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Behavioral Problems in childhood > Task 3: childhood stress > Flashcards

Task 3: childhood stress Flashcards

1
Q

anxiety disorders

A
  • usually chronic, high occurrence before adulthood
  • high comorbidity with different anxiety disorders, also other psychiatric disorders
  • highest comorbidity with depression
  • early intervention may lower risk for onset, persistence, severity of secondary disorders
  • response resembles reactions of normal subjects to conditioned fear cues
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2
Q

Genetics and anxiety disorders

A
  • children with a.d. most likely have parents with a.d.

- genes and environment may be more or less influential depending on developmental stage & quality of primary caregiving

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3
Q

HPA-axis sensitivity programming

A
  • environment can lead to permanent alterations
  • maternal care as mediator in regulation of HPA
  • good care -> reduced cortisol, attenuation (Verminderung) HPA responsiveness
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4
Q

effects of prenatal anxiety on HPA

A
  • prenatal maternal anxiety: associated with cognitive, behavioral, emotional problems in child
  • prenatal cortisol level linked with impaired cognitive development in children
  • > BUT: moderated by attachment: negative outcome only when insecure attached
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5
Q

limbic-prefrontal system in anxiety disorders

A

-elevated activation in limbic structures
-hypoactivation in prefrontal regions aimed at normalizing limbic response
-increased amygdala activation provoked by anxiety-producing stimuli
-prefrontal-amygdala circuit probably mediates mechanisms involved in anxiety
-

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6
Q

attentional bias to threat

A
  • attentional bias associated with heightened HPA activity

- can shape stress responsively and risk for a.d.

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7
Q

early adversity & a.d.

A
  • childhood anxiety predicts occurrence of negative events and negative events predicts anxiety
  • secure attachment can act ad protective factor
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8
Q

parenting (modeling and info transfer) and a.d

A
  • parents display of anxiety/verbal behavior emphasizes threat in environment
  • > this modeling may be a failure in attachment style: parent doesn’t show appropriate care behavior within a stressful situation, fails to co-regulate child’s stress
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9
Q

parenting style and a.d

A
  • lack of warmth and rejecting behavior -> reinforces believe that world and people are hostile and unsupportive
  • over-controlling/rejecting: engender anxious style of attachment
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10
Q

mentalizing and stress

A
  • Effective affect regulation -> reduced reliance on external cues of safety & calling upon mental representations of internalized attachment figures -> internal working models
  • Mentally drawing upon past experiences in which stress was effectively co-regulated
  • secure attachment can predict ability of theory of mind
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11
Q

mothers mentalizing abilities

A

= ability to treat child as an psychological agent with mental states independent of their own -> predicts secure attachment and child’s capacity to mentalize

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12
Q

secure attachment and HPA

A

-> adaptive hypoactivity

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13
Q

broaden and build

A
  • secure attachment leads to seeking supportive attachment relationships throughout the life span
  • directs individuals into new environment (broaden) and requires adapting to new challenges (build)

-if insecure attached: coping strategies associated with hyper vigilance prohibit ability to broaden&build

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14
Q

Buffers against stress

A
  • secure attachment: adaptive allostasis and neural plasticity
  • capacity to retain high levels of mentalizing when faced with threat/anxiety: keeping regulatory brain regions (PFC) engaged during experience of stress and attachment activation
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15
Q

insecure attachment and stress regulation

A
  • infants use secondary strategies: hyperacttivating (gain attention) and deactivation of modes of stress and anxiety
  • anxious attachment: associated with internalizing problems, predisposes to a.d.
  • anxious attached: under-recruit PFC involved in emotion regulation
  • bias toward negative memories
  • amygdala hyperactivation to negative social events
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16
Q

allostatic load

A
  • wears and tears out the body

- emotional regions of brain (fronto-limbic circuit): editor of allostatic load

17
Q

effect of allostatic load on neural circuits

A

-can damage circuits due to overproduction of neurochemicals involved in stress response

18
Q

slow vs reflective response to stress

A

-Sustained hyperactivity: linked to switch in activation from cortical to subcortical brain systems, from slow, reflective regulation, to a rapid, reflexive response

