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Browsing by Subject "Bipolar Disorder"

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    Altered Visuospatial Context Processing in Psychotic Psychopathology
    (2024-05) Pokorny, Victor
    The present dissertation examines atypical use of visuospatial context in psychotic psychopathology. There is a large literature suggesting individuals with schizophrenia, and to a lesser extent bipolar disorder, perceive visuospatial illusions differently than healthy controls. Such work has the potential to identify behavioral and neural markers of psychotic disorders. The first chapter is a meta-analysis that aims to quantify and summarize more than 50 years of research on atypical use of visuospatial context in psychotic psychopathology. When pooling across all task types, we found weak evidence of reduced use of visuospatial context in schizophrenia (Hedges’ g=0.25), and bipolar disorder (g=0.25). The strongest evidence was observed for altered contrast perception paradigms in schizophrenia (g=0.72). We propose altered feedback to the primary visual cortex as a potential neural mechanism underlying this effect. The second chapter is an original study of atypical orientation-dependent surround suppression of perceived contrast in people with schizophrenia (SCZ, n=31) and bipolar disorder (BP, n=29), first-degree biological relatives of these patient groups (SREL, n=28; BPREL, n=21) and healthy controls (CON, n=29). Individuals with schizophrenia exhibited reduced surround suppression across orientations, consistent with weakened untuned gain control. Group differences in orientation-dependent surround suppression magnitude were moderated by visual acuity. These findings clarify the mechanisms of weakened contextual modulation of perceived contrast in psychosis and suggest that visual acuity is an important driver of atypical orientation-dependent suppression in schizophrenia. The third and final chapter is an fMRI examination of brain responses associated with atypical orientation-dependent surround suppression of contrast in the same sample as Chapter 2. We examined BOLD responses to center-surround gratings in individuals with schizophrenia (SCZ, n= 34), bipolar disorder (BP, n = 25), unaffected first-degree relatives of SCZ (SREL, n = 20), unaffected first-degree relatives of BP (BPREL, n = 13) and healthy controls (CON, n = 23). We observed orientation-dependent modulation of V1 BOLD activation to near surrounds across groups. In particular, the SCZ and CON groups exhibited roughly equivalent orientation-dependent contextual modulation (Cohen’s dz SCZ= .56; CON = .63). Surprisingly, the direction of the contextual modulation for near surrounds was opposite of predicted: greater BOLD activation for the condition that was expected to produce suppression. Our unexpected results suggest that spatial attention and figure-ground modulation are important to consider when studying orientation-dependent surround suppression. By disentangling these effects, clinical studies may become more informative with respect to the neural pathophysiology of mental health disorders. Taken together, the findings described in the present dissertation suggest that atypical suppression of perceived contrast holds great potential for clarifying the neural pathophysiology of schizophrenia. In particular, our pattern of results are most suggestive of altered feedback mechanisms driving this effect rather than V1-intrinsic mechanisms. Future research will seek to further disentangle the degree to which spatial attention, figure-ground modulation and attentional lapses contribute to altered surround suppression of contrast in psychotic psychopathology.
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    Neural Anomalies During Vigilance in Schizophrenia: Diagnostic Specificities and Genetic Associations
    (2020-10) Klein, Samuel
    Impaired vigilance is a core cognitive deficit in schizophrenia and may serve as an endophenotype (i.e., mark genetic liability). We used a continuous performance task with perceptually degraded stimuli in schizophrenia patients (N=48), bipolar disorder patients (N=26), first-degree biological relatives of schizophrenia patients (N=55) and bipolar disorder patients (N =28), as well as healthy controls (N=68) to clarify whether previously reported vigilance deficits and abnormal neural functions were indicative of genetic liability for schizophrenia as opposed to a generalized liability for severe psychopathology. We also examined variation in the Catechol-O-methyltransferase gene to evaluate whether brain responses were related to genetic variation associated with higher-order cognition. Relatives of schizophrenia patients had an increased rate of misidentification of nontarget stimuli as targets when they were perceptually similar, suggestive of difficulties with contour perception. Larger early visual responses (i.e., N1) were associated with better task performance in patients with schizophrenia consistent with enhanced N1 responses reflecting beneficial neural compensation. Additionally, reduced N2 augmentation to target stimuli was specific to schizophrenia. Both patients with schizophrenia and first-degree relatives displayed reduced late cognitive responses (P3b) that predicted worse performance. First-degree relatives of bipolar patients exhibited performance deficits, and displayed aberrant neural responses that were milder than individuals with liability for schizophrenia and dependent on sex. Variation in the Catechol-O-methyltransferase gene was differentially associated with P3b in schizophrenia and bipolar groups. Poor vigilance in schizophrenia is specifically predicted by a failure to enhance early visual responses, weak augmentation of mid-latency brain responses to targets, and limited engagement of late cognitive responses that may be tied to genetic variation associated with prefrontal dopaminergic availability. Experimental results illustrate specific neural functions that distinguish schizophrenia from bipolar disorder and provides evidence for a putative endophenotype that differentiates genetic liability for schizophrenia from severe mental illness more broadly.