4.1Pediatrics Autism and ADHD 2014A

7/24/2019 4.1Pediatrics Autism and ADHD 2014A

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Ardales, Austria, Avancea|Azucenas Page 1 of 11

AUTISM AND ADHD

July 13, 2012

Dr. Eusebio

OUTLINE

I. Autistic Spectrum Disorder

II. Autism

Prevalence

Etiology

Diagnosis

Early Signs

Comprehensive evaluation

DSM IV Criteria

Laboratory

Accompanying problems

Management

III. ADHD

Introduction

Prevalence

Causes

Signs and symptoms

Developmental Trend

Co-morbidities

Diagnosis

DSM IV

Treatment

o Standard treatment

o Medications

o Non traditional treatment

Burden of ADHD

AUTISTIC SPECTRUM DISORDER

THE EVOLVING NOMENCLATURE OF AUTISM

1943Kanners autism

1944Aspergers syndrome

1988 Autistic Disorder/Pervasive Developmental Disorder

(DSM-IIIDSM-III R)

1994Autistic Disorder/PDD (DSM IV; ICD 10)

1995Autistic Spectrum Disorders

He wandered about smiling, making stereotyped movements with

his fingers. He shook his head from side to side, whispering or

humming the same 3 note tune. He spun anything he could seize

upon to spin (Kanner 1943).

PDD (Pervasive Developmental Disorder) and ASD (Autistic Spectrum

Disorder) are one in the same. We use PDD is less stigmatizing.

Other subgroub Non-Autistic PDDs:

Aspergers Syndrome - is still an ASD but with normal

language development, however it is still peculiar

PDD NOS

Fragile X Syndrome

Retts syndrome

Chhildhood Disintegrative Disorder

A catch-all term when referring to the spectrum of autism

disorders

Under the pervasive developmental disorders (PDD) spectrum which

also includes Aspergers, childhood disintegrative, Retts and PDD no

otherwise specified (NOS) disorders

o

All share the inability to attain expected social and

communication, emotional, cognitive and adaptive abilities

Can be understood as disturbances of brain development with genetic

underpinnings.

AUTISM

A complex developmental disability that typically appears

during the first three years of life

The result of neurological disorder that affects the functioning

of the brain

TRIADS OF IMPAIRMENTS

o Impaired social relatedness

o Impaired communication and play

o Presence of stereotypic and/or ritualistic activities

A lifetime disability

Results from a brain dysfunction but the exact etiology is

unknown

Early and appropriate intervention have a positive impact on

overall outcome

THE CONCEPT OF DEVELOPMENTAL DISORDERS

Autism is a developmental disorder, a condition a child is

believed to be born with, or born with a potential fo

developing

This concept should be emphasized to parents. It has nothing to

do with pregnancy, poor child rearing, or anything in the

environment.


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PREVALENCE

The US Center for Disease Control has declared autism as the

fastest growing serious developmental disability

Autism rate doubles every 2 years:

o 1990: 1 out of 10,000

2007: 1 out of 150

A new CDC report:

o

One in every 110 American children

o One in every 70 boys

4:1 ratio of boys to girls

Represent a 57% increase from 2002 to 2006

An astonishing 600% rise in the past 20 years

Autism Epidemicor not?

The work epidemic must be used with caution. We must avoid unnecessary

panic and be mindful that labels can be misleading.

ETIOLOGY

Exact cause still is unknown

ASDs are biologically based neurodevelopmental disorders that

are highly heritable

GENETICS

Involve multiple genes; demonstrate great phenotypic variation

A rare mutation involving the deletion or duplication of 25

genes on chromosome 16 over 1% of autism cases in the US

(Autism Update, Harvard Magazine, May-June 2011)

Estimates of recurrence risks: 5-6% (range: 2-8%) when there is

an older sibling with an ASD and even higher when there are

already 2 children with ASDs in the family. (Dr. Eusebio said

that the risk is 6-10%)

AUTISM AND VACCINES

Researches on Vaccinations:

o The final report from IOM, Immunization Safety Review

Vaccines and Autism, released in May 2004, stated that

the committee did not find a link.

