4. 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…………
6. ADHD ?
• A condition affecting children and adults
• Characterized by problems with:
Attention, Impulsivity Overactivity
7. 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
8. Subtypes of ADHD
Predominately Predominately Combined type
Inattentive Hyperactive-Impulsive
Attention Deficit Hyperactivity Disorder
9. 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
13. 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)
14. 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
15. 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
16. Genetics contd..
Learning of behavior
Motivation
Emotion
Working memory
Affects executive function & attention
DRD4 affect the post synaptic sensivity in the
prefrontal &frontal cortex.
20. 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)
21. 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.
22. TOOLS - THE STROOP TEST to asses attention
Black Words
Black Words
24. 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
27. 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
28. 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?
29. 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?
30. 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.
32. 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
33. Childhood ADHD: Treatment
The Triangle principle
Pharmacotherapy
Parents
School
Education
Instruction
and BT
35. How do Stimulants Act?
• Non specific in action
• Increase levels of dopamine and
norepinephrine
• Increase dopamine levels in
– PFC
– Striatum
– Nucleus accumbens
36. Stimulants – The Problem
•Abuse Potential
•Tics
•Anorexia
•Insomnia
37. Stimulants - Methylphenydate
Methyl Phenydate
Blocks NT transporter
Decrease DA & NE uptake
Increased DA in striatum &
PFC
Improves hyperactivity &
attention
38. 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)
39. 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
40. 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
41. 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
44. 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
45. 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.
46. Precautions
• Suicidal thought
• Severe liver injury
– To be discontinued in patients with jaundice or
laboratory evidence of liver injury, and should not be
restarted
47. Other agents
• TCAs (desipramine or imipramine) cardiotoxicity
• Bupropion – anti depressant activating than sedating, insomnia,
lower seizure threshold & tics
48. 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.
49. 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
Hinweis der Redaktion
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
