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

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Child and Adolescent Psychopatholog y Focus: Childhood Schizophrenia and Eating Disorders

Transcript of Child and Adolescent Psychopathology Focus: Childhood Schizophrenia and Eating Disorders.

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

Child and Adolescent Psychopathology

Focus: Childhood Schizophrenia and Eating Disorders

Page 2: 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

Distinguishing symptoms between schizophrenia and autismo Hallucinations (auditory: 80-84% in children)o Delusions (55-63% in children)o Formal thought disorder

Childhood schizophrenia symptoms similar to adulthood schizophrenia since DSM-III

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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 thinkingo Schizophrenic children speak lesso Schizophrenic children show poorer discourse skillso Schizophrenic children show poor conversational repair (i.e., self-

correction)

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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

oSymptoms – poor affect regulation, poor attention, poor impulse control, psychotic symptoms

oAt 2-8-year follow-up:• Almost half developed a mood disorder• Over half developed a disruptive behavior

disorder• No one developed schizophrenia

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Childhood SchizophreniaExample of childhood schizophrenia: January Schofield

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Childhood SchizophreniaPrevalence

< .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

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Childhood SchizophreniaDevelopmental progression (cont’d)

Two different developmental progressionso 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)o Later difficulties• Less severe speech and language problems prior to 30 months• Fewer psychotic symptoms (6-9 years)• Socially impaired with excessive anxiety

o 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

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Childhood SchizophreniaOutcome

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

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Childhood SchizophreniaRisk 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

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Childhood SchizophreniaObstetric 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

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Childhood SchizophreniaPathophysiology

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

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Eating DisordersDiagnostic 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:

o Restricting Type (AN-R)o Binge-eating/purging type (AN-BP)

• Physical symptoms – yellowish skin, lanugo, hypersensitivity to cold, hypotension (low blood pressure), slow heart rate

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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.

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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

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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

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Eating DisordersRisk factors

Anorexia nervosa• Obstetric complicationso Premature birth (small for gestational age)o Cephalhematoma (collection of blood under the scalp)o Subtle brain injuries at birth produce feeding difficultieso 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

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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)

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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

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Eating DisordersDevelopmental 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)

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Eating DisordersDevelopmental 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

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Eating DisordersComorbidity

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