CHILD PSYCHIATRY Ishraq - PowerPoint Presentation

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CHILD PSYCHIATRY

Ishraq Arabiat

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Autism Spectrum Disorder

DEFENETION EPIDEMYOLOGY ETIOLOGYDIAGNOSIS AND CLINICAL FEATURES DIFFERENTIAL DIAGNOSIS

COURSE

AND

PROGNOSISTREATMENT

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previously known as the pervasive developmental

disorders ,phenotypically heterogeneous group of neurodevelopmental syndromes, with polygenic heritability.

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D

S

M

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DSM5

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EPIDEMIOLOGY

Prevalence the current prevalence estimated at approximately 1 %

in

the United States.

Autistic disorder,

about 8 cases

per 10,000 children (0.08 percent

).

Sex Distribution Boys : girls = 4:1

AGE Autism spectrum disorder is typically evident during the

second year of life

, and in severe cases, a

lack of developmentally appropriate interest in social interactions

may be noted even in the first year.

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clinicians and parents share concerns about a child who

by 12 to 18 months has not developed any language, and delayed language accompanied by diminished social behavior are frequently the heralding symptoms in autism spectrum disorder.

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ETIOLOGY AND PATHOGENESIS

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Genetic

up to 15% of cases appear to be associated with a known genetic mutationResearchers who screened the DNA of more than 150 pairs of siblings with autism spectrum disorder found evidence of two regions on chromosomes 2 and 7

containing genes

that may contribute to autism spectrum disorder. Additional genes hypothesized

to be involved in autism spectrum disorder were found on

chromosomes 16 and 17

.

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Autism may occurs with other conditions .

The most common of these inherited disorders is 1.Fragile X syndrome, In 2

to 3

%

of individuals with autism spectrum

disorder repeat

in the

5’

untranslated region of the FMNR1 gene,. Children with fragile X syndrome characteristically exhibit

1.intellectual disability, 2.gross

and fine motor impairments,

3.

an

unusual

facies

,

4.macroorchidism

,

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significantly

diminished expressive language ability.

2.Tuberous

sclerosis

,

characterized

by multiple benign

tumors. Up to 2 % of children with autism spectrum disorder also have tuberous sclerosis.

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Biomarkers in Autism Spectrum Disorder

Several biomarkers of abnormal signaling in the 5-HT system , Because 5-HT is known to be involved in brain development, it is possible that the changes in 5-HT regulation may lead to alterations in neuronal migration and growth in the brain.

the

mTOR linked synaptic plasticity mechanisms

,

and alterations of the γ-

aminobutyric

acid (GABA) inhibitory system.

The first biomarker identified in autism spectrum disorder was elevated serotonin in whole blood, almost exclusively in the

platelets.

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Several studies found

increased total brain volume in children younger than 4 years of age with autism spectrum disorder, whose neonatal head circumferences were within normal limits or slightly below. By about age 5 years, however, 15 to 20 percent of children with autism spectrum

disorder developed

macrocephaly

.

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Immunological Factors

Several reports have suggested that immunological incompatibility (i.e., maternal antibodies directed at the fetus) may contribute to autistic disorder. The lymphocytes of some

autistic children react with maternal antibodies, which raises the possibility

that embryonic

neural tissues may be damaged during gestation. These reports usually reflect single

cases rather than controlled studies, and this hypothesis is still

under investigation

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Prenatal and Perinatal Factors

prenatal factors: 1.

advanced maternal and

paternal age at birth.

2.

maternal gestational bleeding.

3. gestational diabetes

4.

first-born baby.

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Perinatal

risk factors :

1.

Umbilical cord complications

2.

birth trauma

3.

fetal distress

4.

small for gestational age

5.

low birth weight

6.

low 5-minute

Apgar

score

7.

congenital malformation

8.

ABO blood group system or

Rh

factor incompatibility

9.

hyperbilirubinemia

.

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1. Electroencephalography(EEG)abnormalities (10 -83%) of children with the previously defined autistic disorder, and although

no

EEG finding is

specific

to autistic disorder.

2.

seizure

disorders .(4-32%) of individuals with autism spectrum disorder have grand mal seizures

at some time, 3.

(

20 -25 %)

show

ventricular enlargement

on

(CT)

scans

.

Comorbid

Neurological Disorders

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Psychosocial Theories

Studies comparing parents of children with autism spectrum disorder with parents of normal children have shown no significant differences in child-rearing skills.

