DESCRIPTION OF ADHD AND MANAGEMENT

1. GUIDES IN ADHD
Dr Hussein Abdeldayem, MD
Head of Ped Neurology Unit, Faculty of Medicine

2. ADHD is the most commonly
neuro- behavioral disorder in childhood
ADHD: Clinical Practice Guideline…..
American Academy of Pediatric, 2011

3. Shifts in Conceptualizing ADHD Through the years:
• 1902 Defects in moral character
• 1934 Organically driven
• 1940 Minimal Brain Syndrome
• 1957 Hyperkinetic Impulse Disorder
• 1960 Minimal Brain Dysfunction (MBD)
• 1968 Hyperkinetic Reaction of Childhood (DSM II)

4. • 1980 ADD (DSM III)
- with hyperactivity - without hyperactivity
- residual type
• 1987 ADHD (only combined symptoms)
• 1994 AD/HD – 3 TYPES (DSM IV)
Combined Type ( 50-70%), Inattentive type (~30%),
Hyperactive-Impulsive Type (~10%)
•

5. The only problem was that
they could see young
children on the fields
while they studied
indoors
The ears of a boy are on
his back,
He hears only when he is
beaten.
Anonymous

6. • DSM-5: Future of Psychiatric Diagnosis
• Publication of the fifth edition of
• Diagnostic and Statistical Manual of Mental
Disorders (DSM-5)
• in May 2013

7. Updated May 1, 2012
A 06 Attention Deficit/Hyperactivity Disorder
Recommendations for severity criteria for
this disorder are forthcoming
AD/HD consists of a pattern of behavior that is present in multiple settings where it
gives rise to social, educational or work performance difficulties.
A. Either (A1) and/or (A2).
A1. Inattention
A2. Hyperactivity and Impulsivity
Six (or more) of the following symptoms have persisted for at least 6 months to a
degree that is inconsistent with developmental level and that impact directly on
social and academic/occupational activities.
A 07 Attention Deficit/Hyperactivity Disorder Not Elsewhere Classified
No severity criteria are being
recommended for this disorder at the
current time

8. ??????ADHD
Deficient Vz Disturbance
• %
• Boys > girls
• Age onset > 4 yr

9. 7% to 9%
???
• 7-9% of children and adolescents
• Adults : 4 - 5 % of adults
• All levels of socioeconomic
• All levels of IQ
Estimates of worldwide prevalence of
ADHD among school aged children vary
from 2.4–19.8%
Biol Psychiatry 2011

10. Boys >Girls ????
6 : 1 to 12 : 1 to
3:1

11. AD/HD
in school aged children
Educational disorder
7 years old age

12. onset
>4y
>2 year
2010

13. ADHD
Preschoolers
• Y Sleep problems
• S Colic
• C Constantly in motion
• C Unresponsive to requests
• U Trouble staying seated
• T Demanding of attention
• D Rapidly shift from one activity to another
• R Resist passive activities
• R Wander off alone
• W Inappropriate touching/handling objects

14. ‫‪SCHOOL AGE‬‬
‫‪ ‬سهولة التشتت بالمثيرات الخارجية‬
‫‪ ‬الحركة الساكنة‬
‫‪ ‬عدم القدرة على إتباع التعليمات‬
‫‪ ‬عدم القدرة على إنتظار الدور‬
‫‪ ‬الستجابة السريعة قبل إكتمال المهمة‬
‫‪ ‬عدم القدرة على الحتفاظ بالنتباه للمهمة‬
‫‪ ‬النتقال من مهمة إلى إخرى دون إستكمالها‬
‫‪Not time specific‬‬
‫ع3 +‬

15. ‫‪SCHOOL AGE‬‬
‫‪ ‬تكرار الخطاء‬
‫‪ ‬عدم القدرة على‬
‫المحافظة على‬
‫الدوات و النظافة‬
‫‪ ‬عدم اتباع التعليمات‬
‫‪ ‬التحدث بكثرة‬

21. AD/HD
Adolescence and Adult
15%
85%
undiagnosed
Occupational impairment, increased family
dysfunction, driving risks and SUD

22. ADHD in Adolescence
• Low self-esteem
• Bad interpersonal relationships
• SUD
• Delinquency

23. Adult ADHD
• Family
• Work
• Friends
• Accident
• Addiction
Attention-Deficit Disorder Isn't Just for Kids.
Why Adults Are Now Being Diagnosed, Too
Wall Street Journal April 2010

24. What is ADHD ?

25. What is ADHD ? EF
Impairment of Executive Function set and
development ‫المدير التنفيذى‬

26. EF
(Six aspects,
domains)
Organizing Focusing, Regulating
Prioritizing, Sustaining, Alertness,
And And Sustaining effort,
Activating Shifting attention And
To work To task Processing speed
3-
1-
2- Effort
Activation
Focus (Starting &stopping
(planning and
(persisting tasks) activity)
Organizing))

