Visual processing abnormalities in schizophrenia

Last updated
Fig.1 Surround Suppression Demo. With eyes fixed on the blue square, the center of the circle on the right appears to be lower contrast than the circle on the left, even though they are physically identical. SurroundSuppressionExampleFigure.jpg
Fig.1 Surround Suppression Demo. With eyes fixed on the blue square, the center of the circle on the right appears to be lower contrast than the circle on the left, even though they are physically identical.

Visual processing abnormalities in schizophrenia are commonly found, and contribute to poor social function. [1]

Contents

There is evidence that schizophrenia affects perception of contrast and motion, control of eye movements, detection of visual contours, and recognition of faces or facial expressions. The specificity of many visual processing abnormalities in schizophrenia is still an area of active debate within the scientific community. [2] [3] [4] [5] [6]

Perception of contrast

Contrast sensitivity

Contrast is a feature of visual stimuli that characterizes the difference in brightness between dark and light regions of an image. Perception of contrast is affected by the temporal frequency and spatial frequency properties of a stimulus, and the sensitivity to contrast in sine wave stimuli is characterized by the contrast sensitivity function. Contrast sensitivity has been shown to be impaired in schizophrenia. [7] [8] [9] [10] There is evidence that these impairments may be more severe among people with predominantly negative symptoms, [8] [9] or those who are not medicated. [10] Butler and colleagues [11] [ medical citation needed ] have proposed that people with schizophrenia may have a specific deficit in the magnocellular visual processing pathway, and electroencephalography (EEG) data have been presented that may support this view. [11] [ medical citation needed ] Results from pharmacological studies in cats [12] have demonstrated the role of NMDA in contrast perception of magnocellular-tuned stimuli. Application of drugs that deactivate this glutamate receptor type led to reduced neural responses in the visual system of cats, and some argue this suppression is similar to the reduced behavioral responses observed among people with schizophrenia. They claim these results are consistent with the glutamate hypothesis of schizophrenia, [12] which proposes that dysfunction in this neurotransmitter system leads to abnormal neural activity underlying this disorder. Skottun and colleagues [6] dispute the magnocellular deficit theory however, saying that there is not enough evidence from different research groups to support it, and that the experiments focused on this topic have shown very mixed results.

Surround suppression

The perceived contrast of a stimulus is sometimes suppressed when another stimulus is presented surrounding it, an effect known as surround suppression (see Figure 1), which is similar to the simultaneous contrast illusion. In schizophrenia, estimations of perceived contrast in surround suppression are less suppressed than for healthy adults. [13] [14] [15] Further, the magnitude of this perceptual suppression effect has been shown to correlate with the concentration of GABA (γ-aminobutyric acid), an inhibitory neurotransmitter, in the visual cortex. [15] These results may illustrate the role of GABA in mechanisms that regulate the overall level of neural activity [16] in visual cortex, and it has been suggested that such mechanisms may be disrupted in schizophrenia. [12] Such a disruption would be consistent with the GABA hypothesis of schizophrenia, [17] [18] which states that dysfunctional GABAergic inhibition may disrupt neural activity in subjects with this disorder, and this in turn may lead to visual processing abnormalities. [15]

Motion processing

Motion perception is an important visual function and occurs from the earliest stages of cortical visual processing, with individual neurons being tuned to a preferred direction of motion. [19] The cortical area MT (medial temporal cortex, also known as V5) plays a significant role in motion processing, and deactivation of this region using Transcranial magnetic stimulation can affect perception of motion. [20] Subjects with schizophrenia have shown abnormalities in perceptual judgments of motion, speed and direction, [21] [22] [23] [24] with deficits in these judgments generally being reported. It has been suggested that these findings are related to the aforementioned magnocellular deficit purported to exist in this disorder. [24] Inhibition of motion perception by the addition of a surround stimulus has also been examined in schizophrenia, with one group finding evidence both of impaired motion perception and weaker perceptual suppression effects in schizophrenia. [22] This agrees with the findings mentioned previously related to weaker suppression of perceived contrast in this disorder. [13] [14] [15] However, another recent report has disputed this finding, instead showing evidence consistent with stronger surround influence on motion perception in schizophrenia. [21]