Until 1999, DPT, Hib, and Hep B contained thimerosal as a

preservative

Today, with the exception of some flu vaccines, none of the

vaccines to protect preschool aged children against 12

infectious diseases contain thimerosalas a preservative.

The MMR vaccine does not and never did contain thimerosal.

Varicella, (IPV) and PCV have also never contained thimerosal.

No scientifically substantiated association between the

administration of the MMR vaccine and development of AD.

Parents must be well educated that vaccines has nothing to do

with autism

This false belief came about because MMR is being given at

15months of age and the signs of autism are manifested at

18months.

Thimerosal was taken off from vaccines since 1990

BIOLOGIC BASIS Major brain structures implicated in autism: cerebellum

cerebral cortex, limbic system, corpus callosum, basal ganglia

and brainstem

Neurotransmitters: serotonin, dopamine, and epinephrine

Strong belief of Neurobiological alterations but cannot be

exactly pinpoint.

An interesting study was done wherein a Neuroscientist took

the head circumferences of infants diagnosed and suspected of

having Autism. He find out that there is an increase in the head

circumference of these children. His theory: this is because of

abnormal brain development or growth disregulation.

(Nelsons) Head circumference in AD normal or slightly small than normal a

birth until 2 months of age

Afterwards, show an abnormally rapid increase in head circumference

from 6-14 month of age

Increased brain volume in 2-4 years olds

o Increased volume of cerebellum, cerebrum and amygdala

o Marked abnormal growth in the frontal, temporal, cerebellar and

limbic regions of the brain

Followed by abnormally slow or arrested growth

o Areas of underdeveloped and abnormally circuitry in parts o

brains

Huge rise in prevalence rate

Globally affected

Raising figures

Environmental?

Result of unidentified risk

factors

Change in diagnostic

criteria

Improved detection

Rise in awareness

Better record keeping

More media attention


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Regression in overall behavior play, social skills,

communication

Emotional ability, out of control tantrums

Poor motor coordination

Fixate on objects (ie. Ceiling fans/bright lights of party)

Resists changes to specific routines/rituals

Self-injurious behavior

No fear of danger/pain

Dislikes to cuddle/be hugged

Unanimated facial expression or monotone voice

Extreme under/over activity

Diminished responses to pain (Nelson)

Lack of startle responses to sudden loud noises (nelson)

CLINICAL SIGNS ACCORDING TO NELSON

SOCIAL SKILLS

Impaired ability to engage in reciprocal social interactions

o abnormal eye contact

o failure to orient to name

o

failure to use gestures to point or show

o

lack of interactive playo

failure to smile

o lack of sharing

o lack of interest in other children

impairment in joint attention

deficits in empathy

deficits in understanding what another person might be thinking a

lack of theory of mind

VERBAL ABILITIES

range from being nonverbal to having some speech

speech have an odd prosody or intonation

characterized by echolalia, pronoun reversal, nonsense rhyming

PLAY SKILLS

little symbolic play

ritualistic rigidity

preoccupation with parts of objects

prefer solitary play

restrictive or repetitive interests or behaviors

ritualistic behavior

o often need to maintain a consistent, predictable environment

tantrum-like rages can accompany disruptions of routine

INTELLECTUAL FUNCTIONING

can vary from mental retardation to superior intellectual functioning in

select areas

some show typical development in certain skills and show areas of

strengths in specific areas

COMPREHENSIVE EVALUATION

Diagnosed by the clinical examination (Nelson)

DSM-IV criteria

Autism Diagnostic Interview Revised (ADI-R) and Autism Diagnostic

Observation Schedule (ADOS)gold standard diagnostic tools (Nelson)

Assorted checklist (eg. CARS, ADDS, M-CHAT, PDDST)

o Failure to meet age-expected language or social milestones are

important red flags for PDD (Nelson)

Cognitive testing

o Establish overall cognitive function and eligibility for services

(Nelson)

Adaptive skills testing

o Vineland Adaptive Behavior Scale (VABS) is essential to establish

priorities for treatment planning (Nelson)

DSM IV CRITERIA

When an individual displays 6 or more of 12 symptoms listed

across three (3) major areas:

o Social

o

Communication

o Behavior

DSM-IV-TR DIAGNOSTIC CRITERIA FORAUTISTIC DISORDER

A.

