W3: Flashcards
Effects of substance use in pregnancy
harmful mental and fatal consequences
high rates of relapse postpartum
early dysfunctional maternal-infant relationship
most frequent substance used in pregnancy
tobacco
then alcohol, cannabis
Effects of alcohol use
- risk of miscarriage
- infant mortality
- congenital abomalies
- low birthweight
- reduced gestational age
- preterm delivery
- fetal alcohol spectrum disorders
- adverse neurodevelopment outcomes
- cognitive and behavioural challenges
- executive functioning deficits in children
- psychological consequences in adulthood
Effects of smoking
- damage to the umbilical cord structure
- miscarriage
- ectopic pregnancy
- low birthweight
- placental abruption
- preterm
- infant mortality
Effects of second-hand smoking
- respiratory and ear infections
- sudden infant death syndrome
- behavioural dysfunction
- cognitive impairment
Coccaine
- premature rupture of membrane
- placental abruption
- preterm
- low birthweight
- small gestational age
Opioids
- low birthweight
- respiratory problems
- third trimester bleeding
- toxemia
- mortality
- neonatal abstincence syndrome = postnatal withdrawal syndromes of the child
Treatments in pregnancy
- motivational interviewing
- contigency management
- micronized progesterone
- methadone maintenance
- buprenorphine maintenance
- lactation
Motivational interviewing
- patient centered
- collaborative
- help clients to explore and resolve ambivalence
- draws from the trans theoretical model of change
- improve treatment readiness and retention
Contigency management
- positive reinforcement as means of operant conditioning
- usually monetary vouchers
- most successful for smoking cessation
- longer duration of cocaine abstinence
- addition to methadone or buprenorphine treatment
Micronized progesterone
-for postpartum cocaine use
Methadone maintenance
- medically controlled
- steady opiate dosing
- decreases maternal and neonatal morbidity
- greater relapse prevention
Buprenorphine maintenance
- for opiods
- lower retention rates
Breastfeeding
reduces HPA response to stress
-cognitive and motor development in the infant
Brain development during adolescence
- decrease in grey matter -> synaptic pruning
- changes in extracellular matrix
- increases in white matter ->myelination of axons = more efficient communication between brain regions
Neural changes occur well into
mid and late 20’s
Mesolimbic and reward system mature before the
prefrontal and cognitive control
Greater use of alcohol and marijuana by age 18 associated with
compromised inhibitory functioning
Initiation of drinking by late adolescence predicted by
- smaller frontal grey matter and less cerebellar white matter volume
- less volume in regions involved in impulsivity, reward sensitivity, decision making
Reward related subcortical structures are involved in
initiation of drinking in adolescents
Smaller left nucleus accumbens predicts
greater substance use
Markers of vulnerability to initiation
-alteration in neurocognitive performance and neural response patters during inhibition, working memory and reward processing
Effects of substance use on developing brain
- dose dependent relationship with cognitive functioning
- heavy use = worse complex attention, memory, processing speed and visuospatial functioning
- early onset more harmful
- premature cortical grey matter decline
Abstinence proves
improved verbal memory and psychomotor task performance
Marijuana related changes in white matter microstructure confer risk for
psychological disorders like shizophrenia
The emotional component of reward processing is affected by
binge drinking
Heavy drinking is both predicted and preceded by
heavy drinking
Cousin said that there is a natural resilience to
substance use disorder in adolescents -> something adaptive about the adolescent brain
Thoughts on risky behaviour shifted from poor decision making to
adaptation
Risky behaviour is biasing adolescents into
short term rewarding outcomes
Single best predictor to engage in teen substance use is
social environment
Teens perception of peer substance used is predicting
use even after 7 years after initiation
Executive network
- cold executive control
- frontoparietal areas: PPC, DLPFC, inferior frontal gyrus, dorsal anterior cingulate cortex
Salience network
- emotion regulation
- salience attribution
- integration of affective info into decision making
ventral anterior cinculate cortex vACC
Anterior Insula
Orbitofrontal cortex
Limbic areas:amygdala and striatum
Medial prefrontal cortex and superior temporal brain areas
social cognitive functions
- mature later than salience
- sensitive to social and affective context
Brain plasticity explains modulation of
neuronal connections through complex interaction between genes and environment
Course from substance use to substance use disorder is a transition from
goal-oriented, voluntary use to compulsive use
Motivation to use is explained by
salience networks becoming increasingly attentive and responsive to substance use and paired cues
A decreased functioning of frontoparietal executive networks leads to
poor behavioural control over motivation -> more substance use -> disorder
Neural factors that predispose teens to use
- increased emotional arousal, reward sensitivity and value of social info
- valence and rewarding effects of use and cues
Social plasticity hypothesis
same neurosocial mechanisms that place adolescents at initial risk of initiation and escalation of use underlie protective driving factors driving the natural resistance from substance use during adulthood
Contemporary models of SUD in teens
- improv of top down executive control over salience network
- > capacity to resist
- > long term become important
- > impulsive decision making decreases
- > emotional control improves
Key protective factors of social plasticity of normative teen resilience
- social attunement
- heightened brain plasticity
- role transitions and changes in motives
- social context
- durable network
- salient role in social environment => social benefits of use decrease
Social attunement alone is
insufficient to drive behavioural change
-social + plasticity
Regions paired with social attunement and learning
hippocampus and striatum
medial PFC
parahippocampal gyrus
