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BMS3052 > 34. Autism Spectrum Disorder > Flashcards

34. Autism Spectrum Disorder Flashcards

1
Q

Define

Autism Spectrum Disorder (ASD)

A

a developmental disorder that affects communication and behavior. Common symptoms include difficulty with communication, difficulty with social interactions, obsessive interests and repetitive behaviours

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2
Q

Define

DSM

A

the taxonomic and diagnostic tool published by the American Psychiatric Association

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3
Q

Define

ICD

A

the foundation for the identification of health trends and statistics globally, and the international standard for reporting diseases and health conditions.

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4
Q

Define

Brain derived neurotrophic factor (BDNF)

A

plays an important role in neuronal survival and growth, serves as a neurotransmitter modulator, and participates in neuronal plasticity, which is essential for learning and memory. It is widely expressed in the CNS, gut and other tissues.

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5
Q

Define

Purkinje cells

A

neurons in vertebrate animals located in the cerebellar cortex of the brain

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6
Q

Define

Theory of Mind

A

the ability to attribute mental states such as beliefs, intents, desires, emotions and knowledge, among others, to oneself and to others

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7
Q

Define

Discrete trial training

A

breakdown of complex skills by teaching each subskill in a series of highly-structured teaching trials, also known as early intensive behavioural intervention if delivered before 5 years of age

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8
Q

Define

Naturalistic interventions

A

embedding teaching into naturally occurring events e.g. play, mealtime, can address communicative functions and peer interactions

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9
Q

Define

Learning experiences

A

integration of ASD preschoolers with typically developing peers but with individualized curriculum to incorporate ASD’s idiosyncratic needs, promotion of social interactions and extensive parent training

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10
Q

Define

Early start Denver model

A

individualized interventions in consultation with caregiver, therapist, specialist and teaching occurs inside and outside family routines

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11
Q

Define

Construct validity

A

measure of how well the mechanism used to induce the disease phenotype reflects the currently understood disease etiology

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12
Q

Define

Face validity

A

measure of how well the model is able to replicate the disease phenotype

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13
Q

Define

Predictive validity

A

measure of how well an animal model can be used to predict unknown aspects of the disease

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14
Q

Definition

a developmental disorder that affects communication and behavior. Common symptoms include difficulty with communication, difficulty with social interactions, obsessive interests and repetitive behaviours

A

Autism Spectrum Disorder (ASD)

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15
Q

Definition

the taxonomic and diagnostic tool published by the American Psychiatric Association

A

DSM

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16
Q

Definition

the foundation for the identification of health trends and statistics globally, and the international standard for reporting diseases and health conditions.

A

ICD

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17
Q

Definition

plays an important role in neuronal survival and growth, serves as a neurotransmitter modulator, and participates in neuronal plasticity, which is essential for learning and memory. It is widely expressed in the CNS, gut and other tissues.

A

Brain derived neurotrophic factor (BDNF)

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18
Q

Definition

neurons in vertebrate animals located in the cerebellar cortex of the brain

A

Purkinje cells

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19
Q

Definition

the ability to attribute mental states such as beliefs, intents, desires, emotions and knowledge, among others, to oneself and to others

A

Theory of Mind

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20
Q

Definition

breakdown of complex skills by teaching each subskill in a series of highly-structured teaching trials, also known as early intensive behavioural intervention if delivered before 5 years of age

A

Discrete trial training

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21
Q

Definition

embedding teaching into naturally occurring events e.g. play, mealtime, can address communicative functions and peer interactions

A

Naturalistic interventions

How well did you know this?
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22
Q

Definition

integration of ASD preschoolers with typically developing peers but with individualized curriculum to incorporate ASD’s idiosyncratic needs, promotion of social interactions and extensive parent training

A

Learning experiences

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23
Q

Definition

individualized interventions in consultation with caregiver, therapist, specialist and teaching occurs inside and outside family routines

A

Early start Denver model

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24
Q

Definition

measure of how well the mechanism used to induce the disease phenotype reflects the currently understood disease etiology

A

Construct validity

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25
Q

Definition

measure of how well the model is able to replicate the disease phenotype

A

Face validity

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26
Q

Definition

measure of how well an animal model can be used to predict unknown aspects of the disease

A

Predictive validity

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27
Q

What is the estimated prevalence of ASD?

