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Biol Psychiatry. 2015 Jan 15;77(2):147-57. doi: 10.1016/j.biopsych.2014.05.023. Epub 2014 Jun 12.

Progressive reduction in cortical thickness as psychosis develops: a multisite longitudinal neuroimaging study of youth at elevated clinical risk.

Author information

1
Departments of Psychology, Yale University, New Haven, Connecticut; Departments of Psychiatry, Yale University, New Haven, Connecticut. Electronic address: tyrone.cannon@yale.edu.
2
Departments of Psychology, Yale University, New Haven, Connecticut.
3
Semel Institute for Neuroscience and Human Behavior and Department of Psychology, University of California, Los Angeles, Los Angeles, California.
4
Department of Psychiatry, University of California, Irvine, Irvine, California.
5
Department of Psychiatry (JA), University of Calgary, Calgary, Alberta, Canada.
6
Department of Psychiatry, University of California, San Diego, San Diego, California.
7
Department of Psychiatry, Zucker Hillside Hospital, Glen Oaks, New York.
8
Department of Psychiatry, University of California, San Francisco, San Francisco, California.
9
Departments of Psychiatry, Yale University, New Haven, Connecticut.
10
Department of Psychiatry, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
11
Renaissance Computing Institute, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
12
Department of Psychiatry, Beth Israel Deaconess Medical Center and Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.
13
Department of Psychology, Emory University, Atlanta, Georgia.
14
Division of Treatment and Prevention Research, National Institute of Mental Health, Rockville, Maryland.

Abstract

BACKGROUND:

Individuals at clinical high risk (CHR) who progress to fully psychotic symptoms have been observed to show a steeper rate of cortical gray matter reduction compared with individuals without symptomatic progression and with healthy control subjects. Whether such changes reflect processes associated with the pathophysiology of schizophrenia or exposure to antipsychotic drugs is unknown.

METHODS:

In this multisite study, 274 CHR cases, including 35 individuals who converted to psychosis, and 135 healthy comparison subjects were scanned with magnetic resonance imaging at baseline, 12-month follow-up, or the point of conversion for the subjects who developed fully psychotic symptoms.

RESULTS:

In a traveling subjects substudy, excellent reliability was observed for measures of cortical thickness and subcortical volumes. Controlling for multiple comparisons throughout the brain, CHR subjects who converted to psychosis showed a steeper rate of gray matter loss in the right superior frontal, middle frontal, and medial orbitofrontal cortical regions as well as a greater rate of expansion of the third ventricle compared with CHR subjects who did not convert to psychosis and healthy control subjects. Differential tissue loss was present in subjects who had not received antipsychotic medications during the interscan interval and was predicted by baseline levels of an aggregate measure of proinflammatory cytokines in plasma.

CONCLUSIONS:

These findings demonstrate that the brain changes are not explained by exposure to antipsychotic drugs but likely play a role in psychosis pathophysiology. Given that the cortical changes were more pronounced in subjects with briefer durations of prodromal symptoms, contributing factors may predominantly play a role in acute-onset forms of psychosis.

KEYWORDS:

Inflammation; MRI; Prefrontal cortex; Prodromal; Psychosis; Schizophrenia

PMID:
25034946
PMCID:
PMC4264996
DOI:
10.1016/j.biopsych.2014.05.023
[Indexed for MEDLINE]
Free PMC Article

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