ADHD: Aetiology

Question 1

HERITABILITY

Answer 1

FARAONE ET AL. (2005)
- 75-90%
- relatives of people w/ADHD = x2-8 ^ likely to also have ADHD > relatives of people w/o ADHD
DEMONTIS ET AL. (2019)
- GWAS identified several genetic loci (chromosomal positions) for ADHD
- BUT causality for specific genes = unclear

Question 2

NURTURE: PRE/PERI-NATAL RISK FACTORS

Answer 2

DOYLE ET AL. (2017)
- smoking/alcohol during pregnancy = ADHD risk factors
NIGG (2006)
- low birth weight = associated w/increased ADHD risk
TARVER ET AL. (2014)
- children born preterm = ^ likely to have ADHD diagnosis esp. inattention

Question 3

NURTURE: CHILDHOOD RISK FACTORS

Answer 3

NIGG ET AL. (2016)
- lead exposure; variation in iron metabolism gene moderates association between blood lead lvls/ADHD symptoms
MARK ET AL. (2010)
- toxic chemical exposure (pesticides/phthalate)
RUTTER (1998)
- early neglect/psychosocial deprivation

Question 4

NURTURE: FAMILY CAN EXACERBATE

Answer 4

JOHNSTONE & MASH (2001)
- during parent-child interactions kids w/ADHD = more oppositional/less compliant/less able to follow requests
- kids’ difficult beh can elicit negative interactions w/parents; can be ^ critical/controlling/demanding & less responsive
- likely that parents/kids exacerbate each other’s beh (bi-directional influences)

Question 5

NURTURE: FAMILY & MEDICATION

Answer 5

HINSHAW & ARNOLD (2015)
- studies show that reducing kid/ADHD symptoms via medication decreases parent’s control/negativity indicating kids’ parenting influence
- BUT parents’ characteristics (ie. ADHD/depression symptoms) = also important
- modifying parenting (ie. managing disruptive/noncompliant/aggressive beh) can shape ADHD trajectory

Question 6

NURTURE: DIET

Answer 6

BATEMAN ET AL. (2004)
- general adverse effect of artificial food-colouring/benzoate preservatives on 3Y beh
- detectable by parents but not simple clinic assessments

Question 7

NURTURE: PARENTAL FLOW CHART

Answer 7

NIGG (2020)
1. parental exposure/inflammation; child ADHD-liable genotype ->
2. infant = negative effect
3. toddler = weakened effortful control (dysexecutive BUT normative emotional reg)
4. pre-schooler = elevated ADHD symptoms/irritability
5. school-age = ADHD

Question 8

NEUROBIOLOGY MECHANISMS: BRAIN STRUCTURE

Answer 8

SHAW ET AL. (2011)
- 3-4Y delay in maximum thickness of pre-frontal cortex (typically occurs at 6Y BUT ADHD = 9Y)
- pre-frontal cortex thinning = delayed in adolescence; cortical size correlated w/ADHD symptoms

Question 9

NEUROBIOLOGY MECHANISMS: ATTENTION

Answer 9

• attention = selective/sustained/switching/attentional control
• executive function = response inhibition/planning/working memory/error correction
  RAICHLE & SNYDER (2007)
• neuroimaging suggests resting state/default mode (ie. mind-wandering) when attention-focused networks should be engaged
  VAN DEN DRIESSCHE ET AL. (2017)
• BUT others showed blank thought patterns during attention lapses

Question 10

INTERGRATIVE DEVELOPMENTAL MODEL OF HYPER/IMPULSIVE ADHD

Answer 10

BARKLEY (1997)
- reduced beh response/inhibition (ability to delay motor response) = core ADHD feature
- reduced beh inhibition results in impaired executive functions incl:
1. non-verbal working memory (holding info in mind)
2. internalised speech/verbal working patters (self-talk/guidance)
3. self-regulation of effect (ability to regulate emotions)
4. reconstitution (^ order thinking processes ie. analysis/synthesis)
5. motor control/fluency (planning/executing actions)

Question 11

THE DELAY AVERSION HYPOTHESIS

Answer 11

SONUGA-BURKE (2000)
- poor inhibitory control underpins ADHD kids’ dysregulation while delay aversion = dominant characteristics of their motivational style
- THIS is the dominant view
- alternative = motivational style to avoid delay -> impulsive beh (choose immediate > large delay rewards)/secondary deficits in WM/planning

Question 12

THE DUAL PATHWAY MODEL

Answer 12

SONUGA-BARKE (2002)
1. cortico-ventral striatal loop disturbance -> impaired signal delayed reward -> delay aversion -> ADHD
2. cortico-dorsal striatal loop disturbance -> inhibitory deficits -> executive deficits -> ADHD

Question 13

DELAY AVERSION: EVIDENCE

Answer 13

BITSAKOU ET AL. (2009)
- Maudsley’s Index of Delay Aversion (MIDA) = computer-based choice-delay task presented as space game where kid has to destroy enemy ship
- choice between:
1. wait 2s to destroy 1 ship = 1 point (small soon)
2. wait 30s to destroy 2 ships = 2 points (large later)
- sig group/age effect; ADHD ^ likely SS

Question 14

BITSAKOU ET AL. (2008; 2009): SUMMARY

Answer 14

• though kids w/ADHD = impaired relative to controls on delay aversion/inhibitory control tasks ONLY proportion has clinically relevant deficit in tasks (using 10% centile cut-off on control performance)
• findings support emphasis on neuropsychological heterogeneity in ADHD & multiple pathway models

Question 15

BITSAKOU ET AL. (2008; 2009)

Answer 15

INHIBITON
- Stop Signal Reaction Time (SSRT)
- go/no-go (G/NG)

Question 16

! SUMMARY !

Answer 16

• while ADHD = high heritability, specific genes = unidentified BUT evidence of genetic liability
• complex interaction between genes/environmental factors (in utero/through childhood)
• ADHD = heterogenous; dual pathways may enable better characterisation/understanding of mechanisms/traits involved
• reconsider Research Domain Criteria Initiative (RDoC)

Question 17

RESEARCH DOMAIN CRITERIA INITIATIVE (RDoC)

Answer 17

• framework aim = to provide info about basic biological/cognitive processes leading to mental health/illness
• matrix focuses on 6 major human functioning domains
• each has several beh constructs
• constructs = studies along functioning span (normal-abnormal) w/understanding that each = situated in/affected by environmental/neurodevelopmental contexts
• construct measurements can include genetic/physiological/beh/self-report assessments
• gained info may help inform creating mental health screening tools/diagnostic systems/treatment matric