[W3] - L3

Question 1

Is Attention Deficit Hyperactivity Disorder (ADHD) a heterogeneous disorder?

Answer 1

Yes, ADHD is a heterogenous disorder (consisting of dissimilar or diverse ingredients/constituents); in that it is has different faces, it manifests differently for different people. Individuals have their own profile of difficulties and strengths.

Its prevalence amongst children is 5 -7% (about one a classroom), in adults: 2- 3%..

Question 2

Sample Case: An ADHD diagnosed child –> medication improved inattention/hyperactivity/impulsivity, but their academic problems persisted

Answer 2

Further testing revealed intact memory and attentional functions.

A reading disorder explained the learning problems, and a dyslexia intervention helped.

Question 3

Sample Case: An undiagnosed child –> forgets things/disorganized/impulsive –>attention tests/processing speed/memory were normal –> poor executive functioning

Answer 3

Executive dysfunction with normal attention = ADHD of the inattentive subtype

Question 4

Sample Case: Previous oppositional defiant disorder (ODD) diagnosis because of disregard for rules at school –> neuropsychological assessment revealed ADHD and anxiety

Answer 4

The child felt bad, but struggled to express remorse.

Their internalizing problems weren’t identified initially, hence they developed externalising problems.

Positive reinforcement with medication had good outcomes.

Question 5

Sample Case: Diagnosed ADHD –> irritable and poor interpersonal skills at school but not at home.

Answer 5

Neuropsychological assessment showed difficulties with selective attention, evidence for left-sided hemi-neglect emerged (omitted left-sided details, struggled using left fingers)

The conclusion was there had been an early cerebrovascular accident – ADHD/OCD may still apply because no other mental disorder was identified; we just now know a potential cause.

Question 6

How are ADHD symptoms represented in the DSM-V?

Answer 6

In the DSM-V, 6 inattention symptoms are required (for an inattentive subtype diagnosis - although symptoms are likely present from both sides, just dominant on one), 6 hyperactive impulsive required - and then 6 + 6 required for a combined presentation diagnosis. 18 total symptoms are listed (can receive other specified/unspecified diagnoses also)

The symptoms need to interfere with functioning. There are different severities of diagnosis (mild, moderate, severe). Other factors like ODD/CD, IQ, environmental issues (home problems/financial difficulties etc.) must be accounted for. Symptoms must present before the age of 12, and several life areas must be affected. You must exclude other mental disorders that could explain the behaviour (differential diagnosis) – so neuropsychological assessment is not strictly necessary!

For adults, only 5 symptoms in one group are required (as the symptoms are primarily based on childhood presentation).

Inattention Criteria:
- Attention to details/ careless
- Sustaining attention
- Seems not to listen
- Follow through instructions
- Organizing tasks/activities
- Avoids mental effort
- Looses things
- Easily distracted
- Forgetful

Hyperactive/Impulsivity Criteria:
- Fidgeting / squirming
- Leaves seat
- Runs / climbs
- Unable to play quietly
- On the go / driven by motor
- Talking excessively
- Blurts out answer
- Waiting turn
- Interrupting / intruding

[The DSM-5 diagnoses of ADHD do not address the neurological subtypes of attention that have been addressed in the literature]

Question 7

Where are inattentive ADHD symptoms vs. hyperactive symptoms more common?

Answer 7

Inattention is more common at school (expectations to be task oriented) and hyperactivity more common at home (space for free play).

Question 8

ADHD symptoms across the lifespan (heterogeneous with age and gender)

Answer 8

Pre-schoolers (0-6 yrs): hyperactivity
- In boys more running/climbing
- In girls more talking/chattering (“hyperverbal”)

› School age (7-12 yrs): inattention
- In boys with externalizing behaviours: intrusive and disturbing
- In girls internalizing behaviours: quiet and dreamy

› Adolescents (12-21 yrs): impulsivity
- In traffic and socially: accidents, drugs/alcohol, cross-border behaviour – aggression, sexual
- In boys more perpetrators; in girls more victims

› Adults (21+ yrs): weak executive functions
- Planning and organising life: unstructured household and financially
adventurous

