ADHD Flashcards

1
Q

Heritability of ADHD

A
  • Highly heritable trait
  • ->Twin studies 76% heritability
  • Several genes of small effect that interact with environmental factors
  • Shared genetic and environmental risk with other disorders
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2
Q

Behavioural Features

A

Developmental Traits:
>Can co-occur
>Language, motor/social

Emotional Symptoms
>Frustration, irritability, mood lability

Education Problems
>In absence of SLD/LD

Cognitive Deficits

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3
Q

ADHD in adults

A

15% of children will retain diagnosis of adults
>65% persisting impairing levels of symptoms
–>Not necessarily meeting diagnosis

Prevalence in Adults = 2.5% - 4.3%

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4
Q

Changes in symptoms

A

Stable trajectory in attention symptoms
>Middle childhood => adolescence & adulthood

Hyperactivity may decline over time ==> restlessness

-Impulsivity ?=> Verbal impulsivity

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5
Q

ADHD Medication works on:

A

Treatment operates on Dopaminergic pathways
>Link between genetic involved in dopamine and risk of ADHD

Decreased availability to dopaminergic receptors in the brains of adults with ADHD

Stimulant treatment = increase in amount of synaptic dopaminergic and noradrenaline

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6
Q

Genes & ADHD

A

Common Variants are associated in ADHD

>Dopaminergic & adrenergic systems implicated

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7
Q

Endophenotypes:

A

Cognitive/brain markers that lie between behaviour & genetics
>They can help up to identify the genes implicated

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8
Q

TS & ADHD

A

Tuberous Sclerosis Complex (TS)
>Brain tumours have an impact on prevalence neurodevelopmental disorders

Higher rates of ADHD – 60%
–>60% ASD
–>80% cognitive impairment
All have same genetic mutuation
- But 40% don’t develop – so what is going on?
Shrinking tumours in brain ==> reducing learning problems

TS & ADHD – strong RTV
Gene ==> epilepsy ==> response variability ==> increased ADHD symtoms
Therefore, the link between epilepsy and ADHD is mediated by RTV

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9
Q

Meta-analysis by Willcutt et al (2005):

Cognitive Impairments:

A

> Response inhibition: Withhold a response
Vigilance
Working memory
Planning

Further Cognitive Impairments:
> Response Aversion
> Response Time Variability

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10
Q

ADHD & Responsive Time Variability

A

Andreou et al. (2007)

  • Response time is highly variable – long and short
    >RTV decreases and normalises in fast + incentive task (condition 2)
    –>When the task is arousing and motivation
    –>This rapid improvement is specific to ADHD
    —->Compared to control and ASD
  • Links to mood and behaviour fluctuations
  • Genetic overlap and Higher response time variability
  • ->Endophenotype?
  • ->Lapses in attention – linked to suboptimal/decreased arousal level
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11
Q

Top Down & Bottom up processes to RTV

A

RTV = Response Time Variability

Bottom –up:
Subcortical structures that regulate arousal

Top-down
Executive control

==> Combination of both

All individual have subcortical arousal problems that persist
=>Those that ‘remitted’ – their executive functions got better

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12
Q

Brain Maturation and ADHD

A

Grey matter & Cortical Thickness abnormalities in:
- Right Orbital prefrontal cortex
EF

  • Corpus callosum
    Timing
  • Cerebellum
    Planning & motor
    Basal Ganglia
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13
Q

Connectivity & ADHD

A

DTI

Frontal regions have reduced connectivity to ‘posterior’ (back) regions
>Sustaining attention
–>We can’t push our information from the front to the back efficiently

Differences in the “rich club network”
>Networks that are richly populated in the brain
>ADHD lot less connections – the regions are not connected in the same way
>Opposite to SAD

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14
Q

fMRI – Meta-analysis (Cortese et al., 2012)

A

Hypo-activation/Decreased activation
>Ventral attention network
>Inferior Frontal cortex
>Basal ganglia
>Right hemisphere – frontal-parietal networks
Right = more involved in arousal and motivation

Hyper-activation/Increase arousal
>Default mode network
>Visual region
>Somatosensory regions
>Supplementary motor areas
Related to hyperactivity?
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15
Q

Default Mode Network & ADHD

A

Regions activated when you are not doing anything

Typical
DMM off when not doing anything ==> task positive networks (TPN) when doing something
ADHD they don’t switch off and on properly

Connections between DMM & TPN
-Development of these connections more delayed in ADHD

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16
Q

Neural Correlated of Response inhibition & attention in ADHD

A

Motor inhibition: Under-activation of supplementary motor area

Interference inhibition/shifting: anterior cingulate cortex

17
Q

How does ADHD medication impact the brain?

A

1 dose increase activation in areas impaired in ADHD
>Right inferior PFC
>Ventral Anterior Cingulate Cortex (Shifting)
> Putamen

Decrease in:
>Supplementary motor cortex

18
Q

fMRI reductions of activity in ADHD

A

Lower striatal activation

Frontal Regions = inhibitory control and motor function
>Fronto-striatal circuitry
>Cingulo-fronto-parietal network

Temporal and Parietal regions = attention tasks

Default mode Network = state regulation

Orbito-frontal-striatal = Reward/Motivation
Amygdala circuitry

Fronto-cerebellar circuitry = Temporal Processing

19
Q

Summary of Neural Abornomalities in ADHD

A

Decreased Long-range connectivity

Delayed Maturation in DMM

Hypoactivation in fronto-parietal executive control
Hypoactivation of ventral attention network

Hyperactivation of DMM and motor networks

20
Q

EEG in ADHD

A
THETA associated with ADHD
>Consistently altered band in ADHD
Theta power = much more elevated in ADHD
ES = 1.3
>Cortical under-activation/underarousal
>Potential link to increase response variability (RTV)
>Shared genetic influence with ADHD
21
Q

Genetic Overlap between ADHD and Theta Power

A

Genetic correlation of ADHD & EEG influence
>ADHD & evoked theta
>RTV & Theta variability
Evoked Fronocentral theta-band variability

22
Q

ERP & ADHD

A

CPT – OX
>Cued continuous performance task
(Respond/inhibit according to certain stimulus)

ADHD:
>Reduced amplitude of P3 to ‘no go’
>Reduced inhibitory control
>Reduced amplitude P3 to ‘cue’ trial
>Poor attentional orienting – the brain state is not appropriately tuned in to the task as TD
>Linked to subsequent performance 

Support ADHD as a general state regulation problem

With treatment:
No-Go P3 normalises
With medication
When reward was added to a task

23
Q

Adult ADHD & ERP P3

A

Cued P3
Remitted: Cued P3 amplitude is the same as control

Persistent ADHD: still reduced P3 amplitude

24
Q

ASD & ADHD

A

CPT task
>Inhibition

ADHD & ADHD + ASD

  • > Reduced amplitude of P3 ‘no-go’
  • -> ASD do not

Reduced inhibitory processing – unique to ADHD
Higher Conner’s inhibition = reduced P3

Conflict Monitoring
TD: amplitude reduces between go and no-go, as task demands reduce
- No difference in children with ASD
- ‘blunted’ for ADHD

25
Q

Emotional Processing & ERP in ADHD

A

N170
Reduced across all faces in children with ASD not ADHD

N400
BLUNTED responses to fearful faces in a particular context that you are in