The dynamics of cortical folding waves and prematurity-related deviations revealed by spatial and spectral analysis of gyrification.

In the human brain, the appearance of cortical sulci is a complex process that takes place mostly during the second half of pregnancy, with a relatively stable temporal sequence across individuals. Since deviant gyrification patterns have been observed in many neurodevelopmental disorders, mapping cortical development in vivo from the early stages on is an essential step to uncover new markers for diagnosis or prognosis. Recently this has been made possible by MRI combined with post-processing tools, but the reported results are still fragmented. Here we aimed to characterize the typical folding progression ex utero from the pre- to the post-term period, by considering 58 healthy preterm and full-term newborns and infants imaged between 27 and 62 weeks of post-menstrual age. Using a method of spectral analysis of gyrification (SPANGY), we detailed the spatial-frequency structure of cortical patterns in a quantitative way. The modeling of developmental trajectories revealed three successive waves that might correspond to primary, secondary and tertiary folding. Some deviations were further detected in 10 premature infants without apparent neurological impairment and imaged at term equivalent age, suggesting that our approach is sensitive enough to highlight the subtle impact of preterm birth and extra-uterine life on folding.

Are Developmental Trajectories of Cortical Folding Comparable Between Cross-sectional Datasets of Fetuses and Preterm Newborns?

Magnetic resonance imaging has proved to be suitable and efficient for in vivo investigation of the early process of brain gyrification in fetuses and preterm newborns but the question remains as to whether cortical-related measurements derived from both cases are comparable or not. Indeed, the developmental folding trajectories drawn up from both populations have not been compared so far, neither from cross-sectional nor from longitudinal datasets. The present study aimed to compare features of cortical folding between healthy fetuses and early imaged preterm newborns on a cross-sectional basis, over a developmental period critical for the folding process (21-36 weeks of gestational age [GA]). A particular attention was carried out to reduce the methodological biases between the 2 populations. To provide an accurate group comparison, several global parameters characterizing the cortical morphometry were derived. In both groups, those metrics provided good proxies for the dramatic brain growth and cortical folding over this developmental period. Except for the cortical volume and the rate of sulci appearance, they depicted different trajectories in both groups suggesting that the transition from into ex utero has a visible impact on cortical morphology that is at least dependent on the GA at birth in preterm newborns.

An Exact Formula for Calculating Inverse Radial Lens Distortions.

This article presents a new approach to calculating the inverse of radial distortions. The method presented here provides a model of reverse radial distortion, currently modeled by a polynomial expression, that proposes another polynomial expression where the new coefficients are a function of the original ones. After describing the state of the art, the proposed method is developed. It is based on a formal calculus involving a power series used to deduce a recursive formula for the new coefficients. We present several implementations of this method and describe the experiments conducted to assess the validity of the new approach. Such an approach, non-iterative, using another polynomial expression, able to be deduced from the first one, can actually be interesting in terms of performance, reuse of existing software, or bridging between different existing software tools that do not consider distortion from the same point of view.

Structural basis for the association of MAP6 protein with microtubules and its regulation by calmodulin.

Microtubules are highly dynamic αß-tubulin polymers. In vitro and in living cells, microtubules are most often cold- and nocodazole-sensitive. When present, the MAP6/STOP family of proteins protects microtubules from cold- and nocodazole-induced depolymerization but the molecular and structure determinants by which these proteins stabilize microtubules remain under debate. We show here that a short protein fragment from MAP6-N, which encompasses its Mn1 and Mn2 modules (MAP6(90-177)), recapitulates the function of the full-length MAP6-N protein toward microtubules, i.e. its ability to stabilize microtubules in vitro and in cultured cells in ice-cold conditions or in the presence of nocodazole. We further show for the first time, using biochemical assays and NMR spectroscopy, that these effects result from the binding of MAP6(90-177) to microtubules with a 1:1 MAP6(90-177):tubulin heterodimer stoichiometry. NMR data demonstrate that the binding of MAP6(90-177) to microtubules involve its two Mn modules but that a single one is also able to interact with microtubules in a closely similar manner. This suggests that the Mn modules represent each a full microtubule binding domain and that MAP6 proteins may stabilize microtubules by bridging tubulin heterodimers from adjacent protofilaments or within a protofilament. Finally, we demonstrate that Ca(2+)-calmodulin competes with microtubules for MAP6(90-177) binding and that the binding mode of MAP6(90-177) to microtubules and Ca(2+)-calmodulin involves a common stretch of amino acid residues on the MAP6(90-177) side. This result accounts for the regulation of microtubule stability in cold condition by Ca(2+)-calmodulin.