A total of six or more items from (1), (2) and (3) with at leas

two from (1) and one each from (2) and (3)

1. Evaluative impairment in social interaction as manifested

by at least two of the ff:

a. Marked impairment in the use of multiple nonverba

behaviors such as eye-toeye gaze, facial expression

body posture and gesture to regulate socia

interaction

b. Failure to develop peer relationships appropriate to

developmental level

c.

Lack of spontaneous seeking to share enjoymentinterests and achievements with others (eg. Lack o

showing, bringing or pointing out objects of interests

to other people)

d. Lack of social or emotional reciprocity (Note: in the

description, it gives one of the ff. as examples: not

actively participating in simple social play/games

prefers solitary activites or involving other activites

only as tools or mechanical aids)

2. Qualitative impairments in communication as manifested

by at least one of the following:

a. Delay in, or total lack of, the development of spoken

language (not accompanied by an attempt to

compensate through alternative modes o

communication such as gesture or mime)

b. In individuals with adequate speech, marked

impairment in the ability to initiate or sustain a

conversation with others

c. Stereotyped and repetitive use of language o

idiosyncratic language

d. Lack of varied, spontaneous make-believe play o

social imitative play appropriate to developmenta

level


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3. Restricted repetitive and stereotyped patterns of behavior,

interests, and activities, as manifested by at least one of

the following:

a. Encompassing preoccupation with one or more

stereotyped and restricted patterns of interest that is

abnormal either in intensity or focus

b.

Apparently inflexible adherence to specific,

nonfunctional routines or rituals

c.

Stereotyped and repetitive motor manners (e.g. hand

or finger flapping or twisting, or complex whole-body

movements)

d.

Persistent preoccupation with parts of objects

B. Delays or abnormal functioning in at least one of the following

areas, with onset prior to age 3 years: (1) social interaction, (2)

language as used in social communication, or 93) symbolic or

imaginative play

C. The disturbance is not better accounted for by Retts Disorder

or Childhood Disintegrative Disorder.

SPECIALIST/MULTIDISCIPLINARY TEAM

Developmental pediatrician

Pediatric neurologist

Child psychiatrist

Child psychologist

Speech pathologist

Occupational therapist

SPED teacher

Geneticist

Parent support groups

LABORATORY/DIAGNOSTICS

BAERhearing test

EEGsome have seizures

Neurological imaging

Metabolism screening (thyroid, lead)

Chromosomal studiesto rule out Fragile X syndrome

Critical Elements of the Evaluation (Nelson)

Detailed developmental history

o Review of communicative and motor milestones

Medical history

o Discussion of possible seizures, sensory deficits or other medical

conditions

Family history

o

Presence of other developmental disorders

Review of current and past psychotropic medications

o

Review of medication dosages and behavioral response, along

with adverse effects

PROBLEMS THAT MAY ACCOMPANY (ASD)

Sensory problems

Hypersensitivity to certain sounds, textures, tastes and smells

Sounds like vacuum cleaner, ringing of telephone, sudden

storm, waves lapping the shoreline will cause these children to

cover their ears and scream

Mental Retardation

Many children with ASD have some degree of menta

impairment

Seizures

Prevalence: 11-39%

HigHer prevalence if 42% with co-morbid mental retardation

and motor deficits

Onset of epilepsy in ASDs has two peaks: before 5 years of age

and adolescent

PATHOLOGY (Nelson)

