Neurodevelopmental disorders are classified into Autism spectrum disorder Attention deficithyperactivity disorder Specific learning disabilities writingreading Communication disorderslanguagespeechsoundchildhood onset fluency disorders ID: 931789
Download Presentation The PPT/PDF document "Child psychiatry Done by : Rina Karbora..." is the property of its rightful owner. Permission is granted to download and print the materials on this web site for personal, non-commercial use only, and to display it on your personal computer provided you do not modify the materials and that you retain all copyright notices contained in the materials. By downloading content from our website, you accept the terms of this agreement.
Slide1
Child psychiatry
Done by : Rina Karborani
Slide2Neurodevelopmental disorders are classified into:
Autism spectrum disorder
Attention deficit/hyperactivity disorder
Specific learning disabilities (writing/reading)
Communication disorders(language/speech-sound/childhood onset fluency disorders)
Tic (
motor,vocal
) /Tourette’s
disorder
Intellectual disability
Motor disorders (developmental coordination disorder & stereotyping motor movement)
Slide3Autism spectrum disorder
is a neurological and developmental disorder that begins early in childhood and lasts throughout a person's life. It affects how a person acts and interacts with others, communicates,
and
learns.
Although autism can be diagnosed at any age, it is said to be a “developmental disorder” because symptoms generally appear in the first two years of
life
and in severe cases, a lack of
developmentally appropriate
interest in social interactions may be noted even in the first
year.
Slide4Delay of spoken language, inability to start
conversation,loss
of motor
skills,loss
of bowel control
Language delay, repetitive movements
Slide5DSM5 DIAGNOSTIC CRITERIA
:
Criteria A :
persistent deficit in
social communication
and
social interaction
across multiple contexts as manifested by :
1. Deficits in social-emotional reciprocity .
For example:
abnormal social approach and failure of normal back and forth conversation , reduced sharing of interests ,emotions or affect , and failure to initiate or respond to social interactions.
2. Deficits in nonverbal communicative behaviors used for social interaction. For example: poorly integrated verbal and nonverbal communication such as ; abnormalities in eye contact and body language or deficits in understanding and use of gestures to a total lack of facial expressions.
3. Deficits in developing, maintaining and understanding relationships.
For example :
difficulties adjusting behavior to suit various social contexts,
difficulties
in sharing imaginative play or in making friends
, and
absence of interest in peers .
Slide6•
Criteria B
:
restricted, repetitive patterns of behavior, interests or activities, as manifested by at least 2 of the following:
1)
Stereotyped or repetitive motor movements ,use of objects ,or speech .
-Simple motor stereotypes
-Lining up toys or flipping objects
2) 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 . 3)Highly restricted fixated intersts that are abnormal in intensity of focus .
-strong attachement with unusual objects -excessively circumscribed or perseverative interests. 4) 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
Slide7Criteria C :
Symptoms must be present in the early developmental period ( but may not become fully manifested until social demands exceed limited capacities )
Criteria D :
Symptoms
cause
i
mpairments
in social
life.
Criteria E :
Theses disturbances are not better explained by intellectual disability , global developmental delay or intellectual disability.
Slide8Epidemiology
Prevalence
:
about 8 cases per 10,000 children (0.08 percent).
Boys : girls = 4:1
clinicians and parents share concerns about a child who
by 12 to 18 months
has not developed any
language,or
delayed language accompanied by diminished social behavior are frequently the heralding symptoms in autism spectrum disorder
Slide9Etiology & pathogenesis
1) Genetic factors
up to 15% of cases appear to be associated with a known genetic mutation
Researchers
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.
Slide10Autism 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, 5. 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.
Slide112)Biomarkers
The first biomarker identified in autism spectrum disorder was elevated serotonin in whole blood, almost exclusively in the platelets.
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
There are also changes witnessed in the GABA inhibitory system
Slide123)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.
Slide134)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.
•Perinatal risk factors :
1. Umbilical cord complications 2. birth trauma 3. fetal distress 4. small for gestational age 5. low birth weight 6. low Apgar score 7. congenital malformation 8.ABO blood group system or
Rh factor incompatibility 9. hyperbilirubinemia
Slide14Slide15ASSOCIATED SYMPTOMS
•
physical anomalies:
1.
ear malformations
, and others that may reflect abnormalities in fetal development of those organs along with parts of the brain.
2.A greater than expected number of children remain
ambidextrous
at an age when cerebral dominance is established.
Slide16-
Disturbances in
Language Development and
Usage ;
difficulty putting meaningful sentences together, even when they have large vocabularies
-
pronoun reversals: A child might say, “You want the toy” when she means that she wants it. Difficulties in articulation are also common.
As well as:
self-injurious
behaviorsInsomnia
Slide17DIFFERENTIAL DIAGNOSIS
1
. social
communication disorder.
(
lack of conventional greeting others, taking turns in a conversation, and responding
to verbal
and nonverbal
cues)
2. schizophrenia with childhood onset 3. congenital deafness or severe hearing disorder or language disorder (Because children with autism spectrum disorder may appear mute or lack language development) 4. intellectual disability and psychosocial deprivation.
(The main differentiating features between autism spectrum disorder and intellectual disability are that children with intellectual disability syndromes generally display impairments in both verbal and nonverbal areas, whereas children with autism spectrum disorder are relatively weak in social interactions compared to other areas of performance.)
