Wk 2: Ch 10 Disorders of childhood

  1. What are neurodevelopmental disorders?
    • A group of conditions with onset in the developmental period
    • The disorders typically manifest early in developmental, often before the child enters school
    • They are characterised by developmental deficits that produce impairments of
    • Personal
    • Social
    • Academic
    • Occupational functioning
    • The range of developmental deficits varies form very specific limitations of learning control of executive functions to global impairments of social skills or intelligence
  2. Developmental psychopathology
    Focuses on the disorders of childhood within the context of life-span development, enabling us to identify behaviours that are considered appropriate at one stage but not at another
  3. DSM-5 childhood disorders
    • Intellectual disability
    • Specific learning disorder
    • Autism spectrum disorder
    • Motor disorders
    • Communication disorders
    • ADHD
  4. Externalising disorders
    • Characterised by more outward-directed behaviours, such as aggressiveness, non-compliance, overactivity and impulsiveness.
    • The category includes attention-deficit hyperactivity disorder, conduct disorder and oppositional defiant disorder
  5. Internalising disorders
    • Characterised by more inward-focused experiences and behaviours, such as depression, Social withdrawal and anxiety.
    • category includes childhood anxiety and mood disorders.
  6. Role of culture in internalising and externalising behaviour problems
    • The values of a culture may play a role on whether a certain pattern of child behaviour develops or is considered a problem.
    • Study found children in Thailand more like to be seen for internalising behaviour- possibly bc of Bhuddist culture, which discourages aggression. 
    • Whereas Western culture more likely to be seen for externalising behaviour.
    • However,  researchers only used assessment measures that were normed on local samples, leaving open the possibility that behaviour differences between the two cultures were missed because they were not validly assessed for both ­cultures.
    • Across all cultures, boys seen for somatic complaints less for shyness, for girls more shyness.
  7. Attention-deficit hyperactivity disorder
    • ADHD
    • Children with ADHD have 3 main symptoms: inattention, hyperactivity and impulsivity
    • Extreme for a particular developmental period, persistent across different situations, linked to significant impairments in functioning.
    • Difficulty controlling their activity in situations that call for sitting still.
    • Inordinate difficulty getting along with peers and establishing friendships (maybe bc their behaviour is often aggressive and intrusive)
    • Miss subtle social cues, such as noticing when other children are tiring of constant jiggling.
    • Overestimate their ability to navigate social situations with peers.
    • Poor social skills, aggressive behaviour, and self overestimation of performance in social situations all predicted problems with peers 6y later and worse in these categories again.
    • Instant messaging experiment found that ADHD more likely to IM statements that were hostile and off topic.
    • Often singled out quickly and rejected by their peers-
    • from study of boys on summer camp. Impression made 1st day of camp and remained unchanged for 6 week period.
  8. DSM-5 criteria for ADHD
    • individual experiences 6 or more manifestation of inattention present for at least 6 months to a maladaptive degree and greater that what would be expected given a person's developmental level.
    • Several of the above symptoms present before age 12
    • Symptoms are present in two or more setting eg. home/school/work
    • Individuals experience significant impairment in social, academic or occupational functioning.
    • For people age 17+ only 5 signs needed to meet diagnosis
  9. ADHD DSM-5 three specifiers to indicate which symptoms predominate
    • 1. predominantly inattentive: children whose problems are primarily those of poor attention
    • 2. predominantly hyperactive-impulsive: children whose difficulties result primarily from hyperactive/impulsive behaviour
    • combined: children who have both sets of problems (comprises the majority of children with ADHD)

    • Combined specifier children more likely than other subtypes to develop conduct problems and oppositional behaviour, placed in special classes for child'n with behavioural problems and difficulties interacting with peers.
    • Predominantly inattentive specifier have more difficulties with focused attention or speed of information processing
  10. ADHD and comorbidities
    • ADHD and conduct disorder frequently co-occur and share some features in common.
    • However ADHD is associated more with off-task behaviour in school, cognitive and achievement deficits, and a better long-term prognosis.
    • When these 2 disorders co-occur, worst features of each manifests- serious antisocial behaviour, most likely to be rejected by peers, worst academic achievement, have the poorest prognosis.
    • Girls with both ADHD and conduct disorder exhibit more antisocial behaviour and risky sexual behaviour than girls with only ADHD. 

