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Attention Deficit/ Attention Deficit/ Hyperactivity Disorder Hyperactivity Disorder
(AD/HD):(AD/HD):
Dr. Elizabeth SheppardDr. Elizabeth SheppardDevelopmental
Cognitive Neuropsychology
(C8CLDC)
Child Clinical Neuropsychology
(C8DCHN)
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• Learn about diagnostic/ behavioural Learn about diagnostic/ behavioural features of ADHDfeatures of ADHD
• Discuss cognitive explanations of Discuss cognitive explanations of ADHD as a disorder of EFADHD as a disorder of EF
• Discuss abnormalities in brain Discuss abnormalities in brain structure and function in ADHDstructure and function in ADHD
• Think about question of Think about question of discriminant validity – if autism & discriminant validity – if autism & ADHD are both executive disordersADHD are both executive disorders
ObjectivesObjectives
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Diagnostic Criteria Diagnostic Criteria
2 groups of symptoms types2 groups of symptoms types
A) Inattention - 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
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Diagnostic CriteriaDiagnostic Criteria
Bi) Hyperactivity - 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 -Bii) Impulsivity - blurts out answers before questions have been completed; difficulty awaiting turn; interrupts or intrudes on
others (e.g., butts into conversations)
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Additional featuresAdditional features
1. Symptoms are developmentally inappropriate and persist for 6 months or longer
2. Age of onset around 3-4yrs (Palfrey et al., 1985)
3. Symptoms are exhibited in two or more settings (e.g., at school or at home)
4. Prevalence 1-7% (Hinshaw, 1994)
5. Males more likely to be affected – ratio of at least 3:1 (Szatmari et al., 1989)
Diagnostic CriteriaDiagnostic Criteria
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Diagnostic CriteriaDiagnostic Criteria
A. Inattention B. Hyperactivity / Impulsivity
AD/HD – Inattentive Type
[27 %]
AD/HD – Hyperactive Type
[18%]
AD/HD – Combined Type
[55 %]
• In Summary:
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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?
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Core Cognitive DifficultiesCore 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
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Core Cognitive Difficulties?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
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Core Cognitive Difficulties?Core Cognitive Difficulties?• Behavioural Inhibition Deficits: Tested with tasks
requiring control of actions, e.g., the Go/No-go Task:
Time
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Core Cognitive Difficulties?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!
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Core Cognitive Difficulties?Core Cognitive Difficulties?• Behavioural Inhibition Deficits: Tested with tasks requiring
control of actions, e.g., the Stop Signal Task:
Time
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Core Cognitive Difficulties?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]
StopStop!!
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• 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.
Core Cognitive Core Cognitive Difficulties?Difficulties?
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Biological evidenceBiological evidenceDifferences in sizesize of structures involved
in control of action [e.g., reviewed in Swanson et al., 1998]
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Brain StructureBrain StructureDifferences in sizesize of structures involved in
control of action: Caudate [e.g., Castellanos et al., 2003]
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Brain FunctionBrain FunctionDifferences in activityactivity for control-related
circuits [e.g., Durston et al., 2003]
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Brain FunctionBrain 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]
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Brain FunctionBrain 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]
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GeneticsGenetics
Greater frequency of “high-risk” variants of genes“high-risk” variants of genes related to functions of key neurotransmitters (dopamine) (Swanson(dopamine) (Swanson
et al., 2000):et al., 2000):
• Dopamine Transporter (DAT-1)
• Dopamine Receptor (DRD4)
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Gene – Cognition Gene – Cognition InteractionsInteractions
Cognitive Level: e.g., Differences in inhibitory skills
relate to DRD4 polymorphism [e.g., Langley et al., 2004]
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Gene – Brain InteractionsGene – Brain InteractionsBrain 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]
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There are important interactions interactions between genotype and between genotype and environmentalenvironmental 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]
Interactions - Interactions - Gene/Environment Gene/Environment
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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?
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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 depletion2.) 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
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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
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•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?
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• 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?
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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!
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How can the DV problem be solved?
• 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
• Goldberg et al. (2005) compare groups with autism, ADHD & TD on measures of inhibition, planning, mental flexibility & working memory
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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
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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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References• Aron, 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, 1465-1468.
• Barkley, R. A. (1997). Behavioral inhibition, sustained attention, and executive functions: Constructing a unifying theory of ADHD. Psychological Bulletin, 121, 65-94.