Head circumference in AD normal or slightly small than normal a

birth until 2 months of age

Afterwards, show an abnormally rapid increase in head circumference

from 6-14 month of age

Increased brain volume in 2-4 years olds

o Increased volume of cerebellum, cerebrum and amygdale

o Marked abnormal growth in the frontal, temporal, cerebellar and

limbic regions of the brain Followed by abnormally slow or arrested growth

o Areas of underdeveloped and abnormally circuitry in parts o

brains

o

Most affected areas for higher-order cognitive, language

emotional and social functions

MANAGEMENT Primary goals of treatment are to maximize the childs ultimate

functional independence and quality of life

o Minimizing the core features of the disorder

o Facilitating development and learning

o Promoting socialization

o

Reducing maladaptive behaviorso Educating and supporting families

Treatment is primarily non medical

TREATMENT APPROACHES

Applied Behavioral Analysis (ABA)

DIR Method (Floortime)

Miller method

Relationship Development Intervention

Son-Rise

TEACCH Program

Discrete Trial Training (DTT)

CLINICAL THERAPIES

Speech and language therapy

Augmentative communication

Picture exchange communication

Sign language

Sensory Integration Therapy

Occupation Therapy

Physical therapy


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Occupational therapy is done first. If the child (70-80%) is looking at

you and is responding at you, thats the time you add speech

therapy. And if the child is ready for school, must assess if the child is

to go to a special school or regular school.

COMPLEMENTARY THERAPY (BIOLOGICAL)

Immunoregulatory interventions

o Dietary restriction of food allergens

o Administration of immunoglobulin or antiviral agents

Detoxification therapies

o chelation

Gastrointestinal treatment

o Digestive enzymes

o Antifungal agents

o Probiotics

o yeast-free diet, gluten/casein-free diet

o Vancomycin

Dietary supplements

o Vit. A, B6, B12, C, magnesium, folic acid, folinic acid,

dimethylglycine and trimethylglycine, inositol, fatty acids,

omega-3, various minerals and others

o Hyperbaric therapy

Therapy is still the best known management and not these niological

treatment methods.

Family Support

Respite

Support groups and web sites

Psychological services

Seminar and conference services

List ServicesAutism Society of the Philippines it is hard for parents to accept, as

if they have a child who is terminally ill. It is normal that parents

undergo the normal process of acceptance. If a parent cannot

accept, just lay your cards and explain the developmental problems

in intellect and language of the child that need to be corrected.

If it improved, good then. If not, that is Autism. Because some grow

normal but still have signs of autism like eye fleeting.

Pharmacotherapy

Pharmacological intervention targets associated comorbid conditions

and problematic behaviors

1. SSRIs mood and anxiety symptoms and compulsive-like

behaviors

2. Typical antipsychotics (Haloperidol) reducing stereotypy and

facilitating learning

3.

Atypical neuroleptics for symptoms of agitation, irritability,

aggression, self-injury and severe temper outbursts

4. Stimulants (in moderate doses) children with hyperactivity and

impusivity

5. -adrenergic agonists reduce hyperarousal symptoms including

hyperactivity, irritability, impusivity, and repetitive behavior

CURRENT LEVEL OF EVIDENCE

Biomedical Treatment Insufficient published evidence

need for treatment evaluation

studies, not for food selective

children

Tomatis Method Not supported by any published

research studies at present

Hyperbaric Oxygen Lack of well controlled

experimentations

Neurofeedback Needs more empirical research

Floor time (DIR) Looks promising, relatively new

but needs more research

Social skills A well structured group seems

very beneficial

Current Treatment Options

Early and Intensive Behavioral

Intervention (EIBI)

US Surgeon General has

recommended this a s effective

treatment

Treatment and Education of

Autism and RelatedCommunication Handicapped

Children (TEACCH)

National research council has

recommended this as plausibleintervention with positive

program evaluation date

Risperidone (Risperdal) Can be used as a treatmen

approach for problem behavio

only after a function based

approach was ineffective

PROGNOSIS

Most persons with PDD remain within the spectrum as adults

o Continue to experience problems with independent living

employment, social relationships, and mental health

Better prognosis is associated with higher intelligence, functiona

speech and less-bizarre symptoms and behavior.


