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Classification

Classification. DSM-IV Attention Deficit Hyperactivity Disorder (ADHD) is subclassified 1. Inattention 2. Overactivity/impulsivity 3. Combined Permits comorbidity ICD-10 Hyperkinetic Disorder Does not subclassify Insists on presence of both Inattention and Hyperactivity

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Classification

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  1. Classification DSM-IV Attention Deficit Hyperactivity Disorder (ADHD) is subclassified 1. Inattention 2. Overactivity/impulsivity 3. Combined Permits comorbidity ICD-10 Hyperkinetic Disorder Does not subclassify Insists on presence of both Inattention and Hyperactivity Does not permit comorbidity Difference in classification influences prevalence figures

  2. Epidemiology Prevalence of ADHD in children Community surveys American 2% (Costello et al, 1988) 6% (Anderson et al, 1987) Puerto Rico 9% (Bird et al, 1988) British 0.5 to 1% ‘Hyperkinetic Disorder (F90) (Taylor et al, 1991) Male to female ratio 2:1 - 3:1

  3. ‘ In later years this syndrome tends to wane spontaneously and disappear. We have not seen it persist in those patients we have followed to adult life.’ Laufer & Denhoff (1957) Confirmed in DSM-II (1968)

  4. New York Cohorts

  5. Co-morbidity 1.The influence of ADHD persistence In cohort 1 subjects with persistent ADHD symptoms were twice as likely to have APD and 4 times as likely to have SA than those without. 2. APD and SA In cohort 1 subjects with APD were 3 times as likely to have SA than subjects without APD. 3. No increased association between ADHD and affective disorders.

  6. Consequences of ADHD

  7. Strengths/Limitations • Strengths • Size • Blind assessment • Replicatory cohort • CD ‘virtually absent’ • Low drop out • Limitations • Clinically referred • White, male, middle class • Dependent on self-report

  8. Summary 1. ADHD persists into adult life but there is a sharp decline between late adolescence and mid 20s 2. There is co-morbidity for APD and SA and each is dependent on persistence of ADHD 3. Educational and occupational opportunities are reduced 4. Criminality is increased in adult ADHD and is associated with APD. It is also predicted by childhood CD and HI.

  9. Adult ADHD Clinical Studies Two principal sources 1. ‘Graduates’ diagnosed in childhood, followed into adult life 2. Adults presenting with ADHD features for the first time Similarities: 1. Cardinal ADHD features 2. Co-morbidity with APD and SA Differences: Adult presentation group are 1. Older - average age 36-40 2. Minimal gender difference 3. Co-morbidity with affective disorders

  10. Prevalence 1. Prospective longitudinal cohorts • These provide no direct evidence of prevalence but indicate rate of attrition • If childhood prevalence is 5-10% and • Cohort diagnosis falls to 5-10% at 25 years • ADHD prevalence at 25 years = 0.25-1%

  11. Community Based StudiesMethod : Self-report (DSM-IV criteria)

  12. Both studies produce: 1. Prevalence figures 4-5 times higher than longitudinal studies 2. Unexpected predominance of HI type

  13. Assessment Preliminary postal screening Rating Scales : Childhood ADHD behaviour 1. Connors Global Index Threshold Score 15 2. Wender-Utah Threshold Score 48 3. Barkley Scale

  14. Assessment Principles • ADHD is a developmental disorder of childhood; even when it is assessed for the first time in adulthood, a history of childhood ADHD behaviour is essential for diagnosis • A parental history should always be sought • Assessment in an adult, compared with a child, is unavoidably more limited • ADHD features are better viewed in dimensional than in categorical terms • ADHD is a developmental disorder: its features are continuous rather than episodic

  15. Assessment 1. Structured psychiatric interview Family history Personal, developmental, educational, occupational, and social history Current ADHD symptoms Comorbid symptoms 2. Current symptoms using self-report and informant-report measures Adult Barkley Current Behavioural Scale Connors Global Index Hospital Anxiety and Depression Scale DSM-IV ADHD Criteria

  16. DSM-IV Diagnostic Criteria A: 1) At least 6 out of 9 items concerning inattention strongly endorsed A: 2) At least 6 out of 6 items concerning hyperactivity and 3 items concerning impulsivity strongly endorsed B: Hyperactive/impulsive or inattentive symptoms that caused impairment were present before age 7 years C: Some impairment from the symptoms is present in two or more settings (e.g. at school [or work] and at home). D: There must be clear evidence of clinically significant impairment in social, academic, or occupational functioning E: The symptoms do not occur exclusively during the course of a Pervasive Developmental Disorder, Schizophrenia or other Psychotic Disorder and are not better accounted for by another mental disorder (e.g. Mood Disorder, Anxiety Disorder, Dissociative Disorder, or a Personality Disorder)

