1 Attention Deficit/ Hyperactivity Disorder (AD/HD): Dr Attention Deficit/ Hyperactivity Disorder (AD/HD): Dr. Elizabeth SheppardDevelopmental Cognitive Neuropsychology(C8CLDC)Child Clinical Neuropsychology(C8DCHN)
2 Objectives Learn about diagnostic/ behavioural features of ADHD Discuss cognitive explanations of ADHD as a disorder of EFDiscuss abnormalities in brain structure and function in ADHDThink about question of discriminant validity – if autism & ADHD are both executive disorders
3 2 groups of symptoms types Diagnostic Criteria2 groups of symptoms typesA) 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
4 Diagnostic CriteriaBi) 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 excessivelyBii) Impulsivity - blurts out answers beforequestions have been completed; difficultyawaiting turn; interrupts or intrudes on others(e.g., butts into conversations)
5 Diagnostic Criteria Additional features Symptoms are developmentally inappropriate and persist for 6 months or longerAge 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)
6 Diagnostic Criteria B. Hyperactivity / Impulsivity A. Inattention In Summary:B. Hyperactivity / ImpulsivityA. InattentionAD/HD – Inattentive Type[27 %]AD/HD – Combined Type[55 %]AD/HD – Hyperactive Type[18%]
7 Evidence for ED in ADHDEvidence for Executive dysfunction in ADHD comes fromCognitive studies – are individuals with ADHD impaired on cognitive tasks of EF?Biological studies – which areas of brain are implicated in ADHD?
8 Core Cognitive Difficulties Behavioural Inhibition Deficit [Barkley, 1997]Behavioural Inhibition:e.g., Ability to inhibit a prepotent responseWorking Memory:e.g., acting on events held in memorySelf – regulation:e.g., emotional self-controlSpeech Internalization:e.g., description and reflectionReconstitutione.g., analysis and synthesis of behaviour
9 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
10 Core Cognitive Difficulties? Behavioural Inhibition Deficits: Tested with tasks requiring control of actions, e.g., the Go/No-go Task:Time
11 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!
12 Core Cognitive Difficulties? Behavioural Inhibition Deficits: Tested with tasks requiring control of actions, e.g., the Stop Signal Task:Time
13 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!
14 Core Cognitive Difficulties? Review – Pennington & Ozonoff (1996)reviewed studies that presented EF tasks to those with ADHD15/18 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.
15 Biological evidenceDifferences in size of structures involved in control of action [e.g., reviewed in Swanson et al., 1998]
16 Brain StructureDifferences in size of structures involved in control of action: Caudate [e.g., Castellanos et al., 2003]
17 Brain FunctionDifferences in activity for control-related circuits [e.g., Durston et al., 2003]
18 Brain FunctionLou et al. (1984) found decreased blood flow to frontal lobes in ADHD childrenZametkin et al. (1990) found an overall reduction in cerebral glucose utilisation, especially in right frontal areas of parents of ADHD childrenMethylphenidate (Ritalin) as treatment of choice (or similar pharmacological agents), effects on control-related processes [e.g., Aron et al., 2003]
19 Brain FunctionMethylphenidate (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]
20 GeneticsGreater frequency of “high-risk” variants of genes related to functions of key neurotransmitters (dopamine) (Swansonet al., 2000):Dopamine Transporter (DAT-1)Dopamine Receptor (DRD4)
21 Gene – Cognition Interactions Cognitive Level:e.g., Differences in inhibitory skills relate to DRD4 polymorphism [e.g., Langley et al., 2004]
22 Gene – Brain Interactions Brain Level (Structure):e.g., Differences in polymorphisms are reflected in structural differences across the brainDAT1 genotype caudate volumeDRD4 genotype prefrontal volume[Durston et al., 2005]
23 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 weightThose possessing the high-risk genotype are more susceptible to the adverse effects of prenatal risk as indexed by lower birth weight [Langley & Thapar, 2006]
24 Interim summaryEvidence supports notion of ADHD as a disorder of executive functionCognitive evidence – poor performance on tests of inhibitionBiological evidence – frontal lobes implicatedBut issue of discriminant validity – how can symptomatically different disorders (autism & ADHD) stem from the same underlying cause?
