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Externalizing childhood disorders
ADHD, conduct disorder
ADHD diagnostic criteria
6+ innatentive symptoms for 6+ months, maladaptive, abnormal for developmental level or
6+ hyperactive symptoms for 6+ months
symptoms present before 12
in two or more settings
impairing social, academic, occupational functioning
ADHD prevalence rate explanation
diagnosis by unqualified pediatricians and differing educational policies
ADHD male to female ratio
3:1
ADHD into adulthood
symptoms decline with age but rarely go away
ADHD comorbidities
internalizing disorders (0.3), learning disorders (0.15-0.3), conduct disorder (0.25-0.45)
ADHD subtypes
inattentive, hyperactive, combined
ADHD + conduct disorder outcomes
antisocial behaviors, peer rejection, poor academic outcomes, worse prognosis
ADHD genetic etiology
highly heritable (0.7-0.8)
dopamine linked gene (DRD4 DRD5 DAT1)
gene for synaptic elasticity promoting protein (SNAP-25)
ADHD neurobiological etiology
dopaminergenic brain regions are smaller
less activation in frontal brain regions → impaired selective attention, working memory, and inhibiting behavioral response
ADHD and environmental toxin correlations
artificial food coloring weak
lead blood concentration weak
maternal smoking moderate but bidirectional
ADHD family factor etiology
little evidence for causality
ADHD medical treatment
stimulant medications improve concentration, executive function, relationships, and behavior
more effective than therapy, most effective in combination
half of the standard dose may be sufficient
ADHD psychological treatment
parent training and changes in classroom management, monitoring and reinforcement of behavior
intensive behavioral therapy (=ritalin+less intensive BT)
Conduct disorder diagnostic criteria
persistent violation of basic rights of others or social norms as shown by 3+ symptoms
aggression to people and animals, destruction of property, deceitfulness or theft, and serious violation of rules
impairment
Conduct disorder prevalence
0.02-0.1
Conduct disorder prognosis
if life course persistent, violent and antisocial behavior often develops
Conduct disorder comorbidities
substance abuse
internalizing disorders (especially anxiety and depression)
ADHD
Conduct disorder genetic etiology
aggression is more heritable than rule-breaking
conduct problems combined with unemotional/callous are more heritable than conduct problems alone
earlier means more genetically linked
MAOA (monoamine transmitters), 5HTTLPR (serotonin)
Conduct disorder neurophysiological etiology
deficits in regions for emotion and empathy → difficulty detecting emotions other than anger
reduced activation of brain regions for emotion and reward → difficulty associating behavior with consequence
deficits in verbal skill, executive function, and memory
Conduct disorder psychological etiology
unemotional/callous → low moral awareness and remorse
aggressive → hostile bias
Conduct disorder and peer influence
being rejected by peers is causally related to aggression
modeling or coercion in association
Conduct disorder treatments
family interventions, multi systemic treatment
Conduct disorder family interventions
family checkup → three assessment and feedback meetings regarding child and parenting, less aggression and misconduct
parent management training → awarding prosocial not antisocial behavior, better parental interactions and less aggression and antisocial behavior
Conduct multi systemic treatment
intensive therapy in community (family, school, and peer group) to address underlying factor
behavioral, cognitive, and educational treatment
Childhood depression symptoms that are the same as adults
depressed mood
anhedonia
fatigue
concentration problems
SI
Childhood depression symptoms that are diffrent from adults
more guilt
less early morning wakefulness and depression
less appetite and weight loss
Childhood depression prognosis
mostly persists to adulthood
Childhood depression male to female ratio
1:2
Childhood depression family etiology
children with depressed parents 4x as likely to develop
Childhood depression gene-environment etiology
short 5HTTP gene allele combined with stressful life event
Childhood depression social etiology
early life adversity (mostly not limited to home)
Childhood depression psychological etiology
cognitive distortions and negative attributional style increases risk
usually becomes stable in middle school, serves as a cognitive diathesis
Childhood depression treatment
Prozac is more effective than therapy, most effective in combination with therapy
Increase suicidality and cause many physical side effects
CBT is most effective therapy
Childhood anxiety symptoms similar to adults
impaired functioning
severe distress
avoidance
Childhood anxiety symptoms different from adults
do not need to regard fear as irrational