27. EF
(cont.)
Utilizing working
Monitoring
Managing frustration Memory
And
And And
Self-regulating
Modulating emotions Accessing recall
action
6-
4- 5-
Action
Emotion Memory
(Problem solving)
(managing behavior) (working memory)

28. Effects of ADHD on EF
1-response inhibition
2- planning
3- time response/set shifting
4- working memory
5- inner talk
6- emotional stability/lability
7- expectation

29. When are ADHD
impairments Noticeable?
• some: preschool
• Some : middle elementary school
• Some : college or later
Most in 1ry school

30. Executive Functions
challenges
may reveal Weakness
• EF weakness may not noticeable until
one’s self-management is challenged by
increased demands of adult life
EEG
ECG

31. Executive Functions
Development and Demands
• In early childhood, others perform all
executive functions for the child (parents,
sibs and other caretakers)
• Thereafter, the child should be able (or is
forced to) perform these functions for self
Onset before 7

32. PATHOGENESIS

33. summary
• structural and functional imaging studies
suggest that dysfunction of cingulate,
frontal, and parietal cortical regions and
imbalances in the dopaminergic and
noradrenergic systems, contribute to the
pathophysiology of ADHD

34. Imaging Studies
1. Reduction of total brain size
2. Reduction of certain brain regions
3. Decrease blood flow in the striatum
4. Structural changes in the caudate and
putamen

36. ADHD is a Chemical Problem
• Dysfunction of dopaminergic and
noradrenergic systems
• Dopamine and norepinephrine are
important in drugs that treat ADHD
In ADHD children, the rate of glucose
metabolism in basal ganglions and in the frontal cortex is reduced

37. EF networks depends 1ry
on 2 chemicals
Dopamine Norepinephrine
Not release and reload effectively
Medications : slow reuptake so longer in
contact with receptors

38. • Methyl phenydate & Atomoxetene
Mode of action:
– prevents the reuptake of norepinephrine into
the presynaptic neuron
X

39. AETIOLOGY

40. I AM A BUSY MOTHER
or
WE ARE NOT A GOOD FAMILY
or
HE IS A SPOILED BABY

41. 1

42. 1- Hereditary ADHD
Twin. adoption

43. ADHD Is highly heritable
DEPRESSION
IQ
SCHIZOPHRENIA
ADHD
HEIGHT
DBH, 5HTT, SNAP-25

44. = dopamine transporter gene (DAT1)
= dopamine receptor gene (DRD)
* D4
*D5
= serotonin transporter gene5HTT
= others: DBH, HTR1Bm SNAP-25

45. 2- Acquired Brain Injury
A. prenatal Factors:
CNS injury during Fetal Development:
- Premature babies
-Trauma/infection/complications
- Fetal exposure to drugs,
- maternal smoking and maternal alcohol
addiction

46. 2- Acquired Brain Injury (cont.)
B- CNS lesion during labour:
• Type of Delivery can have impact if sudden, or
extremely long and slow delivery
• Birth anoxia
• Weight at birth if SGA
C-. Post Birth Factors:
• Cranial bleed
• Seizures
• Concussion/coma
• Environmental : chronic Lead poison

47. Environmental factors :
• exposures to neurodevelopmental toxins
such as heavy metals and organohalide
pollutants. (lead? mercury? toxins?
-“teratogens”)
• adverse responses to food additives
• intolerances to foods (sugar ??),
• sensitivities to environmental chemicals,
molds, and fungi

48. Organochlorines and Child
Development
• Dichlorodiphenyl dichloroethylene(p,p'DDE)
measured in umbilical cord blood.
• Serum levels were negatively associated
with both mental and psychomotor
development.
• The higher the serum level, the worse the
child's development at 13 months old.

49. Recent studies suggest that causal
pathways in some cases involve
complex interactions between
genetic and environmental factors.
2009

50. Why the Explosion in ADHD?
• Less effective parenting - mother not in home, father working
more. Everyone more stressed.
• Egypt: educational curriculum and process
• Higher demands on children
• Toxins in the prenatal and early childhood environment (over
200 contaminants found in umbilical cord blood )

51. MANAGEMENT

52. Recognition
and Referral
OSHA PLAN OF
MANAGEMENT
OF ADHD CHILD*
*Modified from AAP 2011

53. Recognition
and Referral
Diagnosis
(Assessment)
1+2+3

54. • At present there is no biomedical
laboratory test for ADHD
Neuropharmacology 57 (2009) 579–589
DD 70%

