Lecture 4 Flashcards

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1
Q

What is true about mental illnesses starting in adolescence?

A

They are often more severe and have a higher impact on the rest of their lives.

Also, one in five adolescents have a mental illness that will persist into adulthood.

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2
Q

What can diminished goals lead to?

A

Depression

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3
Q

What can excessive motivation lead to?

A

Substance use and excessive risk-taking

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4
Q

Why is adolescence one of the healthiest periods?

A
  • Improvements in strength, speed, reaction time and reasoning abilities.
  • Increased resistance to cold, heat, hunger, dehydration and most types of injuries.
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5
Q

What is the health paradox?

A

Adolescence is one of the healthiest periods, yet it is associated with a 2- to 3-fold increase in mortality compared to childhood and adulthood.

So, adolescents are strong and smart but still the mortality rate has increased.

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6
Q

Why is risky behaviour necessary in the developmental period? And what are the downfalls of risky behaviour?

A

Because adolescents need to explore and experience. But some risky behaviours have negative consequences, such as traffic accidents, drinking and criminal behaviour.

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7
Q

When is the age peak for traffic accidents, drinking and crime?

A

Traffic accidents: peak in fatal traffic accidents between 15-19 years old.

Drinking: peak when 16 years old.

Crime (US data): peak between 15-20 years old.

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8
Q

What are the underlying processes that help explain the health paradox?

A
  • Neuroimaging studies on brain structure and function related to psychopathology.
  • Relation with real-life behaviour.
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9
Q

What are the two trajectories of antisocial behaviour?

A
  • Antisocial behaviour only shown in adolescence.
  • Persistent pattern of antisocial behaviour.

The biggest part is from the first trajectroy.

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10
Q

What are the functions of the striatum?

A

Dorsal: control network; action selection, maintaining future goals, inhibiting prepotent responses.

Ventral: valuation network; decision making, learning motivated behaviour.

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11
Q

Why is the striatum important?

A

It’s important for selecting actions, thinking about and maintaining future calls, decision making and motivated behaviour.

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12
Q

What are the functions of the prefrontal cortex?

A

Cognitive control: resistance to temptation, delay of gratification, impulse control.

Motivation (social/contextual) can modulate cognitive control.

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13
Q

Why is the prefrontal cortex important?

A

It controls the deeper lying structures, like the striatum. This keeps the balance in the system.

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14
Q

When does the striatum develop?

A

During adolescence, the striatum develops more and becomes more responsive.

The link between the PFC and striatum starts to develop but this takes into adulthood to gain good balance.

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15
Q

What explains risky behaviour?

A

The striatum explains a part of it, but there are other factors, such as motivation and emotionally arousing situations, which also influence the balance.

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16
Q

What are the results from the studies discussed in the lecture on binge drinking?

A
  • More risky behaviour is related to early onset of binge drinking.
  • Predictor behaviour outcomes vs. striatum activity => both were significant in explaining early binge drinking.
  • More activation in ventral striatum during the task of ‘wheel of fortune’ => earlier start of binge drinking.
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17
Q

What was considered binge drinking in the study by Morales et al. (2018) on decision making - alcohol use?

A

At least 5 drinks per occasion for males and at least 4 drinks per occasion for females.

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18
Q

What did the study by Morales et al. (2018) on decision making - alcohol use investigate?

A

The brain development when adolescents start to use alcohol.

The relationship between brain activity at the start of the study and the development of binge drinking overtime.

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19
Q

Study by Morales et al. (2018) on decision making - alcohol use

A

They used 47 adolescents, aged 14-15 with no history of alcohol or drug use. Every three months they were asked if they started binge drinking. Decision making is also included in this study by either taking a risk for a higher amount of money or taking no risk for a lower amount of money.

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20
Q

What are the results of the study by Morales et al. (2018) on decision making - alcohol use?

A
  • Participants who made risky choices started binge drinking earlier.
  • fMRI use shows activation in the medial and lateral prefrontal cortex, anterior insula, striatum, and left cuneus.
  • The more active the striatum was, the earlier the start of binge drinking.
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21
Q

What is the conclusion of the study by Morales et al. (2018) on decision making - alcohol use?

A

The onset of binge drinking can be predicted by behavioural performance and brain activation during a laboratory-based assessment. This helps to understand premorbid neurobiological risk factors for earlier engagement in binge drinking.

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22
Q

What percentage of US adolescents meet the clinical threshold for anxiety?

A

30%

23
Q

What is the relationship between anxiety disorders during adolescence and adulthood?

A

Anxiety disorders during adolescence represent an increased risk for anxiety disorders in adulthood.

24
Q

What is separation anxiety an example of?

A

An anxiety disorder that already presents during childhood.

25
Q

What is the difference between childhood-onset anxiety disorders and adolescent-onset anxiety disorders?

A

Adolescent-onset anxiety disorders have a more negative course & outcome than childhood-onset anxiety disorders.

26
Q

What is a prominent anxiety disorder during adolescence?

A

Social anxiety disorder (SAD)

27
Q

What is a risk factor for SAD?

A

Inhibited temperament, which is the tendency, also present in young children, to shy away from unfamiliar people or objects.

28
Q

What factors should you look at to try to understand how psychopathology develps?

A

Biological, psychological and social factors.

29
Q

What is a risk factor for psychopathology?

A

A stable, early life inhibition.

30
Q

What are some of the brain regions that are implicated in anxiety?

