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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
ADHD as a biological disorder
the belief moved on from moral disorder to biological due to a belief in brain damage causing adhd
26
describe Barkley's model of behavioural inhibition
- 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
describe the discussion about grey matter for ADHD
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
describe the discussion about white matter for ADHD
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
describe delay aversion
those with ADHD choose immediate small rewards rather than delayed larger rewards
30
describe the reward network for delay aversion (ADHD)
fronto-ventral stiatal reward circuits mesobolic branches in nucleus accumbens
31
describe the dual deficit model
associated with inattention subtype - excecutive function deficit of dorsolateral prefrontal cortex
32
why is development a challenge in diagnosis
- 50% cases of childhood ADHD resolve by adulthood - other times, adhd isn't diagnosed until adulthood
33
describe the development of ADHD
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
define pragmatics
they way in which language is used in practice, such as implied or intended meaning
35
what were the changes in the most recent autism update
aspergers disorder and pervasive developmental disorder no longer separated from autism - all come under autistic spectrum disorder (ASD) - new disorder: social communication disorder
36
describe the core characteristics of asc
- triad of imairment - social communication - reciprocal social interactions - restricted interests / rigid and repetitive behaviours
37
signs of asc by 12-24 months
reduced typical social interest lack of warm, emotional responses lack of sharing emotional interest lack of response to name atypical language developmentd
38
describe neurocognitive theories on asc
focus on the developing structure and function of the mind allowed us to test hypotheses about associated brain function
39
describe neurodevelopmental theories
focus on developing brain structures and function of the brain and nervous system
40
what are the neurocognitive theories of asc
- social deficit theories - weak central coherence theory - executive function - extreme male brain
41
describe the theory of mind
can be refered to as mentalising - automatic unconscious ability people with autism cannot pass the sally Anne task
42
describe the atypical structure in people with DLD
- left inferior frontal gyrus - left superior temporal gyrus - perisylvian cortext
43
describe the changes in ADHD brain regions according to delay aversion
- fronto-ventral striatal reward circuit - mesobolic branches and nucleus accumbens
44
describe the changes in ADHD brain regions according to excecutive function theory
- atypical white matter tracts in fronto-posterior and front-striatal-cerebral - reduced grey matter in front-striatal
45
describe the fMRI evidence for autism brain changes
- increased activity in parietal and occipital cortex - decreased activity in frontal circuits
46
describe changes in brain regions for ASC according to neural networks evidence
increased temporal lobe activation decreased frontal lobes and amygdala
47
describe the implied reading network atypical structure for dyslexia
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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