Neuroscience of

Developmental
Disorders.
Lecture 4: Attention Deficit
Hyperactivity Disorder.
Today’s Objectives

• Explore what attention deficit hyperactivity disorder is and

what aspects of development it can affect.

• To consider theories of ADHD, highlighting the need for a

multi-deficit view of developmental disorders.

• To examine the neurobiology behind the theories

• Comorbiditiy Watch: Consider the comorbidity between

ADHD and other Developmental Disorders and why we may
need to consider DD in a different way.
Attention Deficit
Hyperactivity
Disorder (ADHD)
Characteristics of ADHD

ADHD is defined on the basis of 2 dimensions:

1. Inattention
2. Hyperactivity/impulsivity
So not all children with ADHD are hyperactive!

These two dimensions result in 3 subtypes of

ADHD:
3. Hyperactive/impulsive (HYP)
4. Inattentive (INATT)
5. Combined
Characteristics of ADHD - Behaviours
Inattention:
• Often fails to pay attention to details & makes
careless mistakes
• Often has difficulty sustaining attention
• Does not seem to listen when spoken to
• Rarely follows through on instructions & fails
to finish work
• Difficulty organising tasks
• Reluctant to engage in tasks that require
sustained effort
• Often loses things needed for a task
• Easily distracted
• Often forgetful in daily activities
Hyperactivity:
• Restless, fidgets with hands or feet, or squirms in
seat
• Often leaves seat in classroom
• Runs about or climbs excessively in situations
where quiet behaviour is expected
• Difficulty planning or engaging in leisure
activities quietly
• Often ‘on the go’ or acts as if ‘driven by a motor’
• Talks excessively
• Blurts out answers before hearing the whole
question
• Has difficulty awaiting turn
• Interrupts of intrudes on others
 Prevalence in ADHD
1
• 5.9-7.1% (Wilcut, 2012)

• Reports in the media that prevalence rates are

going up ->
But
• Polanczyk et la. (2014)
• 54 studies published between 1985 and
2012
• Only studies that defined ADHD according
to strict criteria, prevalence remained
virtually unchanged
 Prevalence in ADHD
2
• 5.9-7.1% (Wilcut, 2012)

• Reports in the media that prevalence rates are

going up ->
But
• Polanczyk et la. (2014)
• 54 studies published between 1985 and
2012
• Only studies that defined ADHD according
to strict criteria, prevalence remained
virtually unchanged
Prevalence – More boys
than girls?
Official figures usually show that the ADHD population
is made up of more males than females. Taylor (2006)
found:
• 3:1 community sample
• 9:1 referred sample

However…
Girls are more likely to have inattentive ADHD and/or
be less disruptive and/or be less likely to have co-
occurring conditions (Biederman et al., 2005).

So, are there really less females with ADHD or are they
underdiagnosed?
 Ment Pit Stop 1
Which of these are sub-types of ADHD? Choose all that you think apply.
a) Combined
b) Attentive
c) Hyperactive/Impulsive
d) Hypoactive
e) Inattentive
 Terminology Check 1
Test Sensitivity
is the ability of a test to correctly
identify those with the disease (true
positive rate)

Test Specificity
is the ability of the test to correctly
identify those without the disease
(true negative rate).
 How is ADHD
diagnosed? 1
• Typically, via a psychiatric assessment (interviews, observations).
• DSM-V criteria (sensitivity rates 70-90%, Weiler et al., 2000):
• Symptoms causing impairment present before age 7
• Can be diagnosed as early as 4 years (American Academy
of Pediatrics, 2011), but most diagnoses mid childhood
(Wiloughby, 2013) and only 7-20% of 6 yos with ADHD
show persistent features earlier in development (Galera et
al., 2011)
• Impairment from symptoms occurs in two or more settings
• Clear evidence of significant functional impairment (social,
academic)
• Symptoms not accounted for by another psychiatric / mental
disorder
 How is ADHD
diagnosed? 2

However – There is no gold standard

criteria/test/cognitive marker, but
there are some direct measures of
inattentiveness & impulsivity that can
be used as part of the diagnosis.
 How is ADHD
diagnosed? 3
Conners Continuous Performance Test (Connors,
1996) for children aged 8+.

