2. INTRODUCTION :
¶ ADHD is the most common neurobehavioral disorder
of childhood, among the most prevalent chronic
health conditions affecting school-aged children, and
the most extensively studied mental disorder of
childhood.
¶ ADHD is characterized by inattention, including
increased distractibility and difficulty sustaining
attention; poor impulse control and decreased self-
inhibitory capacity; and motor over activity and
motor restlessness.
3. ¶ Affected children commonly experience
academic underachievement,
problems with interpersonal relationships with
family members and peers.
low self-esteem.
¶ ADHD often co-occurs with other emotional,
behavioral, language, and learning disorders
4. EPIDEMIOLOGY:
Studies of the prevalence of ADHD across the
globe have generally reported that 9% of school-
age children are affected, although rates vary
considerably by country.
The prevalence rate in adolescent samples is 2-6%.
5. HISTORY OF ADHD:
Mid-1800s: Minimal Brain Damage
Mid 1900s: Minimal Brain Dysfunction
1960s: Hyperkinesia
1980: Attention-Deficit Disorder
With or Without Hyperactivity
1987: Attention Deficit Hyperactivity Disorder
1994 (DSM IV): ADHD
Primarily Inattentive
Primarily Hyperactive
Combined Type
6. Diagnosing ADHD: DSM-V
Inattention:
(A1)
Lacks attention to detail; makes
careless mistakes.
has difficulty sustaining attention
doesn’t seem to listen.
fails to follow through/fails to
finish instructions or schoolwork.
has difficulty organizing tasks.
avoids tasks requiring mental
effort.
often loses items necessary for
completing a task.
easily distracted.
is forgetful in daily activities.
Persisted for at
least 6 months to a
degree that is
inconsistent with
developmental
level and that
negatively impacts
directly on social
and
academic/occupati
onal activities
7. Diagnosing ADHD: DSM-V
Hyperactivity/
Impulsivity:(A2)
Fidgets or squirms excessively
leaves seat when inappropriate
runs about/climbs extensively
when inappropriate
has difficulty playing quietly
often “on the go” or “driven by a
motor”
talks excessively
blurts out answers before question
is finished
cannot await turn
interrupts or intrudes on others
Persisted for at least
6 months to a
degree that is
inconsistent with
developmental level
and that negatively
impacts directly on
social and
academic/occupatio
nal activities
8. B. Several inattentive or hyperactive-impulsive
symptoms were present prior to age 12 years.
C. Several inattentive or hyperactive-impulsive
symptoms are present in two or more settings.
D. There must be clear evidence of clinically significant
impairment in social, academic, or occupational
functioning.
E. 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, personality disorder).
Diagnosing ADHD: DSM-V
9. Specify whether:
• Combined presentation: If both Criterion A1
(inattention) and Criterion A2 (hyperactivity-
impulsivity) are met for the past 6 months.
• Predominantly inattentive presentation: If Criterion
A1 (inattention) is met but Criterion A2
(hyperactivity-impulsivity) is not met for the past 6
months.
• Predominantly hyperactive/impulsive presentation:
If Criterion A2 (hyperactivity-impulsivity) is met and
Criterion A1 (inattention) is not met for the past 6
months.
Diagnosing ADHD: DSM-V
10. Specify if:
• In partial remission: When full criteria were
previously met, fewer than the full criteria have been
met for the past 6 months, and the symptoms still
result in impairment in social, academic, or
occupational functioning.
Diagnosing ADHD: DSM-V
11. Specify current severity:
• Mild: Few, if any, symptoms in excess of those
required to make the diagnosis are present, and
symptoms result in no more than minor impairments in
social or occupational functioning.
• Moderate: Symptoms or functional impairment
between “mild” and “severe” are present.
• Severe: Many symptoms in excess of those required
to make the diagnosis, or several symptoms that are
particularly severe, are present, or the symptoms result
in marked impairment in social or occupational
functioning
NOTE: . For older adolescents and adults (age 17 and older), at
least five symptoms of A1 or A2 are required.
Diagnosing ADHD: DSM-V
12. ETIOLOGY :
• No single factor determines the expression of ADHD;
• Mothers of children with ADHD are more likely to
experience birth complications, such as toxaemia,
lengthy labour, and complicated delivery.
• Maternal smoking and alcohol use during pregnancy
and prenatal or postnatal exposure to lead are
commonly linked the development of ADHD.
• There is a strong genetic component to ADHD.
[dopamine transporter gene (DAT1) and a particular
form of the dopamine 4 receptor gene (DRD4)].
There are some other genes that might contribute to
ADHD.
13. ETIOLOGY : (CONT.)
• Severe traumatic brain injury with subsequent onset
of substantial symptoms of impulsivity and
inattention are reported in some children.
