Adolescence
Brain development/ Neurobiology --> Maturation
Psychopathology
Models
Neurobiological Model/ Dual Model (figure in course manual)
Triadic Model
Stress-incubation/corticolimbic dysfunction model
Drug Use
plasticity & adolescence as sensitive period
Brain structure
White Matter
Gray Matter
Brain activity (functional changes)
Stress/ Other Risk factors
Schizophrenia
Substance Abuse
Affective & Anxiety Disorders
personality traits as risk factors: high levels of novelty seeking, low levels of harm avoidance
Characteristics of Adolescence
in part triggered by stress exposure e.g. bullying
due to social isolation/exclusion--> social anxiety
peak age of onset of any disorder: 14 years
reduction in delta wave sleep during normal adolescence but this reduction is even more pronounced
exaggeration of typical synaptic elimination
improvements in IQ, working memory, problem solving, perspective taking, face processing --> steady improvement of cognitive control capacity
early emerging bottom up (exaggerated reactivity to motivational stimuli) vs. later maturing top down (cognitive control)
experience-dependent & experience-expectant
choose more actively the environmental stimuli--> different plasticity than in childhood
delayed gratification, response inhibition, social cognition improve
risk taking: sensitivity to environmental incentives
impulsivity: poor top down cognitive control
PFC: cognitive control, optimizing greatest gains
striatum: detecting, learning about novel/rewarding cues, reward-based associations
high density of dopamine receptors in striatum in early adolescence & loss of those receptors by young adulthood (in PFC peak around early adulthood)
hormonal changes--> functional activity in frontostriatal circuits
ventral striatal activation: monetary reward, risky behavior but not impulsivity (cause it's more about top down control from PFC)
cannabis before age 18 --> gray matter atrophy, decline in IQ --> affecting neuronal genesis, neuronal migration, glia formation
low aversive biological responses eg. milder withdrawal symptoms, less pronounced acute effects--> immaturity of GABA receptor systems
influence on mesolimbic dopamine transmission
enhances an already enhanced ventral striatum response --> strengthening reinforcement properties of the drug
less sensitive to behavioral effects but more sensitive to neurotoxic effects
greater hippocampal- dependent memory deficits due to alcohol
also smaller frontal & hippocampal volumes, altered white matter microstructure, poorer memory
connected to childhood sexual abuse, childhood adversity, exposure to early stress
Neurobiology of drug use
- pleasurable feeling of drugs --> dopamine in nucleus accumbens is high
- memory of association that drug = pleasure --> hippocampus
- hippocampus gates responsesof nucleus accumbens + uses environmental cues
- motivational salience --> excitatory PFC input into the accumbens
- drug use associations --> amygdala
- compulsive drug use --> highly reactive HPA
heightened plasticity may not only result in increased opportunities but also in increased vulnerabilities
effects of social isolation and reduced fear extinction in development of mental illnesses (rodent studies)
human brain retains a baseline level of plasticity throughout life
the balance of excitatory and inhibitory neurotransmission is a trigger of heightened plasticity
second period of heightened malleability
volume and integrity linearly increase into adulthood
changes in gray and white matter are accompanied by improvements in cognitive function
adolescence is not a sensitive period per se: there are periods in adolescence during which a specific input from the environment is expected
some sensitive periods may only ever be experiences by a subset of adolescents --> individual differences
Memory
reminiscence bump: more likely to recall autobiographical memories from ages 10-30
heightened mnemnonic capacity
superior recall of music, books, films etc
bullying has lasting effects on physical & mental health in adulthood
exposure in adolescence compared with adulthood: less neuronal activation in PFC, Cingulate, Thalamus
fear extinction learning attenuated
usage because of peers
age-related increases in the BOLD signal in PFC and parietal cortex during working memory task
BOLD increases also during response inhibition eg. Stroop Task
inconclusive results concerning risk seeking (nucleus accumbens)
alterations in neural connectivity and neurotransmission
cortical thickness decrease --> changes in synaptic pruning
maybe not accelerated pruning of synapses but gradual decrease in synapse number that begins in childhood