Spectral-based thickness profiling of the corpus callosum enhances anomaly detection in fetal alcohol spectrum disorders.

Introduction: Fetal alcohol spectrum disorders (FASD) range from fetal alcohol syndrome (FAS) to non-syndromic forms (NS-FASD). The neuroanatomical consequences of prenatal alcohol exposure are mainly the reduction in brain size, but also focal abnormalities such as those of the corpus callosum (CC). We previously showed a narrowing of the CC for brain size, using manual measurement and its usefulness to improve diagnostic certainty. Our aim was to automate these measurements of the CC and identify more recurrent abnormalities in FAS subjects, independently of brain size reduction. Methods: We developed a fast, automated, and normalization-free method based on spectral analysis to generate thicknesses of the CC continuously and at singular points (genu, body, isthmus, and splenium), and its length (LCC). We applied it on midsagittal section of the CC extracted from T1-anatomical brain MRI of 89 subjects with FASD (52 FAS, 37 NS-FASD) and 126 with typically development (6-20 y-o). After adjusting for batch effect, we compared the mean profiles and thicknesses of the singular points across the 3 groups. For each parameter, we established variations with age (growth charts) and brain size in the control group (scaling charts), then identified participants with abnormal measurements (<10th percentile). Results: We confirmed the slimming of the posterior half of the CC in both FASD groups, and of the genu section in the FAS group, compared to the control group. We found a significant group effect for the LCC, genu, median body, isthmus, and splenium thicknesses (p < 0.05). We described a body hump whose morphology did not differ between groups. According to the growth charts, there was an excess of FASD subjects with abnormal LCC and isthmus, and of FAS subjects with abnormal genu and splenium. According to the scaling charts, this excess remained only for LCC, isthmus and splenium, undersized for brain size. Conclusion: We characterized size-independent anomalies of the posterior part of the CC in FASD, with an automated method, confirming and extending our previous study. Our new tool brings the use of a neuroanatomical criterion including CC damage closer to clinical practice. Our results suggest that an FAS signature identified in NS-FASD, could improve diagnosis specificity.

Mapping corpus callosum surface reduction in fetal alcohol spectrum disorders with sulci and connectivity-based parcellation.

Introduction: Fetal alcohol spectrum disorders (FASD) range from fetal alcohol syndrome (FAS) to non-syndromic non-specific forms (NS-FASD) that are still underdiagnosed and could benefit from new neuroanatomical markers. The main neuroanatomical manifestation of prenatal alcohol exposure on developmental toxicity is the reduction in brain size, but repeated imaging observations have long driven the attention on the corpus callosum (CC), without being all convergent. Our study proposed a new segmentation of the CC that relies on both a sulci-based cortical segmentation and the "hemispherotopic" organization of the transcallosal fibers. Methods: We collected a monocentric series of 37 subjects with FAS, 28 with NS-FASD, and 38 with typical development (6 to 25 years old) using brain MRI (1.5T). Associating T1- and diffusion-weighted imaging, we projected a sulci-based cortical segmentation of the hemispheres on the midsagittal section of the CC, resulting in seven homologous anterior-posterior parcels (frontopolar, anterior and posterior prefrontal, precentral, postcentral, parietal, and occipital). We measured the effect of FASD on the area of callosal and cortical parcels by considering age, sex, and brain size as linear covariates. The surface proportion of the corresponding cortical parcel was introduced as an additional covariate. We performed a normative analysis to identify subjects with an abnormally small parcel. Results: All callosal and cortical parcels were smaller in the FASD group compared with controls. When accounting for age, sex, and brain size, only the postcentral (η2 = 6.5%, pFDR = 0.032) callosal parcel and % of the cortical parcel (η2 = 8.9%, pFDR = 0.007) were still smaller. Adding the surface proportion (%) of the corresponding cortical parcel to the model, only the occipital parcel was persistently reduced in the FASD group (η2 = 5.7%, pFDR = 0.014). In the normative analysis, we found an excess of subjects with FASD with abnormally small precentral and postcentral (peri-isthmic) and posterior-splenial parcels (pFDR < 0.05). Conclusion: The objective sulcal and connectivity-based method of CC parcellation proved to be useful not only in confirming posterior-splenial damage in FASD but also in the narrowing of the peri-isthmic region strongly associated with a specific size reduction in the corresponding postcentral cortical region (postcentral gyrus). The normative analysis showed that this type of callosal segmentation could provide a clinically relevant neuroanatomical endophenotype, even in NS-FASD.

