ADHD

1. Attention Deficit Hyperactivity
Disorder
James H. Johnson, Ph.D., ABPP
University of Florida

2. ADHD: Nature of the Problem
 ADHD is a neurodevelopmental
disorder of childhood that is
characterized by developmentally
inappropriate levels of:
 Hyperactivity,
 Impulsivity,
 Inattention.

3. ADHD: How Common is it?
 Prevalence is estimated at 3 to 9 per cent
of the elementary school population.
 ADHD occurs more often in males than
females, with the sex ratio being about 4
to 1 to 9 to 1.
 It is one of the most common disorders
of childhood
 Accounts for a large number of referrals
to pediatricians, family physicians and
child mental health professionals.

4. ADHD: Not a New Problem
 Characteristics of this disorder have been
recognized for at least a century.
 The disorder has been referred to by a
variety of labels;
– Minimal Brain Dysfunction (MBD)
– Hyperkinetic Reaction of Childhood
– Attention Deficit Disorder (ADD)
– Attention Deficit Hyperactivity Disorder
(ADHD)

5. ADHD: Evolution of the Disorder
 Still (1902): ADHD Case study
 Encephalitis epidemic of 1917
 Frontal lobe ablation studies with
primates (1930’s)
 Strauss’ work on Minimal Brain
Dysfunction (1940's -1950's)
 Beginnings of child psychopharmacology;
Using Amphetamines for treatment –
1930-1940.
 MBD becomes Hyperkinetic Disorder (the
1960’s)

6. ADHD: Evolution of the Disorder
(cont.)
 Hyperkinesis becomes ADD – The decade
of the 70’s
 Focus on Dietary Factors – Feingold and
the 1970’s
 Studies of psychophysiological responses
of hyperactive children – the 1970’s
 Development of objective diagnostic
criteria: DSM III
 Recognition of Attention Deficit Disorder
– The early 80’s

7. ADHD: Evolution of the Disorder
(cont.)
 The decade of the 80’s: DSM III &
DSM III-R stimulates ADHD research
and the development of new
assessment methods – new
treatment methods - increased
focus on biological factors.
 The 1990’s - Present: Neuroimaging,
genetics and and a reevaluation of
DSM.

8. ADHD: Core Features
 As noted earlier, ADHD is a
disorder characterized by
developmentally
inappropriate levels of :
– Hyperactivity,
– Impulsivity,
– Inattention.

9. DSM IV Symptoms of
Hyperactivity
 Often fidgets with hands or feet, squirms
in seat.
 Often leaves seat in classroom or in other
situations in which remaining seated is
expected
 Often runs about or climbs excessively in
situations in which it is inappropriate.
 Often has difficulty playing or engaging in
leisure activities quietly.

10. Hyperactive Symptoms
 Is often "on the go" or often acts as
if "driven by a motor“.
 Often talks excessively when
inappropriate to the situation
 A combined total of 6 or more of
hyperactivity/impulsivity criteria
are required for diagnosis.

11. What do we Know about
Hyperactivity?
 Children with ADHD are more active,
restless, and fidgety than normal children
during the day and during sleep.
 There are different types of hyperactivity.
– Gross Motor Activity
– Restless/Squirmy
– Occasionally see verbal hyperactivity
 Hyperactivity often varies according to
situation.
 Degree of hyperactivity may vary with age.

12. Symptoms of Impulsivity
 Often blurts out answers before questions
have been completed.
 Often has difficulty awaiting turn.
 Often interrupts or intrudes on others.
Six symptoms of hyperactivity and
impulsivity are required for diagnosis.

