good ppt for undergraduate medical students

1. Autism spectrum disorder and Attention deficit hypereactivity
disorder in children
Dr. Sabona Lemessa (Assistant professor in pediatrics and child health,
JUMC)
8/12/2022 1

2. Outlines
 Introduction
 Epidemiology
 Risk factors
 Clinical manifestations
 Diagnosis
 Co-morbidities
 Screening
 Treatment
 Prognosis
 Reference
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3. Definition
 Autism spectrum disorder(ASD):
Is a neurobiological disorder with onset in early childhood
is impairment in social communication and social interaction
accompanied by restricted and repetitive behaviors
There is marked variability in the severity of symptoms across
patients, and
cognitive function can range from severe intellectual impairment
through the superior range.
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 The DSM-5 diagnosis of ASD is characterized by-
persistent deficits in social communication and interaction
deficits in social reciprocity; nonverbal communicative behaviors;
and skills in developing, maintaining, and understanding
relationships
 restricted, repetitive patterns of behavior, interests, or activities
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 Autism spectrum disorder includes:
Autistic Disorder
Asperger's Syndrome
 Pervasive Developmental Disorders-Not Otherwise Specified
(PDD-NOS)
 Retts Syndrome and
Childhood Disintegrative Disorder
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 Persistent Deficits in Social Communication and Social Interaction:-
refers to a qualitative impairment in social communication and
reciprocal social interactions,
which is persistent and observable across multiple contexts.
There is not necessarily an absolute lack of social behaviors, but
social communication and interactions are clearly atypical for the
individual’s age and developmental level.
Deficits in social-emotional reciprocity often manifest as
the absence of attempts to initiate social interaction and
 a lack of responsiveness to social overtures.
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 Deficits in nonverbal communication behaviors are a hallmark of ASD
can vary from a total lack of facial expressions and nonverbal
communication to a lack of integration of gestures
(e.g., eye contact, smiling, nodding, shaking the head, shoulder
shrugging) with verbal communication
 Restricted, Repetitive Patterns of Behavior, Interests, or Activities:-
A common form of repetitive speech is echolalia, which may be
immediate or delayed.
Immediate echolalia refers to immediate noncommunicative
repetition of words or phrases.
Delayed echolalia (or scripted speech) refers to the use of highly
ritualized phrases that have been memorized-
such as from television or overheard conversations.
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9. Stereotyped Motor Movements or Speech
 may include hand flapping, finger movements, body rocking and lunging,
jumping, running and spinning, and
repetitive speech such as echoing words immediately after they are
said.
 Stereotyped movements can change over time and
In older children are seen more often in individuals with lower
cognitive functioning.
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10. Social-Emotional Reciprocity
 range from active avoidance or reduced social response to having an
interest in, but
 lacking ability to initiate or sustain, an interaction with peers or adults.
 A young child with ASD may not respond when his name is called
 may exhibit limited showing and sharing behaviors, and may
prefer solitary play
 An older child with ASD may have an interest in peers but may not know
how to initiate or join in play.
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11. Developing, Maintaining and Understanding Relationships
 they have limited insight regarding social relationships.
 They have difficulty understanding the difference between a true friend and
a casual acquaintance.
 They have trouble picking up on the nuances of social interactions and
understanding social expectations for polite behavior.
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12. Epidemiology
 At least one of the disorders on the spectrum was 3.4/1,000 for children 3
to 10 years of age
 The prevalence of ASD is estimated at 1 in 59 persons by the U.S. Centers
for Disease Control and Prevention (CDC).
 The prevalence increased significantly over the past 25 years,
 primarily because of improved diagnosis and case finding
 as well as inclusion of less severe presentations within the autism spectrum.
 Male 3-4 times greater risk than female
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13. Onset Patterns in ASD
 may occur early, with abnormalities in social and communication skills
becoming apparent in the first year of life, or
 children appear to develop normally until at least 12 months of age,
 followed by loss or regression of language and/or social skills.
 The prevalence of regression in ASD is about 30%.
 More typical is a “plateauing” or deceleration of development after 6
months of age.
 This is often accompanied by some loss of social communication skills,
typically joint attention, shared affect, and the use of language.
 children with autistic regression have an earlier age of onset and
are less likely to have bilateral, temporal EEG patterns, or
electrical status during sleep
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14.  Exact cause of autism is unknown
 Thought to result from disrupted neural connectivity and
is primarily impacted by genetic variations affecting early brain
development.
