006). Perceptual grouping in disorganized schizophrenia. Psychiatry Research, 145 (2–3), 105–117. doi: 10.1016/j.psychres.2005.10.016 .

Uhlhaas, P. J., Phillips, W. A., Schenkel, L. S., & Silverstein, S. M. (2006). Theory of mind and perceptual context-processing in schizophrenia. Cognitive Neuropsychiatry, 11 (4), 416–436. doi: 10.1080/13546800444000272 .

Uhlhaas, P. J., Phillips, W. A., & Silverstein, S. M. (2005). The course and clinical correlates of dysfunctions in visual perceptual organization in schizophrenia during the remission of psychotic symptoms. Schizophrenia Research, 75 (2–3), 183–192. doi: 10.1016/j.schres.2004.11.005 .

Uhlhaas, P. J., & Silverstein, S. M. (2005a). Perceptual organization in schizophrenia spectrum disorders: Empirical research and theoretical implications. Psychological Bulletin, 131 (4), 618–632. doi: 10.1037/0033-2909.131.4.618 .

Uhlhaas, P. J., & Silverstein, S. M. (2005b). Phenomenology, biology, and specificity of dysfunctions in gestalt perception in schizophrenia. Gestalt Theory, 27 , 57–69.

Uhlhaas, P. J., & Singer, W. (2006). Neural synchrony in brain disorders: Relevance for cognitive dysfunctions and pathophysiology. Neuron, 52 (1), 155–168. doi: 10.1016/j.neuron.2006.09.020 .

Uhlhaas, P. J., & Singer, W. (2010). Abnormal neural oscillations and synchrony in schizophrenia. Nature Reviews Neuroscience, 11 (2), 100–113. doi: 10.1038/nrn2774 .

Vakhrusheva, J., Zemon, V., Bar, M., Weiskopf, N. G., Tremeau, F., Petkova, E., … Butler, P. D. (2014). Forming first impressions of others in schizophrenia: Impairments in fast processing and in use of spatial frequency information. Schizophrenia Research, 160 (1–3), 142–149. doi: 10.1016/j.schres.2014.10.012 .

Van Horn, S. C., Erisir, A., & Sherman, S. M. (2000). Relative distribution of synapses in the A-laminae of the lateral geniculate nucleus of the cat. Journal of Comparative Neurology, 416 (4), 509–520.

Van Opstal, F., Van Laeken, N., Verguts, T., van Dijck, J. P., De Vos, F., Goethals, I., & Fias, W. (2014). Correlation between individual differences in striatal dopamine and in visual consciousness. Current Biology, 24 (7), R265–R266. doi: 10.1016/j.cub.2014.02.001 .

Viertio, S., Laitinen, A., Perala, J., Saarni, S. I., Koskinen, S., Lonnqvist, J., & Suvisaari, J. (2007). Visual impairment in persons with psychotic disorder. Social Psychiatry and Psychiatric Epidemiology, 42 (11), 902–908. doi: 10.1007/s00127-007-0252-6 .

Vitay, J., & Hamker, F. H. (2007). On the role of dopamine in cognitive vision. In L. Paletta & E. Rome (Eds.), Attention in cognitive systems: Theories and Systems from an Interdisciplinary viewpoint (pp. 352–366). Berlin, Germany: Springer.

Volberg, G., & Greenlee, M. W. (2014). Brain networks supporting perceptual grouping and contour selection. Frontiers in Psychology, 5 , 264. doi: 10.3389/fpsyg.2014.00264 .

Volberg, G., Wutz, A., & Greenlee, M. W. (2013). Top-down control in contour grouping. PLoS One, 8 (1), e54085. doi: 10.1371/journal.pone.0054085 .

Wagner, P. S., & Spiro, C. S. (2008). Divided minds: Twin sisters and their journey through schizophrenia . New York, NY: St. Martin’s Press.

Wang, J., Brown, R., Dobkins, K. R., McDowell, J. E., & Clementz, B. A. (2010). Diminished parietal cortex activity associated with poor motion direction discrimination performance in schizophrenia. Cerebral Cortex, 20 (7), 1749–1755. doi: 10.1093/cercor/bhp243 .

Wang, J., Dobkins, K. R., McDowell, J. E., & Clementz, B. A. (2012). Neural response to the second stimulus associated with poor speed discrimination performance in schizophrenia. Psychophysiology, 49 (2), 198–206. doi: 10.1111/j.1469-8986.2011.01302.x .

Wang, A. Y., Lohmann, K. M., Yang, C. K., Zimmerman, E. I., Pantazopoulos, H., Herring, N., … Konradi, C. (2011). Bipolar disorder type 1 and schizophrenia are accompanied by decreased density of parvalbumin- and somatostatin-positive interneurons in the parahippocampal region. Acta Neuropathologica, 122 (5), 615–626. doi: 10.1007/s00401-011-0881-4 .

Waters, F., Collerton, D., Ffytche, D. H., Jardri, R., Pins, D., Dudley, R., … Laroi, F. (2014). Visual hallucinations in the psychosis spectrum and comparative information from neurodegenerative disorders and eye disease. Schizophrenia Bulletin, 40 (Suppl 4), S233–245. doi: 10.1093/schbul/sbu036 .

Weiss, K. M. (1989). Advantages of abandoning symptom-based diagnostic systems of research in schizophrenia. American Journal of Orthopsychiatry, 59 (3), 324–330.

Weiss, K. M. (1990). Advantages of reconceptualizing schizophrenia in clinical practice. Journal of Clinical Psychology, 46 (1), 21–28.

Weiss, K. M. (1992). On the distinctions between diagnosis, description and measurement of schizophrenia. Psychopathology, 25 (5), 239–248.

Weiss, K. M., Chapman, H. A., Strauss, M. E., & Gilmore, G. C. (1992). Visual information decoding deficits in schizophrenia. Psychiatry Research, 44 (3), 203–216.

Wilson, N. R., Runyan, C. A., Wang, F. L., & Sur, M. (2012). Division and subtraction by distinct cortical inhibitory networks in vivo. Nature, 488 (7411), 343–348. doi: 10.1038/nature11347 .

Witkovsky, P. (2004). Dopamine and retinal function. Documenta Ophthalmologica, 108 (1), 17–40.

Yang, E., Tadin, D., Glasser, D. M., Hong, S. W., Blake, R., & Park, S. (2013). Visual context processing in schizophrenia. Clinical Psychological Science, 1 , 5–15.

Yoon, J. H., Maddock, R. J., Rokem, A., Silver, M. A., Minzenberg, M. J., Ragland, J. D., & Carter, C. S. (2010). GABA concentration is reduced in visual cortex in schizophrenia and correlates with orientation-specific surround suppression. Journal of Neuroscience, 30 (10), 3777–3781. doi: 10.1523/JNEUROSCI.6158-09.201030/10/3777 .

Yotsumoto, Y., Watanabe, T., & Sasaki, Y. (2008). Different dynamics of performance and brain activation in the time course of perceptual learning. Neuron, 57 (6), 827–833. doi: 10.1016/j.neuron.2008.02.034 .

Download references

Acknowledgments

I thank Emily Kappenman, Brian Keane, Matthew Roché, Pamela Butler, Docia Demmin, Bill Phillips, and Judy Thompson for their helpful comments on earlier drafts of this paper.

Author information

Authors and affiliations.

Rutgers Biomedical and Health Sciences, Rutgers University, 151 Centennial Avenue, Piscataway, NJ, 08854, USA

Steven M. Silverstein Ph.D.

You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Steven M. Silverstein Ph.D. .

Editor information

Editors and affiliations.

Department of Psychology, University of Nebraska-Lincoln, Lincoln, Nebraska, USA

William D. Spaulding

Rights and permissions

Reprints and permissions

Copyright information

About this chapter

Silverstein, S.M. (2016). Visual Perception Disturbances in Schizophrenia: A Unified Model. In: Li, M., Spaulding, W. (eds) The Neuropsychopathology of Schizophrenia. Nebraska Symposium on Motivation, vol 63. Springer, Cham. https://doi.org/10.1007/978-3-319-30596-7_4

Download citation

DOI : https://doi.org/10.1007/978-3-319-30596-7_4

Published : 31 May 2016

Publisher Name : Springer, Cham

Print ISBN : 978-3-319-30594-3

Online ISBN : 978-3-319-30596-7

eBook Packages : Behavioral Science and Psychology Behavioral Science and Psychology (R0)

Share this chapter

Anyone you share the following link with will be able to read this content:

Sorry, a shareable link is not currently available for this article.

Provided by the Springer Nature SharedIt content-sharing initiative

Publish with us

Policies and ethics

Find a journal
Track your research

Brain network mechanisms of visual perceptual organization in schizophrenia and bipolar disorder

Find this author on Google Scholar
Find this author on PubMed
Search for this author on this site
For correspondence: [email protected]
Info/History
Preview PDF

Visual shape completion is a canonical perceptual organization process that integrates spatially distributed edge information into unified representations of objects. People with schizophrenia show difficulty in discriminating completed shapes but the brain networks and functional connections underlying this perceptual difference remain poorly understood. Also unclear is whether similar neural differences arise in bipolar disorder or vary across the schizo-bipolar spectrum. To address these topics, we scanned (fMRI) people with schizophrenia, bipolar disorder, or no psychiatric illness during rest and during a task in which they discriminated configurations that formed or failed to form completed shapes (illusory and fragmented condition, respectively). Multivariate pattern differences were identified on the cortical surface using 360 predefined parcels and 12 functional networks composed of such parcels. Brain activity flow mapping was used to evaluate the likely involvement of resting-state connections for shape completion. Illusory/fragmented task activation differences (“modulations”) in the dorsal attention network (DAN) could distinguish people with schizophrenia (AUCs>.85) and could trans-diagnostically predict cognitive disorganization severity. Activity flow over functional connections from the DAN could predict secondary visual network modulations in each group, except among those with schizophrenia. The secondary visual network was strongly and similarly modulated in each subject group. Task modulations were dispersed over a larger number of networks in patients compared to controls. In summary, abnormal DAN activity emerges during perceptual organization in schizophrenia and may be related to improper attention-related feedback into secondary visual areas. Patients with either disorder may compensate for abnormal perception by relying upon non-visual networks.

Competing Interest Statement

The authors have declared no competing interest.

Funding Statement

This work was funded by a National Institutes of Health Mentored Career Development Award (K01MH108783) to BPK.

Author Declarations

I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained.

The details of the IRB/oversight body that provided approval or exemption for the research described are given below:

The study followed the tenets of the Declaration of Helsinki and was approved by the Rutgers University Institutional Review Board.

I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals.

I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance).

I have followed all appropriate research reporting guidelines and uploaded the relevant EQUATOR Network research reporting checklist(s) and other pertinent material as supplementary files, if applicable.

↵ * Co-senior authors

Dedications : None

Declarations of Interest : The authors declare no competing conflicts of interest.

The manuscript has been shortened and the introduction and discussion have been rewritten. Certain analyses have even placed in the 'Supplementary material' near the bottom of the manuscript.

Data Availability

Neural data will be released on OpenNeuro.org along with resting-state functional connectivity matrices and unthresholded task activation maps.

View the discussion thread.

Thank you for your interest in spreading the word about medRxiv.

NOTE: Your email address is requested solely to identify you as the sender of this article.

Citation Manager Formats

EndNote (tagged)
EndNote 8 (xml)
RefWorks Tagged
Ref Manager
Tweet Widget
Facebook Like
Google Plus One

Subject Area

Psychiatry and Clinical Psychology
Addiction Medicine (349)
Allergy and Immunology (671)
Anesthesia (181)
Cardiovascular Medicine (2660)
Dentistry and Oral Medicine (316)
Dermatology (224)
Emergency Medicine (401)
Endocrinology (including Diabetes Mellitus and Metabolic Disease) (950)
Epidemiology (12261)
Forensic Medicine (10)
Gastroenterology (765)
Genetic and Genomic Medicine (4122)
Geriatric Medicine (387)
Health Economics (681)
Health Informatics (2668)
Health Policy (1007)
Health Systems and Quality Improvement (989)
Hematology (364)
HIV/AIDS (855)
Infectious Diseases (except HIV/AIDS) (13714)
Intensive Care and Critical Care Medicine (800)
Medical Education (399)
Medical Ethics (109)
Nephrology (440)
Neurology (3908)
Nursing (210)
Nutrition (580)
Obstetrics and Gynecology (742)
Occupational and Environmental Health (697)
Oncology (2043)
Ophthalmology (587)
Orthopedics (242)
Otolaryngology (306)
Pain Medicine (250)
Palliative Medicine (75)
Pathology (473)
Pediatrics (1116)
Pharmacology and Therapeutics (466)
Primary Care Research (453)
Psychiatry and Clinical Psychology (3449)
Public and Global Health (6548)
Radiology and Imaging (1407)
Rehabilitation Medicine and Physical Therapy (818)
Respiratory Medicine (871)
Rheumatology (411)
Sexual and Reproductive Health (410)
Sports Medicine (343)
Surgery (452)
Toxicology (54)
Transplantation (186)
Urology (167)

An official website of the United States government

The .gov means it’s official. Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Publications
Account settings

Preview improvements coming to the PMC website in October 2024. Learn More or Try it out now .

Advanced Search
Journal List
Elsevier Sponsored Documents

Visual Perception and Its Impairment in Schizophrenia

Pamela d. butler.

a Nathan Kline Institute for Psychiatric Research, Orangeburg

b Department of Psychiatry, New York University School of Medicine, New York, New York

c City University of New York, New York, New York

Steven M. Silverstein

d University of Medicine and Dentistry of New Jersey—University Behavioral HealthCare and Robert Wood Johnson Medical School Department of Psychiatry, Piscataway, New Jersey

Steven C. Dakin

e Institute of Ophthalmology, University College London, United Kingdom.

Much work in the cognitive neuroscience of schizophrenia has focused on attention, memory, and executive functioning. To date, less work has focused on perceptual processing. However, perceptual functions are frequently disrupted in schizophrenia, and thus this domain has been included in the CNTRICS (Cognitive Neuroscience Treatment Research to Improve Cognition in Schizophrenia) project. In this article, we describe the basic science presentation and the breakout group discussion on the topic of perception from the first CNTRICS meeting, held in Bethesda, Maryland on February 26 and 27, 2007. The importance of perceptual dysfunction in schizophrenia, the nature of perceptual abnormalities in this disorder, and the critical need to develop perceptual tests appropriate for future clinical trials were discussed. Although deficits are also seen in auditory, olfactory, and somatosensory processing in schizophrenia, the first CNTRICS meeting focused on visual processing deficits. Key concepts of gain control and integration in visual perception were introduced. Definitions and examples of these concepts are provided in this article. Use of visual gain control and integration fit a number of the criteria suggested by the CNTRICS committee, provide fundamental constructs for understanding the visual system in schizophrenia, and are inclusive of both lower-level and higher-level perceptual deficits.

