Childhood and Adolescent Disorders Flashcards
historical perspective
early 19th century - inadequate parenting, insufficient moral discipline in upbringing
reflection of environments
end of 19th century - abnormal brain functioning
current issues in assessing and treating children and adolescents
must study age specific variations - dif symptoms based on cognitive stage
youth more influenced by environments - lack of autonomy
children cannot self report
general prevalence of childhood disorders
18-22% between ages 4-17
anxiety disorders most common
types of comorbidity
homotypic continuity - current diagnosis predictive of receiving the same diagnosis in the future - panic disorders, psychosis, verbal tics, ecopresis, enuresis
heterotypic continuity - predictive of receiving a different diagnosis in the future - depression to anxiety, ADHD to ODD
ADHD clinical description
persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or development
early childhood onset, 1/3 maintain diagnosis into adulthood
inattention symptoms
making careless mistakes, difficulty with attention, easily distracted, side tracked, problems with organization, messy, losing things, forgetful
hyperactivity symptoms
fidgeting, running around at inappropriate times, not remaining seated, talking excessively, blurting things out
ADHD specifiers
ADHD-I: predominantly inattentive, ADHD-H: predominately hyperactive, ADHD-HI: combined
ADHD-I - more common in girls, associated with academic problems
ADHD-H, HI - three times more common in boys, higher rates of comorbid conduct problems - motor hyperactivity symptoms often decrease over time
comorbidity and ADHD
- 50% have at least one other psychiatric disorder
- ODD or CD 40-60%, learning disorders 25%, anxiety disorders 25%, depression 30%, substance use disorders 40%
ADHD prevalence
2% preschool aged, 6% in children and adolescents, 4% adults
ADHD developmental trajectory
increased risk for developing another psychiatric disorder
begin substance use earlier than youth who do not have ADHD
four times greater risk of serious injury - motor vehicle accidents
lower occupational attainment and greater academic problems
ADHD brain structure and function
- 3-8% reduction in brain size
- abnormalities of the prefrontal cortex and basal ganglia
- marked delay when attaining peak thickness through cerebellum - 10.5 years ADHD, 7.5 years controls
genetics and ADHD
- heritability as high as 70-80%
- extensive study of genes responsible for the recycling and transportation of the neurotransmitter dopamine, genes implicated in developmental process
prenatal risk factors ADHD
prenatal toxin exposure - poor diet, exposure to antidepressants, antihypertensives, illicit drugs, alcohol, tobacco, caffeine, mercury, lead, pregnancy or delivery complications
exposure to manganese, organophosphates, phthalates - particularly problematic for boys
psychosocial risk factors ADHD
- low socio-economic status, large family size, paternal criminality, poor maternal mental health, child maltreatment, foster care placement, family dysfunction
- inattentive symptoms - influenced by psychosocial risk factors
- hyperactive-impulsive symptoms - influenced by by biological risk factors
gene-environment interactions and ADHD
maternal smoking and genetic predisposition
dopamine receptor in prefrontal cortex and inconsistent parenting
ADHD assessment
reports from more than one informant using valid and reliable assessment tools
basic assessment - administering a rating to parents and teachers - self report in adolescence
clinical interview - developmental history, onset of problems, degree of impairment in different settings, differential psychiatric and medical diagnosis, psychosocial issues, family mental health history
pharmacological treatment ADHD
stimulant medication - effective in approximately 80% - increase release of dopamine and NE from storage sites and blocking their reuptake by inhibition of the dopamine transport system
types of ADHD medication
- short or long action methylphenidate, dextroamphetamine, amphetamine - increase vigilance, reaction time, short term memory, learning of new material in children with ADHD
- atomoxetine - act on noradrenaline and serotonin - additional benefits in reducing ODD and anxiety symptoms
ADHD medication side effects
side effects - decreased appetite, weight loss, trouble falling asleep, headaches, increases in pulse and blood pressure - sometimes more irritable or angry
psychoeducational interventions ADHD
adults responsible for the child educated about symptoms, disorder course, deficits associated with ADHD
importance of routines, physical exercise, supervised or planned activities
academic skill faciliation and remediation ADHD
scheduled breaks from classroom activities, the use of reward systems, appropriate positioning of desks, auditory vs written instructions, use of agendas
testing to identify challenges - specific interventions
behavioural parent training ADHD
parents learn techniques to help the child modify their own behaviour by providing consistent rewards and attention when the child completes a task or ceases a negative behaviour
other treatments ADHD
- behavioural classroom management, behavioural peer intervention, organizational training
- no evidence for family therapy, individual psychotherapy, social skills training
- most effective - those that help children enhance their deficient self motivation and working memory
oppositional defiant disorder
frequently argue with adults, temper tantrums, deliberately annoy others, angry and irritable, spiteful, blame others for outbursts, defiant to authority
generally diagnosed by age 8
ODD three symptom categories
angry/irritable mood
argumentative/defiant behaviour
vindictiveness
conduct disorder
