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ADHD: Epidemiology


Heritability data from twin and adoption studies of ADHD suggest a major genetic ... endowment, temperament, abilities) and external systemic processes (family, ... – PowerPoint PPT presentation

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Title: ADHD: Epidemiology

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ADHD history
  • defect in moral control (Still, 1902)
  • minimal brain dysfunction (1940-1960)
  • hyperactivity (1960s)
  • deficits in attention and impulse control
    (1970s- 1980s).
  • deficits in self-regulation and inhibitory
    control (1990s)

  • defined by developmentally inappropriate
    impairing behavioural symptoms of inattention and
    /or hyperactivity/impulsivity
  • symptoms must be present lt 7, be cross
    situational and stable over time
  • more usefully conceptualised as a developmental
    neurocognitive disorder than simply a behaviour
    disorder but there are bi-directional
    environmental influences

ADHD- subtypes
  • ADHD, inattentive type
  • predominatly a cognitive/information
    processing disorder
  • ADHD, hyperactive-impulsive type
  • primarily a disorder of behavioural
    inhibition, associated with increased risk of
  • ADHD, combined type

ADHD co-morbidity
  • co-morbidity between 50-80 (Tannock, 1998
    Barkley, 2005)
  • oppositional-defiant or conduct disorder (50 )
  • mood disorders (15-20)
  • anxiety disorders (25)
  • Tourettes
  • specific learning difficulties (20-30)
  • not yet clear whether the effects of co-morbid
    conditions are additive or synergistic, but
    prognosis poorer for ADHD co-morbid disorders

ADHD epidemiology
  • occurs in 2-10 of children (Hinshaw, 1994
    Pelham et al., 2005 Rowland et al.,2002)
  • category v. continuim
  • occurs across cultures
  • boys gt girls, approximately 31
  • a life span disorder, although symptom
    expression changes across development

ADHD genetic studies
  • Heritability data from twin and adoption studies
    of ADHD suggest a major genetic contribution
    (explains up to 50-80 of variance) (Bierderman
    and Farrone, 2002 Farrone etal., 2005)
  • genetic contribution to ADHD higher than for any
    other psychiatric diorder (International
    Consensus Statement on ADHD, 2002)
  • evidence for specific candidate genes (DRD4 and
    DAT, serotonin transporter gene) in the
    dopaminergic system (Cook et al., 1995 Farrone
    et al., 2005), fits with neurobiological models
    and imaging studies which implicate brain
    structures with rich dopamine innervation eg.
    fronto-striatal circuits. Also symptoms reduced
    by stimulants which act primarily on the
    dopaminergic system

ADHD neuropathology
  • MRI studies demonstrate abnormalities in the
    prefrontal cortex (right side particularly),
    basal ganglia and corpus callosum - consistent
    with theoretical models of abnormal
    frontal-striatal connections (Tannock, 1998
    Sowell et al., 2003)
  • PET - abnormal cerebral perfusion, e.g.
    hypoperfusion of the striatal regions (Lou,
    1990), premotor and superior frontal cortex
    (Zametkin et al., 1990).
  • EEG and ERP studies consistently show
    abnormalities but little agreement about nature
  • Note Inconsistencies across studies may reflect
    heteregeneous subject groups (age, gender ADHD
    sub-type, co-morbidities), different neuroimaging
    techniques, methods of analysis

ADHD neuropsychological models
  • meta-analysis showed deficits in response
    inhibition, vigilance, working memory and
    planning (Willcutt et al., 2005)
  • deficits in self regulation and inhibition rather
    than in arousal, perception, attention (Douglas,
  • deficit of executive control rather than in
    specific information processing skills (Sergeant,
    1988) ie. a disorder of doing not of
    knowing, of performance not skill
  • deficits most evident on tasks of high cognitive
    demand because of failure to develop optimal
    strategies (MacLeod Prior, 1996) or to regulate
    response choices optimally (Barkley et al. 1992).
  • deficit patterns implicate neural systems
    responsible for behavioural regulation and
    inhibition eg. pre-frontal cortex and basal

ADHD integrated model
  • ADHD results from abnormalities in normal
    neurodevelopmental processes e.g. neurogenesis,
    neuronal migration etc. mediated by genetic,
    hormonal or environmental factors or some
    combination of these
  • social factors (e.g. parenting style, parental
    psychopathology, family conflict) not considered
    a cause but may exacerbate genetic or
    neurobiological vulnerability and influence
    management and outcome (Diamond Josephson,
  • i.e. an interplay of biological and
    socio-ecological factors lead to the final common
    pathway of the clinical syndrome of ADHD

ADHD assessment
  • cross-temporal
  • cross-situational
  • ecologically valid
  • utilise multiple informants - child report not
  • utilise structured or semi-structured interviews
    and rating scales
  • address biological, emotional, neuropsychological
    academic issues
  • assess family factors co-morbidities
  • (Pelham et al., 2005)

