By Donald J. Cohen, Dante Cicchetti
This quantity applies a number of degrees of study to neurobiological developmental association, and functioning in normality and psychopathology. It additionally covers themes primary to a developmental standpoint on neuroscience.
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Fetal hypoxia) and an increased risk for the later development of Schizophrenia. These findings suggest that the adverse effects of obstetric complications on the developing fetal brain may play a role in the etiology of Schizophrenia. As Rakic (1988a, 1988b, 1996; Sidman & Rakic, 1982) and Nowakowski (1987; Nowakowski & Hayes, 1999) have concluded, during periods of rapid brain development in which neuronal migration is occurring and synaptic connections are formed the fetal brain is especially vulnerable.
Although HC was similar in all infants enrolled in the study during the first few months of life, those who later developed Autism exhibited a marked accelerated rate of increase in HC beginning several months after birth. , 2003). This increase in HC was associated with greater cerebral and cerebellar volume in these children by 2 to 5 years of age. , 2001). , 2001). However, in adolescence and adulthood, brain size of those with Autism does not differ from that of nonautisitc individuals (Aylward, Minshew, Field, Sparks, & Singh, 2002).
Although the increases in brain volume are marked, the specific underlying cellular components of increased brain volumes are unknown to date. , 2003). In addition, the cause of the increase in brain volume is not completely understood, but clearly reflects some type of dysregulation in one or more stages of brain developmental processes; however, it appears that the early transient period of brain overgrowth is an important underlying factor in the emergence of many of the behavioral symptoms seen in Autism.