• 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, 387-392.
• 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, 1693-1695.
• 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, 678-685.
• 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, 871-878.
• 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, 279-293.
• 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, 836-854.
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References• Hinshaw, S. P. (1994). Attention deficits and hyperactivity in children. London:
Sage.• Langley, K., Marshall, L., van der Bree, M., Thomas, H., Owen, M., O’Donovan, M.,
& Thapar, A. (2004). Association of the dopamine D4 receptor gene 7-repeat allele with neuropsychological test performance of children with ADHD. American Journal of Psychiatry, 161, 133-138.
• Langley, K., & Thapar, A. (2006) COMT Gene Variant and Birth Weight Predict Early-onset Antisocial Behavior in Children with Attention Deficit Hyperactivity Disorder. Directions in Psychiatry, 26, 219-225.
• Lee, J. S., Kim, B. N., Kang, E., Lee, D. S., Kim, Y. K., Chung, J-K, Lee, M. C., & Cho, S. C. (2005). Regional Cerebral Blood Flow in Children With Attention Deficit Hyperactivity Disorder: Comparison Before and After Methylphenidate Treatment. Human Brain Mapping, 24, 157-164.
• Logan, G. D., Cowan, W. B.,& Davis, K. A. (1984). On the ability to inhibit simple and choice reaction time responses: A model and a method. Journal of Experimental Psychology: Human Perception and Performance, 10, 276-291.
• Lou, H. C., Henricksen, L., & Bruhn, P. (1984). Focal cerebral hypoperfusion in children with dysphasia and/or attention deficit disorder. Archives of Neurology, 41, 825-829.
• Ozonoff, S., & Jensen, J. (1999). Brief report: Specific executive function profiles in three neurodevelopmental disorders. Journal of Autism and Developmental Disorders, 29, 171-177.
• Ozonoff, S., Pennington, B. F., & Rogers, S. J. (1991). Executive function deficits in high-functioning autistic individuals: Relationship to theory of mind. Journal of Child Psychology and Psychiatry, 32, 1081-1105.
• Ozonoff, S., & Strayer, D. L. (1997). Inhibitory function in nonretarded children with autism. Journal of Autism and Developmental Disorders, 27, 59-77.
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References• Ozonoff, S., Strayer, D. L., McMahon, W. M., & Filloux, F. (1994). Executive function
abilities in autism: An information processing approach. Journal of Child Psychology and Psychiatry, 35, 1015-1031.
• Palfrey, J. S., Levine, M. D., Walker, D. K., & Sullivan, M. (1985). The emergence of attention deficits in early childhood: A prospective study. Journal of Developmental and Behavioral Pediatrics, 6, 339-348.
• Pennington, B. F., & Ozonoff, S. (1996). Executive functions and developmental psychopathology. Journal of Child Psychology and Psychiatry, 37, 51-87.
• Swanson, J., Castellanos, F. X., Murias, M., LaHoste, G., & Kennedy, J. (1998). Cognitive neuroscience of attention deficit hyperactivity disorder and hyperkinetic disorder. Current Opionion in Neurobiology, 8, 263-271.
• Swanson, J. M., Flodman, P., Kennedy, J., Spence, M. A., Moyzis, R., Schuck, S., Murias, M., Moriarity, J., Barr, C., Smith, M., & Posner, M. (2000). Dopamine genes and ADHD. Neuroscience and Biobehavioral Reviews, 24, 21-25.
• Szatmari, P., Offord, D. R., & Boyle, M. (1989). Correlates, associated impairments, and patterns of service utilization of children with attention deficit disorders: findings from the Ontario Child Health Study. Journal of Child Psychology and Psychiatry, 30, 205-217.
• Szatmari, P., Tuff, L., Finlayson, M. A. J., & Bartolucci, G. (1990). Asperger’s syndrome and autism: Neurocognitive aspects. Journal of the American Academy of Child and Adolescent Psychiatry, 29, 130-136.
• Weinberger, D. R. (1992). A Neural Systems Approach to the Frontal Lobes. Presented at the American Academy of Neurology, San Diego.
• Zametkin, A. J., Nordahl, T. E., Gross, M., King, A. C., Semple, W. E., Rumsey, J., Hamburger, S., & Cohen, R. (1990). Cerebral glucose metabolism in adults with hyperactivity of childhood onset. New England Journal of Medicine, 323, 1361-1366.