Question 9

Comorbidity and ADHD

Answer 9

Comorbidity is relatively common in children with ADHD (1/3 with no comorbidity, 1/3 are comorbid with 1 other disorder, 16% with 2 or more, 18% with 3 or more)

In general, comorbidity is the rule, not the exception (45% of psychiatric patients exhibit comorbidity)

ADHD comorbidity statistics:
> Development Co-ordination Disorder ~50%
› Learning disability 46%
› Conduct disorder 27%
› Anxiety 18%
› Depression 14%
› Speech problems 12%
–
› School problems 69%
› Repeat grade 29%
› High aggravation score (high parental stress - difficult to manage) 53%

Question 10

How do we distinguish between normal or “abnormal” behaviors when diagnosing?

Answer 10

We ask:

Is the behaviour age appropriate (our expectations differ by age)

Does the behaviour fit the context (under time pressure?)

How often does the behaviour manifest itself (it must be persistent – examine its frequency/duration)

What was the developmental trajectory of these behaviours (when did they first manifest/develop)

How are interventions having an effect?

Are there functional impairments visible as a consequence of the behaviour’s presence?

Question 11

The Diagnostic Cycle for ADHD

Answer 11

Signaling/Screening: The first time someone think there might be ADHD (questionnaires are completed and scores are compared to the norm scores for that child’s age/gender)

Medical history/developmental history: Parents or caretakers are questioned via an interview.

Medical history: Teachers/ daycare staff/ sports instructors are interviewed.

Observation of the Child: The child is observed (or interviewed if they are older – this stage is not strictly necessary to confirm an ADHD diagnosis under the DSM; more to exclude other potential diagnoses like anxiety, autism spectrum disorder, tics – and to identify any neurological softsigns (in the face potentially) of genetic/neurological disorders). Note that you may not observe what you expect. In a new environment with an adult in control, their behaviour is unlikely to be typical of how it is at school or at home.

Question 12

Defining ADHD symptom severity with 3 criteria

Answer 12

[Behaviour Frequency, Level of Impairment, and Comparison to Peers]

› Frequency:
- Most days are bad
- Support needed

› Impairment:
- Needs intervention
- Impacts school work / class

› Comparison to peers:
- Deviates from peers
- Avoided by peers/teachers

[Note that comparison to peers can be dangerous as you will need an exact age match – as development happens rapidly and ages across the classroom can vary; hence levels of hyperactivity can vary! Relatively younger students in the classroom have a slightly increased chance of an ADHD diagnosis. The younger the child is, the stronger the effect of a small age difference is (i.e., 6-7 years).]

Question 13

Cognitive Ability vs. Intelligence/IQ

Answer 13

Cognitive ability/functioning does not exclusively mean intelligence/IQ!

There is some overlap though; with working memory being its own cognitive function but also a component of intelligence.

Question 14

The relationship between ADHD and IQ

Answer 14

ADHD can be diagnosed across children with a range of IQ score; although they typically score 7 to 12 points lower than their normative peers.

Unexpectedly low IQ in comparison with parental IQ in children with ADHD may be an indicator of birth complications.

Note that cognitive difficulties can sometimes be misrepresented in an IQ score (i.e., impulsive children reply quicker with less thinking, and will therefore score lower)

Question 15

Dual Pathway Model (Sonuga-Barke et al., 2011)

Answer 15

There are two different frontal networks involved in ADHD - the Executive Function network (meso-cortical branch) and the Reward Sensitivity network (meso-limbic branch). These can manifest as one of two distinct cognitive subtypes:

Executive Function Subtype:
› Response inhibition
› Dysregulation of action and thought
› Meso-cortical branch
› Off-task behaviour
› Consistent behavior
symptoms
› Cognitive Training can compensate

Reward Sensitivity Subtype:
› Delay aversion
› Different motivational style
› Meso-limbic branch
› Disruptive behaviour
› Symptoms depend on environment.
› Cognitive Strategies can compensate.

Question 16

Define Self-Regulation

Answer 16

Brain functions that control behaviour, emotions and attention.

It’s needed when we cannot rely on automatic actions, and when we must be goal-directed.

In Bailey & Jones’ model of regulation, regulatory gestalt is determined by cognitive regulation, emotional regulation, and social regulation —- which are in turn determined by executive functions like inhibitory control, attention control, set shifting, working memory [visual/verbal].

