Attention Deficit/ Hyperactivity Disorder (AD/HD): Dr Attention Deficit/ Hyperactivity Disorder (AD/HD): Dr. Elizabeth Sheppard Developmental Cognitive Neuropsychology (C8CLDC) Child Clinical Neuropsychology (C8DCHN)

Objectives Learn about diagnostic/ behavioural features of ADHD Discuss cognitive explanations of ADHD as a disorder of EF Discuss abnormalities in brain structure and function in ADHD Think about question of discriminant validity – if autism & ADHD are both executive disorders

2 groups of symptoms types Diagnostic Criteria 2 groups of symptoms types A) Inattention - makes careless mistakes in schoolwork, or other activities; difficulty sustaining attention in tasks or play activities; does not seem to listen when spoken to directly; does not follow through on instructions ; has difficulty organising tasks and activities; avoids, dislikes, or is reluctant to engage in tasks that require sustained mental effort; loses things necessary for tasks or activities; easily distracted by extraneous stimuli; forgetful

Diagnostic Criteria Bi) Hyperactivity - fidgets with hands or feet or squirms in seat; leaves seat in situations in which remaining in seat is expected; runs about or climbs excessively in situations in which it is inappropriate; difficulty playing or engaging in leisure activities quietly; talks excessively Bii) Impulsivity - blurts out answers before questions have been completed; difficulty awaiting turn; interrupts or intrudes on others (e.g., butts into conversations)

Diagnostic Criteria Additional features Symptoms are developmentally inappropriate and persist for 6 months or longer Age of onset around 3-4yrs (Palfrey et al., 1985) Symptoms are exhibited in two or more settings (e.g., at school or at home) Prevalence 1-7% (Hinshaw, 1994) Males more likely to be affected – ratio of at least 3:1 (Szatmari et al., 1989)

Diagnostic Criteria B. Hyperactivity / Impulsivity A. Inattention In Summary: B. Hyperactivity / Impulsivity A. Inattention AD/HD – Inattentive Type [27 %] AD/HD – Combined Type [55 %] AD/HD – Hyperactive Type [18%]

Evidence for ED in ADHD Evidence for Executive dysfunction in ADHD comes from Cognitive studies – are individuals with ADHD impaired on cognitive tasks of EF? Biological studies – which areas of brain are implicated in ADHD?

Core Cognitive Difficulties Behavioural Inhibition Deficit [Barkley, 1997] Behavioural Inhibition: e.g., Ability to inhibit a prepotent response Working Memory: e.g., acting on events held in memory Self – regulation: e.g., emotional self-control Speech Internalization: e.g., description and reflection Reconstitution e.g., analysis and synthesis of behaviour

Core Cognitive Difficulties? Behavioural Inhibition Deficits: Tested with tasks requiring control of actions, e.g., the Go/No-go Task (Ozonoff et al., 1994): Say “Go” to all Squares, but not to Circles

Core Cognitive Difficulties? Behavioural Inhibition Deficits: Tested with tasks requiring control of actions, e.g., the Go/No-go Task: Time

Core Cognitive Difficulties? Behavioural Inhibition Deficits: Tested with tasks requiring control of actions, e.g., the Stop Signal Task (Ozonoff & Strayer, 1997): Say “Go” to all Pokemons and “No-go” to Meowth, but stop and say nothing when you see the Stop sign!

Core Cognitive Difficulties? Behavioural Inhibition Deficits: Tested with tasks requiring control of actions, e.g., the Stop Signal Task: Time

Core Cognitive Difficulties? Behavioural Inhibition Deficits: Tested with tasks requiring control of actions, e.g., the Go-Nogo Task, or the Stop Signal Task [Logan et al., 1984] Stop!

Core Cognitive Difficulties? Review – Pennington & Ozonoff (1996) reviewed studies that presented EF tasks to those with ADHD 15/18 studies found a significant difference between those with ADHD and comparison participants on one or more measures of Exec Function. Found those with ADHD poorer than comparison participants 40/60 (67%) tasks used across studies.

Biological evidence Differences in size of structures involved in control of action [e.g., reviewed in Swanson et al., 1998]

Brain Structure Differences in size of structures involved in control of action: Caudate [e.g., Castellanos et al., 2003]

Brain Function Differences in activity for control-related circuits [e.g., Durston et al., 2003]

Brain Function Lou et al. (1984) found decreased blood flow to frontal lobes in ADHD children Zametkin et al. (1990) found an overall reduction in cerebral glucose utilisation, especially in right frontal areas of parents of ADHD children Methylphenidate (Ritalin) as treatment of choice (or similar pharmacological agents), effects on control-related processes [e.g., Aron et al., 2003]

