Topic 3 - Seminar 3

Cognitive characteristics associated with ADHD and ASD

Forms of cognitive processes

• 7 cognitive processes

• 11 EFs

Cognitive processes = ways the brain operates to make sense of sensory input, combine with memory, and form abstract thoughts.

1. Thinking

2. Reasoning

3. Memory

4. Perception

5. Theory of Mind

   • thinking about what someone else might know/think to explain their behaviour

6. Language

7. Learning

Executive functions (EFs) = higher-level control processes regulating cognition + behaviour.

1. Initiation

   • ability to get started

2. Planning & organisation (for a task)

3. Set establishment, maintenance & change (cognitive flexibility)

   • make rules for a task, stick to them while working, then be able to adapt (switch rules/strategies) when new info comes in

   • E.g. Sorting cards: make rules to sort them by colour, maintain that you’re sorting by colour and not get distracted, and if someone says, “now sort by shape instead,” you can flexibly change your behaviour.

4. Judgement

5. Reasoning & abstraction (of info)

6. Self-regulation

   • of emotions + thoughts

7. Response inhibition

   • stopping ourselves from acting on primed impulses

8. Attention

9. Arousal (self-activation)

   • enough energy to start/act, but not so much you get irritable or hypervigilant

10. Working memory

11. Time perception

*NB: EFs 7-11 are more from an experimental perspective (things we measure in experiments)

What are the four main cognitive theories of ADHD?

The core ADHD symptoms (inattention, hyperactivity, impulsivity) are explained by four big theories:

1. Executive dysfunction → ADHD stems from problems with executive functions (e.g., inhibition, working memory, planning).

2. Delay aversion → ADHD reflects difficulty tolerating delay; preference for immediate rewards over long-term goals.

3. State regulation model → ADHD linked to difficulties regulating arousal/alertness (too high or too low at wrong times).

4. Dynamic developmental theory → ADHD explained by atypical reinforcement learning + dopamine system differences, unfolding across development.

1.Executive Functioning (Theory)

• No single cognitive profile defines ADHD → not every child has the same deficits (i.e. inattention).

• But most deficits are in EF (Neuropsychology model of ADHD)

• Most consistent and strong associations are seen for (deficits in):

  • Response inhibition

  • Vigilance/sustained attention

  • Working memory

  • Planning/problem-solving

  • Temporal discounting (time value of some cost/benefit -

    difficulty waiting; prefer immediate reward).

Group vs Individual findings:

• Experimental tasks:

  • Deficits are observed at the group level of analysis in experimental tasks

  • ADHD vs TD → huge group differences in EF tasks.

  • Some cases so severe it influences the group results → some severely impaired kids drag the group average down.

  • At individual level not all ADHD children perform poorly → performance is mixed.

• On EF surveys (e.g., BRIEF):

  • EF deficits are more prominent & widespread across both groups and individuals.

  • Parents consistently report daily-life EF issues (memory, organisation) more strongly than lab tasks capture.

Summary of above:

• Experimental tasks: group-level differences are clear, but not consistent at the individual level.

• Parent surveys (e.g., BRIEF): EF deficits appear more prominent and widespread — both across groups and within individuals.

2. State regulation/cognitive energetic (Theory)

Core idea: ADHD characterised by low arousal levels, people far more sensitive to external stimuli.

• Seek stimulation to raise arousal → looks like hyperactivity/impulsivity.

• If not stimulated/seeking stimulation → inattentive (low arousal state).

Arousal & activation account:

• ADHD kids activate themselves by seeking stimulation (bouncing, moving, impulsive).

Cognitive model systems in the brain

Effort system meets task demands and activates/inhibits Arousal and Activation systems

Hippocampus and Anterior Cingulate Cortex (ACC): Involved in state regulation (regulating your state & how cognitively energetic you are)

• Event rate experiments

  • ADHD kids bored at very slow event rate → poor performance; better and less mistakes with fast event rate.

• Heart rate variability (index of arousal)

• ERP experiments (EEG studies looking at event related potentials)

Effort system = what effort do you need to put into something to meet demands of your environment → responds by activating/inhibiting the arousal/activation system

1.Optimal stimulation theory (Zentall & Zentall, 1983):

• Inverted U-shape: best performance at moderate arousal.

• Over- or under-stimulation → poor performance.

2.Cognitive energetic model (Sanders, 1983): general theory of arousal regulation based on optimal stimulation theory

3.State regulation deficit theory (van der Meere & Sergeant, 1988): Specific theory for ADHD drawing upon the cognitive energetic model.

