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Child and Adolescent Psychopathology

Child and Adolescent Psychopathology. Focus: Childhood Schizophrenia and Eating Disorders. Childhood Schizophrenia. Historical Background Symptoms prior to age two – infantile autism Symptoms with later onsets – paranoid and sociopathic symptoms characteristics of schizophrenia

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Child and Adolescent Psychopathology

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  1. Child and Adolescent Psychopathology Focus: Childhood Schizophrenia and Eating Disorders

  2. Childhood Schizophrenia • Historical Background • Symptoms prior to age two – infantile autism • Symptoms with later onsets – paranoid and sociopathic symptoms characteristics of schizophrenia • Distinguishing symptoms between schizophrenia and autism • Hallucinations (auditory: 80-84% in children) • Delusions (55-63% in children) • Formal thought disorder • Childhood schizophrenia symptoms similar to adulthood schizophrenia since DSM-III

  3. Childhood Schizophrenia • Diagnostic issues • Childhood schizophrenia can be mistaken for brief psychotic episode in context of mood or disruptive behavior disorder • Delusions need to be distinguished from imaginary friends, magical thinking, or hypnagogic experiences • Disorganized speech is common in many healthy children younger than age 7 – loose associations, tangentiality, illogical thinking • Schizophrenic children speak less • Schizophrenic children show poorer discourse skills • Schizophrenic children show poor conversational repair (i.e., self-correction)

  4. Childhood Schizophrenia • Diagnostic issues (cont’d) • Differential diagnosis – mood disorders, schizoaffective disorder, PDD, communication disorders, OCD, PTSD, dissociative disorders, seizure disorders, brain tumors, and substance abuse • Multidimensionally Impaired Disorder • Symptoms – poor affect regulation, poor attention, poor impulse control, psychotic symptoms • At 2-8-year follow-up: • Almost half developed a mood disorder • Over half developed a disruptive behavior disorder • No one developed schizophrenia

  5. Childhood Schizophrenia Example of childhood schizophrenia: January Schofield

  6. Childhood Schizophrenia • Prevalence • < .01% for schizophrenia with onset prior to age 12 • 0.5-0.7% in general adult population • Prevalence dramatically increases after age 13 • Developmental progression • 95% of schizophrenic children have insidious, not acute, onset • Poor premorbid peer relationships, school performance, and general adaptation, speech and language problems prior to 30 months, delayed motoric milestones

  7. Childhood Schizophrenia • Developmental progression (cont’d) • Two different developmental progressions • Early difficulties • Severe speech and language problems prior to 30 months • Pervasive lack of responsiveness • Flat or inappropriate affect, loose associations, incoherence (6-9 years) • Later difficulties • Less severe speech and language problems prior to 30 months • Fewer psychotic symptoms (6-9 years) • Socially impaired with excessive anxiety • Frequency of hallucinations and delusions increased in both groups (9-12 years) • Time between onset of nonpsychotic symptoms and diagnosis of schizophrenia: 3-5 years

  8. Childhood Schizophrenia • Outcome • Remission at 5 years: 3% • Remission at 42 years: 67% • At 15 years post index diagnosis – not living independently, long-term residential care, low educational attainment, poor work history • Onset prior to age 14 predicts worse outcome than adult onset. • Parental thought disorder – cause or effect of childhood schizophrenia? • Sex differences • Male:female ratio higher with onset prior to age 12 • Male:female ratio roughly equal with onset after age 12

  9. Childhood Schizophrenia • Risk factors • Concordance rates • 55.8% among monozygotic twins • 13.5% among dizygotic twins • Childhood schizophrenia possibly more genetically based than adulthood schizophrenia • Different sets of susceptibility genes may be found in different groups of those with schizophrenia • Endophenotypes – abnormalities in smooth-pursuit eye movements, neurocognitive functioning, brain structure, brain electrical activity, and autonomic activity

  10. Childhood Schizophrenia • Obstetric complications • Earlier onset of schizophrenia • Pregnancy complications (e.g., diabetes, bleeding) • Abnormal fetal development (e.g., low birth weight) • Delivery complications (e.g., asphyxia) • Diathesis-stress model (moderational model) • Communication deviance in the family • Dysfunctional family rearing environments

  11. Childhood Schizophrenia • Pathophysiology • Brain structure – 9.2% reduction in total brain volume • Brain reduction greater than in adult schizophrenia • Trajectory of changes = exaggeration of processes found in normal brain development • Neurocognitive impairments – IQ, memory, language, executive function, and attention (stabilize after 2 years) • Subtle, early biological insults influence how the child responds to normal developmental transitions • Overwhelming evidence of continuity of childhood and adulthood schizophrenia