A

1 in 100 people worldwide

28
Q

Which gender is ASD more prevalent in?

A

Boys (4:1)

29
Q

By what age are the core symptoms of ASD usually detectable?

A

3 years old

30
Q

What are the two core symptoms of ASD detectable in children before 3 years of age?

A

Persistent deficits in social communications

Restricted and fixated interests

31
Q

What are some behavioural symptoms of ASD?

A

Persistent deficits in social communications

Restricted and fixated interests

Anxiety

Hyperactivity

Agitation

Impulsivity

Aggressive behaviour

32
Q

What are some functional symptoms of ASD?

A

Functional symptoms include sensory hypersensitivity, seizures and gastrointestinal disorders

33
Q

What is the IQ range of ASD?

A

50 - 130+

34
Q

What does the DSM require for an ASD diagnosis?

A
  1. Persistent deficits in social communication/social interaction
  2. Restricted, repetitive behaviours, interests and activities
35
Q

What does the ICD require for an ASD diagnosis?

A
  1. Abnormal development of receptive/expressive language
  2. Impaired development of selective social attachments/reciprocal social interaction
  3. Markedly restricted repertoire of activity and interest
36
Q

What might we look at when using neuroimaging to diagnose ASD?

A
  • Volumetric analysis – regional, cortical volume – thickness or surface area?
  • Connectivity – fibre tract measurements
  • Functional - fMRI, eye tracking
37
Q

What might we look at when using plasma to diagnose ASD?

A
  • Abnormal levels of brain derived neurotrophic factor (BDNF) in blood of ASD children? Increased/decreased levels have both been reported – “jury is still out”
  • Decreased night time production of melatonin –high rate of sleep disturbance?
  • Altered components of the metabolic (creatinine kinase, lactate dehydrogenase) and inflammatory (cytokine IL-1b, IL-4 levels) pathways
38
Q

What is typical of a child with ASD’s brain early in development?

A

It is larger than usual

Decreased pruning

Increased cortical thickness in parietal lobe

Decreased GABA R expression

Abnormal columnar structure in neocortex

Hypermetabolism in the frontal regions

39
Q

Why is the brain enlarged in early development for ASD children?

A

Increased number, size and myelin content of glial cells, increased neuronal dendrites and axons as a result of decreased pruning

40
Q

Why does the increased brain volume disappear around age 6-8?

A

Abnormal slowness in brain growth

41
Q

In older individuals with ASD, what is different about their brains?

A

Abnormalities in limbic structures in older individuals including hippocampus, amygdala and cingulate cortex – reduction in volume and smaller neurons that are more densely packed

42
Q

How is the cerebellum effected by ASD?

A

Decreased volume, reduced number and size of Purkinje cells

43
Q

What is typical of the brain regions and circuitry of ASD?

A
44
Q

What is the heritablilty of ASD?

A

90%

45
Q

What ASD susceptibility genes have been found?

A

Large number of ASD susceptibility genes identified including scaffold proteins SHANK2 & 3, adhesion molecules cadherins, GABA receptor subunits, voltage-gated calcium channel subunits, regulators of chromatin remodelling MSCP2, CHD8, proteins involved in synapse formation neurexins and neuroligins

46
Q

What are the risk factors of ASD?

A
  1. Infection/Immune dysfunction
  2. Endocrine factors
  3. Obstetric factors
  4. Environmental factors
47
Q

What infection/immune dysfunction factors contribute to ASD?

A

Cerebral spinal fluid of ASD children contains atypical levels of autoantibodies to neural antigens and inflammatory cytokines

Maternal infection during the critical period of early neurodevelopment?

