Academic literature on the topic 'Sulcation corticale'

AbstractAbnormal fetal corticogenesis results in malformations of cortical development (MCD). Abnormal cell proliferation leads to microcephaly or megalencephaly, incomplete neuronal migration results in heterotopia and lissencephaly, neuronal overmigration manifests as cobblestone malformations, and anomalous postmigrational cortical organization is responsible for polymicrogyria and focal cortical dysplasias. MCD comprises various congenital brain disorders, caused by different genetic, infectious, or vascular etiologies and is associated with significant neurological morbidity. Although MCD are rarely diagnosed prenatally, both dedicated multiplanar neurosonography and magnetic resonance imaging enable good demonstration of fetal cortical development. The imaging signs of fetal MCD are: delayed or absent cerebral sulcation; premature abnormal sulci; thin and irregular hemispheric parenchyma; wide abnormal overdeveloped gyri; wide opening of isolated sulci; nodular bulging into the lateral ventricles; cortical clefts; intraparenchymal echogenic nodules; and cortical thickening. The postnatal and prenatal imaging features of four main malformations of cortical development—lissencephaly, cobblestone malformations, periventricular nodular heterotopia, and polymicrogyria—are described.

AbstractObjectivesAberrant cortical development, inferred from cortical folding, is linked to the risk of schizophrenia. Cortical folds develop in a time-locked fashion during fetal growth. We leveraged this temporal specificity of sulcation to investigate the timing of the prenatal insult linked to schizophrenia and the cognitive impairment seen in this illness.MethodsAnatomical MRI scans from 68 patients with schizophrenia and 72 controls were used to evaluate the sulcal depth of five major invariable primary sulci representing lobar development (calcarine sulcus, superior temporal sulcus, superior frontal sulcus, intraparietal sulcus and inferior frontal sulcus) with formation representing the distinct developmental periods.ResultsA repeated-measure ANOVA with five sulci and two hemispheres as the within-subject factors and gender, age and intracranial volume as covariates revealed a significant effect of diagnosis (F[1,134] = 14.8, p = 0.0002). Control subjects had deeper bilateral superior temporal, right inferior frontal and left calcarine sulci. A deeper superior frontal sulcus predicted better cognitive scores among patients.ConclusionOur results suggest that the gestational disruption underlying schizophrenia is likely to predate, if not coincide with the appearance of calcarine sulcus (early second trimester). Nevertheless, the burden of cognitive deficits may relate specifically to the aberrant superior frontal development apparent in late second trimester.

Abstract Perinatal brain injuries in preterm neonates are associated with alterations in structural neurodevelopment, leading to impaired cognition, motor coordination, and behavior. However, it remains unknown how such injuries affect postnatal cortical folding and structural covariance networks, which indicate functional parcellation and reciprocal brain connectivity. Studying 229 magnetic resonance scans from 158 preterm neonates (n = 158, mean age = 28.2), we found that severe injuries including intraventricular hemorrhage, periventricular leukomalacia, and ventriculomegaly lead to significantly reduced cortical folding and increased covariance (hyper-covariance) in only the early (<31 weeks) but not middle (31–35 weeks) or late stage (>35 weeks) of the third trimester. The aberrant hyper-covariance may drive acceleration of cortical folding as a compensatory mechanism to “catch-up” with normal development. By 40 weeks, preterm neonates with/without severe brain injuries exhibited no difference in cortical folding and covariance compared with healthy term neonates. However, graph theory-based analysis showed that even after recovery, severely injured brains exhibit a more segregated, less integrated, and overall inefficient network system with reduced integration strength in the dorsal attention, frontoparietal, limbic, and visual network systems. Ultimately, severe perinatal injuries cause network-level deviations that persist until the late stage of the third trimester and may contribute to neurofunctional impairment.

In this article, we emphasize the usefulness and cost-effectiveness of non-contrast MRI as the primary imaging modality in the evaluation of non-febrile pediatric seizure, illustrate the MR spectrum of different structural lesions causing pediatric seizures, and finally describing the main MR imaging features of these disorders. Among 366 cases of pediatric epilepsy studied over a period of fifteen years the commonly detected structural malformations are mesial temporal sclerosis unilateral and bilateral, heterotopias, cortical dysplasia, neurocutaneous syndromes and few neoplasms. MRI showed hippocampal atrophy and increased signal intensity of the hippocampus on T2-weighted images in mesial temporal sclerosis, cortical thickness and sulcation are decreased in microcephaly, enlarged dysplastic cortex in hemimegalencephaly, and focal cortical dysplasia shows ipsilateral focal cortical thickening with radial hyperintense bands. MRI detects smooth brain in classic lissencephaly, the ectopic position of gray matter in heterotopias, and the nodular cortex with cobblestone cortex in congenital muscular dystrophy. MRI can detect polymicrogyria and the related syndromes, as well as schizencephaly types. In conclusion, MR imaging is essential to demonstrate the morphology, distribution, and extent of different disorders causing seizures in children as well as the associated anomalies and related syndromes to guide patient for further surgical treatment and counseling.

