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CHILD PSYCHIATRY

CHILD PSYCHIATRY. Ishraq A rabiat. Autism Spectrum Disorder. DEFENETION EPIDEMYOLOGY ETIOLOGY DIAGNOSIS AND CLINICAL FEATURES DIFFERENTIAL DIAGNOSIS COURSE AND PROGNOSIS TREATMENT.

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CHILD PSYCHIATRY

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  1. CHILD PSYCHIATRY IshraqArabiat

  2. Autism Spectrum Disorder • DEFENETION • EPIDEMYOLOGY • ETIOLOGY • DIAGNOSIS AND CLINICAL FEATURES • DIFFERENTIAL DIAGNOSIS • COURSE AND PROGNOSIS • TREATMENT

  3. previously known as the pervasive developmental disorders ,phenotypicallyheterogeneous group of neurodevelopmental syndromes, with polygenic heritability. D S M 4

  4. DSM5

  5. 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.

  6. 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.

  7. ETIOLOGY AND PATHOGENESIS

  8. Genetic • 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.

  9. 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’ untranslatedregion 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.

  10. 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-aminobutyricacid (GABA) inhibitory system. • The first biomarker identified in autism spectrum disorder was elevated serotonin in whole blood, almost exclusively in the platelets.

  11. Several studies found increased total brain volume in children younger than 4 years of age with autism spectrumdisorder, 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.

  12. 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

  13. Prenatal and Perinatal Factors • 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. • prenatal factors: 1. advanced maternal and paternal age at birth. 2.maternal gestational bleeding. 3. gestational diabetes 4. first-born baby.

  14. Comorbid Neurological Disorders 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.

  15. 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.

  16. DSM5 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: 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 .

  17. Criteria B: restricted, repetitive patterns of behavior, interests or activities, as manifested by at least 2 of the following: • 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 interststhat 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

  18. 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 impairementin social … Criteria E : Theses disturbances are not better explained by intellectual disability or global developmental delay . intellectual disability and autism frequently co-occur .

  19. 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 remainambidextrousat 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.

  20. Intellectual Disability. • Irritability includes aggression • self-injurious behaviors • Instability 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

  21. 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.

  22. COURSE 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. TREATMENT 1. Educational program 2. behavioral therapy

  23. Attention Deficit/Hyperactivity Disorder • DEFENETION • EPIDEMYOLOGY • ETIOLOGY • DIAGNOSIS AND CLINICAL FEATURES • DIFFERENTIAL DIAGNOSIS • COURSE AND PROGNOSIS • TREATMENT

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

  25. Epidemiology • affects 2.5% of adults and 7-8% of prepubertal elementary school children • M: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.

  26. Etiology

  27. Etiology Neurochemical Factors.Main NT is dopamine and Dysfunction in peripheral Epinephrine Neurophysiological Factors. EEG studies: increased theta activity, especially in the frontal region. 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 Psychosocial Factors. Severe chronic abuse, maltreatment and neglect

  28. 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, globuspallidus, caudate, thalamus, and cerebellum

  29. DSM5

  30. 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.

  31. 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.

  32. TREATMENT:

  33. STIMULANTS : • Methylphenidate (Ritalin) • Dextroamphetamine (Dexedrine) • Dextroamphetamine and amphetamine salt combinations (Adderall). • Vyvanse (lisdexamfetaminedimesylate)

  34. Methylphenidate • are 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. • 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.

  35. 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.

  36. AtomoxetineHCl • 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.

  37. 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

  38. Stimulants non stimulants • Dopamine • Fast acting • Onset 30-90 min • One dose /6-12 hrs • S/E decreseapettite/sleeping/anxiety /headahe • First line • 70-80% • NE • 2-4 weeks • One dose/2days • Moodiness • Rare liver disease • 20-30% • If stimulants not respond

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