Journal
PSYCHOLOGICAL MEDICINE
Volume 41, Issue 7, Pages 1449-1460Publisher
CAMBRIDGE UNIV PRESS
DOI: 10.1017/S003329171000200X
Keywords
Brain; cortical thickness; endophenotype; MRI; schizophrenia
Categories
Funding
- Instituto de Salud Carlos III [PI020499, PI050427, PI060507]
- SENY Fundacio [CI 2005-0308007]
- Fundacion Marques de Valdecilla [API07/011]
- AstraZeneca
- Pfizer
- Bristol-Myers Squibb
- Johnson Johnson
- Lilly
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Background. The thickness of the cortical mantle is a sensitive measure for identifying alterations in cortical structure. We aimed to explore whether first episode schizophrenia patients already show a significant cortical thinning and whether cortical thickness anomalies may significantly influence clinical and cognitive features. Method. We investigated regional changes in cortical thickness in a large and heterogeneous sample of schizophrenia spectrum patients (n=142) at their first break of the illness and healthy controls (n=83). Magnetic resonance imaging brain scans (1.5 T) were obtained and images were analyzed by using BRAINS2. The contribution of sociodemographic, cognitive and clinical characterictics was investigated. Results. Patients showed a significant total cortical thinning (F=17.55, d=x0.62, p< 0.001) and there was a diffuse pattern of reduced thickness (encompassing frontal, temporal and parietal cortices) (all p's< 0.001, d's> 0.53). No significant grouprgender interactions were observed (all p's> 0.15). There were no significant associations between the clinical and pre-morbid variables and cortical thickness measurements (all r's< 0.12). A weak significant negative correlation between attention and total (r=x0.24, p=0.021) and parietal cortical thickness (r=x0.27, p=0.009) was found in patients (thicker cortex was associated with lower attention). Our data revealed a similar pattern of cortical thickness changes related to age in patients and controls. Conclusions. Cortical thinning is independent of gender, age, age of onset and duration of the illness and does not seem to significantly influence clinical and functional symptomatology. These findings support a primary neurodevelopment disorder affecting the normal cerebral cortex development in schizophrenia.
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