disorders of childhood Flashcards

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1
Q

developmental psychopathology

A

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.

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2
Q

two types of childhood disorders

A
  • Externalising disorders: (aggressiveness, non-compliance, overactivity and impulsiveness)
  • Internalising disorders: (depression, social withdrawal and anxiety) childhood anxiety and mood disorders.
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3
Q

The role of culture in internalising and externalising behaviour problems

A
  • culture influences child behaviour
  • Thailand- internalising behaviour problems- fearfulness
    o Buddhism, disapproves of aggression in Thailand
  • Western countries, those with externalising behaviour problems- aggressiveness and hyperactivity
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4
Q

hyperactive symptoms

A

movements
o difficulty controlling activity (moving or talking)
o activities and movements are haphazard –> wear out their shoes and clothing, smash their toys, and exhaust their families and teachers.

social life
- vicious cycles with these three domains ;
o poor social skills
o aggressive behaviour
o overestimation of one’s social abilities
- thus don’t get along with peers (the vicious cycle was a good predictor of troubling relationships when older)

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5
Q

DSM-5 criteria for attention-deficit hyperactivity disorder

Either (a) or (b):

A

a) 6+ problems with inattention AND present for 6 months to a maladaptive degree
b) 6+ problems of hyperactivity-impulsivity AND present for 6 months to a maladaptive degree –> fidgeting, running about inappropriately (in adults, restlessness), acting as if ‘driven by a motor’, interrupting or intruding, incessant talking.

  • symptoms must be present before age 12.
  • present in two or more settings (home, school or, work)
  • Individuals experience significant impairment in social, academic or occupational functioning.
  • For people age 17 or older, only five signs of inattention or hyperactivity-impulsivity
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6
Q

comorbidity with ADHD

A

o majority of children have combined specifier
o Internalising disorders, such as anxiety and depression, also frequently co-occur with ADHD. ( 30% )
o 15 to 30 percent of children with ADHD have a learning disorder

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7
Q

sex differences for ADHD

A
  • 3x more common in boys than in girls
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8
Q

ADHD in adulthood

A
  • 65 to 80 % still have symptoms in adolescence
  • adults may be employed and financially independent but with lower socioeconomic level and change jobs more frequently
  • 15% meet DSM criteria as 25-year-old adults.
  • close to 60%— continue to exhibit symptoms that are associated with impairment in several domains

Severity of symptoms may reduce

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9
Q

genetic factors of ADHD

A
  • heritability estimates ~ 70 to 80 percent
    o dopamine receptor genes: DRD4 and DRD5, and a dopamine transporter gene called DAT1
    o SNAP-25, codes for a protein promoting plasticity

HOWEVER studies have found that the DRD4 or DAT1 genes are associated with increased risk of ADHD only among those who also had particular environmental factors — namely, prenatal maternal nicotine or alcohol use

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10
Q

Neurobiological factors of ADHD

A

 dopaminergic areas of the brain (caudate nucleus, globus pallidus and frontal lobes) are smaller
 Less activation in frontal areas of the brain
 White matter abnormalities and lower grey matter density
 Reduced brain volume
 Delayed cortical maturation in children/adolescents
 Reduced cortical thickness in adults

  • neurobiological risk factors: perinatal and prenatal complications, Low birth weight,
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11
Q

Environmental toxins for ADHD

A
  • elements of the diet: additives &artificial colours,
  • Lead
  • Nicotine — maternal smoking — HOWEVER; smoking may not be causal itself
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12
Q

Multimodal Treatment of Children with ADHD (MTA) study.

A

o medication alone
o medication and intensive behavioural treatment, involving both parents and teachers
o intensive behavioural treatment alone.

  • children receiving only medication had fewer ADHD symptoms than children only receiving intensive behavioural treatment
  • The combined treatment was slightly superior to the medication alone
  • The medication alone and the combined treatment were superior to community-based care, though the behavioural treatment alone was not
  • effects of medication did not persist beyond the study, at least for some of the children
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13
Q

Psychological treatment

A
  • classroom management –> short-term success in improving both social and academic behaviour.

o children’s behaviour is monitored at home and in school, and they are reinforced for behaving appropriately
o Point systems and daily report cards (DRCs)
o earn points or stars for behaving in certain ways; token economy
o Parent-training programs are also effective,
o MTA study indicate that intensive behavioural therapies can be very helpful to children with ADHD.
o This finding suggests that intensive behavioural therapy may be as effective as Ritalin combined with a less intensive behavioural therapy.

