Halide Bilge Türközer1, Paulo Lizano2, Iniya Adhan3, Elena I Ivleva4, Olivia Lutz3, Victor Zeng3, Alexandria Zeng3, Nicholas Raymond3, Deepthi Bannai3, Adam Lee5, Jeffrey R Bishop6, Brett A Clementz7, Godfrey D Pearlson8, John A Sweeney9, Elliot S Gershon10, Matcheri S Keshavan11, Carol A Tamminga4. 1. Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, Texas; Division of Child and Adolescent Psychiatry, Massachusetts General Hospital and McLean Hospital, Boston, Massachusetts; Department of Psychiatry, Harvard Medical School, Boston, Massachusetts. Electronic address: bilge.turkozer@gmail.com. 2. Department of Psychiatry, Beth Israel Deaconess Medical Center and Massachusetts Mental Health Center, Boston, Massachusetts; Department of Psychiatry, Harvard Medical School, Boston, Massachusetts. Electronic address: lizanopl@gmail.com. 3. Department of Psychiatry, Beth Israel Deaconess Medical Center and Massachusetts Mental Health Center, Boston, Massachusetts. 4. Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, Texas. 5. Department of Experimental and Clinical Pharmacology, College of Pharmacy, University of Minnesota, Minneapolis, Minnesota. 6. Department of Experimental and Clinical Pharmacology, College of Pharmacy, University of Minnesota, Minneapolis, Minnesota; Department of Psychiatry and Behavioral Sciences, Medical School, University of Minnesota, Minneapolis, Minnesota. 7. Departments of Psychology and Neuroscience, Bio-Imaging Research Center, University of Georgia, Athens, Georgia. 8. Olin Neuropsychiatry Research Center/Institute of Living, Hartford Hospital, Hartford; Departments of Psychiatry and Neuroscience, Yale University, New Haven, Connecticut. 9. Department of Psychiatry, University of Cincinnati, Cincinnati, Ohio. 10. Department of Psychiatry, University of Chicago, Chicago, Illinois. 11. Department of Psychiatry, Beth Israel Deaconess Medical Center and Massachusetts Mental Health Center, Boston, Massachusetts; Department of Psychiatry, Harvard Medical School, Boston, Massachusetts.
Abstract
BACKGROUND: Impairments of the visual system are implicated in psychotic disorders. However, studies exploring visual cortex (VC) morphology in this population are limited. Using data from the Bipolar-Schizophrenia Network on Intermediate Phenotypes consortium, we examined VC structure in psychosis probands and their first-degree relatives (RELs), sex differences in VC measures, and their relationships with cognitive and peripheral inflammatory markers. METHODS: Cortical thickness, surface area, and volume of the primary (Brodmann area 17/V1) and secondary (Brodmann area 18/V2) visual areas and the middle temporal (V5/MT) region were quantified using FreeSurfer version 6.0 in psychosis probands (n = 530), first-degree RELs (n = 544), and healthy control subjects (n = 323). Familiality estimates were determined for probands and RELs. General cognition, response inhibition, and emotion recognition functions were assessed. Systemic inflammation was measured in a subset of participants. RESULTS: Psychosis probands demonstrated significant area, thickness, and volume reductions in V1, V2, and MT, and their first-degree RELs demonstrated area and volume reductions in MT compared with control subjects. There was a higher degree of familiality for VC area than thickness. Area and volume reductions in V1 and V2 were sex dependent, affecting only female probands in a regionally specific manner. Reductions in some VC regions were correlated with poor general cognition, worse response inhibition, and increased C-reactive protein levels. CONCLUSIONS: The visual cortex is a site of significant pathology in psychotic disorders, with distinct patterns of area and thickness changes, sex-specific and regional effects, potential contributions to cognitive impairments, and association with C-reactive protein levels.
BACKGROUND: Impairments of the visual system are implicated in psychotic disorders. However, studies exploring visual cortex (VC) morphology in this population are limited. Using data from the Bipolar-Schizophrenia Network on Intermediate Phenotypes consortium, we examined VC structure in psychosis probands and their first-degree relatives (RELs), sex differences in VC measures, and their relationships with cognitive and peripheral inflammatory markers. METHODS: Cortical thickness, surface area, and volume of the primary (Brodmann area 17/V1) and secondary (Brodmann area 18/V2) visual areas and the middle temporal (V5/MT) region were quantified using FreeSurfer version 6.0 in psychosis probands (n = 530), first-degree RELs (n = 544), and healthy control subjects (n = 323). Familiality estimates were determined for probands and RELs. General cognition, response inhibition, and emotion recognition functions were assessed. Systemic inflammation was measured in a subset of participants. RESULTS: Psychosis probands demonstrated significant area, thickness, and volume reductions in V1, V2, and MT, and their first-degree RELs demonstrated area and volume reductions in MT compared with control subjects. There was a higher degree of familiality for VC area than thickness. Area and volume reductions in V1 and V2 were sex dependent, affecting only female probands in a regionally specific manner. Reductions in some VC regions were correlated with poor general cognition, worse response inhibition, and increased C-reactive protein levels. CONCLUSIONS: The visual cortex is a site of significant pathology in psychotic disorders, with distinct patterns of area and thickness changes, sex-specific and regional effects, potential contributions to cognitive impairments, and association with C-reactive protein levels.
Authors: Chloe Y Li; Itika Garg; Paulo Lizano; John B Miller; Deepthi Bannai; Megan Kasetty; Raviv Katz; Iniya Adhan; Konstantinos A A Douglas; Jay C Wang; Leo A Kim; Matcheri Keshavan Journal: Clin Ophthalmol Date: 2022-07-28