Fear can be adaptive, as noticing and avoiding potential dangers in the environment has obvious survival benefits. Yet, for some people, excessive fear and hypervigilance for threats can interfere with adaptive functioning, even developing into an anxiety disorder.
Emerging research on children who were exposed to deprivation, neglect, or abuse has begun to reveal how early experience shapes the developmental trajectory of the brain’s systems for responding to dangers. While it has long been known that attention to possible threats is sharpened by early trauma—for example, children who experienced physical abuse are faster to detect angry faces in a visual attention task—recent research has helped to illuminate the biological mechanisms of these changes in vigilance. The research findings have raised intriguing questions about whether such patterns should be considered adaptive or maladaptive.
The stress acceleration hypothesis posits that in children exposed to early trauma, the brain’s threat systems develop at an accelerated pace, potentially at the expense of other developing brain systems. For example, one study examined brain activity during a fear learning task among 89 children who had spent part of their early years in an orphanage and compared them to age-matched children who were never institutionalized. In response to a fear-evoking stimulus, both groups showed increased activity in the amygdala, a small almond-shaped brain structure well-known to respond to dangers.
The groups differed, though, in the extent to which other brain regions were activated together with the amygdala in response to signals of danger. For the previously institutionalized children, the amygdala was activated together with the hippocampus, a structure critical to learning and memory, and subregions of the medial frontal lobe, which are thought to help regulate emotions.
Interestingly, this broad activation of brain regions in response to threats better matched the typical adult pattern rather than the age-appropriate pattern for typically developing children. The findings, therefore, support the idea that the development of the brain’s threat-response system is accelerated after early-life stress.
Additional findings from the same research group have identified the role of stress hormones in these developmental effects. In this study, levels of the stress hormone cortisol partly explained the adult-like pattern of connectivity (co-activation) between the amygdala and prefrontal cortex in response to threats in previously institutionalized children. These children had stronger cortisol release in response to the brain-scanning experiment compared to the never-institutionalized control group of children.
This increased cortisol release statistically explained part of the precocious pattern of brain activation to threatening information in the deprived children. Thus, alterations in the activation of stress hormones following trauma or neglect may be partly responsible for differences in the pattern of brain maturation. (For a fuller discussion of the role of cortisol in early-life stress and deprivation, see here.)
A key question is whether these developmental differences in early-stressed children’s brains are best interpreted as pathological changes that put them at risk for emotional problems, or whether they should be considered instead as protective, adaptive changes in response to a more dangerous early-life environment.
Although children who are exposed to trauma early in life are known to have an increased risk of developing anxiety disorders, it may not be these brain mechanisms in particular that account for that increased risk. On this question, findings seem to conflict. One study found that stronger amygdala reactions to pictures of threatening faces predicted higher anxiety symptoms among children who experienced early neglect but not among typically developing children. This seems to fit with the idea that increased reactivity of this brain region is maladaptive.
Yet, other studies suggest that more adult-like connectivity between brain regions during fear learning may actually be protective. Previously institutionalized children who showed such increased connectivity patterns reported less anxiety two years later than those who did not show the patterns. One possibility, then, is that the more adult-like pattern of engaging frontal lobe regions during fear learning reflects an adaptive strategy, perhaps an attempt to regulate lower-level fear systems that are overactive.
A better understanding of these brain differences in the future may lead to a fuller appreciation of both the direct consequences of early trauma and the biological mechanisms of resilience that help children cope with both typical and adverse environmental conditions. Future research should also focus on better understanding the varied effects of different kinds of early stressors, such as physical abuse, poverty, and parental deprivation, which may have varied intensities and time courses. In the meantime, there is no doubt that early traumatic experiences leave their mark on brain development.
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