Article Figures & Data
Figures
- Figure 1.
a, b, Representative parasagittal anatomy in control (a) and AgCC (b) subjects (x = −6.0 mm). c, In AgCC, callosal fibers fail to cross midline during development, instead forming Probst bundles (white arrows, z = +20 mm). d–f, A combined midspace template was constructed by iterative nonlinear registration to an initial MNI-space target template of all T1-weighted structural images from both AgCC and control subjects: mean control contribution (d), mean AgCC contribution (e), and combined control and AgCC midspace templates (f).
- Figure 2.
a, b, Mean interregional correlations in BOLD signal from 48 Harvard–Oxford atlas labels in both hemispheres for AgCC subjects (a) and control subjects (b). Homotopic correlations appear on the diagonal of the upper right quadrants of the Fisher z-transformed correlation matrices. c, Pairwise comparison of homotopic correlations (z-transformed) for all 48 regions. Only three regions—intracalcarine (23), precuneus (30), and cuneal (31) cortices—show uncorrected significant differences (*α = 0.05), none of which survive FDR correction (q = 0.05). Regions with partial clipping by the calculation mask in either group are indicated with solid bars (see Results, Atlas-based BOLD correlation). d, e, Location and extent in sagittal (d) and axial (e) sections of the three regions with reduced functional correlation in AgCC identified in c. These regions correspond to areas of significantly increased local deformation in AgCC (Fig. 6).
- Figure 3.
Spatial correlation matching of group-level ICs. a, Full correlation matrix, C, for all neuronal ICs identified in the ICA of control and AgCC groups. Searching rows and columns for the maximum correlation coefficient identifies candidate pairings of ICs from each group. A pairing is defined as invertible if the corresponding matrix element contains the maximum correlation in both row and column. b, Reduced correlation matrix, C̃, composed of the reordered invertible IC pairings.
- Figure 4.
a, Invertible matches between AgCC and control group independent component spatial maps, ordered by decreasing spatial correlation coefficient from highest (A7–C40, r = 0.695) to lowest (A4–C5, r = 0.328). b, Additional pairings (by inspection) from the remaining ICs without invertible matches. c, Unmatched ICs: a bilateral cerebellar component in AgCC (A10) and a medial occipital (C8) and lateral parietal (C12) component in controls. d, Suboptimal invertible matches occur when networks in either group are split into subcomponents by the ICA. For example, the dorsal parietal-frontal networks are lateralized in control subjects (C4 and C11) but split anterior–posterior in AgCC (A16 and A41). Similarly, the default mode network is a single component in the control group (C41), but split into frontal and parietal components in AgCC (A2 and A43).
- Figure 5.
Interhemispheric temporal BOLD correlations for each of the group-level ICs. Masks were defined within the left and right hemispheres for suprathreshold voxels for each group-level IC. Extracted BOLD time series (corrected for white matter and CSF time courses) were correlated and mean Fisher z-transformed correlation calculated for all subjects. a, No significant difference was observed between groups in an unpaired comparison of all neuronal ICs (p = 0.778). b, Interhemispheric correlations for the invertible IC pairs from each group. Only one IC pair showed a significant difference in interhemispheric correlation (*A21–C39, left cerebellum, p = 0.0026 FDR corrected). c, Left–right percentage symmetry of the group IC masks used for calculating the BOLD temporal correlations in a and b did not differ between groups (for symmetry definition, see Materials and Methods). d, Left–right percentage symmetry for the ICs that comprise the 17 invertible IC pairings.
- Figure 6.
Mean absolute deformation within suprathreshold regions for each of the 19 IC pairs illustrated in Figure 4. The combination of A16 and A41 has been paired with C4 and C11, as has A2 and A43 with C41, as described in the Results, Morphological variability and independent component differences. IC pairs with significantly higher regional deformation in AgCC compared with controls (*) all correspond to posterior midline locations, which also show significantly reduced homotopic temporal correlation (Fig. 2c).
Tables
- Table 1.
Correspondences of group-level AgCC neuronal independent components to control group and literature components
IC number Best control IC match Correlation coefficient Explained variance Assignment Corresponding IC in Smith et al. (2009) Invertible A7 C40 0.695 4.28% Auditory (frontal) 720 A12 C34 0.689 3.48% Caudate-putamen — A34 C9 0.654 0.82% Ventral visual 320 A26 C2 0.595 1.47% Auditory (temporal) 720 A5 C14 0.586 4.70% Premotor — A8 C3 0.548 4.10% Visual 120 (part) A19 C36 0.527 2.73% Visual 220 A2 C41 0.497 5.61% DMN (with A43) 420 A32 C27 0.476 0.88% Cerebellum (right) 520 (part) A40 C38 0.424 0.04% Posterior cingulate 420 (part) A41 C4 0.407 0.08% Parietal-frontal (with A16) 920,1020 A43 C20 0.382 0.67% DMN (with A19) 420 A21 C39 0.348 2.49% Cerebellum (left) 520 (part) A16 C11 0.346 3.09% Parietal-frontal (with A41) 920,1020 A15 C21 0.339 3.20% vmPFC 820 (part) A25 C16 0.332 1.88% Frontal pole 820 (part) A4 C5 0.328 4.79% dlPFC — Noninvertible A9 C10 4.09% Somatomotor 620 A10 — 3.96% Cerebellum 520 (part) A27 C18 1.43% dlOC — Total 53.79% Seventeen of the 20 components were matched invertibly to control ICs and two noninvertible components were matched by inspection (A9 and A27). DMN, Default mode network; vmPFC, ventromedial prefrontal cortex; dlPFC, dorsolateral prefrontal cortex; dlOC, dorsolateral occipital cortex.
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