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Psych year one > developmental disorders > Flashcards

developmental disorders Flashcards

1
Q

what is a developmental disorder

A

impairments in a child’s physical, cognitive, language, or behavioral development

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2
Q

what is the medical model

A

the basis for research into DD
measures people against the ‘norm’
identifies problems with people
this provides knowledge and support

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3
Q

limitations of the medical model

A

individualistic
not reflective of the real world
deficit or difference

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4
Q

what is the social model of DD

A

aims to support society
difference between impairment and disability
caused b the way osicaty is organised]

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5
Q

approaches to studying developmental disorders

A

look at the process
look at the timing

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6
Q

what is developmental language disorder?

A

poor vocab
porr phonology - struggle to rpeated and ifferentiate between sounds
poor grammar

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7
Q

DLD deficit

A

deficit in procedural memory system,

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8
Q

DLD and declaritive memory

A

it is spared, intact aspects of language

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9
Q

what two things do we need for reading

A

decoding and comprehension

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10
Q

in dyslexia, our of the two things encessary for reading, they have a problem with?

A

decoding

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11
Q

what is dyslexia

A

Problems with accurate word recognition, poor decoding and poor spelling.

Life-time persistent

prevalence 3-6%

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12
Q

sensory theory of dyselxia

A

Rapid Auditory processing theory - deficit in rapid sounds

Rise time theory - impairment in the tracking of the amplitude rise, time in the minimum sound to max

Visual/magnocellular theory - rapid changes in visual stimulation, focuses on visual information rather than processing language

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13
Q

cerebellar theory of dyslexia

A

dysfunctional cerebbelium

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14
Q

the phonological deficit hypothesis of dyslexia

A

ore deficit = poor phonological coding

Semantic, syntactic and pragmatic language (and reading comprehension) unaffected

there are other non-core deficits in dyslexia

implicit phonology - using speech accuratley without thinking, everyday speech

this is phonological processing

measured - Nonword repetition, naming, short-term memory, paired-associate learning

explicit phonology - aware of language sounds

phonological awareness

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15
Q

evidence for PDH

A

performed worse a phoneme deletion task
non word repetition
rapid naming of colours blocks

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16
Q

PDH and neurobiology

A

areas involved in phonological processing and word processing would have a deficit
left hemisphere bc of its association with language

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17
Q

richlan and neurobiology of dyslexia

A

underactive = parietaltemporal lobe + left occipito -temporal cortex
left inferioir frontal gyrus - overactive

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18
Q

van der mark et al. research on the occipito-temporal system

A

found distruted connections in people with dyslexia

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19
Q

what is dyselxia comborbid with

A

DLD

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20
Q

what is the key quetsion regarding the relationship between DLD and dyslexia?

A

Are they seperate conditions with another effect when they work together or are they the same conditions with a difference in severity?

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21
Q

what does evidence suggest about DLD and dyselxia?

A

they are seperate disroders and worse when cobmorbid

  • comprehension experiment , comorbid and DLD highest
  • decoding, dyslexia then comorbid
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22
Q

what model explains why even tho DLD and dyslexia are seperate theyre commonly comorbid

A

the multiple deficit modele

23
Q

what is the multiple deficit model

A

many DD have risk factors some of whic are more important than others, these risk factors can overlap across DD

24
Q

triad of ASD

A

reciprocal social interactions - social communication - restricted interest and repetitive behaviors