Much work in the cognitive neuroscience of schizophrenia has focused on attention, memory, and executive functioning. Less work has focused on perceptual processing. Indeed, during the National Institute of Mental Health MATRICS (Measurement and Treatment Research to Improve Cognition in Schizophrenia) consensus process, perception was not identified as one of the core cognitive domains relevant to schizophrenia or its treatment ( 1 ). This omission is in one sense appropriate, because a goal of MATRICS was to identify existing neuropsychological tests that are useful for clinical trials of schizophrenia, and tests of perception are not widely used by neuropsychologists. In contrast, as we demonstrate in the following text, the omission of assessment of perceptual function from the MATRICS battery means that a set of functions that are frequently disrupted in schizophrenia are not being routinely assessed in clinical trials. This situation is likely to be remedied through the CNTRICS (Cognitive Neuroscience Treatment Research to Improve Cognition in Schizophrenia) project. In the following sections, we describe the outcome of presentations and breakout groups on the topic of perception from the first CNTRICS meeting. These recognize the importance of perceptual dysfunction in schizophrenia, the nature of perceptual abnormalities associated with this disorder, and the critical need to develop perceptual tests for future clinical trials. Although there are also auditory, olfactory, and somatosensory deficits in schizophrenia, the CNTRICS meeting focused on visual processing. A great deal of work has been done on visual processing in schizophrenia, and the visual system is well-characterized from a physiological point of view in normal subjects and is a useful system for evaluating basic concepts of perceptual dysfunction in schizophrenia.

Basic Science of Perceptual Processing

Visual system basics.

Our current view of the architecture of the early visual system and cortical processing streams is given in Figure 1 . The visual system consists of several different pathways, including the magnocellular (M) and parvocellular (P) pathways beginning in the retina and projecting, via the lateral geniculate nucleus (LGN) of the thalamus, to different layers of primary visual cortex (V1).

An external file that holds a picture, illustration, etc.
Object name is gr1.jpg

(A) Architecture of the early visual system [left part adapted by permission from Macmillan Publishers Ltd: Nat Rev Neurosci 8:276–286, copyright 2007 ( 87 ); (B) Visual cortical processing streams. LGN, lateral geniculate nucleus; Pulv, pulvinar; SC, superior colliculus.

The M system is driven by neurons in the LGN with large cell bodies and, in general, conducts low-resolution visual information rapidly to cortex and is involved in initial attentional capture (typically by stimulus onset/offset and/or movement) and processing of overall stimulus organization ( 2–5 ). The P system originates with LGN neurons with smaller cell bodies and, in contrast, conducts high-resolution visual information to cortex and is involved in processing of fine-grained stimulus details and object identification ( 2,6 ). Specific properties of the M and P pathways give rise to these functions. For instance, the M pathway has low spatial resolution, detects low contrast and motion, is color-blind, and has a fast response ( 7,8 ). The P pathway has high spatial resolution, does not respond to low contrast, is color tuned, and has a slow response 1 .

The M and P pathways project mainly to the dorsal (“where,” parieto-occipital) and ventral (“what,” tempero-occipital) streams, respectively, although there is significant interaction between these streams. Functions of the dorsal stream include eye movement control, action guidance, initial attention modulation, motion perception, and visual/somatosensory integration. In the parietal/occipital region, the dorsal stream incorporates areas V3 and middle temporal/medial superior temporal area (MT/MST). As information moves up the hierarchy, more complex processing is achieved. For instance, while V1 is involved with measuring local motion (of small objects), as signals move to higher cortical areas, processing of greater areas of visual space become possible such that V3 is involved in global motion (of larger, more complex objects), and MT/MST mediate global motion and eye movements. The function of the ventral stream is object recognition. It is also modulated by attention due to inputs from frontal cortex and dorsal stream. Again, as information moves up the hierarchy, more complex processing is achieved. The ventral stream processes orientation and size (V1), contour and form (V2), then shape (V4), and finally objects and faces (IT) ( 9,10 ).

A central concept in understanding how neurons respond to visual information is that, when stimuli fall in a region of space known as the receptive field, they induce neurons to fire. For example, ganglion cells in the retina do not respond well to uniform fields of light but do respond to spots of light ( 11 ). Some neurons in the LGN respond to larger spots of light (i.e., have larger receptive fields), and others respond to smaller spots of light (i.e., have smaller receptive fields). Light around the spot, such as occurs when a uniform field of light is presented, will inhibit neurons from firing. This confers on the neuron the ability to signal change in luminance. The size and complexity of receptive fields increases as one progresses through the visual hierarchy: in the retina/LGN receptive fields respond preferentially to spots of light, in V1 they are tuned for orientation (preferring lines or bars) ( 12 ), and in area V2 they respond preferentially to corners or junctions ( 13 ), whereas in V4 they prefer more complex feature arrangements ( 14 ).

Functional Concepts: Definitions of Gain Control and Integration

Visual processing involves several types of neural interactions, including lateral excitatory facilitation, inhibition, and top-down feedback. We divide these interactions into two classes, on the basis of their effects: the first is concerned with optimization of response levels (gain control), and the second is concerned with grouping of neural responses through enhanced neural co-activation (integration).

Gain Control

Gain control refers to processes that allow sensory systems to adapt and optimize their responses to stimuli within a particular surrounding context. Gain control is primarily concerned with controlling the dynamic range of neural response and can in that sense be considered a lower-level class of process than other modulatory processes (such as integration), even though it is likely that it operates at all levels of the visual system. Gain control mechanisms might reflect both intrinsic neuronal properties and lateral interactions between neurons. These processes permit sensory subsystems to modulate their response levels to take into account spatial and temporal context. Gain control processes also assist sensory subsystems in optimizing overall response levels within a limited dynamic signaling range and in increasing contrast between adjacent and successive stimuli. These interactions amplify or attenuate the signal and thus affect integrity of sensory registration.

Gain control in the visual system has been largely studied in early stages of processing such as at the level of the LGN or primary visual cortex. There are a number of ways in which neurons can be influenced by their neighbors in order to control the signaling range and/or indicate salience. These include intracellular mechanisms, direct excitatory and inhibitory connections between neurons, and feedback.

One example in which gain control likely plays a role is in the signaling of salience within a “pop-out” phenomenon ( Figure 2 ). Let us suppose we are interested in signaling the presence of the orientation discrepancy in the lower right corner of the texture. We further suppose the visual system achieves this by pooling responses across a population of orientation-tuned neurons in V1. The top row shows the “raw” neural response where gain control is not operating; the pooled response is uniform—all neurons are responding equally. In the bottom row, divisive gain control is operating. Now the large number of neighboring neurons that receive the same horizontal stimulation inhibit each other and decrease signaling, allowing the response arising from the small diagonally textured patch to “pop out.”

An external file that holds a picture, illustration, etc.
Object name is gr2.jpg

Gain control can contribute to orientation “pop-out.” In this example, the top row of the right side of the figure shows the “raw” neural response where gain control is not operating. In the bottom row, divisive gain control is operating and the large number of neighboring neurons that receive the same horizontal stimulus inhibit each other and decrease signaling, allowing the response from the small diagonally textured patch to “pop out.” Under this view the visual system operates as a cascaded gain-control/integration system, deriving increasingly complex types of salience.

Another example of gain control involves the M pathway where neurons show a steeply rising increase in response to low-contrast stimuli, which reaches a saturation-level once luminance contrast reaches approximately 16% ( 7 ). This leads to a characteristic S-shaped, nonlinear contrast gain control curve ( Figure 3 A). The initial steeply rising part of the curve reflects substantial amplification of low-contrast stimuli, permitting M-pathway neurons to respond robustly even at low contrasts. The nonlinear gain control mechanisms, however, result in saturating responses at higher contrasts. Neurons in the P-pathway exhibit less gain control than M-pathway neurons. Thus, they are less responsive at lower contrasts, but their responses do not saturate at higher contrasts. In construction of future tasks to study gain control, including behavioral tasks, it is important to include both low- and high-contrast stimuli to demonstrate how perceptual responses change in patients when stimulus contrast changes from low to high levels.

An external file that holds a picture, illustration, etc.
Object name is gr3.jpg

Contrast response functions and N-methyl d-aspartate (NMDA) effects ( [A] . Adapted from Kwon et al. [ 16 ], used with permission; [B and C] adapted from Butler et al. Arch Gen Psychiatry , May 2005, 62, 495–504, copyright © 2005, American Medical Association, all rights reserved [ 22 ]). The NMDA antagonists produce shallower gain at low contrast and a much lower plateau in visual evoked potential responses indicating decreased signal amplification. The patient visual evoked potential contrast response curve in the magnocellular condition shows similar decreased gain at low luminance contrast and a lower plateau, indicating decreased signal amplification.

Visual pathways within the brain use glutamate as their primary neurotransmitter, and N-methyl d-aspartate (NMDA) seems to have a central role in gain control. For instance, NMDA receptors amplify responses to isolated stimuli as well as amplifying the effects of lateral inhibition (e.g., increase surround antagonism of center receptive field responses) ( 15 ). Thus, an NMDA deficit would result in decreased amplification and less lateral inhibition. Indeed, NMDA antagonists produce shallower gain at low contrast and a much lower plateau indicating decreased signal amplification ( 16,17 ) ( Figure 3 A).

Integration

Integration refers to processing one step beyond the registration of brightness, color, orientation, motion, and depth cues. Integration is the process linking the output of neurons that individually code local (often small) attributes of a scene into global (typically larger) complex structure, more suitable for the guidance of behavior. Recurrent innervation of primary cortex by higher levels leads to recurrent interaction between regions that can further increase the salience of grouped stimuli. Integration underpins Gestalt grouping phenomena and object recognition. Cells in later visual areas code more global/complex properties by integrating the response of neurons with smaller receptive fields that code, for example, (local) form and motion. Mechanisms of integration include direct connectivity between neurons (e.g., excitation/inhibition and synchronization) as well as feedback ( 18 ). In V1, there are contextual influences on local processing, and at higher levels, possibly as early as V2, integration occurs in terms of global grouping of contextual structure (e.g., contours) ( Figure 4 ).

An external file that holds a picture, illustration, etc.
Object name is gr4.jpg

Contextual effects on orientation (reprinted from Neuron , 48, Dakin S and Frith U, Vagaries of visual perception in autism, 497–507, copyright 2005, with permission from Elsevier [ 88 ]). Oriented structure within our complex visual environment leads to various types of interactions between detectors in V1 (blue region), including integration (“+” connections) and gain control (“−” connections).

Implications

Gain control and integration are both involved in the perception of complex stimuli. Sensory systems use gain control to adapt and optimize responses so that they can then be successfully integrated at higher levels of the visual system via recurrent interactions between areas.

Gain Control in Schizophrenia

Gain control plays an important role in our perception of contrast and motion in that it allows sensory subsystems to maximize the response-difference arising from different stimuli. Several methods have been used for assessing contrast detection in schizophrenia. First, patients with schizophrenia show decreased contrast sensitivity (i.e., need more contrast to detect a grating) across a range of grating-sizes in behavioral studies ( 19,20 ). 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.

Stimulus response properties of M- and P-neurons overlap significantly, making differentiation difficult, particularly in behavioral studies. Nevertheless, features that bias stimuli toward the M-pathway include high temporal frequency, low spatial frequency, low absolute luminance, and low contrast. Although behavioral studies have found contrast sensitivity deficits across spatial frequencies, often thresholds are relatively low (e.g., < 10% contrast; [ 20 ]), limiting P-pathway involvement. In one study in which thresholds were higher (e.g., > 16% contrast), relative preservation at high spatial frequencies was observed ( 22 ). Similarly, larger contrast sensitivity deficits were found when stimuli were presented dynamically rather than statically, also suggesting greater M-pathway, than P-pathway, impairment ( 19 ).

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 3 B and and3C). 3 C). To the extent that P-pathway dysfunction occurs, patient curves show decreased gain at low luminance contrast and a lower plateau, indicating decreased signal amplification, as in the M-pathway. The decreased slope at low contrast and decreased plateau in patients closely resembles results seen after microinfusion of an NDMA antagonist into cat LGN and visual cortex ( 16,17 ) ( Figure 3 A and and3B), 3 B), consistent with glutamatergic theories of schizophrenia ( 23–25 ).

A third approach uses an illusion in which the contrast of a small textured disk appears reduced when presented within a high-contrast surround compared with when it is presented in isolation ( 26 ) ( Figure 5 ). Note that stimuli used in this study were presented greatly above their contrast detection threshold. Patients with schizophrenia were much less susceptible to the illusion, with 12 of 15 patients being more accurate (less biased) than the most accurate control ( 27 ). These results are consistent with decreased center-surround antagonism and hence decreased contrast gain control in schizophrenia patients. Gain control in this illusion might be due to short-range lateral interactions (e.g., γ-aminobutyric acid [GABA]-ergic projections).

An external file that holds a picture, illustration, etc.
Object name is gr5.jpg

The “contrast-contrast” illusion reveals contrast gain control deficits in schizophrenia (reprinted from Curr Biol , 15, Dakin S, Carlin P, Hemsley D, Weak suppression of visual context in chronic schizophrenia, R822–824, copyright 2005, with permission from Elsevier [ 27 ]). (A) The small region at the center of the large circular patch is physically identical to the small patch at the top left but generally seems to be of much lower contrast as a consequence of contrast gain control. (B) One can quantify this effect by plotting the probability that subjects said the central patch was higher contrast than a matching variable contrast reference patch. A typical control subject (green line) indicated that the central patch had a substantially lower contrast than it actually did (indicated by the shift in the green curve to lower reference contrasts). Data from a representative patient with schizophrenia (red line) indicated that they were not susceptible to the illusion and matched the contrast largely correctly.