 Genetics
In identical twins with one child being autistic, the other child has
chance of being affected ranges from 36-96%
10% for fraternal twins
90% of the behavioral phenotype of autism is related to inherited
genes
 Individuals with genetic vulnerability may be more sensitive to
environmental factors influencing early brain development.
Etiology and Pathogenesis
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 Mutations that include large genetic deletions or duplications and small
sequencing changes have been implicated;
these can be inherited or occur de novo.
 Elevated platelet serotonin (5-HT) and mTOR which appear to be
disrupted leads to alterations in neuronal migration and growth in the brain.
 Genetically caused syndromes include ASD part of a broader phenotype:-
Fragile X syndrome, Down, Smith-Lemli-Opitz,
Rett, Angelman, Timothy, Joubert syndrome
Tuberous sclerosis
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 Brain and Brain Injury-
Animal models and studies of individuals with ASD indicate
changes in brain volume and neural cell density in the limbic
system, cerebellum, and frontotemporal regions
Injury to the cerebral cortex includes disorders associated with the
amygdala
Altered neurotransmission or false neurotransmitters
Increased size of total brain, parietal-temporal lobe, and cerebellar
hemisphere volume are usually seen in autistic child
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17. Risk Factors
 Maternal obesity or overweight
 Short interval from prior pregnancy, Preclampsia
 Premature birth
 Prenatal infections(e.g. rubella, CMV)
 Older parents
 Gestational diabetes
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 Sibling Studies-
An autism diagnosis is about 20 times more likely in siblings when
one child had autism
The risk is 25% if there are already two siblings with ASD.
Delays in verbal and nonverbal communication have been noted in
siblings of those with ASD, beginning at about 12 months of age.
However, no consistent specific deficits have emerged as
characteristic of Sib-ASD.
Response to name at 12 months of age and response to joint
attention were predictive of the degree of social impairment and
eventual ASD diagnosis at 3 years of age.
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 Neonatal Intensive Care and Prematurity
higher rate of autism and
a much higher rate of positive screening for ASD in infants with
extreme prematurity.
perinatal complications like preeclampsia, intracranial hemorrhage,
cerebral edema, low Apgar scores, and seizures.
The presence of these risk factors should lead to systematic
screening of toddlers and preschoolers who were born prematurely
or with neonatal complications.
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20.  From study protocol which prospectively registered in the International
Prospective Register of Systematic Reviews, A total of ten studies were
included in the meta-analysis publishe The British Journal of Psychiatry (2018)
 The sample size of the included studies ranged from 847 to 377,708. Age at the
diagnosis of ASD varied between 1 year and 24 years.
 Of the included studies, six were case–control studies, whereas the other four
were cohort studies,
 Of the included studies, seven reported positive associations between pre-
eclampsia and ASD, whereas the other three reported null associations.
 Conclusion- Pre-eclampsia increased the risk of ASD in offspring. The
finding suggests a need for early screening for ASD in offspring of women
with pre-eclampsia.
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 Parental Age and Other Factors:-
Risk of ASD is higher with increasing age of mothers
may act through increasing the risk for de novo mutations.
Environment mutagens such as mercury, cadmium, nickel,
trichloroethylene, and vinyl chloride may play a role.
Vitamin D deficiency may cause mutations, as vitamin D
contributes to repair of DNA damage.
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 Autoimmune Factors:
The presence of maternal thyroid peroxidase antibody (TPOab)
increased risk by nearly 80%.
Maternal gestational or type 2 diabetes, maternal prenatal stress in
the first trimester, and paternal obesity all may increase the risk of
ASD.
A decrease in autism risk has been associated with periconceptual
folate intake and
may be strongest in those with genetically inefficient
folate metabolism.
due to central nervous system (CNS) mitochondrial
dysfunction.
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23. Severity Levels for Autism Spectrum Disorder
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27.  From cross sectional study done in the three outpatients centers receiving
patients referred for neurodevelopmental disorders in Kinshasa, DRC, from
June 2008 to June 2010, total of 450 subjects aged from 1-18 years old
included in the study,
 All patients were subject to an intellectual quotient evaluation and an
electroencephalogram reporting.
 120 (29.3%) received the diagnosis of ASD, with boys outnumbering girls
(OR 3:1. The mean age was 7.9 years (SD 3.4) (p< 0.001).
 Intellectual disability (75.83 %) and epilepsy (72.50%) were the main co-
morbidities significantly associated with autism (p< 0.001).
 co-morbidities were most frequent in subjects with an IQ<70 (p=0.05).
 conclusion was it is important to screen for ASD and co-morbidities among
neurodevelopmental disorders and to undertake survey on ASD.
