Schizophrenia is a complex mental disorder associated with not only cognitive dysfunctions, such as memory and attention deficits, but also changes in basic sensory processing. Although most studies on schizophrenia have focused on disturbances in higher-order brain functions associated with the prefrontal cortex or frontal cortex, recent investigations have also reported abnormalities in low-level sensory processes, such as the visual system. At very early stages of the disease, schizophrenia patients frequently describe in detail symptoms of a disturbance in various aspects of visual perception that may lead to worse clinical symptoms and decrease in quality of life. Therefore, the aim of this review is to describe the various studies that have explored the visual issues in schizophrenia.
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Report WHOMH. Mental Health: New understanding, New Hope, Geneva World Health Organization. 2001.
Stefansson H, Ophoff RA, Steinberg S, et al. Common variants conferring risk of schizophrenia. Nature. 2009;460:744–7.
International Schizophrenia C, Purcell SM, Wray NR, et al. Common polygenic variation contributes to risk of schizophrenia and bipolar disorder. Nature. 2009;460:748–52.
Insel TR. Rethinking schizophrenia. Nature. 2010;468:187–93.
Yeap S, Kelly SP, Sehatpour P, et al. Visual sensory processing deficits in Schizophrenia and their relationship to disease state. Eur Arch Psychiatry Clin Neurosci. 2008;258:305–16.
Butler PD, Schechter I, Zemon V, et al. Dysfunction of early-stage visual processing in schizophrenia. Am J Psychiatry. 2001;158:1126–33.
Butler PD, Javitt DC. Early-stage visual processing deficits in schizophrenia. Curr Opin Psychiatry. 2005;18:151–7.
Slaghuis WL. Contrast sensitivity for stationary and drifting spatial frequency gratings in positive- and negative-symptom schizophrenia. J Abnorm Psychol. 1998;107:49–62.
Chen Y, Levy DL, Sheremata S, et al. Compromised late-stage motion processing in schizophrenia. Biol Psychiatry. 2004;55:834–41.
Butler PD, Zemon V, Schechter I, et al. Early-stage visual processing and cortical amplification deficits in schizophrenia. Arch Gen Psychiatry. 2005;62:495–504.
Giersch A, Lalanne L, van Assche M, et al. On disturbed time continuity in schizophrenia: an elementary impairment in visual perception? Front Psychol. 2013;4:281. This manuscript review the mechanisms involved in the sense of time continuity and clinical evidence that they are impaired in schizophrenia.
Javitt DC. Glutamate and schizophrenia: phencyclidine N-methyl-D-aspartate receptors, and dopamine-glutamate interactions. Int Rev Neurobiol. 2007;78:69–108.
Carlsson A. The current status of the dopamine hypothesis of schizophrenia. Neuropsychopharmacol: Off Publ Am Coll Neuropsychopharmacol. 1988;1:179–86.
Djamgoz MB, Hankins MW, Hirano J, et al. Neurobiology of retinal dopamine in relation to degenerative states of the tissue. Vis Res. 1997;37:3509–29.
Frederick JM, Rayborn ME, Laties AM, et al. Dopaminergic neurons in the human retina. J Comp Neurol. 1982;210:65–79.
Haft M, van Hemmen JL. Theory and implementation of infomax filters for the retina. Network. 1998;9:39–71.
Behrens U, Wagner HJ. Terminal nerve and vision. Microsc Res Tech. 2004;65:25–32.
Bodis-Wollner I. Visual deficits related to dopamine deficiency in experimental animals and Parkinson’s disease patients. Trends Neurosci. 1990;13:296–302.
Deutsch SI, Rosse RB, Schwartz BL, et al. A revised excitotoxic hypothesis of schizophrenia: therapeutic implications. Clin Neuropharmacol. 2001;24:43–9.
Bressan RA, Pilowsky LS. Glutamatergic hypothesis of schizophrenia. Rev Bras Psiquiatr (Sao Paulo, Brazil: 1999). 2003;25:177–83.
Jojich L, Pourcho RG. Glutamate immunoreactivity in the cat retina: a quantitative study. Vis Neurosci. 1996;13:117–33.
Ehinger B, Ottersen OP, Storm-Mathisen J, et al. Bipolar cells in the turtle retina are strongly immunoreactive for glutamate. Proc Natl Acad Sci U S A. 1988;85:8321–5.