• Structural or functional abnormalities have been
identified in children with ADHD without pre-existing
identifiable brain injury.
These include dysregulation of the frontal
subcortical circuits, small cortical volumes in this
region,
widespread small-volume reduction throughout
the brain.
abnormalities of the cerebellum.
• Psychosocial family stressors can also contribute to
or exacerbate the symptoms of ADHD.
14. Lower activity in brain regions associated
with executive function
(particularly abnormalities in
frontostriatal circuit):
Prefrontal cortex
Basal ganglia
Cerebellum(vermis)
These areas of the brain
are associated with
executive function abilities:
Attention, spatial working memory, and short-term
memory.
Response inhibition and set shifting.
PATHOGENESIS
15. • Abnormal central dopaminergic and noradrenergic
tone.
¶ Dopamine has been associated with approach and
pleasure-seeking behaviors.
¶ Norepinephrine plays a role in emotional/
behavioral regulation.
• Smaller brain volume in prefrontal cortex, caudate
nucleus, and vermis of the cerebellum. (a 5-10%
reduction in these brain structures)
Cont.
17. DIAGNOSIS :
• A diagnosis of ADHD is made primarily in clinical
settings after a thorough evaluation, including
– a careful history and clinical interview to rule in or
to identify other causes or contributing factors;
– completion of behavior rating scales;
– a physical examination;
– any necessary or indicated laboratory tests.
• It is important to systematically gather and evaluate
information from a variety of sources, including the
child, parents, teachers, physicians, and when
appropriate other caretakers.
18. Clinical Interview and History:
¶ history of the presenting problems,
¶ growth and development,
¶ pregnancy complications, such as maternal illness
(eclampsia, diabetes),
¶ maternal smoking, alcohol, or illicit drug use.
¶ The perinatal period-- presence of labor problems,
delivery complications, prematurity, jaundice, and low
birth weight.
¶ Disruptive social factors, such as family discord,
situational stress, and abuse or neglect.
¶ A family history of 1st-degree relatives with ADHD,
mood or anxiety disorders, learning disability,
antisocial disorder, or alcohol or substance abuse
(indicate an increased risk of ADHD and/or comorbid
conditions)
19. Behavior Rating Scales:
• Behavior rating scales are useful in establishing the
magnitude of the symptoms, but are not sufficient
alone to make a diagnosis of ADHD.
• Many scales available
– Conners Comprehensive Behavior Rating Scales
(Conners CBRS)-- 6 to 18 years for teacher forms
and parent forms & 8 to 18 years for self-report
forms
– Connors-EC for ages 2-6 yrs
– Connors Comprehensive and ADHD Rating Scale IV
for ages 4-5 yrs
– Connors-3 for ages 6-18 yrs
– Academic Performance Rating Scale for grades 1-6
20. PHYSICAL EXAMINATION AND LABORATORY FINDINGS
• To rule out physical disorders that can mimic the
symptoms of ADHD.
• To identifies other physical problems that increase the
risk of serious adverse events when a stimulant
medication used.
Exploration of cardiac status as well as monitoring of
height and weight.
• identify any possible vision or hearing problems.
• testing for elevated lead levels in children those who
are exposed to environmental factors that might put
them at risk (substandard housing, old paint).
21. DIFFERENTIAL DIAGNOSIS
• Chronic illnesses, such as migraine headaches,
absence seizures, asthma and allergies, hematologic
disorders, diabetes, childhood cancer, can impair
children's attention and school performance, either
because of the disease itself or because of the
medications used to treat or control the underlying
illness (medications for asthma, steroids,
anticonvulsants, antihistamines) .
• In older children and adolescents, substance abuse
can result in declining school performance and
inattentive behavior.
• Sleep disorders, including those secondary to
chronic upper airway obstruction from enlarged
tonsils and adenoids, often result in behavioral and
emotional symptoms.
22. • Depression and anxiety disorders can cause many of
the same symptoms as ADHD, but can also be
comorbid conditions.
• Obsessive-compulsive disorder can mimic ADHD,
particularly when recurrent and persistent thoughts,
impulses, or images are intrusive and interfere with
normal daily activities.
• Adjustment disorders secondary to
– major life stresses (death of a close family
member, parents’ divorce, family violence,
parents’ substance abuse, a move)
– parent-child relationship disorders involving
conflicts over discipline, overt child abuse and/or
neglect, or overprotection.
24. TREATMENT :
No treatments have been found to cure this disorder,
but many treatments exist results in the greatest
degree of improvement in the symptoms of the
disorder.
Psychosocial Treatments
• The parents and child should be educated with
regard to the ways ADHD can affect learning,
behavior, self-esteem, social skills, and family
function.
• The clinician should set goals for the family to
improve the child's interpersonal relationships,
develop study skills, and decrease disruptive
behaviors.
