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Schizophr Res. 2012 Aug;139(1-3):1-6. doi: 10.1016/j.schres.2012.05.002. Epub 2012 May 29.

Longitudinal progression of frontal and temporal lobe changes in schizophrenia.

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1
Department of Psychiatry and Behavioral Sciences, Northwestern University Feinberg School of Medicine, 446 E. Ontario, Suite 7-100, Chicago, IL 60611, USA. d-cobia@northwestern.edu

Abstract

Cortical abnormalities are considered a neurobiological characteristic of schizophrenia. However, the pattern of such deficits as they progress over the illness remains poorly understood. The goal of this project was to assess the progression of cortical thinning in frontal and temporal cortical regions in schizophrenia, and determine whether relationships exist between them and neuropsychological and clinical symptom profiles. As part of a larger longitudinal 2-year follow-up study, schizophrenia (n=20) and healthy participants (n=20) group-matched for age, gender, and recent-alcohol use, were selected. Using MRI, estimates of gray matter thickness were derived from primary anatomical gyri of the frontal and temporal lobes using surface-based algorithms. These values were entered into repeated-measures analysis of variance models to determine group status and time effects. Change values in cortical regions were correlated with changes in neuropsychological functioning and clinical symptomatology. Results revealed exaggerated cortical thinning of the middle frontal, superior temporal, and middle temporal gyri in schizophrenia participants. These thickness changes strongly influenced volumetric reductions, but were not related to shrinking surface area. Neuropsychological and clinical symptom profiles were stable in the schizophrenia participants despite these neuroanatomic changes. Overall it appears that ongoing abnormalities in the cerebral cortex continue after initial onset of schizophrenia, particularly the lateral aspects of frontal and temporal regions, and do not relate to neuropsychological or clinical measures over time. Maintenance of neuropsychological performance and clinical stability in the face of changing neuroanatomical structure suggests the involvement of alternative compensatory mechanisms.

PMID:
22647883
PMCID:
PMC3413315
DOI:
10.1016/j.schres.2012.05.002
[Indexed for MEDLINE]
Free PMC Article
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