Sucher NJ, Lipton SA, Dreyer EB. Molecular basis of glutamate toxicity in retinal ganglion cells. Vis Res. 1997;37:3483–93.
Peng YW, Blackstone CD, Huganir RL, et al. Distribution of glutamate receptor subtypes in the vertebrate retina. Neuroscience. 1995;66:483–97.
Lipton SA, Rosenberg PA. Excitatory amino acids as a final common pathway for neurologic disorders. N Engl J Med. 1994;330:613–22.
Lee WW, Tajunisah I, Sharmilla K, et al. Retinal nerve fiber layer structure abnormalities in schizophrenia and its relationship to disease state: evidence from optical coherence tomography. Invest Ophthalmol Vis Sci. 2013;54:7785–92. The first study evaluating the RNFL thickness in schizophrenic patients using spectral domain OCT (SD-OCT) and also evaluated schizophrenic patients in different phases of the disease.
Parisi V, Restuccia R, Fattapposta F, et al. Morphological and functional retinal impairment in Alzheimer’s disease patients. Clin Neurophysiol: Off J Int Fed Clin Neurophysiol. 2001;112:1860–7.
Lu Y, Li Z, Zhang X, et al. Retinal nerve fiber layer structure abnormalities in early Alzheimer’s disease: evidence in optical coherence tomography. Neurosci Lett. 2010;480:69–72.
Inzelberg R, Ramirez JA, Nisipeanu P, et al. Retinal nerve fiber layer thinning in Parkinson disease. Vis Res. 2004;44:2793–7.
Cabezon L, Ascaso F, Ramiro P, et al. Optical coherence tomography: a window into the brain of schizophrenic patients. Acta ophthalmology. 2012; 90:
Ascaso F, Cabezon L, Quintanilla MA, et al. Retinal nerve fiber layer thickness measured by optical coherence tomography in patients with schizophrenia: a short report. Eur J Psychiatry. 2010;24:227–35.
Chu EM, Kolappan M, Barnes TR, et al. A window into the brain: an in vivo study of the retina in schizophrenia using optical coherence tomography. Psychiatry Res. 2012;203:89–94.
Skottun BC, Skoyles JR. On identifying magnocellular and parvocellular responses on the basis of contrast-response functions. Schizophr Bull. 2011;37:23–6. The study discuss the issue of assess the magnocellular and parvocellular sensitivity in schizophrenic individuals using steady-state visually evoked potentials (VEPs).
Ferrera VP, Nealey TA, Maunsell JH. Responses in macaque visual area V4 following inactivation of the parvocellular and magnocellular LGN pathways. J Neurosci: Off J Soc Neurosci. 1994;14:2080–8.
Nassi JJ, Lyon DC, Callaway EM. The parvocellular LGN provides a robust disynaptic input to the visual motion area MT. Neuron. 2006;50:319–27.
Sincich LC, Park KF, Wohlgemuth MJ, et al. Bypassing V1: a direct geniculate input to area MT. Nat Neurosci. 2004;7:1123–8.
Nassi JJ, Callaway EM. Parallel processing strategies of the primate visual system. Nature reviews. Neuroscience. 2009;10:360–72.
Shapley R. Visual sensitivity and parallel retinocortical channels. Annu Rev Psychol. 1990;41:635–58.
Maunsell JH, Ghose GM, Assad JA, et al. Visual response latencies of magnocellular and parvocellular LGN neurons in macaque monkeys. Vis Neurosci. 1999;16:1–14.
Schiller PH, Malpeli JG. Functional specificity of lateral geniculate nucleus laminae of the rhesus monkey. J Neurophysiol. 1978;41:788–97.
Shapley R, Reid RC, Kaplan E. Receptive fields of P and M cells in the monkey retina and their photoreceptor inputs. Neuroscience research. Suppl: Off J Japan Neurosci Soc. 1991;15:S199–211.
Denison RN, Vu AT, Yacoub E, et al. Functional mapping of the magnocellular and parvocellular subdivisions of human LGN. NeuroImage. 2014;102p2:358–69. The study shows the use of fMRI to identify magnocellular and parvocellular regions of human LGN.
Cheong SK, Tailby C, Martin PR, et al. Slow intrinsic rhythm in the koniocellular visual pathway. Proc Natl Acad Sci U S A. 2011;108:14659–63.