3. Delay Aversion (Theory)

Attempts to describe phenomena of children with ADHD being “able to wait but just don’t want to”

• Very discrete theory → kids are impulsive/hyperactive because they choose not to wait

Motivation account of ADHD

Argues children with ADHD choose smaller but immediate reward over larger but delayed rewards (i.e. temporal discounting)

• Older children with ADHD don’t do this, younger do

Model was expanded to account for inhibitory deficits in ADHD

• Inhibitory control/response inhibition was seen as a primary deficit in ADHD

Future rewards:

• Signalled by the dopamine system within the brain reward circuits (orbito-frontal cortex and ventral striatum)

• Circuits altered in ADHD because not enough dopamine available in VS

• Future rewards down weighted in ADHD children compared to NT who can see/prioritise the bigger reward coming later and wait

Sonuga-Barke (1992, 2003, 2005 etc)

4. Dynamic Developmental Model (Theory)

Behaviourism tradition

• Sagvolden et al., (1998 etc)

ADHD is associated with altered dopaminergic functioning that leads to inappropriate NA (noradrenaline) modulation

Three dopamine systems are affected with lower-than-expected dopamine with ADHD compared to NT:

1. Mesolimbic system: leads to a steepened delay-reward gradient in reinforcement of behavior and deficient extinction of previously reinforced behaviour. Deficits in sustained attention, impulsivity, delay aversion, hyperactivity in novel situations, disinhibition.

   • Smaller window and steeper gradient for effective link between stimulus and reward

     • Harder to positively reinforce behaviour if wait to link – not enough dopamine the link won’t be made

     • Can lead to problems extinguishing previously rewarded behaviour – altered in ADHD because of lower than normal amount of dopamine in this system

2. Mesocortical system: difficulties in orienting attention, impaired saccadic eye movements, poor executive functioning

3. Nigrostriatal system: impaired motor functioning, habit learning, motor clumsiness, soft signs, response inhibition difficulties

Many of the drugs for ADHD target the dopamine system to increase amounts of dopamine and noradrenaline in the brain, giving much better behaviour and executive control

What are the “accounts” or “models” of the four prominent cognitive theories of ADHD?

1. Executive dysfunction theory: Neuropsychology model (of ADHD)

2. State regulation/cognitive energetic theory: Information processing model (theoretical family) - but the account = arousal & activation

3. Delay aversion theory: Motivation account of ADHD

4. Dynamic Developmental theory: Behaviourism tradition model

What are the main cognitive theories of autism?

1. Weak central coherence account / Enhanced Perceptual Functioning

2. Mind-Blindness/Empathising-systemizing theory

3. Executive dysfunction

   • Sticky attention (subvariation)

4. Monotropism theory

Theory 1: Weak central coherence

This theory was enthusiastically received by ASD community

Typically developing people process incoming information for meaning and gestalt (global) form, often at the expense of attention to, or memory for, details and surface structure (“central coherence”)

• Central coherence = making sense of the whole, observed with typically developing people

  • Global form = quickly form a gestalt from the info and get the ”gist” of what’s going on

Individuals with autism exhibit “weak central coherence” → process information in the nitty gritty at the expense of understanding the whole.

Information processing deficit, where information is processed in a piecemeal way, at the expense of contextual meaning

• An information processing theory

Processing bias for featural and local information, and relative failure to extract gist or “big picture” (of sensory info) in everyday life

• This bias can be overcome by explicit instructions or demands for global processing….preference for local over global

• Not that they’re not able to look at the ‘gist’, just a preference/default

Alternative theory: Enhanced perceptual functioning → enhanced low-level perception in ASD and normal functioning of global processing

What does “weak central coherence” mean?

• And what does this theory account for in ASD?

Inability to integrate information into a meaningful whole

• Does not attempt to explain social elements of ASD

Weak central coherence theory accounts for:

• Fascination with unusual objects and local fixation

  • E.g. wheel of a train set but not really looking at the whole train itself

• Superior performance on Embedded Figures Task and WISC Block Design subtest, visual search tasks, visual discrimination tasks

• Poor performance on reading homographs in context (words with same spelling but two different meanings) and rearranging sentences to form a coherent context

  • Need to understand context of sentence to understand the homograph

Lead researchers of this theory: Uta Frith and Francesca Happé

Theory 2: Empathising-systemising theory

Theory to account for strengths and difficulties in ASD

• Attempts to explain the impairments in executive function and central coherence (and the strengths with systemising)

Deficits in the normal development of empathy (poor dev of empathy)

• Theory of Mind, cognitive component

• Original version of this theory was the Mind-Blindness theory (unable to read the mind of another person)

