Literature DB >> 22640702

Aberrant cortical gyrification in schizophrenia: a surface-based morphometry study.

Lena Palaniyappan1, Peter F Liddle.   

Abstract

BACKGROUND: Schizophrenia is considered to be a disorder of cerebral connectivity associated with disturbances of cortical development. Disturbances in connectivity at an early period of cortical maturation can result in widespread defects in gyrification. Investigating the anatomic distribution of gyrification defects can provide important information about neurodevelopment in patients with schizophrenia.
METHODS: We undertook an automated surface-based morphometric assessment of gyrification on 3-dimensionally reconstructed cortical surfaces across multiple vertices that cover the entire cortex. We used a sample from our previous research of 57 patients (50 men) with schizophrenia and 41 controls (39 men) in whom we had tested a specific hypothesis regarding presence of both hypo and hypergyria in the prefrontal cortex using a frontal region-of-interest approach.
RESULTS: Regions with significant reductions in gyrification (hypogyria) were seen predominantly in the left hemisphere, involving the insula and several regions of the multimodal association cortex. Although the prefrontal hypergyria documented earlier did not survive the statistical correction required for a whole brain search (cluster inclusion at p = 0.0001), significant hypergyric frontal clusters emerged when the threshold was lowered (cluster inclusion at p = 0.05). In the insula, a reduction in gyrification was related to reduced cortical thickness in patients with schizophrenia. LIMITATIONS: We studied a sample of patients taking antipsychotic medications, which could have confounded the results. Our sample was predominantly male, limiting the generalizability of our findings.
CONCLUSION: Our observations suggest that the disturbances in cortical gyrification seen in patients with schizophrenia might be related to a disrupted interaction between the paralimbic and the multimodal association cortex and thus might contribute to the pathogenesis of the illness.

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Mesh:

Year:  2012        PMID: 22640702      PMCID: PMC3493098          DOI: 10.1503/jpn.110119

Source DB:  PubMed          Journal:  J Psychiatry Neurosci        ISSN: 1180-4882            Impact factor:   6.186


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