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ADHD

  1. 1. Attention Deficit Hyperactivity Disorder Dr. Santanu Ghosh, MD Assistant Professor, Psychiatry Tripura Medical College, Agartala
  2. 2. The Difficult Child…..
  3. 3. A mother brings her 8-year old son for evaluation after he is suspended from the school for jumping on his seat, teasing other children, and not following directions. He spends two to three hours a night with homework that he never successfully completes. His mother wants to know what is wrong with her child. The child is a victim of…………
  4. 4. Attention Deficit Hyperactivity Disorder
  5. 5. ADHD ? • A condition affecting children and adults • Characterized by problems with: Attention, Impulsivity Overactivity
  6. 6. ADHD Prevalence Physician office visits in 2001 9.7 L Mental health referral for children 30-50% Sex Ratio Male> Female 3-4:1 Children Prevalence : 7.5% • 40- 70% of adolescence Persists in • Up to 50% of adults
  7. 7. Subtypes of ADHD Predominately Predominately Combined type Inattentive Hyperactive-Impulsive Attention Deficit Hyperactivity Disorder
  8. 8. ClinicalADHD: Etiology Presentation Inattentiveness Difficulty sustaining Hyperactivity Impulsivity attention  Often fidgets Makes careless mistakes in Runs about/climbs Blurt s out answers school work Difficulty in obeying Difficulty awaiting turn Fails to complete task Often on the go Often interrupt others Disinterest which requires Talks excessively mental effort Forgetful, Often loses things • Impairment • Duration >6 months
  9. 9. ADHD Impact ADHD Impact Ch Academic ild ren limitations Occupational/ Relationships vocational Adults Low self Legal difficulties ADHD esteem Motor vehicle accidents Injuries Smoking and substance abuse Adolescents
  10. 10. ADHD: Etiology Etiology Neuroanatomical Neurochemical Environmental (family) Genetic ADHD origins CNS insults
  11. 11. ADHD and the Brain PET scan shows Decreased blood flow to decreased glucose prefrontal cortex and metabolism throughout Diminished arousal of pathways connecting to brain the Nervous System limbic system (caudate nucleus and striatum)
  12. 12. ADHD and the Brain ADHD and the Brain cont.. MRIs of ADHD patients show: Abnormal development in the frontal and striatal Smaller anterior regions right frontal lobe Decreased communication and processing of Significantly information between hemispheres smaller corpus callosum Immature basal ganglia Smaller caudate nucleus
  13. 13. Genetics Dopamine genes Parents with ADHD have > 50% chance of having a child with ADHD •DA type 2 gene •DA transporter gene (DAT1) About 25% of children with ADHD have parents who meet the Dopamine receptor (DRD4, formal diagnostic criteria for “repeater gene”) is over- ADHD represented in ADHD patients
  14. 14. Genetics contd.. Learning of behavior Motivation Emotion Working memory Affects executive function & attention DRD4 affect the post synaptic sensivity in the prefrontal &frontal cortex.
  15. 15. Catecholaminergic Neurotransmission Catecholaminergic Neurotransmission Relative to ADHD Relative to ADHD Dopamine Norepinephrine • Striatal-prefrontal • Prefrontal • Enhances signal • Dampens noises • Improves attention - Distractibility - Focus - Shifting - Vigilance • Executive operations - Acquisition • Increases inhibition - On task behavior - Behavioral - On task cognitive - Cognitive - perception - Motoric Solanto.Stimulant Drugs & ADHD. Oxford; 2001
  16. 16. Dopamine in the Brain
  17. 17. Other Causes Brain insults such as injury to frontal Environmental factors like Brain insults such as injury to frontal region, premature birth, Injury complications during pregnancy, low social class Pb Zn Sub clinical lead exposure: Serum Zinc- low levels in hyper inattention, antisocial actives behavior, Hyperactivity (Bellinger 2004)
  18. 18. Assessment & Diagnosis  A good clinical history A thorough developmental history  Toddlers may be unable to be seated  Pre school & school children may be hyperactive, naughty  Older children are more inattentive.
  19. 19. TOOLS - THE STROOP TEST to asses attention Black Words Black Words
  20. 20. The Coloured words
  21. 21. ADHD - Rating Scale Prognosis of ADHD Conner’s Home School Teachers Version Version Rating Scale • Contains a set of • Contains a set of • Aged 3-17 years 18 questions 18 questions • Addressing • Contains 28 or 39 • Addressing attention questions learning abilities, attention and • Addresses organizing behavior Conduct problem, abilities, hyperactivity, behavior and inattentive-passive, memory and hyperactivity
  22. 22. Differential Diagnosis Anxiety Conduct disorder Opposition Disorder Depression Defiant Disorder
  23. 23. Comorbidities: ADHD 49% 11% 7% Depression 11% Conduct Disorder Anxiety
  24. 24. Prognosis of ADHD With a combination of medication and If not properly psychosocial and treated individuals behavioral across age-span are interventions most at risk children’s With increasing age symptoms are •Hyperactivity decreases ameliorated •Inattention, impulsivity, 80% of affected children disorganization & symptoms of ADHD relationship difficulties persist into adolescence persist and adulthood Nelson’s Textbook of Pediatrics, 17th Ed p 109-110
  25. 25. Understanding Adult ADHD Do you have difficulty concentrating or focusing your attention on one thing? Do you often start multiple projects at the same time, but rarely finish them? Do you have trouble with organization?  Do you procrastinate on projects that take a lot of attention to detail?
