Visual processing abnormalities in schizophrenia
[1] 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.
[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.
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.
[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.
[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.
[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.
Detecting visual contours, edges, or boundaries is an important function in human and computer vision which facilitates figure-ground segmentation and object recognition.
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.
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.
[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 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").
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.
[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.
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.