    • Internalising disorders, such as anxiety and depression, also frequently co-occur with ADHD. 
    • As many as 30 percent of children with ADHD may have comorbid internalising disorder.
    • 15 to 30 percent of children with ADHD have a learning disorder .

    • Having both ADHD and conduct disorder is associated with substance use.
    • Hyperactive symptoms of ADHD predicted subsequent substance use at age 14 and substance use disorder at age 18 after controlling for symptoms of conduct disorder.
  11. ADHD prevalence
    • About 7% in Aus sample
    • Risen dramatically in the past decade, ranging from 8 to 11 percent compared to older estimates of 3 to 7 percent .
    • A recent meta-analysis did not find evidence for an increase in the number of children who met criteria for ADHD over time.
    • Children may receive diagnosis after a brief visit with paediatrician, but correct diagnoses require careful and thorough assessments.
    • ADHD 3 times more common in boys than girls
  12. ADHD in adulthood
    • Some children show reduced severity of symptoms in adolescence and early adulthood
    • 65 to 80 percent of children with ADHD still have symptoms associated with impairments in adolescence.
    • In adulthood, most people with ADHD are employed and financially independent, but some studies have found that adults with ADHD are generally at a lower socioeconomic level and change jobs more frequently than is typical.
    • Up to 15 percent of people continued to meet DSM criteria as 25-year-old adults.
    • ADHD symptoms may decline with age, but they do not entirely go away for many people.
  13. Aetiology of ADHD- genetic
    • Genetic factors
    • Heritability estimates as high as 70-80%
    • Genes associated with the neurotransmitter dopamine (dopamine receptor genes DRD4 & DRD5, dopamine transporter gene DAT1)
    • Gene SNAP25 which codes for a protein that promotes plasticity of neurone synapses has been associated.
    • Several genes interacting with each other and with environmental factors will provide the most complete picture of the role of genes in ADHD.
  14. Aetiology of ADHD- neurobiological factors
    • Studies suggest that brain structure, function and connectivity differ in children with and without ADHD, particularly in areas of the brain linked to the neurotransmitter dopamine.
    • Dopaminergic areas of the brain, such as the caudate nucleus, globus pallidus and frontal lobes, are smaller in children with ADHD.
    • Children with ADHD exhibit less activation in frontal areas of the brain.
    • Children with ADHD perform poorly on neuropsychological tests that rely on the frontal lobes (such as inhibiting behavioural responses).
    • Lower grey matter density
    • Smaller dopaminergic areas of the brain
    • White matter abnormalities
    • Reduced brain volume
    • Delayed cortical maturation in children/adolescents
    • Reduced cortical thickness in adults

    Perinatal and prenatal complications: low birth weight (mitigated by greater maternal warmth)
  15. Aetiology of ADHD- Environmental toxins
    • Limited evidence that food additives impact hyperactive behaviour.
    • Some evidence suggests that higher blood levels of lead may be associated to a small degree with symptoms of hyperactivity and attentional problems however most children with higher blood levels of lead do not develop ADHD, and most children with ADHD do not show such elevated blood levels.
    • Exposure to tobacco, alcohol, substance misuse in utero was associated with ADHD symptoms.
    • Study with surrogate mothers found that ADHD symptoms were related to maternal smoking in both groups, but the association was significantly higher in children whose genetically related mothers smoked during pregnancy.
    • Findings suggest that smoking might not be a causal factor by itself but that it is related to other maternal behaviour and psychopathology that might increase the risk of ADHD.
  16. ADHD Aetiology- Family factors in ADHD
    • Just as parents of children with ADHD may give them more commands and have negative interactions with them so these children have been found to be less compliant and more negative in interactions with their parents.
    • Fathers who had a diagnosis of ADHD were less effective parents.
    • Family characteristics thus may well contribute to maintaining or exacerbating the symptoms and consequences of ADHD; however, there is little evidence to suggest that families actually cause ADHD
  17. Treatment of ADHD- stimulant medications
    • Reduce disruptive behaviour and impulsivity, and improve ability to focus attention
    • Shown short term improvements in concentration, goal-directed activity, classroom behaviour, and social interactions with parents, teachers and peers, as well as reduction in aggressiveness and impulsivity in about 75% of children with ADHD.
    • Appear to help in these domains by interacting with the dopamine system in the brain
    • Longitudinal study showed that medication as it is administered in the community does not appear to offer any benefits above and beyond other forms of treatment.
  18. Treatment of ADHD- psychological treatment
    • Reinforced for behaving appropriately eg. through point systems and daily report cards. 
    • Finding suggests that intensive behavioural therapy may be as effective as Ritalin combined with a less intensive behavioural therapy.
  19. Economic cost of ADHD in Australia
    • Latest report suggests that more than 800k Australians have ADHD
    • Estimate economic cost is 20.4 million
  20. Intellectual disability DSM criteria
    • 1. deficits in intellectual functioning
    • 2. deficits in adaptive functioning relative to their age and cultural group in one or more of the following areas- communication, social participation, work/school, independence.
    • 3. Onset during development (ie. childhood, before 18 years)

