“…These maturational and plastic features of brain development might help to compensate for the adverse effects of stress hormones on neural architecture. Severe early life trauma, for example, is associated with hypercortisolism (Cicchetti and Rogosch 2001;De Bellis et al 1999;Delahanty et al 2004), and yet children with posttraumatic stress disorder after maltreatment do not seem to have smaller hippocampi (Carrion et al 2001;De Bellis et al 2002). Alternatively, developmental changes could render the growing hippocampus more vulnerable to glucocorticoid-induced injury (Bremner and Vermetten 2001;Cicchetti and Rogosch 2001;Goodyer et al 2001), as evidenced by findings from imaging studies that adult women who were sexually abused as children had a smaller hippocampus compared with women without a history of abuse (Stein et al 1997;Vythilingam et al 2002).…”
Background-Research in animal models has demonstrated that elevated levels of glucocorticoids can inflict damage within the hippocampus. In adult humans, elevated cortisol levels have been associated with reduced hippocampal volumes; however, normative data in children are not available. The objective of this study was to examine possible associations of serum cortisol levels with hippocampal volumes and morphology in healthy children.
“…These maturational and plastic features of brain development might help to compensate for the adverse effects of stress hormones on neural architecture. Severe early life trauma, for example, is associated with hypercortisolism (Cicchetti and Rogosch 2001;De Bellis et al 1999;Delahanty et al 2004), and yet children with posttraumatic stress disorder after maltreatment do not seem to have smaller hippocampi (Carrion et al 2001;De Bellis et al 2002). Alternatively, developmental changes could render the growing hippocampus more vulnerable to glucocorticoid-induced injury (Bremner and Vermetten 2001;Cicchetti and Rogosch 2001;Goodyer et al 2001), as evidenced by findings from imaging studies that adult women who were sexually abused as children had a smaller hippocampus compared with women without a history of abuse (Stein et al 1997;Vythilingam et al 2002).…”
Background-Research in animal models has demonstrated that elevated levels of glucocorticoids can inflict damage within the hippocampus. In adult humans, elevated cortisol levels have been associated with reduced hippocampal volumes; however, normative data in children are not available. The objective of this study was to examine possible associations of serum cortisol levels with hippocampal volumes and morphology in healthy children.
“…Heightened sympathetic tone in the form of increased catecholamine secretion has been described consistently in individuals with PTSD (Southwick et al, 1999). Peripheral and central concentrations of norepinephrine are augmented in individuals with PTSD at baseline (Delahanty et al, 2005;Geracioti et al, 2001;Southwick et al, 1999) and following exposure to threatening stimuli (Blanchard et al, 1991;Geracioti et al, 2008). This increased norepinephrine production in PTSD in response to stressful or threatening stimuli can induce cytokine release (Bierhaus et al, 2003).…”
Section: Mechanisms Of Increased Inflammation In Fearand Anxiety-basementioning
The study of inflammation in fear-and anxiety-based disorders has gained interest as growing literature indicates that proinflammatory markers can directly modulate affective behavior. Indeed, heightened concentrations of inflammatory signals, including cytokines and C-reactive protein, have been described in posttraumatic stress disorder (PTSD), generalized anxiety disorder (GAD), panic disorder (PD), and phobias (agoraphobia, social phobia, etc.). However, not all reports indicate a positive association between inflammation and fear-and anxiety-based symptoms, suggesting that other factors are important in future assessments of inflammation's role in the maintenance of these disorders (ie, sex, co-morbid conditions, types of trauma exposure, and behavioral sources of inflammation). The most parsimonious explanation of increased inflammation in PTSD, GAD, PD, and phobias is via the activation of the stress response and central and peripheral immune cells to release cytokines. Dysregulation of the stress axis in the face of increased sympathetic tone and decreased parasympathetic activity characteristic of anxiety disorders could further augment inflammation and contribute to increased symptoms by having direct effects on brain regions critical for the regulation of fear and anxiety (such as the prefrontal cortex, insula, amygdala, and hippocampus). Taken together, the available data suggest that targeting inflammation may serve as a potential therapeutic target for treating these fear-and anxiety-based disorders in the future. However, the field must continue to characterize the specific role pro-inflammatory signaling in the maintenance of these unique psychiatric conditions.
“…Stress increases the secretion of corticotrophin releasing hormones by the hypothalamus, stimulating the pituitary gland which in turn produces adrenocorticotropic hormones, activating the adrenal glands and increasing the levels of adrenaline and cortisol (the stress hormone; Delahanty, Nugent, Christopher, & Walsh, 2005). This adaptive mechanism known as the hypothalamus-pituitary-adrenal (HPA) axis (see Figure 1), when chronic, represents a marker of wear and tear or allostatic load associated with changes in the metabolic process, reduced dendritic branching, and deficits in attention and learning (Cicchetti & Rogosh, 2007;Danese & McEwen, 2012;Hackman & Farah, 2009;Hackman, Farah, & Meaney, 2010).…”
Studies suggest that socioeconomic status is a strong predictor of academic achievement. This theoretical paper proposes that despite the fact that low-socioeconomic status represents a risk factor that seems to undermine attentional skills and thus academic achievement, emerging evidence suggests the potential of new approaches, interventions and cognitive training programs to reverse the negative effects of poverty. The evidence presented in this paper may be of particular interest for teachers because it provides a larger scope to better understand the implications of socioeconomic status on learning and school achievement. This paper intends to make teachers aware that today more than ever they count on important knowledge and valuable resources like cognitive training intervention programs to help students. These intervention programs correct dysfunctional attention bringing hope to socially disadvantaged students who struggle in school.
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