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28. Common Co-occurring Conditions in Autism Spectrum Disorder (ASD)
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 Epilepsy:-
Epilepsy of all seizure types occur frequently in children with autism.
The overall rate, even in idiopathic cases of autism with normal IQ, is
higher (13% to 17%) than the risk in the general population (1% to
2%).
There is a bimodal distribution of age of onset, with peaks occurring at
younger than 5 years and during adolescence and
with the rate increased in those with intellectual disability or underlying
medical conditions.
The prevalence of epilepsy was 21.5% in subjects with ASD and ID
compared with 8% in those with ASD and no ID.
Both abnormal synaptic plasticity and excitatory/inhibitory imbalance
can be contributing factors.
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 Changes associated with seizures and epileptogenesis may disrupt normal
activity-dependent developmental processes.
 Changes in functional connectivity determined by EEG are being explored
as a biomarker for early identification of ASD.
 The presence of cerebral palsy or focal motor findings also increases risk.
 Seizures in children with autism should be treated as they would be in
children without autism,
 with even more attention than usual paid to the possible behavioral and
cognitive side effects of antiseizure drugs.
 Repetitive and stereotypic behaviors could mimic temporal lobe seizures,
and
 inattention from absence seizures may be construed as autistic behavior.
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34. SCREENING AND DIAGNOSTIC EVALUATION FOR ASD
 The American Academy of Pediatrics recommends screening for ASD for
all children at age 18 mo and 24 mo.
 because these are critical times for early social and language development,
and earlier intervention is more effective for ASD
 The Modified Checklist for Autism, Revised/Follow-Up Interview
(MCHAT-R/FU), a 20-item parent report measure, with additional parent
interview completed for intermediate scores.
 The MCHAT-R/FU can be used from age 16-30 mo.
 Assessment of ASD includes direct observation of the child to evaluate
social skills and behavior
 Indicated in children with-
delayed language/communication milestones,
regression in social or language skills, and
children whose parents raise concerns regarding ASD
 child with an older sibling who has ASD
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 These structured play-based assessments provide social prompts and
opportunities to evaluate-
the frequency and quality of a child's social responsiveness
to initiation, and maintenance of social interactions; the capacity for
joint attention and
shared enjoyment; the child's behavioral flexibility; and
presence of repetitive patterns of behavior
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36. Screening Instruments for ASD
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37. Diagnostic Instruments for ASD
 Auditory evaluation
 General medical evaluation
should be considered, especially for developmental delay
TFT, CBC , Ferritin level and Lead level
 Metabolic screening
If clinically indicated (e.g. severe intellectual disability and
seizures, developmental regression)
 Electroencephalography:-
Epileptiform EEG abnormalities and interictal discharges (IEDs)
have been reported in children with ASD (up to 30%) but
do not typically correlate with clinical seizure activity.
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 Neuroimaging(MRI/ spectroscopy)- Routine use is controversial
Indicated for complex ASD:-
clinical focal findings, major dysmorphology, micro- or
extreme (≥ 4 SD) macrocephaly, skin lesions, seizures
focal EEG abnormalities, motor regression
 Genetic screening
Genome-wide microarray, fragile X syndrome (FMR1 gene)
PTEN gene(indicated if HC > +3SD)
MECP2 gene - Consider for females with intellectual disability
 Assessment of co-morbidities
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39. THE NEUROLOGIC EVALUATION IN AUTISM
 large head circumference (HC) or frank macrocephaly, somatic overgrowth,
 Motor Disturbances in Tone, Gait, Praxis, and Stereotypies
Hypotonia is common in children with ASD but not uniquely so.
Dyspraxia in ASD strongly correlates with the core social,
communicative, and behavioral impairments
Both motor function and visual-motor integration contribute to the
dyspraxia.
 Motor stereotypies are very common in ASD and
have an earlier onset (younger than 3 years) than tics (5 to 7 years) and
tend to be consistent and fixed, frequently involving hands, arms, or the
entire body
 Self injurious behavior (SIB) is reported to occur in varying proportions of
individuals with ASD (i.e., 35 to 50%).