25. Behaviorally Oriented Treatments :
• The goal of such treatment is for the clinician to
identify targeted behaviors that cause impairment in
the child's life (disruptive behavior, difficulty in
completing homework, failure to obey home or
school rules)
• The clinician should guide the parents and teachers
in implementing rules, consequences, and rewards to
encourage desired behaviors.
• Behavioral interventions are only modestly
successful at improving behavior, but they may be
particularly useful for children with complex
comorbidities and family stressors, when combined
with medication.
26. Medications :
The most widely used medications are the pre
synaptic dopaminergic agonists, commonly called
psychostimulant medications
¶ Over the first 4 wk of treatment, the physician should
increase the medication dose as tolerated (keeping
side effects minimal to absent) to achieve maximum
benefit.
¶ If this strategy does not yield satisfactory results, or if
side effects prevent further dose adjustment in the
presence of persisting symptoms, the clinician
should use an alternative class of stimulants that
was not used previously.
¶ If satisfactory treatment results are not obtained
with the second stimulant, clinicians may choose to
prescribe atomoxetine, a noradrenergic reuptake
inhibitor. .
27. STIMULANTS:
Methylphenidate:
• Available in immediate and sustained release.
• Absorption: From the GI tract, slow and incomplete
• Dose(Ritalin): 5mg (0.3mg/kg/dose) PO BID before
breakfast and lunch.
– Increase by 5-10mg/day (0.2mg/kg/day) at weekly
intervals.
– Max = 60mg/day (2mg/kg/day).
• Once dose is determined, can switch to longer acting
agent (Concerta ~20% IR and 80% ER, Metadate ~30%
IR and 70% ER , Ritalin LA ~50% IR and 50% delayed
4hrs).
28. Amphetamines:
• Dextroamphetamine (single salt) - 5mg PO once or
twice daily MAX: 40mg/day.
• Mixed amphetamine salts -
– >6 years old 5mg PO once or twice daily;
MAX:40mg/day (5-6 yr start at start with 2.5 mg ),
– 10mg PO(for SR product); MAX: 30mg/day.
• Lisdexamphetamine (prodrug) –
– 6-8 years old: 20 mg PO-- MAX 70 mg/day.
– >8 years old: 30mg PO --MAX: 70 mg/day.
– May increase in increments of 10-20 mg/day at
weekly intervals till max dose until optimal
response is obtain.
29. Dexmethylphenidate
• D-threo-enantiomer of methylphenidate.
• Better absorbed.
• Initial Dose: 2.5mg PO BID OR 10mg PO (XR).
Side effect of stimulant
• Common: Anorexia, Sleep disturbance, Weight
loss, Nervousness/ Restlessness,Growth
retardation Increased blood pressure.
• Severe: Tics, Arrhythmia, Psychosis, Sudden
cardiac death, drug abuse potential.
30. NON-STIMULANTS
• Usually second-line treatments
– If stimulants are poorly tolerated or ineffective
– As monotherapy or adjunct to stimulants
Atomoxetine
• MOA: selective nor epinephrine reuptake inhibitor.
• Second-line treatment or alternative for patients with
history of drug abuse.
• Dose: 0.5mg/kg, then titrate up every 3 days to
1.2mg/kg in either 1 or 2 daily doses
• Max = 1.4mg/kg or 100mg (whichever is less)
• Side Effects:
– Common: weight loss, abdominal pain, appetite
suppression, sleep disturbance
– Serious: rare but severe liver injury
– suicidal ideation
31. • Clonidine and Guanfacine
– MOA: alpha-2 adrenergic agonist.
– Provides modest reduction in ADHD symptoms by reducing
impulsivity, hyperactivity and improving sleep.
– Must taper slowly- risk for rebound hypertension.
• Desipramine
– MOA: inhibit NE and serotonin.
– SE: anticholinergic effects, lowers seizure threshold, CV
effects.
• Bupropion
– MOA: inhibits NE and DA.
– Equivalent to methylphenidate.
– SE: tics, lowers seizure threshold.
• Others-- Iron May augment effects of stimulant
therapy in adolescent patients with low ferritin.
32. Follow up:
– Every 1-3 weeks during initial titration.
– Every 3-6 months thereafter.
• Assess treatment response through validated
behavioral ADHD rating scales (Patients, parents
and teachers)
• Monitor height and weight during stimulant
therapy
Stopping Therapy
• Consider stopping if patient is stable and doing
well. Stop for 1-4 weeks then reevaluate.
33. PROGNOSIS
• From 60-80% of children with ADHD continue to
experience symptoms in adolescence, and up to 40-
60% of adolescents exhibit ADHD symptoms into
adulthood.
• In children with ADHD, a reduction in hyperactive
behavior often occurs with age. Other symptoms
become more prominent with age, such as
inattention, impulsivity, and disorganization.
