Journal
BIOLOGICAL PSYCHIATRY
Volume 76, Issue 6, Pages 438-446Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.biopsych.2014.02.010
Keywords
Neuroimaging; penalized splines; psychosis; system; topology
Categories
Funding
- National Institutes of Health (NIH) Intramural Research Program
- NIH-Cambridge Graduate Partnership PhD program
- Wellcome Trust
- Medical Research Council United Kingdom
- Medical Research Council [G0001354, G1000183B, G0001354B] Funding Source: researchfish
- National Institute for Health Research [NF-SI-0513-10051] Funding Source: researchfish
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Background: Schizophrenia is a disorder of brain connectivity and altered neurodevelopmental processes. Cross-sectional case-control studies in different age groups have suggested that deficits in cortical thickness in childhood-onset schizophrenia may normalize over time, suggesting a disorder-related difference in cortical growth trajectories. Methods: We acquired magnetic resonance imaging scans repeated over several years for each subject, in a sample of 106 patients with childhood-onset schizophrenia and 102 age-matched healthy volunteers. Using semiparametric regression, we modeled the effect of schizophrenia on the growth curve of cortical thickness in similar to 80,000 locations across the cortex, in the age range 8 to 30 years. In addition, we derived normative developmental modules composed of cortical regions with similar maturational trajectories for cortical thickness in typical brain development. Results: We found abnormal nonlinear growth processes in prefrontal and temporal areas that have previously been implicated in schizophrenia, distinguishing for the first time between cortical areas with age-constant deficits in cortical thickness and areas whose maturational trajectories are altered in schizophrenia. In addition, we showed that when the brain is divided into five normative developmental modules, the areas with abnormal cortical growth overlap significantly only with the cingulo-fronto-temporal module. Conclusions: These findings suggest that abnormal cortical development in schizophrenia may be modularized or constrained by the normal community structure of developmental modules of the human brain connectome.
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