CAMHS 2 - conduct disorder Flashcards

1
Q

when was conduct disorder first in DSM

A

DSM-4 (2000)

formally known as externalising disorders (in childhood/adolescent) - due to it being hard to express struggles e.g. depression

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2
Q

2 types of disruptive behaviour disorders

A

conduct disorder (CD)
oppositional defiant disorder (ODD)

CD –> before 10 years old = childhood

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3
Q

ODD - characteristics (3 categories)

A

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 behaviour:

  • 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 misbehaviour

Vindictiveness:

  • Is often spiteful or vindictive
  • Has shown spiteful or vindictive behaviour at least twice in the past six months
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4
Q

issue of NHS medicalising bad behaviour

A

idea that not doing what your told is not a mental disorder

report showed 1/18 (12.8%) of english children have mental disorders

doubt if ODD is real due to it just being bad behaviour at a young age

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5
Q

quality of life and conduct disorder (CD) (5 categories) (3 age groups)

A

categories:

  • comorbid with psychiatric and physical disorders, learning difficulties, and medical consequences
  • criminal behaviour
  • social and family impairments
  • academic/occupational problems
  • risky and irresponsible behaviours

different levels of these with age, examples:

childhood:

  • ADHD, ODD
  • peer rejection
  • school exclusion

adolescence:

  • depression
  • criminal behaviour
  • intimate partner violence
  • unplanned pregnancy

adulthood:

  • premature mortality
  • ASPD
  • suicide attempts
  • poor parenting
  • unemployment
  • STDs
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6
Q

incidence and heritability of CD

A

1- 2.5% worldwide incidence

5 - 74% heritability
heritability in more extensive studies = 40-50%
heritability in those with CU traits = 45-67%

often comorbid with ADHD

32,000 symptom profiles can give rise to a diagnosis

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7
Q

environmental risk factors for CD (in vitro, birth, family, non-familial)

A

in vitro (maternal factors):

  • smoking
  • alcohol
  • drug use
  • stress

birth:

  • birth complications
  • maternal or paternal psychopathy
  • malnutrition

childhood + adolescence:
familial:

  • harsh and inconsistent discipline
  • parent-child conflict
  • maltreatment
  • low SES and poverty

extra-familial:

  • community violence
  • association with deviant peers
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8
Q

genetic risk factors for CD (5 categories it can effect)

A
  • autonomic
  • neurocognitive
  • social information processing
  • temperament
  • personality traits

gene-environment interplay and correlations in CD

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9
Q

different types of gene-environment correlations (3)

A

passive = association between inherited genes and environment in which they are raised e.g. smart parents provide intellectually stimulating environments; parents who smoke/drink around their kids

active = seek out environments that support genetic tendencies e.g. smart children may take more challenging classes; may spend more time with others who also smoke/drink/are antisocial

evocative = association between gene influenced behaviour and others reactions to you - multiplier effect e.g. you are argumentative which makes others more aggressive with you back

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10
Q

genome-wide association study (GWAS)

A

observational study of a genome-wide set of genetic variants in different individuals to see if any variant is associated with a trait

associations between single-nucleotide polymorphisms (SNPs) and traits like major human diseases

can also be applied to any other genetic variants and any other organisms

GWA studies compare the DNA of participants having varying phenotypes for a particular trait or disease

participants may be people with a disease (cases) and similar people without the disease (controls)

phenotypefirst approach:

  • clinical used to classify before genes
  • if one type of variant is more frequent in people with a disease = associated
  • associated SNPs = mark region of genome that may influence risk of disease
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11
Q

single nucleotide polymorphism

A

DNA molecules differ by a singe base-pair location

(like an allele)

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12
Q

GWAS finding genes which we don’t understand yet with CD

A

DONT NEED TO KNOW - JUST AN EXAMPLE OF A GENE THAT ISN’T UNDERSTOOD

RBFOX1 = associated with CD

Fox-1 homolog A, also known as:
* ataxin 2-binding protein 1 (A2BP1)
* hexaribonucleotide-binding protein 1 (HRNBP1)
* RNA binding protein fox-1 homolog (Rbfox1)

protein encoded by RBFOX1 gene

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13
Q

different genes associated with CD (5)

