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Although pediatric stroke is associated with higher survival rates compared with adult stroke, a substantial body of evidence indicates significant neuropsychologic morbidity in pediatric stroke survivors. Neuroplasticity does not guarantee good outcome in children. The general trends observed in the literature are reviewed as is the profile observed in common causes of pediatric stroke congenital heart disease, moyamoya disease, and sickle cell disease. The neuropsychologic profile of pediatric stroke patients is heterogeneous due to the multiplicity of associated causes. Stroke in early infancy and large strokes are associated with cognitive impairment while more limited disorders, such as phasic deficit, are observed in childhood stroke. Executive dysfunction is common in pediatric stroke, but social interaction skills are usually preserved. Congenital heart disease and sickle cell disease are associated with global neuropsychologic dysfunction while cognition is usually preserved in moyamoya. Executive dysregulation is instead more frequently reported in this population. Further study of maladaptive processes after pediatric stroke will allow identification of predictors of functional and neuropsychologic outcomes and permit personalization of care.Childhood traumatic brain injury (TBI) commonly occurs during brain development and can have direct, immediately observable neurologic, cognitive, and behavioral consequences. However, it can also disrupt subsequent brain development, and long-term outcomes are a combination of preinjury development and abilities, consequences of brain injury, as well as delayed impaired development of skills that were immature at the time of injury. There is a growing number of studies on mild TBI/sport-related concussions, describing initial symptoms and their evolution over time and providing guidelines for effective management of symptoms and return to activity/school/sports. Mild TBI usually does not lead to long-term cognitive or academic consequences, despite reports of behavioral/psychologic issues postinjury. Regarding moderate to severe TBI, injury to the brain is more severe, with evidence of a number of detrimental consequences in various domains. Patients can display neurologic impairments (e.g., motor deficits, to rehabilitation and care). Interventions should identify and target these specific factors, given their major role in postinjury outcomes. Abusive head trauma (AHT) occurs in very young children (most often less then 6 months) and is a form of severe TBI, usually associated with delay before appropriate care is sought. Outcomes are systematically worse following AHT than following accidental TBI, even when controlling for age at injury and injury severity. Children with moderate to severe TBI and AHT usually require specific, coordinated, multidisciplinary, and long-term rehabilitation interventions and school adaptations, until transition to adult services. Interventions should be patient- and family-centered, focusing on specific goals, comprising education about TBI, and promoting optimal parenting, communication, and collaborative problem-solving.This chapter focuses on new concepts and new paradigms shedding light on the complex issue of socioenvironmental factors that affect the psychologic development of the child. Longitudinal controlled studies have sorted out "what leads to what under which circumstances," adding to the heuristic value of the addition of risks and of the Bronfenbrenner's ecologic model of development and disentangling the socioeconomic status (SES) from poverty. We emphasize the importance of taking attachment styles and attachment disorganization into account for a better understanding of both normal development and early psychopathology. Intervention studies demonstrate the real life effect of the gene-environment interaction with or without epigenetic processes. read more Thus, this chapter deals with paradigmatic situations as ADS, Prader-Willi, or prematurity as they allow us to learn more about early development and epigenetic influences.Optimal brain function critically hinges on the remarkably precise interconnections made among millions of neurons. These specialized interconnected neuronal junctions, termed synapses, are used for neuronal communication, whence the presynaptic neurons releases a specific neurotransmitter, which then binds to the appropriate protein receptor on the membrane of the postsynaptic neuron, activating and eliciting a response in this connected neuron. In this chapter, we discuss how synapses form and are modified as the brain matures. Genetic programs control most of the wiring in the brain, from allowing axons to choose where to target their synapses, to determining synapse identity. However, the final map of neuronal connectivity in the brain crucially relies on incoming sensory information during early childhood to strengthen and refine the preexisting synapses thus allowing both nature and nurture to shape the final structure and function of the nervous system (Fig. 5.1). Finally, we discuss how advances in the knowledge of basic mechanisms governing synapse formation and plasticity can shed light on the pathophysiology of neurodevelopmental disorders.Exposure to environmental toxicants can have deleterious effects on the development of physical, cognitive, and mental health. Extensive laboratory and clinical studies have demonstrated how the developing brain is uniquely sensitive to toxic agents. This chapter focuses on the main neurologic impairments linked to prenatal and postnatal exposure to lead, methylmercury, and polychlorinated biphenyls, three legacy environmental contaminants whose neurotoxic effects have been extensively studied with respect to cognitive and behavioral development. The main cognitive, emotion regulation, sensory, and motor impairments in association with these contaminants are briefly reviewed, including the underlying neural mechanisms such as neuropathologic damages, brain neurotransmission, and endocrine system alterations. The use of neuroimaging as a novel tool to better understand how the brain is affected by exposure to environmental contaminants is also discussed.
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