pruning maybe also accompanied by reduced nr. of glial cells
volume increases through childhood, declines throughout adolescence (gradual decline of frontal and parietal --> inverted U-shape, but not of temporal)
apparent loss of gray matter maybe reflects an increase in myelination of intra-cortical axons or increase in white matter volume overall
How? Probably anomalies of typical maturation processes + psychosocial factors (eg. school, relationships) + biological environmental factors (eg. pubertal hormonal changes, drugs)
typically begins in adolescence or early adulthood (earlier onset leads to more severity)
exaggerated typical decrease in frontal grey matter volume
related to heightened sensitivity for reward
structural anomalities in superior temporal gyrus, vPFC, amygdala
anomalous amygdala responses to social stimuli
curvilinear developement of subcortical regions --> motivational behavior (peak 13-17 years)
linear pattern of development until young adulthood
subcortical and prefrontal regions are considered as a circuit
imbalance: adolescent is biased by functionally mature subcortical relative to less mature cortical circuitry
motivated behavior has 3 distinct neural circuits: approach (ventral striatum), avoidance (amygdala), regulatory (prefrontal cortex)
all can be modulated by emotional/reinforcing contexts eg. promise of a reward facilitated adolescent cognitive control behavior more than for adults
peers are a motivational cue and can diminish cognitive control
sensation seeking: curvilinear pattern with peak at 10-15 years
linear decrease of impulsivity with age
sexual maturity
in adolescents and adults, trials for which money was at stake speeded performance and facilitated accuracy, but the effect was larger for adolescents
positive associations between hippocampal volumes and age of first use
people with ADHD have decreased prefrontal activity and are 4x as likely to develop a substance use disorder
3 main factors contribute to age-based progression of increased drug use: 1. sensitized stress response system, 2. sensitive periods of vulnerability, 3. maturational processes during adolescence
exposure to early stress enhances psychopathology in general, and shifts initiation of drug use to younger ages
compulsive drug use increases due to reactive HPA
affects hippocampus development (may enhance contextual responding to drug-related cues)
brain regions & circuits need to mature to notice the effects of early stress
steeper slope for males
white matter decline does not necessarily mean decline in myelination (could also be dependent on the axon diameter)
Figure course manual
Adolescence
Adults
Children
Striatum & PFC inter and intra connections are still developing, none is fully mature
striatum intraconnections are mature but PFC intraconnections are not mature yet. Striatum can already send interconnections to the PFC but PFC is not able to reprocicate interconnections to the striatum. This leads to larger influence of emotions and less cognitive control in relation to those emotions.
All of the intra and interconnections are mature but striatum plays a smaller role than PFC. PFC interconnections are stronger than striatum intraconnections.That's why PFC can exert more influence on the striatum.
also similar pattern of development in cannabinoid receptors
networks: action observation, biological motion processing, executive --> interplay between those explains individual differences in peer influence resistance
increase in independence
also more exposure to (social) risk factors
other risk factors: maternal deprivation, household dysfunction, abuse, parental loss --> aversive childhood experiences
PFC & Striatal connections are modified/shaped by experience
positive factors?
constructive parenting style, genetic factors (MAOA protective), social support, protective & positive environment, sport activities outside that allow to be "risky" eg. climbing
Pathway from life experience to risky health behaviors
- Adverse experience --> 2. Modified `frontolimboic Function --> 3. Reduced stressed reactivity, altered cognition, unstable affect regulation --> 4. Impulsive behaviors & risk taking --> 5. Poor health behaviors, addiction risk
consequences of adverse experience: 1) stress reactivity reduced eg. not stressed about taking drugs, 2) cognitive processing is shifted toward a focus on short term goals and a more impulsive response selection, 3) regulation of affect is less stable and prone to negative states
those are the immediate consequences of modified frontolimboic functions