The C terminus of tubulin, a versatile partner for cationic molecules: binding of Tau, polyamines, and calcium.

The C-terminal region of tubulin is involved in multiple aspects of the regulation of microtubule assembly. To elucidate the molecular mechanisms of this regulation, we study here, using different approaches, the interaction of Tau, spermine, and calcium, three representative partners of the tubulin C-terminal region, with a peptide composed of the last 42 residues of α1a-tubulin. The results show that their binding involves overlapping amino acid stretches in the C-terminal tubulin region: amino acid residues 421-441 for Tau, 430-432 and 444-451 for spermine, and 421-443 for calcium. Isothermal titration calorimetry, NMR, and cosedimentation experiments show that Tau and spermine have similar micromolar binding affinities, whereas their binding stoichiometry differs (C-terminal tubulin peptide/spermine stoichiometry 1:2, and C-terminal tubulin peptide/Tau stoichiometry 8:1). Interestingly, calcium, known as a negative regulator of microtubule assembly, can compete with the binding of Tau and spermine with the C-terminal domain of tubulin and with the positive effect of these two partners on microtubule assembly in vitro. This observation opens up the possibility that calcium may participate in the regulation of microtubule assembly in vivo through direct (still unknown) or indirect mechanism (displacement of microtubule partners). The functional importance of this part of tubulin was also underlined by the observation that an α-tubulin mutant deleted from the last 23 amino acid residues does not incorporate properly into the microtubule network of HeLa cells. Together, these results provide a structural basis for a better understanding of the complex interactions and putative competition of tubulin cationic partners with the C-terminal region of tubulin.

Larger is twistier: spectral analysis of gyrification (SPANGY) applied to adult brain size polymorphism.

The description of cortical folding pattern (CFP) is challenging because of geometric complexity and inter-subject variability. On a cortical surface mesh, curvature estimation provides a good scalar proxy of CFP. The oscillations of this function can be studied using a Fourier-like analysis to produce a power spectrum representative of the spatial frequency composition of CFP. First, we introduce an original method for the SPectral ANalysis of GYrication (Spangy), which performs a spectral decomposition of the mean curvature of the grey/white interface mesh based on the Laplace-Beltrami operator eigenfunctions. Spangy produces an ordered 7 bands power spectrum of curvature (B0-B6) and provides an anatomically relevant segmentation of CFP based on local spectral composition. A spatial frequency being associated with each eigenfunction, the bandwidth design assumes frequency doubling between consecutive spectral bands. Next, we observed that the last 3 spectral bands (B4, 5 and 6) accounted for 93% of the analyzed spectral power and were associated with fold-related variations of curvature, whereas the lower frequency bands were related to global brain shape. The spectral segmentation of CFP revealed 1st, 2nd and 3rd order elements associated with B4, B5 and B6 respectively. These elements could be related to developmentally-defined primary, secondary and tertiary folds. Finally, we used allometric scaling of frequency bands power and segmentation to analyze the relationship between the spectral composition of CFP and brain size in a large adult dataset. Total folding power followed a positive allometric scaling which did not divide up proportionally between the bands: B4 contribution was constant, B5 increased like total folding power and B6 much faster. Besides, apparition of new elements of pattern with increasing size only concerned the 3rd order. Hence, we demonstrate that large brains are twistier than smaller ones because of an increased number of high spatial frequency folds, ramifications and kinks that accommodate the allometric increase of cortical surface.