Slide18Comorbid Neurological Disorders
Electroencephalography (EEG) abnormalities and seizure disorders occur with greater than expected frequency in individuals with autism spectrum disorder. Four percent to 32 percent of individuals with autism spectrum disorder have grand mal seizures at some time, and about 20 to 25 percent show ventricular enlargement on computed tomography (CT) scans.
Slide19Course and prognosis
is typically a lifelong
best prognosis:
1. IQ>70 and develop communicative language by ages 5-7.
2. improved if the home environment is supportive
Slide20Treatment
Psychosocial interventions:
intensive
behavioral
programs ( Cognitive behavioral therapy)
parent
training
academic/educational
interventions
Components of these comprehensive treatments include expanding social
skills, communication, and language.
Slide21Psychopharmacological
Interventions
Psychopharmacological interventions in autism spectrum disorder are mainly directed
at ameliorating behavioral
symptoms rather than core features of
autism spectrum disorder. Target symptoms include
irritability
,
aggression
,
temper tantrums , self-injurious behaviors, hyperactivity, and impulsivityTwo second-generation antipsychotics, risperidone and aripiprazole have been approved by the (FDA) for treatment of irritability in individuals with autism spectrum disorder.* Several randomized placebo controlled
trials of methylphenidate(stimulant medication) have been conducted for the treatment of hyperactivity, impulsivity, and inattention in children and adolescents with autism spectrum disorder.
Slide22Attention Deficit/Hyperactivity Disorder
is a neuropsychiatric condition, characterized by a pattern of diminished sustained attention, and increased impulsivity or hyperactivity.
Epidemiologic studies suggest that ADHD occurs in about 5
%of youth
including children and adolescents, and about 2.5
%
of
adults.
-The
rate of ADHD in parents and siblings of children with ADHD is 2 to 8 times greater than in the general population.ADHD is more prevalent in boys than in girls, with the ratio ranging from 2:1 to as high as 9:1.
Slide23AGE
: 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.
Up to 70 percent of
children with
ADHD meet criteria for a comorbid psychiatric disorder, including
learning disorders
, anxiety disorders, mood disorder conduct disorders, and substance
use.
disorders.
Slide24Etiology
1)Genetic factors :
the
etiology of ADHD is largely
genetic(multiple genes) ,
with a heritability of approximately 75
% that influence the production of neurotransmitters.
-2) neurochemical factors:
dopamine is a major focus of clinical
investigation. (low dopamine level)
Animal studies have shown that other brain regions such as locus ceruleus, which consists predominantly of noradrenergic neurons (norepinephrine) , also play a major role in attention.3) Neurophysiological Factors EEG studies: increased theta activity, especially in the frontal region.
Slide254)
Developmental
Factors
Premature birth and
mothers who had maternal
infection during pregnancy. Reports indicated that September is a peak month for births of children with ADHD with and without comorbid learning disorders.
5)
Neuroanatomical correlations with ADHD:
the brainstem, which contains the reticular thalamic nuclei function, isinvolved in sustained attention. A review of (MRI), (PET), and single photon emission computerizedtomography (SPECT) suggests that populations of children with ADHD show evidence ofboth decreased volume and decreased activity in prefrontal regions, anterior cingulated,globus pallidus
, caudate, thalamus, and cerebellum. PET scans have also shown thatfemale adolescents with ADHD have globally lower glucose metabolism than bothcontrol female and male adolescents without ADHD.
Slide26DSM-5 criteria
the
DSM
-
5
diagnosis of
ADHD
requires ≥6 symptoms of hyperactivity and impulsivity or ≥6 symptoms of inattention
Slide27Differential 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.
Slide28Course 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.
Slide29Treatment
Pharmacologic treatment
is considered the first line
of treatment
for ADHD. Central nervous system stimulants are the first choice of agents
in that
they have been shown to have the greatest
efficacy.
Drugs are divided into
stimulant
and non-stimulant drugs.Stimulants are the better choice and used most commonly , they work by increasing dopamine levels, they consist of 3 groups: Ritalin group ( methylphenidate)Adderall group ( mixed amphetamine salts) Dexedrine group ( dextroamphetamine ) Vyvanse (lisdexamfetamine dimesylate) is a pro-drug
of dextroamphetamine and is FDA approved for children above 6 years old.
Slide30Methylphenidate
•
dopamine agonists
•
FDA approved for children 6 years and older
•Methylphenidate preparations are highly effective in up to three fourths of children, with relatively few adverse effects.
•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. -risk of addiction In children with a history of motor tics, methylphenidate should be used in caution. Stimulant drugs are contraindicated In children with cardiac abnormalities.
Slide31Non-stimulant medications ( like
atomoxetine
) :
Less effective than stimulants
Nonstimulants
don’t tend to cause agitation,
or insomnia
. They also don’t pose the same risk of abuse or addiction like stimulants do.
they
have a longer-lasting and smoother effect than many stimulants, which can take effect and wear off abruptly.
Slide32Atomoxetine
is a norepinephrine uptake inhibitor approved by the FDA for the treatment of
ADHD in children age 6 years and older.
Its half-life is approximately 5 hours and it is usually administered twice daily
*Most
common side effects
include,
abdominal discomfort, dizziness, and irritability. In some cases, increases
in blood pressure and heart rate
have been reported black box warning for potential increases in suicidal thoughts and hepatotoxicity
Slide33Thank you