19
Q

5HTTLPR - seretonin transported gene polymorphism

A
  • infants SS: more fear
  • Strong links between 5-HTTLPR genotype and endophenotypes of depressive disorders like amygdala reactivity, structure & connectivity of the amygdala, ACC and PFC
20
Q

interaction of 5HTTLPR genotype with quality of maternal care

A
  • insecure attached, ss: 8&12 months: most fear, incline in negative affect expression, decline in positive emotionality
  • secure, ss: no high fear at 8m, but at 12m similar level as insecure
  • Infants with ss are probably more susceptible to inadequate maternal care
21
Q

5HTTLPR by environment interaction for anxiety sensitivity

A
  • Interaction between childhood emotional (or physical) maltreatment and 5 HTTLPR genotype
  • SS individuals with higher levels of maltreatment had significant higher levels of AS
22
Q

maternal stress/anxiety/depression and glucocorticoid treatment during pregnancy

A

-lower birthweight, smaller size of baby
-increased HPA activity
-disturbances in child development and behavior
(unsociable, ADHD, sleep disturbances, psychiatric disorders = depressive symptoms, drug abuse, mood/anxiety disorders)

23
Q

lower birthweight + lower levels of maternal care

A

reduced hippocampal volume in adulthood

24
Q

full-day care centers

A
  • glucocorticoid levels rise in children over the day, more so in toddlers than in older preschool-aged children
  • if also less supportive care = larger increases, especially for children who are more disorganized and emotionally negative
  • poor care for long hours early in development have increased risk of behavioral problems later
25
Q

sensitive parenting and HPA

A

-smaller increases in or less prolonged activation of HPA to everyday perturbations

26
Q

offspring of depressed mums (post natal)

A
  • risk of heightened HPA activity or developing depression during adolescence
  • pre-school: alterations in frontal lobe activity that correlate with diminished empathy and other behavioral problems
27
Q

Severe deprivation, neglect, abuse

A

-lower basal levels of glucocorticoids = HYPOcorticolism

28
Q

stress in adolescence & HPA

A
  • heightened basal and stress-induced activity of HPA -> related to dramatic changes in sex steroid levels
  • heightened HPA activity during adolescence: increased sensitivity to onset of stress-related mental disorders
29
Q

in adolescence long-lasting effects become evident:

A
  • grew up in poor economic conditions/mothers depressed postnatally: higher glucocorticoid levels
  • early adversity may lead to alterations in grey matter volume and neural integrity of FC, reduced size ACC
30
Q

Frontal cortex

A

-develops during teens, might be particularly vulnerable to stress

31
Q

Hippocampus

A
  • develops in first year of life

- might be less affected by exposure to adversity in adolescence

32
Q

relationship glucocorticoid levels and cognitive performance in adulthood

A

inverted U-shape

33
Q

acute glucocorticoid elevation and memory

A

increased memory for emotional info and impairs retrieval of neutral info

34
Q

low self esteem in adulthood

A
  • predictor of increased reactivity to stress

- reduced hippocampal volume

35
Q

depression in adulthood

A

elevated basal glucocorticoid levels

36
Q

PTSD

A

HYPOactivity of the HPA, reduced basal glucocorticoid levels
-> in case of abuse, you down regulate HPA axis (=coping mechanism) -> body tries to become less sensitive

37
Q

Neurotoxicity hypothesis

A

Prolonged exposure to glucocorticoids reduces the ability of neurons to resist insults, increasing the rate at which they are damaged by other toxic challenges or ordinary attrition

-implies that a reduced hippocampal size is the end product of years/decades of PTSD, depressive symptoms or chronic stress

38
Q

neurotoxicity hypothesis - limitations

A

does not explain the hyposecretion of glucocorticoids that occurs in patients suffering from PTSD, who also present reduced hippocampal volume

39
Q

vulnerability hypothesis ?

A

Reduced hippocampal volume in adulthood is a pre-existing risk factor for stress-related disorders that is induced by genetics and/or early exposure to stress

Behavioral Problems in childhood (6 decks)

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