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40. Treatment
 Educational
Behavioral approaches based on the principles of applied
behavioral analysis (ABA)-
 involve direct incremental teaching of skills within a
traditional behavioral framework using reinforcement of
desired behavior, careful data collection, and
analysis and adjustment of the treatment program based on
review of data
Augmentative communication approaches using photographs or
picture
Higher cognitive, play, and joint attention skills and lower
symptom severity at baseline are predictors for better outcomes in
core symptoms, intellectual function, and language function.
 Treating co-occurring conditions
Seizure, GI problems and Improving sleep hygiene
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 Pharmacology
Stimulant medication(atomoxetine) and α-agonists for ADHD in
ASD
Selective serotonin reuptake inhibitors (SSRI) can be used for
anxiety and OCD
Atypical antipsychotic(risperidone and aripiprazole)
 reduces irritability, aggression, and self-injury
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 Neuroleptic Agents:-
block dopamine receptors, such as haloperidol, thioridazine, and
trifluoperazine.
Haloperidol decreased motor stereotypies, hyperactivity,
withdrawal, and negativism in children with autism, but use is
limited by the risk of extrapyramidal symptoms.
Risperidone and aripiprazole for the treatment of irritability
(including aggression, self injurious behavior, temper tantrums, and
mood swings)
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43. Common Pharmacologic Treatments in Autism Spectrum Disorder (ASD)
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44. Prognosis
 Autism spectrum disorder is a lifelong condition.
 Although a minority of individuals respond so well to therapy that they no
longer meet criteria for the diagnosis,
Adult outcome studies are sobering, indicating that many adults
with ASD are
socially isolated, lack gainful employment or independent living,
and
have higher rates of depression and anxiety.
 Outcome as measured by developmental progress and functional
independence is better for individuals who have higher cognitive and
language skills and lower ASD severity at initial diagnosis.
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45. Attention Deficit–Hyperactivity Disorder
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46. Introduction
 Is the most common neurobehavioral disorder in childhood
 disorder of executive function attributable to abnormal dopamine
transmission in the frontal lobes and frontostriatal circuitry.
inattention, including increased distractibility and difficulty
sustaining attention;
poor impulse control and decreased self-inhibitory capacity; and
motor over activity and motor restlessness
 Affected children usually experience:-
academic underachievement,
problems with interpersonal relationships with family members and
peers
low self-esteem
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47. Epidemiology
 ADHD affects up to 5 to 8% of school-aged children
60 to 85% of those diagnosed as children continuing to meet
criteria for the disorder in adolescence, and
up to 60% continuing to be symptomatic into adulthood.
usually not a reportable disease
 more common in boys than girls
male to female ratio 4:1 for the predominantly hyperactive type and
male to female ration 2:1 for the predominantly inattentive type
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48. PATHOGENESIS
 Not definitively known.
 A genetic imbalance of catecholamine metabolism in the cerebral cortex
appears to play a primary role.
 largely genetic, with a heritability of approximately 75%
 various environmental factors may play a secondary role; the significance
of environmental factors is controversial.
20% of children with severe traumatic brain injury are reported to
have subsequent onset of substantial symptoms of impulsivity and
inattention.
However, ADHD may also increase the risk of traumatic brain
injury.
 Most children with ADHD have no evidence of gross structural damage in
the central nervous system (CNS)
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 Genetic factors-
supported by twin studies that demonstrate concordance as high as
92% in monozygotic twins and 33% in dizygotic twins
Family-based and case-control studies have identified a number of
genes that appear to play a role in the development of ADHD
 Neurochemical Factors-dopamine hypothesis:-
 Dopamine D2, D4, and D5 receptor genes (DRD2, DRD4, and DRD5)
 dysfunction in both the adrenergic and dopaminergic systems.
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 Neuroanatomical Aspects-
Functional brain imaging reveals that groups of children with
ADHD have reduced global activation and
reduced local activation in the area of the basal ganglia and anterior
frontal lobe
Brain MRI studies in children with ADHD indicate-
reduction or even loss of the normal hemispheric asymmetry in
the brain, as well as smaller brain volumes of specific
structures
such as the prefrontal cortex and basal ganglia.
Children with ADHD have approximately a 5–10% reduction
in the volume of these brain structures
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51. NEUROBIOLOGY OF ATTENTION DEFICIT–HYPERACTIVITY
DISORDER
 core deficit in ADHD is impairment of behavioral inhibition, which leads
to the other symptoms of ADHD.
 impaired behavioral inhibition is limited to ADHD/HI and ADHD/C (i.e.,
those with hyperactive or impulsive symptoms) and
 excludes children with ADHD/I (i.e., those with inattention only)
 unbalance between the high activation of the basal ganglia and
cerebellum and the low activation of the prefrontal cortex for the
forethought condition in ADHD.
