Lecture 7 - ADHD Flashcards
What is the prevalence of ADHD in childhood populations?
Around 1%
What are the primary symptoms of ADHD?
Inattention
Hyperactivity
What are the 3 subtypes within ADHD?
- combined (both inattention and hyperactivity)
- inattentive
- hyperactive
What are the most common subtypes of ADHD?
Combined and inattentive
What is the controversy surrounding the ADHD subtypes; what do those arguing against the subtypes believe?
You can only have a combined subtype; you cannot have ADHD if you only have the inattentive or only have the hyperactive domain of symptoms.
Argue that, when someone is diagnosed with the inattentive or hyperactive subtype, the symptoms from the other domain are already there, they just have not been observed/have not manifested yet.
What did those arguing against the controversy, and for the subtypes, counter with?
There are different subtypes, each one responds to medication differently.
What was the action of the latest DSM, in order to resolve the controversy surrounding the subtypes of ADHD?
The DSM changed the subtypes to ‘presentations’ of ADHD.
- Ali not necessarily sure how this helps in changing/resolving the matter, however.
What type of disorder is ADHD believed to be?
Developmental
What did Gogtay et al., (2002) find about developmental abnormalities in ADHD?
Used longitudinal MRIs to measure total brain volume, total gray matter volume, total white matter volume and frontal gray matter volume in children with ADHD, childhood-onset schizophrenia, and healthy controls.
Across development from 4-22, the change in volumes of ADHD children, for all measures, followed the same trajectory as healthy controls, but were slightly behind/lower throughout (eventually, age 25-30, they caught up)
COS trajectories started normal, but quickly dropped, for all measures but total white matter volume.
Name the two models of maturation abnormalities in ADHD.
- ‘Maturational Lag’ model
- ‘Developmental Deviation’ model
What does the ‘Maturation Lag’ model assume about ADHD?
Children with ADHD are a few years behind their brain development. Means that eventually, when development ends, they will catch up (in volume).
- most children with ADHD have outgrown it by the time they are 19/20. However, some adults still do have ADHD (although some argue that adult ADHD is a different disorder to childhood ADHD)
What does the ‘Developmental Deviation’ model assume about ADHD?
ADHD is a deviation, rather than a lag, from normal brain activity - at some point, things go haywire and development either over or undershoots.
Which of the two models of maturational abnormality in ADHD is supported by the literature?
Neither model is fully supported by findings in the literature. In reality, it’s somewhere in the middle?
What did ***Maier et al., (2015) find about brain differences in ADHD patients?
Unmedicated adult patients with ADHD - no specific brain areas are different, but have general reductions in frontal regions.
What is a common deficit between childhood and adult ADHD?
They both have problems with response inhibition
Which neurotransmitter is implicated in ADHD, and generally, how is it aberrant?
Dopamine - too little transmission
Basal ganglia (nucleus accumbens), frontal cortex and caudate and putamen.
(***Sagvolden and Sergeant, 1998)
What was the model of ADHD proposed by Sagvolden, Johansen, Aase and Russell (2005)?
Dysfunction of dopaminergic systems resulting from drug abuse, genetics, or environmental pollutants may cause ADHD symptoms by interacting with fronto-striatal circuits.
What is the most common ADHD treatment, and what does it do?
Methylphenidate. Blocks dopamine transporters, leading to increased dopamine. Leads to increases in signal : noise ratio of striatal cells, and decreases background noise. Posited as a mechanism for improving attention by enhancing task-related neuronal cell-firing.
Since dopamine cells fire in response to salient stimuli, methylphenidate could amplify dopamine-induced increases to salient stimuli and thus be context dependent.
Volkow et al., (2005)
What did Volkow et al., (2004) find about the effect of methylphenidate on striatal activity on a neutral and mathematical task?
11C chemical (radioactive ligand, radioligand) competes with dopamine. Supplied it to participants. Were able to track it, and pick up where dopamine would normally bind to. –> Found lots of activation in the striatum.
When dopamine was released, the brightness of the striatum diminishes, representing less detection of 11C and more transmission of dopamine.
On neutral task, no difference in activation/11C detection in the striatums between patients given a placebo and patients given methylphenidate.
However, on a mathematical task, application of methylphenidate led to decreased 11C binding, indicating increased levels of dopamine transmission.
–> suggests that methylphenidate leads to increased dopamine, but only when dopamine is required - for example when the task demands attention/concentration (e.g. on the mathematical task, rather than the neutral task). Increased dopamine here increases saliency of the task, enabling greater performance.
What did Ter Huurne et al., (2015) study and find regarding methylphenidate and performance on a cognitive task?
Effect of methylphenidate on performance on a cognitive task (determining gender of a face).
Faces presented either next to another face, or next to a scrambled face, acted as distractors. RTs faster when scrambled face used as distractor.
Gave PPS methylphenidate or a placebo before performing the task. Application of MPH increased reaction times, but also increased accuracy of performance, across both distractor types, compared to PPS with placebo’s.
RTs longer for face distractors compared to scrambled face distractors, but the difference was larger for those on MPH. More effort required when presented with a salient distractor.