• Respond to targets and ignore non-targets

• Uses response speed, false alarms, misses and
hits
• Inattentiveness: is characterized by higher-
than-average misses
• Impulsivity: characterized by commission
errors (false alarms and anticipatory responses)
 How is ADHD
diagnosed? 4
But ADHD is most commonly diagnosed via
interviews and questionnaires:

• Conners 3rd Edition parent / teacher / self

report scale
• Strengths and Difficulties Questionnaire
(includes a hyperactivity scale) is often used
as an initial screener
How is ADHD
diagnosed? 5
 • Subjective criteria (i.e., might be a problem for one
family / teacher, but not another)
Diagnostic • Many non-specific problems that overlap with other
disorders (poor sleep, poor motor control,
Challenges literacy/learning difficulties, aggression)
• Many ADHD-specific traits feature in other
disorders…

ADHD GAD Mania Depression CD/ODD

Restlessness X X X X
Poor Concentration X X X X X
Increased motor activity X X X
Distractibility X X X X
Irritability X X X X
 Diagnostic
Challenges – EEG? 1
Could EEG diagnosis overcome the challenges
posed using behavioural diagnosis?
• Its readily accessible and inexpensive.

Reminder:
• it captures neuronal ensembled activation of the
cerebral cortex
• Different rhythms characterize different cognitive states
• Sleep – slow delta waves
• Concentration – high frequency beta activity
• Meditative state – theta
 Diagnostic
Challenges – EEG? 2
Could EEG diagnosis overcome the challenges posed
using behavioural diagnosis?

• Jasper et al. (1938) reported a slowing of the EEG

rhythms at fronto-central sensors in “behavioural
problem children” described as hyperactive,
impulsive and highly variable.

• But, 75 years on, clinical applications of EEG in

psychiatry are controversial, with methodological
limitations and a lack of diagnostic studies (Weder,
2013; Cortese & Castellanos, 2012; Loo & Makeig,
2012)…
 Diagnostic Challenges
– EEG? 3
Early reports of the use of EEG waves to
diagnose ADHD were promising with
initial studies showing:

Theta/beta ratio (TBR): Increased theta

(4-7Hz, slow waves) and/or decreased
beta (14-30Hz, fast waves)
Barry et al., 2003; Lubar, 1991).
 Diagnostic Challenges
– EEG? 4
There were early reports of medium to
large effect sizes for group differences:

• Ranging from .62-3.08

(Snyder & Hall, 2006; Boutros et al., 2005)

With diagnostic sensitivity rates of 90%

which exceeds the behavioural
interview/questionnaire measures on the
DSM V criteria (70-90%)
(Quintana et al., 2007; Monastra et al., 2001; Arns
et al., 2013 - review).
 Diagnostic Challenges – EEG? 5
Neuropsychiatric EEG-Based Assessment
(NEBA) offered in private clinics (e.g., in the
Science Park!)
• Costs roughly £350
• Calculates ratios of theta and beta brain
waves
• Approved by US FDA
But
• No agreed cut-offs (i.e., method not
fully standardised)
• No checks of reliability / validity
• No thorough research evaluation
(only one study to date carried out by
NEBA Health, which hasn’t been
published in a peer reviewed journal,
“triple-blinded protocol showed only
61% agreement between individual
clinicians and a multidisciplinary team.
However, that rate improved to 88%
once the NEBA system was added.”
 Diagnostic Challenges – EEG? 6
And… more recent findings haven’t been as positive:
• Replication failures of TBR differences in children (Ogrim et al., 2012) and adults (Loo et al., 2009).
Recent meta-analysis by Arns et al (2013) reported a non-significant TBR effect size that was
significantly associated with year of study publication (r=.96, p.002).
• Low sensitivity in some studies (Ogrim et al (2012) sensitivity of 65% and specificity of 58% in
differentiating between children with and without ADHD based on TBR, in contrast with an accuracy
of 85% based on classification by omission errors (on a CPT) alone) (see also Buyck & Wiersema,
2014).
• Not as simple as the TBR: Clarke et al (2012) characterized the variability within EEG data of 264
children (155 with ADHD) to reveal five behaviourally and symptomatically unique clusters. Only 36%
of the ADHD sample showed TBR. Not everyone with ADHD is the same (think about what we have
learnt about in our ‘Comorbidity Watch’ section).
• EEG not ready to serve as a tool to diagnose (potentially true of any univariate measures); although see
Lenartowicz & Loo (2014) for promising multivariate approaches.
 Diagnostic Challenges – Development 1
incessant and demanding ; play < 3
Preschool mins, not listening, no sense of danger

