1. CHAPTER FIFTEEN Pervasive Developmental Disorders

2. Overview n nDefinitions n nSymptoms n nSubtypes n nEpidemiology & Course n nEtiology n nTreatment

3. Overview n nDefinitions nSymptoms nSubtypes nEpidemiology & Course nEtiology nTreatment

4. Definitions n nPervasive Developmental Disorders (PDDs) or Autistic Spectrum Disorders … are disorders that involve profound disturbances in relationships, stereotyped activities and unusual behaviors, and communication difficulties. n nPDDs begin early in life and involve severe impairments in particular areas of functioning. n nAutistic Disorder is the most researched PDD.

5. Overview nDefinitions n nSymptoms nSubtypes nEpidemiology & Course nEtiology nTreatment

6. Symptoms Autism is characterized by… n nEarly onset n nProfound indifference to social relationships (impaired social interactions) n nOdd or stereotypical behavior n nSeverely impaired or nonexistent communication skills n nDisorder typically has chronic and unremitting course

7. T.O.M.: Sally-Ann Task

8. Symptoms: Others n nApparent sensory deficits n nSelf-injury n nSavant performance

10. Overview nDefinitions nSymptoms n nSubtypes nEpidemiology & Course nEtiology nTreatment

11. Subtypes nAsperger’s Disorder nChildhood Disintegrative Disorder nRett’s Disorder

12. Subtypes Asperger’s Disorder Childhood Disintegrative Disorder Rett’s Disorder  Descriptively identical to Autism  No Major Communication Problems  Higher intellectual functioning  Is this a separate disorder?  Poorly understood  Severe problems in social interaction and communication  Stereotyped behaviors  Onset – after 2 years of normal development  Clearly distinct condition  5 Months of normal development, then:  Decrease head growth  Loss of purposeful hand movements  Loss of social engagement  Poor coordination  Marked delay in language  Typically only in females

13. Overview nDefinitions nSymptoms nSubtypes n nEpidemiology & Course nEtiology nTreatment

14. Epidemiology n nFrequency of Autism and PDDs   Between 30 to 60 in 10,000 children suffer from autism n nWhy such an increase?   Environment (MMR vaccinations)?   Broadened diagnostic criteria (i.e. Asperger’s)?   Increased awareness?

15. Prevalence in the U.S.

16. Prevalence in Illinois

17. Epidemiology n nGender Differences   Three to four times as many boys as girls n nAutism also is much more common among siblings of a child with autism, suggesting possible genetic causes.

18. Course & Outcomes n nLifelong Disorder n nOne study followed 63 children with autism into adulthood.   One person functioning in “normal” range   22 achieved fair to good adjustment   The remainder lived in institutions or other special settings n nAsperger’s Disorder has better prognosis

19. Course & Outcomes nTwo Important Developmental Periods  Early Preschool  Developed Language Skills by 5 or 6  Early Adolescence  Cognitive and social skills may improve  No way to predict path for a given child  Seizure disorders nHigher IQ during early school years also positive prognostic indicator

20. Overview nDefinitions nSymptoms nSubtypes nEpidemiology & Course n nEtiology nTreatment

21. Etiology: Psychosocial n nParental hostility and/or inappropriate reinforcement n n“Refrigerator Parents” n nNo evidence to support this claim! n nLack of empirical evidence to support psychological causal factors.

22. Etiology: Biological n nA number of findings indicate that biological abnormalities play an important role in the etiology of autism.   Seizure disorders by adolescence or early adult life   Increases in the prevalence of autism among children with genetic and infectious diseases   Prevalence of autism higher among immediate relatives   Prevalence is particularly high among twin pairs   A disproportionate number of neurological abnormalities have been identified among children with autism

23. Etiology: Biological n nConcordance Rates   MZ = 60%   DZ = 0% nBut why are DZ twin concordance rates so low?  Combination of genes or spontaneous genetic mutation

24. Etiology: Biological nNeurochemicals  Endorphins  Elevated levels  Critics argue this theory is too narrow  Self-Destructive Behavior?  Neuropeptides  Oxytocin & Vasopression

25. Etiology: Biological n nAbnormalities in brain structure   Left cerebral hemisphere?   Subcortical brain structures   Limbic System   Cerebellum   Front Lobe n nSeveral different sites may be damaged n nStructural abnormalities result of abnormal brain development

26. Overview nDefinitions nSymptoms nSubtypes nEpidemiology & Course nEtiology n nTreatment

27. Treatment n nMedications   Antipsychotics, antidepressants, amphetamines, psychedelics, and megavitamins   None of these effective n nSecretin   Neurotransmitter for digestion   No better then placebo n nSSRI   Obsessive Compulsive Disorder   Stereotyped behaviors

28. Treatment nFacilitated Communication  Touted as cure for Autism  Systematic studies show treatment may not be effective  “Ouija Board” effect nApplied Behavior Analysis (ABA)  Intensive behavior modification using operant conditioning  Most promising treatment

29. Treatment: ABA nGoals 1. Identify specific target behaviors 2. Gain control of behaviors 3. Gradually set more difficult goals nABA has been successful in teaching self-care skills, but less successful in teaching social responsiveness.

30. Treatment: ABA nLovaas (1987) compared outcomes for three groups of children with Autism n19 Received intensive ABA (40 hrs. wk. for 2 yrs.) n19 Less intensive n21 Were treated somewhere else

31. Treatment: ABA nFindings:  9 children from the intensive ABA group (47%) completed first grade in normal school  8 more from the intensive group (42%) passed first grade in special classes  Only 1 (2%) in other groups completed first grade in normal school  18 (45%) completed first grade in special classes nFollow-up studies indicate that many gains continues into late childhood and adolescence (McEachlin et al., 1993)