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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
hyperactivity/impulsivity symptoms? DSM5
``` 6 for at least 6 months fidgeting runs/climbs inappropriately unable to play quietly difficulty with patience ```
26
Prevalence of ADHD?
5-7% of children, 2.5% of adults (more males)
27
Comorbidity of ADHD?
80% have comorbid disorders (eg mood/learning)
28
Causes of ADHD?
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
Structural brain findings of ADHD?
Reduced brain volume (caudate nucleus, amygdala, HC) Disrupted cortical thinning and white matter connectivity between hemispheres
30
Functional brain findings of ADHD?
Reduced blood flow in frontal lobes and BG EEG: greater theta/beta ratio
31
Cognitive process of ADHD?
Reduced focused, sustain attention Reduced verbal, working memory Reduced executive functioning
32
ADHD is associated with? Dopamine hypothesis
Reduced extracellular dopamine | - treatment with dopamine agonists inhibits the reuptake of dopamine
33
Maturational delay hypothesis of ADHD?
There is delayed cortical thickness meaning delayed development of higher cognitive functions (inhibitory control, attention) - tends to improve with age
34
Network dysfunction model of ADHD?
Suggests a hypoactive prefrontal cortex - required for organisation/planning meaning it accounts for the inattention and disorganisation
35
What are the three separate subsections of the attentional network model?
Alerting model Orienting model Executive control network
36
What is the alerting model?
Governs general level of arousal and vigilance - maintained by norepinephrine
37
What is the orienting system?
Directing attention to prioritise external information - voluntary/involuntary Dorsal: top-down Ventral: bottom-up
38
What is the executive control network?
Higher level regulation | - prioritises information for our current goals
39
Attention models fronto system, ventral system and dorsal system roles? Cortese et al
FS: goal directed executive control processes VS: orienting to salient stimuli DS: select external stimuli based on goals, experience, memory
40
Reward model of ADHD?
striatum, ACC, OFC central to reward processing
41
Mind-at-rest model fo ADHD?
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
Treatment of ADHD?
Pharmacological: - dopamine and norepinephrine agonists (stop reuptake and increase dopamine availability) Nonpharmacological: - behaviour interventions (typically less effective than pharm)
43
What is dyslexia?
A specific reading ability (written texts) | - marked by poor phonological awareness - poor naming, WM, EF
44
Causes of dyslexia?
Genetic base: 50% heritability (prenatal brain development genes) Environment: lower SES
45
Brain changes in Dyslexia?
Various subtle visual, auditory and motor/cerebellar deficits - likely to stem from a deficit of phonological processing rather than sensorimotor
46
Dual-route model of word cognition?
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
Visual theory of Dyslexia?
Make word reversal errors - failure in establishing hemispheric dominance
48
Orthographic learning theory of dyslexia?
Establishing ability to mapping between phonemes and graphemes
49
Phonological theory of dyslexia?
There is a grapheme/phoneme conversion route and this is the issue with reading
50
Visual attention theory of dyslexia?
Performance on visual tasks is often different in people with dyslexia
51
Neural mechanisms in dyslexia?
Disrupted activation of the LH language network - temporoparietal region - occipito-temporal - lH inferior frontal gyrus
52
Treatment of dyslexia?
Intensive instructions to learn how to read phonics

PSY325 - Neuropsychology & Clinical Neuroscience (12 decks)

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