In the developing human brain, the cortical sulci formation is a complex process starting from 14 weeks of gestation onward. The potential influence of underlying mechanisms (genetic, epigenetic, mechanical or environmental) is still poorly understood, because reliable quantification in vivo of the early folding is lacking. In this study, we investigate the sulcal emergence noninvasively in 35 preterm newborns, by applying dedicated postprocessing tools to magnetic resonance images acquired shortly after birth over a developmental period critical for the human cortex maturation (26-36 weeks of age). Through the original three-dimensional reconstruction of the interface between developing cortex and white matter and correlation with volumetric measurements, we document early sulcation in vivo, and quantify changes with age, gender, and the presence of small white matter lesions. We observe a trend towards lower cortical surface, smaller cortex, and white matter volumes, but equivalent sulcation in females compared with males. By precisely mapping the sulci, we highlight interindividual variability in time appearance and interhemispherical asymmetries, with a larger right superior temporal sulcus than the left. Thus, such an approach, included in a longitudinal follow-up, may provide early indicators on the structural basis of cortical functional specialization and abnormalities induced by genetic and environmental factors.

In the human brain, the morphology of cortical gyri and sulci is complex and variable among individuals, and it may reflect pathological functioning with specific abnormalities observed in certain developmental and neuropsychiatric disorders. Since cortical folding occurs early during brain development, these structural abnormalities might be present long before the appearance of functional symptoms. So far, the precise mechanisms responsible for such alteration in the convolution pattern during intra-uterine or post-natal development are still poorly understood. Here we compared anatomical and functional brain development in vivo among 45 premature newborns who experienced different intra-uterine environments: 22 normal singletons, 12 twins and 11 newborns with intrauterine growth restriction (IUGR). Using magnetic resonance imaging (MRI) and dedicated post-processing tools, we investigated early disturbances in cortical formation at birth, over the developmental period critical for the emergence of convolutions (26-36 weeks of gestational age), and defined early 'endophenotypes' of sulcal development. We demonstrated that twins have a delayed but harmonious maturation, with reduced surface and sulcation index compared to singletons, whereas the gyrification of IUGR newborns is discordant to the normal developmental trajectory, with a more pronounced reduction of surface in relation to the sulcation index compared to normal newborns. Furthermore, we showed that these structural measurements of the brain at birth are predictors of infants' outcome at term equivalent age, for MRI-based cerebral volumes and neurobehavioural development evaluated with the assessment of preterm infant's behaviour (APIB).

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clinicaltrials.gov Identifier: NCT00413946.

Congenital hypothyroidism (CH) can lead to intellectual deficits despite early high-dose treatment. Our study aimed to determine whether motor impairments can occur despite early highdose treatment. Sixty-three children with CH and early (median age of onset of treatment 9 d), high-dose treatment (median starting dose of levothyroxine 14.7 g/kg/d) were tested with the Zurich Neuromotor Assessment (ZNA) at a median age of 13.8 y (range 7.0 -14.2 y). Median z-scores in the children with CH were Ϫ0.95 in the pure and Ϫ0.56 in the adaptive fine motor component, significantly lower than in the ZNA test norms (p Ͻ 0.001 and p ϭ 0.01, respectively). The 26 children with athyreosis were more affected than the 33 children with dysgenesis, particularly in the pure motor (Ϫ1.55 versus Ϫ0.76, p ϭ 0.03), adaptive fine motor (Ϫ1.31 versus 0.13, p Ͻ 0.01), and static balance task (Ϫ0.47 versus 0.67, p ϭ 0.01). Boys performed worse than girls. Older age at onset of treatment was related to poorer adaptive fine motor performance. Movement quality (assessed by associated movements) was not affected. We conclude that severe CH can cause neuromotor deficits persisting into adolescence. These deficits cannot completely be reversed by postnatal treatment, but earlier age at treatment may reduce the degree of impairment. (Pediatr Res 70: 614-618, 2011)