Professor Alasdair Vance Head, Academic Child Psychiatry Department of Paediatrics University of Melbourne Royal Children s Hospital
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1 Assessment and treatment of ADHD in children and adolescents In Australia: an overview Professor Alasdair Vance Head, Academic Child Psychiatry Department of Paediatrics University of Melbourne Royal Children s Hospital
2 Outline of Symposium 1. ADHD: definition, epidemiology 2. ADHD: Key biological risk factors 3. ADHD: Key psychosocial risk factors 4. A model for intervention 5. A medication approach (Australian perspective)
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4 1. ADHD: definition Diagnostic nosology-some comments: DSM-IV definition of a mental disorder- A mental disorder is conceptualized as a clinically significant behavioural pattern that occurs in an individual and is associated with impairment in one or more areas of functioning
5 1. ADHD: definition Diagnostic nosology-some comments in children and adolescentsimpairment is developmentally inappropriate, judged relative to children of the same age, gender and IQ in social, academic, occupational or other important areas of functioning multi-informant reports required
6 1. ADHD: definition Attention Deficit Hyperactivity Disorder (ADHD) DSM-IV CRITERIA -six or more symptoms, at least six months duration, maladaptive/inconsistent with developmental level -inattention dimension and/or hyperactivity-impulsivity dimension -evident in at least two settings -onset before seven years of age -impairment in social, academic, occupational functioning -symptoms not due to a PDD, Psychotic, Mood, or Anxiety Disorder
7 1. ADHD: definition TYPES of ADHD -combined type -predominantly inattentive type -predominantly hyperactive-impulsive type
8 1. ADHD: definition Key comorbid conditions: -tic disorders -oppositional defiant disorder/conduct disorder -anxiety and/or depressive disorders -language learning disorders (spelling/reading/arithmetic/writing) -speech and language disorders (articulation/grammar) -developmental coordination disorder
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10 1. ADHD: definition Common possible developmental pathways: all associated with educational, social, occupational under-achievement, alcohol/ substance abuse/dependence disorders, altered adult personality childhood adolescence adulthood ADHD-CT ADHD-IA ADHD-IA ADHD-CT Depressive d Depressive d ADHD-CT Conduct d ASPD
11 1. ADHD: epidemiology - 2%-6.3% (epidemiological samples) - 2-3: 1 (boys: girls) - social adversity status (non-specific increase) - ethnic, cultural factors (pattern same, prevalence differs)
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13 2. ADHD: Key biological risk factors d = 1.0 d =0.5 Biological risk factors Psychosocial risk factors Healthy ADHD ADHD
14 2. ADHD: Key biological risk factors Genetics: -heritability estimates 65%-90% phenotypic variance in population Studies OR -DAT1 10-repeat allele, N= DRD4 7-repeat allele, N= Taq1 polymorphism DBH, N= SNAP-25 gene N= HT1B N=3 1.44
15 2. ADHD: Key biological risk factors - Cognitive deficits in ADHD are associated with these key candidate genes: Healthy children: DAT1 3 VNTR 10-repeat allele DAT1 intron 8 VNTR 3-repeat allele R spatial inattention DAT1 3 UTR VNTR 10-repeat allele (η 2 =.07/.08/.08) - this 10/3DAT1 haplotype ADHD (OR 2.58)
16 2. ADHD: Key biological risk factors Neuroimaging -structural MRI: prefrontal cortex, basal ganglia, medial temporal and inferior parietal lobes (global 3% decrease) primarily white matter (d=.45 cf.28 gray matter) developmental trajectories independent of medication treatment
17 Total cerebral growth curves 1100 Controls > ADHD p<.003 m L Age (y) Castellanos et al., JAMA 2002 NV Males ADHD Males NV Females ADHD Females
18 2. ADHD: Key biological risk factors Neuroimaging -functional MRI: prefrontal cortex, basal ganglia, medial temporal and inferior parietal lobes bilateral task dependent decrease in activation post-puberty - midline activation - compensatory? pre-puberty - not evident
19 Silk, Vance et al, B J Psych 2005 N=14, CBCL inattention subscale T score: (10.72)
20 Region of activation BA C (mm) Z Control Group greater than ADHD-CT Group Parieto-Occipital R Precuneus R Cuneus Posterior Parietal R Inf. Parietal Frontal/Subcortical R Caudate Nucleus, Body Vance et al, Mol Psych 2007 N=24, CBCL inattention subscale T score: (9.43)
21 N=14, CBCL inattention subscale T score: (9.75)
22 2. ADHD: Key biological risk factors Cognitive neuroscience response inhibition tasks (eg STOP tasks) working memory tasks (eg n-back; VSWM tasks) deficits in both implicating PFC-striatal and PFC-striatal-parietal neural networks investigated as markers for medication response in children with ADHD
23 2. ADHD: Key biological risk factors Cognitive neuroscience working memory (Mehta et al., 2000) PET VSWM task 10 healthy adult males 2 sessions 2W apart MPD 40mg or placebo with scanning 90+ minutes later rcbf -left DLPFC, left SMA, left PPC associated with improved VSWM performance
24 2. ADHD: Key biological risk factors Cognitive neuroscience selective attention/working memory (Bush et al., 2008) fmri MSIT 21 adults ADHD RCT 6 weeks OROs-MPD or placebo damcc associated with improved performance
25 2.ADHD: Key biological risk factors Composite z-scores ADHD children in the low dose and high dose Condition (dex. 2.5mg/ 7.5mg) (Mollica et al., Human Psychopharmacology 2004)
26 2. ADHD: Key biological risk factors Summary - biological factors important - small effect: candidate genes - medium effect: candidate genes- CogNS measures; brain structural/functional changes - large effect: CogNS constructs - developmental stage-independent deficits - compensatory changes post-puberty - medication changes non-specific currently