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 Risk factors-
prematurity and whose mothers were observed to have maternal
infection during pregnancy
Perinatal insult to the brain during early infancy
Severe chronic abuse, maltreatment and neglect
Zinc deficiency, IDA
Head trauma in young children- 20% in future for ADHD
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53. clinical features
 Clinical manifestations of ADHD may change with age
 ADHD is a syndrome with two categories of core symptoms:-
hyperactivity/impulsivity and inattention
hyperactivity, attention deficit
impulsivity
behavioral symptoms of aggression and defiance
memory and thinking deficits, specific learning disabilities, and
speech and hearing deficits
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54. Hyperactivity and impulsivity
 almost always occur together in young children.
 The predominantly hyperactive-impulsive subtype of ADHD is characterized
by the inability to sit still or inhibit behavior
 observed by the time the child reaches four years of age and increase during the
next three to four years, peaking in severity when the child is seven to eight
years of age
 Symptoms of hyperactivity and impulsivity may include:-
 Excessive fidgetiness (eg, tapping the hands or feet, squirming in seat)
 Difficulty remaining seated when sitting is required (eg, at school,
work, etc)
 Feelings of restlessness (in adolescents) or inappropriate running
around or climbing in younger children
 Difficulty playing quietly
 Difficult to keep up with, seeming to always be "on the go"
 Excessive talking, Difficulty waiting turns
 Blurting out answers too quickly, Interruption or intrusion of others
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55. Inattention
 characterized by reduced ability to focus attention and reduced speed of
cognitive processing and responding.
 described as having a sluggish cognitive tempo and frequently appear to be
day dreaming or "off task".
 The typical presenting complaints center on cognitive and/or academic
problems.
 Among children born at <32 weeks gestational age, symptoms of
inattention appear to be more prominent than hyperactivity and impulsivity
 The symptoms of inattention typically are not apparent until the child is
eight to nine years of age
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 Symptoms of inattention may include:-
Failure to provide close attention to detail, careless mistakes
Difficulty maintaining attention in play, school, or home activities
Seems not to listen, even when directly addressed
Fails to follow through (eg, homework, chores, etc)
Difficulty organizing tasks, activities, and belongings
Avoids tasks that require consistent mental effort
Loses objects required for tasks or activities (eg, school books,
sports equipment, etc)
Easily distracted by irrelevant stimuli
Forgetfulness in routine activities (eg, homework, chores, etc)
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57. Diagnosis criteria
 The American Psychiatric Association has defined consensus criteria for
the diagnosis of ADHD, which are published in the Diagnostic and
Statistical Manual of Mental Disorders Fifth Edition (DSM-5).
For children <17 years, the DSM-5 diagnosis of ADHD requires
 ≥6 symptoms of hyperactivity and impulsivity or
 ≥6 symptoms of inattention.
For adolescents ≥17 years and adults,
≥5 symptoms of hyperactivity and impulsivity or
≥5 symptoms of inattention are required
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 The symptoms of hyperactivity/impulsivity or inattention must:-
Occur often
Be present in more than one setting (eg, school and home)
Persist for at least six months
Be present before the age of 12 years
Impair function in academic, social, or occupational activities
Be excessive for the developmental level of the child
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59. classification
 Depending upon the predominant symptoms, ADHD can be categorized
into one of the three subtypes
1) Predominantly inattentive – ≥6 symptoms of inattention for children
<17 years; ≥5 symptoms for adolescents ≥17 years and adults
2) Predominantly hyperactive-impulsive – ≥6 symptoms of hyperactivity-
impulsivity for children <17 years; ≥5 symptoms for adolescents ≥17
years and adults
3) Combined – ≥6 symptoms of inattention and ≥6 symptoms of
hyperactivity-impulsivity for children <17 years; ≥5 symptoms in each
category for adolescents ≥17 years and adults
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60. Possible developmental impacts of attention-deficit/hyperactivity disorder
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61. Comorbidities
 can be primary or secondary
 high prevalence of comorbidity with other neuropsychiatric
disorders .
Of children with ADHD, 15–25% have learning disabilities, 30–
35% have developmental language disorders,
15–20% have diagnosed mood disorders, and 20–25% have
coexisting anxiety disorders.
Children with ADHD can also have concurrent diagnoses of sleep
disorders, memory impairment, and decreased motor skills.