Eye movements

Eye movements are important behaviors for locating and tracking objects in the visual world. Two of the major types of eye movements are saccades and smooth pursuit. Saccades are very rapid and precise eye movements between two positions, and are important in establishing fixation. Smooth pursuit on the other hand, allows the viewer to track a moving object along its trajectory within the visual field. Deficits in eye movement behavior among people with schizophrenia have been reported since the beginning of the 20th century. [25] Genetic factors are believed to be involved in these abnormalities, as unaffected relatives show similar dysfunction. [25] Specifically, saccade abnormalities have been observed in this disorder, with people showing changes in saccade rate, amplitude and accuracy. [25] Such deficits have been linked to medication with lithium, as well as to damage in frontal lobe regions. [25] Further, people with schizophrenia often exhibit errors in smooth pursuit eye movements. [25] [26] The neural correlates of smooth pursuit behavior in schizophrenia have been studied using functional Magnetic Resonance Imaging (fMRI), with abnormal activation having been observed in multiple cortical regions implicated in motion processing, such as Frontal Eye Fields and area MT. [26] Some have speculated that errors in smooth pursuit in this disorder may depend on deficits in frontal lobe processing, such as errors in anticipating the direction of stimulus motion, and that this in turn may be consistent with working memory deficits in schizophrenia. [25] Others have disputed this claim, presenting evidence instead pointing to the aforementioned deficits in motion processing, and abnormalities in cortical area MT as a possible source of smooth pursuit errors. [27] [ medical citation needed ] In this experiment, it was found that motion perception and smooth pursuit task performance were correlated, but no relationship between measures of smooth pursuit and attention was observed.

Contour detection

Detecting visual contours, edges, or boundaries is an important function in human and computer vision which facilitates figure-ground segmentation and object recognition. Contour integration depends on a subject's ability to link representations of separate visual stimuli into a coherent percept. Subjects with schizophrenia have been shown to perform worse than healthy adults on tasks that depend on contour integration, [12] [28] [29] [30] and these deficits may be related to factors such as illness severity, chronicity, and degree of disorganized symptoms. [12] In these experiments, subjects often viewed stimuli that could be connected to form a coherent perception of a line, like a simplified connect the dots puzzle. In general, the magnitude of visual processing abnormalities (such as abnormal contour detection performance) in schizophrenia are fairly small. Therefore, it may be necessary to examine experimental data from a large number of subjects in order to observe difference between healthy adults and those with schizophrenia using statistical methods. It has been proposed that weaker lateral excitation due to deficient NMDA-receptor functioning could disrupt neural processing, and that this might underlie problems with contour integration in schizophrenia. This idea is consistent with the glutamate hypothesis of schizophrenia, [12] as dysfunction in this neurotransmitter system may explain the symptoms observed.

Presentation of collinear stimuli flanking a target can enhance responses to the target in cortex, an effect known as flanker or collinear facilitation, which has been shown to be weaker in those with schizophrenia than in unaffected adults or those with bipolar disorder. [30] Publications from multiple research groups indicate that those with schizophrenia perform more poorly than healthy adults when asked to identify contours composed of separated line segments embedded in backgrounds made up of randomly oriented segments. [28] [29] This includes evidence from an fMRI experiment indicating abnormally reduced activation in visual areas V2-4. [29] Another group used EEG to examine illusory contour processing deficits in schizophrenia. [31] [ medical citation needed ] They found decreased amplitude and altered source location for the P1 component in patients, which they claim reflects abnormal dorsal stream processing in this disorder.

Crowding phenomenon

Crowding refers to the phenomenon where recognition of visual stimuli presented in the periphery is impaired by the presence of other nearby objects (sometimes called "flankers"). Abnormal crowding has been observed in schizophrenia, with different groups reporting stronger [32] or weaker [33] [ medical citation needed ] crowding effects.

Gaze shifts

During gaze shifts, for example when an object appears in the periphery, humans usually move both their eyes and head to capture the object of interest. In experiments, in which participants needed to shift their gaze to detect a visual target, people with schizophrenia exhibit abnormal eye-head coordination, and no modulation of saccadic latency (the delay between onset of the stimulus in the periphery and the start of the gaze shift) occurred, which is usually task dependent in healthy controls as they adjust to different task in terms of saccadic latency. [34] [35]