A
  • Amygdala: anxiety and stress;
  • Bed nucleus of stria terminalis: a tiny structure, which is connected to the amygdala;
  • Hypothalamus: information processing;
  • Hippocampus: memory processes;
  • Prefrontal cortex: cognitive part of anxiety;
  • Striatum: motivation and rewards.
31
Q

What is anxiety related to?

A

Changes in the structure, function and connections of brain regions.

32
Q

What five systems are not in balance during anxiety and the involved brain regions?

A
  • Fear conditioning
  • Uncertainty anticipation
  • Cognitive control
  • Motivation processing
  • Stress regulation
33
Q

What happens if there is an imbalance in the developmental progress of the five systems during adolescence?

A

This provides an essential basis for the high incidence of anxiety disorders during this period.

34
Q

The fear conditioning system

A

The amygdala => Hippocampus => Prefrontal cortex

35
Q

The motivation processing system

A

Prefrontal cortex => Striatum
Amygdala => Striatum

36
Q

The cognitive control system

A

Prefrontal cortex <=> Amygdala

37
Q

The uncertainty anticipation system

A

Prefrontal cortex => Bed nucleus of the stria terminalis
Amygdala => Bed nucleus of the stria terminalis

38
Q

The stress regulation system

A

Prefrontal cortex => Hypothalamus
Amygdala => Hypothalamus

39
Q

The cognitive control network between the PFC and the amygdala

A

The medial PFC controls the activation of the amygdala, while the amygdala projects to the mPFC.

During adolescence, the PFC matures and connections between the PFC and the amygdala are reorganized.

In anxiety, there is a delayed maturation of the PFC, reduced integrity of the structural connection PFC-amygdala and reduced functional connectivity PFC-amygdala.

40
Q

Uncertainty anticipation between Bed Nucleus of the Stria Terminalis (BNST), amygdala and PFC

A

The amygdala has an immediate response to a threat, the BNST has sustained responses to unpredictable threat information and the BNST receives input from mPFC.

During adolescence, the BNST response is stronger.

In anxiety, there is possibly a weakened functional connectivity between the BNST and the amygdala. Furthermore, there are possible changes in connectivity between the BNST and the PFC.

41
Q

What is important about the neural circuits of adolescent anxiety?

A
  • Hypoactivation of emotional cognitive control system.
  • Immature fear conditioning system.
  • Reward system and stress response are hypersensitive.
42
Q

Limitations of the neural circuits of adolescent anxiety

A
  • How do these functional circuits integrate?
  • Studies often focus on one element of the network.
  • More working adults => adolescents, but there are most likely adolescent specific brain abnormalities.
  • Limitations of cross-sectional data .
43
Q

What does the study of Groenewold et al. (2023) on SAD show?

A

Different patterns in adolescents with social anxiety/ adults with social anxiety.

44
Q

Groenewold et al. (2023) on SAD

A

MRI data is brought together from all over the world to get a bigger sample and more variety. The subcortical volumes are investigated.

45
Q

What are the results of Groenewold et al. (2023) on SAD?

A

People with SAD have a smaller putamen and a larger pallidum, which is part of the striatum, than the control group, but age also plays a role in this.

46
Q

What is the conclusion of Groenewold et al. (2023) on SAD?

A

Adolescent anxiety is not by definition defined by the same brain changes as social anxiety.

47
Q

Lahat et al. (2016) on inhibited temperament

A

Longitudinal study showing developmental trajectories over time.

The observations of this study started when babies were still 4 months old. They looked at whether the babies had an inhibited temperament. When they were ten years old, they got an MRI scan, and they were asked about social anxiety symptoms. The same was done at the age of thirteen. A pinata task was done online in which the pinata has to be hit in time to earn starts.

48
Q

What are the results of Lahat et al. (2016) on inhibited temperament?

A
  • There is a positive relationship between the inhibited temperament and social anxiety later in life.
  • There were no differences found between the groups of high behavioural inhibition or low behavioural inhibition.
  • During the anticipation of reward, brain activity is found in the ventral striatum.
  • There is more activity found in the dorsal caudate in high behavioural inhibition than low behavioural inhibition and there was also a relationship with social anxiety.
49
Q

What is the study of Davey et al. (2008) on affective disorders about?

A

Adolescence and affective disorders: Adolescent vulnerability for affective disorders

50
Q

What is the prevalence for affective disorders according to Davey et al. (2008)?

A
  • One month prevalence for MDD is 2% in late childhood and 6% in late adolescence.
  • The prevalence is higher for girls than for boys.
  • The lifetime prevalence for people in their mid-twenties is 25%.
51
Q

What are the results of Davey et al. (2008) on affective disorders?

A
  • Adolescent depression is often a forerunner of adult depression (recurrence 70%).
  • It is not just maturation of the brain that plays a role in the emergence of depression in adolescence because it also takes place when the brain is matured.
52
Q

Bio-psychosocial model on the development of depression

A

The model shows the changes in the three domains which contribute to the development of depression. Many things have to do with the processing of reward. Social cues are for example less rewarding.

53
Q

What are the results of Forbes et al. (2009) on reward and depression

A
  • Depressed patients showed less ventral striatum activation to positive stimuli.
  • Correlation with decreased interest and pleasure: participants with the least ventral striatal activation reported the least interest and pleasure in, and subsequent performance of, activities.
  • There was more activity in the PFC.

More activity in the PFC may play a role in affect regulation and social cognition => over-regulation of reward responding in young people with depression.