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Congenital infections are infections transmitted from mother to child during pregnancy (transplacentally) or delivery (peripartum). They have the potential to adversely affect fetal development and long-term neurodevelopmental outcome through inflammatory, destructive, developmental, or teratogenic lesions of the brain. Because the fetal/neonatal brain has a limited capacity to respond to injury, early inflammatory changes may be difficult to visualize and only manifest as neurocognitive disability later in life. Teratogenic effects, which may include aberrations of neuronal proliferation and migration, are more easily visible on imaging, but may be equally difficult to use to predict long-term neurocognitive outcomes. This chapter reviews the general pathophysiology of congenital infection and describes the epidemiology, the antenatal and postnatal diagnosis, and the treatment of congenital infections as well as the long-term neurodevelopmental outcomes.Substance use during pregnancy and the short- and long-term impacts of different substances on maternal, fetal, and longer-term health outcomes of individuals prenatally exposed have been the subject of much investigation. Alcohol has been recognized as harmful during pregnancy and has been clearly recognized as a neurobehavioral teratogen, and the pattern of effects has been termed fetal alcohol spectrum disorder. More recently, the effects of prenatal cannabis exposure have been vigorously explored as a priority research area following decriminalization/legalization of cannabis in Canada and the United States. As the data become more and more robust, we are learning that cannabis during pregnancy can have negative effects on maternal and fetal outcomes and on longer-term neurodevelopmental and cognitive functions.Since the historical scandal of thalidomide in the 1960s, practitioners and future mothers are fearful of drugs during pregnancy. In-uterine exposure to drugs can induce major malformation of the fetus or even intrauterine fetal death. Prescribing drugs to a pregnant woman requires particular attention, and it is necessary to consider both the maternal needs and the proven and potential fetal risks. In this chapter, we review the mechanisms for medication transfer from mother to fetus, fetal risk according to pregnancy timeline, and the main dangerous drugs during pregnancy. We also focus on three prescription debates, which are relevant for neurodevelopmental disorder, because they each point to a paradigmatic situation-diethylstilbestrol, which shows transgenerational adversary effects; valproate, which impacts neurodevelopment as a whole; and antidepressants for which the adverse impact on neurodevelopment is still controversial given the impact of depression itself. Finally, we consider the implications for practice and toxicologic research to promote risk prevention.The consequences of prematurity on brain functional development are numerous and diverse, and impact all brain functions at different levels. Prematurity occurs between 22 and 36 weeks of gestation. This period is marked by extreme dynamics in the physiologic maturation, structural, and functional processes. These different processes appear sequentially or simultaneously. They are dependent on genetic and/or environmental factors. Disturbance of these processes or of the fine-tuning between them, when caring for premature children, is likely to induce disturbances in the structural and functional development of the immature neural networks. These will appear as impairments in learning skills progress and are likely to have a lasting impact on the development of children born prematurely. The level of severity depends on the initial alteration, whether structural or functional. In this chapter, after having briefly reviewed the neurodevelopmental, structural, and functional processes, we describe, in a nonexhaustive manner, the impact of prematurity on the different brain, motor, sensory, and cognitive functions.Neurodevelopmental disorders occur more frequently in boys than in girls and often differ in presentation between the sexes. The sex differences in prevalence and presentation of autism spectrum disorder, intellectual disability, communication disorders, specific learning disabilities, attention deficit/hyperactivity disorder, Tourette's syndrome, and epilepsy are discussed, as well as sex differences in the patterns of comorbidities between these disorders. Prominent theories have been proposed to explain sex biases. These include genetic factors, sex hormones, sociological factors, cognitive differences between the sexes, and environmental insult. Despite the large body of research reviewed in this chapter, many aspects of sex-related effects in neurodevelopmental disorders remain poorly understood.Neurodevelopmental disorders encompass a broad range of conditions, which include autism, epilepsy, and intellectual disability. These disorders are relatively common and have associated clinical and genetic heterogeneity. Cytoskeletal Signaling inhibitor Technology has driven much of our understanding of these diseases and their genetic underlying mechanisms, particularly highlighted by the study of large cohorts with comparative genomic hybridization and the more recent implementation of next-generation sequencing (NGS). The mapping of copy number variants throughout the genome has highlighted the recurrent, highly penetrant, de novo variation in syndromic forms of neurodevelopmental disease. NGS of affected individuals and their parents led to a dramatic shift in our understanding as these studies showed that a significant proportion of affected individuals carry rare, de novo variants within single genes that explain their disease presentation. Deep sequencing studies further implicate mosaicism as another mechanism of disease. However, it has also become clear that while rare variants explain a significant proportion of sporadic neurodevelopmental disease, rare variation still does not fully account for the familial clustering and high heritability observed. Common variants, including those within these known disease genes, are also shown to contribute significantly to overall risk. There is also increasing awareness of the important contribution of epigenetic factors and gene-environment interactions.
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