• A variety of risk factors can affect children with
untreated ADHD as they become adults. These risk
factors include engaging in risk-taking behaviors
(sexual activity, delinquent behaviors, substance
use), educational underachievement or employment
difficulties, and relationship difficulties.
34. PREVENTION
• Parent training can lead to significant improvements in
preschool children with ADHD symptoms, and parent
training for preschool youth with ADHD can reduce
oppositional behavior.
REFERENCES
• NELSON TEXTBOOK OF PEDIATRICS, 20th EDITION.
• KAPLAN & SADOCK'S COMPREHENSIVE TEXTBOOK OF
PSYCHIATRY, 9th EDITION.
• MASH & WOLFE ABNORMAL CHILD PSYCHOLOGY,4th
EDITION
• Journal of PEDIATRICS Volume 127, Number 3, March
2011
38. Kevin T. Blake, Ph.D., P.L.C.
All Rights Reserved
www.drkevintblake.com 38
MTA Study
• Medication Management Treatment Group did
best. 50% decline in symptoms.
• Medication with Behavioral Modification Group did
no better.
• Behavior Modification Group did better than
placebo.
• Community Treatment only had 25% decline in
symptoms.
• Medication helps with social interaction.
NIMH Research Treatment for Attention Deficit Hyperactivity Disorder (ADHD): The Multimodal
Treatment Study – Questions and Answers. From website:
www.nimh.nih.gov/chilfhp/mt.aqu.cfm
39. Kevin T. Blake, Ph.D., P.L.C.
All Rights Reserved
www.drkevintblake.com 39
The MTA Study
• Group 1: “Experimental Medication”
– Three medications used
• Methyltphenidate (Ritalin)
• D Amphetamine (Dexedrene)
• Pemoline (Cylert)**
– If medication one did not work or there was a side effect, changed
to the next medication and so on.
–Each month parent and child was seen by
physician. Child checked for response to
treatment and side effects. Each month
questionnaires given to parents and
teachers.
40. Kevin T. Blake, Ph.D., P.L.C.
All Rights Reserved
www.drkevintblake.com 40
The MTA Study
• Group 2: Behavior Modification
– Parents taught how to use token economies at
home and daily report cards, teachers taught
how to teach AD/HD child, how to use token
economies in the classroom, and daily report
cards, AD/HD children were sent to special camp
for AD/HD kids, parents and teachers given “800”
number for consultation 24/7, continued on for
14 months!
41. Kevin T. Blake, Ph.D., P.L.C.
All Rights Reserved
www.drkevintblake.com 41
The MTA Study
• Group 3: “Experimental Medication Plus
Behavior Modification Group”
42. Kevin T. Blake, Ph.D., P.L.C.
All Rights Reserved
www.drkevintblake.com 42
The MTA Study
• Group 4: “Community Services”
– The parents are told their child has Combined
Type AD/HD and they are encouraged to go out
to their community and get what services they
want for their child…This was the “Control
Group.”
• Medication, aroma therapy, etc.
43. Behavioral Treatment Components
• Psychoeducation about ADHD
• Structure/routines
• Clear rules/expectations
• Attending/rewards
• Planned ignoring
• Effective commands
• Time out/loss of privileges
• Point/token systems
• Daily school-home report card
• Intensive summer treatment programs
Notas do Editor
Specific brain findings (neuro-imaging studies):
--Neuro-imaging studies suggest the importance of the frontostriatal region of the brain in ADHD and the pathways connecting this region with the limbic system (via the striatum) and the cerebellum.
--Children with ADHD have smaller right prefrontal cortex, structural abnormalities in areas of the basal ganglia (e.g., caudate nucleus), smaller total and right cerebral volumes, smaller cerebellum, and delay in brain maturation in the prefrontal cortex (children with ADHD lag 2-3 years behind children without ADHD in development of the PFC).
Attention = the ability to focus or filter information, including attentional alerting and sustained attention.
Memory = the ability to hold information in mind (spatial refers to how things are ordered in space relative to one another), which depends on attention.
Response inhibition = the ability to interrupt a response during dynamic moment-to-moment behavior (i.e., maintaining focused behavior requires continually suppressing alternate behaviors that may be activated by context). *Most well-studied executive function skill in ADHD.Set shifting = The ability to shift one’s mental focus within a task such as sorting by color vs. sorting by number (i.e., task switching).
**Note that spatial working memory and response inhibition are the most researched, and have moderate to large effect sizes (i.e., differences between ADHD kids and non-ADHD kids in spatial working memory and response inhibition are moderate to large).
Most research evidence suggests deficiencies in the availability of dopamine and norepinephrine among children with ADHD relative to comparison children, although epinephrine and serotonin have also been implicated.