55. DD for ADHD
• 1- anxiety disorders
• 2- conduct disorder
• 3- oppositional defiant disorder
• 4- impulse-control or mood disorders
• 5- learning disorders
• 6- mental retardation
• 7- gifted children
• 8- pervasive developmental disorders

56. DD for ADHD (contin.)
• 9- depression
• 10-Bipolar disorders, Schizophrenia
• 11- Drugs : PB, CZP
• 12- Misfits between the child and
school, or even the child and
•
teacher.
• • 13- substance abuse: stimulants, cocaine
phenyclidine
• 14- hyperthyroidism
• 15- BHL

57. Bipolar Disorder

58. Rule outs for the Diagnosis of
ADHD
Myth : ADHD child Can do
• Video Games
• Watch TV
• Computers
• Play Sports
• Build Leggos

59. Rule outs for the Diagnosis of
ADHD
Myth : 2-respond to medications.
• 20-30% of AD/HD children do NOT
respond
• Only 50 -55% respond academically when
medicated.
• 20-25% respond to medications (False
Positives) in no ADHD children

60. DSM-IV criteria
Criteria for ADHD Diagnosis (cont.)
1- the symptoms of ADHD must have been
present for at least 6 months before the
diagnosis can be established
2-have an onset before age 7

61. Criteria for ADHD (cont.) Diagnosis
3- Causes significant problems at least in two
different settings (home and school ) of ASE
DSN-IV criteria

62. OSHA TRIANGLE
ASSESSMENT Medical
Environment
CHILD FAMILY

63. OSHA TRIANGLE
ASSESSMENT
Medical
DD 70%
1- DSM 4
2- conner’s*
psychological Profile
Intellecual and cognitive F
Developmental/academic Skills
learning readiness and achievement
Individual, scholastic and social adjustment
(behav rating scale) Environment
Motor adjustment and coordination Teacher Q
language and speech assessment and
evaluation including academic language
CHILD FAMILY
Parental Attitude and Family adjustment

64. DSM
subtypes
60% 30% 10%
60%
COMBINED HYPERKINETIC
INATTENTIVE

65. Parental Altitude

67. OCD

68. Dyslexia

69. Dyslexia

70. anxiety

72. The Diagnosis of ADHD
NO ROLE OF
• Laboratory tests
• Brain CT/MRI

73. EEG

74. Imaging Studies
(MRI)
1. Reduction of total brain size
2. Reduction of certain brain regions – prefrontal cortex
(thin)
3. Structural changes in the caudate and putamen
4. Decrease blood flow in the striatum

75. The Diagnosis of ADHD
• Must get the story from all sides -the child, the family, the
school, and significant others.
• Careful, thorough exploration of all the issues before leaping to
conclusions.
Assessment Team

76. Recognition
and Referral
Assessment
Initiation of
treatment

77. Opinion
Agenda
Should we treat ADHD?
How do we treat ADHD?

79. Rule 2
Untreated ADHD
Parents’ consequences
• Chronic stressed or worried about child’s ADHD
• Frustration
• Blaming, guilt
• Social isolation
• Parents’ marriage has been negatively affected
• Economic burden

80. Rule 3
No “magic cure”
• There is no “quick fix”.
• No single intervention will correct the
problems for every child-need a toolbox

81. Rule 4
Treatment needs to target not
only the core symptoms but
also co-morbid and
coexisting disorders and
other psychosocial
adversities

82. Role 5
MEDICATION Parents’ Fear of
Medications for ADHD:
• Dependence
• Change personality or IQ
• Being labeled, attribution problems
• Reactions of others – teachers, peers,
family
• Use special prescription
• Cost
• Lastly: anorexia, insomnia, tics, height,
suicide

84. Medicine
Drug
OSHA Protocol of
B- treatment
Environment
Child role Family
Teacher orientation
role
Class guidance
1-Behavior modification sessions
2-Academic sessions 1- Family counseling
3- Group therapy ( ADHD DAY) 2- Group therapy

85. Family Group Therapy

86. Full Day Activity

87. MEDICATION
MEDICINE
CRITERIA FOR CHOICE
• 1- not before age 6 years
• 2- compliance
• 3- available
• 4- no other effects
• 5- specific and not
symptomatic
• 6- Results of a Pan-European Survey
ADHD impact across the day

88. Medications
Stimulants Non-stimulants
Methylphenidate
Others

89. Drugs Used For Treatment Approved by FDA
Stimulants
:
c) Methylphenidate
b) Dextro-amphetamines ( not available)

90. Forms of Methylphenidate
•
a) short acting 3-6 hrs:
Ritalin (10mg)
c) once daily :
Concerta (ER)

91. Methylphenidate (Ritalin)
action : Increases release of norepinephrine and dopamine in the
cerebral cortex to reticular activating system
• Onset: 0.5-1hr,
• Maximum: 3 hr
• duration 4-6 hr;
• metabolized by liver;
• excreted by kidneys
0.3 -0.8 mg/kg/dose
lowest dose
7days/week

92. Ritalin (methylphenidate)
• paradoxical affect to increase attention
span and calming effect.
• Dose -breakfast and lunch; increase by
0.1g/kg/ dose or by 5-10mg/dose at
weekly intervals. Max dose
2mg/kg/day or 60mg/day.