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ATTENTION DEFICIT HYPERACTIVITY DISORDER

INTRODUCTION

Most common neurobehavioral disorder of childhood affecting school-

aged children

ADHD is a childhood onset neurobehavioral disorder which is

characterized by inattention, impulsivity, and hyperactivity.

ADHD Historic Timeline

1930: minimal brain damage

1968: hyperkinetic reaction of childhood (DSM-II)

1994: ADHD

2010: DSM-V

ADD (Attention Deficit Disorder) and ADHD are one and the same

PREVALENCE

Accounts for 30-40% of referrals

More common in boys than girls (5:1)

Estimated prevalence of children with ADHD is about 2-12%

(5.2%)

Can persist in adulthood:

o 8.10% of children have ADHD

o 9.6% of adolescents have ADHD

o 4.4 % of adults have ADHD

o Up to 65% of children with ADHD continue to experience

the DO into adulthood

Often underdiagnosed in children and adolescent

WHAT CAUSES ADHD?

Prevailing misconceptions such as:

o Kulang sa Pansin

o Temporary and will be outgrown

o Young, boytypical

o Laziness

o Diet: high in sugar intake

o Allergy

o Poor parenting, poor home life

o Poor teaching style in school

Hyperactivity can be normal for 2-4 years of age because this is the

run about stage but if this activity is impairing the childs functioning

then it is abnormal.

ADHD is heterogeneous behavioral DO with multiple possible

etiologies:

o Neurobiological factors

o Genetic origins (mean heritability is higher than

Schizophrenia)

o CNS insults

o Environmental factors (poor nutrition or exposure to Lead)

HERITABILITY OF ADHD

Mean heritability of ADHD is 0.75

There is a strong genetic component to ADHD

o 2 candidate genes: dopamine transporter gene (DAT1) and

dopamine 4 receptor gene (DRD4)

NEUROBIOLOGY OF ADHD

PET scan shows decreased cerebral metabolism in brain area

controlling attention

It is believed that there is a diminished blood flow to the frontal lobe,

which is the center of executive function, attention, and

concentration.

Nuerobiochemical Imbalance: Lack of Norepinephrine and

Dopamine. That is why medication plays a very important role in

management.

ENVIRONMENTAL CONTRIBUTION

Maternal drug use

Maternal smoking

Alcohol use during pregnancy

Prenatal or postnatal exposure to lead

Food colorings and preservatives have inconsistently been associated

with hyperactivity in previously hyperactive children

Psychosocial family stressors

Prenatal or perinatal insults (premature asphyxiated, stormy

course of neotatal)

Maternal depression

INTERPLAY OF ETIOLOGIC FACTORS

Exact etiology is unknown but it is believed that it is of

Neurobiological problem and environmental factors play an

important role.

SIGNS AND SYMPTOMS

Characterized by (CORE SYMPTOMS):

o Inattention

o Impulsivity


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o Hyperactivity

Other symptoms:

