Regional thinning of the cerebral cortex in schizophrenia: Effects of diagnosis, age and antipsychotic medication
Received 31 January 2007; received in revised form 3 September 2007; accepted 12 September 2007. published online 16 October 2007.
Abstract
Morphological abnormalities of the cerebral cortex have been reported in a number of MRI-studies in schizophrenia. Uncertainty remains regarding cause, mechanism and progression of the alterations. It has been suggested that antipsychotic medication reduces total gray matter volumes, but results are inconsistent. In the present study differences in regional cortical thickness between 96 patients with a DSM-IV diagnosis of schizophrenia (n=81) or schizoaffective disorder (n=15) and 107 healthy subjects (mean age 42 years, range 17–57 years) were investigated using MRI and computer image analysis. Cortical thickness was estimated as the shortest distance between the gray/white matter border and the pial surface at numerous points across the entire cortical mantle. The influence of age and antipsychotic medication on variation in global and regional cortical thickness was explored. Thinner cortex among patients than controls was found in prefrontal and temporal regions of both hemispheres, while parietal and occipital regions were relatively spared. Some hemispheric specificity was noted, as regions of the prefrontal cortex were more affected in the right hemisphere, and regions of the temporal cortex in the left hemisphere. No significant interaction effect of age and diagnostic group on variation in cortical thickness was demonstrated. Among patients, dose or type of antipsychotic medication did not affect variation in cortical thickness. The results from this hitherto largest study on the topic show that prefrontal and temporal cortical thinning in patients with schizophrenia compared to controls is as pronounced in older as in younger subjects. The lack of significant influence from antipsychotic medication supports that regional cortical thinning is an inherent feature of the neurobiological disease process in schizophrenia.
bInstitute of Psychiatry, University of Oslo, P.O. Box 85, Vinderen, N-0319 Oslo, Norway
cInstitute of Psychology, University of Oslo, P.O. Box 1094, Blindern, N-0317 Oslo, Norway
dDepartment of Biostatistics, Institute of Basic Medical Sciences, University of Oslo, P.O. Box 1122, Blindern, N-0317 Oslo, Norway
eHuman Brain Informatics (HUBIN), Department of Clinical Neuroscience, Psychiatry Section, Karolinska Institutet and Hospital, SE-171 76 Stockholm, Sweden