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PSY325 > Week 12 - Neurodevelopmental Disorders > Flashcards

Week 12 - Neurodevelopmental Disorders Flashcards

1
Q

What is a type of abnormality of anatomical development?

A

Hydrocephaly

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2
Q

What is hydrocephaly?

A

Abnormal build up of cerebrospinal fluid (CFS) in the ventricles of the brain

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3
Q

What are some genetic and chromosomal disorders?

A

Turner’s syndrome

Williams syndrome

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4
Q

What are acquired neurodevelopmental disorders?

A

Fetal alcohol syndrome

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5
Q

What is Turner’s syndrome?

A

Partial or total deletion of X chromosome affecting females

Do not develop secondary sex characteristics, short stature, other physical features

Comorbid with learning disabilities and behavioural symptoms

Low-average IQ

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6
Q

What are some treatments for Turner’s syndrome?

A

Growth and sex hormone therapy

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7
Q

What is Williams syndrome?

A

Distinct physical features

Sociable, empathetic, talkative

Remarkable language abilities for characteristically low IQs

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8
Q

What are some strengths of people with WIlliams syndrome?

A

Sociable, empathetic, talkative

Remarkable language abilities for characteristically low IQs

Other cognitive strengths include near-perfect pitch, a sense of rhythm and a remarkable ability to recognise faces

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9
Q

What problems are associated with Williams syndrome?

A

Severe attentional problems,

poor spatial abilities

Difficulty drawing objects

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10
Q

What are the brain changes associated with Williams syndrome?

A

General thinning of cortex

  • Boundary of parietal and occipital lobes
  • Orbitofrontal cortex

Spared in superior temporal gyrus (auditory cortex)

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11
Q

Why may people with Williams syndrome have a remarkable sense of pitch and rhythm?

A

No deficits in superior temporal gyrus (auditory cortex)

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12
Q

What is fetal alcohol syndrome?

A

characteristic physical features

microcephaly, low birth weight, reduced growth

Poor muscle tone and coordination

Below average IQ, inattention, hyperactivity, learning disabilities, poor behavioural regulation

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13
Q

What are some communication neurodevelopmental disorders?

A

Language disorder

Speech sound disorder

Childhood onset fluency disorder (stuttering)

Social (pragmatic) communication disorder

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14
Q

What are some motor neurodevelopmental disorders?

A

Developmental coordination disorder

Stereotypical movement disorder

Tic disorder

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15
Q

What are the core symptoms of autism spectrum disorder?

A

Reduced capacity for social interaction and communication

Restricted and repetitive patterns of behaviour, interests or other activities

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16
Q

What are the early signs of autism in infants?

A

poor eye contact

poor response to name

lack of showing and sharing

no gesturing by 12 months

loss of language or social skills

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17
Q

What are the early signs of autism in pre-school-aged children?

A

Limited pretend play

odd or intensely focused interests

rigidity

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18
Q

What are the early signs of autism in school-aged children?

A

Concrete literal thinking

trouble understanding emotions

lack conversational skills or appropriate social approach

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19
Q

What is the genetic basis of autism?

A

heritability 50%

many genes identified

gene-environment interaction

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20
Q

What are the environmental factors of autism?

A

Perinatal or birth complications

parental age

exposure to infection, pollution, pesticide, nutritional factors

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21
Q

What did Pinel describe as the neural mechanisms in autism?

A

Variability in underlying neural correlates

Post mortem and structural studies implicate cerebellum, amygdala, frontal and temporal cortex, white matter connectivity

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22
Q

What are the structural findings of autism?

A

Enlarged brain volume

Increased volume in frontal and temporal lobes

Reduced cortical thickness in the temporal cortex

Increased cortical thickness in the frontal cortex

Fewer/smaller neurons in cerebellum and frontal and temporal cortices

Smaller subcortical volume, greater volume in caudate nucleus

Excess white matter and disrupted connectivity between areas

23
Q

What are the functional findings of autism?

A

Mixed findings of increased and decreased glucose metabolism and blood flow compared to control

often limbic, frontal and temporal areas

24
Q

What are the treatments for autism?

A

Intensive learning experiences and behavioural interventions in early childhood

No recommended pharmacological treatment for core symptoms

antipsychotics and prescription stimulants sometimes prescribed for other symptoms

25
Q

What are the core symptoms of ADHD?

A

Inattentiveness

Impulsivity and hyperactivity

26
Q

What are the challenges/risks associated with ADHD?

A

academic performance

school-related problems

risk taking

social relationships

antisocial behaviour

drug abuse

27
Q

What is the genetic basis of ADHD?

A

Heritability 70-80%

Multiple genes focussed on the dopaminergic system

Epigenetic effects

28
Q

What environmental factors contribute to ADHD?

