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NEUROPSYCH & CLINICAL NEURO > Week 12: Neurodevelopmental disorders > Flashcards

Week 12: Neurodevelopmental disorders Flashcards

1
Q

Malformation of the brain tissue during neurodevelopment is….

A

Often incompatible with life and will end in miscarriage or still births

However some can and do survive with deficits

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2
Q

What is hydrocephaly?

A

Occurs when there is excess CSF in the ventricles of the brain, increasing intracranial pressure

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3
Q

When does hydrocephaly occur?

A

Can occur prenatally due to congenital issues such as spina bifida

or

Peri or postnatally most likely due to an intraventricular haemorrhage among premature infants but may also be due to infections, cysts and brain injury

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4
Q

How do they relieve intracranial pressure in hydrocephaly?

A

Can use a shunt to drain the CSF from the ventricles

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5
Q

What are the 2 genetic and chromosomal disorders focussed on in this unit?

A

Turners’ syndrome

Williams syndrome

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6
Q

What causes turners’ syndrome?

A

Partial or total deletion of the X chromosome - meaning females are affected

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7
Q

People with turners’ syndrome do not develop….

A

Secondary sex characteristics

E.g. the development of ovaries is specifically affected

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8
Q

What is turners’ syndrome co-morbid with?

A

Learning disabilities and behavioural symptoms (ADHD or hyperactivity)

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9
Q

Explain intelligence in turners’ syndrome

A

Have low to average IQ but their verbal IQ is often way higher than their performance IQ

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10
Q

What treatments are used for turners’ syndrome?

A

Growth hormones

Sex hormone therapy

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11
Q

What causes williams syndrome?

A

Deletion of part of chromosome 7

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12
Q

Williams syndrome is….

A

rare

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13
Q

Are there any gender differences in Williams syndrome?

A

No it is equal in males and females

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14
Q

Those with williams syndrome are very….

A

Sociable, empathetic and talkative

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15
Q

What are the strengths of those with williams syndrome? but what are the slight downsides to these?

A

They have remarkable language skills despite their low IQ - this may mask their underlying disability

They have perfect pitch and sense of rhythm (musical ability) - however this makes them sensitive to sounds in their environment

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16
Q

What are some of the things those with williams syndrome struggle with?

A

Attention
Spatial abilities
Drawing objects
Problem solving

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17
Q

What distinct physical features do those with williams syndrome have?

A

An upturned nose and a broad mouth

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18
Q

What can be co-morbid with williams syndrome

A 
CVD
Gastrointestinal problems
Kidney issues 
Bladder problems
Joint problems (that affect motor control & delays motor development)
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19
Q

What changes occur in the brain for williams syndrome?

A

Cortical thinning (in parietal/occipital boundary and in the orbitofrontal cortex - explaining impairments in spatial cognition and hyper sociability)

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20
Q

Which area is spared in williams syndrome brains?

A

Superior temporal gyrus

auditory cortex - relates to musical ability

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21
Q

What are acquired (or preventable) disorders?

A

Occur when there is an injury to the brain either pre or postnatally
Typically due to radiation, toxins, malnutrition, tumours, brain injury

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22
Q

What is the most common acquired but preventable condition in children?

A

Fetal alcohol syndrome (an umbrella term for many conditions)

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23
Q

What causes fetal alcohol syndrome?

A

Occurs due to prenatal exposure to alcohol

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24
Q

Symptoms of fetal alcohol syndrome relate to the…

A

Dose and frequency of prenatal alcohol use

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25
Q

Alcohol consumption during pregnancy is more damaging when?

A

Throughout the first trimester of if used consistently throughout the whole pregnancy

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26
Q

What are the symptoms of fetal alcohol syndrome?

A 
Increased risk of low birth rate and reduced growth 
Poor muscle tone and coordination 
Seizures or tremors (neurological) 
Below average IQ + learning difficulties
Inattention 
Hyperactivity 
Poor behavioural regulation
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27
Q

What treatments are there for fetal alcohol syndrome?

A

Prevention is better than cure

There is some opportunity to identify mothers that need help to reduce consumption

Child:

  • Learning support
  • Behavioural management therapy
  • Speech and learning therapy
  • Can use medication for ADHD like symptoms
  • Social skills training
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28
Q

What is autism spectrum disorder (ASD)?

A

a complex developmental condition that involves persistent challenges in social interaction, speech and nonverbal communication, and restricted/repetitive behaviors

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29
Q

When does ASD become apparent?

A

Between 1 and 3 years

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30
Q

Are there any gender differences in ASD?

A

75% are male

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31
Q

What is ASD generally co-morbid with?

A

Intellectual impairments and learning disabilities

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32
Q

How does ASD present in infants?

A 
Poor eye contact 
Not responding to their name
Lack of showing and sharing 
No gesturing by 12 months 
Loss of language or social skills
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33
Q

How does ASD present in preschool children?

A

Limited pretend play
Odd or intensely focussed interests
Rigidity or inflexibility

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34
Q

How does ASD present in school-age children?