Childhood anxiety prevalence
3-5%
Childhood anxiety heritability
moderate (0.29-0.5)
Childhood anxiety social etiology
parental control and overprotectiveness (moderate)
parental rejection (mild)
bullying (moderate)
Childhood anxiety psychological etiology
overestimate danger of social situations and underestimate ability to cope
Childhood PTSD risk factors
family stress and coping styles
Separation anxiety disorder diagnostic criteria
developmentally inappropriate and excessive anxiety about separation from attachment figures with 3+ for 4+ weeks (6+ months in adults)
distress when deparated
worry something bad will happen to figure
refusal to go to school, work, or elsewhere
refusal to sleep away from home
nightmares about separation from figure
physical complaints when separated from figure
Childhood anxiety treatment
CBT → reframing fears, exposure training, relapse prevention
BT and group CBT → best for social anxiety
bibliotherapy → parent roleplays as therapist
Specific learning disorder diagnostic criteria
difficulties learning basic academic skills inconsistent with age, schooling, intelligence for 6+ months
interference with academic achievement or daily life
Specific learning disorder types
dyslexia (reading)
dyscalulia (math)
written expression impairment
Dyslexia etiology
heritable component, genes associated with reading ability
disrupted connectivity between regions for phonological awareness and regions that support speech production
Dyslexia treatment
phonological awareness training
instructional support accomodation (podcast, recorded lectures, tutors, no time limit)
Intellectual disability diagnostic critieria
intellectual deficits determined by intellectual testing and broader clinical assessment
deficits in adaptive functioning relative to age and cultural groups in: communication, social participation, work or school, independence, need for support
onset during child development
Down syndrome genetic etiology
extra copy of chromosome 21 causes intellectual disability and characteristic physical abnormalities
Fragile X syndrome genetic etiology
mutation of the Fm1 gene on the X chromosome causes large underdeveloped ears, a long thin face, and often intellectual disability or specific learning disorder
Recessive gene and intellectual disability
phenylketonurea causes deficiency of liver enzyme phenylalanine causing build up of phenylperuvic acid
can cause brain damage and intellectual disability
Intellectual disability and infectious disease
in utero exposure to infectious diseases like HIV, rubella, or herpes
Environmental hazards and intellectual disability
exposure to mercury or lead
Intellectual disability treatment
residential treatment → when individuals cant function in their community, part time or full time
behavioral treatment → specific behavioral objectives and step by step learning to improve functioning
cognitive treatment → speech guided problem solving
computer assisted instruction
ASD symptoms
1+ deficit in social communication and social interactions
2+ restricted repetetive behaviors, interests, or activities
ASD social communication and interaction symptoms
deficit in social or emotional reciprocity
deficits in nonverbal behaviors
deficit in development of peer relationships appropriate at age level
ASD repetitive or restricted behaviors
stereotyped or repetitive speech, movement, or use of objects
excess adherence to routines, rituals, or extreme resistance to change
very restricted interests that are abnormal in focus
hyper or hypo reactivity to sensory input or unusual interest in sensory environment
onset in early childhood
symptoms limit and impair functioning
ASD communication deficits
echolalia and pronoun reversal
ASD comorbidity
intellectual disability (often with profound sensorimotor function)
specific learning disorder (0.3)
anxiety disorders
ASD prevalence
1/68 children
ASD male to female
4:1
ASD onset
begins in early childhood and can be detected in the first months of life
ASD prognosis
children with higher IQ and speech acquisition before 6 have better outcomes
most do not require residential care and some can go to college and have a job
most continue to have impaired social relationships throughout their life
ASD genetic etiology
highly heritable (0.5-0.8)
specific genes underlying autism not identified
ASD neurobiological etiology
larger brains, neurons not pruning correctly
larger cerebellum, explore their surroundings less
larger amygdala in childhood, predicts difficulties communicating and socializing
smaller amygdala in adulthood, preducts difficulties in emotional perception
ASD medicinal treatment
antipsychotic medications treat behavioral problems but are less effective than therapy
ASD behavioral treatment
intense operant conditioning in all aspects of childs life for 40+ hrs a week for 2+ yrs
larger IQ increase and better educational outcomes