Martinez A, Hillyard SA, Dias EC, et al. Magnocellular pathway impairment in schizophrenia: evidence from functional magnetic resonance imaging. J Neurosci: Off J Soc Neurosci. 2008;28:7492–500.
Skottun BC, Skoyles JR. Contrast sensitivity and magnocellular functioning in schizophrenia. Vis Res. 2007;47:2923–33.
Kim D, Wylie G, Pasternak R, et al. Magnocellular contributions to impaired motion processing in schizophrenia. Schizophr Res. 2006;82:1–8.
Doniger GM, Foxe JJ, Murray MM, et al. Impaired visual object recognition and dorsal/ventral stream interaction in schizophrenia. Arch Gen Psychiatr. 2002;59:1011–20.
Merigan WH, Maunsell JH. How parallel are the primate visual pathways? Annu Rev Neurosci. 1993;16:369–402.
Merigan WH, Maunsell JH. Macaque vision after magnocellular lateral geniculate lesions. Vis Neurosci. 1990;5:347–52.
Merigan WH, Katz LM, Maunsell JH. The effects of parvocellular lateral geniculate lesions on the acuity and contrast sensitivity of macaque monkeys. J Neurosci: Off J Soc Neurosci. 1991;11:994–1001.
Merigan WH, Byrne CE, Maunsell JH. Does primate motion perception depend on the magnocellular pathway? J Neurosci: Off J Soc Neurosci. 1991;11:3422–9.
Tolhurst DJ. Reaction times in the detection of gratings by human observers: a probabilistic mechanism. Vis Res. 1975;15:1143–9.
Legge GE. Sustained and transient mechanisms in human vision: temporal and spatial properties. Vis Res. 1978;18:69–81.
Slaghuis WL, Thompson AK. The effect of peripheral visual motion on focal contrast sensitivity in positive- and negative-symptom schizophrenia. Neuropsychologia. 2003;41:968–80.
Slaghuis WL, Bishop AM. Luminance flicker sensitivity in positive- and negative-symptom schizophrenia. Exp Brain Res. 2001;138:88–99.
Slaghuis WL. Spatio-temporal luminance contrast sensitivity and visual backward masking in schizophrenia. Exp Brain Res. 2004;156:196–211.
Revheim N, Butler PD, Schechter I, et al. Reading impairment and visual processing deficits in schizophrenia. Schizophr Res. 2006;87:238–45.
Lima FB, Gracitelli CP, Paranhos Junior A, et al. Evaluation of magnocellular pathway abnormalities in schizophrenia: a frequency doubling technology study and clinical implications. Arq Bras Oftalmol. 2013;76:85–9. The study discussed an interesting and controversial topic about magnocellular pathway deficit using frequency doubling technology in patients with schizophrenia and evaluate the relationship between the deficit in visual processing with socio-demographic factors and clinical factors associated with chronicity, such as negative symptoms, duration of the disease, and antipsychotic drug use.
Evans MA, Shedden JM, Hevenor SJ, et al. The effect of variability of unattended information on global and local processing: evidence for lateralization at early stages of processing. Neuropsychologia. 2000;38:225–39.
Gutherie AH, McDowell JE, Hammond Jr BR. Scotopic sensitivity in schizophrenia. Schizophr Res. 2006;84:378–85.
Delord S, Ducato MG, Pins D, et al. Psychophysical assessment of magno- and parvocellular function in schizophrenia. Vis Neurosci. 2006;23:645–50.
Braus DF, Weber-Fahr W, Tost H, et al. Sensory information processing in neuroleptic-naive first-episode schizophrenic patients: a functional magnetic resonance imaging study. Arch Gen Psychiatr. 2002;59:696–701.
Barch DM, Mathews JR, Buckner RL, et al. Hemodynamic responses in visual, motor, and somatosensory cortices in schizophrenia. NeuroImage. 2003;20:1884–93.
Schwartz BD, McGinn T, Winstead DK. Disordered spatiotemporal processing in schizophrenics. Biol Psychiatr. 1987;22:688–98.
Saccuzzo DP, Braff DL. Early information processing deficit in schizophrenia. New findings using schizophrenic subgroups and manic control subjects. Arch Gen Psychiatr. 1981;38:175–9.