13. Symptoms of Inattention
 Often fails to give close attention to
details or makes careless mistakes.
 Often has difficulties sustaining
attention in tasks or play activities.
 Often does not seem to listen when
spoken to directly.
 Often does not follow through on
instructions and fails to finish
homework, chores, or duties in the
workplace

14. Symptoms of Inattention
 Often has difficulty organizing tasks and
activities
 Often avoids, dislikes, or is reluctant to
engage in tasks that require sustained
mental effort.
 Often loses things necessary for tasks or
activities
 Is often easily distracted by extraneous
stimuli.
 Is often forgetful in daily activities
 (6 or more necessary for diagnosis)

15. What Do We Know About ADHD
Attention Problems?
 ADHD "attentional" problems may be most
obvious on specific types of attentional
tasks.
 Children with ADHD seem to have their
greatest difficulties with sustaining their
attention in responding to tasks - in being
vigilant.
 Attention problems are usually seen most
clearly in situations requiring the child to
attend over time to dull, boring, and
repetitive tasks.

16. Situational Variations in Symptoms
 ADHD symptoms show significant
variation across situations.
 Children with ADHD do not display
symptoms in all situations
 The absence of symptoms in some
situations does not mean that the
child does not have ADHD.

17. Situations That Increase ADHD
Symptoms
 When the demands of the situation are to
be good, to be still, and to be quiet.
 The greater the demands, the more
problematic the behavior of the child will
likely become.
 An exception might be in situations
where the child is being continuously
rewarded for complying with demands.
 In familiar situations where novelty and
task stimulation are low.

18. Other Situations That
Increase Symptoms
 Situations where there are low rates of
intrinsic or external reinforcement.
 When the child is fatigued.
 Studies, monitoring 24 hour activity
levels have suggested that the hours of 1
– 5 seem to be peak times for increased
activity in children with ADHD.

19. Overview of Diagnostic Criteria
 Symptom Criteria - Core Symptoms of
Hyperactivity & Impulsivity and/or Inattention
(Six or More Symptoms of either category).
 Duration Criterion - Symptoms have Persisted for
at Least 6 Months.
 Developmental Criterion - Symptoms are
Inconsistent with Developmental Level.
 Impairment Criterion - Clear Evidence of
Clinically Significant Impairment in Social,
Academic, or Occupational Functioning

20. Overview of Criteria (cont.)
 Age Criterion - Some Symptoms that Cause
Impairment Were Present Before Age 7.
 Situation Criterion - Some Impairment from
Symptoms is Present in Two or More Settings.
 NOTE. The failure to attend to full range of
symptoms is not uncommon
 Presence of hyperactivity, impulsivity, and
inattention is not necessarily to be equated with
ADHD.

21. Types of ADHD
 Combined Type
– Symptoms of hyperactivity, impulsivity and
inattention.
 Hyperactive/Impulsive
– Symptoms of hyperactivity and impulsivity.
 Predominately Inattentive
– Symptoms of inattention.

22. ADHD Mimicry
 Sensory Impairments
 Medication side effects
– Phenobarbital
– Dilantin
– Some Asthma Medications
 Seizure Disorder
 RTH (Resistance to Thyroid Hormone)
 PTSD
 Bipolar Disorder
 Anxiety Disorders
 Depressive Disorders

23. Comorbid Conditions
 What are comorbid conditions?
 Controversy over use of the term.
 Why is it essential to consider the possibility of
comorbid conditions in assessing children with
ADHD?
 Importance of distinguishing between comorbid
conditions and mimicry.
 What is the frequency of comorbidities in
children with ADHD?

24. Comorbid Conditions
 Learning Disabilities - 19 to 26%
 Oppositional Defiant Disorder - 40% Conduct
Disorder - 25% children; 45-50% Adolescents.
 Anxiety Disorders - 30%
 Depressive Disorder - 10 - 30%
 Bipolar Disorder – up to 20%.
 Tics and Tourette’s Disorder – 7% of children
with ADHD have a tic disorder.
 40 to 50% of those with Tourette’s disorder have
ADHD

25. Developmental Issues
 There are factors in infancy, such as difficult
temperament, that appear to be early precursors of
ADHD.
 Initial development of ADHD is most often during the
preschool years.
 While there is often a decline in the level of
hyperactivity and some improvement in attention and
impulse control in adolescence, perhaps 80 % continue
to be impaired by their symptoms and meet current
diagnostic criteria.
 A significant number of children with ADHD (probably
over 50%) continue to display problems into the adult
years.

