THE ADHD SPECTRUM

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THE ADHD SPECTRUM
The Social Brain 2Glasgow 3-2006
Professor Hans-Christoph Steinhausen Department
of Child and Adolescent Psychiatry University of
Zurich,Switzerland
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DefinitionCore symptoms
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ClassificationDimensional 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
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Epidemiology

• Prevalence rates according to criteria
• DSM-III-R 3 - 11 per cent
• DSM-IV 8 - 18 per cent
• ICD-10 (?) 2 per cent

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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
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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)

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Aetiology / Neurochemistry
Regions rich in dopamine (DA) and noradrenaline
(NA) are consistently implicated
8
AetiologyNeuropsychology

• ADHD involves dysfunction in a widely distributed
  neural network

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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
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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.

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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 genesDRD-4 and -5 (positive and
  negative reports)
• Significant associations with ADHD but small
  effect sizes (not more than 5 per cent of the
  variance)

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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

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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
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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

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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
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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

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TreatmentInterventions
Psychoeducation
Patient-focused
Psychopharmacotherapy
Cognitive behaviour therapy
Psychoeducation
Parent-focused
Parent training
Psychoeducation
School-focused
Behavioural interventions
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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)