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1 ADHD: AN OVERVIEW A/Professor Alasdair Vance Head, Academic Child Psychiatry Department of Paediatrics University of Melbourne Telephone: Facsimile:

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5 Attention Deficit Hyperactivity Disorder (ADHD) DSM-IV CRITERIA -six or more symptoms, at least six months, maladaptive/inconsistent with developmental level -inattention dimension and/or hyperactivity-impulsivity dimension -evident at least two settings -onset before seven years of age -impairment social, academic, occupational functioning -symptoms not due to a PDD, Psychotic, Mood, or Anxiety Disorder

6 TYPES of ADHD -combined type -predominantly inattentive type -predominantly hyperactive-impulsive type COMORBIDITY of ADHD -language-based Learning Disorders -Oppositional-Defiant or Conduct Disorders -anxiety and depressive symptoms and/or Disorders

7 HISTORICAL CONTEXT-biological factors -Clouston (1899): undue brain reactiveness to mental and emotional stimuli -Still (1902): defect of moral control due to a delay in the brain s development -Tredgold (1908): inherited brain defectneuropathic diathesis -Bradley (1937): benzedrine-improved behaviour and school performance

8 AETIOLOGY-biological factors GENETIC STUDIES: -twin studies; family studies; adoption studies -genetic differences appear to account for 30%-50% of the inter-individual variations in trait measures of childhood hyperactivity and inattentiveness NEUROIMAGING STUDIES: -MRI: Hynd et al. (1993); reversal of L>R pattern of asymmetry in the region of the head of the caudate nucleus -PET: Lou et al.(1989);hypoperfusion in the frontal lobes corrected with short-term psychostimulant medication

9 AETIOLOGY-biological factors (continued) NEUROPSYCHOLOGICAL STUDIES: -Douglas et al. (1983): poor performance on the Continuous Performance Task (CPT) as evidence of a deficit in sustained attention (NB; controversy over rate of performance decline over time in hyperactive children relative to controls) -Kempton et al (1999): children with ADHD have a worse performance on pencil and paper and computerised, verbal and non-verbal tests of executive function - definition of executive function : describes the complex cognitive processes enabling optimisation of performance in situations where multiple cognitive processes are required (Baddeley, 1986)

10 AETIOLOGY-other proposed miscellaneous factors -food additives: Feingold (1975)-synthetic colourings, flavourings, preservatives and naturally occurring salicylates in fruits -psychosocial factors: parental mental health including substance abuse; parenting style; family systemic factors such as triangulation and scapegoating -controlled clinical trials confounded by logistic and methodological difficulties vulnerability and risk dimensional model: an appropriate means of understanding aetiological dimensions in children with ADHD

11 NATURAL HISTORY: poor prognosis in the following areas: -parental and family relationships -school peer relationships and teacher relationships -wider social relationships -educational achievement -occupational achievement -anti-social personality disorder, anxiety and depressive disorders, polysubstance abuse/dependence disorders

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14 BIOLOGICAL TREATMENT GENERAL PRINCIPLES OF BIOLOGICAL TREATMENT: -biological vulnerability and environmental risk factors vary according to critical developmental periods that need to be determined at an individual as well as at a group level -the determination of the goals of biological treatment involves behavioural symptoms, including core and non-core features of ADHD, along with comorbid symptoms. These need to be assessed carefully at an individual level before biological treatment is commenced

15 BIOLOGICAL TREATMENT (continued) GENERAL PRINCIPLES OF BIOLOGICAL TREATMENT (continued): -cognitive measures, such as measures of executive functioning (for example non-verbal working memory), are needed as well as behavioural measures. These two forms of assessing biological treatment effectiveness may be dissonant Three primary biological treatments used in the management of primary school-aged children with ADHD: -Psychostimulant medication -Clonidine -Tricyclic antidepressants

16 PSYCHOSTIMULANT MEDICATION -Dexamphetamine and Methylphenidate (Ritalin) -catecholaminergic medication that leads to alterations in the function of the dopaminergic and noradranergic neurotransmitter systems in the prefrontal cortical regions of the brain -clinical effect evident within approximately one hour and lasts approximately three to four hours in most primary school-aged children -similar half-life, and, benefits and side-effects profiles, although there is debate about anecdotal and published reports of differences in all of these areas (Efron et al., 1997)