Suggests that MPH may improve cognitive processing, perhaps through increased dopamine, by opening up attention to greater amounts of stimuli, but this can backfire by allowing excessive application of attention, leading to slower processing when more salient distracting stimuli is present.
What is a distractor cost?
Slowing of reaction times as a result of using a distractor method/distractor stimuli.
What is the finding regarding ADHD diagnosis rate between countries, and why might this be the case?
More developed countries have more diagnoses of ADHD.
More awareness in developed countries.
Why is there controversy surrounding the treatment of ADHD?
Clinical diagnosis for which there are no laboratory or radiological confirmatory tests or specific physical features
Diagnostic criteria change frequently. No cure, can only outgrow the condition or manage it using drugs (but these are often stimulant drugs which have potential for abuse)
Define attention
Ability to look at/prioritise one (relevant) aspect of the environment/sensory information whilst ignoring another, (irrelevant) aspect.
What is EEG?
The measurement of the electric activity of the brain. Reflects the synchronous activity of millions of neurons.
Define ERP
The brain’s transient time-locked response to a stimulus.
What are the neural correlates of spatial attention?
If you must pay attention to something, the ERP
response increases.
Brain response is bigger when the location of the bar is cued, than when it is not.
If something is cued, the baseline activity adjusts itself so you are most responsive to it.
(Mangun et al., 1987)
What is the problem with using ERP markers in ADHD?
There is not much consistency in the ERP differences found.
What is alpha activity (10Hz) associated with?
Sensory cortices, specifically a lack of work/processing being carried out by such cortices.
What is theta activity (4-7Hz) associated with?
Frontal cortices, thought to represent the ‘conductor’; modulates neuronal activity in hippocampal, subcortical, limbic and cortical areas.
What does 15Hz mean for a brain signal?
The signal is fluctuating 15 times per second.
What did Cavanagh et al., (2011) show about theta rhythms and what they might represent?
Measured activation of the frontal cortex during a task where participants are told that their responses are correct or incorrect.
Brain activity shows increased frontal cortex activation around 200ms after incorrect feedback, compared to correct feedback. Implies that frontal responses, shown to be consistent with theta band activity (Mazaheri et al., 2009) could represent drives to change behaviour to reduce incorrect feedback on future trials.
What did Jensen, Ole and Mazaheri (2010) find about how the frontal cortex changes occipital activity?
Frontal cortex changes the occipital cortex, either increases alpha if you want to ignore something, or decreases alpha if you want to pay attention to something (increased alpha activity leads to decreased activity in sensory cortices)
What did Mazaheri et al., (2010) study and find regarding neurobiological underpinnings of ADHD, using an attention task? What do these results suggest and why are they important?
Children with ADHD, combined subtype. Very simple attention task. Presented with Vs, representing a visual stimulus to follow, or As, representing an auditory stimulus to follow. Valid cues meant that the correct domain of stimulus would follow, invalid cues meant that the opposite domain of stimulus would follow.
Measured accuracy and reaction time of discriminatory judgement between the two visual/auditory stimuli (either red or blue lizard for visual, and high vs low tone for auditory).
Faster, and more accurate, for valid cues across the board. However, ADHD children were less accurate and were slightly slower.
Also found that typical children reduced their alpha activity in visual cortices in the interval between cue and stimulus presentation. This would represent an increased ability of the visual cortex to prioritise information and attend to visual cues. No significant difference in ADHD children.
Correlation between alpha and all other parts of scalp. Typical children: Alpha modulation was correlated with theta activity over the front. This correlation between alpha and theta activity was not found in ADHD children.
Suggests no interaction/communication between frontal and visual cortex in ADHD. Suggests no alpha modulation in the visual cortex, representing an inability to prioritize visual information as well as typical children. ADHD children can still do the task, so must use an alternative, less efficient method.
Perhaps the lack of communication between frontal and visual cortices underlies the inability of ADHD individuals to discriminate between salient and irrelevant stimuli, a potential reason for their inattention.
What does the diagnosis of ADHD involve?
ADHD child should have 6 inattention or 6 hyperactivity criteria.
What did Mazaheri et al., (2014) study and find
Task: cues that told PPS to use left or right hand. Period of rest, presented with a stimulus array, had to respond according to the direction of the arrows. Compared typical, inattentive and combined ADHD children.
Cues resulted in alpha modulation in the visual cortex, highest amount in typical children, some modulation in combined subtype, but the inattentive subtype had the least amount (visual cortex was processing the cues the least). Alpha modulation represented a decrease in alpha activity, to enhance sensory attention/discrimination.
Typical children had the most amount of alpha suppression over their motor cortex, Combined subtype had the least alpha suppression. Suggests that the neural correlate of symptoms in the hyperactivity domain could be underpinned by a reduction in alpha suppression, leading to increased activity in motor regions.
Again found connectivity between frontal and visual systems in typical children, but the connectivity was lacking in both types of ADHD children.
Suggests lack of connectivity between frontal and visual cortex is common to both subtypes of ADHD, and that it is possible to look at the visual and motor system and differentiate between the combined and inattentive subtype neurologically.