ADC measurement relevance to predict hemorrhage transformation after mechanical thrombectomy.

BACKGROUND: ADC (apparent coefficient diffusion) value has been known to predict hemorrhage transformation (HT) after thrombolysis and recently, after mechanical thrombectomy (MT). We aimed to evaluate that utility separately in basal ganglia and superficial territory. We used HT occurrence with or without NIHSS change as primary outcome measures. METHODS: This single-center retrospective study included consecutive stroke patients receiving MT for internal carotid artery (ICA) or middle cerebral artery (M1 or M2) occlusion. In patient with or without HT, using the Heidelberg Bleeding Classification, on follow-up CT scan at 24-48 h, we assessed the ADC value separately in basal ganglia and superficial territory on MRI before MT to search for the correlation. Multivariable analysis was performed using variables with significant differences between the HT group and non-HT group. RESULTS: One hundred seventeen patients were included in the final analysis. HT distribution was as follows: 9 patients (7.69%) HI1 or 2; 14 patients (11.97%) PH1; 21 patients (17.95%) PH2; 29 patients (24.79%) subarachnoid hemorrhage; and 21 patients (17.95%) symptomatic intracranial hemorrhage (sICH). Mean ADC minimal value in basal ganglia in the HT group was significantly lower than in the non-HT group (377.6 × 10-6 mm2/s [± 52.4] vs 413.3 × 10-6 mm2/s [± 72.5]; p = 0.0229) with an area under the curve (AUC) of 0.6622 (95% CI: 0.5-0.8; p = 0.014). MRI-MT time was significantly longer in the HT group (p = 0.0002), but there was no association between ADC value and onset-MRI or MRI-MT times (Spearman's coefficients <0.7, p > 0.05). Glycemia at admission (>1.5 g/L) (OR = 4.2; 95% CI [1.611; 10.961]) and carotid occlusion (OR = 2.835; 95% CI [1.134; 7.091]) were independently associated with HT. CONCLUSIONS: ADC value in basal ganglia, unlike brain superficial territory, are correlated to HT risk after MT.

Long-term follow-up of neurodegenerative phenomenon in severe traumatic brain injury using MRI.

BACKGROUND: Traumatic brain injury (TBI) lesions are known to evolve over time, but the duration and consequences of cerebral remodelling are unclear. Degenerative mechanisms occurring in the chronic phase after TBI could constitute "tertiary" lesions related to the neurological outcome. OBJECTIVE: The objective of this prospective study of severe TBI was to longitudinally evaluate the volume of white and grey matter structures and white matter integrity with 2 time-point multimodal MRI. METHODS: Longitudinal MRI follow-up was obtained for 11 healthy controls (HCs) and 22 individuals with TBI (mean [SD] 60 [15] months after injury) along with neuropsychological assessments. TBI individuals were classified in the "favourable" recovery group (Glasgow Outcome Scale Extended [GOSE] 6-8) and "unfavourable" recovery group (GOSE 3-5) at 5 years. Variation in brain volumes (3D T1-weighted image) and white matter integrity (diffusion tensor imaging [DTI]) were quantitatively assessed over time and used to predict neurological outcome. RESULTS: TBI individuals showed a marked decrease in volumes of whole white matter (median -11.4% [interquartile range -5.8; -14.6]; p < 0.001) and deep grey nuclear structures (-17.1% [-10.6; -20.5]; p < 0.001). HCs did not show any significant change over the same time period. Median volumetric loss in several brain regions was higher with GOSE 3-5 than 6-8. These lesions were associated with lower fractional anisotropy and higher mean diffusivity at baseline. Volumetric variations were positively correlated with normalized fractional anisotropy and negatively with normalized mean diffusivity at baseline and follow-up. A computed predictive model with baseline DTI showed good accuracy to predict neurological outcome (area under the receiver operating characteristic curve 0.82 [95% confidence interval 0.81-0.83]) CONCLUSIONS: We characterised the striking atrophy of deep brain structures after severe TBI. DTI imaging in the subacute phase can predict the occurrence and localization of these tertiary lesions as well as long-term neurological outcome. TRIAL REGISTRATION: ClinicalTrials.gov: NCT00577954. Registered on October 2006.

