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A controlled comparison of thickness, volume and surface areas from multiple cortical parcellation packages.

ABSTRACT: BACKGROUND:Cortical parcellation is an essential neuroimaging tool for identifying and characterizing morphometric and connectivity brain changes occurring with age and disease. A variety of software packages have been developed for parcellating the brain's cortical surface into a variable number of regions but interpackage differences can undermine reproducibility. Using a ground truth dataset (Edinburgh_NIH10), we investigated such differences for grey matter thickness (GMth), grey matter volume (GMvol) and white matter surface area (WMsa) for the superior frontal gyrus (SFG), supramarginal gyrus (SMG), and cingulate gyrus (CG) from 4 parcellation protocols as implemented in the FreeSurfer, BrainSuite, and BrainGyrusMapping (BGM) software packages. RESULTS:Corresponding gyral definitions and morphometry approaches were not identical across the packages. As expected, there were differences in the bordering landmarks of each gyrus as well as in the manner in which variability was addressed. Rostral and caudal SFG and SMG boundaries differed, and in the event of a double CG occurrence, its upper fold was not always addressed. This led to a knock-on effect that was visible at the neighbouring gyri (e.g., knock-on effect at the SFG following CG definition) as well as gyral morphometric measurements of the affected gyri. Statistical analysis showed that the most consistent approaches were FreeSurfer's Desikan-Killiany-Tourville (DKT) protocol for GMth and BrainGyrusMapping for GMvol. Package consistency varied for WMsa, depending on the region of interest. CONCLUSIONS:Given the significance and implications that a parcellation protocol will have on the classification, and sometimes treatment, of subjects, it is essential to select the protocol which accurately represents their regions of interest and corresponding morphometrics, while embracing cortical variability.

SUBMITTER: Mikhael SS

PROVIDER: S-EPMC6348615 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature

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Project description:Introduction22q11.2 deletion syndrome (22q11DS) represents one of the largest known genetic risk factors for psychosis, yet the neurobiological mechanisms underlying symptom development are not well understood. Here we conducted a cross-sectional study of 22q11DS to decompose cortical volume into its constituent parts, cortical thickness (CT) and surface area (SA), which are believed to have distinct neurodevelopmental origins.MethodsHigh-resolution T1-weighted scans were collected on 65 participants (31 22q11DS, 34 demographically comparable typically developing controls, 10-25 years old). Measures of cortical volume, CT, and SA were extracted from regions of interest using the FreeSurfer image analysis suite. Group differences and age-related trajectories in these structures, as well as their association with psychotic symptomatology, were assessed.ResultsRelative to controls, 22q11DS participants showed bilateral volumetric reductions in the inferior temporal cortex, fusiform gyrus, anterior cingulate, superior parietal cortex, and cuneus, which were driven by decreased SA in these regions. 22q11DS participants also had increased volumes, driven by increased CT, in bilateral insula regions. 22q11DS youth had increased CT in frontal regions, particularly middle frontal and medial orbitofrontal cortices. A pattern of age-associated cortical thinning was observed in typically developing controls in brain regions associated with visual and sensory information-processing (i.e., left pericalcarine cortex and fusiform gyrus, right lingual and postcentral cortices). However, this relationship was disrupted in 22q11DS participants. Finally, correlational analyses revealed that increased CT in right medial orbitofrontal cortex was associated with increased positive symptom severity in 22q11DS.ConclusionDifferential disruptions of CT and SA in distinct cortical regions in 22q11DS may indicate abnormalities in distinct developmental neural processes. Further, neuroanatomic abnormalities in medial frontal brain structures disproportionately affected in idiopathic schizophrenia were associated with psychotic symptom severity in 22q11DS youth, suggesting that disrupted biological processes in these cortical regions may underlie development of psychotic symptoms, both in 22q11DS and in the broader population.

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A controlled comparison of thickness, volume and surface areas from multiple cortical parcellation packages.

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