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z. z. PSY3032 Lectures - Abnormal Psychology > Week 3 Lecture 3b - Disorders of Childhood (55:30) DN > Flashcards

Week 3 Lecture 3b - Disorders of Childhood (55:30) DN Flashcards

1
Q

Lecture Summary

A
  • Early diagnosis of disorders of childhood is critical for prognosis and intervention
  • Much is known about developmental disorders., yet understanding of causal role is still in its infancy
  • Biological aetiology does not always equate to biological treatments e.g., ASD
  • Treatment is currently focussed on managing symptoms rather than eradicating the disorder
  • Children with developmental disorders can lead enriched lives with appropriate support and intervention.
    142: 00
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2
Q

What is one of the most extreme disorder a child can be diagnosed with?

A

Conduct Disorder

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3
Q

How does Conduct Disorder Manifest?

A
  1. Repetitive and persistent behaviour pattern that violates the basic rights of others or conventional social norms.

3 or more of (15) of the following over last 12months, and at least one in previous 6mths

  • a) Aggression to people and animals
  • b) Destruction of property
  • c) Deceitfulness or theft
  • d) Serious violation of rules
  1. Significant impairment in social, academic or occupational functioning
  2. If older than 18y, criteria for Anti-Social Personality Disorder not met.
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4
Q

Summarise phenotype of Conduct Disorder?

A
  • Extreme behaviour
  • Aggression to people, animals, property
  • Violation of social norms
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5
Q

What is the prevalence of Conduct Disorder?

A
  • 9.5% (Nock et al., 2006)
  • 4-16% boys
  • 1.2 - 9% girls
  • Incidence and Prevalence peak at 17yrs

57:20

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6
Q

What are the three sub-types of Conduct Disorder?

A
  • Childhood-onset type - development (3y+)
    • usually male, aggressive behaviour
  • Adolescent-onset type
    • less likely to show aggressive behaviour
    • have more normative peer relationships
    • more balanced male:female ratio than childhood type
  • Lifetime persistence type (DSM-5 Unspecified onset???)
    • most common in boys (x 10-15)

58:00

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7
Q

What disorders have found to be comorbid with conduct disorder

A

concurrent disorders

  • ADHD
  • neurodevelopmental difficulties
  • 50% will develop Anti- social P.D.
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8
Q

What is the long term prognosis for children with** conduct disorder**?

A
  • Life-course type have severe problems
  • Psychopathology
  • Lower education
  • Partner/Child abuse
  • Violent behaviour
  • Adolescent-limited type - “grow- out’ of disorder
  • 50% will develop Anti- social P.D.

59:00

slide39

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9
Q

What does the literature say about the Aetiology of Conduct Disorder?

A

literature is mixed

  • Social
  • Environmental
  • Psychological
  • Neurobiological
    • Genetic link - Heritability estimates - 40-50% genetic

59:45

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10
Q

Aetiology of Conduct Disorder? 2

A

Behavioural/Psychological

  • Neuropsychological Deficits
  • Psychological Factors
    • Behaviour imitation
    • Reinforcement of aggression
    • Kenneth Dodge - social-cognitive framework
  • Peer Influences
  • Social Influences

1:03 slide43

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11
Q

What did Caspi et al., (2002) find when looking at the genetic/environmental interaction in Conduct disorder?

A
  • Genetic x Environmental interaction
  • MAOA gene (warrior gene) (x chromosome) and maltreatment (environmental)
    • Is antisocial behaviour predicted by?
      • MAOA activity? NO (gene)
      • Maltreatment? NO (environment)
      • MAOA + maltreatment? YES genetic environmental interaction
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12
Q

How are Social-Cognitive factors relevant to aggressive behaviours observed in Conduct Disorder?

A
  • individuals not concerned with repercussions
  • social emotions e.g., empathy, guilt moral awareness are missing
  • the individuals social cognitive framework is atypical

1:05

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13
Q

What are risk factors for Conduct Disorder due to Peer Influences?