A reaction-diffusion model of human brain development.

Cortical folding exhibits both reproducibility and variability in the geometry and topology of its patterns. These two properties are obviously the result of the brain development that goes through local cellular and molecular interactions which have important consequences on the global shape of the cortex. Hypotheses to explain the convoluted aspect of the brain are still intensively debated and do not focus necessarily on the variability of folds. Here we propose a phenomenological model based on reaction-diffusion mechanisms involving Turing morphogens that are responsible for the differential growth of two types of areas, sulci (bottom of folds) and gyri (top of folds). We use a finite element approach of our model that is able to compute the evolution of morphogens on any kind of surface and to deform it through an iterative process. Our model mimics the progressive folding of the cortical surface along foetal development. Moreover it reveals patterns of reproducibility when we look at several realizations of the model from a noisy initial condition. However this reproducibility must be tempered by the fact that a same fold engendered by the model can have different topological properties, in one or several parts. These two results on the reproducibility and variability of the model echo the sulcal roots theory that postulates the existence of anatomical entities around which the folding organizes itself. These sulcal roots would correspond to initial conditions in our model. Last but not least, the parameters of our model are able to produce different kinds of patterns that can be linked to developmental pathologies such as polymicrogyria and lissencephaly. The main significance of our model is that it proposes a first approach to the issue of reproducibility and variability of the cortical folding.

A central role for polyamines in microtubule assembly in cells.

Owing to preferential electrostatic adsorption of multivalent cations on highly anionic surfaces, natural multivalent polyamines and especially quadrivalent spermine can be considered as potential regulators of the complex dynamical properties of anionic MTs (microtubules). Indeed, the C-terminal tails of tubulin display many negative residues in a row which should enable the formation of a correlated liquid-like phase of multivalent counterions on its surface. Although it is known that polyamine counterions promote MT assembly in vitro, little is known about the relevance of this interaction in vivo. In the present study, we have explored the relationship between polyamine levels and MT assembly in HeLa and epithelial NRK (normal rat kidney) cells using DFMO (alpha-difluoromethylornithine), an irreversible inhibitor of ornithine decarboxylase, and APCHA [N-(3-aminopropyl)-N-cyclohexylamine], a spermine synthase inhibitor. Under conditions of intracellular polyamine depletion, the MT network is clearly disrupted and the MT mass decreases. Addition of spermine to polyamine-depleted cells reverses this phenotype and rapidly promotes the extensions of the MT network. Finally, we show that polyamine levels modulate the coating of MTs with MAP4 (MT-associated protein 4), an MT-stabilizing protein, and the spatial distribution of EB1 (end-binding protein 1), an MT plus-end-binding protein. In addition, polyamines favour the formation of gap junctions in NRK cells, a process which requires MT extensions at the cell periphery. The present study provides a basis for a better understanding of the role played by polyamines in MT assembly and establishes polyamine metabolism as a potential cellular target for modulating MT functions.

Surface Regularity via the Estimation of Fractional Brownian Motion Index.

The recent definition of fractional Brownian motions on surfaces has raised the statistical issue of estimating the Hurst index characterizing these models. To deal with this open issue, we propose a method which is based on a spectral representation of surfaces built upon their Laplace-Beltrami operator. This method includes a first step where the surface supporting the motion is recovered using a mean curvature flow, and a second one where the Hurst index is estimated by linear regression on the motion spectrum. The method is evaluated on synthetic surfaces. The interest of the method is further illustrated on some fetal cortical surfaces extracted from magnetic resonance images as a means to quantify the brain complexity during the gestational age.

The influence of biophysical parameters in a biomechanical model of cortical folding patterns.