o Non compliance

o Impulse aggression

o Social interaction

o Academic efficiency

o Academic accuracy

o Irritable

o

Problems with sleep

EARLY INDICATORS

Diagnosis not made until 4years of age but early signs can be

seen

Before I was born, mom said I love to do cartwheels in her

belly

In infancy, may be characterized by unpredictable behavior,

shrill crying, irritability and overactivity

May show only brief periods of quiet sleep

Clinical manifestations may change with age

o Preschool children motor restlessness and, aggressive and

disruptive behavior

o Older adolescents and adults disorganized, distractible, and

inattentive symptoms

SYMPTOMS OF HYPERACTIVITY

Squirms and fidgets

Cannot stay seated

Runs or climbs excessively

Cannot play or work quietly

Is on the go or driven by a motor

Talks excessively

Pushing, hitting other children thinking that it is still part of play

Impatient

SYMPTOMS OF IMPULSIVITY

Blurts out answers

Cannot wait for his turn

Intrudes, interrupts others

SYMPTOMS OF INATTENTION

Carelessness

Difficulty sustaining attention in activity

Does not listen

Does not follow through with tasks

Is disorganized

Avoids/dislikes tasks requiring sustained mental effort

Loses important items

Easily distracted

Forgetful in daily activities

ADHD CLINICAL SUBTYPES

3 subtypes: (Nelson)

o ADHD, predominantly inattentive type

Often includes cognitive impairment

More common in females

o

ADHD, predominantly hyperactive-impulsive type

More common in males

o

ADHD, combined type

COMPARING BOYS AND GIRLS

BOYS GIRLS

Frequency of Referral more Less

Symptom recognition Earlier Later

ADHD type Combined (5:1) Pred. Inattentive (2:1)

Signs Externalizing:

aggression,

overreactivity

Internalizing:

Underachievement,

daydreaming

Females are diagnosed late because they manifest inattention than

the usual hyperactivity

ADHD DEVELOPMENTAL TREND BY AGE

As the child grows to adult, the hyperactivity and impulsivity would

decrease and what would remain is the Inattention.They usually

are impatient, restless, and disorganized.

ADHD: CO-MORBIDITY

Its presence is more the rulerather than the exception

Only ~30% will have pure ADHD

In those with co-morbidities:

o >80% have one co-morbidity

o 60% have at least 2 co-morbidities

Co-morbidities persist and more obvious when the patient

grows into an adult.

Most common co-morbidity is ODD (Oppositional Defiant

Disorder)


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DIAGNOSIS OF ADHD

History

o History of the presenting problems

o The childs overall health and development

o Social and family history

o Maternal and birth history

o Good family history (genetic) you can see if one of

parents have ADHD mother talking a lot or father

fidgeting

Interviews (parents, teachers and patient)

o Determine functional impairment at home and in

school/job setting

o Behavioral rating scale should be answered by both

parents and teachers because one of the criteria of

diagnosis is that this condition should be happening in two

settings

Rating scales to corroborate clinical symptoms

PE, VS, physical explanations for DO, secondary conditions,

drug contraindictation

DSM-IV TR criteria, ICD-10 criteria

Make assessment for co-morbid conditions

Interview should emphasize factors that might affect the development

or integrity of the CNS or reveal chronic illness, sensory impairments, or

medication use that might affect the childs functioning (Nelson)

DSM-IV CRITERIA

States that the behavior must be:

o developmentally inappropriate

o must begin before age 7 years

o must be present for at least 6 months

o must be present in 2 or more settings

o

must not be secondary to another disorder

Persistent pattern of inattention and/or hyperactivity or

impulsitivity

o

No. of symptoms (6 or more)

o Duration of symptoms (> 6 mos)

o Onset (before 7 y/o)

o Setting (2 or more settings)

o Severity (developmentally inappropriate)

o Impact (significant impairment in social, academic and

occupational functioning)

o Exclusion (other medical disorders)

Behavior Rating Scales

Useful in establishing the magnitude and pervasiveness of the

symptoms

Not sufficient alone to make a diagnosis of ADHD

1.

ADHD Diagnostic Rating Scale

2.

