Abstract
Psychosis has been associated with neural anomalies across a number of brain regions and cortical networks. Nevertheless, the exact pathophysiology of the disorder remains unclear. Aberrant visual perceptions such as hallucinations are evident in psychosis, while the occurrence of visual distortions is elevated in individuals with genetic liability for psychosis. The overall goals of this project are to: (1) use psychophysical tasks and neuroimaging to characterize deficits in visual perception; (2) acquire a mechanistic understanding of these deficits through development and validation of a computational model; and (3) determine if said mechanisms mark genetic liability for psychosis. Visual tasks tapping both low- and high-level visual processing are being completed as individuals with psychotic disorders (IPD), first-degree biological siblings of IPDs (SibIPDs) and healthy controls (HCs) undergo 248-channel magneto-encephalography (MEG) recordings followed by 7 Tesla functional magnetic resonance imaging (MRI). By deriving cortical source signals from MEG and MRI data, we will characterize the timing, location and coordination of neural processes. We hypothesize that IPDs prone to visual hallucinations will exhibit deviant functions within early visual cortex, and that aberrant contextual influences on visual perception will involve higher-level visual cortical regions and be associated with visual hallucinations. SibIPDs who experience visual distortions—but not hallucinations—are hypothesized to exhibit deficits in higher-order visual processing reflected in abnormal inter-regional neural synchronization. We hope the results lead to the development of targeted interventions for psychotic disorders, as well as identify useful biomarkers for aberrant neural functions that give rise to psychosis.
Highlights
E feedforward signals from V1 to higher visual areas in parietal and temporal cortices, while surface segregation relies on feedback connections originating in temporal areas and extending to V1 [26]
By studying individuals that vary along the psychosis spectrum, as well as individuals with intermediate clinical phenotypes (i.e., siblings of individuals with a psychotic disorder (IPDs) (SibIPDs)), we can determine how dimensional variation along the psychosis spectrum differentially influences the manifestation of visual hallucinations and visual distortions/illusions
Functional neuroimaging, and a computational model, this project has the potential to yield a mechanistic understanding of visual hallucinations and distortions in subjective visual experience seen across the psychosis spectrum
Summary
E feedforward signals from V1 to higher visual areas in parietal and temporal cortices, while surface segregation relies on feedback connections originating in temporal areas and extending to V1 [26]. It has been suggested that early visual processing is partially dependent on local gain control mechanisms [30,31], coupled with long-range inputs from higher areas along the visual pathway [32]. We propose to examine the neural mechanisms underlying visual hallucinations and distortions in individuals with a psychotic disorder (IPDs) and first-degree biological siblings of individuals with a psychotic disorder (SibIPDs) and healthy controls (HC). The primary goals of the proposed work are to use psychophysical tasks and neuroimaging techniques to (1) precisely characterize behavioral and neural abnormalities in individuals with psychotic disorders during visual perception; (2) acquire a mechanistic understanding of these abnormalities through development and validation of a computational model; and (3) determine if said mechanisms mark genetic liability for psychosis (i.e., constitute a biomarker). H1: Individuals prone to visual hallucinations have reduced gain control in neural circuits of early visual cortex (V1, V2), which will be reflected by improved accuracy on a surround suppression task (i.e., reduced suppression); H2: Reduced intracortical connectivity within visual cortex (e.g., connectivity between V1 and V2), will be reflected in aberrant detection of co-linearity between visual elements and poor suppression of irrelevant elements of a visual scene; H3: Reduced activity in more anterior visual brain regions (LOC/fusiform, frontal cortex) and early visual cortex, will be characterized by deviant object identification due to weak use of high-level object templates to identify relevant targets in ambiguous scenes
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