    Severity of intellectual disability is assessed in 3 domains: conceptual, social, practical
  21. Aetiology of intellectual disability- genetic
    • Primary cause of intellectual disability can be identified in only 25 percent of the people affected. The causes that can be identified are typically neurobiological.
    • Down syndrome linked

    • Linked with fragile X syndrome- caused by the silencing of a single gene on the X chromosome
    • Most common cause of genetically inherited intellectual disability
    • Most often seen in males
    • Occurs 1/2500

    • Williams syndrome
    • A deletion of multiple genes on chromosome
    • Occurs in 1/7500-20k births
    • Diagnosed through FISH which assesses whether the elastin gene is present or not
    • Distinctive cognitive profile and intriguing social phenotype (increased approach to unfamiliar people

    • Recessive-gene diseases
    • Several hundred recessive-gene diseases have been identified, and many of them can cause intellectual disability.
    • Eg. Phenylketonuria (PKU)- deficiency of a liver enzyme.
    • Cannot break down phenylalanine and build up, can damage brain bc the unmetabolised amino acid interferes with the process of myelination.
  22. Aetiology of intellectual disability- infectious diseases
    • While in utero the foetus is at increased risk of intellectual disabilities resulting from maternal infectious diseases, such as rubella, cytomegalovirus, toxoplasmosis, herpes simplex and HIV.
    • Consequences most serious during first trimester, when foetus has no detectable immunological response.