  17. Barkley Scale Item 1: Failed to give close attention to details or made careless mistakes in their work Item 2: Fidgeted with hands or feet or squirmed Item 3: Interrupted or intruded on others

  18. Limitations of Barkley Scale 1. Self-report. Positive response self evident 2. Response set. Positive responses are all in the affirmative. 3. The wording still reflects the initial development of the scale for use with children 4. Does not take sufficient account of adult symptomatology

  19. Clinical Psychology Assessment 1. General Intellectual Functioning • Wechsler Abbreviated Scale of Intelligence 2. Attention a. Selective - ‘Telephone Search’ b. Divided - ‘Telephone Search While Counting’ c. Switching - ‘Visual Elevator’ d. Sustained - Continuous Performance Test 3. Impulsivity • Matching Familiar Figures 4. Executive Function • BADS

  20. Van der Linden et al (2000) First Cohort Study: Demography First 96 consecutive referrals to clinic. Gender: 69 males : 27 females Ethnicity: 1 A-C 4 Asians remainder caucasian Mean age: 27.4 (10.3) Education: 25% to A level/university 40% unemployed 64% single 47% lived with parents

  21. First Cohort Study: Diagnoses 30 (31%) met DSM4 criteria for ADHD. 66 (69%) did not.

  22. First Cohort Study: ADHD vs non-ADHD ADHD non ADHD Age 22.4 (7.0) 29.4 (10.6) Gender M 26 (87%) 43 (65%) p<0.001 F 4 (13%) 23 (35%) p<0.030 Drug abuse 62% 31% p<0.013 Personality Disorder 58% 29% p<0.020 Developmental relatively delayed Milestones

  23. Illicit substance abuse in previous 3 monthsADHD non ADHD n=29 n=54 (missing=1) (missing=12)Cannabis *(1) 18 (62%) 16 (3)%)Amphetamines 4 (14%) 4 (7%)Opiates 1 ((3%) 0 (0%)Cocaine 5 (17%) 3 (6%)Benzodiazepines 1 (3%) 1 (2%)Ecstasy *(2) 4 (14%) 0 (0%)Other 3 (10%) 1 (2%)Any regular illicit drug use *(3) 18 (62%) 17(31%)*(1) chi square: 8.21, df=1, p=0.004; *(2) chi square: 7.96, df=1, p=0.005;*(3) chi square: 6.17, df=1, p=0.013.

  24. ICD-10 personality disorder ADHD non ADHD n=26 n=38 (missing=4) (missing=28) Paranoid 3 (12%) 1 (3%) Schizoid 0 (0%) 1 (3%) Dissocial *(1) 10 (38%) 4 (11%) Impulsive *(2) 11 (42%) 6 (16%) Borderline 2 (8%) 0 (0%) Histrionic 1 (4%) 1 (3%) Anankastic 0 (0%) 2 (5%) Anxious 3 (12%) 3 (8%) Dependent 0 (0%) 1 (3%) Any personality disorder *(3) 15 (58%) 11 (29%) *(1) chi square=7.05 df=1 p=0.008; *(2) chi square=5.57 df=1 p=0.018; *(3) chi square=5.29df=1 p=0.020

  25. Developmental milestones ADHDnon ADHD n=22 n=46 (missing=8) (missing=20) Sitting early 1 (5%) 0 (0%) late 3 (14%) 1 (2%) Crawling early 1 (5%) 0 (0%) late 3 (14%) 1 (2%) Walking early 1 (5%) 0 (0%) late *(1) 6 (27%) 3 (7%) Talking early 1 (5%) 2 (4%) late *(2) 8 (36%) 4 (9%) *(1) chi square=4.81 df=1 p=0.028; *(2) chi square=6.97 df=1 p=0.008

  26. Attitude to ADHD Referral initiation % by the patient 46 by the family 44 by GP/specialist 10 Reaction to diagnosis pleased not pleased neutral ADHD diagnosed 77% 0 23% ADHD not diagnosed 8% 58% 30%