A

RBFOX1 - development
GABRA2 - gaba (inhibitory)
SLAC6A4 – serotonin receptor
Oxytocin receptor OXTR
C1QTNF7 – glucose metabolism and insulin signalling

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14
Q

mono amine oxidase (MAO)

A

MAO = enzyme that breaks down monoamine neurotransmitters

different forms of MAO gene e.g. MAO-L = low, less active

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15
Q

gene-environment interaction in CD with maltreatment

A

low mono amine oxidase gene (MAO-L) = more CD

severe maltreatment = more CD

these two interact so severe maltreatment and MAO-L = highest rates of CD

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16
Q

neurocognitive features of CD (5)

A
  • Verbal IQ
  • Working Memory
  • Executive functions
  • Emotion recognition
  • less sensitive to punishment cues, particularly when they are already keen for a reward
    overly sensitive to reward

OR can be overly sensitive to punishment and insensitive to reward

idea that the systems are dysregulated - can be up or down

17
Q

brain areas and functions

A

DIAGRAM ON SLIDE
all details aren’t needed
general idea of frontal areas ( do similar things) and amygdala and striatum (dopaminergic - decision making, reward)

emotion and empathy:

  • amygdala
  • striatum
  • ventromedial PFC
  • ventral anterior cingulate cortex
  • superior/middle frontal gyrus
  • middle/inferior temporal gyrus
  • fusiform gyrus
  • insula

reinforcement learning/decision making:

  • ventromedial PFC
  • striatum
  • medial PFC
  • dorsal anterior cingulate cortex
  • supplementary motor area
  • insula

executive functions:

  • dorsal anterior cingulate cortex
  • superior/middle temporal gyrus
  • insula
  • precuneus

threat response:

  • amygdala
  • vm PFC
  • dorsal anterior cingulate cortex
  • insula

resting state activity

  • amygdala
  • medial PFC
  • posterior cingulate cortex
  • precuneus
18
Q

gene influence on CD - brain function and amygdala

A

high amygdala activity = MAO-L gene

bigger differences between MAO-L and high in men than in women

19
Q

cognitive hostile attributional bias

A

tendency of individuals to interpret not only ambiguous cues as signalling hostility, but also many cues that are generated with benign intentions

anterior cingulate activity and MAOA genotype

MAO-L = low/no activity in anterior cingulate
MAO high = negative activity in anterior cingulate

LOOK AT SLIDE 31 - BRAIN STRUCTURE DIAGRAMS

20
Q

management of CD without comorbid disorders in early and late childhood

A

DSM-V or ICD-11 diagnosis of CD and assessment for LPE (limited prosocial emotions)

psychosocial interventions:
without LPE:

  • early childhood = social learning theory based parent training
  • late childhood/adolescence = social learning theory based parent training and child skills training

with LPE:

  • early childhood = social learning theory based parent training - additional training focused on parental warmth and child empathy skills
  • same in later childhood but with more general child skills training too

if response to these is poor, add medication:

  • risperidone (without ADHD)
  • psychostimulants and/or risperidone (CD with comorbid ADHD)
21
Q

management of CD with comorbid disorders (3 categories)

A

all start with psychosocial intervention and if not, do these

internalizing comorbidity (e.g. anxiety, depression, PTSD)
–> evidence based disorder specific psychosocial intervention, or psychotherapy and/or disorder-specific medication (SSRI)

externalising comorbidity (e.g. ADHD, ODD)
–> first line = stimulant for ADHD (may reduce impulsive aggression and so can be beneficial alongside psychosocial interventions for CD and ADHD)
–> second line = risperidone for impulsive-aggressive behaviour and hyperactivity (first line in children with comorbid ID)

comorbid developmental disorders (e.g. elimination disorders, language disorders)
–> evidence based intervention for respective disorder

22
Q

pharmacological therapies for CD

A

stimulants - Ritalin
antipsychotics

23
Q

do boot camps work for CD

A

no
if you do not fear punishment that wont change it