Kanner’s

early

speculations that

parental emotional factors

might be implicated as

contributing to

the development of autism spectrum disorder have been clearly refuted.

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Criteria A : persistent deficit in social

communication

and social

interaction across multiple contexts as manifested by :

DSM5 DIAGNOSTIC CRITERIA :

1. Deficits in

social-emotional reciprocity .

For example: from abnormal social approach and failure of normal back and forth conversation to reduced sharing of interests ,emotions , or affect ,to failure to initiate or respond to social interactions.

2. Deficits in

nonverbal communicative behaviors

used for social interaction.

For example: from poorly integrated verbal and nonverbal communication to abnormalities in

eye contact

and body language or deficits in understanding and use of

gestures

to

a total lack of facial expressions and nonverbal communications.

3. Deficits

in developing, maintaining and understanding relationships.

For example : from difficulties adjusting behavior to suit various social contexts, to difficulties in sharing imaginative play or in making friends to absence of interest in peers .

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Criteria B

: restricted, repetitive patterns of behavior, interests

or

activities

, as manifested by at

least 2

of the following:

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Stereotyped or repetitive motor

movements ,use of objects ,or speech .

Simple motor stereotypes

Lining up toys or flipping objects

Echolalia

Idiosyncratic phrases

Insistence on sameness , inflexible

adherence to routines or ritualized patterns of verbal or nonverbal behavior.

-extreme distress at small changes.

-difficulties with transitions .

-rigid thinking patterns

-same food every day .

Highly

restricted fixated

intersts

that are abnormal in intensity of focus .

-strong

attachement

or preoccupation with unusual objects

-excessively circumscribed or

perseverative

interests.

Hyper or

hypoactivity

to sensory input

or unusual interest in sensory aspects of the environment

-apparent indifference to pain/temperature

-adverse response to specific sounds or textures

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Criteria C :

Symptoms must be present in the early develpopmental period ( but may not become fully manifest until social demands exceed limited capacities )Criteria D :

Symptoms

cause

impairement

in social …

Criteria E :

Theses disturbances are not better explained by intellectual disability

or global developmental delay . intellectual disability and autism frequently co-occur .

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ASSOCIATED SYMPTOMS

minor physical anomalies:such as ear malformations, and others that may reflect abnormalities in fetal development of those organs along with parts of the brain.

A greater than expected number of children remain

ambidextrous

at an age when cerebral dominance is established.

Behavioral Symptoms:

1. Language Development and Usage difficulty putting meaningful sentences together, even when they have large vocabularies

2.

pronoun reversals

: A child might say, “You want the toy” when she means that she wants it. Difficulties in articulation are also common.

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Intellectual Disability.

Irritability includes aggressionself-injurious behaviorsInstability of Mood and Affect. Hyperactivity and Inattention are both common behaviors in young children.

Insomnia a frequent sleep problem among children and adolescents

.

Minor Infections and Gastrointestinal Symptoms.

Precocious Skills

or splinter skills of great proficiency, such as

prodigious rote memories or calculating abilities, hyperlexia and musical abilities

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DIFFERENTIAL DIAGNOSIS

1. social (pragmatic) communication disorder.

2.

DSM-5 communication disorder.

3.

schizophrenia with childhood onset

4. congenital deafness or severe hearing disorder;

5. intellectual disabillity and psychosocial deprivation.

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COURSE AND PROGNOSIS

is typically a lifelongbest prognosis: 1. IQ>70

and develop communicative language

by ages 5-7.

2.

improved if the home environment is supportive.

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TREATMENT

1. Educational program

2. behavioral therapy

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Attention Deficit/Hyperactivity DisorderDEFENETION EPIDEMYOLOGY ETIOLOGYDIAGNOSIS AND CLINICAL FEATURES

DIFFERENTIAL DIAGNOSIS

COURSE

AND

PROGNOSIS

TREATMENT

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DEFENETION

ADHD: is a neuropsychiatric condition, characterized by a pattern of diminished sustained attention, and increased impulsivity or hyperactivity.

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Epidemiology

affects 2.5% of adults and 7-8% of prepubertal elementary school childrenM:F ratio

2-9:1.

First-degree biological relatives are at high risk for developing ADHD as well as other psychiatric disorders.

