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Psych year one > developmental disorders > Flashcards

developmental disorders Flashcards

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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
Q

dyad of ASD

A

social interaction and communication have merged so then that and resitriec interest and repetitive behaviours

26
Q

characteristics of ASD

A

social communication disorder- difficulties using spoken and written language, social

27
Q

how early do we observe ASD

A

12-24 months

28
Q

history of ASD explanations

A

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
Q

social deficit theory

A
  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
Q

neurology of ASC

A

low activation in frontal lobes
and amygdalamore activity in temporal lobe

31
Q

results of scanned brains whislt thinking about 16 social interactions

A

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
Q

how accurate at scannig peoples brain to see fi they had ASC

A

97%

33
Q

mirror neuron theory

A

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
Q

charectoristics of ADHD

A

innatention and hyperactive

35
Q

subdivisions of adhd

A

combined
innatentive
hyperactive

36
Q

adhd diagnosis

A

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
Q

conners continuous performance test

A
  • 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
Q

a person with innatentive ADHD would respond to the conners continuous perforemance test by

A

higher-than-average misses - not paying attention

39
Q

a person with impulse/hyperactive ADHD would respond to the conners continuous perforemance test by

A

commission errors (false alarms and anticipatory responses) hitting no targets/when they are not there

40
Q

what is a key diagnostic challenge of adhd

A

it symptoms are similar to o many other disorders

41
Q

EEG findings on ADHD brain

A

hyperactive = slow EEG rhythms
increased theta wave and decreased beta

42
Q

what is sensitivity rate of EEG and ADHD

A

90%
in private clinics can be used as a diagnostic tool

43
Q

developmental challenges of ADHD

A
  • key adhd behaviours change overtime
  • ## 50% of childhood ADHD cases resolve by adulthood
44
Q

adhd controversy

A

is ADHD a real disorder or caused by the education system, poor parenting, construct of society and its societal expecttations

45
Q

concequences of ADHD

A
  • 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
Q

neurobiology of ADHD, ciruit

A
  • 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
Q

brain areas involved in inhibition

A

righter inferior frontal cortex
motor area
anterioir cingulate gyrus
striato-thalamic areas

48
Q

brain areas and attention

A
  • Right dorsolateral prefrontal cortex
  • Posterior basal ganglia
  • Thalamic and parietal regions
49
Q

diffusion spectrum imaging

A

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
Q

Gau, DSI finding

A

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
Q

delay aversion and adhd

A

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
Q

difference between inattention and hyperactive ADHD (charectoristics)

A

inattentive = difficulty with attention, often loses things, easily distracted, no organization.

hyperactive = restless, fidgety, talkative, interrupts people

53
Q

adhd comorbidity

A

dyslexia - ADHD - ASC

Psych year one (19 decks)

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