Perception of faces and facial emotions

Faces

Face perception is a function of the visual system which is critical for social behavior. People with schizophrenia have shown abnormalities in tasks designed to probe facial processing and recognition. [36] [37] [2] Specifically, performance deficits have been observed in this disorder when subjects were asked to identify degraded pictures of faces, and the deficits observed were specific to those with predominantly disorganized symptoms. [37] Another experiment using the same stimuli during EEG found poorer performance and slower reaction times among those with schizophrenia, as well as abnormalities in beta band activity. [36] The authors state that these results are related to deficits in long range coordination of neural activity, as described for contour detection. Another experiment using EEG and structural MRI to examine facial processing abnormalities in schizophrenia found decreased N170 component responses, and this was correlated with decreased gray matter volumes in the fusiform gyrus. [38] [ medical citation needed ] There is evidence that the fusiform face area is a visual cortical region that may be specialized for detecting faces. The authors of this study conclude that their data support a specific face processing deficit in schizophrenia. However, another study using fractured images of faces found that people with schizophrenia were better than healthy adults at identifying images of famous people that had been distorted. [2] These experiments state that this may be evidence of weaker "configural" processing in schizophrenia, who instead may rely more on local image features for face identification, as these were preserved in their image manipulation.

Facial emotions

Recognizing emotional expressions in images of human faces is a particularly important component of face perception with clear implications in human social interactions. People with schizophrenia reportedly perform poorly compared with healthy adults when asked to identify facial emotions. [3] [4] [5] [39] Some researchers have claimed that this is not a deficit specific to facial emotion perception per se, but rather evidence of a generalized deficit or overall poorer task performance in schizophrenia. [3] [4] However, others have argued that a review of the literature shows evidence of an additional specific deficit in processing negative emotions, such as anger and fear, among those with schizophrenia. [5] In addition, evidence has been presented of a link between a specific emotion processing deficit in schizophrenia and the volume of temporal lobe structures, including fusiform gyrus and middle temporal gyrus, as measured using MRI. [39]

Visual backward masking

In visual backward masking (VBM) a briefly presented target is followed by a mask, which decreases performance on the target. [40] VBM is a powerful experiment for schizophrenia research. [41] It allows for control over timing at millisecond level, there are well-supported theories of the underlying mechanisms, and it can be easily studied using EEG and fMRI. [42] Not only patients but also their unaffected siblings show strong and reproducible masking deficits, thus masking deficits have been suggested as an endophenotype for schizophrenia. [42] [43] [44]

Trigger hypothesis

In the early stages of the disease, and in untreated patients, hypersensitivity to low spatial frequencies has been documented. During the further course (and medication) of schizophrenia, this hypersensitivity turns into hyposensitivity and begins to affect other spatial frequencies of visual perception. Alterations to the visual signal, which are largely inconsistent over the course of schizophrenia (remission and relapse phases), may lead to the formation of inconsistent internal models of the world. These signal alterations (noise-to-signal ratios) are associated with fluctuations in Dopamine and Acetylcholine levels, decreased activity of inhibitory GABAergic interneurons, and hypofunction of NMDAr associated with gradual loss of cell populations in the precortical visual circuit. The volatile and noisy signal from the visual periphery may then act as an amplifier of primarily decreased connectivity within frontal areas, which may then prograde retrogradely to lower cortical areas of the visual information processing circuit. [45]

See also

Related Research Articles

<span class="mw-page-title-main">Schizophrenia</span> Mental disorder with psychotic symptoms

Schizophrenia is a mental disorder characterized by hallucinations, delusions, disorganized thinking and behavior, and flat or inappropriate affect. Symptoms develop gradually and typically begin during young adulthood and are never resolved. There is no objective diagnostic test; diagnosis is based on observed behavior, a psychiatric history that includes the person's reported experiences, and reports of others familiar with the person. For a diagnosis of schizophrenia, the described symptoms need to have been present for at least six months or one month. Many people with schizophrenia have other mental disorders, especially depressive disorder, anxiety disorders, and obsessive–compulsive disorder.

<span class="mw-page-title-main">Visual cortex</span> Region of the brain that processes visual information

The visual cortex of the brain is the area of the cerebral cortex that processes visual information. It is located in the occipital lobe. Sensory input originating from the eyes travels through the lateral geniculate nucleus in the thalamus and then reaches the visual cortex. The area of the visual cortex that receives the sensory input from the lateral geniculate nucleus is the primary visual cortex, also known as visual area 1 (V1), Brodmann area 17, or the striate cortex. The extrastriate areas consist of visual areas 2, 3, 4, and 5.