A large number of studies have reported motion processing deficits in schizophrenia ( 28–32 ). Motion is signaled by direction-sensitive cells in V1 and then pooled by MT neurons with: 1) larger receptive fields, and 2) center-surround antagonism (as a likely substrate for gain control). A recent study ( 33 ) provides evidence for decreased gain control in schizophrenia in a motion discrimination task. Whereas center-surround antagonism in control subjects resulted in reduced ability to perceive motion of a high-contrast stimulus as its size increased, patients with schizophrenia did not show this reduction in motion perception. Importantly, like Dakin et al. ( 27 ), these authors find that a disruptive context has less influence on patients than on controls, arguing against nonspecific deficits or lack of attention as an underlying cause of differences. Increased center-surround antagonism, indicative of increased gain control, has also been found in motion studies in schizophrenia ( 34 ).

Significant correlations between impaired motion perception and M-pathway dysfunction also point to motion processing deficits in schizophrenia resulting from impaired gain control ( 28 ). Patients with schizophrenia show preferential M-pathway dysfunction ( 21,22,28,35–38 ), although deficits have also been observed in parvocellular processing ( 19,20 ). The M-pathway has several properties (speed of processing, low spatial resolution) that make it a suitable physiological substrate for gain control ( 39 ). The P-pathway also exhibits nonlinear gain characteristics, although less so than the M-pathway. Mechanisms of gain control dysfunction include NMDA and GABA-ergic dysfunction. Indeed, NMDA dysfunction seems to be linked to gain control in the M-pathway. Other neurotransmitters (e.g., 40 ), which are also implicated in schizophrenia, also modulate visual processing. For example, dopamine deficiency has been linked to impaired perceptual and electrophysiological response to contrast signals including those presented in a center surround paradigm ( 41,42 ). A recent neurophysiological study suggests that nicotine increases gain control in the visual cortex ( 43 ). This might be important in understanding “self-medication” with smoking and strengthens the hypothesis of weak gain control in schizophrenia. It is a challenge to understand and reconcile the involvement of different types of neurotransmitters in visual perception. It is also unclear whether perceptual deficits exhibited by people with schizophrenia for the processing of transient (moving/flickering) stimuli arise from intrinsic dorsal stream dysfunction or from aberrant M-pathway input ( 21,44 ).

In summary, gain control studies in schizophrenia clearly show that patients have difficulty modulating neuronal responses to take advantage of the surrounding context. There is also evidence that gain control deficits, seen in contrast detection and M-pathway deficits, are important in predicting outcome ( 22,45 ), and are related to higher-level problems in perceptual organization ( 28,46 ) and to symptomatology ( 20,47–51 ).

Integration in Schizophrenia

Visual integration deficits are seen in contrast, contour, form, and motion processing in schizophrenia. For example, in the last 10 years the connectivity supporting the integration of orientation across space (into extended visual contours) has been studied psychophysically with so-called “flank facilitation” paradigms ( 52 ). Here one measures the detectability of a low-contrast oriented target in the presence of two similar higher-contrast flanking patches arranged so the triplet forms an elongated contour. With some target-flank separations control subjects find it easier to detect the central element when the flanks are present than when they are absent (facilitation). Patients with schizophrenia do not exhibit such a difference, suggesting a failure in ability to integrate the collinear flankers ( 53 ). This would seem to implicate weaker interactions between orientation detectors possibly mediated by abnormal long-range horizontal connectivity in V1.

There are numerous examples of poor form processing in schizophrenia that would seem to directly implicate integration deficits. These include deficits in object recognition, grouping, perceptual closure, face processing, and reading ( 54–62 ). Classic studies show that there is less influence of global on local processing ( 54,58 ). Indeed, patients perform better than control subjects under conditions when global integration would normally interfere with responses to individual elements ( 54,56,58 ). A number of studies have used a psychophysically rigorous contour integration paradigm ( 63 ). This task examines the ability to perceive a contour made up of separate elements within a background of noise elements. Both the contour segments, and background noise elements are small oriented Gabor elements, which are designed to be well-matched to the spatial frequency processing characteristics of orientation-selective simple cells in primary visual cortex (V1); therefore they are ideal for the examination of these features and their integration. Embedded contours constructed from such elements cannot be detected by purely local feature detectors or by the known types of orientation-tuned neurons with large receptive fields (e.g., 64 ); their detection requires the integration of local orientation measurements ( Figure 6 ). Deficits in contour integration have been extensively documented in schizophrenia ( 57,65–67 ). This is thought to result from decreased NMDA-modulated lateral excitation among the spatial filters signaling these elements and the consequent reduction in synchronization of this neural activity ([ 68 ]; see also for reviews [ 69,70 ]). Simpler Gestalt tasks, involving perception of basic shapes with nonfragmented contours, are not affected in schizophrenia, however ( 71 ).

An external file that holds a picture, illustration, etc.
Object name is gr6.jpg

Performance of the schizophrenia group (dashed line) and healthy control group (solid line) across six conditions of contour element jitter manipulation. The subject's task was to indicate, with a two-button response device, on each trial, whether the narrow part of the egg-shaped contour is pointing to the left or the right. With increasing element jitter (± the number of degrees noted on the x axis), the correlations between adjacent contour elements decrease, and perception of the contour amidst dense background noise becomes more difficult. The left-hand side shows the increasing element jitter of the adjacent contours amidst the background noise. Schizophrenia patients were not able to perform at above chance levels in the two most difficult conditions (reprinted from Computers in Human Behavior , 22, Kozma-Wiebe P, et al ., Development of a world-wide web based contour integration test, 971–980, 2006, with permission from Elsevier [ 65 ]).

Interactions between dorsal and ventral streams and frontal cortex provide one model for how form integration deficits might arise in schizophrenia. Processing is substantially faster via the dorsal stream, which would permit it to prime ventral stream areas ( 72–74 ). A fundamental role of the M system/dorsal stream might be to produce a low-resolution template of the visual scene that influences perceptual processes, such as categorization of natural images, object recognition, and perceptual grouping in the ventral occipito-temporal cortex, by allowing P pathway fine-detailed input to be used more effectively ( 3,75–80 ). With a perceptual closure paradigm Doniger et al. ( 59 ) found that patients had impaired ability to recognize fragmented pictures. Patients also had decreased amplitude of the dorsal stream-generated P100-evoked potential component, which occurred earlier in time than impairment in the ventral stream-generated closure negativity (N cl ) component associated with object recognition. Initial P input to the ventral stream was normal as indicated by an intact N1 component. Thus, the impaired behavioral closure and decreased N cl seem to be due to lack of interactions between dorsal and ventral stream areas leading to decreased priming of ventral stream. This provides an example of integration deficits due to lack of recurrent interactions in schizophrenia.

As discussed in the preceding text, numerous studies have shown motion processing deficits in schizophrenia ( 28,30–32,81 ). Whereas gain control is involved in motion deficits (e.g., 33), processing of motion also clearly involves integration, because motion is signaled by direction-sensitive cells in V1 whose responses are then pooled by MT neurons with larger receptive fields to signal complex motion.

In summary, there are numerous examples of integration deficits in schizophrenia. Impairments in visual integration have been linked to increases in disorganized symptoms ( 57,66,67 ), poorer premorbid social functioning ( 82 ), presence of childhood trauma in schizophrenia ( 83 ), and illness severity and chronicity ( 84 ).

How the Constructs Fit the Criteria

First, this construct is readily measured in humans with such tasks as contrast sensitivity, contrast illusions, visual evoked potential contrast paradigms activating the M pathway, and pop-out stimuli. Second, there is strong evidence of impairment in schizophrenia. Third, there is relatively strong clarity of the link to neural circuitry. In vision, gain control is generally related to mechanisms in the LGN and visual cortex, and deficits have been found in these areas in diffusion tensor imaging, functional magnetic resonance imaging, and post-mortem anatomical studies. Fourth, there is a moderate amount of clarity of the understanding of the mechanisms. Use of the construct of gain control with the concomitant emphasis on short-term lateral interactions, center-surround mechanisms, and intrinsic neuronal properties specified in the definition provide mechanisms known to be involved and that need further testing. Fifth, there are explicit animal models that include recording of evoked potentials in cats and monkeys, particularly after NMDA antagonist infusion. Further models need to be developed. Sixth, there are strong links to neural systems through neuropsychopharmacology. Links have been found to NMDA, GABA-ergic, and nicotine function. Seventh, measures are highly amenable for use in human imaging studies. Finally, there are moderate links to functional outcome, and more work is needed in this area.

First, integration is readily measured in humans with grouping, perceptual closure, face processing, and contour integration tasks. Second, there is strong evidence of impairment in schizophrenia. Third, there is moderate evidence of a link to neural circuitry. Integration involves V2 and higher areas. There is much evidence for this in healthy subjects, but less evidence for actual disturbance in these specific circuits in schizophrenia, because most studies have been behavioral. Fourth, there is a relatively strong amount of clarity of the mechanisms. Mechanisms include long-range lateral interactions and recurrent processing. Deficits in paradigms such as contour integration are thought to be related to NMDA-modulated lateral excitation among the spatial filters signaling these elements as well as GABA-related inhibition of noise. Fifth, animal models of integration deficits have not been developed. Sixth, link to neural systems through neuropsychopharmacology is not well developed. Giersch et al. ( 85 ) have demonstrated effects of lorazepam and other benzodiazepines on GABA inhibitory activity on a visual closure task, but further work needs to be done. Seventh, measures are highly amenable for use in human imaging studies. Eighth, there is a moderately strong link to functional outcome in schizophrenia. For instance, there is high face validity regarding functional outcome for deficits in gestalt processing, perceptual closure, face processing, reading, and contour integration. In addition, there is evidence that perceptual organization deficits are linked to poorer premorbid social functioning (which is associated with poor outcome) and at least one study linking these deficits with longer stays in state hospitals.

Other Perceptual Constructs Discussed at the Meeting

In addition to visual gain control and integration, a number of other constructs were discussed during the Perceptual Breakout Session at the meeting and were also felt to be potential candidates for consideration. These included: 1) early auditory processing that can be assessed with tone matching and auditory event-related potential paradigms; 2) auditory integration that can be assessed with phonemic/linguistic processing, prosody, auditory object processing, streaming/cocktail party, and reafferentation paradigms; 3) olfactory processing; 4) somatosensory processing/reafferentation; and 5) cross-modal integration.

Conclusions

Gain control and integration are readily measured in humans, and there is strong evidence of their impairment in schizophrenia. A strength of both constructs is that they are grounded in both computational and cognitive theory and known brain function in humans and animals. Both constructs have been reliably measured with a range of paradigms. Both constructs are essential for perceptual function. Further study of these constructs in schizophrenia will be helpful in understanding the substrates of perceptual deficits in schizophrenia and the contribution of perceptual deficits to higher-level dysfunction. However, it is important to note that both gain control and integration are complicated constructs.

There are a number of practical advantages of these constructs: 1) testing is straightforward (cards/computers); 2) behavioral tests can elicit superior performance in schizophrenia, ruling out attentional/top down effects; 3) the underlying neural circuitry is becoming clearer; 4) imaging visual areas is straightforward, because they are large and many of them are located near the cortical surface; and 5) drug models (e.g., ketamine) and animal models (macaque) are established.

In conclusion, consistent deficits in visual processing are observed in schizophrenia. Reductions in gain control and integration can account for findings from a number of experimental paradigms (including contrast detection, gestalt processing, motion perception, and eye-movement control). The neurophysiology of both processes is likely to involve effects of glutamatergic activity at NMDA receptors and interactions between M- and P-pathways. Moreover, some tasks have been designed so that reduced gain control or integration leads to superior performance compared with control subjects, ruling out the possibility that the impairment reflects a generalized deficit.

Acknowledgments

Preparation of this article was supported in part by Grant RO1MH66374 from the National Institute of Mental Health (PDB), an Independent Investigator Award from the National Alliance for Research on Schizophrenia and Depression (SMS), and the Wellcome Trust (SCD).

We gratefully acknowledge Dr. Daniel C. Javitt's role as the Clinical Consultant on Perception in this process as well as the contributions of all of the members of the Perception Discussion Group at the first CNTRICS meeting.

None of the authors has a biomedical financial interest or potential conflict of interest.

1 There is also evidence (reviewed in Hendry and Reid [ 86 ]) for a third class of “koniocellular” neurons in LGN with very small cell bodies. These cells are thought to drive a third visual pathway that remains poorly understood but is thought to be involved in integration of somatosensory-proprioceptive information.

Search Menu
Sign in through your institution
Advance articles
Editor's Choice
Supplements
Submission Site
Author Guidelines
Open Access
Why publish with this journal?
About Schizophrenia Bulletin
About the University of Maryland School of Medicine
About the Maryland Psychiatric Research Center
About the NIH Public Access Policy
Editorial Board
Advertising and Corporate Services
Journals Career Network
Self-Archiving Policy
Dispatch Dates
Journals on Oxford Academic
Books on Oxford Academic

University of Maryland School of Medicine

Article Contents

Introduction: the complex relationship between visual loss and psychosis, the bayesian brain, predictive coding approaches to the symptoms of schizophrenia, the primacy of vision in inferring the causes of sense-data and shaping our representation of the world, sensory impairment as a window onto psychosis, the challenge faced by the developmentally visually deprived brain, a computational solution to the challenge of visual deprivation: evidence for increased top-down/neuromodulatory drive in congenitally blind individuals, how might computational changes occurring in the visually deprived brain protect against schizophrenia, altered conscious vision, reality, and psychosis, psychosis and schizophrenia, conclusion and predictions, acknowledgments, conflict of interest statement.

< Previous

Blindness, Psychosis, and the Visual Construction of the World

Article contents
Figures & tables
Supplementary Data

Thomas A Pollak, Philip R Corlett, Blindness, Psychosis, and the Visual Construction of the World, Schizophrenia Bulletin , Volume 46, Issue 6, November 2020, Pages 1418–1425, https://doi.org/10.1093/schbul/sbz098

Permissions Icon Permissions

The relationship between visual loss and psychosis is complex: congenital visual loss appears to be protective against the development of a psychotic disorder, particularly schizophrenia. In later life, however, visual deprivation or visual loss can give rise to hallucinosis, disorders of visual insight such as blindsight or Anton syndrome, or, in the context of neurodegenerative disorders, more complex psychotic presentations. We draw on a computational psychiatric approach to consider the foundational role of vision in the construction of representations of the world and the effects of visual loss at different developmental stages. Using a Bayesian prediction error minimization model, we describe how congenital visual loss may be protective against the development of the kind of computational deficits postulated to underlie schizophrenia, by increasing the precision (and consequent stability) of higher-level (including supramodal) priors, focusing on visual loss-induced changes in NMDA receptor structure and function as a possible mechanistic substrate. In simple terms, we argue that when people cannot see from birth, they rely more heavily on the context they extract from the other senses, and the resulting model of the world is more impervious to the false inferences, made in the face of inevitably noisy perceptual input, that characterize schizophrenia. We show how a Bayesian prediction error minimization framework can also explain the relationship between later visual loss and other psychotic symptoms, as well as the effects of visual deprivation and hallucinogenic drugs, and outline experimentally testable hypotheses generated by this approach.

