ADHD Flashcards
Heritability of ADHD
- 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
Behavioural Features
Developmental Traits:
>Can co-occur
>Language, motor/social
Emotional Symptoms
>Frustration, irritability, mood lability
Education Problems
>In absence of SLD/LD
Cognitive Deficits
ADHD in adults
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%
Changes in symptoms
Stable trajectory in attention symptoms
>Middle childhood => adolescence & adulthood
Hyperactivity may decline over time ==> restlessness
-Impulsivity ?=> Verbal impulsivity
ADHD Medication works on:
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
Genes & ADHD
Common Variants are associated in ADHD
>Dopaminergic & adrenergic systems implicated
Endophenotypes:
Cognitive/brain markers that lie between behaviour & genetics
>They can help up to identify the genes implicated
TS & ADHD
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
Meta-analysis by Willcutt et al (2005):
Cognitive Impairments:
> Response inhibition: Withhold a response
Vigilance
Working memory
Planning
Further Cognitive Impairments:
> Response Aversion
> Response Time Variability
ADHD & Responsive Time Variability
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
Top Down & Bottom up processes to RTV
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
Brain Maturation and ADHD
Grey matter & Cortical Thickness abnormalities in:
- Right Orbital prefrontal cortex
EF
- Corpus callosum
Timing - Cerebellum
Planning & motor
Basal Ganglia
Connectivity & ADHD
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
fMRI – Meta-analysis (Cortese et al., 2012)
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?
Default Mode Network & ADHD
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
Neural Correlated of Response inhibition & attention in ADHD
Motor inhibition: Under-activation of supplementary motor area
Interference inhibition/shifting: anterior cingulate cortex
How does ADHD medication impact the brain?
1 dose increase activation in areas impaired in ADHD
>Right inferior PFC
>Ventral Anterior Cingulate Cortex (Shifting)
> Putamen
Decrease in:
>Supplementary motor cortex
fMRI reductions of activity in ADHD
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
Summary of Neural Abornomalities in ADHD
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
EEG in ADHD
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
Genetic Overlap between ADHD and Theta Power
Genetic correlation of ADHD & EEG influence
>ADHD & evoked theta
>RTV & Theta variability
Evoked Fronocentral theta-band variability
ERP & ADHD
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
Adult ADHD & ERP P3
Cued P3
Remitted: Cued P3 amplitude is the same as control
Persistent ADHD: still reduced P3 amplitude
ASD & ADHD
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
Emotional Processing & ERP in ADHD
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