<span class="mw-page-title-main">Hallucination</span> Perception that only seems real

A hallucination is a perception in the absence of an external stimulus that has the compelling sense of reality. Hallucination is a combination of two conscious states of brain: wakefulness and REM sleep. They are distinguishable from several related phenomena, such as dreaming, which does not involve wakefulness; pseudohallucination, which does not mimic real perception, and is accurately perceived as unreal; illusion, which involves distorted or misinterpreted real perception; and mental imagery, which does not mimic real perception, and is under voluntary control. Hallucinations also differ from "delusional perceptions", in which a correctly sensed and interpreted stimulus is given some additional significance.

<span class="mw-page-title-main">Anhedonia</span> Inability to feel pleasure

Anhedonia is a diverse array of deficits in hedonic function, including reduced motivation or ability to experience pleasure. While earlier definitions emphasized the inability to experience pleasure, anhedonia is currently used by researchers to refer to reduced motivation, reduced anticipatory pleasure (wanting), reduced consummatory pleasure (liking), and deficits in reinforcement learning. In the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), anhedonia is a component of depressive disorders, substance-related disorders, psychotic disorders, and personality disorders, where it is defined by either a reduced ability to experience pleasure, or a diminished interest in engaging in previously pleasurable activities. While the International Statistical Classification of Diseases and Related Health Problems, Tenth Revision (ICD-10) does not explicitly mention anhedonia, the depressive symptom analogous to anhedonia as described in the DSM-5 is a loss of interest or pleasure.

<span class="mw-page-title-main">Parietal lobe</span> Part of the brain responsible for sensory input and some language processing

The parietal lobe is one of the four major lobes of the cerebral cortex in the brain of mammals. The parietal lobe is positioned above the temporal lobe and behind the frontal lobe and central sulcus.

<span class="mw-page-title-main">Temporal lobe</span> One of the four lobes of the mammalian brain

The temporal lobe is one of the four major lobes of the cerebral cortex in the brain of mammals. The temporal lobe is located beneath the lateral fissure on both cerebral hemispheres of the mammalian brain.

Magnocellular cells, also called M-cells, are neurons located within the magnocellular layer of the lateral geniculate nucleus of the thalamus. The cells are part of the visual system. They are termed "magnocellular" since they are characterized by their relatively large size compared to parvocellular cells.

A gamma wave or gamma rhythm is a pattern of neural oscillation in humans with a frequency between 30 and 100 Hz, the 40 Hz point being of particular interest. Gamma rhythms are correlated with large-scale brain network activity and cognitive phenomena such as working memory, attention, and perceptual grouping, and can be increased in amplitude via meditation or neurostimulation. Altered gamma activity has been observed in many mood and cognitive disorders such as Alzheimer's disease, epilepsy, and schizophrenia.

The two-streams hypothesis is a model of the neural processing of vision as well as hearing. The hypothesis, given its initial characterisation in a paper by David Milner and Melvyn A. Goodale in 1992, argues that humans possess two distinct visual systems. Recently there seems to be evidence of two distinct auditory systems as well. As visual information exits the occipital lobe, and as sound leaves the phonological network, it follows two main pathways, or "streams". The ventral stream leads to the temporal lobe, which is involved with object and visual identification and recognition. The dorsal stream leads to the parietal lobe, which is involved with processing the object's spatial location relative to the viewer and with speech repetition.

Reduced affect display, sometimes referred to as emotional blunting or emotional numbing, is a condition of reduced emotional reactivity in an individual. It manifests as a failure to express feelings either verbally or nonverbally, especially when talking about issues that would normally be expected to engage emotions. In this condition, expressive gestures are rare and there is little animation in facial expression or vocal inflection. Additionally, reduced affect can be symptomatic of autism, schizophrenia, depression, post-traumatic stress disorder, depersonalization derealization disorder, schizoid personality disorder or brain damage. It may also be a side effect of certain medications.

<span class="mw-page-title-main">Chubb illusion</span> Optical illusion

The Chubb illusion is an optical illusion or error in visual perception in which the apparent contrast of an object varies substantially to most viewers depending on its relative contrast to the field on which it is displayed. These visual illusions are of particular interest to researchers because they may provide valuable insights in regard to the workings of human visual systems.

