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
What are the core symptoms of ADHD?
Inattentiveness Impulsivity and hyperactivity
26
What are the challenges/risks associated with ADHD?
academic performance school-related problems risk taking social relationships antisocial behaviour drug abuse
27
What is the genetic basis of ADHD?
Heritability 70-80% Multiple genes focussed on the dopaminergic system Epigenetic effects
28
What environmental factors contribute to ADHD?
Prenatal events and substance exposures, Heavy metal and chemical exposures, nutritional factors and lifestyle/psychosocial factors
29
what are the structural findings of ADHD?
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
What are the functional findings of ADHD?
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
What are the cognitive deficits related to ADHD?
Focused attention Sustained attention Verbal memory Working memory Executive function
32
What is the dopamine hypothesis of ADHD?
It is associated with reduced extracellular dopamine Treatment with dopamine agonists inhibits the reuptake of dopamine
33
What is the maturational delay hypothesis?
Delayed development of higher cognitive functions (Inhibitory control, attention, temporal foresight) Symptoms tend to improve with age
34
What does neuroimaging suggest about the naturational delay hypothesis of ADHD?
Reduced size of cortico-striatal regions and reduced functional activation
35
What do the network dysfunction models of ADHD suggest?
Hypoactive PFC - organisation and planning, value based decision making. accounts for inattention and disorganisation
36
What are the different types of network dysfunction models of ADHD?
Attention model Reward model 'mind at rest'
37
What did cortese et al (2012) suggest about the attention model of ADHD?
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
What did ortiz et al (2015) find about the Reward model of ADHD?
Hypoactivity in the striatum for reward anticipation Hyperactivity dLPFC and OFC for reward receipt
39
What is the reward model of ADHD?
Related to the striatum, ACC, OFC central to reward processing Delayed gratification, impulse control Significance not assigned to longer term goals
40
What is the mind-at- rest model of ADHD?
Default mode network (DMN) - active when at rest, deactivated when task focussed Mind wandering, day dreaming, contemplating, reflecting
41
What does imaging research show about the mind-at-rest model for children with ADHD?
ADHD children are slow to switch off DMN - corrects with methylphenidate
42
How can you switch off DMN in children?
Methylphenidate
43
What are some pharmacological treatments for ADHD?
Dopamine and norepinephrine agonists: Dextroamphetamine, methylphenidate (ritalin) mixed with amphetamine (adderall) Sometimes NE agonists (atomoxetine) antidepressants or anticonvulsants
44
What is the core symptom of dyslexia?
Specific reading disability
45
What is the genetic basis of dyslexia?
Strong genetic influence Heritability 50%
46
What are the environmental factors associated with dyslexia?
Lower SES = 5-10 variance in reading
47
What are the causes of dyslexia?
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
What is included in the dual-route model of word recognition?
Lexical (orthographic/direct) route Phonetic (phonological/indirect) route
49
What is the lexical route of the dual-route model of dyslexia?
Word recognised as a whole unit and translated directly to a meaning Used for reading familiar and irregular words
50
What is the phonetic route in the dual-route model of dyslexia?
Letters translated into sounds (phonemes) using grapheme-phoneme conversion (GPC) rules and sounds are blended together Used for reading unfamiliar and nonwords
51
What are the causal theories of dyslexia?
Visual theory auditory processing theory cerebellar theory Magnocellular visual theory Phonological theory Orthographic learning Visual attention theory
52
What are the neural mechanisms of dyslexia?
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
How is dyslexia treated?
Early intensive explicit instruction Phonics based reading instruction