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)

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ADHD

• 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

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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
  ODD/CD
• ADHD, combined type

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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

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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

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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

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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

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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,
  1988)
• 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
  ganglia

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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,
  2005)
• i.e. an interplay of biological and
  socio-ecological factors lead to the final common
  pathway of the clinical syndrome of ADHD

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ADHD assessment

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

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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

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ADHD treatment

• stimulants do
• reduce behavioural symptoms
• improve attentiveness/productivity
• reduce negative impact on others (Swanson et al.,
  1993)
• are more effective in the hyperactive/impulsive
  and combined subtypes than in the inattentive
  group (Tannock, 1998)

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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)

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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
  completed

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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
  continuity.
• 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)

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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
  (2005
• 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

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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

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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
  community)
• improved definition and measurement of
  constructs, identification of sub-types
• thresholds for onset, duration, symptoms,
  severity and impairment may change as
  understanding improves

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Tim

• 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
  tasks.
• 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

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Tim

• 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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Tim

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

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