A

A lot of peer influence in Conduct disorder

e.g., Gang culture - Belonging to a group

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14
Q

What ‘Social Influences’ are risk factors for Conduct Disorder

A
  • urban living
  • unemployment
  • reduced education
  • disruptive family life
  • family monitoring
  • deviant peers
  • surprising that one particular study found no environmental factor
    106: 30

slide43

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15
Q

What is Oppositional Defiance Disorder?

A
    1. A pattern of angry/irritable mood, argumentative/defiant behaviour, or vindictiveness lasting at least 6 months as evidence by at least four from:
      * a) Angry/irritable mood
      * b) Argumentative/Defiant behaviour
      * c) Vindictiveness
    1. The disturbance in behaviour is associated with distress in the individual or others in his or her immediate social context, or it impacts negatively on social, emotional, occupational or other important areas of functioning.
    1. The behaviours do not occur exclusively during the course of a psychotic, substance use, depressive, or bipolar disorder. Also, the criteria are not met for disruptive mood dysegulation disorder.
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16
Q

Why is the prevalence of Oppositional Defiance disorder higher than Conduct Disorder?

A

because it isn’t as extreme as Conduct Disorder

(Clare said this, but really need to think this through??)

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17
Q

What is the prevalence of Oppositional Defiance Disorder?

A
  • Prevalence – 1-16%
  • Pre-puberty –mainly boys
  • Post-puberty – exclusively boys
  • Comorbidity with ADHD is high (50-65%)
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18
Q

How is OD both similar & different to ADHD?

A
  • Similar
    • in the way it manifests
  • Different
    • OD is more calculated/planned behaviour
    • ADHD child is generally reacting not planning it
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19
Q

What is the prognosis for individuals diagnosed with Oppositional Defiance Disorder?

A
  • Better than CD
  • Mild forms remit
  • Moderate becomes progressively worse after 5y
  • Sometimes crosses over to Conduct Disorder
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20
Q

When would a child move from a diagnosis of Oppositional Defiance Disorder to one of Conduct Disorder?

A

When the behaviour becomes aggressive/violent toward people, animals, property

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21
Q

What are the two main forms of treatment for Oppositional Defiant Disorder?

A
  • Stimulants
  • Parent Management Training
    • based on operant conditioning (rewarding good behaviours)

1:09:40

slide45

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22
Q

What is the DSM-5 definition of Autism Spectrum Disorder (ASD)?

A
  • A. Persistent deficits in social communication and social interactions across multiple contexts, as manifested by:
    • a. Deficits in social-emotional reciprocity
    • b. Deficits in nonverbal communicative behaviours sued for social interaction
    • c. Deficits in developing, maintaining, and understanding relationships
  • B. Restricted, repetitive patterns of behaviour, interests, or activities, as manifested by at least two of the following:
    • a. Stereotyped and repetitive motor movements, use of objects or speech.
    • b. Insistence on sameness, inflexible adherence to routines, or ritualised patterns of verbal or nonverbal behaviour.
    • c. Highly restricted, fixated interests that are abnormal in intensity or focus.
    • d. Hyper- or hypo reactivity to sensory input or unusual; interests in sensory environment, such as fascination wit lights or spinning objects.
    • e. Hyper- or hypo-reactivity to sensory input or unusual interest in sensory aspects of the environment.
  • C. Symptoms must be present in the early developmental period
  • D. Symptoms cause clinically significant impairments in social, occupational, or other important areas of current functioning.
  • E. Disturbances are not better explained by intellectual disability
  • Specificity
  • Severity

1:10:10

slide47

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23
Q

How is Autism diagnosed?

A
  • based on series of semi-structured interviews between
    • Clinical Psychologist
    • Caregiver &
    • Child
  • not clear cut - prolonged, highly specialised proposed
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24
Q

Summarise Autism Spectrum Disorder?

A
  • Social Communication Deficits
  • Patterns of behaviour (repetitive/restricted)
  • Symptoms present early
  • Clinically significant impairments in functioning
  • Not better explained by intellectual disability
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25
Q

With the change to Autism Spectrum Disorders in DSM-5, what two additional factors form part of a diagnosis?

A
  • Specificity
  • Severity
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26
Q

Why is a severity scale necessary?