Objectives: We evaluated the hypothesis that in fetuses with congenital heart disease (CHD) there is a correlation between the expected pattern of in utero brain blood supply and the severity of neurodevelopmental impairment. Methods: A total of 58 fetuses with CHD and 58 controls underwent a Doppler ultrasound and fetal MRI at 36-38 weeks. Fetuses with CHD were divided into two functional classes: class A with an expected severe reduction in oxygenated brain blood supply (left outflow tract obstruction and transposition of great vessels) and class B with theoretically near-normal or mildly impaired oxygenated brain blood supply (other CHD). Head biometry and cerebroplacental Doppler were assessed by ultrasound, and brain volumetry, cortical development and metabolism by MRI. Results: Both class A and B CHD fetuses had significant differences in head biometry, brain perfusion, cortical development and brain metabolism compared with controls. However, there was a significant linear tendency for head biometry, cerebral Doppler, volumes, cortical sulcation and metabolic ratios across the three clinical groups, with signs of more severe brain alterations in type A CHD fetuses. Conclusions: All fetuses with CHD showed significant brain developmental changes, but differences were more pronounced in CHD associated with an expected severe reduction in oxygenated blood supply to the brain.

ABSTRACT The new epidemic of Zika virus infection raises grave concerns, especially with the increasingly-recognized link between emerging cases of microcephaly and this infectious disease. Besides small cranial dimensions, there are striking morphologic anomalies in the fetal brain. Key anomalies include cortical developmental malformations and a peculiar distribution of pathologic calcifications. These potentially indicate a new pattern of congenital central nervous system infection. Methods: Eight women underwent fetal MRI. Four infants also underwent postnatal CT. Five of the women underwent amniocentesis. Results: All neonates were born with microcephaly. On fetal MRI, ventriculomegaly, marked reduction of white matter thickness, severe sylvian fissure simplification, abnormal sulcation, and diffuse volumetric loss of cerebellar hemispheres were consistently seen. On postnatal CT, diffuse subcortical and basal ganglia calcifications were observed. The Zika virus was detected in two amniocenteses by polymerase chain reaction assays. Conclusion: We hope to assist the medical community in recognizing the spectrum of encephalic changes related to congenital Zika virus infection.

The asymmetry of the cerebral sulcal morphology is particularly obvious in higher primates. The sulcal asymmetry in macaque monkeys, a genus of the Old World monkeys, in our previous studies and others is summarized, and its evolutionary significance is speculated. Cynomolgus macaques displayed fetal sulcation and gyration symmetrically, and the sulcal asymmetry appeared after adolescence. Population-level rightward asymmetry was revealed in the length of arcuate sulcus (ars) and the surface area of superior temporal sulcus (sts) in adult macaques. When compared to other nonhuman primates, the superior postcentral sulcus (spcs) was left-lateralized in chimpanzees, opposite of the direction of asymmetry in the ars, anatomically-identical to the spcs, in macaques. This may be associated with handedness: either right-handedness in chimpanzees or left-handedness/ambidexterity in macaques. The rightward asymmetry in the sts surface area was seen in macaques, and it was similar to humans. However, no left/right side differences were identified in the sts morphology among great apes, which suggests the evolutionary discontinuity of the sts asymmetry. The diversity of the cortical lateralization among primate species suggests that the sulcal asymmetry reflects the species-related specialization of the cortical morphology and function, which is facilitated by evolutionary expansion in higher primates.