26. Prognosis of ADHD
 Outcome of ADHD in adolescents is highlighted by
the results of a study by Barkley, Fischer, et al, (1990).
 This study followed a large sample of ADHD (158)
and normal children (81) prospectively for 8 years
after diagnosis.
 123 hyperactive children and 66 normals were located,
interviewed and complete questionnaires.
 In the hyperactive group 12 (9.7%) were female and
111 were male. In the normal group 4 of the subjects
were female and 62 were male.


27. Prognosis In Adolescence
 The vast majority of the hyperactive subjects
(71.5%) met DSM III-R criteria for ADHD at
follow up.
 More than 59% met criteria for Oppositional
Defiant Disorder as compared to 11% of the
controls.
 Approximately 43 % of the hyperactive group
could be diagnosed as CD as compared to 1.6%
of the control group.

28. Prognosis Continued
 Hyperactive subjects were more likely to have
had an auto accident, to have had more
automobile accidents, to have had more bodily
injuries in accidents, and to be at fault for
accidents more often than did controls.
 Adolescents in the hyperactive group were also
more likely to have received traffic citations,
especially for speeding

29. Prognosis Continued
 Cigarette and alcohol use were the only
categories of substance use that differentiated
hyperactives and normals.
 When the the hyperactive sample was separated
into groups (purely ADHD and ADHD + CD)
purely ADHD subjects showed no greater use of
cigarettes, alcohol, or marijuana than did normal
controls.
 Mixed hyperactive/Conduct disordered children
displayed two to five times the rate of substance
use as did pure hyperactives or normals.

30. Prognosis Continued
 Three times as many hyperactives had failed a grade
(29.3% versus 10%), had been suspended (46.3%
versus 15.2%) or had been expelled (10.6% versus
1.5%).
 Results indicated that hyperactivity alone increases the
risk of suspension (30.6% vs 15.2%), and dropping out
 (4.8% vs 0% ) as compared to controls
 However, the added diagnosis of CD greatly increases
the risk (67% suspended, 13% dropped out).
 The presence of CD accounted almost entirely for the >
risk of expulsion within the hyperactive group

31. Prognosis In Adulthood
 As many as 67% of children diagnosed with ADHD
will display symptoms in adulthood serious enough to
interfere with academic, vocational or social
functioning.
 There are indications that the type of ADHD that
persists into adulthood is more highly genetic than the
type that remits in childhood.
 ADHD in adults is sometimes considered a “hidden
disorder” as symptoms are often obscured by other
problems.
 Prevalence is thought to be 2 – 4% with sex ratio of 2 –
1 or lower).

32. Risk Factors
 Maternal cigarette use
 Maternal alcohol use
 Unusually long or short labor
 Forceps delivery
 Toxemia
 Meconium staining
 Birth during the month of
September.
 Minor physical anomalies

33. Etiology - Genetics
 Between 10 and 35 per-cent of the
immediate family members of children
with ADHD also display this disorder.
 Risk for siblings of children with disorder
is approximately 32%
 If a parent has ADHD the risk to offspring
is on the order of 50+%
 Twin studies suggest concordance rates
for monozygotic twins is around 80% with
concordance rates of approximately 30%
for dizygotic twins.
 Overall, twin studies suggest an average
heritability of .80

34. Etiology: Molecular Genetics
 Molecular genetics has begun to identify
specific genes related to ADHD.
 A “dopamine type 2 gene” has been found
to be related to ADHD as well as
Tourette’s and alcoholism.
 More recently a "dopamine transporter
gene" and a “dopamine repeater
gene”have been identified.
 This gene, found to be related to ADHD in
multiple studies, seems to be related to
post-synaptic sensitivity in the frontal
and prefrontal cortical regions and to be
associated with executive functions.