A

Concrete or literal thinking
Trouble understanding emotions
Lack conversational skills or appropriate social approach

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35
Q

What are the causes of ASD?

A

Can be genetic or environmental

  • also gene-environment interaction
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36
Q

Explain genetics and ASD

A

50% inheritability rates - greater risk among siblings or first-degree relatives

Genes that regulate brain development, neurotransmitter function and synapses have been identified

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37
Q

The environmental causes of ASD?

A

Perinatal birth complications
parental age (advanced age of parents)
Exposure to infections, pollution, nutritional factors
Maternal infection or immune activation during pregnancy

38
Q

ASD is characterised by increased brain volume. Where?

A

In frontal and temporal lobes

39
Q

White and gray matter in ASD

A

There is excess white matter and disrupted connectivity between areas

there is reduced cortical thickness in the temporal cortex and increased in frontal cortex

40
Q

What functional findings are there regarding autism brains

A

There is a mixed findings of increased and decreased glucose metabolism and blood flow compare to controls often in the limbic frontal and temporal areas

41
Q

What social factors are largely affected in autism

A

Impairments in theory of mind and emotion perception and processing

42
Q

What cognitive functions are moderately affected in autism

A

Processing speed verbal learning and memory

43
Q

What treatment is there for autism

A

You can use intensive learning experience and behavioural interventions in early childhood target communication and social behaviours

There are no recommended medications for the core symptoms but antipsychotics and prescription stimulants can sometimes be prescribed for other behavioural symptoms

44
Q

What is attention deficit hyperactivity disorder

A

Persistent patterns of inattentiveness and impulsivity and hyperactivity

45
Q

When is the typical onset of ADHD

A

Typically occurs before 12 years of age

46
Q

How many children have ADHD

A

5 to 7%

47
Q

How many adults have ADHD

A

2.5%

48
Q

Are there any gender differences in ADHD

A

It is two times more likely in males

49
Q

What are the three subtypes of ADHD

A

A combined subtypes with both of the core symptoms

A predominantly inattentive presentation

A predominantly hyperactive impulsive presentation

50
Q

What are are some of the inattentiveness symptoms of ADHD

A

Low attention to detail, can’t sustain attention, doesn’t listen when spoken to, can’t follow instructions a complete tasks, loss of items necessary for activities, easily distracted

51
Q

What are some of the hyperactivity and impulsivity aspects of ADHD

A

Often fidgets with hands or feet
Leaves their seat in situations when they’re not supposed to
Often runs or climbs in situations where it is inappropriate
Can’t be engaged in activities quietly
Often talks excessively
Has difficulty waiting their turn
Interrupts often

52
Q

What are some common psychiatric and medical comorbidities in ADHD

A 
Tourettes
Mood disorders
Learning disabilities
Diabetes
Hypertension 
Epilepsy
53
Q

What are some challenges or risks for those with ADHD

A 
Academic performance
School-related problems
Risk-taking
Social relationships
Antisocial behaviour
Drug abuse
54
Q

What is the inheritability rate of ADHD

A

70 to 80%

55
Q

What genes are involved in ADHD

A

There is a focus on the dopaminergic system associated with reduced dopamine and dopamine agonists are affective in treatment

other serotonergic genes are under investigation

56
Q

What are some environmental factors towards the cause of ADHD

A

Prenatal events such as low birth rate and complications

Substance exposures, heavy metal and chemical exposure

Nutritional factors such as vitamin D and omega three

Lifestyle and Psychosocial factors such as stress poverty and trauma

57
Q

What are the functional findings of ADHD brains

A

The frontostriatal structures and pathways are different such as reduced bloodflow in frontal lobes and basal ganglia during tasks that require cognitive control

These areas have rich dopaminergic projections and the medication to treat ADHD modulates the basal ganglia and frontal lobe activity working to increase the activity in these areas

58
Q

Explain EEG patterns in ADHD compare to normal controls

A

There is greater theta and beta ratios which is a marker of cognitive control.

When engaging in control there is a reduction in this ratio showing that ADHD children do not have the same level of cognitive control

59
Q

What cognitive processes are different in ADHD

A

Reduction in both focused and sustained attention

Verbal and working memory differences

Executive functioning differences such as planning, reward processing, risky or impulsive decision making, inhibitory control and attentional control

60
Q

What is the dopamine hypothesis of ADHD

A

Thought to be associated with reduced extracellular dopamine

Treatment with dopamine agonists inhibits the re-uptake of dopamine so there is more dopamine in the extracellular space

61
Q

What is the maturational delay hypothesis of ADHD

A

Delayed cortical thickness meaning delayed development of high cognitive functions and symptoms tend to improve or normalise with age as many children do not have severe symptoms of ADHD in adult hood

This is thought to be due to the late development of frontal lobes

62
Q

What is the network dysfunction model of ADHD

A

Suggests a hyperactive or reduced activity in the pre-frontal cortex that is required for organisation and planning accounting for in attention and disorganisation

