Over the past several decades, significant advances have been made in our understanding of the basic stages and mechanisms of mammalian brain development. Studies elucidating the neurobiology of brain development span the levels of neural organization from the macroanatomic, to the cellular, to the molecular. Together this large body of work provides a picture of brain development as the product of a complex series of dynamic and adaptive processes operating within a highly constrained, genetically organized but constantly changing context. The view of brain development that has emerged from the developmental neurobiology literature presents both challenges and opportunities to psychologists seeking to understand the fundamental processes that underlie social and cognitive development, and the neural systems that mediate them. This chapter is intended to provide an overview of some very basic principles of brain development, drawn from contemporary developmental neurobiology, that may be of use to investigators from a wide range of disciplines.

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The effects of focal brain injury are investigated in the first stages of language development, during the passage from first words to grammar. Parent report and/or free speech data are reported for 53 infants and preschool children between 10 -44 months of age. All children had suffered a single, unilateral brain injury to the left or right hemisphere, incurred before six months of age (usually in the pre-or perinatal period). This is the period in which we should expect to see maximal plasticity, but it is also the period in which the initial specializations of particular cortical regions ought to be most evident. In direct contradiction of hypotheses based on the adult aphasia literature, results from 10 -17 months suggest that children with righthemisphere injuries are at greater risk for delays in word comprehension, and in the gestures that normally precede and accompany language onset. Although there were no differences between left-vs. right-hemisphere injury per se on expressive language, children whose lesions include the left temporal lobe did show significantly greater delays in expressive vocabulary and grammar throughout the period from 10 -44 months. There were no specific deficits associated with left frontal damage, but there was a significant effect of frontal lobe injury to either hemisphere in the period from 16 -31 months, when normal children usually show a burst in vocabulary and grammar. This bilateral effect of frontal damage is independent of motor impairment. Hence there are specific effects of lesion site in early language development, but they are not consistent with the lesion-syndrome correlations observed in adults with homologous injuries, nor with the literature on acquired lesions in older children. Results are used to argue against innate localization of linguistic representations, and in favor of an alternative view in which innate regional biases in style of information processing lead to familiar patterns of brain organization for language under normal conditions, while permitting alternative patterns to emerge in children with focal brain injury. 3 FROM FIRST WORDS TO GRAMMAR IN CHILDREN WITH FOCAL BRAIN INJURYIn 1861, Paul Broca described a case of nonfluent aphasia with preserved comprehension, associated with damage to a region of left frontal cortex that now bears Broca's name. By 1874, Carl Wernicke had described a very different form of aphasia, a severe comprehension deficit with preserved fluency and melodic line (albeit with clear impairment of word retrieval). This syndrome was associated with damage to the posterior portion of the left temporal lobe, a region now referred to as Wernicke's area. The reliability and significance of these two complementary lesion-syndrome mappings have been called into question many times (Freud 1891(Freud /1953Goldstein, 1948;Head, 1963;Marie, 1906;Mohr et al., 1978), including recent studies using in vivo brain imaging which show that the classic lesion-syndrome correlations are violated at least 20% of the time (Basso, C...

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Mirror movements are seen in normal children in the first decade. The movements persist after age 10 in patients with congenital hemiparesis. At first, mirror movements are more prominent in the good hand (when the impaired hand attempts a unimanual task), but after age 10, mirroring diminishes in the good hand, and these movements are equally prominent in good and impaired hands. Maturational changes in callosally mediated inhibition of uncrossed motor pathways and reorganizational changes of the pyramidal motor system after early unilateral brain injury explain these age-dependent changes in asymmetries of mirror movements.

Autoimmune disease in women during pregnancy is associated with an increased risk for LD in their sons. Maternal antibodies, particularly anti-Ro/La, likely affect the fetal brain of male offspring and result in later learning problems. These findings should promote greater awareness of the risk for LD in sons of women with autoimmune disease and the possible need for early educational intervention in those children.

The use of prescription medication to augment cognitive or affective function in healthy persons-or neuroenhancement-is increasing in adult and pediatric populations. In children and adolescents, neuroenhancement appears to be increasing in parallel to the rising rates of attention-deficit disorder diagnoses and stimulant medication prescriptions, and the opportunities for medication diversion. Pediatric neuroenhancement remains a particularly unsettled and value-laden practice, often without appropriate goals or justification. Pediatric neuroenhancement presents its own ethical, social, legal, and developmental issues, including the fiduciary responsibility of physicians caring for children, the special integrity of the doctor-child-parent relationship, the vulnerability of children to various forms of coercion, distributive justice in school settings, and the moral obligation of physicians to prevent misuse of medication. Neurodevelopmental issues include the importance of evolving personal authenticity during childhood and adolescence, the emergence of individual decision-making capacities, and the process of developing autonomy. This Ethics, Law, and Humanities Committee position paper, endorsed by the American Academy of Neurology, Child Neurology Society, and American Neurological Association, focuses on various implications of pediatric neuroenhancement and outlines discussion points in responding to neuroenhancement requests from parents or adolescents. Based on currently available data and the balance of ethics issues reviewed in this position paper, neuroenhancement in legally and developmentally nonautonomous children and adolescents without a diagnosis of a neurologic disorder is not justifiable. In nearly autonomous adolescents, the fiduciary obligation of the physician may be weaker, but the prescription of neuroenhancements is inadvisable because of numerous social, developmental, and professional integrity issues.

Congenital adrenal hyperplasia results from an adrenal enzyme deficiency, that causes an underproduction of glucocorticoids and sometimes mineralocorticoids and a resultant overproduction of androgens, until treatment with replacement glucocorticoids is instituted. The goal of this study was to determine the frequency and etiology of white-matter changes and temporal lobe atrophy demonstrable on magnetic resonance imaging (MRI) in a group of children and young adults with congenital adrenal hyperplasia. About one third of the patients evidenced white-matter abnormalities or temporal lobe atrophy. All patients, except one with a known stroke, had normal neurologic examinations. Exposure to excess exogenous glucocorticoids in the process of being treated for congenital adrenal hyperplasia is the most theoretically appealing explanation for these MRI findings. However, the relationship of MRI findings to treatment status (over-versus under-suppressed) does not run in clear parallel.