  12. Eating Disorders • Diagnostic Issues • Anorexia nervosa (AN) • Weight loss or failure to gain weight (85% of expected weight for height and age) • Intense fear of gaining weight or becoming “fat” • Disturbed perception of weight and shape • Denial of seriousness of illness (poor insight) • Amenorrhea • Subtypes of anorexia nervosa include: • Restricting Type (AN-R) • Binge-eating/purging type (AN-BP) • Physical symptoms – yellowish skin, lanugo, hypersensitivity to cold, hypotension (low blood pressure), slow heart rate

  13. Eating Disorders • Bulimia nervosa (BN) • Twice weekly for 3 months, consumption of unusually large amounts of food • Twice weekly for 3 months, compensatory behaviors to prevent weight gain (e.g., self-induced vomiting, laxative/diuretic abuse, fasting, excessive exercise) • Undue influence of weight and shape on self-evaluation • Binge = 1,000-2,000 calories; foods that are typically high in fat and sugar content • Individuals with bulimia nervosa wait on average of 6 years before seeking treatment • Physical symptoms include erosion of dental enamel, esophagus, colon damage, enlarged salivary glands.

  14. Eating Disorders • Binge eating disorder (BED) • Provisional eating disorder • Twice weekly for 6 months, uncontrollable binge eating • Marked distress regarding binge-eating • Absence of compensatory behaviors • Physical symptoms include obesity and its consequences

  15. Eating Disorders • Prevalence • 1.4-2% of girls and women, 0.1-0.2% of boys and men experience anorexia nervosa during their lifetime • 1.1-4.6% of girls and women, 0.1-0.2% of boys and men experience bulimia nervosa during their lifetime • 0.2-1.5% of girls and women, 0.9-1% of boys and men experience binge eating disorder during their lifetime

  16. Eating Disorders • Risk factors • Anorexia nervosa • Obstetric complications • Premature birth (small for gestational age) • Cephalhematoma (collection of blood under the scalp) • Subtle brain injuries at birth produce feeding difficulties • Eating pathology in mothers produce premature birth and small gestational size because of malnourishment • Premorbid neuroticism • Low weight and high dietary restraint at age 13 • Pressure to be thin (peers, family, media),low parental and peer support do not predict onset of anorexia nervosa

  17. Eating Disorders • Bulimia nervosa • Pressure to be thin body dissatisfaction  dieting and negative affect  bulimia nervosa (mediational model) • Early feeding difficulties – digestive problems, Pica • Binge eating disorder • Dysregulated affect • Dietary restriction increases reinforcing value of food • Part of array of behaviors in individuals high in impulsivity • Children are at risk for eating disorders in general if relatives have a specific eating disorder (“anorexia and bulimia nervosa do not ‘breed true’”, p. 651)

  18. Eating Disorders • Genetic vulnerability • Concordance rates for anorexia nervosa: 33-84% • Concordance rates of bulimia nervosa: 28-83% • Concordance rates for binge eating disorder: 41% • Brain structure • Anorexia nervosa – gray and white matter loss, increased ventricular size, increased cerebrospinal fluid (CSF) volume, enlarged sulci • Bulimia nervosa – cerebral atrophy

  19. Eating Disorders • Developmental progression in anorexia nervosa • Two peak periods of onset: ages 14 and 18, probably related to school transitions • Emerges after puberty suggests hormonal changes as triggers for onset • Recovery: 50-70%; improvement: 20%; chronic course: 10-20% • Course of illness: average of 10 years • Mortality rate: 6% per decade die of illness (acute starvation and suicide)

  20. Eating Disorders • Developmental progression in bulimia nervosa • One peak period of onset: ages 14-19 • Chronic course of recovery and relapse (8.1 years) • Subthreshold bulimia nervosa shows less chronicity • Mortality rate: less than 1% • Developmental progression in binge eating disorder • One peak period of onset: ages 16-18 • Recovery: 50% by 6 months, 80% by 3-5 years • Course of illness: average of 8.1 years • Risk factor for obesity onset

  21. Eating Disorders • Comorbidity • Anorexia nervosa – major depression and anxiety disorders • Bulimia nervosa – major depression and anxiety disorders • Binge eating disorder – major depression • Sex differences • Anorexia and bulimia nervosa – 10:1 males to females • Distribution more balanced in adulthood • Cultural considerations • Higher rates of binge-eating and lower rates of anorexia nervosa in African American women than White women

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