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PSY325 - Neuropsychology & Clinical Neuroscience > Week Twelve - Developmental Childhood Disorders > Flashcards

Week Twelve - Developmental Childhood Disorders Flashcards

1
Q

Neurodevelopmental disorders of childhood involve?

A

Abnormalities of anatomical development
- hydrocephaly

Genetic and chromosomal disorders

  • turner’s syndrome
  • williams syndrome

Acquired disorders
- FASD

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2
Q

What is Turners syndrome?

A

Partial of total deletion of X chromosome affecting females
- do not develop secondary sex characteristics, shorts stature

Often comorbid with learning/behavioural disabilities

Lower IQ, high VIQ tho

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3
Q

Treatment for turner’s syndrome?

A

Growth and sex hormone therapy

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4
Q

What is Williams syndrome?

A

Elvin typed facial features (upturned nose etc) - physical features

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5
Q

Strengths & weaknesses of Williams syndrome?

A

Strengths:

  • Social, empathetic and talkative
  • remarkable language abilities (but low IQ)
  • Near perfect pitch, rhythm, recognise faces

Weaknesses:

  • Severe attentional problems
  • Poor spatial ability
  • Drawing
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6
Q

Brain changes in Williams Syndrome?

A

General thinning of cortex (parietal and occipital lobes, orbitofrontal cortex)
- spared in temporal gyrus (auditory cortex so explains musical abilities)

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7
Q

What are acquired disorders?

A

When there is injury to the brain other prenatally or postnatally

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8
Q

What is FASD?

A

A diagnostic term used to describe impacts on the brain and body of individuals prenatally exposed to alcohol
- worst during first trimester

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9
Q

Characteristics of FASD?

A

Microcephaly, low birthweight, reduced growth

Poor muscle tone and coordination

Below IQ, inattention, hyperactivity, learning disabilities, poor behaviour

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10
Q

FASD diagnosis?

A

presence of severe impairment in at least 3 neurodevelopment domains and 3 facial features

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11
Q

Treatment for FASD?

A

Learning and behavioural therapy

Medication for ADHD like symptoms

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12
Q

What is ASD?

A

Restricted and repetitive patterns of behaviour, interests or other activities

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13
Q

Early signs of ASD?

A

Infants: poor eye contact, poor response

Pre-school: limited play

School age: concrete/literal thinking

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14
Q

ASD gender difference?

A

males 75%

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15
Q

Explain the heterogenous of ASD?

A

Continuum of impairments for any one symptom

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16
Q

Abilities in ASD?

A

Have savant abilities (cog and artistic eg memory, drawing)

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17
Q

Causes of ASD?

A

Genetics: heritability is 50% (many genes have been identified in brain development, NT function, synaptic changes)

GENE-ENVIRONMENT interaction

Environmental:

  • prenatal birth complications
  • parental age
  • infection, pollution, nutritional factors
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18
Q

Post mortem findings of ASD in brain?

A

Cerebellum (fewer neurons), amygdala, frontal (increased cortical thickness) & temporal cortex (decreased cortical thickness) and white matter connectivity (excess) is implicated

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19
Q

People with ASD spend?

A

Less time looking at faces (eyes especially)

- lower activity in fusiform face area

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20
Q

Functional findings of ASD in brain?

A

Increased/decreased glucose metabolism and blood flow in limbic frontal/temporal areas

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21
Q

What social factors are affected in ASD?

A

Theory of mind and emotion processing

22
Q

Treatment of ASD?

A

Learning and behavioural interventions in early childhood
- no recommended pharmacological treatment for core symptoms

Antipsychotics sometimes prescribed

23
Q

what is ADHD?

A

Persistent pattern of inattentiveness and hyperactivity/impulsivity

24
Q

Inattentiveness symptoms? DSM5

A 
6 for at least 6 months
difficulty with attention
poor listening
poor follow through with tasks
organisation skills are poor
25
Q

hyperactivity/impulsivity symptoms? DSM5

A 
6 for at least 6 months 
fidgeting
runs/climbs inappropriately
unable to play quietly
difficulty with patience
26
Q

Prevalence of ADHD?