Research on vision in psychosis has aimed to characterize the mechanisms of hallucinations 1 or elucidate visual deficits. 2 , 3 Little research has focused on visual loss and the development of psychosis.

The age of onset of visual loss may be crucial. Strikingly, the absence of vision at birth appears to protect against psychosis, whereas later-life visual loss appears to predispose to the development of psychotic symptoms. In this article, we explore this complex relationship, and the role of vision in constructing models of the world—which become dysfunctional in psychosis.

Very few other medical disorders that may be protective against psychosis have been identified: rheumatoid arthritis is the most notorious example. 4 Why might congenital blindness be protective? 5 , 6 Demonstrating a negative association between two disorders with low prevalence is a challenge, but if the risk of schizophrenia and congenital blindness were independent, the probability of not finding any cases of co-occurrence in the literature is exceedingly small. 7 Congenital peripheral (as opposed to cortical) blindness have been reported to co-occur with schizophrenia, although these reports do not utilize contemporary diagnostic criteria 8 , 9 ; furthermore, some reported cases are of early blindness (eg, earlier than 6 years of age) rather than being truly congenital.

More recently, a population-wide study of nearly half a million people found no occurrences of congenital/early cortical blindness and schizophrenia or broadly defined psychosis, and a lower-than-expected rate in individuals with congenital/early peripheral blindness. 10 On the other hand, lower visual acuity in adolescence is associated with increased psychosis risk. 11

The lack of association is particularly surprising given that congenital blindness often results from perinatal infections or trauma, or chromosomal disorders, 12 all of which are independently associated with psychosis. 13–15 Congenital rubella syndrome, eg, predisposes to both schizophrenia and congenital blindness but there are no documented cases of their co-occurrence. 16

The relationships between visual loss and the development of psychosis might be explained through the lens of predictive coding, a potentially unifying framework for behavioral and physiological data in both schizophrenia and blindness.

Predictive coding accounts of psychosis take as their starting point the assumption that the brain is a hierarchical Bayesian inference machine. In Bayesian inference, prior predictions about the world are represented as probability distributions of the causes of inputs lower in the hierarchy. These priors are then combined with data to form a posterior probability distribution. How much weight the prior has relative to the data is determined by the inverse variance of the prior probability distribution, or precision. The relative precision of priors and sensory likelihood (ie, the precision of prior and sensory prediction errors) determine whether sensory data are discounted. If sensory precision is high relative to prior precision, then sensory prediction errors invoke a much greater belief updating. Conversely, if the precision of prior prediction errors is greater than sensory precision, sensory evidence is effectively ignored. Noisy parties may yield a relatable example. If you are at a crowded party with someone you have just met, you may find it harder to understand what they say, because your model of their speech will not be as precise as it would be say for a beloved partner. 17 When someone is well known, the precision of your prior beliefs about them is higher and you can more readily attribute prediction errors to the background and the chances of misunderstanding are lowered. 17

Recent accounts of psychotic symptoms in schizophrenia 18 , 19 have adopted a broadly Bayesian approach, although details of the precise deficit tend to differ between accounts (see refs. 20 and 21 for reviews). All theories focus on a neuromodulatory deficit such that the variables in the hierarchy are inappropriately optimized. Aberrant precision of prediction errors causes a state where previously irrelevant stimuli become abnormally salient in terms of their ability to update beliefs higher in the hierarchy. In this setting, prior precision may increase to compensate for the over-weighting of sensory evidence, culminating in delusions and hallucinations. Alternatively, a primary abnormality of prior precision may underwrite false inference about the world or self. 22 , 23

Of all sensory modalities, vision affords the perceiver the most amount of information about the world; eg, vision can convey more information (eg, spatial location, size, motion, color, and number) about someone approaching from a distance than touch, hearing, or smell.

Visual inputs have primacy in sculpting priors. There need only be a tiny change in the wavelength of light reaching my retina for me to change my mind about whether the ship on the horizon is flying pirates’ colors. A visual prior will usually affect the perception of an object in another modality (eg, the rubber-hand illusion). For a fully sighted individual, it is rare for what someone hears to trump what they see. As I walk down a busy shopping street, my priors are updated with every saccade. However, if I were blindfolded I would be immediately overwhelmed by a wealth of confusing auditory and tactile data. Vision confers a consistency 24 and a context to integrate data from other modalities. 25 Notably, there are cases of psychotic illness including schizophrenia following congenital cortical deafness, 26 consistent with the primacy of vision, as opposed to hearing, in organizing our multi- and supramodal world models.

It is possible then to account for why adult visual loss can result in visual hallucinations, following visual deprivation 27 or in Charles-Bonnet syndrome. 28 If the brain has developed normally, then visual loss will decrease the precision of visual input. Higher-level predictions will thus “explain away” this noisy input, resulting in false inferences, ie, hallucinations. 29

In neurodegenerative disease such as Parkinson’s disease and Alzheimer’s, visual impairment is also a risk factor for the development of visual hallucinations 30 , 31 and indeed visual hallucinations in such disorders occur more frequently in conditions of poor ambient light. 31 , 32 Interestingly, the occurrence of complex (as opposed to simple) visual hallucinations in neurodegenerative disorders is relatively greater than in hallucinosis secondary to visual loss. 28 In the latter, the precision of higher-level priors is relatively unimpaired and so noisy sensory input mainly affects lower levels, creating shapes, flashes, etc. In neurodegenerative disease, complex hallucinations such as people or animals may be more frequent because of the combination of imprecise sensory data and abnormal modulation of the precision of priors higher in the hierarchy, secondary to abnormalities in modulatory neurotransmitters such as dopamine and acetylcholine; and, given that brain structure recapitulates model structure, 33 secondary also to structural brain changes with neurodegeneration, ie, the model itself is degenerating.

When healthy adults are blindfolded, a majority of subjects report visual hallucinations, after a day. 27 Full insight—awareness of the nonveridical nature of the experience—into these experiences is maintained. Likewise, in organic visual hallucinosis, insight is usually retained. Substantial imbalances between the precision of high-level prior beliefs and of sensory data may contribute to loss of insight such that an extraordinary percept can no longer be dismissed with confidence as unlikely. In Parkinson’s disease, worsening insight regarding visual hallucinations accompanies worsening neuromodulatory dysfunction 34 and disease progression into cortical areas and circuits that have been implicated in the specification of higher-level priors. 31 , 33

When individuals deprived of tactile or visual stimulation are played meaningful auditory stimuli (such as jokes), there is a resultant decrease in psychopathology compared with those played “white noise,” 35 ie, there is a top-down attenuation of the effects of noisy, bottom-up signals, 36 which may explain the efficacy of keeping elderly patients occupied or talking to them in managing their distressing visual hallucinations.

The visual hallucinogenic effects of dopamine agonists and anticholinergics can be similarly understood as affecting the relative precision of prior beliefs, as can the psychotomimetic effects of various drugs of abuse. 36 Psychedelic drugs like lysergic acid diethylamide (LSD), which act via serotonergic 5HT2A receptors, are potent inducers of visual hallucinations. 37 Blind subjects given LSD all experienced hallucinations in multiple modalities, although congenitally blind subjects did not report visual hallucinations. Of 13 late-blind subjects who experienced visual hallucinations, only two experienced complex hallucinations. 38 An in-depth account of LSD reported by a congenitally blind musician similarly reveals an absence of visual hallucinations but an abundance of experiences involving other senses. 39

Visual loss in later life is not protective against the development of schizophreniform psychosis. Indeed, in Usher syndrome, visual degeneration occurs after adolescence (although sometimes as early as in the first decade) and is associated with schizophrenia-like symptoms. 40–42

For a congenitally blind person, there is no rich visual signal with which to shape one’s priors about the world. Each of the other sensory modalities samples a much smaller part of the sensorium, in a noisier fashion, and priors must be built up, piecemeal, from the information contained therein. It is essential then that these hard-won priors (both supramodal and within individual modalities 43 ) remain stable, so as to enable effective interaction within the world. That is, the organism should exhibit a relatively greater top-down influence of priors because the bottom-up, sensory information samples much less of it. As a congenitally blind individual walks down that same shopping street described above, his situation must be very different from a sighted individual with his eyes closed. The same auditory and tactile information that a blindfolded person perceives as chaotic and confusing does not overwhelm a congenitally blind person.

Congenitally blind individuals show reduced integration between nonvisual modalities. 44 , 45 For example, sighted individuals are vulnerable to an auditory-tactile illusion, whereby multiple tones presented simultaneously with a single tactile stimulus leads to the perception of more than one touch. Congenitally blind individuals evince a significantly attenuated illusion. 45 Putzar et al have shown that in adult patients born with congenital cataracts who at least 5 months later had them removed, thereby restoring sight, there was evidence of significantly impaired audio–visual integration. 46 This is also consistent with the possibility that early visual deprivation permanently reduces multimodal integration. On a single-cell level, Carriere and colleagues found that visual deprivation altered the response properties of single neurons in the cat anterior ectosylvian sulcus, a cortical area implicated in higher-order multisensory processing: dark rearing caused a shift in the neuronal population away from neurons whose responses could be effectively driven by stimuli in a number of different sensory modalities towards neurons whose responses were primarily driven only by unisensory stimuli and which could now only be modulated by a simultaneously presented stimulus in a second modality. 47

The reason this occurs may be obvious: vision most clearly provides the spatial scene within which sensory data from other modalities can be most efficiently contextualized and integrated; it enables the construction of multimodal or supramodal representations. According to Hotting et al, “developmental visual input is essential for the use of space to integrate input of the non-visual modalities, possibly because of its high spatial resolution.” 45 In the visually deprived brain evidence of impaired online multisensory integration suggests a less efficient development of supramodal and multimodal (ie, higher level) representations, despite evidence of substantial functional and anatomical cortical reorganization. 48 , 49 There is a requirement, therefore, for these hard-won higher-level representations to exhibit a stability that is not threatened by the individual’s “noisy” nonvisual sense data. The “imposition of structure on noise,” through inference to the best explanation or abduction, must be relatively greater.

Congenitally blind individuals are less susceptible to the somatic version of the rubber hand illusion wherein, in normally sighted but blindfolded individuals, proprioceptive and tactile information are integrated to create a false sense of bodily ownership. 50 In congenitally blind individuals, despite identical tactile and proprioceptive inputs, no illusion was experienced at all, suggesting a unique stability of their supramodal higher-level bodily representations in the face of “surprising” sensory data. There is evidence that early blindness leads to improved spatial cognition for tasks that use an egocentric reference frame, 51–53 indirectly supporting the idea that such visual deprivation necessitates the construction of a more stable representation of the world as it relates to ones interactions within it .

It may seem obvious that such an internal world would be more resilient to the kind of reality distortions that characterize the positive symptoms of schizophrenia. But how might such an invariant representation be achieved, computationally, and how might this be protective against schizophrenia?

In considering the neuronal instantiation of predictive inference in the brain, it is useful to distinguish between driving and modulatory signals. 54 Driving signals convey information about the presence or magnitude of prediction error and are typically thought to be mediated by strong intrinsic forward connections, relying on fast AMPA receptor-mediated glutamatergic currents; driving connections elicit a spiking response in their targets. Modulatory signals serve to modify response properties of their targets; they are thought to be mediated by slow, backward connections; they elicit small postsynaptic responses that grow larger with repeat stimuli and show nonlinear response characteristics. 55 They are implicated in fine-tuning the context-sensitivity of neuronal responses, eg, in the formation of receptive field characteristics. NMDA receptors (NMDARs) exhibit a number of properties that strongly suggest that NMDAR-mediated signaling is primarily top-down and modulatory in character. Other neurotransmitters including dopamine, GABA 56 and acetylcholine also perform modulatory roles. Dopamine might specify the precision of prediction errors 57 in the sensorimotor and interoceptive domain, namely, those involved in planning actions. 58

An increase in top-down modulatory signaling would be one way to ensure the stability of higher-level priors in the visually impaired brain. Carriere et al demonstrated that on a single-neuron level, visual deprivation shifts the responses of higher-level, multisensory neurons towards a profile indicative of an increased modulatory influence and a decreased sensory driving response. 47 This modulatory change may be NMDAR-dependent. A Transcranial Magnetic Stimulation (TMS) study has demonstrated that visual deprivation does indeed cause increases in NMDAR-dependent cortical excitability in humans. 59

This shift is explicable if the influence of prior beliefs is a result of their precision weighting relative to prediction error. In the visually deprived brain, we would expect increased precision of priors.

There is evidence that early visual impairment induces such a state. The neuromodulatory influence of NMDARs may be determined by their subunit composition. The NR2B subunit has the slowest kinetics for the release of its Mg+ ion such that those NMDARs containing the NR2B subunit are the most nonlinear and the most effective summators of EPSPs. NR2B-containing receptors are densest in layers 2 and 6 of the macaque visual cortex; these layers receive the densest termination of backward projections, consistent with the computational requirements for “top-down” signaling, ie, descending nonlinear predictions capable of negating ascending prediction errors. Thus, NR2B subunit-containing receptors may have a particularly important role in the modulation and specification of priors. 55

In the early-developing brain, the ratio of NR2A-containing to NR2B-containing NMDARs (the NR2A/NR2B ratio) is at its lowest. Postnatally there is an excess of NR2B receptors and, during development the amount of NR2A increases, increasing the NR2A/NR2B ratio in several brain regions. This coincides with a period of increased exploration of the world in most species and may mediate synaptic remodeling, 60 or regulate the threshold for long-term potentiation/depression (LTP/LTD)—known as metaplasticity. 61

Dark-rearing rodents retards this shift from NR2B to NR2A in visual cortex such that higher levels of NR2B persist for longer. 61 Computationally, this could be thought of as a persistence of top-down modulatory influence beyond the normal, developmentally expected period (perhaps via more efficient induction of LTP/LTD). That visual deprivation leads to an increase in the modulatory, rather than the driving, signal we hypothesize is an adaptive response to early visual loss to maintain stability of higher-level priors.