behaviour that violates the basic rights of others or major societal norms, lack of remorse or guilt, callousness
aggression towards people and animals
destruction of propety
deceitfulness or theft
serious violation of rules
CD classifications
onset in childhood, adolescence, unspecfied
mild, moderate, severe
CD and ODD sex differences
boys 3-4x more likely for CD, girls more likely at a later age
slightly more boys diagnosed with ODD
assortative mating - females with CD tend to date males with CD
ODD and CD comorbidity
92% with ODD met criteria for another disorder - mood, anxiety, impulse control, substance use
highly comorbid with ADHD
CD and substance abuse
CD and ODD share a genetic influence
three pathways linked to internalizing disorders
failure model: engaging in externalizing behaviour increases probability of experiencing social failure - related to developing internalizing problems
acting out model: youth may mask their mood problems by behaving aggressively
reciprocal model: associations between externalizing problems and internalizing problems are reciprocal
dysruptive mood dysregulation disorder
chornic and severe irriability manifested clinically by frequent temper outbursts, persistently angry or irriable mood
2-5% prevalence
onset before age 10
ODD and CD prevalence
ODD in preschool - 9-12%, 3-6% adolescence
CD 8.1% boys, 2.8% girls
true prevalence hampered by changes in DSM criteria
ODD and CD developmental trajectory
ODD -> CD -> ASPD
trajectory is robust - more concern for those diagnosied with ODD and CD than just CD
arguments that they are distinct
ODD linked to mood disorders, CD antisocial
ODD and CD genetics
CD - 71%
strong genetic basis for antisocial behaviour
heritability estimates range from 44-72%
ODD and CD neurobiology
aggression - decreased glucose metabolism in frontal lobe
damage to amygdala - impulsive aggressive behaviour
serotonin abnormalities, low norepinephrine
hot executive functions
smaller brain structures and lower brain activity in these areas
motivation and affective cognitive processing associated with self management skills when emotions run high - anterior cingulate cortex, insular cortex, frontal cortex
ODD and CD cognitive factors
poor executive functioning, low IQ, reading disorders, lack of empathy, poor social cognition
ODD and CD prenatal risk factors
maternal smoking, substance use, pregnancy and birth complications - CD
most important is maternal stress and smoking during pregnancy
ODD and CD psychosocial risk factors
poor parenting - low monitoring, harsh and inconsistent, discpline, abuse - externalizing difficulties
moderate relation with insecure attachemnt - strong relation to disorganized attachment
peer rejection, association with deviant peers, poverty
ODD and CD gene environment interaction
MAOA - 80% with low activity version who were maltreated had a conduct disorder vs 40% with high activity
differential susceptibility theory and biological sensitivity context theory - sources of vulnerability can increase risk of poorer outcomes or better outcomes with supportive environments
ODD and CD problem solving skills training
modelling and practice, role playing, reinforcement contingencies
try to reduce hostile attributions
never fully reach normal functioning
ODD and CD pharmacological treatment
first consideration if there is comorbid ADHD
antipsychotic - moderate effect on disruptive and aggressive behaviour
lithium for short term anger management
ODD and CD parent training
promote social behaviour while reducing negative behaviour
idea that parents can reinforce antisocial behaviour
seperation anxiety disorder
distress when seperated from attachment figure, constant worry about caregiver, withdraw, timid, distress, worry about harm, nightmares about seperation
1/3 develop other anxiety or mood disorders
three trajectories for seperation anxiety disorder
high increasing group - 15.5% - 16x more likely to meet criteria for social anxiety disorder in adulthood
moderate - 37.3%
low - 47.2%
GAD in childhood
many worries, difficult to control worries, tired, restless, fatigued, irritable
6 months
1 physiological symptom
anxiety disorders comorbidity
mood disorders
71% met criteria for depression and anxiety
1/3 with SAD present with GAD, another 1/3 will develop GAD
73% heterotypic comorbidity
anxiety disorders prevalence
9% aged 4-11, 15% aged 12-17
equally common in boys and girls in youth
anxiety disorders developmental trajectory
anxiety age 11 - predictive of anxiety age 15
SAD predicts SAD
anxiety in early childhood -> behavioural issues middle childhood -> depressive late childhood
temperament and anxiety
anxious temperament in infancy
behavioural inhibition - withdrawal or fear in novel situations - persists throughout life, 2-4x more risk of anxiety disorders
brain structure and function and anxiety
amygdala - prolonged activation can lead to anxiety
higher resting heart rates and blood pressure
anxiety and genetics
38% of children with parents with an anxiety disorder had one
heritability 59%
genetic factors explain 68% stability in anxiety symptoms
prenatal risk factors and anxiety
mother experiencing stress while pregnanct
elevated cortisol in mother on developing brain
psychosocial risk factors and anxiety
genetic risk might be chanelled through environment
vicarious learning, operation and classical conditioning
relationship with poverty and psychoapthology
gene environement interactions and anxiety
fear conditioning
anxiety following stressful life period
cognitive behavioural treatment and anxiety
most evidence
helping parents learn to cope, gradual exposure to stimuli
pharmacological treatment of anxiety
SSRIs
fluvoaxamine - reduction in 8 weeks
92% of those taking medication stayed well
combined SSRI and CBT - best results aged 7-17