27 3. ADHD: Key psychological risk factors Summary - parental psychopathology: alcohol/depressive/anxiety disorders - marital functioning: - family functioning: - peer group functioning: empathy/attunement/sensitivity/responsiveness flexibility/adaptiveness/regulation of affect/problem solving sociocultural context affects the character of these aspects and their detection
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34 4. A model for intervention -assessment and treatment focuses on delineation of risk factors and resilience factors-biologically (eg, executive function deficits; good arousal regulation) psychologically (eg, externalise blame; balanced critical self-reflection) and socially (eg, hostile critical interpersonal environment; confiding, nurturing consistent interpersonal environment) -monitoring of these risk and resilience factors and their response to treatment through developmental phases
35 4. A model for intervention -a practical approach [A] psychological and social treatment approach implemented for 4-6 weeks (may take 6 months of new habit formation before sustained behavioural change) key elements are the interpersonal and the intra-individual milieu interpersonal: positive reinforcement, response cost, token economy, contingency planning (turn taking, active listening, active ignoring, empathy skills, etc), making and keeping friends intra-individual: controlled breathing, muscle biofeedback, guided visual imagery
36 4. A model for intervention - a practical approach [B] key other vulnerabilities addressed vision, hearing, specific verbal and/or visuospatial learning difficulties, developmental coordination difficulties, speech and language difficulties
37 4. A model for intervention a practical approach [C] medication use to facilitate availability of the young person to learn from the psychological and social interventions through better arousal regulation better mood regulation better executive functioning
38 4. A model for intervention Summary - medication can aid a child s ability to invest in a psychosocial treatment program and learn from this program - can take 6 months of practice before new habits are formed - biological and psychosocial treatments maximize resilience and minimize risk factors through shared effects on the brain and the mind
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40 5. A medication approach (Australian perspective) - stimulant medication is the first line treatment short-acting forms: methylphenidate, dexamphetamine long-acting forms: OROS-methylphenidate, LA-methylphenidate clear and substantial evidence for methylphenidate efficacy up to a dose of 60mg daily for treatments periods of approximately 12 months methylphenidate and dexamphetamine similar efficacy and adverse effects profile although individual preferences manifest
41 5. A medication approach (Australian perspective) - Stimulant medication benefits decrease core symptoms of ADHD decrease aggression increase quality of social interactions increase compliance - Stimulant medication indications ADHD diagnosis and psychosocial interventions insufficient
42 5. A medication approach (Australian perspective) - Stimulant medication adverse effects initial insomnia, appetite suppression nervousness, restlessness, dysphoria, easy crying, agitation, depressive symptoms, stomach ache headache, dizziness, rash, motor tics, mannerisms in overdose: delirium, sweating, tremor, twitching, vomiting
43 5. A medication approach (Australian perspective) - Stimulant medication adverse effects growth retardation (MTA 3y f/u: 2cm /2.7kg ) weight loss epileptic seizures psychotic episodes abuse potential not adverse effects but careful monitoring needed in vulnerable patients
44 5. A medication approach (Australian perspective) - Atomoxetine is the second line treatment specific potent noradrenaline re-uptake inhibitor indicated when stimulant medication ineffective, associated with significant adverse effects common adverse effects: nausea, drowsiness, initial insomnia, appetite suppression
45 5. A medication approach (Australian perspective) - Imipramine is a third line treatment tricyclic compound similar to atomoxetine (a phenylpropanolamine derivative) but with less specific noradrenaline effect and significant cardiac adverse effects - Clonidine is a third line treatment central α-2 noradrenergric agonist significant effect; primarily hyperactivity/impulsiveness significant drowsiness, hypotensive and cardiac adverse effects gradual withdrawal because of rebound hypertension and tics
46 5. A medication approach (Australian perspective) - Neuroleptic medication is a third line treatment atypical neuroleptic medication: eg risperidone / aripiprazole low doses (up to risperidone 1.5mg daily equivalent) severe aggression, affective lability, PDD, ID typical neuroleptic medication: eg pericyazine - thioridazine equivalent (now withdrawn) third line treatments only used with careful monitoring and involvement in a treatment-resistant unit
47 5. A medication approach (Australian perspective) Conclusion - start low, go slow, finish slow, although ensure optimal doses are used - medication facilitates each child s ability to learn in the classroom, playground and home environment: new habits can take 6 months to evolve - Comprehensively assess and treat with approved medication and/or psychosocial treatments all comorbid conditions
48 5. We need an adequate evidence base for medication treatment, psychosocial treatment and their combination.
49 In the context of careful systematic comprehensive training
50 TRANSLATIONAL CLINICAL SCIENTISTS From laboratory bench, social/cultural factors to clinical practice
51 Tools for Translation: 2008 Genes Cells Systems Individual Social WGAS Sequencing Transgenics Epigenetics Databases Stem Cells Transcript profiles Proteomics Optical imaging Databases Electrode Arrays Zebrafish PET fmri DTI Databases Sensors Eye gaze Cognitive tools Repositories Data Sharing - Integration Web 2.0 Knowledge management
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