48
Q

What endocrine factors contribute to ASD?

A

Maternal stress – intrauterine exposure to cortisol and thyroxine

49
Q

What obstetric factors contribute to ASD?

A

Low birth weight, preterm/caesarean delivery, uterine bleeds?

50
Q

What are the environmental factors that contribute to ASD?

A

Maternal exposure to prescription medication, illicit drugs, heavy metals (mercury), environmental toxins (pollution), cigarette smoke

51
Q

What are the three theories of ASD?

A
  1. Impeded plasticity
  2. Excitation and inhibition dysregulation
  3. Theory of mind
52
Q

How does impeded plasticity explain ASD?

A

Abnormal regulation of cell division and apoptosis

Early overgrowth of brain structures e.g. frontal cortex, amygdala and cerebellum

Hyper- followed by hypo- neuronal connectivity

53
Q

How does excitation and inhibition dysregulation explain ASD?

A

Imbalance of glutaminergic and GABAergic synapses

ASD patients are susceptible to development of epileptic seizures

54
Q

How is theory of mind related to ASD?

A

The capacity to understand subjective mental states including thoughts and desires is known as ToM

ToM develops early in children without disabilities but is delayed in children with ASD

55
Q

Which synapses are imbalanced in ASD?

A

Glutaminergic

GABAergic

56
Q

What is the role of oxytocin in pregnancy?

A
  • Oxytocin is an important peptide hormone that participates in the induction of labour
  • During brain development, the GABAergic signals shift from “depolarization and excitation” to “hyperpolarization and inhibition” as a result of reduction in intracellular [Cl-]. At birth, OXY mediates a sudden short-lasting reduction in [Cl-], presumably to facilitate the shift which protects neurons from anoxic episodes
57
Q

How is oxytocin involved in ASD?

A
  • It is also a hormone that plays an important role in social behaviour
  • ASD children have lower baseline OXY levels
  • Intranasal OXY has been trialled as a therapy for the core symptom of ASD (doesn’t work)
58
Q

What are the interventional model behavioural treatments for ASD?

A

Discrete trail training

Naturalistic interventions

Learning experiences

Early start Denver model

59
Q

How is the skill-based model used to treat ASD?

A

Functional communication training, positive behaviour support, self management, speech generation

60
Q

What are the most common pharmacological treatments for ASD?

A

Antipsychotics

Stimulants

Antihypertensives

Antidepressants

CNS depressants

61
Q

What three attributes should a good animal possess?

A

Construct validity

Face validity

Predictive validity

62
Q

What areas of ASD do animal models explore?

A

Neonatal lesions

Maternal intervention

Genetic models

63
Q

What do neonatal lesion ASD animal studies explore?

A
  • Amygdala – dysfunction in amygdala linked to ASD behaviours
  • Cerebellum – abnormalities (loss of Purkinje cells) detected in ASD patients
  • Medial prefrontal cortex – social deficits, overgrowth of mPFC pronounced in ASD patients
64
Q

What do maternal intervention ASD animal studies explore?

A
  • prenatal valproic acid exposure – mechanistically affect the epigenome at critical developmental stages
  • prenatal exposure to infection – Borna disease virus
65
Q

What do genetic model ASD animal studies explore?

A
  • BDNF overexpression – high seizure susceptibility, anxiety and depressive-like behaviour but no deficits in social behaviour
  • Fragile X mental retardation (FMR) 1 gene KO – decrease social interaction, increased repetitive behaviours, anxiety, hyperactivity, decrease spatial learning
  • GABARb3 subunit KO – seizure susceptibility, hyperactivity, stereotyped behaviour, learning and memory deficits, impaired social interaction
  • MeCP2 (transcriptional repressor) KO – increased anxiety, decreased motor coordination, impaired social interactions and learning and memory
  • Neuregulin (cell adhesion molecules) KO – mutations in NLGN3&4 associated with ASD
  • OXT, OXTR KO – oxytocin has key role in social interactions and recognition

BMS3052 (26 decks)

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