Abnormal cortical folding patterns, such as lissencephaly, pachygyria and polymicrogyria malformations, may be related to neurodevelopmental disorders. In this context, computational modeling is a powerful tool to provide a better understanding of the early brain folding process. Recent studies based on biomechanical modeling have shown that mechanical forces play a crucial role in the formation of cortical convolutions. However, the effect of biophysical parameters in these models remain unclear. In this paper, we investigate the effect of the cortical growth, the initial geometry and the initial cortical thickness on folding patterns. In addition, we not only use several descriptors of the folds such as the dimensionless mean curvature, the surface-based three-dimensional gyrification index and the sulcal depth, but also propose a new metric to quantify the folds orientation. The results demonstrate that the cortical growth mode does almost not affect the complexity degree of surface morphology; the variation in the initial geometry changes the folds orientation and depth, and in particular, the slenderer the shape is, the more folds along its longest axis could be seen and the deeper the sulci become. Moreover, the thinner the initial cortical thickness is, the higher the spatial frequency of the folds is, but the shallower the sulci become, which is in agreement with the previously reported effects of cortical thickness.

A connectome-based approach to assess motor outcome after neonatal arterial ischemic stroke.

OBJECTIVE: Studies of motor outcome after Neonatal Arterial Ischemic Stroke (NAIS) often rely on lesion mapping using MRI. However, clinical measurements indicate that motor deficit can be different than what would solely be anticipated by the lesion extent and location. Because this may be explained by the cortical disconnections between motor areas due to necrosis following the stroke, the investigation of the motor network can help in the understanding of visual inspection and outcome discrepancy. In this study, we propose to examine the structural connectivity between motor areas in NAIS patients compared to healthy controls in order to define the cortical and subcortical connections that can reflect the motor outcome. METHODS: Thirty healthy controls and 32 NAIS patients with and without Cerebral Palsy (CP) underwent MRI acquisition and manual assessment. The connectome of all participants was obtained from T1-weighted and diffusion-weighted imaging. RESULTS: Significant disconnections in the lesioned and contra-lesioned hemispheres of patients were found. Furthermore, significant correlations were detected between the structural connectivity metric of specific motor areas and manuality assessed by the Box and Block Test (BBT) scores in patients. INTERPRETATION: Using the connectivity measures of these links, the BBT score can be estimated using a multiple linear regression model. In addition, the presence or not of CP can also be predicted using the KNN classification algorithm. According to our results, the structural connectome can be an asset in the estimation of gross manual dexterity and can help uncover structural changes between brain regions related to NAIS.

Group-level cortical surface parcellation with sulcal pits labeling.

Sulcal pits are the points of maximal depth within the folds of the cortical surface. These shape descriptors give a unique opportunity to access to a rich, fine-scale representation of the geometry and the developmental milestones of the cortical surface. However, using sulcal pits analysis at group level requires new numerical tools to establish inter-subject correspondences. Here, we address this issue by taking advantage of the geometrical information carried by sulcal basins that are the local patches of surfaces surrounding each sulcal pit. Our framework consists in two phases. First, we present a new method to generate a population-specific atlas of this sulcal basins organi- zation as a fold-level parcellation of the cortical surface. Then, we address the labeling of individual sulcal pits and corresponding basins with respect to this atlas. To assess their validity, we applied these methodological advances on two different populations of healthy subjects. The first database of 137 adults allowed us to compare our method to the state-of-the-art and the second database of 209 children, aged between 0 and 18 years, illustrates the adaptability and relevance of our method in the context of pediatric data showing strong variations in cortical volume and folding.

Is the Blood Oxygenation Level-Dependent fMRI Response to Motor Tasks Altered in Children After Neonatal Stroke?

