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Summary - Psychological and Neurobiological Consequences of Child Abuse

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This is a summary of the course Psychological and Neurobiological Consequences of Child Abuse within the IBP programme of Leiden. It is a full summary of the scientific articles and the lectures, which I all attended to take notes of. It is seperated by week and 45 pages in total. Together with m...

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  • January 18, 2024
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  • 2023/2024
  • Summary
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Psychological and neurobiological consequences of
child abuse

Week 1 2
Litterature 2
Lecture 5
Week 2 7
Litterature 7
Lecture 10
Week 3 13
Litterature 13
Lecture 16
Week 4 21
Litterature 21
Lecture 24
Week 5 27
Litterature 27
Lecture 31
Week 6 34
Litterature 34
Lecture 36
Week 7 39
Litterature 39
Lecture 40
Week 8 44
Litterature 44
Lecture 46

This summary was made in block 2 of the academic year 2023-2024. I attended all the
lectures to make this summary, using the slides and the real-life explanation of the professor to
make the summary concise but detailed enough to understand all important concepts. Besides
this, each piece of literature is also summarized every week to understand the key take-aways of
the articles.
I also made a practice exam with answers that can be found separately on my account.
Together with this, it’s the perfect way to prepare for the exam. Good luck!

, Week 1
Introduction

Litterature
Child Maltreatment and Risk for Psychopathology in Childhood and Adulthood
(Jaffee, 2017).
The focus of this review is on the relationship between maltreatment and mental health problems
in childhood and adulthood; Children and adults who are exposed to abuse or neglect in
childhood are at risk for a range of poor mental health outcomes, including internalizing (MDD,
PTSD, anxiety) and externalizing psychopathology (ADHD, CD, and ODD), posttraumatic
stress disorder, psychotic symptoms, and personality disorders. Children under the age of 3
have the highest risk of being mistreated.
Increased risk for PTSD through two pathways:
● Heightened risk for mental disorders
● Maltreatment sensitizes the neurobiological response to subsequent trauma
Measuring maltreatment is difficult due to biased retrospective reports and omission.
The paper reviews three mechanisms by which childhood maltreatment increases the risk for
psychopathology.
● Hypervigilance to threat
Early research proposed that children could become sensitized to threatening stimuli
because of their early exposure to anger and other negative emotions. This sensitization
to threat could increase children’s risk for anxiety. These types of sensitization could be
assessed through a test similar to an Implicit Attitude Measure in which both a happy and
an angry face are shown in a test. Children with a history of maltreatment or who were
exposed to harsher forms of parenting show biased attention to angry faces; they are
selectively attentive to anger cues and are more likely to identify ambiguous facial
expressions as angry. The biased attention to threat involves limbic and prefrontal
cortical circuitry, as maltreated children show heightened amygdala reactivity, even
when cues are shown pre consciously. The tendency to allocate more attention to angry
faces has been shown to explain why abused youth attribute more hostile intent to other’s
behaviors and thus engage in more aggressive behavior. Furthermore, an attention bias to
angry faces can be seen in both abusive as well as more normative forms of harsh
parenting, such as authoritarian parenting. These reactions toward more negative stimuli
can be modulated.
● Deficits in emotion recognition
Maltreated youth are poorer than non-maltreated youth at accurately identifying facial
expressions of emotion, which is believed to be due to the fact that parents of maltreated
youth have less prototypical angry facial expressions and vocalizations. Furthermore,
abused children also have trouble matching emotional outcomes with their common

, elicitors, and maltreated youth are poorer at identifying facial expressions of emotion.
This, combined with a lowered ability to regulate emotions, could lead to rejection by
peers, which in turn again exacerbates problem behaviors.
● Reward responsiveness
Reduced responsiveness to reward is thought to be a neural mechanism by which
maltreatment increases the risk for depression. Behaviorally, maltreated children and
adults who were maltreated as children are less sensitive to cues for reward than non
maltreated controls, especially toward anticipated reward. Mesolimbic dopaminergic
circuitry that projects to the basal ganglia (incl ventral striatum) is involved in the
responsiveness of reward.
The ACC is involved in reinforcement learning. The slow maturation of ACC leaves it
vulnerable to physiological consequences of chronic stressors. Due to this, e.g. women
with history of sexual abuse are less likely to “learn from their mistakes’’ in certain tasks.