Brain Function Methylphenidate (Ritalin) as treatment of choice (or similar pharmacological agents): normalises baseline differences in blood flow [Lee et al., 2005] IMPORTANT: Need for combined treatment approaches [MTA Cooperative Group, 1999]

Genetics Greater frequency of “high-risk” variants of genes related to functions of key neurotransmitters (dopamine) (Swanson et al., 2000): Dopamine Transporter (DAT-1) Dopamine Receptor (DRD4)

Gene – Cognition Interactions Cognitive Level: e.g., Differences in inhibitory skills relate to DRD4 polymorphism [e.g., Langley et al., 2004]

Gene – Brain Interactions Brain Level (Structure): e.g., Differences in polymorphisms are reflected in structural differences across the brain DAT1 genotype  caudate volume DRD4 genotype  prefrontal volume [Durston et al., 2005]

Interactions - Gene/Environment There are important interactions between genotype and environmental variables: Early-onset antisocial behaviour in AD/HD is predicted by a specific genetic variant previously linked with prefrontal cortical function and birth weight Those possessing the high-risk genotype are more susceptible to the adverse effects of prenatal risk as indexed by lower birth weight [Langley & Thapar, 2006]

Interim summary Evidence supports notion of ADHD as a disorder of executive function Cognitive evidence – poor performance on tests of inhibition Biological evidence – frontal lobes implicated But issue of discriminant validity – how can symptomatically different disorders (autism & ADHD) stem from the same underlying cause?

How can the DV problem be solved? Biological level Pennington & Ozonoff (1996) argue 6 possible biological explanations: 1.) Differences in severity – e.g. differing levels of dopamine depletion 2.) Time in development when insult occurs – but all present early in life 3.) Different single brain changes within the PFC i.e. different parts altered but general ‘family resemblance’ between symptoms

How can the DV problem be solved? 4.) Changes in brain outside but related to PFC – Weinberger (1992) distinguishes intrinsic & extrinsic frontal disorders – neuropathology outside PFC can cause dysfunction within PFC as part of complex system e.g. basal ganglia in ADHD 5.) 2 localised changes in brain development – one in PFC ( ED) and one outside ( behavioural effects) 6.) Diffuse changes in the brain i.e. a general change in brain development e.g. neuronal number, structure, connectivity. EFs may be vulnerable to such changes due to complexity

How can the DV problem be solved? Cognitive level It may be that different disorders are deficient in differing EFs or have different profiles of ED severity at cognitive level Some early studies on autism informative as have ADHD as comparison group: Szatmari et al. (1990) - 80% of the comparison sample met criteria for ADHD and/or conduct order - also associated with impairments in EF. Those with autism made significantly more errors on the WCST Ozonoff et al. (1991) children with autism were impaired on WCST and especially the Tower of Hanoi in relation to comparison participants 25% of whom had a diagnosis of ADHD.

How can the DV problem be solved? Ozonoff & Jensen (1999) – examined EF profiles in groups of children with ASD, Tourette Syndrome, ADHD and typically developing (TD) comparison participants Tested on Tower of Hanoi (planning); WCST (mental flexibility); & Stroop task (inhibition) On Tower of Hanoi & WCST the group with ASD sig. poorer than all other groups (no diff between other groups) On Stroop task, ADHD group only were sig. poorer than TD group Conclude disorders can be differentiated on basis of exec profiles – double dissociation

How can the DV problem be solved? Geurts et al. (2004) compare groups with autism, ADHD & TD on various tasks including: stop signal task, self-ordered pointing, Tower of London, WCST, verbal fluency Group with ASD showed deficits in inhibition, planning, fluency, cognitive flexibility but not working memory Those with ADHD showed problems with verbal fluency & inhibition only Conclude those with autism show more generalised EF problems than ADHD – no double dissociation!

How can the DV problem be solved? Goldberg et al. (2005) compare groups with autism, ADHD & TD on measures of inhibition, planning, mental flexibility & working memory Only group differences were on working memory task (form of self-ordered pointing) Participants with autism made more errors than TD group for 8 items & 6 items; Those with ADHD made more errors for 8 items only Conclude working memory impaired in those with autism & ADHD but more severe in autism

How can the DV problem be solved? Some argue autism has additional cognitive features not related to ED e.g. weak central coherence Booth et al. (2003) – drawing task Planning – making changes to accommodate new feature WCC – drawings rated for strategy, fragmentation & configural violations Autism & ADHD showed planning deficits in comparison to TD Only autism group showed WCC Conclude WCC specific to autism

Summary Autism & ADHD both involve ED Differences may arise from: Cognitive Which EFs affected Severity of impairment Additional deficits such as WCC Biological Exact location of damage Extent of damage Damage to other regions Further research needed to establish profiles of impairment in different developmental disorders

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