childhood and adolescent psychological problems 2 Flashcards
when did conduct disorder enter the DSM?
- DSM 4 TR
- 2000
what was conduct disorder previously known as?
- externalising disorders
example of behaviours in conduct disorder
- bullying
- arson
- shoplifting
- fighting
- property destruction
etc…
different names for conduct disorder
- childhood CD before age 10
- adolescent CD after age 10
oppositional defiant disorder
- Angry and irritable mood:
–> often and easily loses temper
–> is frequently touchy and easily annoyed by others
–> is often angry and resentful - Argumentative and defiant behavior:
–> often argues with adults or people in authority
–> often actively defies or refuses to comply with adults’ requests or rules
–> often deliberately annoys or upsets people
–> often blames others for his or her mistakes or misbehavior - Vindictiveness:
–> is often spiteful or vindictive
–> has shown spiteful or vindictive behavior at least twice in the past six months
examples of callous and unemotional traits
- persistent pattern of behaviour
- disregard for others
- lack of empathy
- problems in emotional and behavioural regulation
- different to other antisocial youth
- similar to adult psychopathy
- less sensitive to punishment cues
–> especially when they are keen to a reward - positively related to intellectual skills in the verbal realm
is bad behaviour always a psychological disorder?
- no
- NHS accused of medicalising bad behaviour
- 1 in 18 pre-school kids have been said to have psychological problems
- experts doubt if oppositional defiance disorder in toddlers is real as it is only characterised by bad behaviour
quality of life and conduct disorder
- if untreated, CD can lead to:
–> criminal behaviours
–> violence
–> gangs
–> depression and anxiety
–> substance abuse
–> premature mortality
–> Antisocial Personality Disorder
–> unemployment
–> homelessness
incidence and heritability of conduct disorder
- incidence:
–> 1-2% to 2-2.5% worldwide - heritability
–> between 5% and 74% - most extensive studies show a heritability of 40-50%
- those with callous and unemotional traits tend to have a heritability of 45-67%
- often comorbid with ADHD
- 32, 000 symptom profiles could give rise to diagnosis
environmental factors for conduct disorder
- in utero:
–> smoking
–> alcohol
–> drugs
–> stress - birth:
–> birth complications
–> maternal/paternal psychopathology
–> malnutrition - familial
–> harsh & inconsistent discipline
–> parent-child conflict
–> maltreatment
–> low socio-economic status and poverty - extra-familial
–> community violence
–> association with deviant peers
genetic/dispositional risk factor for conduct disorder
- autonomic
- neurocognitive
- social information processing
- temperament
- personality traits
passive gene-environment correlation
- inherit a genetic predisposition to smoke or drink alcohol
- passively in the environment we see parents smoking and drinking
- we have the genetic predisposition and the environment already matches it
–> we don’t do anything to change the environment so we’re passive
active gene-environment correlation
- genes make us actively change our environment
- we make the changes to account for our genetic predisposition
- e.g. having the genetic component for CD and then seeking out an antisocial peer group
- we ACTIVELY make our genetic disposition match our environment
evocative gene-environment correlation
- we have a genetic predisposition and then people evoke this or change environment to trigger this genetic predisposition
- multiplier effect
- genotype evocatively interacts with the environment
- positive feedback loop
what is a genome-wide association study?
- an observational study of a genome-wide set of genetic variants in different individuals to see if any variant is associated with a trait
- GWAs typically focus on associations between single-nucleotide polymorphisms (SNPs) and traits like major human diseases, but can equally be applied to any other genetic variants and any other organisms
GWAs and human data
- GWA studies compare the DNA of participants having varying phenotypes for a particular trait or disease
- compare cases with controls
- this approach is known as phenotype-first, in which the participants are classified first by their clinical manifestation(s), as opposed to genotype-first
- if one type of the variant (one allele) is more frequent in people with the disease, the variant is said to be associated with the disease
- associated SNPs are then considered to mark a region of the human genome that may influence the risk of disease
what is a single-nucleotide polymorphism (SNP)?
- basically an allele
- the upper DNA molecule differs from the lower DNA molecule at a single base-pair location (a C/A polymorphism)
- a single letter in the gene has changed
issues with genome wide association studies in psychology
- when we do GWAs in psychology and psychiatry, we might find a gene which we don’t understand yet
–> e.g. RBFOX1
–> this is then hard to apply
single genes associated with conduct disorder
- RBFOX1 = development
- GABRA2 = gaba, inhibitory
- SLAC6A4 = serotonin receptor
- Oxytocin receptor OXTR
- C1QTNF7 = glucose metabolism and insulin signaling
mono amine oxidase (MAO)
- mono-amine oxidase (MAO) is an enzyme that breaks down mono-amine neurotransmitters
- an enzyme is a protein
–> proteins are made by genes - there are different forms of the MAO gene: –> MAO – L (low form) is less active
genetic influences on conduct disorder (gene x environment interaction)
- the low form of MAO is associated with higher conduct disorder rates
- no maltreatment is associated with lower conduct disorder rates
- severe maltreatment AND low form of MAO associated with the highest rates of conduct disorder
neurocognitive symptoms of conduct disorder
- deficits in:
–> verbal IQ
–> working memory
–> executive functions
–> emotion recognition - they are often less sensitive to punishment cues, particularly when they are already keen for a reward
- overly sensitive to reward
OR - overly sensitive to punishment cues
- insensitive to reward
brain areas and their basic function
- frontal lobe = executive functions, decision making, learning and some emotion regulation
- amygdala = emotional regulation and threat response
- striatum = reward
- all disrupted in conduct disorder
genetic influences on conduct disorder (brain function)
- people with low forms of MAO have higher amygdala activation
–> over activation of amygdala
–> involved in emotion regulation and threat response
the cognitive / hostile attributional bias
tendency of individuals to interpret not only ambiguous cues as signaling hostility, but also many cues that are generated with benign intentions
management of conduct disorder without comorbid disorders
- different management techniques with and without LPE
- LPE = limited prosocial emotions
- use psychosocial interventions first
- if psychosocial interventions don’t work, then can move towards pharmacological treatment
management of conduct disorder with comorbid disorders
- different psychosocial interventions based on the type of comorbidity:
–> internalising comorbidity = depression, anxiety
–> externalising = like ADHD or OCD
–> comorbid developmental disorders = like language disorders - use psychosocial interventions first
- then can use disorder-specific interventions for comorbid disorders
pharmacological therapies for conduct disorder
- stimulants (e.g. Ritalin)
- Antipsychotics
other therapies for conduct disorder
- boot camp
–> more intense
–> very strict and disciplined - parent based / family based psychosocial interventions