It is likely that there are many such adaptations, and some of the behavioral and neurophysiological differences observed in congenitally blind people, 5 may subserve the same function. There are no data on whether dark-rearing alters the NMDAR subunit composition in areas outside of visual cortex; this a question of great interest for future studies. Furthermore, it is known that across species, early visual deprivation leads to plastic changes in cerebral cortex whereby visual cortex comes to instantiate sensory processing for other modalities. 62 , 63 If the relative changes in NMDAR subunit composition (along with other relevant changes in receptor function) are retained in brain areas which go on to serve nonvisual processing, then it is likely that the resulting computational changes (ie, greater influence of top-down modulation) would also affect processing in other modalities, even supramodally. This is consistent with the idea that, fundamentally, the cortex is “metamodal”: rather than being specialized for a particular kind of sensory input it is specialized for a particular kind of computation. 64

While the dopamine hypothesis has hegemony, there is increasing recognition that NMDAR dysfunction may be primary to dopaminergic dysfunction, 65 with converging evidence for NMDAR antagonism and/or hypofunction in generating symptoms of psychosis. 18 , 66 , 67

There is increasing evidence for schizophrenia-associated alterations in NMDAR subunit composition, 68 consistent with NMDAR hypofunction. Mutations in the GRIN2B gene, which codes for the NR2B subunit, suggest a reduction in the number or function of NR2B-containing receptors. 69 Interestingly, administration of NMDAR antagonists, which are psychotomimetic, causes increase of synaptic NR2A-containing, but not NR2B-containing, synaptic receptors. 70 However, other alterations in glutamatergic signaling, or other neuromodulators should not be ignored.

Predictive coding theories of schizophrenia state that abnormal precision of prediction errors or priors gives rise to false inferences about one’s own thoughts, movements, and even emotions manifest as hallucinations and delusions. We suggest that increased precision of higher-level priors in the congenitally visually deprived brain protects against schizophrenia. That is, abnormalities that characterize the disorder have less impact on congenitally blind individuals because of the stability of their higher-level supramodal representations.

Patients with schizophrenia have highly variable estimates of the visual consequences of their actions. This variability correlates with the strength of delusions of control. Furthermore, they rely more on external visual information than controls in making their judgments. They may have imprecise internal predictions about the sensory consequences of action, which prompts greater reliance on external cues. 71 We suggest that in visually impaired individuals this situation is reversed: relatively greater precision of internal predictions, as a consequence of the impossibility of visual calibration. This is fundamentally opposed to the low precision internal predictions posited in schizophrenia.

Our focus in this paper has been on the role of precision as encoding uncertainty in hierarchical predictive coding—and how this is affected by early visual experience. The explanatory scope of this formulation is appealing because it links neurodevelopment with Bayesian belief updating and the opportunity for false inference—of the sort associated with positive psychotic symptoms. A key aspect of this formulation is that it rests upon the top-down control of precision at various levels of the cortical hierarchy. In turn, this means the brain must be equipped with predictions or beliefs about precision, namely, beliefs about beliefs. This is important because it speaks to a form of metacognition, namely, beliefs about the precision of beliefs lower in the hierarchy, or “hyperpriors.” One example is “ large amplitude prediction errors can only be generated by things I can’t predict ” (such as external agents); such a hyperprior may give rise to erroneous external attributions of the causes of sense data in psychosis. 22 Thus, hyperpriors in the hierarchies of developmentally typical individuals predispose to visual hallucinations following visual deprivation or later-life visual loss. With congenital visual loss, however, by virtue of developing within an inherently less predictable world, different hyperpriors obtain that are less likely to garner external attributions and psychosis. (There is resonance here with the autism literature also, in which aberrant precision of prediction errors likewise perturbs difficult social inferences. 72 ) On this view, the role of hyperpriors (about precision) may also inform the extent to which people have an insight into their false percepts.

In the neuropsychology of vision, there are patients whose brain damage and subsequent dysfunction help us think about vision and consciousness. Blindsight describes the covert visual abilities of brain damaged individuals who deny conscious visual perception. It is contrasted with Anton’s syndrome, wherein blind individuals claim to be sighted and behave as though they are (walking through, but colliding with, objects in the world). Both of these syndromes are characterized by acquired damage to the visual cortex in individuals whose development (and interaction with the visual world) was otherwise typical. The syndromes are consistent with a Bayesian Prediction Error Minimization Model of conscious perception, wherein candidate percepts are predicted and to some extent visual experience is consistent with those model predictions. The syndromes differ in the richness with which those predictions are experienced. Blindsight has low richness which conflicts with behavioral detection of stimuli. Anton’s has high richness that conflicts with reality.

We suggest that in blindsight, model predictions and the extent to which perception conforms to predictions are impaired. And in Anton’s syndrome, prediction error minimization is impaired such that individuals fail to infer that they are indeed blind. In Charles-Bonnet syndrome, model making and perception aligning with ones’ model is hyper-engaged, however, and prediction error processing, particularly at higher hierarchical levels (which we may term reality monitoring) is somewhat intact, since Charles-Bonnet syndrome cases often appreciate that they are hallucinating.

Our discussion has focused on positive psychotic symptoms of schizophrenia. Negative symptoms and thought disorder are also central features of the illness. Whilst they have received less consideration from predictive coding theorists, they can be brought into the explanatory fold . 73 In brief, thought disorder would arise when the contextual predictions that constrain cognition are imprecise (subtending aberrant prediction errors that derail one’s train of thought) and negative symptoms may arise from maladaptive predictions about the consequences of one’s actions: if we experience our agency unpredictably, why act at all. 73 There is a dearth of research pertaining to the precision of the relevant predictions in congenitally blind individuals, but we would predict that they would show similarly increased stability in the relevant domains.

We have argued that visual experience is critical in the construction of our internal world model. Visual loss can disrupt the development or maintenance of that model. We have proposed a predictive coding solution to the conundrum that congenital visual loss protects against psychosis, while later-life visual loss predisposes towards it. We argue that congenitally blind individuals exhibit greater stability of higher-level priors, possibly via increased NMDAR-mediated signaling. We believe that the functional or computational core of this theory offers an attractive and testable hypothesis, leading to a number of experimentally testable predictions:

Congenitally blind people will show decreased psychotomimetic effects of ketamine.

Congenitally blind people will show a more pronounced force matching illusion in comparison with blindfolded controls; this is in contrast with schizophrenic patients who show a reduced illusion. 74

Congenitally blind individuals will show lower psychosis-proneness than the sighted population. If congenitally blind individuals exhibit markedly stable prediction error signaling, they should show reduced schizotypy. 75 A similar prediction has been made by Silverstein and colleagues. 7

Congenitally blind individuals will show appropriate frontal cortical fMRI prediction error responses during causal learning, unlike people with psychosis whose prediction error is aberrant (per Corlett et al 76 ).

Our biological knowledge of the computational changes outlined above will change as our basic understanding of both blindness and schizophrenia evolve. NMDAR-mediated signaling is unlikely to represent the full picture. Nevertheless, we hope that the preceding discussion illustrates the potential for computational psychiatry to shed light on one of psychiatry’s most recalcitrant mysteries.

P.R.C. was supported by the Yale University Department of Psychiatry the Connecticut Mental Health Center (CMHC) and Connecticut State Department of Mental Health and Addiction Services (DMHAS), an IMHRO/Janssen Rising Star Translational Research Award, and NIMH R01MH12887).

The authors would like to thank Paul Fletcher, Anthony David, Rick Adams, Janet Pollak, and Matthew Nour for their valuable comments on earlier versions of the manuscript. Any errors that remain are solely those of the authors.

The authors declare that they have no conflicts of interest.

Waters F , Collerton D , Ffytche DH , et al. . Visual hallucinations in the psychosis spectrum and comparative information from neurodegenerative disorders and eye disease . Schizophr Bull . 2014 ; 40 ( Suppl 4 ): S233 – S245 .

Google Scholar

Silverstein SM , Rosen R . Schizophrenia and the eye . Schizophr Res Cogn . 2015 ; 2 ( 2 ): 46 – 55 .

Butler PD , Silverstein SM , Dakin SC . Visual perception and its impairment in schizophrenia . Biol Psychiatry . 2008 ; 64 ( 1 ): 40 – 47 .

Cullen AE , Holmes S , Pollak TA , et al. . Associations between non-neurological autoimmune disorders and psychosis: a meta-analysis . Biol Psychiatry . 2019 ; 85 ( 1 ): 35 – 48 .

Silverstein SM , Wang Y , Keane BP . Cognitive and neuroplasticity mechanisms by which congenital or early blindness may confer a protective effect against schizophrenia . Front Psychol . 2012 ; 3 : 624 .

Landgraf S , Osterheider M . “To see or not to see: that is the question.” The “Protection-Against-Schizophrenia” (PaSZ) model: evidence from congenital blindness and visuo-cognitive aberrations . Front Psychol . 2013 ; 4 : 352 .

Silverstein SM , Wang Y , Roché MW . Base rates, blindness, and schizophrenia . Front Psychol . 2013 ; 4 : 157 .

Leivada E , Boeckx C . Schizophrenia and cortical blindness: protective effects and implications for language . Front Hum Neurosci . 2014 ; 8 : 940 .

Leivada E . Vision, language and a protective mechanism towards psychosis . Neurosci Lett . 2016 ; 617 : 178 – 181 .

Morgan VA , Clark M , Crewe J , et al. . Congenital blindness is protective for schizophrenia and other psychotic illness. A whole-population study . Schizophr Res . 2018 ; 202 : 414 – 416 .

Hayes JF , Picot S , Osborn DPJ , et al. Visual acuity in late adolescence and future psychosis risk in a cohort of 1 million men . Schizophr Bull Jun 12 2018 .

Rahi JS , Cable N ; British Childhood Visual Impairment Study Group . Severe visual impairment and blindness in children in the UK . Lancet . 2003 ; 362 ( 9393 ): 1359 – 1365 .

Khandaker GM , Zimbron J , Lewis G , Jones PB . Prenatal maternal infection, neurodevelopment and adult schizophrenia: a systematic review of population-based studies . Psychol Med . 2013 ; 43 ( 2 ): 239 – 257 .

Lowther C , Costain G , Baribeau DA , Bassett AS . Genomic disorders in psychiatry-what does the clinician need to know? Curr Psychiatry Rep . 2017 ; 19 ( 11 ): 82 .

Cannon M , Jones PB , Murray RM . Obstetric complications and schizophrenia: historical and meta-analytic review . Am J Psychiatry . 2002 ; 159 ( 7 ): 1080 – 1092 .

Brown AS , Cohen P , Greenwald S , Susser E . Nonaffective psychosis after prenatal exposure to rubella . Am J Psychiatry . 2000 ; 157 ( 3 ): 438 – 443 .

Brown M , Kuperberg GR . A hierarchical generative framework of language processing: linking language perception, interpretation, and production abnormalities in schizophrenia . Front Hum Neurosci . 2015 ; 9 : 643 .

Stephan KE , Friston KJ , Frith CD . Dysconnection in schizophrenia: from abnormal synaptic plasticity to failures of self-monitoring . Schizophr Bull . 2009 ; 35 ( 3 ): 509 – 527 .

Corlett PR , Taylor JR , Wang XJ , Fletcher PC , Krystal JH . Toward a neurobiology of delusions . Prog Neurobiol . 2010 ; 92 ( 3 ): 345 – 369 .

Adams RA , Stephan KE , Brown HR , Frith CD , Friston KJ . The computational anatomy of psychosis . Front Psychiatry . 2013 ; 4 : 47 .

Sterzer P , Adams RA , Fletcher P , et al. The predictive coding account of psychosis . Biological psychiatry . 2018 ; 84 ( 9 ): 634 – 643 .

Corlett PR , Horga G , Fletcher PC 3rd , et al. Hallucinations and strong priors . Trends Cogn Sci . 2019 ; 23 ( 2 ): 114 – 127 .

Powers AR , Mathys C , Corlett PR . Pavlovian conditioning-induced hallucinations result from overweighting of perceptual priors . Science . 2017 ; 357 ( 6351 ): 596 – 600 .

Nardini M , Jones P , Bedford R , Braddick O . Development of cue integration in human navigation . Curr Biol . 2008 ; 18 ( 9 ): 689 – 693 .

Tcheang L , Bülthoff HH , Burgess N . Visual influence on path integration in darkness indicates a multimodal representation of large-scale space . Proc Natl Acad Sci U S A . 2011 ; 108 ( 3 ): 1152 – 1157 .

du Feu M , McKenna PJ . Prelingually profoundly deaf schizophrenic patients who hear voices: a phenomenological analysis . Acta Psychiatr Scand . 1999 ; 99 ( 6 ): 453 – 459 .

Merabet LB , Maguire D , Warde A , et al. Visual hallucinations during prolonged blindfolding in sighted subjects . J Neuroophthalmol . 2004 ; 24 ( 2 ): 109 – 113 .

Ffytche DH . Visual hallucinatory syndromes: past, present, and future . Dialogues Clin Neurosci . 2007 ; 9 ( 2 ): 173 – 189 .

Reichert DP , Seriès P , Storkey AJ . Charles bonnet syndrome: evidence for a generative model in the cortex? PLoS Comput Biol . 2013 ; 9 ( 7 ): e1003134 .

Burghaus L , Eggers C , Timmermann L , Fink GR , Diederich NJ . Hallucinations in neurodegenerative diseases . CNS Neurosci Ther . 2012 ; 18 ( 2 ): 149 – 159 .

Diederich NJ , Fénelon G , Stebbins G , Goetz CG . Hallucinations in Parkinson disease . Nat Rev Neurol . 2009 ; 5 ( 6 ): 331 – 342 .

Diederich NJ , Goetz CG , Raman R , et al. Poor visual discrimination and visual hallucinations in Parkinson’s disease . Clin Neuropharmacol . 1998 ; 21 ( 5 ): 289 – 295 .

Friston K . A theory of cortical responses . Philos Trans R Soc Lond B Biol Sci. Apr 29 2005 ; 360 ( 1456 ): 815 – 836 .

Factor SA , McDonald WM , Goldstein FC . The role of neurotransmitters in the development of Parkinson’s disease-related psychosis . Eur J Neurol . 2017 ; 24 ( 10 ): 1244 – 1254 .

Rosenzweig N , Gardner L . The role of input relevance in sensory isolation . Am J Psychiatry . 1966 ; 122 ( 8 ): 920 – 928 .

Corlett PR , Frith CD , Fletcher PC . From drugs to deprivation: a Bayesian framework for understanding models of psychosis . Psychopharmacology (Berl) . 2009 ; 206 ( 4 ): 515 – 530 .

