Mandy DD Part 3 Flashcards

1
Q

Neurcog theories - executive dysfunction

A

Executive dysfunction is top down cog processes that allow goal orientated decision making. Can be hot (ventral relating to inhibition) or cold (memory, planning and flexibility). Dysfunction is weakness in 1+ areas. Barkleys model of behavioural inhibition, primary is in self control, effects memory, speech, regulation which underpin motor control and reconstitution

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2
Q

Testing executive dysfunction

A

3 measures: response inhibition, vigilance and planning. Ps press button each time see cross and RT measures, beep presented 25% time which tells ps to inhibit response, intervals between go and no go vary and got longer as harder. Vigilance: CPT: connors letter sequence for 15mins, press button when target seq occurs, looking for omission errors or commission. Planning: tower of hanoi: stack objects as asked to move position in few moves W rules

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3
Q

Meta analysis of ED studies

A

Wilcut: studies 85-2004, found group diffs in all ED tasks across hot and cold. Effect size 0.51-0.57 medium , most consistent was stop signal RT and vigilance as more omission errors, tower of Hanoi. Fewer than half of adhd showed sig impairment tho

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4
Q

Adhd and grey matter

A

Grey:processes info, dendrites and soma. White: transports info,in aps. Frontostriatal circuit implicated in EF, one of last to mature, highest cortical area for motor actions, pathways connect to frontal and basal ganglia (motor control, cog and behaviour). Edmund: reduced grey matter vol compared to dolaminergic inner action in frontostriatal. Hart: adhd adults had less activation for inhibition and attention

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5
Q

Diffusion spectrum imaging

A

3d modelling used to represent nerve tracts using data collected by mri, uses diffusion of water molecules in brain as diffusion depends on the type of tissue and see fibre distributions
Children with adhd show atypical white matter tract structure in chen 2016 fronto striato circuit (part of EF netrwork)

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6
Q

White matter

A

Gau: 32 adhd ps and matched controls, used DSI for frontostriatal tracts and divided into 4: caudate dorsolateral, caud medial prefrontal, orbitofrontal and ventrolateral. Had altered white matter integrity in all 4 in both hemis, so poor attention, inhibition and schools functioning. EF measures and symptoms mediated associated between frontostriatal white matter and school functioning, regardless of age, gender and normal (a spectrum)

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7
Q

Delay aversion

A

Small immediate rewards compared to delay larger sonuga, faster decline in effectiveness of reinforcement as delay increases. No diff when delays not associated w rewards. Diff processing of rewards and states adhd is affective disorder. Reward network:fronto ventral striatal circuits, mesolimbic terminating in nuc accumbens

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8
Q

Evidence of delay aversion

A

Sonuga: child adhd wanted sooner reward even if less. Solanto: adhd and normal children did stop signal RT for inhibition and slay aversion, did discriminant function analysis to sort ps to adhd and control:found classified 68% correct, choice delay 71% correct and together 87.5%, no correlation between 2 measures , has been replicated in preschoolers to suggest multiple deficit approach:

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9
Q

Multiple deficits

A

equifinality is multiple forces that converge on parallel symptom displays MDT-pennington. Dual deficit theory Inhibitory linked to inattention and delay aversion linked yo hyperactivity

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10
Q

Adhd comorbidity

A

25-45% with dyslexia and asd. Adhd and dyslexia presence of adhd in reading disorder is 45%. Fam risk, phoneme awareness, letter knowledge and EF predicts reading performance. Poor reading skills and EF dyslexia goes up but no EF goes down, fam of dyslexia more likely to have adhd, overlaps W dld . Occurs W asd and tic disorders

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11
Q

Why DD are separate

A

Started w medical model, started with differentiation from norm, created deficit based which leads to bureaucracy which leads to research
Views are changing and control ps aren’t completely separate

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12
Q

Trans diagnostic approach

A

Moreno: in adult paych, looks at individual casss and puts symptoms first. Neuro disordered are diff patterns of symptoms reflecting common underlying continuum rather than causal. Songers view of natural variation continuum. Applies to clinical and research. Change is hard as system build around diff view, need resources and money

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13
Q

Problems with diagnosis in uk

A

No population screening as can lead to over identification and stigma from teachers. In us, most never diagnosed and in uk, parents bring up concerns but doesn’t lead to referral , only for hyperactivity. Overactivity may be goal orientated, inattentive may be insomnia and EF may be bipolar,

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14
Q

Treatment

A

Amphetamine led to better school outcomes and more relaxed behaviour, diff drugs in diff countries. Cns stimulant main treatment and atomoxetine. May cause insomnia, heart problems, misuse. Can strengthen abilities via games and tasks, organisation, attention training, inhibitions. Fatty acid supplement

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15
Q

Genetic links

A

Small genetic influence from twin studies, bad postnatal life diet, artificial colours, reduced thickness of cortex, reduced connectivity at rest in DMN

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16
Q

Camouflaging and interventions

A

When ppl try to hide their problems. Hobson and lee interviews parents of children with dld. Used in 8 ways (pro social, conversation skills, relying on others, avoidance, non verbal, disruptive, copying, other cog abilities). Delayed recognition and so support, - effects on energy, mental health. Interventions don’t work as not accessible as need language

17
Q

Spectrum 10k

A

Aimed to investigate genetic and environmental factors that contribute to wellbeing of asd - bad as wanted dna which could be used for bad