<span class="mw-page-title-main">Colour centre</span> Brain region responsible for colour processing

The colour centre is a region in the brain primarily responsible for visual perception and cortical processing of colour signals received by the eye, which ultimately results in colour vision. The colour centre in humans is thought to be located in the ventral occipital lobe as part of the visual system, in addition to other areas responsible for recognizing and processing specific visual stimuli, such as faces, words, and objects. Many functional magnetic resonance imaging (fMRI) studies in both humans and macaque monkeys have shown colour stimuli to activate multiple areas in the brain, including the fusiform gyrus and the lingual gyrus. These areas, as well as others identified as having a role in colour vision processing, are collectively labelled visual area 4 (V4). The exact mechanisms, location, and function of V4 are still being investigated.

In cognitive neuroscience, visual modularity is an organizational concept concerning how vision works. The way in which the primate visual system operates is currently under intense scientific scrutiny. One dominant thesis is that different properties of the visual world require different computational solutions which are implemented in anatomically/functionally distinct regions that operate independently – that is, in a modular fashion.

<span class="mw-page-title-main">Posterior parietal cortex</span> Part of the human brain

The posterior parietal cortex plays an important role in planned movements, spatial reasoning, and attention.

The glutamate hypothesis of schizophrenia models the subset of pathologic mechanisms of schizophrenia linked to glutamatergic signaling. The hypothesis was initially based on a set of clinical, neuropathological, and, later, genetic findings pointing at a hypofunction of glutamatergic signaling via NMDA receptors. While thought to be more proximal to the root causes of schizophrenia, it does not negate the dopamine hypothesis, and the two may be ultimately brought together by circuit-based models. The development of the hypothesis allowed for the integration of the GABAergic and oscillatory abnormalities into the converging disease model and made it possible to discover the causes of some disruptions.

Visual object recognition refers to the ability to identify the objects in view based on visual input. One important signature of visual object recognition is "object invariance", or the ability to identify objects across changes in the detailed context in which objects are viewed, including changes in illumination, object pose, and background context.

<span class="mw-page-title-main">Parasol cell</span>

A parasol cell, sometimes called an M cell or M ganglion cell, is one type of retinal ganglion cell (RGC) located in the ganglion cell layer of the retina. These cells project to magnocellular cells in the lateral geniculate nucleus (LGN) as part of the magnocellular pathway in the visual system. They have large cell bodies as well as extensive branching dendrite networks and as such have large receptive fields. Relative to other RGCs, they have fast conduction velocities. While they do show clear center-surround antagonism, they receive no information about color. Parasol ganglion cells contribute information about the motion and depth of objects to the visual system.

<span class="mw-page-title-main">Nucleus basalis</span> Group of neurons in the brain

In the human brain, the nucleus basalis, also known as the nucleus basalis of Meynert or nucleus basalis magnocellularis, is a group of neurons located mainly in the substantia innominata of the basal forebrain. Most neurons of the nucleus basalis are rich in the neurotransmitter acetylcholine, and they have widespread projections to the neocortex and other brain structures.

The causes of schizophrenia that underlie the development of schizophrenia, a psychiatric disorder, are complex and not clearly understood. A number of hypotheses including the dopamine hypothesis, and the glutamate hypothesis have been put forward in an attempt to explain the link between altered brain function and the symptoms and development of schizophrenia.

Form perception is the recognition of visual elements of objects, specifically those to do with shapes, patterns and previously identified important characteristics. An object is perceived by the retina as a two-dimensional image, but the image can vary for the same object in terms of the context with which it is viewed, the apparent size of the object, the angle from which it is viewed, how illuminated it is, as well as where it resides in the field of vision. Despite the fact that each instance of observing an object leads to a unique retinal response pattern, the visual processing in the brain is capable of recognizing these experiences as analogous, allowing invariant object recognition. Visual processing occurs in a hierarchy with the lowest levels recognizing lines and contours, and slightly higher levels performing tasks such as completing boundaries and recognizing contour combinations. The highest levels integrate the perceived information to recognize an entire object. Essentially object recognition is the ability to assign labels to objects in order to categorize and identify them, thus distinguishing one object from another. During visual processing information is not created, but rather reformatted in a way that draws out the most detailed information of the stimulus.