A

5-7% of children, 2.5% of adults (more males)

27
Q

Comorbidity of ADHD?

A

80% have comorbid disorders (eg mood/learning)

28
Q

Causes of ADHD?

A

Genetic: heritability (70-80%), multiple genes (dopaminergic system), epigenetic effects

Environment: prenatal and substance exposures, heavy metal/chemical exposure, nutritional factors (vita D, omega 3), lifestyle/psychosocial factors

29
Q

Structural brain findings of ADHD?

A

Reduced brain volume (caudate nucleus, amygdala, HC)

Disrupted cortical thinning and white matter connectivity between hemispheres

30
Q

Functional brain findings of ADHD?

A

Reduced blood flow in frontal lobes and BG

EEG: greater theta/beta ratio

31
Q

Cognitive process of ADHD?

A

Reduced focused, sustain attention

Reduced verbal, working memory

Reduced executive functioning

32
Q

ADHD is associated with? Dopamine hypothesis

A

Reduced extracellular dopamine

- treatment with dopamine agonists inhibits the reuptake of dopamine

33
Q

Maturational delay hypothesis of ADHD?

A

There is delayed cortical thickness meaning delayed development of higher cognitive functions (inhibitory control, attention) - tends to improve with age

34
Q

Network dysfunction model of ADHD?

A

Suggests a hypoactive prefrontal cortex - required for organisation/planning meaning it accounts for the inattention and disorganisation

35
Q

What are the three separate subsections of the attentional network model?

A

Alerting model
Orienting model
Executive control network

36
Q

What is the alerting model?

A

Governs general level of arousal and vigilance

  • maintained by norepinephrine
37
Q

What is the orienting system?

A

Directing attention to prioritise external information
- voluntary/involuntary

Dorsal: top-down
Ventral: bottom-up

38
Q

What is the executive control network?

A

Higher level regulation

- prioritises information for our current goals

39
Q

Attention models fronto system, ventral system and dorsal system roles? Cortese et al

A

FS: goal directed executive control processes
VS: orienting to salient stimuli
DS: select external stimuli based on goals, experience, memory

40
Q

Reward model of ADHD?

A

striatum, ACC, OFC central to reward processing

41
Q

Mind-at-rest model fo ADHD?

A

Normally out DMN is active when at rest, deactivated when task focused - ADHD children are slow to switch of DMN (can be corrected with methylphenidate)

42
Q

Treatment of ADHD?

A

Pharmacological:
- dopamine and norepinephrine agonists (stop reuptake and increase dopamine availability)

Nonpharmacological:
- behaviour interventions (typically less effective than pharm)

43
Q

What is dyslexia?

A

A specific reading ability (written texts)

- marked by poor phonological awareness - poor naming, WM, EF

44
Q

Causes of dyslexia?

A

Genetic base: 50% heritability (prenatal brain development genes)
Environment: lower SES

45
Q

Brain changes in Dyslexia?

A

Various subtle visual, auditory and motor/cerebellar deficits
- likely to stem from a deficit of phonological processing rather than sensorimotor

46
Q

Dual-route model of word cognition?

A

Lexical (direct) route: Word recognised as a whole unit and translated directly to meaning - used for reading familiar/irregular words

Phonetic (indirect) route: Letters translated into sounds using grapheme/phoneme conversion - unfamiliar and nonwords

47
Q

Visual theory of Dyslexia?

A

Make word reversal errors - failure in establishing hemispheric dominance

48
Q

Orthographic learning theory of dyslexia?

A

Establishing ability to mapping between phonemes and graphemes

49
Q

Phonological theory of dyslexia?

A

There is a grapheme/phoneme conversion route and this is the issue with reading

50
Q

Visual attention theory of dyslexia?

A

Performance on visual tasks is often different in people with dyslexia

51
Q

Neural mechanisms in dyslexia?

A

Disrupted activation of the LH language network

  • temporoparietal region
  • occipito-temporal
  • lH inferior frontal gyrus
52
Q

Treatment of dyslexia?

A

Intensive instructions to learn how to read phonics

PSY325 - Neuropsychology & Clinical Neuroscience (12 decks)

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