ADHD treatment
  • psychoeducation
  • stimulant medication - efficacy established in
    rigorous, double blind, placebo-controlled
    multi-centre trails e.g. MTA study
  • behavioural therapy (operant conditioning)- some
    evidence for efficacy (Jensen, 2005 Swanson,
    2005), but stimulants alone more efficacious for
    pure ADHD, combined therapy more useful for
    co-morbid ADHD
  • diet, biofeedback - no evidence for efficacy
  • social skills training - no evidence for efficacy
  • individual/family therapy - may be helpful with
    secondary symptoms eg. low self esteem,
    depression, family discord
  • environmental modification helfpul as adjunct
    to 1,2 3

ADHD treatment
  • stimulants do
  • reduce behavioural symptoms
  • improve attentiveness/productivity
  • reduce negative impact on others (Swanson et al.,
  • are more effective in the hyperactive/impulsive
    and combined subtypes than in the inattentive
    group (Tannock, 1998)

ADHD treatment
  • little current evidence that stimulants
  • induce aggression or anti-social behaviour
    (Connor et al., 2002) but may increase mood
    lability at least initially
  • lead to external behavioural attributions (Horn
    et al., 1991)
  • increase the risk of substance abuse
    (metanalysis by Faraone Wilens, 2003), 1999)
    although ADHD itself increases risk (Barkley,
    1998 Molina Pelham, 2004), particularly with
    co-morbid CD
  • improve learning and achievement as effectively
    as they reduce behaviour symptoms is equivocal
    (Swanson et al., 1993 Tannock, 1998)

ADHD management
  • poor internal organisation of incoming
    stimuli - therefore
  • provide high external structure/supervision
  • reduce competing stimuli/choices
  • break complex tasks into unitary components
  • encourage stop, think, do self talk
  • utilise operant conditioning principles to shape
    behaviour eg. reward time spent on task, tasks

ADHD prognosis
  • 70 of childhood cases persist into adolescence
    and 65 of adolescent cases persist into
    adulthood, although some symptoms may
    improve/change (Barkley et al., 2004). Others
    report lower rates, but still significant
  • adult prevalence rates complicated by change of
    informant and symptom patterns, but
    sub-threshold disorders, at least, remain high
  • in addition, high rates of CD, anti-social
    personality disorder, criminality and substance
    abuse e.g. ninefold increase in APD and four fold
    increase in substance misuse disorder over 16
    year follow-up (Joughin et al. 2003)

ADHD - prognosis
  • early co-morbidity with ODD and CD has the most
    adverse outcome (Moffit, 1990, Barkley, 1998)
  • marital discord, family disadvantage, positive
    family history of ADHD, negative parent-child
    interaction, low IQ poor peer relationships also
    increase risk for poor outcome (SIGN guidelines
  • distinction between symptomatic versus functional
    remission - poor functional outcome may be
    mediated through secondary factors such as low
    self esteem, academic failure, attitude of
    critical others even when cases to not meet
    diagnostic criteria for ADHD

ADHD current research
  • moving away from description and validation to a
    focus on aetiology, pathogenesis, prognosis and
    treatment efficacy
  • cognitive models which postulate faulty
    information processing and executive deficits
  • neurobiological models that emphasize genetic
    influences on brain structure or neurochemistry
  • but
  • models not well integrated in empirical studies
  • high rates of co-morbidity act against
    consistency in the findings
  • current models seek a unitary cause or cognitive
    marker of the disorder reductionist models

ADHD future directions
  • longitudinal studies combining genetic,
    neuroimaging and neuropsychological approaches
    within a developmental framework
  • need to take account of context ie. transactions
    between intrinsic child factors (genetic and
    biological endowment, temperament, abilities) and
    external systemic processes (family, school and
  • improved definition and measurement of
    constructs, identification of sub-types
  • thresholds for onset, duration, symptoms,
    severity and impairment may change as
    understanding improves

  • early history
  • well, but irritable baby, poor sleeper
  • advanced early development
  • busy impulsive toddler
  • couldnt take him anywhere, difficult to settle
  • Kindergarten
  • poor listener, active , fails to complete
  • acts without thinking, cant wait his turn
  • knows, but does not follow rules
  • alienates peers, exasperates teachers
  • parents feel demoralised and socially ostracised
  • referral to mental health service
  • parenting skills behaviour management
  • strategies

  • Prep
  • liked school, seemed bright but learned poorly
  • non-compliant, failed to complete tasks
  • restless, distracts others
  • lies, takes things, aggressive, no friends
  • referral to Psychology
  • motor restlessness , over-talkative, anxious,
  • distractible, poor self-monitoring
  • IQ in superior range, STAM and visuo-motor
  • deficits ie. input and output processes affected

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  • Treatment (multi-modal )
  • stimulants
  • behaviour modification (home school)
  • parent support
  • diet
  • Five years later
  • academic skills at grade level but ?
  • terrible writer, does not complete tasks
  • conflictual peer relationships
  • less active, but impulsive, volatile, ?depressed

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