Developmental psychopathology of Aggression

1
Developmental psychopathology of Aggression

• Mark Dadds, David Hawes, Sabine Merz, Yael Perry,
  Aaron Frost, Alison Riddell, Damien Haines, Emel
  Solak, Amali Abeygunawardane, Jenny Fraser,
• Catholic Education, UNSW, Griffith University,
  Funded by the National Health and Medical
  Research Council of Australia

2
Development of Conduct Disorder
10
Adulthood
Childhood
Adolescence
3

• Do aggressive children belong in child mental
  health services?

4
Conduct problems and later psychopathology

• Kim - Cohen

5

• We can make sense of different sub-pathways by
  consideration of
• Specific genetic risk profile
• Endo-phenotypic vulnerabilities
• Diagnostic presentation
• Environmental protection and risk (including
  treatments)
• Sensitive periods for intervention

6
An example of sub-pathways CU traits

• Callous unemotional style
• Lacking empathy
• Lacking guilt
• Unkind

Still from LeRoys The Bad Seed (1956)
7
Subtypes of Conduct Disorder

• Common Conduct Disorder CD with CU traits
• Associated with Family Problems - Not Associated
  with Family Problems
• Neurological problems - No neurological
  problems
• Reactive aggression - Reactive and proactive
  aggression
• Emotional dysregulation (anxiety) - Low anxiety
• Impulsivity - Punishment Insensitivity
• High salience of emotion - Low salience emotion
• - Normal empathy - Empathy deficits

Respond to family interventions and
social-cognitive skills training
Unclear treatment outcomes
8
Predictive validity

• Outcomes
• Growth in antisocial behaviour across the 12
  months
• Severity of DSM IV externalising _at_ 12 month
  follow-up

9
Parent ratings 1-year later
 
10
Diagnostic severity 1-year later
11
Viding, Blair, Moffitt Plomin (2005)

• Similar item structure of APSD and SDQ
• N 3687, 7 year old twin pairs from UK
• Teacher ratings
• Analysis of extremes (1.3 SDs gt mean)

12
Viding, Blair, Moffitt Plomin (2005)
     
13
Unadjusted means for ODD severity and Antisocial
factor scores by CU groups, for pre-treatment,
post-treatment, and follow-up
 
14
(No Transcript)
15

• MAOA
• Polymorphism modify the activity of the
  serotinergic MAOA enzyme (Denney et al., 1999),
• Increased amygdala activity to angry-fearful
  faces (Meyer-Lindenberg et al., 2006).
• HTTLPR
• The short allele of the 5-HTTLPR functional
  polymorphism in the promoter of the serotonin
  transporter gene, interacts with environmental
  adversity to predict vulnerability to anxious
  temperament and depression (Caspi et al, 2003
  Wilhelm et al., 2006).
• Increased amygdala activity to angry-fearful
  faces (Pezawas et al., 2005)
• COMT
• The Val108/158Met polymorphism modifies activity
  of the COMT enzyme (Lachman et al., 1996) plays a
  major role in prefrontal cortical functioning,
  and deficits in the latter show established
  relationships with aggression and antisocial
  behaviour.
• Predicts violence as a main effect within high
  risk groups (Thapar et al. 2005), is associated
  with poorer processing of facial emotions
  autism Murphy et al. (in press).

16
MAOA activity and violence
17
COMT genotype and aggression in ADHD
18
(No Transcript)
19
Emotion processing

• Increasing evidence that various forms of
  psychopathology are associated with deficits in
  identifying facial emotions
• Genotypes differently associated with amygdala
  activity to threatening faces
• Emerging evidence that psychopathy associated
  with specific deficits in fear recognition cf
  increased reactivity to fear in MAOA/HTT risk?
  Decreased reactivity in COMT.

20
(No Transcript)
21
(No Transcript)
22
ANSWER ITEM 11
23
(No Transcript)
24
(No Transcript)
25
ANSWER ITEM 12
26
(No Transcript)
27
(No Transcript)
28
ANSWER ITEM 13
29
(No Transcript)
30
(No Transcript)
31
(No Transcript)
32
Correlations between CU, Antisocial and accuracy
of emotion recognition.
33
Threat Interpretations(Non-clinic, Anxious
Oppositional Groups)
(Barrett, Rapee, Dadds Ryan, 1996)
34
Some speculations
Clearly, such deficits could not explain
antisocial behaviour in high CU, however..
35
Idea 1 Fear perception and theory of mind
Fear stimulus
Information about environment from following
others gaze
Aversive threat
Observer
36
Idea 2 The language of the eyes
37
(No Transcript)
38
(No Transcript)
39
The language of the eyes

• Amygdala and attention, social gaze
• Ralph Adolphs work
• Autism v Social Phobia v CU traits
• Interventions that focus on attentional/recognitio
  n skills may be important

40
Focus On Eyes
X
41
(No Transcript)
42
X
Focus On Mouth
43
(No Transcript)
44
Attentional processes in emotion recognition
Condition 1 Free gaze Hi CU lt normal 2 Eyes
focus Hi CU normal 3 Mouth
focus normal HI CU
45
Mean accuracy of facial fear recognition for boys
high and low on CU traits under three Gaze
conditions no instruction, instruction to focus
on eyes, instructed to focus on mouth.
Significant interaction between Gaze and CU
category, F(2,55) 5.149, p .009. Error bars
represent standard errors of the mean
46

• Specific genotypes interact with environmental
  risk to produce specific and measurable emotion
  processing problems
• VIM? Blair
• Sensitive periods?

47
Sensitive periods for attachment conditioning
48
Amygdala activity and attachment conditioning
49
Oxytocin and vasopressin levels after interaction
with mothers
50
Conditioned attachment is corticosterone
dependent
51
CU traits associated with low cortisol
52
Conclusions

• Common conduct disorder is characterised by
  over-seeing threat.
• Callous/unemotional traits are associated with
  under-seeing fear. These, like amygdala-damaged
  patients, appear to be due to attentional
  problems.
• The differences may be endo-phenotypic and
  associated with vulnerabilities coming from MAOA,
  5-HTT and COMT polymorphisms (and others).
• Endo-phenotypes are modified by specific hormonal
  actions and caregiver behaviours.
• These biological-environmental interactions are
  markers of failure to benefit from subtle
  socialization experiences at ages critical to
  emotion recognition and theory of mind
  development.

53
The future

• Gene x environment models leading to powerful EIs
  that target specific vulnerabilities at specific
  sensitive periods.
• Poor parenting disruptions to serotonin
  pathways gt poor regulation gt high threat and
  violence
• Poor parenting disruptions to COMT enzyme, PFC
  limbic systemlow emotionality, bonding,
  attachment to aversive stimuli
• Emotion-processing attachment interventions