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14
Q

The DSM-5 of intellectual disability

A

include three criteria:
DSM-5
1) have intellectual deficits (problem-solving, reasoning, abstract thinking) determined by intelligence testing and broader clinical assessment –> IQ score must be considered within the context of a more thorough assessment

2) experience significant deficits in adaptive functioning relative to their age and cultural group in one or more of the following areas: communication, social participation, work or school, independence at home or in the community, requiring the need for support at school, work or independent life.–> must be assessed across a broad range of domains
3) The onset of these deficits occurs during child development.

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15
Q

aetiology of intellectual disability

chromosomal abnormalities

A

down syndrome

  • (trisomy 21), :having an extra copy of chromosome 21.
  • physical signs (short and stocky stature; oval, upward-slanting eyes; a prolongation of the fold of the upper eyelid over the inner corner of the eye; sparse, fine, straight hair; a wide and flat nasal bridge;
  • Characterised by weaknesses in verbal abilities
  • Increased risk of age-related cognitive decline and dementia

fragile x syndrome

  • mutation in the fMR1 gene on the X chromosome (silencing)
  • large, underdeveloped ears and a long, thin face
  • 1/3 children with fragile X syndrome also exhibit ASD
  • The most common cause of genetically inherited intellectual disability

recessive gene disease

infectious diseases
in-utero; foetus is at increased risk of itnellectual disabilites (maternal infections, diseases, rubella, cytomegalovirus, toxoplasmosis, herpes simplex and HIV.

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16
Q

Environmental hazards&raquo_space; aetiology of intellectual disability

A
  • MERCURY: ingesting affected fish.
  • LEAD: lead-based paints, smog and the exhaust from automobiles that burn leaded gasoline.
  • Lead poisoning can cause kidney and brain damage as well as anaemia, intellectual disabilities, seizures and death.
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17
Q

Treatment of intellectual disability

A
  • Residential treatment
  • however many have jobs and are able to live independently

Behavioural treatments

  • Specific behavioural objectives are defined, and children are taught skills in small, sequential steps (operant conditioning)
  • operant approach (applied behaviour analysis), is also used to reduce inappropriate and self-injurious behaviour.

Cognitive treatments
- “Self-instructional training” teaches children to guide their problem-solving efforts through speech and verbalisation

Computer-assisted instruction

  • computers have been used to help people with intellectual disability learn to use an ATM
  • Smartphones can be enormously helpful by serving as aids for reminders, directions, instructions and daily tasks.
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18
Q

A brief history of autism spectrum disorder; Johns Hopkins, Leo Kanner 1943

A
  • disturbed children behaving in ways that didn’t present as an intellectual disability or schizophrenia.
  • “early infantile autism” –> ‘extreme autistic aloneness’
  • severely limited in language
  • everything to remain unchanged.
  • accepted into DSM-III in 1980 –> autistic disorder.
19
Q

Asperger’s (Hans Asberger 1944)

A
  • less severe and having fewer communication deficits than autism.
  • Included in 1994 in DSM-IV.
  • not differ qualitatively from autistic disorder, these two categories will likely be combined in DSM-5.
20
Q

four initial diagnostic categories of ASD

A

o Asperger’s disorder
o pervasive developmental disorder not otherwise specified
o childhood disintegrative disorder
o were combined into one category called autism spectrum disorder.

21
Q

DSM-5 criteria for autism spectrum disorder

A

Must meet criteria A, B, C, D, and E

A. Deficits in social communication and social interactions

  • not approaching others, not having a back and forth conversation, reduced sharing of interests and emotions
  • Deficits in eye contact, facial expressions, body language
  • Deficit in development of peer relationships

B. Restricted, repetitive behaviour patterns, interests, or activities
- Excessive adherence to routines, rituals in verbal or nonverbal behaviour, or extreme
resistance to change
- Very restricted interest that are abnormal in focus, such as preoccupation with part of
objects
- Hyper or hyporeactivity to sensory input or unusual interest in sensory environment,
such as fascination with lights or spinning objects.

C. Symptoms must be present in the early developmental period

D. Symptoms cause clinically significant impairment in social, occupational, or other
important areas of current functioning.

E. These disturbances are not better explained by intellectual disability or global developmental delay.

22
Q

joint attention

A

interactions that require two people to pay attention to each other, whether speaking or communicating emotion nonverbally, are impaired in children with autism.

fMRI studies–> do not show activation in the fusiform gyrus, other regions in temporal lobes, and the amygdala, the areas of the brain most often associated with identifying faces and emotion

children with ASD are not born with gaze deficits.
- However, between 2 and 24 months, the pattern of gaze between the two groups of infants began to diverge.