25 How can the DV problem be solved? Biological levelPennington & Ozonoff (1996) argue 6 possible biological explanations:1.) Differences in severity – e.g. differing levels of dopamine depletion2.) Time in development when insult occurs – but all present early in life3.) Different single brain changes within the PFC i.e. different parts altered but general ‘family resemblance’ between symptoms
26 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 ADHD5.) 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
27 How can the DV problem be solved? Cognitive levelIt may be that different disorders are deficient in differing EFs or have different profiles of ED severity at cognitive levelSome 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 WCSTOzonoff 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.
28 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 participantsTested 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 groupConclude disorders can be differentiated on basis of exec profiles – double dissociation
29 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 fluencyGroup with ASD showed deficits in inhibition, planning, fluency, cognitive flexibility but not working memoryThose with ADHD showed problems with verbal fluency & inhibition onlyConclude those with autism show more generalised EF problems than ADHD – no double dissociation!
30 How can the DV problem be solved? Goldberg et al. (2005) compare groups with autism,ADHD & TD on measures of inhibition, planning, mentalflexibility & working memoryOnly 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 onlyConclude working memory impaired in those with autism & ADHD but more severe in autism
31 How can the DV problem be solved? Some argue autism has additional cognitive features not related to ED e.g. weak central coherenceBooth et al. (2003) – drawing taskPlanning – making changes to accommodate new featureWCC – drawings rated for strategy, fragmentation & configural violationsAutism & ADHD showed planning deficits in comparison to TDOnly autism group showed WCCConclude WCC specific to autism
32 Summary Autism & ADHD both involve ED Differences may arise from: CognitiveWhich EFs affectedSeverity of impairmentAdditional deficits such as WCCBiologicalExact location of damageExtent of damageDamage to other regionsFurther research needed to establish profiles of impairment in different developmental disorders
33 ReferencesAron, A. R., Dowson, J. H., Sahakian, B. J., & Robbins, T. W. Methylphenidate improves response inhibition in adults with attention-deficit/hyperactivity disorder. Biological Psychiatry, 54,Barkley, R. A. (1997). Behavioral inhibition, sustained attention, and executive functions: Constructing a unifying theory of ADHD. Psychological Bulletin, 121,Booth, R., Charlton, R., Hughes, C., & Happé (2003). Disentangling weak coherence and executive dysfunction: planning drawing in autism and attention-deficit/hyperactivity disorder. Philosophical Transactions of the Royal Society of London, B, 385,Castellanos, F. X., Sharp, W. S., Gottesman, R. F., Greenstein, D. K., Giedd, J. N., & Rapoport, J. L. (2003). Anatomic Brain Abnormalities in Monozygotic Twins Discordant for Attention Deficit Hyperactivity Disorder. American Journal of Psychiatry, 160,Durston , S., Fossella, J. A., Casey, B. J., Pol, H. E., Galvan, A., Schnack, H. G., Steenhuis, M. P., Mindera, R. B., Buitelaar, J. K., Kahn, R. S., & van Engeland, H. (2005). Differential effects of DRD4 and DAT1 genotype on fronto-striatal grey matter volumes in a sample of subjects with ADHD, their unaffected siblings and controls. Molecular Psychiatry, 10,Durston, S., Tottenham, N. T., Thomas, K. M., Davidson, M. C., Eigsti, I.-M., Yang, Y., Ulug, A. M., & Casey, B. J. (2003). Differential patterns of striatal activation in young children with and without ADHD. Biological Psychiatry, 53,Goldberg, M. C., Mostofsky, S. H., Cutting, L. E., Mahone, E. M., Astor, B. C., Denckla, M. B., & Landa, R. J. (2005). Subtle executive impairment in children with autism and children with ADHD. Journal of Autism and Developmental Disorders, 35,Guerts, H. M., Verté, S., Oosterlaan, J., Roeyers, H., & Sergeant, J. A. (2004). How specific are executive functioning deficits in attention deficit hyperactivity disorder and autism? Journal of Child Psychology and Psychiatry, 45,
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