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Cortical Folding (cortical + folding)
Selected AbstractsPrefrontal gyral folding and its cognitive correlates in bipolar disorder and schizophreniaACTA PSYCHIATRICA SCANDINAVICA, Issue 3 2009A. M. McIntosh Objective:, We sought to address whether dorsal or ventral prefrontal gyrification is abnormal in bipolar disorder and to determine its diagnostic specificity and cognitive associations. Method:, Forty-two out-patients with bipolar disorder, 28 with schizophrenia and 37 controls underwent magnetic resonance imaging. All subjects also underwent IQ and executive assessments using tasks whose performance has been localized to the ventral or dorsal prefrontal cortex. Cortical folding was quantified using the gyrification index (GI) and related to the cognitive measures. Results:, Patients with bipolar disorder showed reduced prefrontal gyrification compared with controls but did not differ from patients with schizophrenia. Neither ventral nor dorsal GI was preferentially affected in either disorder. Current IQ was positively and significantly correlated with GI. Conclusion:, Patients with bipolar disorder and patients with schizophrenia have reduced prefrontal gyrification affecting both ventral and dorsal subregions. These reductions were significantly associated with cognitive impairments occurring in both disorders. [source] Cortical folding difference between patients with early-onset and patients with intermediate-onset bipolar disorderBIPOLAR DISORDERS, Issue 4 2009Jani Penttilä Objectives:, Cerebral abnormalities have been detected in patients with bipolar disorder (BD). In comparison to BD with a later onset, early-onset BD has been found to have a poorer outcome. However, it is yet unknown whether neuroanatomical abnormalities differ between age-at-onset subgroups of the illness. We searched for cortical folding differences between early-onset (before 25 years) and intermediate-onset (between 25 and 45 years) BD patients. Methods:, Magnetic resonance images of 22 early-onset BD patients, 14 intermediate-onset BD patients, and 50 healthy participants were analyzed using a fully automated method to extract, label, and measure the sulcal area in the whole cortex. Cortical folding was assessed by computing global sulcal indices (the ratio between total sulcal area and total outer cortex area) for each hemisphere, and local sulcal indices for 12 predefined regions in both hemispheres. Results:, Intermediate-onset BD patients had a significantly reduced local sulcal index in the right dorsolateral prefrontal cortex in comparison to both early-onset BD patients and healthy subjects, and lower global sulcal indices in both hemispheres in comparison to healthy subjects (p < 0.05, Bonferroni corrected). Brain tissue volumes did not differ between groups. Conclusions:, This study provided the first evidence of a neuroanatomic difference between intermediate-onset and early-onset BD, which lends further support to the existence of different age-at-onset subgroups of BD. [source] Folding of the tectal cortex by local remodeling of neural differentiationDEVELOPMENTAL DYNAMICS, Issue 3 2004Tatsuo Mima Abstract The folding pattern of the brain cortex is a precisely regulated process, but the mechanism involved during development remains unclear. A proposed theory predicts that the initiation of cortical folding depends, at least partly, on nonuniform distribution of neuronal differentiation and neurite growth. We tested this theory experimentally, by remodeling the normal pattern of neuronal cell differentiation within the embryonic optic tectum. Multiple foci of activated fibroblast growth factor signaling were created in the tectal cortex to locally change the neural differentiation and axonal growth patterns. At these foci, tectal cells remained undifferentiated and their radial and tangential migration was suppressed. These local changes in the neuronal cell differentiation resulted in a conversion of the tectal cortex from smoothly extended into precociously folded. The results provide in vivo experimental evidence that microscopic changes in the neuronal cell differentiation pattern can induce or remodel the folding pattern of the brain cortex. Developmental Dynamics 229:475,479, 2004. © 2004 Wiley-Liss, Inc. [source] Increased gyrification in Williams syndrome: evidence using 3D MRI methodsDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 5 2002J Eric Schmitt BABS Understanding patterns of gyrification in neurogenetic disorders helps to uncover the neurodevelopmental etiology underlying behavioral phenotypes. This is particularly