Keri S, Kelemen O, Janka Z, et al. Visual-perceptual dysfunctions are possible endophenotypes of schizophrenia: evidence from the psychophysical investigation of magnocellular and parvocellular pathways. Neuropsychology. 2005;19:649–56.
Schechter I, Butler PD, Silipo G, et al. Magnocellular and parvocellular contributions to backward masking dysfunction in schizophrenia. Schizophr Res. 2003;64:91–101.
Gracitelli CP, de Lima Vaz FB, Bressan RA, et al. Visual field loss in schizophrenia: evaluation of magnocellular pathway dysfunction in schizophrenic patients and their parents. Clin Ophthalmol (Auckland, NZ). 2013;7:1015–21. This study address an important topic that there is a lower global sensitivity in schizophrenic patients and their parents compared with controls.
Tootell RB, Switkes E, Silverman MS, et al. Functional anatomy of macaque striate cortex II. Retinotopic organization. J Neurosci: Off J Soc Neurosci. 1988;8:1531–68.
Skottun BC, Skoyles JR. Are masking abnormalities in schizophrenia limited to backward masking? Int J Neurosci. 2009;119:88–104.
Slaghuis WL, Bakker VJ. Forward and backward visual masking of contour by light in positive- and negative-symptom schizophrenia. J Abnorm Psychol. 1995;104:41–54.
Phillipson OT, Harris JP. Perceptual changes in schizophrenia: a questionnaire survey. Psycholog Med. 1985;15:859–66.
Harris JP, Calvert JE, Leendertz JA, et al. The influence of dopamine on spatial vision. Eye. 1990;4(Pt 6):806–12.
Bodis-Wollner I. Altered spatio-temporal contrast vision in Parkinson’s disease and MPTP-treated monkeys: the role of dopamine. In: Bodis-Wollner I, editor. Dopaminergic mechanisms in vision. New York: A.R. Liss Inc; 1988. p. 205–20.
Brandies R, Yehuda S. The possible role of retinal dopaminergic system in visual performance. Neurosci Biobehav Rev. 2008;32:611–56.
Calvert JE, Harris JP, Phillipson OT. Probing the visual system of Parkinson’s disease and chronic schizophrenic patients on depot neuroleptic using the tilt after effect. Clin Vis Sci. 1992;7:119–27.
Shuwairi SM, Cronin-Golomb A, McCarley RW, et al. Color discrimination in schizophrenia. Schizophr Res. 2002;55:197–204.
Buttner T, Kuhn W, Muller T, et al. Visual hallucinosis: the major clinical determinant of distorted chromatic contour perception in Parkinson’s disease. J Neural Transm (Vienna, Austria: 1996). 1996;103:1195–204.
Paulus W, Schwarz G, Werner A, et al. Impairment of retinal increment thresholds in Huntington’s disease. Ann Neurol. 1993;34:574–8.
de Xivry JJ O, Lefevre P. Saccades and pursuit: two outcomes of a single sensorimotor process. J Physiol. 2007;584:11.
Lisberger SG, Evinger C, Johanson GW, et al. Relationship between eye acceleration and retinal image velocity during foveal smooth pursuit in man and monkey. J Neurophysiol. 1981;46:229–49.
Fender DH, Nye PW. The effects of retinal image motion in a simple pattern recognition task. Kybernetik. 1962;1:192–9.
Engelken EJ, Wolfe JW. A modeling approach to the assessment of smooth pursuit eye movement. Aviat Space Environ Med. 1979;50:1102–7.
Baloh RW, Kumley WE, Sills AW, et al. Quantitative measurement of smooth pursuit eye movements. Ann Otol Rhinol Laryngol. 1976;85:111–9.
Yee RD. Eye movement recording as a clinical tool. Ophthalmology. 1983;90:211–22.
Diefendorf AR, Dogde R. An experimental study of the ocular reactions of the insane from photographic records. Brain. 1908;31:451. Oxford Univ. Press.
Mather JA, Putchat C. Motor control of schizophrenics—I. Oculomotor control of schizophrenics: a deficit in sensory processing, not strictly in motor control. J Psychiatr Res. 1982;17:343–60.
Bartfai A, Levander SE, Nyback H, et al. Smooth pursuit eye tracking, neuropsychological test performance, and computed tomography in schizophrenia. Psychiatr Res. 1985;15:49–62.
Tanaka M, Fukushima K. Neuronal responses related to smooth pursuit eye movements in the periarcuate cortical area of monkeys. J Neurophysiol. 1998;80:28–47.
