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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 autism
o 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
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
o Schizophrenic children speak less
o Schizophrenic children show poorer discourse skills
o Schizophrenic children show poor conversational repair (i.e., selfcorrection)
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
o Symptoms – poor affect regulation, poor
attention, poor impulse control, psychotic
symptoms
o At 2-8-year follow-up:
• Almost half developed a mood disorder
•
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Over half developed a disruptive behavior
disorder
No one developed schizophrenia
Childhood Schizophrenia
Example of childhood schizophrenia: January Schofield
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
Childhood Schizophrenia
Developmental progression (cont’d)
 Two different developmental progressions
o 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
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
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
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
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
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:
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
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.
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
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
Eating Disorders
Risk factors
 Anorexia nervosa
• Obstetric complications
o Premature birth (small for gestational age)
o Cephalhematoma (collection of blood under the scalp)
o Subtle brain injuries at birth produce feeding difficulties
o 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
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)
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
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: 1020%
 Course of illness: average of
10 years
 Mortality rate: 6% per decade
die of illness (acute starvation
and suicide)
Eating Disorders
Developmental progression in bulimia nervosa
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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
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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
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