References

  1. ↑ Silverstein, SM; Rosen, R (June 2015). "Schizophrenia and the eye". Schizophrenia Research. Cognition. 2 (2): 46–55. doi: 10.1016/j.scog.2015.03.004 . PMC   4559409 . PMID   26345525.
  2. 1 2 3 Joshua, N.; Rossell, S. (1962). "Configural face processing in schizophrenia". Schizophrenia Research. 112 (1–3): 99–103. doi:10.1016/j.schres.2009.03.033. PMID   19419842. S2CID   39343088.
  3. 1 2 3 Kerr, S.L. & Neale, J.M. (1993). "Emotion Perception in Schizophrenia: Specific Deficit or Further Evidence of Generalized Poor Performance". Journal of Abnormal Psychology. 102 (2): 312–318. doi:10.1037/0021-843X.102.2.312. PMID   8315144.
  4. 1 2 3 Salem, J.E., Kring, A.M., & Kerr, S.L. (1996). "More Evidence for Generalized Poor Performance in Facial Emotion Perception in Schizophrenia". Journal of Abnormal Psychology. 105 (3): 480–483. CiteSeerX   10.1.1.317.9472 . doi:10.1037/0021-843X.105.3.480. PMID   8772021.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  5. 1 2 3 Mandal, M. K.; Pandey, R.; Prasad, A. B. (1998). "Facial expressions of emotions and schizophrenia: A review". Schizophrenia Bulletin. 24 (3): 399–412. doi: 10.1093/oxfordjournals.schbul.a033335 . PMID   9718632.
  6. 1 2 Skottun, Bernt C.; Skoyles, John R. (2007). "Contrast sensitivity and magnocellular functioning in schizophrenia". Vision Research. 47 (23). Elsevier BV: 2923–2933. doi:10.1016/j.visres.2007.07.016. ISSN   0042-6989. PMID   17825350.
  7. ↑ Keri, S., Antal, A., Szekeres, G., Benedek, G., & Janka, Z. (2002). "Spatiotemporal visual processing in schizophrenia". Journal of Neuropsychiatry and Clinical Neurosciences. 14 (2): 190–6. doi:10.1176/appi.neuropsych.14.2.190. PMID   11983794.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  8. 1 2 Slaghuis, W.L., & Thompson, A. K. (2003). "The effect of peripheral visual motion on focal contrast sensitivity in positive-and negative-symptom schizophrenia". Neuropsychologia. 41 (8): 968–980. doi:10.1016/S0028-3932(02)00321-4. PMID   12667532. S2CID   21972610.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  9. 1 2 Slaghuis, Walter L. (2004). "Spatio-temporal luminance contrast sensitivity and visual backward masking in schizophrenia". Experimental Brain Research. 156 (2): 196–211. doi:10.1007/s00221-003-1771-3. PMID   14752582. S2CID   23072195.
  10. 1 2 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. PMID   16829048. S2CID   31845762.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  11. 1 2 Butler, P. D.; Martinez, A.; Foxe, J. J.; Kim, D.; Zemon, V.; Silipo, G.; Mahoney, J.; Shpaner, M.; Jalbrzikowski, M.; Javitt, D. C. (1 February 2007). "Subcortical visual dysfunction in schizophrenia drives secondary cortical impairments". Brain. 130 (2). Oxford University Press (OUP): 417–430. doi: 10.1093/brain/awl233 . ISSN   0006-8950. PMC   2072909 . PMID   16984902.
  12. 1 2 3 4 5 6 Butler, Pamela D.; Silverstein, Steven M.; Dakin, Steven C. (2008). "Visual Perception and Its Impairment in Schizophrenia". Biological Psychiatry. 64 (1). Elsevier BV: 40–47. doi:10.1016/j.biopsych.2008.03.023. ISSN   0006-3223. PMC   2435292 . PMID   18549875.
  13. 1 2 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 . PMID   16243017.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  14. 1 2 Yoon, J. H., Rokem, A. S., Silver, M. A., Minzenberg, M. J., Ursu, S., Ragland, J. D., & Carter, C. S. (2009). "Diminished Orientation-Specific Surround Suppression of Visual Processing in Schizophrenia". Schizophrenia Bulletin. 35 (6): 1078–1084. doi:10.1093/schbul/sbp064. PMC   2762622 . PMID   19620601.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  15. 1 2 3 4 Yoon, J. H., Maddock, R. J., Rokem, A. S., 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.6158-09.2010. PMC   2846788 . PMID   20220012.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  16. ↑ Heeger, D. J. (1992). "Normalization of Cell Responses in Cat Striate Cortex". Visual Neuroscience. 9 (2): 181–197. doi:10.1017/S0952523800009640. PMID   1504027. S2CID   22804285.
