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B&B > B&B3 > Flashcards

B&B3 Flashcards

1
Q

what are developmental disorder

A

disorder resulting from a delayed or atypical mental or physical development - affects both physical and mental abilities

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2
Q

what is the medical model

A

measures individuals against the norm
it holds a deficit view - identifies problems with people

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3
Q

what is the social model

A

support society rather than approach research
put forward distinction between impairment an disability

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4
Q

define some approaches in studying developmental disorders

A
  • understand both typical and atypical developent
  • development is a process not an end product
  • multiple levels of research needed
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5
Q

define the causal model: theoretical framework

A
  • behaviour level: we observe difficulties in learning to read and write -> underlying cause at a cognitive level. external environmental factors influence 3 levels: behaviour cognitive and environmental
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6
Q

define developmental language disorder

A
  • language skills below peers of age equivalent score below mental age - no neurological damage and 7% prevalence
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7
Q

what is the procedural deficit hypothesis

A

specific deficit in procedural network -> basal ganglia, parts of frontal cortex

spared declarative memory -> hippocampus, medial temporal lobes

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8
Q

describe the difference between acquired and developmental dyslexia

A

acquired: illness or head injury
developmental: genetic

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9
Q

describe the rapid auditory theory of dyslexia

A

deficit in perceiving short and rapid varying sounds

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10
Q

describe rise time theory

A

impaired tracking of aptitude rise time cues

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11
Q

describe visual/magnocellular theories

A

respond to rapid change in visual stimulation - main deficit is reduced sensitivity within visual system

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12
Q

define the cerebral theory

A

dysfunction in motor control

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13
Q

define phonological deficit hypothesis

A

deficit in phonological decoding

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14
Q

describe two types of phonology

A

implicit - unconscious
explicit - conscious

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15
Q

describe the triad of impairment in asc

A
  • social communication
  • reciprocal social interactions
  • restricted interest / rigid and repetetive behaviours
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16
Q

signs of asc by 24 months

A

lack of warm and emotional expressions
lack of sharing emotional interest
lack of response to name
lack of interacting
atypical language development

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17
Q

define test sensitivity

A

ability of a test to correctly identify those with the disease (true positive rate)

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18
Q

define test specificity

A

ability of a test to correctly identify those without the disease (true negative rate)

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19
Q

describe some characteristics of inattention ADHD

A
  • fail to pay attention
  • careless mistakes
  • doesn’t listen when spoken to
  • difficulty organising tasks
  • easily distracted
20
Q

describe some characteristics of hyperactivity/impulsivity ADHD

A
  • restless, fidgeting
  • talks excessively
  • difficulty waiting turn
21
Q

describe the DSM-5 criteria for ADHD

A
  • symptoms causing impairment present before the age of 7
  • impairments from symptoms occur in two or more settings
  • clear evidence of significant functional impairment (social and academic)
22
Q

what are some challenges in diagnosing ADHD

A
  • subjective criteria: might be a problem for one family member/teacher but not another
  • many non-specific problems that overlap with other disorders (poor sleep, learning difficulties, aggression)
23
Q

describe Agnew-Blais longitudinal risk study

A

those who met the criteria for childhood ADHD that persisted to adulthood -> lower IQ, increased drug use, anxiety

those who got diagnosed in adulthood but didn’t reach the criteria in childhood -> fewer externalising problems, higher IQ, similar mental health issues

24
Q

ADHD as a moral disorder

A

questions around what contributes to ADHD has long history
- description of children with motor agitation, difficulty in controlling impulses -> get labelled as having no consideration for others

25
Q

ADHD as a biological disorder

A

the belief moved on from moral disorder to biological due to a belief in brain damage causing adhd

26
Q

describe Barkley’s model of behavioural inhibition

A
  • inhibition is a prerequisite for many other skills that underpin Motor control
  • includes working memory, self control, internalisation of speech, emotional regulation, cognitive ability
  • behaviour inhibition leads to generalised deficits and lack of motor control?
27
Q

describe the discussion about grey matter for ADHD

A

grey matter: processes information in the brain - the structures within the grey matter process signals generated in the sensory organs or other areas of grey matter and directs sensory stimuli to nerve cells

the fronto-striatal circuit
basal gangilia

28
Q

describe the discussion about white matter for ADHD

A

white matter: transports the information which is encoded in action potential and propagated along neurons
white matter integrity determines the speed and fidelity of that information
people with ADHD had altered white matter integrity associated with poor attention, vigilance, inhibition and school functioning

29
Q

describe delay aversion

A

those with ADHD choose immediate small rewards rather than delayed larger rewards

30
Q

describe the reward network for delay aversion (ADHD)

A

fronto-ventral stiatal reward circuits
mesobolic branches in nucleus accumbens

31
Q

describe the dual deficit model

A

associated with inattention subtype
- excecutive function deficit of dorsolateral prefrontal cortex

32
Q

why is development a challenge in diagnosis

A
  • 50% cases of childhood ADHD resolve by adulthood
  • other times, adhd isn’t diagnosed until adulthood
33
Q

describe the development of ADHD

A

preschool - incessant and demanding (not listening, no sense of danger, activities <3 minutes)

school years - forgetful and distracted (excessive movement and activities <10 minutes)

adolescence - excessive fidgeting, no focus or planning (activity <30 minutes)

adulthood - inner sense of restlessness and impatient

34
Q

define pragmatics

A

they way in which language is used in practice, such as implied or intended meaning

35
Q

what were the changes in the most recent autism update

A

aspergers disorder and pervasive developmental disorder no longer separated from autism
- all come under autistic spectrum disorder (ASD)
- new disorder: social communication disorder

36
Q

describe the core characteristics of asc

A
  • triad of imairment
  • social communication
  • reciprocal social interactions
  • restricted interests / rigid and repetitive behaviours
37
Q

signs of asc by 12-24 months

A

reduced typical social interest
lack of warm, emotional responses
lack of sharing emotional interest
lack of response to name
atypical language developmentd

38
Q

describe neurocognitive theories on asc

A

focus on the developing structure and function of the mind
allowed us to test hypotheses about associated brain function

39
Q

describe neurodevelopmental theories

A

focus on developing brain structures and function of the brain and nervous system

40
Q

what are the neurocognitive theories of asc

A
  • social deficit theories
  • weak central coherence theory
  • executive function
  • extreme male brain
41
Q

describe the theory of mind

A

can be refered to as mentalising - automatic unconscious ability
people with autism cannot pass the sally Anne task

42
Q

describe the atypical structure in people with DLD

A
  • left inferior frontal gyrus
  • left superior temporal gyrus
  • perisylvian cortext
43
Q

describe the changes in ADHD brain regions according to delay aversion

A
  • fronto-ventral striatal reward circuit
  • mesobolic branches and nucleus accumbens
44
Q

describe the changes in ADHD brain regions according to excecutive function theory

A
  • atypical white matter tracts in fronto-posterior and front-striatal-cerebral
  • reduced grey matter in front-striatal
45
Q

describe the fMRI evidence for autism brain changes

A
  • increased activity in parietal and occipital cortex
  • decreased activity in frontal circuits
46
Q

describe changes in brain regions for ASC according to neural networks evidence

A

increased temporal lobe activation
decreased frontal lobes and amygdala

47
Q

describe the implied reading network atypical structure for dyslexia

A

increased activation in left inferior frontal gyrus (compensatory reliance of effortful articulatory processes)
decreased activation in left inferior parietal lobule (general attention mechanisms )
decreased activation in left occipital temporal cortex (fast word recognition and orthographic processing)

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