17 PSYCHOSTIMULANT MEDICATION (continued) BENEFITS -replicated short-term (3-6 weeks duration) reduction in the core symptom domains of ADHD; unclear benefits on the non-core and comorbid symptoms that occur frequently -replicated short-term (3-6 weeks duration) improvement in the pencil and paper and computerised tasks of the executive functions -replicated short-term (3-6 weeks duration) improvement in the general non-specific construct of academic achievement -a similar replicated short-term (3-6 weeks duration) improvement in the general non-specific construct of social interaction

18 PSYCHOSTIMULANT MEDICATION (continued) BENEFITS (continued) -debated intermediate to long-term (greater than 3 months duration) effects on both the core and the noncore symptoms of ADHD and the associated comorbid symptoms -replicated better performance on the tasks of the executive functions in the intermediate to long-term (greater than 3 months duration) (Kempton et al, 1999) -unclear effects of intermediate to long-term (greater than 3 months duration) psychostimulant medication on the general non-specific construct of academic achievement

19 PSYCHOSTIMULANT MEDICATION (continued) BENEFITS (continued) - unclear effects of intermediate to long-term (greater than 3 months duration) psychostimulant medication on the general non-specific construct of social interaction SIDE-EFFECTS Short-term -physiological effects related to the activation of the noradranergic neurotransmitter systems; initial and middle insomnia, loss of appetite, stomach-aches, headaches, dizziness and daytime drowsiness

20 PSYCHOSTIMULANT MEDICATION (continued) SIDE-EFFECTS (continued) -affective symptoms; social withdrawal, sudden crying, sudden severe sadness, dysphoria, mood lability and aggressive outbursts Intermediate to long-term -concern about growth problems and/or tolerance related to psychological +/- physiological dependence -physiological side-effects (as above); immediate onset -affective side-effects; can have a delayed onset

21 PSYCHOSTIMULANT MEDICATION (continued) DILEMMAS -age effects; usefulness?; dosage -weight effects -diagnostic subtype effects -behavioural and/or cognitive measures of response

22 CLONIDINE -presynaptic α 2-receptor agonist that leads to a decreased level of functional activity of the noradranergic neurotransmitter system in the central nervous system -clinical effect that commences after approximately one to two hours and lasts from six to twelve hours -half-life from twelve to twenty hours, although this varies greatly between individuals and within the same individual at critical developmental periods BENEFITS -hyperactivity, impulsiveness and the frequency and severity of aggressive outbursts are the primary benefits, although there is a paucity of controlled clinical trials

23 CLONIDINE (continued) BENEFITS (continued) -inattention does not appear to be readily improved, although there is no controlled trial data to adequately address this issue -initial insomnia associated with psychostimulant medication use has been treated with Clonidine SIDE-EFFECTS -over-sedation and postural hypotensive symptoms have been reported if higher doses of Clonidine (greater than 100mcg) have been used -Swanson et al. (1995) reported four sudden deaths in twenty three children with ADHD treated with concurrent methylphenidate and Clonidine

24 CLONIDINE (continued) DILEMMAS -clarification of its role in the management of ADHD TRICYCLIC ANTIDEPRESSANTS -wide range of pharmacological action including blockade of adrenergic, serotoninergic, cholinergic, and histaminergic receptor systems; primary action is thought to relate to its inhibition of noradrenaline reuptake and serotonin reuptake -clinical effects are not apparent for four to six weeks -half-life of approximately twenty hours

25 TRICYCLIC ANTIDEPRESSANTS (continued) BENEFITS -decreased level of activity and impulsiveness -performance on cognitive tasks does not appear to be aided -anxiolytic and mood-stabilising effects SIDE-EFFECTS -anti-cholinergic side-effects (for example, dry mouth) -anti-histaminergic side-effects (for example, sedation) -anti-adrenergic side-effects (for example, postural hypotensive symptoms) -conduction defects (for example, prolonged QT interval on an Electrocardiogram-ECG)

26 TRICYCLIC ANTIDEPRESSANTS (continued) DILEMMAS -clarification of role(s) in the management of ADHD -use of blood levels to guide its use in the management of ADHD -safety when used alone or in combination with other agents; Werry et al. (1995) published a series of four sudden deaths in young people using desipramine in 1988

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28 Conclusion -ADHD is a heterogeneous condition -ADHD has an unknown aetiology -ADHD is clinically best conceptualised as a series of developmental vulnerabilities in biological, psychological, social and cultural domains -ADHD treatment always involves psychological interventions at an individual and/or a group level with psychostimulant medication and/or other medication interventions facilitating the availability of the child to learn, remember and recall information in a number of domains