Genetic moderators of maltreatment:
● MAOA gene is involved in the metabolism of dopamine, serotonin, and norepinephrine.
In the low-activity variant of this gene, men are at elevated risk for antisocial outcomes
when exposed to maltreatment.
● 5-HTTLPR S allele may elevate risk for depression compared to L allele carriers, with
an enhanced amygdala reactivity. Also more cognitive vulnerabilities to depression,
particularly under stressful conditions.
Psychosocial moderators of maltreatment:
● High ego control, ego resilience, high self-esteem, and high self-reliance
● Social support. However social support is unassociated with e.g. PTSD symptoms when
no abuse has been present.

The majority of adults who were victimized as children do not themselves perpetrate abuse or
neglect. This can be due to the buffer of experiencing a safe/nurturing relationship, or because of
Child Protective services sometimes stepping in when a generational history of maltreatment is
known.
All in all, there is a need for more prospective, longitudinal data on maltreatment to better
understand the course of resilience and dysfunction over time and the long-term effects of
maltreatment on mental and physical health.

Paradise Lost: The Neurobiological and Clinical Consequences of Child Abuse and
Neglect (Nemeroff, 2016).
This review focuses on early life stress (ELS) and its consequences on psychiatric and physical
health.

, Research has been done on the chemical consequences of maltreatment in laboratory animals,
but these resembled more the consequences of neglect than abuse. However, it found among
others:
● ELS major risk factor for suicide and risk factor for BPD
● Maternal deprivation in rats → increases in basal and stress-induced ACTH and CRF
concentrations
● Early Life Stress in non-human primates
→ increases in CSF CSR concentrations & cortisol reactivity
→ blunted growth hormone and increase in BMI
→ Increase in amygdala volume associated with CSF CSR concentrations
● ELS can change the role of HPA and CRF in handling the effects of stress
● An increase in the release of corticotropin releasing hormone can be an indication of
dysregulation in the HPA as a result to trauma
● ACE increases risk for medical disorders
● Reduced hippocampal volume in depressed women with a history of CM
● Childhood sexual abuse negative predictor of response to CBT?

The HPA axis has always been researched thoroughly when it comes to the mammalian stress
response. It has been found that ELS can result in both hyperactivity and hypoactivity of the
HPA axis. This effect can be influenced by the nature of abuse suffered, presence of
psychosocial support, (epi)genetic factors, and family history of psychiatric disorders. The
two-sided consequences of ELS has brought about the suggestion of a two-pathway model that
involves interaction of the glucocorticoid system and the oxytocin system.
Furthermore, child abuse and neglect is associated with an increased risk for not only
psychiatric disorders, but a variety of medical disorders as well, including ischemic heart disease,
cancer, chronic lung disease, skeletal fractures, autoimmune disorders, and liver disease. The
risk is directly proportional to the number and magnitude of the ELS. Most of these
disorders or physical problems have strong ties with increased inflammation.
Moreover, (epi)genetics can play a strong role. For instance, in a development Study
cohort of 1,037 subjects that had been assessed multiple times from age 3 to adulthood, those
who carried one or two copies of the short allele of the serotonin transporter promoter
polymorphism exhibited higher rates of adult depression and suicidality when exposed to
childhood maltreatment when compared to those long allele homozygotes with equal ELS
exposure.
The most interesting finding from this study is how much concordance there is in terms
of gene x environment interaction studies . However, many questions are still left unanswered,
and highlights the complexity of the fields and its combination of variables. All in all, early life
experiences can elicit profound effects on the development and function of the nervous system.

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