A

because there is a spectrum of disorders from mild to extremely severe

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27
Q

Why is a specificity scale necessary for Autism Spectrum Disorder?

A
  • allows you to specify with or without
    • intellectual impairment
    • language impairment
  • Language used to appear in DSM-IV-TR
  • no longer a feature along spectrum in DSM-5
  • it is now a specifier

1:12:50

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28
Q

What were the hallmark features of ASD in earlier versions of the DSM?

How has this changed in DSM-5?

A
  • Earlier Versions
    • Social
    • Repetitive Actions
    • Communication
  • DSM-5
    • Social
    • Repetitive Actions
  • Communication is no longer a hallmark feature it is now a specifier
    1: 15

slide48

29
Q

Why did Autism get more attention than Aspergers

A

1940’s

Leo Kanner - published in English

Hans Asperger - did not

1:14

30
Q

Autism, a brief history?

A
  • 1943 - Leo Kanner
  • observed early infantile autism
  • shut off from the outside world
  • not recognised in DSM until 1980
31
Q

What are the three descriptors of the the severity scale in ASD?

A
  • 1 - requires support
  • 2 - requires substantial support
  • 3 - requires very substantial support

1:13

32
Q

What is the likely outcome of the changes to ASD in the DSM-5?

A
  • will most likely be an increase in research
  • renewed enhusiasm
  • controversy as two camps
    • one disorder - with degrees of severity
    • not the same disorder 2 very different disorders Autism & Aspergers
33
Q

When forming a picture of Autism Spectrum Disorder, what is an important consideration?

A

Huge individual differences

1:15:30

34
Q

How do the Social & Emotional Disturbances experienced in ASD manifest?

A
  • Impairment in reciprocal social interaction is gross and sustained.
    • eye to eye contact reduced
    • facial expression lacking
    • poor non-verbal communication.
  • Failure to initiate play and interact with peers
  • Problems with joint attention
  • Issues in face recognition – impt. for recognition of emotions
  • fMRI studies reveal variation in localized neural function
  • Is the core problem with Theory of Mind?
35
Q

Why is face recognition so important?

A
  • key for recognition of emotions & different non-verbal cues
    • eyes reveal a lot about what we feel

1:16:30

36
Q

What feature of faces do individuals most typically focus on (as found in scanpath studies)?

A
  • Typical - the eyes
  • Autism - non-essential features
37
Q

What is a scan path?

A
  • pattern of eye movements that occur when processing a complex stimulus
  • Pelphrey et al., (2002) pg.251 (bottom paragraph)
38
Q

What have fMRI studies found in individuals with Autism?

A
  • Reduced activation in **fusiform gyrus **
    • which is essential for recognition of facial emotions
39
Q

What kind of behaviours are impacted by the absence of ‘theory of mind’ in individuals with ASD

A
  • any behaviour that involves seeing others as having different thoughts, emotions to oneself
    • e.g., empathy, telling, jokes, lying

1:18:15

40
Q

What did Pelphrey et al., (2002) investigate?

A
  • Visual Scanning of Faces in Autism
  • Looked at scan paths
    • Control - across eyes. down, back up
    • Autism - disorganised way of viewing faces
      • don’t look at or process the same way
      • don’t have the same neural activations

1:19

slide50

41
Q

How has the diagnosis of Communication (language) Deficits changed in DSM-5?

What features are often impaired in ASD?

A
  • Now a specifier - not a hallmark feature in DSM-5
  • impacts the severity of the ASD from mild to severe
    • Marked & Sustained
  • Features of communication deficits
    • Marked & Sustained
    • Verbal and Non-Verbal
    • Delay/Lack of Development/in tact
    • Speech Impaired (monotone; inappropriate pitch; stochastic)
    • Echolalia
    • Pronoun Reversal (he/she or name)
    • Literal use of words
    • Repetitive use of language irrespective of meaning
    • Humour and irony
    • Lack of understanding for non-verbal behaviors, facial expressions, tone.
42
Q

If a child was previously diagnosed with Aspergers, what information now needs to be communicated in the new diagnosis of Autism?