  26. 26. Understanding Adult ADHD contd..  Do you have problems remembering appointments or obligations?  Do you have trouble staying seated during meetings or other activities?  Are you restless or fidgety?  Do you often lose or misplace things?
  27. 27. Treatment Goals • A child-specific, individualized treatment program should be developed for children • A goal of maximizing function to – improve relationships and performance at school, – decrease disruptive behaviors, – promote safety, – increase independence and – improve self esteem.
  28. 28. Treatment Options Medication Behavioral Therapy Psychotherapy Educational Techniques
  29. 29. Treatment Options • Medications are the first line of choice for ADHD management – Help treating the core symptoms of ADHD • Psychotherapy and behavioral therapies – Effective in management of co morbid disorders with ADHD
  30. 30. Childhood ADHD: Treatment The Triangle principle Pharmacotherapy Parents School Education Instruction and BT
  31. 31. Medications • Stimulants – Methylphenidate & derivatives – Amphetamine & derivatives • Non – Stimulants – Antidepressants – Antipsychotics – Atomoxetine
  32. 32. How do Stimulants Act? • Non specific in action • Increase levels of dopamine and norepinephrine • Increase dopamine levels in – PFC – Striatum – Nucleus accumbens
  33. 33. Stimulants – The Problem •Abuse Potential •Tics •Anorexia •Insomnia
  34. 34. Stimulants - Methylphenydate Methyl Phenydate Blocks NT transporter Decrease DA & NE uptake Increased DA in striatum & PFC Improves hyperactivity & attention
  35. 35. Atomoxetine • Initially developed as an antidepressant however found more effective in ADHD • Initially called as Tamoxetine but name changed to atomoxetine to avoid confusion with tamoxifen (for advanced breast cancer)
  36. 36. Mode of Action of Atomoxetine • Selective NE reuptake inhibitor • Inhibits NE/DA re uptake in PFC (NET>DAT) – DA taken up by NET in PFC • Increase in extra-cellular NE (not DA) in subcortex (nucleus accumbens/striatum) • But no increase in DA in sub-cortex & hence no tics/abuse
  37. 37. Mode of Action (cont’d…) • A highly selective and a potent inhibitor of presynaptic NE transporter • Increases extracellular concentrations of DA 3 fold in prefrontal cortex • Does not alter DA concentrations in striatum and nucleus accumbens – No motoric or abuse potential • Increases levels of catecholamines in PFC Bymaster FP, et al, Neuropsychopharmacology, 2002, 27(5), 699 - 711
  38. 38. Action on Dopamine • In PFC Dopamine moves with the aid of NE transporter • Lack of dopamine transporters in PFC • Atomoxetine blocks NE transporter and increases DA in synaptic cleft
  39. 39. Atomoxetine Release acetylcholine Release acetylcholine Improves attention ,cognition Improves attention ,cognition Dosage-0.5mg/kg-1.2mg/kg Dosage-0.5mg/kg-1.2mg/kg No abuse potential
  40. 40. PRE-FRONTAL CORTEX /DA /DA Atemoxetine Post- Post-
  41. 41. Indications • FDA approved in November 2002 for treatment of ADHD • The first non stimulant drug for ADHD after debut of methylphenidate for about 40 years
  42. 42. Recent Warnings • Atomoxetine increased the risk of suicidal ideation in short-term studies in children or adolescents with Attention Deficit/Hyperactivity Disorder (ADHD). • Patients started on therapy should be monitored closely for suicidal thinking and behavior.
  43. 43. Precautions • Suicidal thought • Severe liver injury – To be discontinued in patients with jaundice or laboratory evidence of liver injury, and should not be restarted
  44. 44. Other agents • TCAs (desipramine or imipramine) cardiotoxicity • Bupropion – anti depressant activating than sedating, insomnia, lower seizure threshold & tics
  45. 45. NON PHARMACOLOGICAL TREATMENT Parent behavior management training •Parenting skills training to implement BT programme at home •Contingency programme •Positive reinforcement •Time out •To ignore negative behavior Social skills training •Aim is to develop social relationship •Waiting for turn, sharing toys ,asking for help.
  46. 46. Non pharmacological treatment CBT - Cognitive Behavior Therapy  helpful in adolescents, they recognizes social cues, determines action in situations Other behavioral  Daily activity scheduling Training teachers / school

Editor's Notes

  • ADHD is most likely caused by a complex interplay of factors Biologic factors that predispose an individual for ADHD include post-traumatic or infectious encephalopathy, lead poisoning, and fetal alcohol syndrome Environmental influences include abuse or neglect, family adversity, and situational stress Emerging literature provides support for the hypothesis that abnormalities in frontal networks or frontal-striatal dysfunction and catecholamine dysregulation are involved Family and twin studies reveal compelling data regarding the genetic origin of ADHD; and recent advances in neuroimaging techniques have promoted closer study of neuroanatomic correlates
  • ADHD is most likely caused by a complex interplay of factors Biologic factors that predispose an individual for ADHD include post-traumatic or infectious encephalopathy, lead poisoning, and fetal alcohol syndrome Environmental influences include abuse or neglect, family adversity, and situational stress Emerging literature provides support for the hypothesis that abnormalities in frontal networks or frontal-striatal dysfunction and catecholamine dysregulation are involved Family and twin studies reveal compelling data regarding the genetic origin of ADHD; and recent advances in neuroimaging techniques have promoted closer study of neuroanatomic correlates
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