  27. Diagnostic rates

  28. Diagnostic statusfirst 203 patients vs recent 96 patients

  29. Gender ratios

  30. ADHD Subtypes

  31. Diagnoses by gender

  32. Referral sources

  33. ADHD is essentially the same disorder in adults as in children, though overactivity is less prominent, and the comorbidity with conduct disorder and ODD is replaced by a comorbidity with antisocial PD and substance abuse Effective treatment is essentially the same. Pharmacotherapy, especially cerebral stimulants (CS) is the mainstay

  34. The Cerebral Stimulants (CS) • A group of drugs that act to increase intrasynaptic DA/NA. Their actions are complex and at different concentrations they may either inhibit or augment monoaminergic (DA/NA) activity • Reasons for beneficial CS effect in ADHD • The disturbance of neuro-transmitter function that underlies ADHD is still poorly understood, but probably involves monoaminergic dysfunction, especially DA, but also probably NA and serotonin. Increased DA activity is likely and the effect of CS is to diminish this

  35. CS: Efficacy (1) Nine studies comprising total of 292 subjects Methylphenidate 6 studies Pemoline 2 studies Amphetamine (adderal) 1 study Response rate varies 25-73% - mean 60% cf children 6-12 years 60-70% Adolescence 75%

  36. CS: Efficacy (2) Reasons for reduced efficacy in adults 1) Lack of consistent diagnostic criteria in adults 2) Inadequate dosage 3) Presence of comorbidity 4) Poorly developed outcome measures Inadequate dosage especially important Earlier studies average dose 0.6 mgm/Kgm - response 50% Later study (Spencer et al, 1995) 1.0/Kgm - response 78%

  37. CS Indications First choice drug treatment of ADHD at any age Adults who 1) Meet criteria for DSM-IV 2) Fail to meet criteria for DSM-IV but meet criteria for childhood onset illness and remain symptomatic

  38. CS Contraindications In adults there are few absolute contraindications 1. Substance abuse - unstudied Antisocial personality disorders - unstudied 2. PH or present psychosis Drug induced psychosis very unlikely 3. Childhood problems eg. Tics, growth delay, less important

  39. The Principal CS Drugs Methyl Phenidate Short acting forms : Ritalin (10mgm tab) Equasym (5 mgm tab) Sustained release : Concerta Dexamphetamine Dexadrine Pemoline Not recommended Also available elsewhere: Adderal, a combination of D/L amphetamine

  40. Side Effects CS drugs well tolerated in adults In order of frequency: Insomnia, Edginess, Diminished appetite, Dysphoria, Headache Most prominent after introduction of drug or increase in dosage. Should remit spontaneously over time. If not - drug reduction or add TCA Reported in children but not in adults: Psychosis, substance abuse Effect on BP/HR minimal

  41. Methyl Phenidate (Ritalin) Short acting forms (Equasym, Ritalin) • Tablets strength 5-10-20 mgm • Peak plasma Conc 1-2 hours post - ingestion • Elimination half-life 3-6 hours • Peak behavioural effects Half-hour - 2-6 hours • Daily dose range 0.3-2.0 mgm/Kgm Sustained release form (Concerta) • Tablets strength 18 mgm • Duration of action 10-14 hours No correlation between serum levels and clinical efficacy and /or toxicity

  42. Other pharmacological treatments Tricyclic antidepressants May be used in combination with CS in presence of 1) Depressive comorbidity 2) Side-effects, especially initial insomnia, weight loss Tertiary, e.g. Desipramine, TCA’s superior to secondary TCA’s Only two controlled trials conducted : Desipramine vs placebo Tomoxetine (NA receptor inhibitor) vs placebo Both shown to be effective TCA’s more effective against behavioural and cognitive dysfunction

  43. Atomoxetine A noradrenergic receptor inhibitor • Starting dose 40mgm, to increase to 80 mgm after one month • Maximum dose 100 mgm • Side effects: nausea, vomiting, abdominal pain, appetite loss, weight loss • Significant therapeutic effect in placebo controlled trials

  44. Other pharmacological treatments • MAOIs • Alpha 2 agonists e.g. clonidine • Beta blockers • Venlafaxine • No controlled trials in adults • Neuroleptics - best avoided

  45. Management 1. Methyl phenidate or dexamphetamine 2. Small initial dose to minimise side-effects 3. Dose schedule : morning, midday, (late afternoon) 4. Small incremental increases over short intervals 5. Total daily dose: relationship to weight 6. Management of side-effects 7. Drug holidays, withdrawal 8. Sensitivity/tolerance 9. Drug level. Relationship with clinical effects/side-effects 10. Long acting preparation

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