35. Genetic Contributions (cont.)
 With developments in molecular genetics
occurring at an increasingly rapid rate
(due to the Human Genome Project), in
the near future, we may have genetic
tests that can provide early screening for
ADHD and possibly associated
comorbidities.
 Genetic factors are clearly strongly
implicated in the development of this
disorder.
 Hereditary is one of the most well
supported etiological factors in the
development of ADHD

36. Etiology – Neurological Insult
 Multiple factors that can result in brain
damage are associated with ADHD.
 For example, anoxia, is associated with
increased frequencies of hyperactivity and
attentional problems.
 ADHD occurs more often in children with
seizure disorders, who are presumed to
have neurological involvement
 As was noted earlier, diseases such as
encephalitis can also result in symptoms
of ADHD as can various types of
infections.

37. Etiology: Brain Damage
 These findings suggest that neurological
insult can result in an increased
probability of developing ADHD.
 However, most children with ADHD do
not have a significant history of brain
injury.
 Indeed, such injuries are unlikely to
account for ADHD in most children.
 In fact probably 95% of hyperactive
children show no evidence of
documentable neurological impairment.
 This does not mean, however, that
neurological factors are not involved.

38. Neuropsychological Test Findings
 Results from research involving
neuropsychological testing has often
suggested that children with ADHD have
problems;
– in inhibiting behavioral responses,
– with working memory,
– with planning and organization,
– with verbal fluency,
– with perserveration,
– In motor sequencing,
– with other frontal lobe functions.

39. Research with Neuropsychological
Testing (Cont.)
 Not only do children with ADHD show
executive functioning deficits but
siblings of ADHD children who do not
have ADHD, have milder yet significant
impairments of the same type.
 This suggests a possible genetic risk for
executive function deficits in families.

40. Cerebral Blood Flow
 Studies of cerebral blood flow in ADHD
and normal children have consistently
shown decreased blood flow to the
prefrontal regions and pathways
connecting these regions to the limbic
system via the striatum and specifically
its anterior region (the Caudate Nucleus)
 Studies using PET scans to assess
cerebral glucose metabolism in the
frontal regions have found diminished
metabolism in, adults and adolescent
females with ADHD.

41. Cerebral Blood Flow
Continued
 Significant correlation's between
diminished metabolic activity in the left
anterior frontal region and severity of
symptoms in adolescents with ADHD have
also been demonstrated
 This demonstration of a relationship
between decreased metabolic activity of
certain brain regions and severity of
ADHD symptoms is crucial to
documenting the importance of the link
between brain activation and behaviors
associated with ADHD

42. Frontal Lobes

43. Basal Ganglia

44. Striatal Network

45. MRI Studies
 Early studies found differences in the
Corpus Callosum, with this structure
being smaller in children with ADHD. –
Not always replicated.
 Other MRI studies have found children
with ADHD to have a smaller left caudate
nucleus than did normal children. These
findings are interesting in light of the
results of earlier blood flow studies
suggesting lower levels of activation in
this specific area in children with ADHD.

46. MRI Continued
 Several more recent MRI studies, with
larger samples, have replicated these
early results by finding that ADHD
children had significantly smaller
anterior right frontal regions, a smaller
caudate nucleus, and smaller golbus
pallidus regions that normals.
 Research has also found decreased
cerebellar volume in ADHD children.
 Work in this area suggests that
abnormalities in the development of the
frontal-striatal regions may well
underlie the development of ADHD.

47. Neurotransmitter Deficiencies
 The possibility of a neurotransmitter
dysfunction in children with ADHD has
been suggested for many years.
 This notion seemed to originate from
observations of the response of children
with ADHD to different type of stimulant
drugs.
 The fact that stimulant drugs have an
impact on ADHD and that they increase
dopamine has contributed to the
neurotransmitter dysfunction
hypothesis.

48. Neurotransmitter Deficiencies
 There is more direct evidence of
neurotransmitter deficiencies from studies
of cerebral spinal fluid in ADHD and
normal children which suggests decreased
dopamine levels in ADHD children
 There is also some evidence of a
deficiency in the availability of
norepinephrine in children with ADHD.
 This is of interest given that a very new
non-stimulant ADHD medication,
Straterra, is thought to act on
norepinephrine levels.

