![]() Studies in adult women with early abuse-related PTSD have shown altered function in the anterior cingulate/medial prefrontal cortex while they were remembering their childhood trauma ( Bremner 1999 Shin 1999). Abused children also show alterations in EEG activity in the frontal cortex ( Teicher 1994, 19). ( De Bellis and Thomas 2003b Carrion 2001). Children with PTSD have smaller whole brain and corpus callosum volume ( Carrion and Steiner 2000 De Bellis 2002) and alterations in structure of the cerebellum ( Anderson 2002) and frontal cortex. Consistent with deficits in hippocampal function are deficits in verbal declarative memory ( Bremner 1995) and failure of hippocampal activation with memory tasks ( Bremner 2003a) in adult women with early abuse-related PTSD. Smaller hippocampal volume is found among adults with early abuse-related PTSD ( Bremner 1997, 2003a Stein 1997), adult women with early abuse and depression ( Vythilingam 2002), and borderline personality disorder ( Driessen 2000 Schmahl 2003) but not in children with PTSD ( De Bellis 1999a, 2002 Carrion 2001) suggesting that early abuse with chronic long-term stress-related psychiatric disorder is required for this finding. Studies in clinical populations of abuse survivors with posttraumatic stress disorder (PTSD) are consistent with animal studies. ![]() Cognitive problems have also been identified in children with PTSD ( Beers 2002). Alterations in serotonergic ( Rosenblum 1994 Bennett 2002) and GABAergic ( Caldji 2000) receptors also contribute to deficits in social attachment and regulation of mood and affect following early stress. The noradrenergic/locus coeruleus system also plays a key role in stress ( Bremner 1996a) and early stressors lead to long-term decreases in genetic expression of alpha-2 noradrenergic receptors in the locus coeruleus, which may lead to loss of feedback inhibition of noradrenergic activity with associated increases in noradrenergic responses to subsequent stressors ( Sanchez 2001 Caldji 2000 Francis 1999). Early environmental deprivation inhibits hippocampal neurogenesis conversely, neurogenesis is enhanced by enriched environment ( Kempermann 1997), learning ( Gould 1999a) and, at times, some antidepressant treatments ( Malberg 2000 Czeh 2001). Early stressors cause long-term increases in glucocorticoid responses to stress ( Plotsky and Meaney 1993 Ladd 1996) as well as decreased genetic expression of cortisol receptors in the hippocampus and increased genetic expression of corticotrophin-releasing factor in the hypothalamus, both of which may contribute to dysregulation of the hypothalamic-pituitary-adrenocortical (HPA) system ( Ladd 19). The hippocampus has the capacity to grow new neurons in adulthood (neurogenesis), but stress inhibits neurogenesis ( Nibuya 1995 Duman 1997 Gould 1997) and memory function ( Diamond 1996 Luine 1994). Substantial research has focused on the relationship between development, early stress, the HPA axis, and the hippocampus, a stress-sensitive brain region that plays a critical role in learning and memory ( McEwen 1992 Sapolsky 1990, 1996 Gould and Tanapat 1999). g., young infants do not have a fully developed glucocorticoid (cortisol in humans) response to stress, although other markers such as c- fos show that they do respond to stressors ( Smith 1997). There is an important interaction between development and stress, e. The hypothalamic-pituitary-adrenal (HPA) axis plays a critical role in the stress response. ![]() The amygdala mediates fear responses, and the prefrontal cortex is involved in mood as well as emotional and cognitive responses ( Bremner 2003b). Now, converging evidence from neurobiology and epidemiology suggests that early life stress such as abuse and related adverse experiences cause enduring brain dysfunction that, in turn, affects health and quality of life throughout the lifespan.Īn expanding body of evidence from rodent, primate, and human research suggests that early stressors cause long term changes in multiple brain circuits and systems ( Sanchez 2001 Bremner 2003a). Unfortunately, this elegant sequence is vulnerable to extreme, repetitive, or abnormal patterns of stress during critical or circumscribed periods of childhood brain development that can impair, often permanently, the activity of major neuroregulatory systems, with profound and lasting neurobehavioral consequences ( Teicher 2000 Heim and Nemeroff 2001 Repetti 2002 Gutman and Nemeroff 2002 Gorman 2002 De Bellis and Thomas 2003a Bremner and Vermetten 2001). The organization and functional capacity of the human brain depends upon an extraordinary set and sequence of developmental and environmental experiences that influence the expression of the genome ( Perry and Pollard 1998 Teicher 2000, 2002).
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