Question 17

How would poor executive functioning manifest itself?

Answer 17

Poor executive functioning can lead to off-task behaviour in which one is disorganized, lacks initiation, is forgetful, requires frequent prompts, perseverates on a task even when the class moves on, procrastinates, poor time management, doesn’t plan for the future (Similar to inattention ADHD symptoms!)

Question 18

The Reward Sensitivity Subtype in the Dual Pathway Model

Answer 18

The reward sensitivity subtype is characterized by impulsiveness, inattention, over-activity (stimming).

Question 19

Delay Aversion and Delay Discounting

Answer 19

Delay Aversion: Manifests as a preference for immediate over delayed reward.

Delay discounting: How much the effect of a reward diminishes depending on how significant the delay is for the reward receival. In children with ADHD, immediate rewards are much more effective and future rewards, like a good grade, are valued much less.

Question 20

ADHD and the maturation of frontal areas

Answer 20

The maturation of frontal areas is delayed in children with ADHD (peak of cortical thickness is achieved later – especially in the prefrontal cortex [roughly 2.5 years later than their peers])

Contrastingly, children with ADHD had early cortical maturation in the primary motor cortex (but the delay in executive function maturation may make this movement difficult to manage or rein in!)

Question 21

The Timing Pathway and the Triple Pathway Model (Extension)

Answer 21

The Timing Pathway is considered responsible for long distance connections with the cerebellum.

Manifestations of this pathway include:
› “Time blindness”
› Forgetting time / time slips away
› Arriving late, even when important
› Planning difficulties
› Inaccurate rhythm tapping
› Inaccurate time estimation
› Inaccurate time production

[Indeed, children and adults with ADHD have more difficulties moving to the beat. This is more evident with music than pure beats]

Question 22

Is there a single cognitive pathway to ADHD?

Answer 22

There’s no single cognitive pathway leading to ADHD (only 35 - 50% experience weak inhibitory control)

Aside from the Triple Pathway Model, some even speculate that there could be a fourth memory/decision making pathway.

Indeed, frontal network deficits are the most prominent explanation - but these networks involve connectivity to many areas of the brain: subcortical reward system, supplementary motor cortex, parietal cortex, cerebellum! The whole brain can be involved in ADHD, not only the frontal lobe.

When assessing ADHD, you should have a broad assessment covering all the relevant areas.

Question 23

Treating ADHD

Answer 23

Medication is no longer the first step - instead its psychoeducation, parent/teacher training, or behavior therapy (more restrained than it was 20 years ago).

Stimulants are the medication typically used if the other approaches have an insufficient effect (i.e., methylphenidate)

Some individuals do not respond to stimulants and therefore non-stimulants can be used (i.e., atomoxetine)

Stimulants Can – restore neural transmission of both dopamine and noradrenaline in the prefrontal brain of individuals with ADHD –- have large effects on ADHD behavioural symptoms but smaller effects on cognition are smaller – lower doses of stimulants appear cognition-enhancing, while higher doses of stimulants are behaviourally activating but cognition impairing! –Medication only has very small effects/improvements for academic performance (still lower than normative peers)

Promising interventions grounded in neuropsychology include: strategy instruction, cognitive training, physically active lessons, and neuro-feedback.

Question 24

Summarizing Lecture 3

Answer 24

› ADHD has different faces [Symptom expression; Comorbidities]

› Deciding what is “normal” is at the heart of diagnosing
neurodevelopmental disorders

› Determining symptom severity is crucial: frequency,
impairment, comparison to peers.

› Beware of the relative age of a comparative child, especially in young
children.

› ADHD is a disorder of brain maturation (delayed frontal areas)

› Behave and perform like younger children

› IQ is pressed by 7-12 points due to neuropsychological
deficits

› Lower IQs than expected can be due to birth complications

› Executive functions and reward sensitivity subtypes explain heterogeneity

> There’s no single cognitive pathway leading to ADHD

› Frontal network deficits are the most prominent
explanation

› Involves connectivity to many areas of the brain:
subcortical reward system, supplementary motor cortex,
parietal cortex, cerebellum.

› Whole brain can be involved in ADHD; not only frontal
lobe