49. Etiology: Psychosocial Factors
 There is little evidence for the role of
psychosocial factors in the
development of ADHD, although
factors such as parent-child conflict
may exacerbate problems in a child
with ADHD.
 Psychosocial factors may also
contribute to the development of
certain comorbid disorders that may
complicate the clinical picture.

50. Etiology: Overview
 In reviewing the literature on the
etiology of ADHD, Barkley suggests …
 “It should be evident from the
research…that neurological and genetic
factors make a substantial contribution
to symptoms of ADHD and the
occurrence of this disorder.
 A variety of genetic and neurological
etiologies (e.g., pregnancy and birth
complications, acquired brain damage,
toxins, infections, and genetic effects)
can give rise to the disorder through
some disturbance in a final common
pathway in the nervous system.

51. Overview Continued
 That final common pathway appears to be the
integrity of the prefrontal cortical-striatal
network.
 It now appears that hereditary factors play the
largest role in the occurrence of ADHD
symptoms in children.
 It may be that what is transmitted genetically is
a tendency toward a smaller and less active
prefrontal-striatal network.

52. Overview Continued
 The condition can also be caused or
exacerbated by pregnancy complications,
exposure to toxins, or neurological disease
 Social factors alone cannot be supported as
causal in this disorder, but such factors may
exacerbate the condition, contribute to its
persistence, and more likely, contribute to
the forms of comorbid disorders associated
with ADHD.
 Cases of ADHD can arise without genetic
predisposition if the child is exposed to a
significant disruption or neurological injury
to this final common neurological pathway,
but this would seem to account for only a
small minority of ADHD children. “

53. Treatment of ADHD
 Stimulant Medications
 Other Medications
 Psychosocial Treatments
 Educational Accommodations

54. Commonly Used Stimulant
Medications
 Ritalin
 Dexadrine
 Adderall
 Concerta
Between 70 and 80 % of children with ADHD respond
positively to stimulant drugs.
Stimulant drugs represent an empirically supported
treatment for core symptoms of ADHD.

55. Side Effects of Stimulants
 Common side effects can include: loss of
appetite, weight loss, sleeping problems,
irritability,
 restlessness, stomachache, headache,
rapid heart rate, elevated blood pressure,
sudden deterioration of behavior
 symptoms of depression with sadness,
crying, and withdrawn behavior.
 intensification of tics (muscle twitches
of the face and other parts of the body),
possible Tourette’s and growth
suppression.

56. Side Effects (Cont.)
 While side effects are always a possibility they are
often
– Transient in nature
– The result of inappropriate medication levels
 If one medication results in side effects, another
might be used without side effects.
 Sometimes other medications are used to minimize
side effects.
 Good clinical judgment by the clinician may help to
minimize side effects.

57. Some Examples of NonStimulant Drugs
in ADHD Treatment
 Non Stimulant ADHD Medication
– Straterra - a norepinephrine reuptake inhibitor- selectively
blocks the reuptake of norepinephrine, which increases its
availability
 Other Non Stimulant Drugs
– Anti-depressants (e.g., Tofranil, Wellbutrin)
– Anti-hypertensives (Clonidine)

58. Psychosocial Treatments
 Parent Training
 Social Skills Training
 Cognitive Behavioral Treatments.
 Psychotherapy for comorbid conditions

59. Educational Interventions
 Special Education Services for existing
learning problems.
 Classroom accommodations.
 Classroom behavior modification programs.

60. ADHD Treatment: Concluding
Comments
 In treating ADHD it is essential to treat the full range
of difficulties that impact on child and family
functioning.
 Treatment of ADDH will often need to be
“multimodal” in nature.
 Findings from the Multimodal Treatment Study
suggest that;
– Stimulant medication is effective in reducing core
symptoms
– Psychosocial treatments are of value in addressing
associated comorbidities.

61. That’s All Folks!