93. Concerta (ER) (18, 27, 36 and 54 mg) ( 11- 12 H)

94. Other Forms of Methylphenidate
•
a) short acting 3-6 hrs:
Focalin ( isomere of methylphenidate) (2.5, 5, 10 mg) (Out
recently)
b) intermediate acting 6-8 hrs:
SR Ritalin (Ciba 20 mg) (not recommended
Metadate ER
c) once daily ( 8+ hrs):
Metadate CD
Ritalin LA (20, 30, 40 mg) (Sprinkle)
e) recent route:
transdermal MPH (daytrana)

95. Other effects > S/E
rebound agitation or exaggeration of pre-medication symptoms as it is wearing off

96. contraindications
• Tics
• Failure to thrive
• ??? Epilepsy
• MAO inhibitors ( absolute contraindication)
• Allergy to ritalin (absolute contraindication)
• glaucoma
Precautions
Use cautiously in patients with marked anxiety, motor tics or with family
history of Tourette syndrome, or history of substance abuse.

97. Medications
Stimulants Non-stimulants
Ritalin
concerta
atomoxetine
Others

98. Drugs Used For Treatment
FDA approval
(non stimulant)
Atomoxetine
= Selective Nor-epinephrine reuptake inhibitors
Since 2002

99. Atomoxetine for ADHD
• ADHD with epilepsy
• ADHD with depression
• ADHD in ASD
• ADHD with tics

100. Atomoxetine
for ADHD
• Safe
• Single dose
• Effective
• Doses follow mg/kg dosing
• benefits tend to persist into evening &
sometimes into morning
No insomnia
Night concentration

101. Rational for a non-stimulant medication for
treatment of ADHD
1- poor response or tolerability in some patients
2- act for a maximum of 12 hrs
3- suboptimal response is not uncommon
4- relative or contraindicated for some co-morbid conditions as
tics, anxiety, substance abuse
5- some parents refuse stimulants
6- risk for abuse

102. Atomoxetine is
specific for
mechanism
treatment
Can be stopped Persist after
with still benefit no medicine

103. Atomoxetine
for ADHD
• Start: 0.5- 0.8 mg/kg/d
• Target 1.2 mg/kg/d
• Available in 10mg, 18mg, 25mg, 40mg and
60mg strengths
• Some improvements may be seen in 1 – 2
wks , full effects not until 6-8 wks

104. Atomoxetine
• Rapidly absorbed after oral intake
• Absorption unaffected by food
• Brain concentrations > plasma
concentrations
• Metabolized by P450 2D6 (neither inhibits
nor induces)
• ~ 80% of dose excreted in urine
Data on file, Ell Lilly and Company

105. Side effects of Atomoxetine
• Anorexia
• Dyspepsia
• Nausea
• Emesis
• Sedation
• Fatigue
• insomnia
• Dizziness
• Mood swings
• Growth delay??
July 2007 Dev Med Ch Neurol

106. Medications
Stimulants Non-stimulants
Ritalin atomoxetine
concerta
Others
1- buproprion
2- resperidone
3- catapres
4- ??? Benefit
- LCPUFA

107. Drugs Used For Treatment
(others)
Antidepressant
Buproprion (Wellbutrin*)
=Antidepressant (norephinephrine/dopamine reuptake inhibitor).
ADHD + ANXIETY OR DEPRESSION
*150 mg /tab

109. Other Antidepressant
Tricyclics :
imipramine, desipramine, nortriptyline
Always monitor cardiovascular side effects

110. Risperidone
)
• Action: Unclear, but may be related to
antagonism for dopamine and serotonin receptors..
• Peak plasma level in 1-2 hr,
• Hepatic metabolism
• excreted by liver
• Side effects: dry mouth, stomatitis, taste alteration (rare)
ADHD + ASD

111. Alpha2 antagonist
• antihypertensives Clonidine (catapres)
• Guanfacine

113. “Cod Liver Oil “
LCPUFA
• cod liver oil contains vitamins A and D and has a
different concentration of omega3 (EFA)
• Promotes normal bone formation, vision and
reproduction
• Promotes immunity
• Promotes appetite
• Promotes concentration amd mental function
• For : autism, ADHD/ADD