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62.  From analytical cross-sectional study done on children attending pediatric
neurology and psychiatry clinics of Mulago National Referral Hospital, the largest
hospital in Uganda, Using the disruptive behavior scale
 520 children were screened for the study, 332 participants were recruited and
enrolled to participate in the study.
 prevalence of DSM-IV ADHD symptoms was 11%.
 Children aged less than 10 years were four times likely to have ADHD (OR 4.1,
95% CI 1.7–9.6, p < 0.001).
 The demographic factors independently associated with ADHD were age less than
10 years, male gender, history of maternal abnormal vaginal discharge during
pregnancy, and no formal education or the highest level of education being
primary school.
 co-morbidities associated with ADHD were epilepsy (25.71%), autism spectrum
disorders (14.29%), conduct disorder (8.57%) and intellectual disability (8.57%).
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63. Diagnostic evaluation
 ADHD is a clinical diagnosis; there are no diagnostic laboratory nor cognitive
tests.
 clinical diagnosis based on criteria in the fifth edition of the Diagnostic and
Statistical Manual of Mental Disorders (DSM-5)
 Criteria are divided into two lists of symptoms:-
inattention and
Hyperactive impulsive behavior
 Based on the number of items identified, there are three classifications:
ADHD/I (primarily inattentive type)
ADHD/HI (primarily hyperactive-impulsive type) and
ADHD/C (combined type)
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64. How to assess children for attention-deficit/hyperactivity disorder?
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65. Stepped Diagnostic Approach to Attention Deficit–Hyperactivity Disorder
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66. Physical Examination and Laboratory Findings
 Laboratory Studies:-
No laboratory tests are available to identify ADHD in children
Features in the history or on examination may lead to specific tests
for disorders manifesting as or coexisting with ADHD,
such as hypothyroidism, hyperthyroidism or phenylketonuria.
 The presence of hypertension, ataxia should prompt further neurologic or
endocrine diagnostic evaluation
 Impaired fine motor movement and poor coordination and other subtle
neurologic motor signs are common but not sufficiently specific to
contribute to a diagnosis of ADHD.
 difficulties with finger tapping, alternating movements, finger-to-
nose, skipping, tracing a maze, cutting paper
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67. TREATMENT
 Psychosocial Treatments
the parents and child should be educated
The clinician should set goals for the family to improve
the child's interpersonal relationships, develop study skills, and
decrease disruptive behaviors.
Parent support groups with appropriate professional consultation to
such groups can be very helpful
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68. cont...
 Behaviorally Oriented Treatments
are modestly successful at improving core ADHD symptoms and
are considered the first-line treatment in preschool-age children
with ADHD.
may be particularly useful for children with comorbid anxiety,
complex comorbidities, family stressors, and when combined with
medication
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69. Medications
 psychostimulant medications, including-
methylphenidate, dexmethylphenidate, amphetamine, and
various amphetamine and dextroamphetamine preparations
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 a methylphenidate compound is unsuccessful, the clinician
should switch to an amphetamine product.
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 Stimulant drugs used to treat ADHD may be associated with an increased
risk of adverse cardiovascular events, including-
sudden cardiac death, myocardial infarction, and stroke, in young
adults and rarely in children.
In some of the reported cases, the patient had an underlying
disorder, such as
hypertrophic obstructive cardiomyopathy, which is made
worse by sympathomimetic agents.
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71. cont...
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72. Prognosis
 A childhood diagnosis of ADHD often leads to persistent ADHD throughout
the life span.
 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 associated with ADHD can become more prominent with
age, such as inattention, impulsivity, and disorganization, and these exact a
heavy toll on young adult functioning.
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73. cont...
 Risk factors in children with untreated ADHD as they become adults
include engaging in risk-taking behaviors-
sexual activity, delinquent behaviors, substance use),
educational underachievement or employment difficulties, and
relationship difficulties.
 With proper treatment, the risks associated with ADHD, including injuries,
can be significantly reduced. Consistent treatment with medication and
 adjuvant therapies appears to lower the risk of adverse outcomes, such as
substance abuse.
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75. Reference
 David K. Urion, Carolyn F. Bridgemohan, Learning and Developmental
Disorders, Nelson 21st edition.
 Marilyn Augustyn, MD, on Autism spectrum disorder, uptodate, 2018.
 Deborah G. Hirtz, Ann Wagner, Pauline A. Filipek, and Elliott H. Sherr,
Autistic Spectrum Disorders, Swaiman’s Pediatric Neurology 6th edition.
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76. Thank you
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