However it does not account for impulsivity and hyperactivity

63
Q

What are the three separate attentional network models

A

Alerting model

Orienting model

Executive control network

64
Q

What is the alerting network within the attentional network model

A

It governs our general level of arousal and our vigilance

It is maintained by nopinephrine that is synthesised in the locus calculus of the pons projecting broadly throughout many areas of the brain

65
Q

What is the orienting network of the attention of network model

A

It is important to directing our attention to prioritise external information by selecting something to attend to

This can be automatic or voluntary it may catch our eye and we orientated towards it or we may wish to attend to it

The dorsal system is top-down and more voluntary

The ventral system is bottom up and re-orientating

66
Q

What is the temporal parietal Junction and how is it involved in the ventral system of the orienting network

A

It acts as an interrupt feature so that if something appears in our environment that we need to attend to it will interrupt our current processing and re-orientate us to that novel stimulus in the environment

67
Q

What is the executive control network of the attentional network model

A

It is involved in high-level regulation of the other systems including the orienting and alerting systems

it is important to prioritise information information for our current goals

68
Q

Explain the ventral system hypos and hyper situations

A

If it’s hypo the deficits in detecting irregularities in the environment and this my underlying problems in modulating behaviour based on changes

If it’s hyper it may end up in some of the distractibility symptoms for example this circuit is a bracket to orient I will attention so increased activation he may increase this instead of focusing on what is really important

69
Q

What is the reward model of ADHD

A

It can explain attention and impulsivity

The striatum, anterior cingulate cortex and orbitofrontal cortex central to reward processing

70
Q

What is the mind at rest theory of ADHD

A

It’s the default mode network this is active when you’re at rest and deactivated when you’re focused on a task so that other networks are important for the task activated imaging research shows that ADHD children are slow to switch off this network and it corrects with methylphenidate

71
Q

What are the pharmacological treatment of ADHD

A

Dopamine and norepinephrine agonists

They stop the reuptake and increases dopamine availability up regulating striatal to pathways

72
Q

What are the nonpharmacological treatments of ADHD

A

The typically less affective in terms of ADHD symptoms but they are helpful for symptoms that are left over after the medication is taken affect

Things such as behavioural interventions
Oh there’s things like cognitive training neuro feedback dietary nutrition information and caffeine

73
Q

What is dyslexia

A

Defined by specific reading disability is despite normal intelligence and exposure to adequate reading instructions

74
Q

What aspect of reading to those with dyslexia struggle with

A

Have problems with decoding written text instead of oral language comprehension

75
Q

How prevalent is dyslexia

A

7%

76
Q

Are there any gender differences in dyslexia

A

It is more common in males

77
Q

What are the common comorbidities of dyslexia

A

ADHD, language impairment and speech sound disorder

78
Q

Are there any cultural differences in dyslexia

A

There are severe cases of dyslexia when language is consistent in grapheme phoneme mapping this is not the case in English

79
Q

What is the genetic heritability rate of dyslexia

A

50%

80
Q

What are the brain differences in dyslexia

A

There are various subtle visual auditory and motor deficits seen however because there are different types of dyslexia there are possibly multiple causes

likely to stem from a deficit of phonological processing so the representation and comprehension of speech sounds

81
Q

What are the two aspects of the dual route model of word recognition

A

Lexical or the direct route

Phonetic or the indirect route

82
Q

What is the lexical route of the dual route model of word recognition

A

The word is recognised as a whole unit and translated directly to meaning

used for reading with familiar and irregular words

this is what we use when we become efficient in reading in order to comprehend it

83
Q

What is the phonetic or indirect route of dual route model of word recognition

A

Letters are translated into sounds

using grapheme phoneme conversion

so this is used for reading unfamiliar and nonwords non-words

84
Q

What is the visual theory of dyslexia

A

Based on observation that people with dyslexia often make word reversal errors it was argued that this was a result of a failure in establishing hemispheric dominance

85
Q

What is the phonological theory of dyslexia

A

Grapheme phoneme conversion route that seems to be the problem issues with reading words through this process of phonological decoding

86
Q

What is the most largely excepted best explanation of dyslexia theories

A

The phonological theory

87
Q

What is the orthographic learning theory of dyslexia

A

It emphasises the ability to establish those mappings between phonemes and graphemes rather than just a problem with the final logical representation of them themselves

88
Q

What is the visual attention theory of dyslexia

A

Performance on visual tasks is often different in people with dyslexia compare to neuro typical

This performance can predict reading ability at a later point in time

89
Q

What are the new mechanism differences in dyslexia

A

There is disrupted activation of the left hemispheric language network

The temporal region for phonological processing in grapheme and phoneme conversion

Occipital temporal for visual word form area and whole word recognition

90
Q

What are the treatments for dyslexia

A

It is recommended the children identified early

They can undergo early intensive instructions to learn how to read phonics maybe resulting in the normalisation of the reading and language left hemispheric networks

NEUROPSYCH & CLINICAL NEURO (12 decks)

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