23
Q

theory of mind

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.
  • TOM typically develops between 2 ½ and 5 years
  • ASD don’t undergo this developmental milestone  unable to understand others’ perspectives and emotional reactions.

False belief tasks:
- Sally Ann task (Baron-Cohen, Leslie & Frith, 1985)
- Smarties task (Perner, Leekam & Wimmer, 1987)
 Reading the Mind in the eyes (Baron-Cohen,
Wheelwright & Joilliffe, 2010)
- Individuals with ASD had difficulty
identifying mental states from images
- Particularly difficult when only looking at
images of eyes

24
Q

babbling

A

utterances of infants before they begin to use words, less frequent in ASD

  • pronoun reversal:refer to themselves as ‘he’, ‘she’, or ‘you’ (or even by their own name).  closely linked to echolalia
  • Pronoun reversal is closely linked to echolalia — when children with ASD use echolalic speech, they refer to themselves as they have heard others speak of them and misapply pronouns.
  • very literal in their use of words and will condition certain actions with terms
25
Q

Echolalia

A
  • child echoes, usually with remarkable fidelity, what he or she has heard another person say.

immediate echolalia ‘Do you want a cookie?’ The child’s response may be, ‘Do you want a cookie?’

delayed echolalia, the child may be in a room with the television on and appear to be completely uninterested. Several hours later or even the next day, the child may echo a word or phrase from the television program.

26
Q

self-stimulatory activities

A

o endless body rocking
o hand flapping
o walking on tiptoe
oThey may spin and twirl string, crayons, sticks, and plates
o twiddle their fingers in front of their eyes
o stare at fans and other spinning things.
o The children may become preoccupied with manipulating an object and may become very upset when interrupted.
o strong attachments to simple inanimate objects and to more complex mechanical objects (e.g., refrigerators and vacuum cleaners).
oIf the object is something they can carry, they may walk around with it in their hands, and this may interfere with their learning to do more useful things.

27
Q

Comorbidity and ASD

A
  • Estimated 50 - 72% young people with ASD also have a comorbid disorder
  • High rates of comorbid depression and anxiety (50%)
  • ADHD 30% - 70%
     Intellectual disability 12%
     Specific learning disorder
     Language disorder
  • ASD is also frequently comorbid with anxiety, including separation anxiety, social anxiety, general anxiety and specific phobias
28
Q

Prevalence of autism spectrum disorder

A
  • begins in early childhood and evident in the first months of life.
  • affects 1 of every 68 children ( 5x boys than girls have ASD
  • large increase in the number of ASD diagnoses over the past 25 years
  • The diagnosis of ASD is remarkably stable

Potential reasons for the increase are:

  • Broader diagnostic criteria
  • Greater public awareness
  • Public schools mandated to provide services for children with ASD
29
Q

prognosis for ASD

A
  • children with higher IQs who learn to speak before age six have the best outcomes.
  • Still, many independently functioning adults with ASD continue to show impairment in social relationships
30
Q

aetiology of ASD

A

Genetic factors
- heritability estimates of around .80

Molecular genetics

  • deletion on chromosome 16 and chromosome
  • SNPs between two genes on chromosome 5
  • no two ASD presentations are likely to have the same underlying genetic and biological cause

Neurobiological factors

  • b/w ages of 2 and 4, the brains become significantly larger + grey and white matter
  • neurons are not being pruned correctly
  • brain growth slows abnormally in later childhood.
  • ‘overgrown’ in ASD: frontal, temporal and cerebellar, –> linked to language, social and emotional functions.
  • amygdalae were larger
  • connectivity issues and/or abnormal cortical organisation in frontal and limbic areas
31
Q

treatment of ASD applied behaviour analysis

A
  • Ivar Lovaas
  • a behaviour therapist
    o intensive operant conditioning-based program with young (under four years old) children with ASD

drugs
- haloperidol (trade name Haldol), an antipsychotic medication used in the treatment of schizophrenia.
o reduces social withdrawal, stereotyped motor behaviour, and such maladaptive behaviours as self-mutilation and aggression
o Many do not respond positively to the drug
Treatment for symptoms such as sleep (e.g. melatonin) and anxiety.