A

Communication is** In tact**

35:10

slide51

43
Q

How does speech delay impact the diagnosis of ASD?

A
  • Speech shows large individual variation in ASD
  • Now used as a specifier in DSM-5
  • Used to differentiate between autism and Aspergers.

121:30

44
Q

What is a very early sign of a child’s fitting ASD diagnostic criteria?

A
  • lack of eye contact
    123: 00
45
Q

What is Stimming?

A
  • Self stimulatory behaviour observed in ASD
    • arm flapping
    • rocking
    • walking on tip toes
46
Q

What are some of the features of the Repetitive Acts/Patterns of behaviour observed in ASD?

A
  • “Stimming” – self-stimulatory activities
  • Obsessional desire for order and ritual
  • Intense attention to items
  • Require routine & consistency
  • Children become upset when order becomes unbalanced
47
Q

What is an implication of changing Aspergers to Autism?

A
  • Impacts the way the individual identifies themselves
    • previously Aspergers now Autism
48
Q

What are some self-stimulatory behaviours in a child with ASD?

A
  • flapping arms
  • walking on tippy toes
  • rocking
49
Q

ASD and Intellectual Ability

slide 54 notes

A
  • Intellectual Impairments
  • Many fit diagnostic criteria for intellectual disability (IQ<70)
  • Estimates dropped from 75-80% to 35%
  • Impairment not uniform – distinct from I.D.
  • Poor on language tests
  • Good on spatial-processing
  • Information processing unaffected
  • Inspection Time – Lowest Threshold for Detection
  • Children with autism
    • (IQ68) vs. normal functioning (IQ118) vs. learning-disabled children (no autism) (IQ68)
  • Response time: ~40msecs vs. ~40msec vs. ~60msec Frith (2003)
  • Isolated exceptional skills

1:28:50

50
Q

What is a threshold for detection?

What is it used to detect in ASD?

A
  • Inspection time
  • threshold for detecting a stimulus shown very quickly
    • e.g., Show a light for short period of time
    • look for shortest period of time taken to detect (this is the threshold)
    • is used to measure Information processing time
  • part of assessing intellectual ability 1:30
51
Q

What did Frith (2003) investigate?

A
  • Looked at Information Processing Time
  • used lowest threshold for detection
    • Autism - IQ68 - 40ms
    • Typical - IQ118 - 40ms
    • Learning Disabled - IQ68 - 60ms
      • this shows that ASD it is not the same as learning disability
      • response time for ASD was same as Typically developing child
      • ASD impacts various abiilities differently
52
Q

Is a child who has an exceptional skill (e.g., musical instrument) classified as ‘high functioning’ Autism?

A
  • No
  • ‘High functioning’ refers to an IQ over 70 in an individual with Autism

1:31 Slide54

53
Q

What is an area of behaviour that demonstrates the huge variation among individuals on the Autism Spectrum?

A
  • Isolated exceptional skills vary greatly e.g.,
    • excellent eye for detail
    • accuracy
    • memory for facts
    • creative talents
54
Q

What is the prevalence of ASD?

A
  • 1 in every 110 children
  • M:F ratio = 4:1
  • very stable diagnosis across lifespan

1:32:30 slide55

55
Q

What are some epidemiological facts about ASD?

A
  • Large increase over past 1⁄4 decade (300% increase)
  • Across all racial, ethnic and socioeconomic groups
  • Stable across the lifespan - 1/84 at 2 yrs old will not meet diagnosis at 9yrs old
56
Q

What two factors have been found to impact the prognosis for an individual with ASD?

A
  • Varied Language ability & IQ
    • determinants of an individual’s outcome in adult life
57
Q

What kind of studies suggest a genetic component in the aetiology in ASD?

A

Sibling Studies

  • Siblings of Autistic Children
    • 75 times more likely to have autism (McBride et al., 1996)

Twin Studies

  • Strong Evidence
    • 60-90% concordance in monozygotic twins
    • 0-20% concordance in dizygotic (normal siblings)
    • Heritability of ASD estimated at 90% (Sousa et al., 2011)
  • Tremendously complex!