Schmid Y , Enzler F , Gasser P , et al. . Acute effects of lysergic acid diethylamide in healthy subjects . Biol Psychiatry . 2015 ; 78 ( 8 ): 544 – 553 .

KRILL AE , ALPERT HJ , OSTFELD AM . Effects of a hallucinogenic agent in totally blind subjects . Arch Ophthalmol . 1963 ; 69 : 180 – 185 .

Dell’Erba S , Brown DJ , Proulx MJ . Synesthetic hallucinations induced by psychedelic drugs in a congenitally blind man . Conscious Cogn . 2018 ; 60 : 127 – 132 .

Domanico D , Fragiotta S , Trabucco P , Nebbioso M , Vingolo EM . Genetic analysis for two italian siblings with usher syndrome and schizophrenia . Case Rep Ophthalmol Med . 2012 ; 2012 : 380863 .

Wu CY , Chiu CC . Usher syndrome with psychotic symptoms: two cases in the same family . Psychiatry Clin Neurosci . 2006 ; 60 ( 5 ): 626 – 628 .

Carvill S . Sensory impairments, intellectual disability and psychiatry . J Intellect Disabil Res . 2001 ; 45 ( Pt 6 ): 467 – 483 .

Struiksma ME , Noordzij ML , Postma A . What is the link between language and spatial images? Behavioral and neural findings in blind and sighted individuals . Acta Psychol (Amst) . 2009 ; 132 ( 2 ): 145 – 156 .

Hötting K , Röder B . Hearing cheats touch, but less in congenitally blind than in sighted individuals . Psychol Sci . 2004 ; 15 ( 1 ): 60 – 64 .

Hötting K , Rösler F , Röder B . Altered auditory-tactile interactions in congenitally blind humans: an event-related potential study . Exp Brain Res . 2004 ; 159 ( 3 ): 370 – 381 .

Putzar L , Goerendt I , Lange K , Rösler F , Röder B . Early visual deprivation impairs multisensory interactions in humans . Nat Neurosci . 2007 ; 10 ( 10 ): 1243 – 1245 .

Carriere BN , Royal DW , Perrault TJ , et al. . Visual deprivation alters the development of cortical multisensory integration . J Neurophysiol . 2007 ; 98 ( 5 ): 2858 – 2867 .

Collignon O , Dormal G , Albouy G , et al. . Impact of blindness onset on the functional organization and the connectivity of the occipital cortex . Brain . 2013 ; 136 ( Pt 9 ): 2769 – 2783 .

Hasson U , Andric M , Atilgan H , Collignon O . Congenital blindness is associated with large-scale reorganization of anatomical networks . Neuroimage . 2016 ; 128 : 362 – 372 .

Petkova VI , Zetterberg H , Ehrsson HH . Rubber hands feel touch, but not in blind individuals . PLoS One . 2012 ; 7 ( 4 ): e35912 .

Röder B , Föcker J , Hötting K , Spence C . Spatial coordinate systems for tactile spatial attention depend on developmental vision: evidence from event-related potentials in sighted and congenitally blind adult humans . Eur J Neurosci . 2008 ; 28 ( 3 ): 475 – 483 .

Röder B , Kusmierek A , Spence C , Schicke T . Developmental vision determines the reference frame for the multisensory control of action . Proc Natl Acad Sci U S A . 2007 ; 104 ( 11 ): 4753 – 4758 .

Pasqualotto A , Proulx MJ . The role of visual experience for the neural basis of spatial cognition . Neurosci Biobehav Rev . 2012 ; 36 ( 4 ): 1179 – 1187 .

Bastos AM , Usrey WM , Adams RA , et al. Canonical microcircuits for predictive coding . Neuron . 2012 ; 76 ( 4 ): 695 – 711 .

Adams RA , Shipp S , Friston KJ . Predictions not commands: active inference in the motor system . Brain Struct Funct . 2013 ; 218 ( 3 ): 611 – 643 .

Fiorillo CD . Towards a general theory of neural computation based on prediction by single neurons . PLoS One . 2008 ; 3 ( 10 ): e3298 .

Diederen KM , Ziauddeen H , Vestergaard MD , et al. Dopamine modulates adaptive prediction error coding in the human midbrain and striatum . J Neurosci . 2017 ; 37 ( 7 ): 1708 – 1720 .

Friston KJ , Shiner T , FitzGerald T , et al. . Dopamine, affordance and active inference . PLoS Comput Biol . 2012 ; 8 ( 1 ): e1002327 .

Boroojerdi B , Battaglia F , Muellbacher W , Cohen LG . Mechanisms underlying rapid experience-dependent plasticity in the human visual cortex . Proc Natl Acad Sci U S A . 2001 ; 98 ( 25 ): 14698 – 14701 .

Gambrill AC , Barria A . NMDA receptor subunit composition controls synaptogenesis and synapse stabilization . Proc Natl Acad Sci U S A . 2011 ; 108 ( 14 ): 5855 – 5860 .

Yashiro K , Philpot BD . Regulation of NMDA receptor subunit expression and its implications for LTD, LTP, and metaplasticity . Neuropharmacology . 2008 ; 55 ( 7 ): 1081 – 1094 .

Collignon O , Vandewalle G , Voss P , et al. . Functional specialization for auditory-spatial processing in the occipital cortex of congenitally blind humans . Proc Natl Acad Sci U S A . 2011 ; 108 ( 11 ): 4435 – 4440 .

Ptito M , Moesgaard SM , Gjedde A , Kupers R . Cross-modal plasticity revealed by electrotactile stimulation of the tongue in the congenitally blind . Brain . 2005 ; 128 ( Pt 3 ): 606 – 614 .

Pascual-Leone A , Hamilton R . The metamodal organization of the brain . Prog Brain Res . 2001 ; 134 : 427 – 445 .

Moghaddam B , Javitt D . From revolution to evolution: the glutamate hypothesis of schizophrenia and its implication for treatment . Neuropsychopharmacology . 2012 ; 37 ( 1 ): 4 – 15 .

Corlett PR , Honey GD , Krystal JH , Fletcher PC . Glutamatergic model psychoses: prediction error, learning, and inference . Neuropsychopharmacology . 2011 ; 36 ( 1 ): 294 – 315 .

Rolls ET , Deco G . A computational neuroscience approach to schizophrenia and its onset . Neurosci Biobehav Rev . 2011 ; 35 ( 8 ): 1644 – 1653 .

Weickert CS , Fung SJ , Catts VS , et al. Molecular evidence of N-methyl-D-aspartate receptor hypofunction in schizophrenia . Mol Psychiatry . 2013 ; 18 ( 11 ): 1185 – 1192 .

Martucci L , Wong AH , De Luca V , et al. . N-methyl-D-aspartate receptor NR2B subunit gene GRIN2B in schizophrenia and bipolar disorder: polymorphisms and mRNA levels . Schizophr Res . 2006 ; 84 ( 2-3 ): 214 – 221 .

von Engelhardt J , Doganci B , Seeburg PH , Monyer H . Synaptic NR2A- but not NR2B-Containing NMDA receptors increase with blockade of ionotropic glutamate receptors . Front Mol Neurosci . 2009 ; 2 : 19 .

Synofzik M , Thier P , Leube DT , Schlotterbeck P , Lindner A . Misattributions of agency in schizophrenia are based on imprecise predictions about the sensory consequences of one’s actions . Brain . 2010 ; 133 ( Pt 1 ): 262 – 271 .

Lawson RP , Mathys C , Rees G . Adults with autism overestimate the volatility of the sensory environment . Nat Neurosci . 2017 ; 20 ( 9 ): 1293 – 1299 .

Corlett PR , Honey GD , Fletcher PC . Prediction error, ketamine and psychosis: an updated model . J Psychopharmacol . 2016 ; 30 ( 11 ): 1145 – 1155 .

Shergill SS , Samson G , Bays PM , Frith CD , Wolpert DM . Evidence for sensory prediction deficits in schizophrenia . Am J Psychiatry . 2005 ; 162 ( 12 ): 2384 – 2386 .

Corlett PR , Fletcher PC . The neurobiology of schizotypy: fronto-striatal prediction error signal correlates with delusion-like beliefs in healthy people . Neuropsychologia . 2012 ; 50 ( 14 ): 3612 – 3620 .

Corlett PR , Murray GK , Honey GD , et al. . Disrupted prediction-error signal in psychosis: evidence for an associative account of delusions . Brain . 2007 ; 130 ( Pt 9 ): 2387 – 2400 .

Month:	Total Views:
October 2019	371
November 2019	88
December 2019	48
January 2020	37
February 2020	335
March 2020	76
April 2020	34
May 2020	27
June 2020	14
July 2020	22
August 2020	22
September 2020	41
October 2020	16
November 2020	38
December 2020	60
January 2021	43
February 2021	19
March 2021	26
April 2021	31
May 2021	36
June 2021	15
July 2021	14
August 2021	12
September 2021	17
October 2021	21
November 2021	146
December 2021	125
January 2022	115
February 2022	79
March 2022	102
April 2022	64
May 2022	48
June 2022	66
July 2022	63
August 2022	59
September 2022	83
October 2022	81
November 2022	46
December 2022	81
January 2023	98
February 2023	83
March 2023	75
April 2023	89
May 2023	49
June 2023	53
July 2023	57
August 2023	70
September 2023	68
October 2023	56
November 2023	68
December 2023	48
January 2024	70
February 2024	256
March 2024	381
April 2024	196
May 2024	106
June 2024	107
July 2024	102
August 2024	86
September 2024	33

Email alerts

Citing articles via.

Recommend to your Library

Affiliations

Schizophrenia International Research Society

Online ISSN 1745-1701
Print ISSN 0586-7614
About Oxford Academic
Publish journals with us
University press partners
What we publish
New features
Open access
Institutional account management
Rights and permissions
Get help with access
Accessibility
Advertising
Media enquiries
Oxford University Press
Oxford Languages
University of Oxford

Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide

Cookie settings
Cookie policy
Privacy policy
Legal notice

This Feature Is Available To Subscribers Only

This PDF is available to Subscribers Only

For full access to this pdf, sign in to an existing account, or purchase an annual subscription.

Subjects and methods
Article Information

Six screens from the experiment illustrating stimulus presentation. The boxes and the fixation dot were onscreen at all times during a block. One of the 4 objects (a check mark, a diamond, an "X", or a "T") appeared in 1 of the 4 boxes (stimulus and location selected randomly and without replacement from f a pool of trial types) every 1250 milliseconds and remained on screen for 150 milliseconds in an object task block, where the X was the target, and screen 4 f would require a response; in a spatial task block, where the lower right location was the target, screen6 would require a response.

Grand-average event-related potentials to the target and nontarget stimuli in the right visual field (left visual field stimuli event-related potentials are similar) in the spatial and object tasks from the patient and control groups.

Target minus nontarget difference waves for the frontal, dorsal, and ventral regions of interest.

Electrode position map. The nose is at the top, back of the head at the back, and the vertex at the center of the figure. Standard positions from the 10/20 system are marked in circles. The region of interest electrodes are identified by squares (frontal), diamonds(dorsal), and triangles (ventral). FP indicates prefrontal electrode; F, lateral frontal electrode; Fz, superior frontal electrode; T, midtemporal electrode; Cz, central electrode; Pz, parietal electrodes; O, cccipital electrode; and Oz, midline occipital electrode.

Difference waves at a posterior midline site, near parietal electrode 21 showing the N2b reduction despite amplitude sparing of the P300 in the patient group compared with the control subjects. The amplitude windows are shown here, the object windows on the object, left visual field plot, and the spatial windows on the spatial left visual field plot. The N2b windows are in long dashes, the P300 windows for the controls are in the light dots, and the P300 window for the patients is in the dark dots.

Task × ROI × Group interaction. Bars denote SE. Amplitude of the N2b at the dorsal and ventral regions of interest (ROIs) in the spatial and object tasks for the controls and patients. Note the larger N2b dorsally in the spatial condition and ventrally in the object condition for the controls only.

See More About

Select your interests.

Customize your JAMA Network experience by selecting one or more topics from the list below.

Academic Medicine
Acid Base, Electrolytes, Fluids
Allergy and Clinical Immunology
American Indian or Alaska Natives
Anesthesiology
Anticoagulation
Art and Images in Psychiatry
Artificial Intelligence
Assisted Reproduction
Bleeding and Transfusion
Caring for the Critically Ill Patient
Challenges in Clinical Electrocardiography
Climate and Health
Climate Change
Clinical Challenge
Clinical Decision Support
Clinical Implications of Basic Neuroscience
Clinical Pharmacy and Pharmacology
Complementary and Alternative Medicine
Consensus Statements
Coronavirus (COVID-19)
Critical Care Medicine
Cultural Competency
Dental Medicine
Dermatology
Diabetes and Endocrinology
Diagnostic Test Interpretation
Drug Development
Electronic Health Records
Emergency Medicine
End of Life, Hospice, Palliative Care
Environmental Health
Equity, Diversity, and Inclusion
Facial Plastic Surgery
Gastroenterology and Hepatology
Genetics and Genomics
Genomics and Precision Health
Global Health
Guide to Statistics and Methods
Hair Disorders
Health Care Delivery Models
Health Care Economics, Insurance, Payment
Health Care Quality
Health Care Reform
Health Care Safety
Health Care Workforce
Health Disparities
Health Inequities
Health Policy
Health Systems Science
History of Medicine
Hypertension
Images in Neurology
Implementation Science
Infectious Diseases
Innovations in Health Care Delivery
JAMA Infographic
Law and Medicine
Leading Change
Less is More
LGBTQIA Medicine
Lifestyle Behaviors
Medical Coding
Medical Devices and Equipment
Medical Education
Medical Education and Training
Medical Journals and Publishing
Mobile Health and Telemedicine
Narrative Medicine
Neuroscience and Psychiatry
Notable Notes
Nutrition, Obesity, Exercise
Obstetrics and Gynecology
Occupational Health
Ophthalmology
Orthopedics
Otolaryngology
Pain Medicine
Palliative Care
Pathology and Laboratory Medicine
Patient Care
Patient Information
Performance Improvement
Performance Measures
Perioperative Care and Consultation
Pharmacoeconomics
Pharmacoepidemiology
Pharmacogenetics
Pharmacy and Clinical Pharmacology
Physical Medicine and Rehabilitation
Physical Therapy
Physician Leadership
Population Health
Primary Care
Professional Well-being
Professionalism
Psychiatry and Behavioral Health
Public Health
Pulmonary Medicine
Regulatory Agencies
Reproductive Health
Research, Methods, Statistics
Resuscitation
Rheumatology
Risk Management
Scientific Discovery and the Future of Medicine
Shared Decision Making and Communication
Sleep Medicine
Sports Medicine
Stem Cell Transplantation
Substance Use and Addiction Medicine
Surgical Innovation
Surgical Pearls
Teachable Moment
Technology and Finance
The Art of JAMA
The Arts and Medicine
The Rational Clinical Examination
Tobacco and e-Cigarettes
Translational Medicine
Trauma and Injury
Treatment Adherence
Ultrasonography
Users' Guide to the Medical Literature
Vaccination
Venous Thromboembolism
Veterans Health
Women's Health
Workflow and Process
Wound Care, Infection, Healing

Others Also Liked

Download PDF
X Facebook More LinkedIn

Potts GF , O'Donnell BF , Hirayasu Y , McCarley RW. Disruption of Neural Systems of Visual Attention in Schizophrenia. Arch Gen Psychiatry. 2002;59(5):418–424. doi:10.1001/archpsyc.59.5.418

Manage citations:

Permissions

Disruption of Neural Systems of Visual Attention in Schizophrenia

From Rice University, Houston, Tex (Dr Potts); University of Indiana, Bloomington (Dr O'Donnell); Kyorin University School of Medicine, Tokyo, Japan(Dr Hirayasu); Harvard Medical School, Boston, Mass, and Brockton Veterans Affairs Medical Center, Brockton, Mass (Dr McCarley).