25
dyad of ASD
social interaction and communication have merged so then that and resitriec interest and repetitive behaviours
26
characteristics of ASD
social communication disorder- difficulties using spoken and written language, social
27
how early do we observe ASD
12-24 months
28
history of ASD explanations
1943 - originate from the emotional coldness of a child’s mother. 1950s/60s - neurological underpinning 1980s - cognitive theories, neurocognitive, brains may differ and lead to observable cognitive effects 1990s, function of the brain and its link
29
social deficit theory
1. struggle to meta-represent, lack of pretend play 2. social difficulties bc tehy struggle to see people as agents with their own minds 3. unability to recognise peoples thughts
30
neurology of ASC
low activation in frontal lobes and amygdalamore activity in temporal lobe
31
results of scanned brains whislt thinking about 16 social interactions
results one: - Activation in posterior midline regions (including the precuneus which is part of the parietal cortical region) for controls but not for the autistic participants. - Interpreted as a lack of self-involvement in social representation of words like “hug”. results 2: white matter tracs are less developed in autistic patient
32
how accurate at scannig peoples brain to see fi they had ASC
97%
33
mirror neuron theory
more activity in the right isual and left anterior parietal areas less in insula and amygdala no actvity in the mirror neuron system in the inferior frontal gyrus
34
charectoristics of ADHD
innatention and hyperactive
35
subdivisions of adhd
combined innatentive hyperactive
36
adhd diagnosis
sysmptoms before 7 diagnosis usually at 6 psychiatric assements behaviours need to be observed in multiple settings mostly interviews and observations used to diagnose
37
conners continuous performance test
- Respond to targets and ignore non-targets - Uses response speed, false alarms (if they press when its a non target) , misses (miss a target) and hits
38
a person with innatentive ADHD would respond to the conners continuous perforemance test by
higher-than-average misses - not paying attention
39
a person with impulse/hyperactive ADHD would respond to the conners continuous perforemance test by
commission errors (false alarms and anticipatory responses) hitting no targets/when they are not there
40
what is a key diagnostic challenge of adhd
it symptoms are similar to o many other disorders
41
EEG findings on ADHD brain
hyperactive = slow EEG rhythms increased theta wave and decreased beta
42
what is sensitivity rate of EEG and ADHD
90% in private clinics can be used as a diagnostic tool
43
developmental challenges of ADHD
- key adhd behaviours change overtime - 50% of childhood ADHD cases resolve by adulthood -
44
adhd controversy
is ADHD a real disorder or caused by the education system, poor parenting, construct of society and its societal expecttations
45
concequences of ADHD
- **Schooling:** INATT associated with academic problems, even more so than HYP (Breslau et al., 2008; Duncan et al., 2007) - **Social:** Likely a result of not being able to detect/divide attention across multiple subtle social cues (Kofler et al., 2011) - **Behaviour:** HYP associated with later substance abuse, even when controlling for conduct disorder (Elkins et al., 2007) - **Mental Health:** Increased risk of internalising problems and additive disorders (Beiderman et al., 2006) - **Employability:** Lower ranking occupations on average (Mannuzza et al., 2000) - **Discrimination:** “laziness and aggression” (Kooij et al., 2010); Stickley et al (2019) 3x higher odds of experiencing mental health discrimination, based on self report
46
neurobiology of ADHD, ciruit
- the fronto-striatal circuit is implicated - last to mature - involved in motor action - mediated motor control, cognitive and behavioural functions. - reduced grey matter in this circuit - this effects the release of dopamine, preventing activty in these areas
47
brain areas involved in inhibition
righter inferior frontal cortex motor area anterioir cingulate gyrus striato-thalamic areas
48
brain areas and attention
- Right dorsolateral prefrontal cortex - Posterior basal ganglia - Thalamic and parietal regions
49
diffusion spectrum imaging
Diffusion spectrum imaging - DSI 3D modelling technique used to visually represent nerve tacts using data collected by an MRI uses diffusion of eater molecules to creat brain image difusiion resprents thebinteracting tissues complex images of fibre distrubitions children with ADHD show atypicak white-matter structure atypical in fronto-striato-cerebellar circuit
50
Gau, DSI finding
used DSI to reconstruct fronto-striato-cerebellar circuit and split it into four sections adhd group had altered white matter in all four tracts bilaterally (both sides of the brain) link between integrity of white matter tracts and how well they do at school that was shown on these tasks
51
delay aversion and adhd
adhd (hyperactive) chose immedate short rewards rather than delayed larger rewards. associated with reward network —> Fronto-ventral striatal reward circuits Mesolimbic branched terminating in the nucleus accumbens
52
difference between inattention and hyperactive ADHD (charectoristics)
inattentive = difficulty with attention, often loses things, easily distracted, no organization. hyperactive = restless, fidgety, talkative, interrupts people
53
adhd comorbidity
dyslexia - ADHD - ASC

Psych year one (19 decks)

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