  17. ↑ Lewis, D. A., Hashimoto, T., & Volk, D. W. (2005). "Cortical Inhibitory Neurons and Schizophrenia". Nature Reviews Neuroscience. 6 (4): 312–324. doi:10.1038/nrn1648. PMID   15803162. S2CID   3335493.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  18. ↑ Gonzalez-Burgos, G., & Lewis, D. A. (2008). "GABA neurons and the mechanisms of network oscillations: implications for understanding cortical dysfunction in schizophrenia". Schizophrenia Bulletin. 34 (5): 944–61. doi:10.1093/schbul/sbn070. PMC   2518635 . PMID   18586694.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  19. ↑ Hubel, D. H.; Wiesel, T. N. (1962). "Receptive fields, binocular interaction and functional architecture in the cat's visual cortex". The Journal of Physiology. 160 (1): 106–154.2. doi:10.1113/jphysiol.1962.sp006837. PMC   1359523 . PMID   14449617.
  20. ↑ Tadin, D., Silvanto, J., Pascual-Leone, A., & Battelli, L. (2011). "Weakened Improved Motion Perception and Impaired Spatial Suppression following Disruption of Cortical Area MT/V5". Journal of Neuroscience. 31 (4): 1279–83. doi:10.1523/JNEUROSCI.4121-10.2011. PMC   3078722 . PMID   21273412.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  21. 1 2 Chen, Y., Norton, D., & Ongur, D. (2008). "Altered center-surround motion inhibition in schizophrenia". Biological Psychiatry. 64 (2): 74–77. doi:10.1016/j.biopsych.2007.11.017. PMC   2483430 . PMID   18206855.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  22. 1 2 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 . PMC   6674537 . PMID   17079669.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  23. ↑ 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. PMID   15050865. S2CID   10006874.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  24. 1 2 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. PMC   2045640 . PMID   16325377.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  25. 1 2 3 4 5 6 Abel, L. A., Levin, S., & Holzman, P. S. (1992). "Abnormalities of Smooth Pursuit and Saccadic Control in Schizophrenia and Affective Disorders". Vision Research. 32 (6): 1009–1014. doi:10.1016/0042-6989(92)90002-Z. PMID   1509692. S2CID   37248315.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  26. 1 2 Hong, L. E., Tagamets, M., Avila, M., Wonodi, I., Holcomb, H., & Thaker, G. K. (2005). "Specific motion processing pathway deficit during eye tracking in schizophrenia: a performance-matched functional magnetic resonance imaging study". Biological Psychiatry. 57 (7): 726–732. doi:10.1016/j.biopsych.2004.12.015. PMID   15820229. S2CID   20560856.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  27. ↑ Stuve, T. A.; Friedman, L.; Jesberger, J. A.; Gilmore, G. C.; Strauss, M. E.; Meltzer, H. Y. (1997). "The relationship between smooth pursuit performance, motion perception and sustained visual attention in patients with schizophrenia and normal controls". Psychological Medicine. 27 (1). Cambridge University Press: 143–152. doi:10.1017/s0033291796004230. ISSN   0033-2917. PMID   9122294. S2CID   23106085.
  28. 1 2 Silverstein, S. M., Kovács, 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 . PMID   10828411. S2CID   36005234.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  29. 1 2 3 Silverstein, S. M., Berten, S., Essex, B., Kovács, I., Susmaras, T., & Little, D. M. (2009). "An fMRI Examination of Visual Integration in Schizophrenia". Journal of Integrative Neuroscience. 8 (2): 175–202. doi:10.1142/S0219635209002113. PMID   19618486.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  30. 1 2 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. doi:10.1017/S0033291705004381. PMID   16045070. S2CID   12984126.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  31. ↑ Foxe, John J.; Murray, Micah M.; Javitt, Daniel C. (2005). "Filling-in in schizophrenia: a high-density electrical mapping and source-analysis investigation of illusory contour processing". Cerebral Cortex. 15 (12): 1914–27. doi: 10.1093/cercor/bhi069 . PMID   15772373.