    • Infectious diseases can also affect a child’s developing brain after birth.
    • Encephalitis and meningococcal meningitis may cause brain damage and even death if contracted in infancy or early childhood.
  23. Aetiology of intellectual disability- environmental hazards
    • Mercury implicated ingested by eating fish
    • Lead
  24. Treatment of intellectual disability
    • Residential treatment- aides
    • Behavioural treatments: Operant conditioning, applied behaviour analysis
    • Cognitive treatments: Self-instructional training teaches these children to guide their problem-solving efforts through speech.
    • Teacher demonstrates and teachers then they would learn to talk themselves through the steps using simple verbal or signed instructions.
    • Possibly generalise this to other tasks.
    • Computer-assisted instruction
    • Behavioural treatments: early interventions that teach skills in small sequential steps
    • Teaching children routines
  25. Autism spectrum disorder
    a lifelong developmental condition that affects, among other things, the way an individual relates to his or her environment and interacts with other people
  26. Autism spectrum disorder- Social and emotional disturbances
    • Rarely approach others, look through or past people, turn back on them, no eye contact, rarely initiate play with other children.
    • Joint attention: interactions that require two people to pay attention to each other (eg. speaking or communicating emotion non-verbally)- impaired in children with autism.
    • People with ASD do not show activation in the fusiform gyrus, other regions in the temporal lobes, and the amygdala, the areas of the brain most often associated with identifying faces and emotion, when completing face perception or identity tasks.
    • Theory proposed that children with ASD have a deficient theory of mind (person's understanding that other people have desires, beliefs, intentions and emotions that may be different from one's own)
  27. ASD DSM 5
    • a. deficits in social communication and social interactions
    • b. restricted, repetitive behaviour patterns, interests, or activities
    • c. onset during early childhood
    • d. the symptoms of ASD limit and impair functioning
  28. Possible early features
    • Not pointing at objects to show interest by 14 months
    • Not responding to their name by 12 months
    • Have delayed speech and language skills
    • Does not direct the attention of others
    • No gaze monitoring
    • Not playing pretend games by 18 months
    • avoid eye contact and want to be alone
    • Have obsessive interests
    • Limited range facial expressions
    • Flapping hands, rock body or spin in circles
    • Repeat words or phrases (echolalia)
    • Get upset by minor changes
    • Have trouble understanding other people's feelings or talking about their own feelings
    • Limited use gestures
  29. ASD- communication deficits
    • Babbling less frequent in infants with ASD and conveys less information than it does in other infants 
    • Lag behind language development.
    • Echolalia: echoing what someone has said. Immediate echolalia or delayed echolalia
    • Pronoun reversal:  refer to themselves as ‘he’, ‘she’, or ‘you'.
    •  Children with ASD are very literal in their use of words. eg. say 'do not drop cat' instead of no
    • Less eye gaze on human faces
    • Individuals with ASD had difficulty identifying mental states from images. Particularly difficult when only looking at images of eyes.
  30. ASD- repetitive and ritualistic acts
    • Can become extremely upset over changes in their daily routines and surroundings.
    • Likely to perform a more limited number of behaviour and less likely to explore new surroundings.
    • Peculiar ritualistic hand movements and other rhythmic movements (self-stimulatory activities).
    • Some form strong attachments to inanimate objects
    • Stereotypes or repetitive speech, motor movements of us of objects
  31. Comorbidity and ASD
    • Estimated 50-72% young people with ASD also have a comorbid disorder
    • Many also have Intellectual disability  (12%) however sensorimotor development is greater relative to those with intellectual disability.
    • Some with ASD have isolated skills and may have exceptional long term memory.
    • A study found over 1/3 also have specific learning disorder.
    • Also frequently comorbid with anxiety, including separation anxiety, social anxiety, general anxiety and specific phobias and depression (50%)
    • ADHD (30-70%)
  32. Prevalence of ASD
    • Affects 1 in every 68
    • About 5 times more boys than girls
    • Large increase in diagnoses
    • Only 1/84 children diagnosed with ASD at age 2 no longer met diagnostic criteria at age 9.
    • Has increased over time- potential reasons are:
    • Broader diagnostic criteria
    • Greater public awareness
    • Public schools mandated to provide services for children with ASD
  33. Prognosis for autism spectrum disorder
    • children with higher IQs who learn to speak before age six have the best outcomes. 
    • IQs over 70 predicted more strengths and fewer weaknesses in adaptive functioning as they grew older.
    • outcomes were better for those who had interacted and engaged more with their peers.
    • many independently functioning adults with ASD continue to show impairment in social relationships.
  34. Aetiology of autism spectrum disorder
    • Genetic factors: Heritability estimates of around .80 
    • Siblings of individuals with ASD show more ASD symptoms (without meeting criteria)
    • Twin studies, which have found between 47 and 90 percent concordance for ASD between identical twins, compared with concordance rates of 0 to 20 percent between fraternal twins.

    Shared environmental factors accounted for over half of the risk for developed autism. No evidence for faulty parenting

    • Neurobiological factors: brain larger -  born with brains of a relatively normal size; however, between the ages of two and four, the brains of children with ASD become significantly larger. Normalise after age of 4. Might indicate that neurons are not being pruned correctly and then possibly over pruning.
    • Areas of the brain that are ‘overgrown’ in ASD include the frontal, temporal and cerebellar, which have been linked with language, social and emotional functions.
    • One study found that the amygdalae were larger among children with ASD- predicts difficulty in social behaviour.
    • EEG/fMRI studies reveal connectivity issues and/or abnormal cortical organisation in frontal and limbic areas.
  35. Treatment of ASD
    • Behavioural treatment:
    • Applied behaviour analysis (ABA): intensive operant conditioning. Shown to be effective.
    • However small sample sizes, few were randomised trials (poor quality)
    • Need randomised control trials to prove that is better than other treatments
    • Drug treatment: at this point, less effective than behavioural treatment. 
    • most common: haloperidol an antipsychotic medication used in the treatment of schizophrenia (some evidence reduce social withdrawal, stereotyped motor behaviour) but most do not respond well.
    • May be useful when comorbid disorders respond well to medical treatment.
    • Treatment for symptoms such as sleep (eg. melatonin) and anxiety
Card Set
Wk 2: Ch 10 Disorders of childhood
Ch 10 Disorders of childhood