Functional MRI is increasingly being used in the assessment of brain activation and connectivity following stroke. Many of these studies rely on the Blood Oxygenation Level Dependent (BOLD) contrast. However, the stability, as well as the accuracy of the BOLD response to motor task in the ipsilesional hemisphere, remains ambiguous. In this work, the BOLD signal acquired from both healthy and affected hemispheres was analyzed in 7-year-old children who sustained a Neonatal Arterial Ischemic Stroke (NAIS). Accordingly, a repetitive motor task of the contralesional and the ipsilesional hands was performed by 33 patients with unilateral lesions. These patients were divided into two groups: those without cerebral palsy (NAIS), and those with cerebral palsy (CP). The BOLD signal time course was obtained from distinctly defined regions of interest (ROIs) extracted from the functional activation maps of 30 healthy controls with similar age and demographic characteristics as the patients. An ROI covering both the primary motor cortex (M1) and the primary somatosensory cortex (S1) was also tested. Compared with controls, NAIS patients without CP had similar BOLD amplitude variation for both the contralesional and the ipsilesional hand movements. However, in the case of NAIS patients with CP, a significant difference in the averaged BOLD amplitude was found between the healthy and affected hemisphere. In both cases, no progressive attenuation of the BOLD signal amplitude was observed throughout the task epochs. Besides, results also showed a correlation between the BOLD signal percentage variation of the lesioned hemisphere and the dexterity level. These findings suggest that for patients who sustained a NAIS with no extensive permanent motor impairment, BOLD signal-based data analysis can be a valuable tool for the evaluation of functional brain networks.

Optical flow approaches to the identification of brain dynamics.

The superior temporal resolution of magneto- and electroencephalography (MEEG) provides unique insight into the dynamics of brain function. The analysis of the spatial dimensions of MEEG recordings can take a multiplicity of approaches: from the original scalp recordings to the identification of their generators through localizing or imaging techniques. Overall, both MEEG native or imaging data may be considered as multidimensional structures with potentially dense information contents. Quantitative analysis of the spatiotemporal flow of information conveyed by MEEG begins with a feature-extraction problem, thereby leading to improved insight in the multidimensional structure of brain dynamics. In this contribution, we approach this endeavor by suggesting that brain dynamic features from local through global spatial scales may be identified using the previously-introduced technique of surface-based optical flow. We illustrate this assertion by the quantitative analysis of time-resolved sequences of brain activity through the identification of episodes of relative topographical stability. In that respect, we revisit the concept of brain microstates with a new approach and distinct operational hypotheses. Local dynamic features from a variety of brain systems may also be explored through this methodology, as illustrated by experimental data on fast responses in the visual system as revealed by MEEG source imaging.

On early brain folding patterns using biomechanical growth modeling.

Abnormal cortical folding patterns may be related to neurodevelopmental disorders such as lissencephaly and polymicrogyria. In this context, computational modeling is a powerful tool to provide a better understanding of the early brain folding process. Recent studies based on biomechanical modeling have shown that mechanical forces play a crucial role in the formation of cortical convolutions. However, the correlation between simulation results and biological facts, and the effect of physical parameters in these models remain unclear. In this paper, we propose a new brain longitudinal length growth model to improve brain model growth. In addition, we investigate the effect of the initial cortical thickness on folding patterns, quantifying the folds by the surface-based three-dimensional gyrification index and a spectral analysis of gyrification. The results tend to show that the use of such biomechanical models could highlight the links between neurodevelopmental diseases and physical parameters.

Alterations in Cortical Morphology after Neonatal Stroke: Compensation in the Contralesional Hemisphere?

Although neonatal arterial ischemic stroke is now well-studied, its complex consequences on long-term cortical brain development has not yet been solved. In order to understand the brain development after focal early brain lesion, brain morphometry needs to be evaluated using structural parameters. In this work, our aim was to study and analyze the changes in morphometry of ipsi- and contralesional hemispheres in seven-year-old children following neonatal stroke. Therefore, we used surface-based morphometry in order to examine the cortical thickness, surface area, cortical volume, and local gyrification index in two groups of children that suffered from neonatal stroke in the left (n = 19) and right hemispheres (n = 15) and a group of healthy controls (n = 30). Reduced cortical thickness, surface area, and cortical volumes were observed in the ipsilesional hemispheres for both groups in comparison with controls. For the group with left-sided lesions, higher gyrification of the contralesional hemisphere was observed primarily in the occipital region along with higher surface area and cortical volume. As for the group with right-sided lesions, higher gyrification was detected in two separate clusters also in the occipital lobe of the contralesional hemisphere, without a significant change in cortical thickness, surface area, or cortical volume. This is the first time that alterations of structural parameters are detected in the "healthy" hemisphere after unilateral neonatal stroke indicative of a compensatory phenomenon. Moreover, findings presented in this work suggest that lesion lateralization might have an influence on brain development and maturation.