Background Patients with schizophrenia show attention deficits. The frontal P2a and posterior N2b event-related potential components are early indices of activity in neural systems supporting attention and they are reduced in schizophrenia in auditory tasks. However, the auditory P300 is reduced as well. Thus, the P2a and N2b reductions may simply reflect a general event-related potential amplitude reduction. The visual P300, however, is often spared in schizophrenia. If neural systems supporting attention are specifically disrupted in schizophrenia, the attention-sensitive P2a and N2b should be differentially reduced in patients, compared with the P300, in a visual attention task.

Methods We analyzed 64-channel event-related potentials from 14 schizophrenic patients and 14 control subjects in a visual object–spatial attention task. We examined the amplitude of the P2a, N2b, and P300 components in the target minus standard difference wave to see if there was a differential reduction of the P2a and N2b compared with the P300.

Results Both the P2a and N2b waveforms were reduced in the patient group (81%[control mean, 1.99 µV; patient mean, 0.38 µV] and 95% [control mean, 0.55 µV; patient mean, 0.03 µV], respectively) while the P300 was not reduced. Measured at the peak of the frontal P2a, the N2b was larger dorsally in the spatial task and larger ventrally in the object task in the control group.

Conclusions The spatial distribution of the P2a and N2b was consistent with activity in the prefrontal cortex and modality-specific posterior cortex, respectively. The differential reduction of the P2a and N2b waveforms supports the hypothesis of specific disruption in neural systems of visual attention in schizophrenia.

DISRUPTION OF attention and working memory are characteristic of patients with schizophrenia. 1 - 4 Attention allocates resources to task-relevant perceptual representations. The ability to attend to and process task-relevant stimuli is critical for generating goal-directed behavior. When attention is disrupted, the ability to generate goal-directed behavior is impaired. Understanding of the neural bases of attention and working memory disruption in schizophrenia might provide insight into the neuropathologic factors of the disorder.

Primate studies suggest that prefrontal cortex and its interactions with perceptual areas in posterior cortex are important for attention and working memory. 5 - 8 For visual stimuli, perceptual processing is divided into 2 streams: the dorsal"where" spatial location stream, projecting to the posterior parietal cortex, and the ventral "what" object feature stream, projecting to the inferior temporal cortex. 9 , 10 Interaction between the posterior parietal cortex and the prefrontal cortex is necessary for visuospatial working memory 8 and similar interaction between the inferior temporal cortex and the prefrontal cortex is needed in visual object working memory. 11 If the prefrontal cortex and its connections with the posterior brain support attention and working memory, then disruptions in these neural networks may underlie those cognitive disturbances in schizophrenia. 12

Event-related potentials (ERPs) have been used to study the neural systems supporting attention. Early studies focused on the P300 component, a large, centroparietal positive component, occurring approximately 400 milliseconds after the presentation of a stimulus. 13 - 15 However, since, in some cases, the P300 can peak after the execution of the behavioral response, 16 it cannot be a direct index of the allocation of processing resources to relevant stimuli.

There are more specific, earlier posterior negative ERP indices of attention, including the N2b. 17 , 18 An N2b has been identified to task-relevant stimuli in auditory, 19 , 20 somatosensory, 21 , 22 and visual modalities. 20 , 23 The N2b usually overlies and has been associated with activity in the cortical areas responsible for perceptual processing. 24 - 26

Some studies report a positivity over frontal sites at about the same latency as the N2b. 25 - 29 The frontal positivity, referred to here as the P2a, is due to different neural generators than the N2b, demonstrated by differences in latency, laterality, and psychological responsiveness. 27 - 30 While the N2b is modulated both by stimulus properties and task demands, the P2a is sensitive only to the task relevance of the stimulus. 29 Thus, the P2a and N2b may provide an index of interaction between posterior stimulus representation areas and the frontal executive in the processing of task-relevant stimuli.

The most commonly reported ERP finding in schizophrenia is an amplitude reduction of the auditory P300. 31 - 33 Some studies have shown a left-sided lateralization of this reduction and this has been linked to structural abnormalities in the left temporal lobe. 34 The visual P300 seems to be less affected in schizophrenia, with most studies showing either no reduction or less reduction of the visual than the auditory P300. 31 , 32 There have been a few reports of auditory N2 reduction in schizophrenia. 30 , 35 , 36 To our knowledge, there are only 2 reports of visual N2 reduction in schizophrenia, both of which found the reduction despite a P300 of normal amplitude. 35 , 37 The single report, by our group, of the auditory frontal P2a in schizophrenia, found it reduced. 30 We know of no studies of the visual P2a or related components in schizophrenia. Thus, it is unclear if there is a specific disruption of the neural networks supporting visual attention in schizophrenia, or whether the disruption is confined to the auditory modality.

This study used a visual selective attention task, where targets were defined either by their spatial location or their visual object features. This task has been shown to elicit a P2a and N2b with a spatiotemporal distribution consistent with interaction between prefrontal cortex and the dorsal where pathway in location selection and the ventral what pathway in object selection. 26 We compared the ERPs from a 64-channel recording array, which provided the spatial resolution needed to assess activity in specific processing pathways. Reduction of the frontal P2a and posterior N2b in the patients, despite sparing of the P300, would provide evidence of specific disruption of the neural systems supporting visual attention in schizophrenia.

The patients (n = 21) were recruited from outpatient treatment and inpatient wards at the Brockton Veterans Affairs Medical Center, Brockton, Mass. Diagnoses were made from the Structured Clinical Interview for DSM-IV (SCID) under the supervision of a licensed clinical psychologist trained in SCID administration (κ interrater reliability in our laboratory has been 0.99 for schizophrenic vs other diagnoses over the last 5 years). Subjects were between the ages of 19 and 58 years, had no history of electroconvulsive treatment or neurological illness, no alcohol or other drug abuse in the last5 years or a lifetime history of addiction, no alcohol use 24 hours prior to testing, and the desire to participate as evidenced by giving written informed consent. Control subjects (n = 22) were recruited by newspaper advertisement using the same exclusion criteria with the addition of no lifetime history of mental illness.

Subjects who performed at less than 90% accuracy in any task or who had fewer than 20 artifact-free electroencephalographic (EEG) trials in any condition were excluded, leaving 14 patients and 18 control subjects. An additional4 controls were excluded to make equal-subpopulation (n) groups, selected such that the groups were not significantly different for age. The groups did differ on verbal IQ, parental socioeconomic status, and years of education( Table 1 ). One control and 2 patients were left-handed; all were male. The diagnostic conditions of the patients were as follows: 6 were paranoid, 4 undifferentiated, 2 residual, and 2 schizoaffective. All patients were medicated at the time of testing, 7 with typical antipsychotic medications, 6 with atypical antipsychotic medications, and 1 with a combination therapy. Seven of the patients were also taking anticholinergic medication.

Stimuli were presented using a personal computer (Macintosh Centris650; Apple Computer, Cupertino, Calif) running PsyScope software 40 communicating with the EEG amplifiers via a Button Box (New Micros, Dallas, Tex). During the experiment, there was a fixation dot at the center of the screen and 4 boxes at the 4 corners of an invisible square. Each box subtended approximately 2° of visual angle and was approximately 6° from fixation. On each trial, 1 of 4 objects would appear in 1 of the boxes and remain onscreen for 150 milliseconds with a 1250-millisecond intertrial interval. The 4 objects were an "X," a "T," a "check mark," and a "triangle" (96 pixels per object). The object and location on any given trial were equiprobable and selected randomly without replacement from a pool of trial types ( Figure 1 ).

Subjects performed 2 blocked target detection tasks: selection by location and selection by object. In the location task, 1 of the 4 boxes was designated the target location. Subjects were instructed to press a key whenever any object appeared at the target location. In the object task, 1 of the 4 objects was designated the target. Subjects were instructed to press a key any time the target object appeared at any location. The target objects and target locations were randomly selected for each subject. Halfway through each run, a new location and object were selected as targets, constrained such that each subject had a target location in each visual field. Each subject participated in 4 task blocks of 200 trials each, 2 location and 2 object blocks, with a break every 100 trials. Task order and response hand were counterbalanced across subjects.

The EEG was referenced to the vertex and sampled at 250 Hz using 2 linked32-channel EEG amplifiers (SynAmps; Neuroscan Labs, Herndon, Va) and 64-channel electrode nets (Geodesic Sensor Nets; Electrical Geodesics Inc, Eugene, Ore). Epochs were 1000 milliseconds, including a 200-millisecond prestimulus baseline. The epochs were scanned by an artifact detection algorithm and trials with eye blinks or out-of-range data (0 ± 75 µV) excluded from further analysis. The EEG was digitally low-pass filtered at 30 Hz to eliminate high-frequency noise. The EEG epochs were averaged by stimulus type (nontarget, target), visual field (left, right), and task block (spatial, object) to create the ERP waveforms, then transformed into an average reference representation to attenuate spatial distortions due to choice of reference sensor. 41 Grand average waveforms were created by averaging together the individual subject averages for each group (schizophrenic, control) in each condition. Since the psychological operation of interest was the detection of the task-relevant targets, the ERP components in common to both the targets and nontargets were removed by creating target minus nontarget difference waves. Target and nontarget waveforms comparing the spatial and object tasks for the control and patient groups at the frontal, dorsal, and ventral regions of interest (ROIs) are shown in Figure 2 . Target minus nontarget waveforms are shown in Figure 3 .

Temporal windows were selected around the P2a, N2b, and P300 peaks in the difference wave by inspection of the waveforms and a peak latency analysis was performed. Where significant effects on latency were found between groups or conditions, latency adjustments were made to the windows and the mean amplitude was extracted (latencies below). To reduce the dimensionality of an electrode factor, ROIs were identified containing subsets of the electrodes. 42 , 43 These ROIs were frontal (bilateral electrode pairs 2-59, 4-62, and 5-58) for the P2a; dorsal (8-34, 13-46, and61-49) and ventral (20-38, 26-37, and 27-32) for the N2b; and centroparietal(8-34, 20-38, 24-33) and temporal (15-47, 16-45, 18-43, and 23-42) for the P300. The frontal, dorsal, and ventral ROIs are shown on a map of the electrode locations in Figure 4 . Six independent repeated-measures analysis of variances (ANOVAs) were performed, a peak latency and a mean amplitude analysis for each component window, with the within factors task (spatial, object), visual field (left, right), and hemisphere (left, right), plus an ROI factor (dorsal, ventral) in the N2b analysis, and a between factor group (control, schizophrenic). A seventh ANOVA was performed on the amplitude only at the temporal lobe ROI to test for laterality differences as seen in the auditory P300 with the same electrode array. 30 An ANOVA was also performed on the reaction time data. Correlations were computed between the frontal P2a and the N2b at the 2 posterior ROIs and probabilities computed with the Fisher r -to- z test. Tests for differences between groups on demographic variables were performed using 2-tailed t tests. An α-level of .05 was used for all comparisons.

The groups differed on reaction time, F 1,23 = 19.32, P <.001, with the patient group (mean [SD], 593.99 [92.32] milliseconds) about 120 milliseconds slower than the control group (mean,471.41 [83.04] milliseconds). There was also a significant difference in reaction time between the tasks, F 1,23 = 89.95, P <.001, with the reaction time in the spatial task (mean, 488.43 [84.05] milliseconds) about 93 milliseconds faster than in the object task (mean, 580.91 [108.79] milliseconds). Mean accuracy was 99% (792/800) for controls in the spatial task and 97% (776/800) in the object task; the patients were 97% (775/800) in the spatial task and 94% (750/800) in the object task.

Effects for task and group were used for latency correction. The latency window for the P2a and N2b was from 160 to 400 milliseconds For the P2a there was a main effect for task, F = 46.93, P <.001, with the spatial task peak (mean, 263.26 [73.12] milliseconds) about 51 milliseconds earlier than the object task peak (mean, 313.96 [60.19] milliseconds). There was an effect for task on the N2b, F = 81.37, P <.001, showing a faster latency in the spatial task (mean, 248.82 [56.360] milliseconds) than in the object task (mean, 296.67 [68.16] milliseconds). The latency window for the P300 was from 320 to 600 milliseconds. There was an effect for task, F = 78.43, P <.001, showing shorter peak latency in the spatial task (mean, 455.81 [69.64] milliseconds) than in the object task (mean, 520.12 [63.13] milliseconds). There was also an effect for group, F = 5.10, P = .03, showing a faster latency in the control group (mean, 469.26 [75.66] milliseconds) than in the patient group(mean, 506.67 [66.95] milliseconds).