Le terme de neurodéveloppement dans son acception la plus large renvoie à l'ensemble des processus permettant le développement du système nerveux depuis les étapes les plus précoces de sa formation in utero jusqu'aux étapes plus tardives de maturation à l'adolescence aboutissant au système nerveux adulte. Les travaux de ces quarante dernières années ont conduit à proposer un modèle neurodéveloppemental des troubles psychiatriques, notamment schizophréniques, sur la base d'arguments génétiques, épidémiologiques et d'imagerie. Ce modèle propose que l'apparition de la maladie soit liée à une/des anomalie(s) dans les processus de formation (neurodéveloppement précoce) et de maturation (neurodéveloppement tardif) du système nerveux, sous l'effet combiné de facteurs génétiques et environnementaux. Dans ce contexte, ce travail de thèse vise à préciser les effets des anomalies neurodéveloppementales sur les troubles psychiatriques, notamment schizophréniques à travers l'étude de différents marqueurs. La première étude a pour objectif d'étudier les corrélations entre deux marqueurs du développement cérébral précoce : un marqueur clinique (les signes neurologiques mineurs) et un marqueur en imagerie (la sulcation du cortex cérébral) dans une population de sujets atteints de schizophrénie. Une corrélation entre ces deux marqueurs est mise en évidence : l'index de sulcation est d'autant plus faible que les sujets présentent des signes neurologiques mineurs significatifs. Notre conclusion est que l'étude combinée de différents marqueurs peut permettre d'isoler des sous-groupes de patients ayant eu des atteintes neurodéveloppementales précoces plus marquées. La deuxième étude a pour objectif de caractériser l'effet de différents marqueurs d'anomalies neurodéveloppementales précoces sur le fonctionnement cognitif de sujets atteints de schizophrénie. L'effet sur le contrôle exécutif (mesuré par la tâche du Trail Making Test) de marqueurs cliniques (signes neurologiques mineurs, latéralisation manuelle) et en imagerie (sulcation du cortex cingulaire antérieur et élargissement des ventricules ventraux) est mesuré en recherchant les effets principaux et les interactions entre chaque marqueur. Nous trouvons des interactions entre différents marqueurs, avec principalement un effet de sommation non-linéaire. Notre interprétation est que les différents marqueurs reflètent des atteintes distinctes, bien que toutes précoces, du développement cérébral avec un effet final commun sur les fonctions exécutives. La troisième étude a pour objectif de préciser la spécificité de la sulcation comme marqueur d'anomalies neurodéveloppementales précoces à travers son étude dans une population de sujets adultes présentant un trouble du spectre autistique (TSA), pathologie débutant dès la petite enfance, en lien évident avec des atteintes neurodéveloppementales précoces. Des anomalies de sulcation du cortex cingulaire antérieur, similaires à celles observées chez les patients atteints de troubles schizophréniques, sont détectées chez les patients présentant un TSA. Ces résultats sont en faveur d'anomalies neurodéveloppementales précoces partagées entre différentes pathologies psychiatriques : les modifications de la sulcation corticale sont spécifiques non pas d'un trouble donné mais de la précocité des atteintes. En conclusion, nous proposons que l'étude des anomalies neurodéveloppementales soit intégrée dans une approche dimensionnelle en psychiatrie
The term neurodevelopment in its broadest sense refers to all of the processes encompassing development of the nervous system from the earliest stages of formation in utero to later stages of maturation during adolescence to produce the fully functional adult nervous system. Work over the last thirty years has led to a neurodevelopmental model of human psychiatric disorders, including schizophrenia, based on genetic, epidemiological and imaging evidence. This model asserts that disease is fundamentally linked to or develops from abnormality(s) in the formation processes (early neurodevelopment) and maturation (late neurodevelopment) of the nervous system due to a combination of genetic and environmental factors. In this context this thesis aims to clarify the effects of neurodevelopmental abnormalities on psychiatric disorders, including schizophrenia, through the study of different markers. The first study aims to investigate correlations between markers of early brain development: a clinical marker (neurological soft signs) and an imaging marker (sulcation of the cerebral cortex) in a population of subjects with schizophrenia. A correlation between these two markers is presented: the sulcation index was found to be lower in subjects that had significant neurological soft signs. We concluded that the combined study of different markers may help to isolate subgroups of patients with greater early neurodevelopmental damage. The second study aims to characterize effects of different markers of early neurodevelopmental abnormalities on cognitive functioning in patients with schizophrenia. Effects on executive control (as measured by the Trail Making Test) were correlated with clinical markers (neurological soft signs, handedness) and imaging (sulcation of the anterior cingulate cortex and enlargment of the ventricles). We found interactions between different markers with a mainly non-linear summation effect. Our interpretation is that different markers reflect separate insults, though all early, on brain development with a common final effect on executive function. The third study aims to clarify the specificity of sulcation as a marker of early neurodevelopmental abnormalities by studying a population of adult subjects with autism spectrum disorder (ASD), a patholody beginning in early childhood and linked with evidence of early neurodevelopmental damage. Sulcation abnormalities of the anterior cingulate cortex, similar to those observed in patients with schizophrenia are detected in patients with ASD. These results suggest early neurodevelopmental abnormalities are shared by different psychiatric disorders and that changes in cortical sulcation are not specific to a given disorder but the early damage. In conclusion, we suggest that the study of neurodevelopmental abnormalities should be integrated into a dimensional approach in psychiatry