Abstract
Several studies have sought to test the neurodevelopmental hypothesis of schizophrenia through analysis of cortical gyrification. However, to date, results have been inconsistent. A possible reason for this is that gyrification measures at the centimeter scale may be insensitive to subtle morphological changes at smaller scales. The lack of consistency in such studies may impede further interpretation of cortical morphology as an aid to understanding the etiology of schizophrenia.In this study we developed a new approach, examining whether millimeter-scale measures of cortical curvature are sensitive to changes in fundamental geometric properties of the cortical surface in schizophrenia. We determined and compared millimeter-scale and centimeter-scale curvature in three separate case–control studies; specifically two adult groups and one adolescent group. The datasets were of different sizes, with different ages and gender-spreads. The results clearly show that millimeter-scale intrinsic curvature measures were more robust and consistent in identifying reduced gyrification in patients across all three datasets.To further interpret this finding we quantified the ratio of expansion in the upper and lower cortical layers. The results suggest that reduced gyrification in schizophrenia is driven by a reduction in the expansion of upper cortical layers. This may plausibly be related to a reduction in short-range connectivity.
Highlights
A major challenge in schizophrenia research is to identify and characterize a core pathophysiology that could account for the wide array of symptoms
Such ideas have been embedded in more specific theories such as cognitive dysmetria (Andreasen and Paradiso, 1998; Andreasen et al, 1999), cerebral asymmetry (Crow, 2008), and the reduced neuropil hypothesis (Selemon and Goldman-Rakic, 1999), each implicating aberrant connectivity as the structural substrate for functional abnormalities
When data were combined across groups, we observed a strong, positive correlation between cortical surface area and each of the gyrification parameters
Summary
A major challenge in schizophrenia research is to identify and characterize a core pathophysiology that could account for the wide array of symptoms. The deficit must be diffuse and pervasive (White and Hilgetag, 2011), a fact that has been reflected in an emphasis on explanatory models that appeal to disruptions in neural connectivity (Harrison, 1999) Such ideas have been embedded in more specific theories such as cognitive dysmetria (Andreasen and Paradiso, 1998; Andreasen et al, 1999), cerebral asymmetry (Crow, 2008), and the reduced neuropil hypothesis (Selemon and Goldman-Rakic, 1999), each implicating aberrant connectivity as the structural substrate for functional abnormalities. Consistent with this view is a lack of gliosis (Roberts et al, 1987), the presence of structural abnormalities at an early stage in first-episode patients, and the presence of behavioral abnormalities prior to the onset of symptoms (Khandaker et al, 2011)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