1:34:10

slide56

58
Q

What did the graphical representation taken from Holt & Monaco, 2011 represent with regard to ASD?

A
  • the complex network of
    • known and predicted interactions between proteins encoded by genes implicated in ASD
    • susceptibility.
  • apparently no exam question on this according to Clare!
    135: 10 slide57
59
Q

Neurological Aetiology of ASD?

A
  • Brain volume ↑ in autistic individuals (Courchesne et al., 2001)
  • Occurs during specific developmental periods (2-4y)
  • Over-sized areas include frontal, temporal and cerebellar regions, and the amgydala.

Why?

  • Overproduction of cells which do not undergo cell death?
  • Failure of synaptic pruning?
  • EEG/fMRI studies reveal connectivity issues and/or abnormal cortical organization in
    • frontal and limbic areas.
60
Q

What has been found with brain volume in individuals with Autism?

What is the suspected basis for this?

A
  • Increased brain volume occurs 2-4yrs
  • Oversized areas frontal, temporal, cerebellar regions & the amygdala
  • May be due to failure of synaptic pruning
    • which occurs in a typically developing child
    • thus efficient neural pathways are not developing
61
Q

What environmental factors have been implicated in the Aetiology of ASD?

A
  • Perinatal factors
  • Infections?
  • Lead?
62
Q

What Perinatal factor was been implicated in ASD?

A
  • several decades ago
  • thalidomide
    • given to pregnant women for morning sickness
    • blamed for increase in ASD
63
Q

What Infections have been implicated in ASD?

What evidence supports this?

A

MMR Vaccine (Wakefield et al., 1998) reported it was causal for ASD in children

  • Institute of Medicine (IoM) no conclusive evidence that MMR is causal
  • Media frenzy resulted in many parents not giving children vaccine

Herpes virus (Rapin & Katzman, 1998).

1:37

slide59

64
Q

How was Lead implicated?

What evidence supports this?

A
  • Children with developmental and/or behavioural problems elevated levels of lead in blood (Lewendon et al., 2001)
  • Relevance to ASD is unclear
    • children with lead poisoning generally don’t go onto develop ASD
    • so link is unclear

1:37:50

slide59

65
Q

What does the graphical representation from Holt & Monaco, 2011 look at?

A
  • Looks at the underlying mechanisms of Autism
    • Genetics Mutations
    • CNV (Copy Number Variance)
    • Epigenetics (impact of environment of expression of genes)
  • ALL three = altered connectivity
    • which leads to a disconnect between different brain areas
  • Decreased integration of information then leads to diffuse behavioural issues across
    • social interaction
    • stereotype behaviour
    • communication

138:00

66
Q

Name the two main treatments for Autistic Disorder?

A
  • Psychological Interventions
  • Pharmacological Interventions
67
Q

What are some features of Psychological Interventions in ASD?

A
  • Intensive Operant Conditioning Intervention (Lovaas, 1987)
  • Success depends upon
    • i) severity of disorder and
    • ii) early intervention
  • All behaviour treatments (especially involving parents) have shown improvement.

See Rivera et al. (2008) Review. (not examinable)

68
Q

What pharmacological Interventions have been used in ASD?

How does this treatment compare to psychological interventions?

A
  • Haloperidol (Haldol)
    • Reduced social withdrawal
    • Maladaptive behaviours
    • No effect on language and/or social skills
  • Naltrexone
    • Reduces hyperactivity
  • May be used for co-morbid disorders
  • In sum, drug therapy is less effective. 141:20
69
Q

Which study prompted a lot of modern day treatments for ASD?

What are the key findings from that study?

A
  • Intensive Operant Conditioning Intervention (Lovaas, 1987)
  • Treatment
    • 40hrs wk - 12 of 19 (had normal IQ at end)
    • 10hrs wk - 2 of 40 (had normal IQ at end)
  • Outcomes were impacted by
    • Severity of disorder
    • Early intervention
    • Intensity of training
  • Lovaas Method now known as Applied Behavioural Analysis

z. z. PSY3032 Lectures - Abnormal Psychology (20 decks)

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