Hong LE, Tagamets M, Avila M, et al. Specific motion processing pathway deficit during eye tracking in schizophrenia: a performance-matched functional magnetic resonance imaging study. Biol Psychiatr. 2005;57:726–32.
Fox PT, Fox JM, Raichle ME, et al. The role of cerebral cortex in the generation of voluntary saccades: a positron emission tomographic study. J Neurophysiol. 1985;54:348–69.
Fukushima J, Fukushima K, Chiba T, et al. Disturbances of voluntary control of saccadic eye movements in schizophrenic patients. Biol Psychiatr. 1988;23:670–7.
Fukushima J, Morita N, Fukushima K, et al. Voluntary control of saccadic eye movements in patients with schizophrenic and affective disorders. J Psychiatr Res. 1990;24:9–24.
Bender J, Reuter B, Mollers D, et al. Neural correlates of impaired volitional action control in schizophrenia patients. Psychophysiology. 2013;50:872–84. The study aimed at identifying neural correlates of Slowed initiation of volitional but not visually guided saccades.
Picard H, Le Seac’h A, Amado I, et al. Impaired saccadic adaptation in schizophrenic patients with high neurological soft sign scores. Psychiatr Res. 2012;199:12–8. This study shows that schizophrenic patients with high neurological soft signs scores have reduced saccade adaptation, providing neurophysiological evidence of cerebellar dysfunction.
Bolding MS, Lahti AC, White D, et al. Vergence eye movements in patients with schizophrenia. Vis Res. 2014;102:64–70.
Abel LA, Levin S, Holzman PS. Abnormalities of smooth pursuit and saccadic control in schizophrenia and affective disorders. Vis Res. 1992;32:1009–14.
Silverstein SM, Hatashita-Wong M, Schenkel LS, et al. Reduced top-down influences in contour detection in schizophrenia. Cogn Neuropsychiatry. 2006;11:112–32.
Onitsuka T, Niznikiewicz MA, Spencer KM, et al. Functional and structural deficits in brain regions subserving face perception in schizophrenia. Am J Psychiatr. 2006;163:455–62.
Gottesman II, Gould TD. The endophenotype concept in psychiatry: etymology and strategic intentions. Am J Psychiatr. 2003;160:636–45.
Chen Y, Nakayama K, Levy DL, et al. Psychophysical isolation of a motion-processing deficit in schizophrenics and their relatives and its association with impaired smooth pursuit. Proc Natl Acad Sci U S A. 1999;96:4724–9.
Keri S, Kelemen O, Benedek G, et al. Different trait markers for schizophrenia and bipolar disorder: a neurocognitive approach. Psychol Med. 2001;31:915–22.
Green MF, Nuechterlein KH, Mintz J. Backward masking in schizophrenia and mania. II. Specifying the visual channels. Arch Gen Psychiatr. 1994;51:945–51.
Green MF, Nuechterlein KH, Breitmeyer B. Backward masking performance in unaffected siblings of schizophrenic patients. Evidence for a vulnerability indicator. Arch Gen Psychiatr. 1997;54:465–72.
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Conflict of Interest
Carolina P. B. Gracitelli, Ricardo Y. Abe, and Alberto Diniz-Filho declare that they have no conflict of interest. Fabiana Benites Vaz-de-Lima is a medical manager for Abbvie. Augusto Paranhos Jr. is a consultant for Allergan, Inc. Felipe A. Medeiros has received financial support from Alcon Laboratories Inc., Bausch & Lomb, Carl Zeiss Meditec Inc., Heidelberg Engineering, Inc., Merck Inc., Allergan Inc., Sensimed, Topcon, Inc, Reichert, Inc., National Eye Institute. Research grant–Alcon Laboratories Inc., Allergan Inc., Carl Zeiss Meditec Inc., Reichert Inc. Consultant–Allergan, Inc., Carl–Zeiss Meditec, Inc.; Novartis.
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This article is part of the Topical Collection on Schizophrenia and Other Psychotic Disorders
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Gracitelli, C.P.B., Abe, R.Y., Diniz-Filho, A. et al. Ophthalmology Issues in Schizophrenia. Curr Psychiatry Rep 17, 28 (2015). https://doi.org/10.1007/s11920-015-0569-x
- Visual impairment
- Visual deficits