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z year 1 Developmental > Developmental disorders > Flashcards

Developmental disorders Flashcards

1
Q

list aspects that create environment

A

diet, maternal drug abuse, orthnography, social envionment, teaching style, deprivation, trauma

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2
Q

what % of people are affected by developmental dyslexia?

A

3-6%

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3
Q

talk about dyslexia prevelance

A

cross-cultures
across lifespan
more males than females.

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4
Q

what does dyslexia inhibit?

A

reading achievement is Substantially below that expected given the person’s
chronological age, measured intelligence and age-appropriate
education

Significantly interferes with academic achievement or
activities of daily living that require reading skills

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5
Q

talk about causation of dyslexia

A

is not explained by a sensory deficit.

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6
Q

talk about memory deficits in dyslexia

A

verbal short term memory deficits- norm memory for visual info poor memory for verbal info.

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7
Q

what deficit do dyslexic patients have regarding naming objects

A

Rapid Automated naming deficits- naming well known objects at speed

Denckla & Rudel 1976

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8
Q

talk abut dyslexia and phonological awareness deficits

A
  • Syllable-tapping task: tap out the number of syllables (or beats) that youcan hear in the word (cat=1; banana=3)
  • Onset-rime (crust-cross) & initial-final phoneme (coat-goat) judgment tasks: both names were pronounced by the experimenter, and the subjects were asked to decide whether the names had any sounds in common.
  • Phoneme-tapping task: tap out the number of sounds that they could hear (cat=3)

deficits in all

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9
Q

discuss visual deficits in dyslexics

A

Cornelissen et al.

dyslexics have higher motion coherence thresholds than controls

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10
Q

Describe Buck’s phonological account to dyslexia

A

DIFFICULTY ANALYZING THE SOUND STRUCTURE OF LANGUAGE. this leads to a failure to learn systematic relationship between spellings and sounds. failure to master spelling sound correspondences is a primary source of the word recognition problems.

-innacurate representations not difficulty analysing.

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11
Q

what is a flaw with Buck’s phonological account to dyslexia?

A

a very specific account in that the problems are constrained to the domain of language

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12
Q

what is there debate about regarding dyslexia?

A

how different phonological functions/ issues are related (e.g. rapid naming vs decoding)

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13
Q

discuss dyslexia in terms of a temporal processing deficit

A
  • have difficulties percieving short streams of sound
  • difficulty perceiving tones of sound–> problems representing speech at a fine-grained level.
  • correlations between rate of auditory processing and reading errors.
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14
Q

discuss dyslexia in terms of a magnocellular deficit

A
  • visual difficulties- blurring/ moving/ inversed words and letters.
  • magnocellular stream is atypical in dyslexia
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15
Q

what does a magnocellular deficit account for

A

behavioural results of impared visual motion and reduced contrast sensitivity at low spatial frequencies

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16
Q

How can the magnocellular deficit system be reduced?

A
  • eye movements. letters appear to move (coverning one eye reduces errors)
  • attention and peripheral vision (reducing field of view reduces errors)
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17
Q

what two explainations are there for dyslexia?

A
  • Phonological processing deficit

- sesorimotor deficit

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18
Q

what is included within the sensorimotor deficit explaination of dyslexia?

A

temporal processing, magnocellular visual system, poss also cerebellum.

19
Q

what did Ramus et al. find to be the only deficit found in every dyslexic patient?

A

phonological processing

20
Q

what chromosomes are thought to have an influence on dyslexia?

A

15,6,1

21
Q

what gives evidence for the heritability of dyslexia?

A
  • family studies

- chromosomes

22
Q

what is the direct biological evidence to the magnocellular theory? and when would these arise

A

Postmortem: magnocellular layers of the LGN were disordered, 30% smaller than average neurones (Galaburda and Livingstone, 1993). These differences arise during the 4th or 5th month of foetal development.

23
Q

what is suggested that is needed for the magnocellular system to develop?

A

fish oils

24
Q

what biological evidence suggests the phonological processing system may cause dyslexia?

A

Normal- asymmetry of L/R planum temporale (L is bigger)

Dyslexics- symmetrical or R is bigger

poss link between symmetry of L/R planum temporale and severity of phonological deficits

25
Q

what study suggests that there may be an environmental element to dyslexia?

A

Paulesu et al.

shallowness/ depth of orthography

26
Q

discuss autism prevalence

A

1 in 100 children born
more males
present through life
at all IQ levels

27
Q

define vaguely autism

A

a severe disorder of communication, socialization and imagination

28
Q

how do those with autism face difficulty in social relationships?

A

poor use of non-verbal behaviour e.g. facial expressions.

lack of spontaneous seeking to share enjoyment / interest

lack of recognition of affect

lack of social/emotional reciprocity

limited sharing

29
Q

how do those with autism face difficulty in language and communication?

A
  • delay / lack of language
  • atypical nonverbal communication
  • repetitive language
  • one sided, awkward conversations
  • limited pretend play
30
Q

talk about autism and repetitive behaviour

A
  • preoccupation with restricted interests
  • inflexible, non-functional routines / rituals
  • stereotyped, persistent motor mannerisms
  • narrow, restricted fields of interest
31
Q

what are the two deficit accounts of autism?

A
  • theory of mind

- executive functions

32
Q

what is the processing style account of autism?

A

-local processing

33
Q

when given a theory of mind experiment (where will sally look for her toy) with 3-4 children who are normal, ASD and down syndrome how many pass?

A

normal- 85%
Down syndrome-86%
ASD- 20%

Baron-cohen

34
Q

how much later do children with autism develop theory of mind?

A

5 years later

fail to understand mental states

35
Q

how do autistic children compare to normal children on executive function?

A

planning and cognitive flexibility is far lower

normal- 40% ish
autism- 33% ish

36
Q

do autistic children have a strong or weak central coherence?

A

weak

37
Q

how do autistic children percieve features

A

features are retained and heavily perceived but at the expense of global configuration and meaning.

38
Q

regarding local and global info when will autistic children perform poorly and well?

A

good performance where attention to local information is an advantage
poor performance on tasks requiring recognition of global meaning or integration of stimuli in context

39
Q

what does Happe argue regarding autism explainations?

A

shouldnt expect there to be one single one

40
Q

discuss autism and genetics

A

not only autism itself is heritible but also relatives show increased rated of the broader autism phenotype or isolated traits.

41
Q

what did Baron-Cohen show about autism using fMRI?

A

when asked to pick emotional state/ if people were male/ female from pics of the eye region.

people with autism showed less extensive activation in frontal regions and no activation in the amygdala.

42
Q

what did Casteli find using fMRI on autistic patients?

A 
ASD (adult) group showed less activation
than typical controls in this ‘mentalising system’:
Medial-prefrontal
Temporo-parietal
Amygdala region
43
Q

what has been consistent in findings across studies of autism regarding the brain?

A

Mentalising- underactivation of social brain- PFC, ST, Amygdala- during social processing tasks

Overaction of frontostraital regions (dIPFC, BG- reward areas) during restricted/ repetitive task

less lateralised patterns during language tasks

fewer long range connections and more shorter ones.

decreased anterior> posterior connections

44
Q

is there a coherent accepted model for ASD yet?

A

no

z year 1 Developmental (7 decks)

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