A

Prenatal events and substance exposures, Heavy metal and chemical exposures, nutritional factors

and lifestyle/psychosocial factors

29
Q

what are the structural findings of ADHD?

A

Reduced brain volume

Smaller volume of subcortical structures (basal ganglia, amygdala, hippocampus) cerebellum, prefrontal cortex and corpus callosum

Peak cortical thickness is delayed 3 years

Disrupted cortical thinning and white matter connectivity between hemispheres

30
Q

What are the functional findings of ADHD?

A

Fronto striatal structures and pathways

Mixed findings in relation to D2, D3 receptor availability and density of dopamine transporters

Gene variants related to the dopaminergic system may modulate fronto-striatal circuitry

31
Q

What are the cognitive deficits related to ADHD?

A

Focused attention

Sustained attention

Verbal memory

Working memory

Executive function

32
Q

What is the dopamine hypothesis of ADHD?

A

It is associated with reduced extracellular dopamine

Treatment with dopamine agonists inhibits the reuptake of dopamine

33
Q

What is the maturational delay hypothesis?

A

Delayed development of higher cognitive functions (Inhibitory control, attention, temporal foresight)

Symptoms tend to improve with age

34
Q

What does neuroimaging suggest about the naturational delay hypothesis of ADHD?

A

Reduced size of cortico-striatal regions and reduced functional activation

35
Q

What do the network dysfunction models of ADHD suggest?

A

Hypoactive PFC - organisation and planning, value based decision making. accounts for inattention and disorganisation

36
Q

What are the different types of network dysfunction models of ADHD?

A

Attention model

Reward model

‘mind at rest’

37
Q

What did cortese et al (2012) suggest about the attention model of ADHD?

A

Fronto parietal system: goal directed executive control processes

Ventral attention system: orienting to salient external stimuli

Doral attention system: Select external stimuli based on goals, experience, memory

38
Q

What did ortiz et al (2015) find about the Reward model of ADHD?

A

Hypoactivity in the striatum for reward anticipation

Hyperactivity dLPFC and OFC for reward receipt

39
Q

What is the reward model of ADHD?

A

Related to the striatum, ACC, OFC central to reward processing

Delayed gratification, impulse control

Significance not assigned to longer term goals

40
Q

What is the mind-at- rest model of ADHD?

A

Default mode network (DMN) - active when at rest, deactivated when task focussed

Mind wandering, day dreaming, contemplating, reflecting

41
Q

What does imaging research show about the mind-at-rest model for children with ADHD?

A

ADHD children are slow to switch off DMN - corrects with methylphenidate

42
Q

How can you switch off DMN in children?

A

Methylphenidate

43
Q

What are some pharmacological treatments for ADHD?

A

Dopamine and norepinephrine agonists:

Dextroamphetamine, methylphenidate (ritalin) mixed with amphetamine (adderall)

Sometimes NE agonists (atomoxetine) antidepressants or anticonvulsants

44
Q

What is the core symptom of dyslexia?

A

Specific reading disability

45
Q

What is the genetic basis of dyslexia?

A

Strong genetic influence

Heritability 50%

46
Q

What are the environmental factors associated with dyslexia?

A

Lower SES = 5-10 variance in reading

47
Q

What are the causes of dyslexia?

A

Various subtle visual, auditory and motor/cerebellar deficits are commonly seen

Multiple types of developmental dyslexia - possibly multiple causes

Likely to stem from a deficit of phonological processing (representation/comprehension of speech sounds) rather than sensorimotor processing

48
Q

What is included in the dual-route model of word recognition?

A

Lexical (orthographic/direct) route

Phonetic (phonological/indirect) route

49
Q

What is the lexical route of the dual-route model of dyslexia?

A

Word recognised as a whole unit and translated directly to a meaning

Used for reading familiar and irregular words

50
Q

What is the phonetic route in the dual-route model of dyslexia?

A

Letters translated into sounds (phonemes) using grapheme-phoneme conversion (GPC) rules and sounds are blended together

Used for reading unfamiliar and nonwords

51
Q

What are the causal theories of dyslexia?

A

Visual theory

auditory processing theory

cerebellar theory

Magnocellular visual theory

Phonological theory

Orthographic learning

Visual attention theory

52
Q

What are the neural mechanisms of dyslexia?

A

Disrupted activation of LH language network

  • Temporoparietal regioln: phonological processing and grapheme phoneme conversion
  • Occipito-temporal: visual word form areas, whole word recognition
  • LH inferior frontal gyrus
53
Q

How is dyslexia treated?

A

Early intensive explicit instruction

Phonics based reading instruction

PSY325 (11 decks)

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