true in Williams syndrome (WS), a condition caused by de novo deletion of approximately 1 to 2Mb in the 7q11.23 region. Individuals with WS characteristically possess an unusual dissociation between deficits in visual-spatial ability and relative preservations in language, music, and social drive. A preliminary postmortem study reported anomalous gyri and sulci in individuals with WS. The present study examined gyrification patterns in 17 participants with WS (10 females, 7 males; mean age 28 years 11 months, SD 8 years 6 months) and 17 age- and sex-matched typically developing control participants (mean age 29 years 1 month, SD 8 years 1 month) using new automated techniques in MRI. Significantly increased cortical gyrification was found globally with abnormalities being more marked in the right parietal (p=0.0227), right occipital (p=0.0249), and left frontal (p=0.0086) regions. These results suggest that one or more genes in the 7q11.23 region are involved during the critical period when cortical folding occurs, and may be related to the hypothesized dorsal/ventral dissociation in this condition. [source] Cerebral Cortical Gyrification: A Preliminary Investigation in Temporal Lobe EpilepsyEPILEPSIA, Issue 2 2007Lisa Ronan Summary:,Purpose: To introduce a measure of global cortical folding in epilepsy by using stereology. Subtle developmental abnormalities associated with temporal lobe epilepsy may encompass brain morphologic changes such as an aberrant degree of cortical folding. Methods: Stereologic methods of volume and surface-area estimation were applied to in vivo MR brain-image data of a cohort of 20 temporal lobe epilepsy (TLE) patients (10 men, 10 women), and 20 neurologically normal controls (10 men, 10 women). Indices of cerebral gyrification and cerebral atrophy were generated. The impact of side of seizure onset, age at onset, history of febrile seizures, presence or absence of lesions, and presence or absence of secondarily generalized seizures on cerebral gyrification was assessed. Results: Although no significant group mean difference was found in the degree of cerebral gyrification between patients and controls, five of 10 of male patients had an abnormal gyrification when compared with male controls. One female patient had a significant change in gyrification compared with female controls. In general, patients with TLE demonstrated a significant degree of global cerebral atrophy compared with controls. Clinical factors were not demonstrated to affect significantly any of the quantitative parameters. Conclusions: The results of this study suggest that an aberrant degree of global cerebral gyrification may occur in certain clinical groups of TLE patients. These findings have implications for general theories of developmental susceptibility in TLE. [source] Neuroimaging of cortical development and brain connectivity in human newborns and animal modelsJOURNAL OF ANATOMY, Issue 4 2010Gregory A. Lodygensky Abstract Significant human brain growth occurs during the third trimester, with a doubling of whole brain volume and a fourfold increase of cortical gray matter volume. This is also the time period during which cortical folding and gyrification take place. Conditions such as intrauterine growth restriction, prematurity and cerebral white matter injury have been shown to affect brain growth including specific structures such as the hippocampus, with subsequent potentially permanent functional consequences. The use of 3D magnetic resonance imaging (MRI) and dedicated postprocessing tools to measure brain tissue volumes (cerebral cortical gray matter, white matter), surface and sulcation index can elucidate phenotypes associated with early behavior development. The use of diffusion tensor imaging can further help in assessing microstructural changes within the cerebral white matter and the establishment of brain connectivity. Finally, the use of functional MRI and resting-state functional MRI connectivity allows exploration of the impact of adverse conditions on functional brain connectivity in vivo. Results from studies using these methods have for the first time illustrated the structural impact of antenatal conditions and neonatal intensive care on the functional brain deficits observed after premature birth. In order to study the pathophysiology of these adverse conditions, MRI has also been used in conjunction with histology in animal models of injury in the immature brain. Understanding the histological substrate of brain injury seen on MRI provides new insights into the immature brain, mechanisms of injury and their imaging phenotype. [source] | |||||||||||||||||||||||||