Systemizing refers to the drive to analyse, explore and construct systems and rules

• Either intact or superior in autism

Has been extended to explain male and female differences at the population level with the Extreme Male Brain theory

• Highly controversial, theory = autistic M/F have an extreme ‘male’ version of the brain, based on a stereotype about what the ‘male’ brain is

Theory 3: Executive dysfunction hypothesis

Executive functions regulate and manage lower-order cognitive functions

• i.e., attention and response-inhibition – which are fundamental cognitive skills that underpin complex higher-order EFs (e.g. those below)

• Sticky attention (next cue card)

Deficits in higher-order executive function will impact lower-order processes such as:

• language

• perception

• explicit memory

• learning

• action

Symptoms of autism are due to deficits in executive control over behaviour

• Explains the restricted, repetitive, stereotyped patterns of behaviour

• Due to anatomical dysfunction within the fronto-striatal and fronto-parietal circuits, people with autism will have difficulties with higher-order cognitive functions

Sticky attention (as a sub-component of EF/dysfunction theory of ASD)

Sub-component of EF/dysfunction theory of ASD

The socio-communicative impairments that define ASD are not present at birth but emerge gradually over the first two years of life

• Quite hard to test in early life

Basic attentional processes provide a foundation for socio-communicative skills

Aberrant attentional mechanisms, especially impaired disengagement of attention, emerge with the core ASD symptoms

• Problems with attentional mechanisms may lead to impaired disengagement of attention and shifting to something new in the environment – emerge with core ASD symptoms

Early deficits in disengaging attention may result in a cascade of impairments and ultimately contribute to the emergence of the ASD phenotype

• Cascading effect on the way you engage socially later in life aligned with ASD phenotype

Early attention issues may be an early neuro-behavioural marker of ASD

• If this is the case, then attention-targeted early interventions that remediate abnormal attention may place child back on normal developmental trajectory

Theory 4: Monotropism theory

• What is monotropism

• How does attention influence autism?

Monotropism = “restricted range of interests”

Atypical strategies for the allocation of attention are central to the autistic condition

• Difference between autistic and non-autistic people is a difference in strategies employed in the distribution of scarce attention

The limited availability of attention plays a central role in everyday life → need to choose where we focus

How we allocate our attention, whether it be over many interests or concentrated on a few, is a trait distributed normally over the population and to a large degree genetically determined

• Diagnosis of autism selects those at the tight-focus end of the distribution

  • Allocating their attention to a small number of things

Social interactions, use of language, and shifting of attention are all tasks that require broadly distributed attention

• Being able to hold a convo, follow the topics, use working memory, engage and form a response → requires a lot of attention across broad things

• For autistic people, these activities are inhibited by the canalization of available attention into a few highly aroused interests

  • Fixate on specific aspects of the convo that are highly arousing interests

Monotropism and autism

• Issues with steps performing a task

• Hyper- and hypo-awareness

To perform a task, any individual needs to:

1. See the point of the task (understand the task goal)

2. Value the point of the task (be motivated by it)

3. See how to perform the task (understand precisely what task it is, what steps must be taken to carry it out)

4. Understand how to take the identified steps

Monotropic individuals are likely to have problems with each of these steps

• I.e. if doing cognitive test with person with autism, may need to really spell out these steps

Hyper-awareness within the attention tunnel and a general lack of expectation, i.e. hypo-awareness, outside it

Variability in cognitive testing with autistic people may reflect “which interests have been fired into monotropic superdrive and which have been left unstimulated by any felt experience”

• Could be due to the cognitive test peaking the interests of the pt, or if they are unstimulated

“Intensely preoccupied with the movement of the spinning coin or lid, I saw nothing or heard nothing. People around me were transparent. And no sound intruded on my fixation. It was as if I was deaf” (Grandin and Scarino, 1986, p20)

• Captures the hyper-fixation (attention tunnel that they are interested in)

Helpful heuristics from Murray et al., 2005

• For monotropic attention

1. Motivate connections with other people, and positive views about society, through the individual’s interests: ‘Start where the child is’

   • Need to tailor things to peak the interest of the child

2. Ensure connections are acquired through the pursuit of an individual’s own interests; endogenously motivated links will be stronger and more stable

   • Stronger than being told to do something

3. Improve understanding in order to correct false or partial connections

• Connections between tasks etc or the big picture?

4. Reduce task demands in complexity, time pressure, and irrelevant stimuli

   • These things may capture/distract the person with autism along the way

5. Make tasks meaningful: if tasks and ideas are conveyed in small portions, ensure that the overall relatedness of the parts is understood

   • So that the whole point is understood