Figure 5 shows ERP from a midline electrode between Cz and Pz (electrode 21) comparing the patient and control groups with the amplitude windows for the P2a/N2b and P300. The latency corrected amplitude windows for the P2a and N2b were 160 to 300 milliseconds for the spatial task and 228 to 368 milliseconds for the object task. There was an effect on the P2a for group, F = 34.25, P <.001, showing reduced amplitude in the patient group. For the N2b, there was a main effect for group, F 1,26 = 10.13, P = .004, showing a smaller amplitude in the patient group and an effect for hemisphere, F = 31.97, P <.001, which was modified by group, F = 26.89, P <.001, showing a larger amplitude over the left hemisphere in the controls only. Task × ROI × Group was significant, F = 14.22, P <.001, showing a larger N2b in the ventral path in the object task and a larger N2b in the dorsal path in the spatial task in the control group ( Figure 6 ). Task × ROI × Field was significant, F = 7.67, P = .01, as were the Task × ROI × Field × Group, F = 6.63, P = .016, and Task × ROI × Hemisphere × Group, F = 4.77, P = .04 interactions, indicating that the larger dorsal N2b in the spatial task and ventral N2b in the object task in the control group was mostly for stimuli in the left visual field and over the left hemisphere.

The P300 amplitude window was latency corrected for differences in group and task. For the spatial task the window was from 360 to 520 milliseconds for the controls and 392 to 552 milliseconds for the patients; for the object task the window was from 416 to 576 milliseconds for the controls and 464 to 624 milliseconds for the patients. In the centroparietal ROI there was an effect for task, F = 6.10, P = .02, showing a larger P300 in the spatial task. The Field × Hemisphere × Group interaction was significant, F = 7.29, P = .01, suggesting a larger P300 contralateral to the visual field of the stimulus for the control subjects. In the temporal lobe ROI, there was a Field × Hemisphere interaction, F = 5.00, P = .03, showing the P300 larger contralateral to the visual field of the stimulus. Task × Hemisphere × Group interaction was significant, F = 6.30, P = .02, indicating that, for the controls, the P300 in the spatial task was larger over the left hemisphere and in the object task was larger over the right hemisphere.

For the controls, the strongest correlations were between the frontal and ventral ROIs in both tasks (object task: r = −0.34, P <.001; spatial task: r = −0.39, P <.001). However, the P2a was significantly correlated with the dorsal N2b only in the spatial task, r = −0.23, P = .003; in the object task the correlation only approached significance, r = −0.15, P = .06. In the patients, the correlation was actually stronger between the frontal P2a and ventral N2b in the object task that for the controls, r = −0.48, P <.001. However, for the patients, the correlation between the P2a and ventral N2b in the spatial task was reduced compared with the controls, r = −0.22, P = .005, and the correlation between the P2a and dorsal N2b was not significant in the spatial task, r = −0.12, P = .11.

In this visual attention study, the patients with schizophrenia showed a reduced P2a and a reduced N2b, despite a P300 of normal amplitude and spatial distribution. This suggests that the neural systems and cognitive operations indexed by the P2a and the N2b were differentially affected in the patient group.

Attention requires the direction of processing resources to task-relevant perceptual representations. Prior research indicates that the N2b indexes the formation of a perceptual representation in modality specific areas of posterior cortex. 44 The P2a, with its inferior prefrontal distribution and enhancement to target stimuli, may index activity in orbitofrontal cortical areas of task-relevance computation or salience evaluation. 26 One of the functions of orbitofrontal cortex appears to be to evaluate the motivational value of a stimulus, independent of its physical features. 45 The topographic distribution and psychological responsiveness of the P2a and N2b are consistent with simultaneous activity in posterior cortical areas of perceptual representation and prefrontal cortical areas of salience evaluation. 26 , 29 For the controls, at the peak of the P2a, the N2b was larger at the ventral ROI when target detection was based upon object feature and larger at the dorsal ROI when target detection was based upon stimulus location ( Figure 3 and Figure 6 ). This relationship was not true for the patients, indicating a disruption in the visual attention network between prefrontal cortex and stimulus-specific posterior cortex. The patients were able to perform the task, thus, there had to be some level of activity in the network. However, if the activity was sufficiently degraded, it might be unable to generate a scalp detectable P2a and N2b. In a more difficult task, the performance of the patients might start to decline more precipitously than that of the controls as the network became more challenged.

From the data presented here it is impossible to determine if the location of the physiological dysfunction is in one of the contributing cortical areas(prefrontal cortex or multiple posterior areas) or in the connections between the areas. There is substantial evidence that structural and functional abnormality in the frontal brain contributes to cognitive disruption in schizophrenia. 46 - 52 There are also hypotheses that posit functional disconnections in the brain in schizophrenia, 53 - 55 one of which proposes a disruption in communication between prefrontal and posterior cortex. 56 , 57 There is less evidence of distributed posterior dysfunction. The correlation analysis here is ambiguous, suggesting disrupted communication in the spatial task but not in the object task, consistent with behavioral data suggesting differential disruption in the dorsal pathway in schizophrenia. 58

This study used a heterogenous group of long-term, medicated patients, and there were significant differences between the control and patient groups. The ERP effects might be medication induced, although a prior study found visual N2 reduction in unmedicated patients. 50 , 59 Despite these limitations, the large and differential degradation of the P2a and N2b in the patient group provides evidence of specific disruption of the neural system supporting detection of task relevant visual stimuli in schizophrenia.

Submitted for publication October 4, 2000; final revision received September7, 2001; accepted October 1, 2001.

This study was supported by a young investigator's award from the National Alliance for Research on Schizophrenia and Depression, Great Neck, NY (Dr Potts). Additional support was provided by grant MH40799-09 from the National Institutes of Health, Bethesda, Md (Dr McCarley) and by the Veterans Administration through the Research Center for Basic and Clinical Neuroscience Studies of Schizophrenia, Washington, DC (Dr McCarley).

Corresponding author and reprints: Geoffrey F. Potts, PhD, Psychology, MS-25, Rice University, 6100 Main St, Houston, TX 77005 (e-mail: [email protected] ).

Register for email alerts with links to free full-text articles
Access PDFs of free articles
Manage your interests
Save searches and receive search alerts

IMAGES

Visual representation of schizophrenia on Craiyon
Schizophrenia
Visual representation of schizophrenia. Multiple human heads cojoined
PPT
5 Different Types Of Schizophrenia One Must Know About
Schizophrenia: Symptoms, Risk Factors, Diagnosis, Treatment, and Coping

VIDEO

Schizophrenia Simulation 7
What does a Schizophrenia Psychotic episode look like?
SCHIZOPHRENIA POV SIMULATION *Hindi AUDIO*
A Simulation of Auditory and Visual Hallucinations in Schizophrenia and Bipolar Disorder Mania
Is schizophrenia fairly represented in the media? Keon West
This is What it's like to Have Schizophrenia

COMMENTS

Visualizing mental representations in schizophrenia patients: A reverse
Reverse correlation, a data-driven psychophysical method, has recently become popular in the field of social face perception to obtain visual read-outs of mental representations of facial appearances of states and traits (Brinkman et al., 2017; Dotsch and Todorov, 2012; Jack and Schyns, 2017; Oldmeadow et al., 2013).Participants are presented with a series of stimuli that consist of random ...
What visual illusions teach us about schizophrenia
VIs were an early component of visual research in schizophrenia (see first referenced studies: Letourneau and Lavoie, 1973; Letourneau, 1974). More recently, these procedures have gained a renewed interest, with Dakin et al. (2005) as the first authors to postulate a decreased susceptibility to illusion in this disorder.
The Phenomenology and Neurobiology of Visual Distortions and
The Phenomenology and Neurobiology of Visual ...
Visualizing mental representations in schizophrenia patients: A reverse
The aims of this study are therefore two-fold: (1) To test whether to reverse correlation approach can be applied schizophrenia patients, and (2) to investigate whether schizophrenia patients have different mental representations of trustworthy faces, compared to healthy controls. Go to: 2. Methods. 2.1.
Portrayals of Schizophrenia by Entertainment Media: A Content Analysis
The exclusion of other visual media featuring characters with schizophrenia may have affected the generalizability of the findings. To provide a more comprehensive assessment of the portrayal of schizophrenia by the visual media, future research should expand the scope of media to include documentaries and movies made for television.
Early-stage visual perception impairment in schizophrenia, bottom-up
Early-stage visual perception impairment in schizophrenia ...
Abnormal visual representations associated with confusion of perceived
Abnormal visual representations associated with confusion of perceived facial expression in schizophrenia with social anxiety disorder Simon Faghel-Soubeyrand 1 , 2 , Tania Lecomte 1 ,
Visualizing mental representations in schizophrenia patients: A reverse
For the first time, we explored the applicability of reverse correlation, which has been successfully used to visualize mental representations in healthy populations, to visualize mental representations in schizophrenia patients. We investigated mental representations of trustworthy faces, a primary dimension of social face evaluation that is ...
Visual system assessment for predicting a transition to psychosis
Visual system assessment for predicting a transition to ...
Visual Hallucinations in the Psychosis Spectrum and Comparative
Visual experiences in schizophrenia best match the phenomena reported in the red box derived from PD, AD, DLB, and peduncular lesions—but not the green (eye and visual pathway pathology) and blue (serotonergic syndrome) boxes. ... Without representation in the outside world (visual hallucinations): Go to Question 4. b) With a representation ...
Remediation of Visual Processing Impairments in Schizophrenia: Where We
Visual Remediation in Schizophrenia: Low-Level Visual Processes. Low-level visual processes (e.g., spatial frequency processing, contrast sensitivity, orientation discrimination) involve the representation of basic visual features and are primarily dependent on retinal and thalamic activity and coding in primary visual cortex (V1) [].Low-level visual perceptual deficits in schizophrenia have ...
The Phenomenology and Neurobiology of Visual Distortions and
Schizophrenia is characterized by visual distortions in ~60% of cases, and visual hallucinations (VH) in ~25-50% of cases, depending on the sample. These symptoms have received relatively little attention in the literature, perhaps due to the higher rate of auditory vs. visual hallucinations in psychotic disorders, which is the reverse of what ...
Visual Perception Disturbances in Schizophrenia: A Unified Model
An alternative explanation is that schizophrenia is characterized by overly broad tuning of visual cortex neurons , leading to imprecise, noisy, and unstable representations in LOC, and to subsequent delays in reentrant processing of visual information [note—outside of orientation tuning (Robol et al., 2013; Rokem et al., 2011; Schallmo ...
Visual Masking in Schizophrenia: Overview and Theoretical Implications
Abstract. 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).
Brain network mechanisms of visual perceptual organization in ...
Visual shape completion is a canonical perceptual organization process that integrates spatially distributed edge information into unified representations of objects. People with schizophrenia show difficulty in discriminating completed shapes but the brain networks and functional connections underlying this perceptual difference remain poorly understood.
Visual Perception and Its Impairment in Schizophrenia
First, integration is readily measured in humans with grouping, perceptual closure, face processing, and contour integration tasks. Second, there is strong evidence of impairment in schizophrenia. Third, there is moderate evidence of a link to neural circuitry. Integration involves V2 and higher areas.
Realistic Schizophrenia Simulation
This video accurately simulates the experience of schizophrenia and other forms of psychosis.
Visual processing deficits in patients with schizophrenia spectrum and
Visual perceptual abnormalities were reported to be more predictive of conversion from a psychosis prodrome to schizophrenia than symptoms of thought and language problems and ideas of reference [25], and are linked to functional outcome in schizophrenia [26, 27]. Impaired visual processing has also been linked to transdiagnostic vulnerability ...
The Phenomenology and Neurobiology of Visual Distortions and
Regarding the latter, we suggest that, in schizophrenia, when the quality of representations in the visual system is more degraded and/or ambiguous than normal due to changes in precortical pathways [e.g., in the retina or optic radiations (170, 171)], a condition is created which increases the likelihood of distorted visual perceptions ...
Systematic review of visual illusions in schizophrenia
Visual illusions are a suitable method for understanding perceptual organization, as different visual illusions engage different neural and cognitive operations ( King et al., 2017 ). Perceptual deficits in schizophrenia have been described since the early 1950s ( Halpern, 1951; Bender et al., 1954; Weckowicz, 1957; Saucer, 1958 ), and studies ...
Blindness, Psychosis, and the Visual Construction of the World
The relationship between visual loss and psychosis is complex: congenital visual loss appears to be protective against the development of a psych ... disorder have less impact on congenitally blind individuals because of the stability of their higher-level supramodal representations. Patients with schizophrenia have highly variable estimates of ...
PDF Abnormal visual representations associated with confusion of perceived
ARTICLE OPEN Abnormal visual representations associated with confusion of perceived facial expression in schizophrenia with social anxiety disorder Simon Faghel-Soubeyrand1,2 , Tania Lecomte 1, M ...
Disruption of Neural Systems of Visual Attention in Schizophrenia
The most commonly reported ERP finding in schizophrenia is an amplitude reduction of the auditory P300. 31-33 Some studies have shown a left-sided lateralization of this reduction and this has been linked to structural abnormalities in the left temporal lobe. 34 The visual P300 seems to be less affected in schizophrenia, with most studies ...

Portrayals of Schizophrenia by Entertainment Media: A Content Analysis of Contemporary Movies

Information

Export Citations

View options

Purchase Options

Not a subscriber?

Share article link

PREVIOUS ARTICLE

Create a new account

Reset password

Save citation to file

Add to My Bibliography

The Phenomenology and Neurobiology of Visual Distortions and Hallucinations in Schizophrenia: An Update

Conflict of interest statement

Similar articles

Publication types

Related information

Miscellaneous

Visual Perception Disturbances in Schizophrenia: A Unified Model

Cite this chapter

Access this chapter

Similar content being viewed by others

A review of abnormalities in the perception of visual illusions in schizophrenia

Early-stage visual perception impairment in schizophrenia, bottom-up and back again

Perceptual Functioning

Acknowledgments

Author information

Corresponding author

Editor information

Rights and permissions

Copyright information

About this chapter

Download citation

Share this chapter

Brain network mechanisms of visual perceptual organization in schizophrenia and bipolar disorder

Competing Interest Statement

Funding Statement

Author Declarations

Data Availability

Citation Manager Formats

Subject Area

Visual Perception and Its Impairment in Schizophrenia

Steven M. Silverstein

Steven C. Dakin

Basic Science of Perceptual Processing

Functional Concepts: Definitions of Gain Control and Integration

Gain Control

Integration

Implications

Gain Control in Schizophrenia

Integration in Schizophrenia

How the Constructs Fit the Criteria

Other Perceptual Constructs Discussed at the Meeting

Conclusions

Acknowledgments

Article Contents

Blindness, Psychosis, and the Visual Construction of the World

Email alerts

Affiliations

This Feature Is Available To Subscribers Only

See More About

Others Also Liked

Manage citations:

Disruption of Neural Systems of Visual Attention in Schizophrenia

IMAGES

VIDEO

COMMENTS