Conner Rating Scales (parent and teacher)

3. ADHD Index

4. Swanson, Nolan and Pelham Checklist

5. ADD-H: Comprehensive Teacher Rating Scale

Conners is the most commonly used

Physical Examination and Laboratory Findings No laboratory tests available

Presence of HPN, ataxia or thyroid DO should prompt further diagnostic

evaluation

Impaired fine motor movement and poor coordination and other soft

signs are common

o finger tapping

o alternating movements

o

finger-to-nose

o skipping

o tracing a maze

o cutting paper

STANDARD ADHD TREATMENTEDUCATION

Understanding the DO

o Medical cause

o Not due to parenting

Environmental restructuring

o Classroom changes

o ADHD-friendly modification in family, work, leisure

activities

o Structure, list, delegating

Parent support groups: www.chadd.org or www.add.org

Educate parents that this condition is inborn and that poo

parenting is not the cause of the problem, how to handle thechild

PSYCHOSOCIAL INTERVENTION

Parent education

o Reinforce positive behavior and correct negative behavior

o Establish and maintain house rules

Academic Skill Training

o Focus on time management, study skill and following

directions


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Social Skill Training

o Target specific behaviors (e.g. playground aggression)

Behavioral management in the time frame of 8-12 sessions

o Stress-conflict resolution

ADHD children does not have to be placed in special schools because

actually these children are very smart with normal IQ unless in cases

with concomitant intellectual disbilities

MEDICATION

Remains as one of the most successful treatment for child with

ADHD

As effective as standard therapy treatment. Dr. Eusebio have

patients in the province with no therapy but on medication and

they are doing alright.

Medications increases the neurotransmitter in the synapses

MEDICATIONS APPROVED BY FDA

Psychostimulant (FIRST LINE)

Amphetamine preparation

o

Addreallo Dexedrine

Methylphenidate preparation (best)

o Ritalin

o MPHOros (Concerta)

o Transdermal delivery system (patch)

Psychostimulants found to improve core symptoms of ADHD

(inattention, impulsivity and hyperactivity). It also improve other

symptoms such as noncompliance, impulsive aggression, social

interactions, academic efficiency, academic accuracy and family

dynamics

Limitations to Psychostimulants

Tolerability issues

o Insomnia, irritability, headache, appetite suppression

o Parent/patient perception of mood and personality

change on medication

o Adverse effect on height and weight

o In other countries used as diet pills that is why it is

regulated

Co-morbid conditions (tics, anxiety) aggrevated

Controlled substance concerns

o Social stigma

o Diversion and abuse potential (DEA Schedule II drugs)

o Prescribing Inconvenience

Noradrenergic Reuptake Inhibitor (SECOND LINE)

Atomoxetine (Strattera)

Giving psychostimulant to somebody who Is already hyperactive, it is

postulated that in ADHD the stimulatory portion of the brain is the

only one activated and the inhibitory center is dormant or asleep

The psychostimulants will work on the inhibitory center to correct

the imbalance.

Alternative Medications (Not Approved by FDA)

Antidepressants

o Bupropion

o Imipramine

o Nortriptyline

Alpha-2 Adrenergic Agents/Antihypertensives

o Clonidine (used prior to Methylphenidate but will only cure

the impulsivity and not the hyperactivity)

o Guanfacine

Arousal Agents

o Modafinil

Non-Traditional Therapies for ADHD

Dietary management

Bio/Neurofeedback Therapy

Tomatis Method

All are controversial and alternative treatments!!!

BURDEN OF ADHD

Impacts on all aspects of life

Childhood: Impair peer relationship, academic limitation

socioemotional problem

Other children do not involve ADHD child because they are too

aggressive

Academic limitations because as more and more academic skills

need to learn the lack of attention impairs the receptivity to

learning, careless mistakes and not review test exams


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Adolescents: at risk of getting into risk taking behaviors like

alcohol and drug abuse, motor and vehicular accidents

Adults: moving from one job to another, or relationship from

one to another.

Adult Outcome of Children with ADHD

Adults who function fairly well: 30%

Adults who continue to have significant problems with

concentration, impulsivity and social interaction: 50-60%

Adults who have psychiatric or antisocial problems or both: 10-

15%

ADHD is not yet curable but certainly is manageable!

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4.1Pediatrics Autism and ADHD 2014A

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Transcript of 4.1Pediatrics Autism and ADHD 2014A