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THE ADHD SPECTRUM

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Title: THE ADHD SPECTRUM


1
THE ADHD SPECTRUM
The Social Brain 2 Glasgow 3-2006
Professor Hans-Christoph Steinhausen Department
of Child and Adolescent Psychiatry University of
Zurich, Switzerland
2
Definition Core symptoms
3
Classification Dimensional approach
  • ADHD...
  • … is not like tuberculosis or epilepsy
    (categorical with clear symptoms for diagnosis)
  • … is rather like hypertension or being overweight
    (dimensional with spectrum of symptoms)

One can have more or less of it the borders
blur however, its classification (ICD-10 or
DSM-IV) is categorical
4
Epidemiology
  • Prevalence rates according to criteria
  • DSM-III-R 3 - 11 per cent
  • DSM-IV 8 - 18 per cent
  • ICD-10 (?) 2 per cent

5
Aetiology / Neuroanatomy
  • Smaller brain (4) right frontal lobe (8)
  • Smaller basal ganglia (6) ? normalisation (18
    years)
  • Smaller cerebellum (12) ? more pronounced (18
    years)
  • Volumetric differences
  • manifest early (6 years)
  • correlate with ADHD severity
  • are irrespective of medication status
  • are irrespective of comorbidities

Total brain volume
ml
Age (years)
Controls gt ADHD Plt0.003
6
Aetiology / Neurophysiology
EEG based ADHD ? maturational lag
Cue P300 posterior sources
Cue P300 longitudinal
(Manova ADHD X cue/distractor plt.01, year plt.05)
  • ADHD activity remains reduced (less attention,
    van Leeuwen et al 1998)
  • younger age activity is stronger (increased
    attentional demand)

7
Aetiology / Neurochemistry
Regions rich in dopamine (DA) and noradrenaline
(NA) are consistently implicated
8
Aetiology Neuropsychology
  • ADHD involves dysfunction in a widely distributed
    neural network

9
Aetiology / Neuropsychology
Disturbance of executive functioning
  • Inhibition (motor, cognitive and emotional)
  • Planning
  • Working memory
  • Speech fluency
  • Selective and sustained attention
  • Cognitive flexibility or interference control

These findings are not specific to ADHD
10
Aetiology / Genetics
  • Twin Studies
  • Correlations and concordance rates for
    ADHD-traits and -symptoms are higher in MZ than
    in DZ.
  • Heritability estimates range from 0.39 to 0.91
  • Parental (maternal) contrast effects account for
    the low DZ correlations.

11
Aetiology / Genetics
  • Molecular Genetics
  • Associations of ADHD with variations in certain
    genes, e.g.dopamine transporter gene DAT1
    (positive and negative reports) and dopamine
    receptor genes DRD-4 and -5 (positive and
    negative reports)
  • Significant associations with ADHD but small
    effect sizes (not more than 5 per cent of the
    variance)

12
Aetiology / Genetics
  • Clinical Implications
  • ADHD is highly heritable
  • Most children with DNA variants do not have ADHD
  • Most children with ADHD do not have the known DNA
    variants
  • Further work is needed before results can be
    incorporated into clinical practice

13
Aetiology / Integrated Framework
Risk factors
Processes
Levels
Genetic disposition
Altered neuronal networks
  • Neuroanatomy
  • chemistry
  • physiology

Acquired biological factors
Altered self-regulation
Neuro- psychology
Inattention, Hyperactivity, Impulsivity
Behaviour
Adverse conditions in family/ school
Negative interactions with caregivers
Interactions
Associated disorders/ problems
Coexisting problems
Döpfner et al 2002
14
Clinical Picture Psychosocial impairments
  • Symptom domains
  • Inattention
  • Hyperactivity
  • Impulsivity
  • Functional impairments
  • Self
  • Low self-esteem
  • Accidents and injuries
  • Smoking/ substance abuse
  • Delinquency
  • School/ work
  • Academic difficulties/ underachievement
  • Employment difficulties
  • Home
  • Family stress
  • Parenting difficulties
  • Social
  • Poor peer relationships
  • Socialisation deficit
  • Relationship difficulties

Lead to
  • Psychiatric comorbidities
  • Disruptive behavioural disorders (conduct
    disorder and oppositional defiant disorder)
  • Anxiety and mood disorders

15
Comorbidity
Very frequent (more than 50)
  • Oppositional defiant or conduct disorder

Frequent (up to 50)
  • Specific learning disorders, Anxiety disorder,
    Developmental coordination disorder

Less frequent (up to 20)
  • Tic disorders, Depressive disorder

Infrequent
  • Autism spectrum disorders, Mental retardation

Over 85 of patients have at least one
comorbidity and approximately 60 of patients
have at least two comorbidities
16
Clinical Assessment
Multidimensional approach
  • Interviews with parents and child
  • Behavioural observation
  • Questionnaires and rating scales
  • Neuropsychological testing
  • Physical examination and neuromotor testing
  • Laboratory tests
  • Differential diagnosis

17
Treatment Interventions
Psychoeducation
Patient-focused
Psychopharmacotherapy
Cognitive behaviour therapy
Psychoeducation
Parent-focused
Parent training
Psychoeducation
School-focused
Behavioural interventions
18
Clinical Course Conclusion
  • ADHD is a chronic disorder, the clinical picture
    changes over the lifespan of the patient
  • Diagnostics and treatment must be adapted
    throughout the patients lifespan
  • Preschoolers - early intervention, behavioural
    methods preferred
  • Schoolchildren - combination of drug and
    behavioural therapy
  • Adolescents/adults - treatment modification
    needed (associated problems)
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