32
Q

what are neurodevelopment disorders

A
  • A group of conditions with onset in the developmental period.

developmental deficits that produce impairments of

  • Personal
  • Social
  • Academic
  • Occupational functioning

Neurodevelopment disorders frequently co-occur
Down syndrome, Autism Spectrum Disorder and Intellectual

Disability often experience elevated attention difficulties. Yet the pathways to these behaviours are very different.

33
Q

what is MTA

A

The MTA was a multisite study designed to evaluate the leading treatments for ADHD, including behaviour therapy, medications, and the combination of the two. included nearly 600 children, ages 7-9, who were randomly assigned to one of four treatment modes:

intensive medication management alone;
intensive behavioural treatment alone;
a combination of both; or
routine community care (the control group).

Combination treatment and medication management alone were both significantly superior to intensive behavioural treatment alone and to routine community care in reducing ADHD symptoms. The study also showed that these benefits last for as long as 14 months.

therefore carefully monitored medication with monthly follow-up is more effective than intensive behavioural treatment alone, for up to 14 months.

34
Q

stimulant medication for ADHD

A
  • Methylphenidate/Ritalin
  • Dexamphetamine sulphate (DEX)
  • Atomoxetine (ATX)
35
Q

how does medication help with ADHD

A

reduces disruptive behaviour and impulsivity, and improve ability to focus attention

  • stimulates show short-term improvements in concentration, goal-directed activity, classroom behaviour, and social interactions with parents, teachers and peers, as well as reductions in aggressiveness and impulsivity in about 75 percent of children with ADHD
  • These drugs appear to help in these domains by interacting with the dopamine system in the brain
36
Q

the AAIIDD definition for intellectual disability

A

Intellectual disability is characterised by significant limitations both in intellectual functioning and in adaptive behaviour as expressed in conceptual, social and practical adaptive skills.

This disability begins before age 18.

Five Assumptions Essential to the Application of the Definition

1) Limitations in present functioning within the context of community environments typical of the individual’s age, peers, and culture.
2) Valid assessment considers cultural and linguistic diversity as well as differences in communication, sensory, motor and behavioural factors.
3) Within an individual, limitations often coexist with strengths.
4) An important purpose of describing limitations is to develop a profile of needed supports.
5) With appropriate personalised supports over a sustained period, the life functioning of the person with ­intellectual disability generally will improve.

encourages the identification of an individual’s strengths and weaknesses on psychological, physical and environmental dimensions with a view towards determining the kinds and degrees of support needed to enhance the person’s functioning in different domains.

37
Q

IEP for intellectual disability

A

In the schools, this program is based on the person’s strengths and weaknesses, and on the amount of instruction needed.
Students are identified by the classroom environment they are judged to need.
This approach can lessen the stigmatising effects of having intellectual disability and may also encourage a focus on what can be done to improve the student’s learning.

38
Q

genome-wide association studies (GWAS

A

) look for differences in gene sequence (single nucleotide polymorphisms — SNPs) and gene structure (copy number variations — CNVs)

39
Q

Genetic or Chromosomal Abnormalities

Williams syndrome&raquo_space;> aetiology of intellectual disability

A
  • A deletion of multiple genes on Chromosome 7
  • Occurs in 1 out of 7,500-20,000 births
  • Distinct facial phenotype
  • Diagnosed through Fluorescent In Situ Hybridization (FISH) which assesses whether the elastin gene is present or not
  • Distinctive cognitive profile and intriguing social phenotype (increased approach to unfamiliar people).
40
Q

problems with diagnosing ADHD

A
  • Difficult to diagnose in children under 4 (i.e. 4 year old developmentally appropriate behaviour is variable)
41
Q

Family factors in ADHD

A
  • parent–child relationship interacts with neurobiological factors
  • parent’s own history of ADHD
  • there is little evidence to suggest that families actually cause ADHD
42
Q

DSM-5 CHANGES

A

o more children and adults receiving the diagnosis in DSM
o the age of onset was changed from under age 7 to under age 12.
o adults only need to show symptoms in five domains instead of the six required for children.
o DSM-5 no longer distinguishes among mild, moderate and severe intellectual disability based on IQ scores alone, as was done in DSM-IV-TR. The severity is assessed in three domains: conceptual (which includes intellectual and other cognitive functioning), social and practical.
-Used to be mental retardation in DSM-IV
- Asperger’s disorder was in DSM-IV but combined with autism for DSM5

43
Q

issues with childhood diagnosis

A

The same or similar symptoms can present across different disorders.
 For instance children with Down syndrome, Autism Spectrum Disorder and Intellectual
Disability often experience elevated attention difficulties. Yet the pathways to these
behaviours are very different.