  32. ↑ Kraehenmann, R., Vollenweider F.X., Seifritz E., Kometer, M. (2012). "Crowding deficits in the visual periphery of schizophrenia patients". PLOS ONE. 7 (9): e45884. Bibcode:2012PLoSO...745884K. doi: 10.1371/journal.pone.0045884 . PMC   3458825 . PMID   23049884.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  33. ↑ 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. Bibcode:2013PLoSO...860951R. doi: 10.1371/journal.pone.0060951 . PMC   3621669 . PMID   23585865. (Erratum:  doi:10.1371/journal.pone.0218483, PMC   6564015, PMID   31194845,  )
  34. ↑ Schwab, S., Würmle, O., Razavi, N., Müri, R. M., & Altorfer, A. (2013). "Eye-head coordination abnormalities in schizophrenia". PLOS ONE. 8 (9): e74845. Bibcode:2013PLoSO...874845S. doi: 10.1371/journal.pone.0074845 . PMC   3769305 . PMID   24040351.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  35. ↑ Malsert, J., Guyader, N., Chauvin, A., & Marendaz, C. (2012). "Having to identify a target reduces antisaccade latencies in mixed saccadic paradigms: A top-down effect released by tonic prefrontal activation?". Psychological Research. 3 (2): 105–111. doi:10.1080/17588928.2012.666965. PMID   24168691. S2CID   205936260.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  36. 1 2 Uhlhaas, P. J., Linden, D. E. J., 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): 8168–75. doi: 10.1523/JNEUROSCI.2002-06.2006 . PMC   6673788 . PMID   16885230.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  37. 1 2 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. PMID   17081620. S2CID   21325572.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  38. ↑ Onitsuka, Toshiaki; Niznikiewicz, Margaret A.; Spencer, Kevin M.; Frumin, Melissa; Kuroki, Noriomi; Lucia, Lisa C.; Shenton, Martha E.; McCarley, Robert W. (2006). "Functional and structural deficits in brain regions subserving face perception in schizophrenia". American Journal of Psychiatry. 163 (3): 455–62. doi:10.1176/appi.ajp.163.3.455. PMC   2773688 . PMID   16513867.
  39. 1 2 Goghari, V. M., MacDonald, A. W., & Sponheim, S. R. (2011). "Temporal Lobe Structures and Facial Emotion Recognition in Schizophrenia Patients and Nonpsychotic Relatives". Schizophrenia Bulletin. 37 (6): 1281–1294. doi:10.1093/schbul/sbq046. PMC   3196942 . PMID   20484523.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  40. ↑ Breitmeyer, Bruno G. (2006). Visual masking : time slices through conscious and unconscious vision. Öğmen, Haluk. (2nd ed.). Oxford: Oxford University Press. ISBN   0-19-853067-6. OCLC   62290483.
  41. ↑ Herzog, Michael H.; Brand, Andreas (June 2015). "Visual masking & schizophrenia". Schizophrenia Research: Cognition. 2 (2): 64–71. doi:10.1016/j.scog.2015.04.001. PMC   5609636 . PMID   29114454.
  42. 1 2 Green, M. F.; Lee, J.; Wynn, J. K.; Mathis, K. I. (2011-07-01). "Visual Masking in Schizophrenia: Overview and Theoretical Implications". Schizophrenia Bulletin. 37 (4): 700–708. doi:10.1093/schbul/sbr051. ISSN   0586-7614. PMC   3122285 . PMID   21606322.
  43. ↑ Chkonia, Eka; Roinishvili, Maya; Makhatadze, Natia; Tsverava, Lidia; Stroux, Andrea; Neumann, Konrad; Herzog, Michael H.; Brand, Andreas (2010-12-09). Hashimoto, Kenji (ed.). "The Shine-Through Masking Paradigm Is a Potential Endophenotype of Schizophrenia". PLOS ONE. 5 (12): e14268. Bibcode:2010PLoSO...514268C. doi: 10.1371/journal.pone.0014268 . ISSN   1932-6203. PMC   3000331 . PMID   21151559.
  44. ↑ da Cruz, Janir R; Shaqiri, Albulena; Roinishvili, Maya; Favrod, Ophélie; Chkonia, Eka; Brand, Andreas; Figueiredo, Patrícia; Herzog, Michael H (2020-01-21). "Neural Compensation Mechanisms of Siblings of Schizophrenia Patients as Revealed by High-Density EEG". Schizophrenia Bulletin. 46 (4): 1009–1018. doi:10.1093/schbul/sbz133. ISSN   0586-7614. PMC   7345810 . PMID   31961928.
  45. ↑ Adámek, Petr; Langová, Veronika; Horáček, Jiří (2022-03-21). "Early-stage visual perception impairment in schizophrenia, bottom-up and back again". Schizophrenia. 8 (1): 27. doi:10.1038/s41537-022-00237-9. ISSN   2334-265X. PMC   8938488 . PMID   35314712.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.