AGE:

Symptoms of ADHD are often present by age

3 years

, but unless they are very severe, the diagnosis is frequently not made until the child is in kindergarten, or elementary school.

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Etiology

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Etiology

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Genetic Factors

the etiology of ADHD is largely genetic, with a heritability of approximately

75 %

.

found an association of the dopamine transporter gene

(DAT1)

and dopamine

4 receptor

seven-repeat allele gene (DRD4) gene with

ADHD

Neurochemical

Factors

.

Main NT is

dopamine

and

Dysfunction in peripheral Epinephrine

Neurophysiological

Factors

.

EEG studies: increased

theta

activity, especially in the

frontal region

.

Psychosocial Factors

.

Severe chronic abuse, maltreatment

and neglect

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Developmental Factors

.

Premature

birth and whose mothers were observed to have maternal

infection

during pregnancy.

Reports indicated that

September

is a peak month for births of children with ADHD with and without

comorbid

learning disorders.

Neuroanatomical

correlations with ADAH:

the superior and temporal

cortices

+

focusing

; external parietal and corpus

striatal

regions

+

motor executive functions; the hippocampus

+

encoding of memory traces.

in prefrontal regions

+

shifting from one stimulus to another, anterior cingulated

gyrus

,

globus

pallidus

, caudate, thalamus, and cerebellum

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DSM5

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Differential Diagnosis

Anxiety.Mania. conduct disorder.

Specific learning disorders

of various kinds must also be distinguished from ADHD; a child may be unable to read or do mathematics because of a learning disorder, rather than because of inattention.

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Course and Prognosis

Symptoms persist into adolescence in 60 -85% of cases, and into adult life in approximately 60 % of cases. Persistence is predicted by a

family history

of the disorder,

negative life events

, and

comorbidity

with conduct symptoms, depression, and anxiety disorders.

Most patients with the disorder, however, undergo partial remission and are vulnerable to substance use disorders, conduct disorder and mood disorders.

Learning problems often continue throughout life. When remission occurs, it is usually between the ages of

12-20.

Overactivity

is usually the first symptom to remit, and distractibility is the last.

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TREATMENT:

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STIMULANTS :

Methylphenidate (Ritalin)Dextroamphetamine (Dexedrine)Dextroamphetamine and amphetamine salt combinations (Adderall

).

Vyvanse

(lisdexamfetamine

dimesylate

)

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Methylphenidate

are dopamine agonistsFDA approved for children 6 years and olderMethylphenidate preparations are highly effective in up

to three fourths

of children, with relatively few adverse effects.

Concerta

,

the 10- to 12-hour extended-release form of methylphenidate, is administered

once

daily in the morning.

Side effects:headaches, abdominal pain, nausea, and insomnia.

Some children experience a

rebound effect

, in which they become mildly irritable and appear to be slightly hyperactive for a brief period when the medication wears off.

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In children with a history of

motor tics, methylphenidate should be used in caution.Another common concern about use of methylphenidate preparations over long periods is potential growth suppression.

When given

“drug holidays”

on weekends or summers, children tend to eat more and also make up the growth.

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Atomoxetine HCl

is a norepinephrine uptake inhibitor approved by the FDA for the treatment of ADHD in children age 6 years and older. Atomoxetine

is well absorbed by the gastrointestinal tract, and maximal plasma levels are reached

in 1 to 2 hours

after ingestion.

Its half-life is approximately 5 hours and it is usually administered twice daily.

Children who received combined

atomoxetine

and fluoxetine experienced greater increases in blood pressure and pulse.Atomoxetine

is metabolized by the cytochrome P450 2D6

. Drugs that inhibit CYP 2D6, including

fluoxetine

,

paroxetine

, and

quinidine

, may lead to increased plasma levels of this medication.

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Most common side effects include diminished appetite, abdominal discomfort, dizziness, and irritability. In some cases, increases in blood pressure and heart rate have been reported.

Unlike the stimulants, Strattera carries with it a black box warning for potential increases in suicidal thoughts and

hepatotoxicity

DDX:

bipolar II disorder, and

cyclothymia

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Stimulants non stimulants

DopamineFast acting Onset 30-90 min One dose /6-12 hrsS/E decrese

apettite

/sleeping/anxiety /headahe

First line

70-80%

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NE

2-4 weeks

One dose/2days

Moodiness

Rare liver disease

20-30%

If stimulants not respond