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466 Conclusionsdomains of cognitive, social, and motor function. Kiki Chang, Kim Gallelli, andMeghan Howe (chapter 14) describe how the epigenesis of bipolar disorder in lateadolescence is often preceded by signs of cognitive dysfunction. The evidence ofearly abnormalities, coupled with genetic data showing a heritable component tothese disorders, demonstrates that neural vulnerability can be congenital (i.e.,present at birth) or acquired by exposure to nonoptimal postnatal experiences, eventhough the clinical expression may not be apparent until after puberty.Assuming that there is a congenital or early acquired neural abnormality, somehave proposed that adolescent neuromaturational processes interact with preexistingbrain abnormality in the epigenesis of certain clinical disorders. For example,in the case of schizophrenia, it has been suggested that there may be a localizedcongenital brain abnormality that interacts with normal neuromaturational eventsfollowing puberty. These postpubertal changes in neural circuitry set the stagefor the expression of the prodromal stages of psychotic disorders. Such a modelis described by Anthony Grace in chapter 11, where it is posited that developmentallytriggered changes in limbic circuitry “unmask” a previously latent frontalabnormality. Others, attempting to account for the changing behavioral manifestationsof vulnerability from infancy through adolescence, propose that the congenitallesion is not silent, but rather affects different behavioral domains asdevelopment proceeds. More specifically, Walker (1994) suggests that abnormalitiesin dopamine neurotransmission and receptors in the striatum give rise todifferent kinds of behavioral expressions as the various neural circuits that includethis subcortical region come online. During adolescence, as the limbic-striatal andfrontal-striatal circuitry mature, the preexisting striatal abnormality results in circuitrymalfunction and affective and cognitive signs of psychosis.Several of the chapters document evidence for psychobiological vulnerabilitiesthat are acquired during infancy and early childhood. Megan Gunnar (chapter6), Michael Meaney (chapter 7) and Nicole Cooper et al. (chapter 15) describeresearch findings that highlight the interplay between early exposure to stress andsubsequent brain development. The generalized and sometimes persistent adverseeffects of early childhood deprivation are clearly illustrated by the work of CharlesNelson, Charles Zeanah, and Nathan Fox (chapter 9). At the same time, their worksuggests the possibilities for interrupting this cycle by environmental interventions.Farah and colleagues (chapter 16) find evidence for early stress effects onbrain development brought about by chronic poverty conditions. They also findsome evidence that deficits in cognitive stimulation during early childhood arerelated to the functioning of language centers in the developing brain.The Onset of Brain Dysfunction in AdolescenceFinally, it is possible that the neuropathology underlying disorders that arise duringadolescence does not involve either a congenital brain abnormality or aberrantneuromaturational processes. Instead, the brain dysfunction presumed to be