Another challenge, Our old

activities < 10 mins; forgetful,
friend – developmental School distracted; excessive movements in
Years
change! inappropriate contexts

excessive fidgetiness; attention < 30

Adolescence
• Key ADHD behaviours mins; no focus/planning; reckless
change over time
• 50% of childhood ADHD inner sense of restlessness;
Adulthood incomplete details;
cases ‘resolve’ by adulthood. impatient; accidents
• Other times, ADHD isn’t
diagnosed until adulthood.
 Diagnostic Challenges – Development 2
Agnew-Blais et al., 2016 (longitudinal Risk study)

• 247 / 2232 met criteria for childhood ADHD that persisted

to adulthood: more symptoms, lower IQ, great
academic/social impairments, anxiety, conduct disorder,
increased drug use

• 122 / 2232 diagnosed in adulthood but didn’t reach criteria

in childhood: fewer externalising problems, higher IQ, but
comparable symptoms and similar rates of mental health
disorders.
 Something to Ponder…
If a person is diagnosed in childhood and then is
resolved in adulthood:

• Has it resolved?
• Or has the person learned to mask/camouflage?

We don’t necessarily know the answer to this but

given the challenge of diagnosis in ADHD it’s an
important point to ponder.
 Ment Pit Stop 2
Which of the below do you think is the biggest challenge towards diagnosing
ADHD? Rank in order of biggest to smallest challenge.
• Characteristics of ADHD overlap with other conditions
• Criteria of diagnosis can be subjective
• Changes in presentation of characteristics across development
• No gold standard test for ADHD
• The characteristics of ADHD vary between individuals
 ADHD – Disorder or
Consequence of Society? 1

You may have heard debates around whether

ADHD is a real disorder.
• Questions around what contributes to ADHD
has a long history (i.e., Lancet article 1902)
• Description of children with motor
agitation, attention problems, difficulty in
controlling impulses, need for immediate
reward (George Still, 1902)
• Attributed the behavioural characteristics to
– the children had ‘no consideration for
others’
• Called the disorder ‘deficit of moral
control’
 ADHD Misconception
This historical example is emblematic of
the stigma associated with ADHD
symptoms

Those with ADHD are commonly

misinterpreted as having control over
their behaviour and being responsible for
their symptoms
 ADHD – Disorder or
Consequence of Society? 2

It did change from a ‘moral’ disorder to

a biological one, but wrongly thought to
be the result of brain damage (Hohman,
1922; Kahn & Cohen, 1934)

Renamed minimal brain dysfunction, as

it was observed that not all children had
brain lesions (Clements & Peters, 1962)

It eventually made its way into the DSM

in the 1980s
 ADHD – Disorder or
Consequence of Society? 3
But, much controversy remains about
whether ADHD should exist as a
diagnostic category…
• Is it a consequence of our education
system?
• Video of a talk given by Sir Ken Rob
inson – ‘Changing Education Paradi
gms’
• Is it a consequence of poor
parenting? (Johnston et al., 2012)
• Is it a construct of the expectations
of society (Social Construct Theory)
 The reality:
Consequences of ADHD
• Schooling: INATT associated with academic problems, even more
so than HYP (Breslau et al., 2008; Duncan et al., 2007)
• Social: Likely a result of not being able to detect/divide attention
across multiple subtle social cues (Kofler et al., 2011)
• Behaviour: HYP associated with later substance abuse, even when
controlling for conduct disorder (Elkins et al., 2007)
• Mental Health: Increased risk of internalising problems and
additive disorders (Beiderman et al., 2006)
• Employability: Lower ranking occupations on average (Mannuzza
et al., 2000)
• Discrimination: “laziness and aggression” (Kooij et al., 2010);
Stickley et al (2019) 3x higher odds of experiencing mental health
discrimination, based on self report
 Ment Pit Stop 3

How might these misconceptions and misunderstanding of

ADHD affect those with it?
Theories of ADHD
and their
Neuropsychology
Neurocognitive Theories 1
Executive Dysfunction
• Deficit in executive control (Barkley, 1997)
Delay Aversion
• Individuals have an aversion to waiting (Sonuga-Barke
et al., 1992; 1994)
Dual Deficit
• Inhibition/EF deficit & delay aversion (Sonuga-Barke,
2002, 2004, 2005)
Time Perception Deficit
• Deficit estimating time intervals when reward is offered
(Smith et al., 2002)
Excessive mind wandering
Intra-individual variability
• Fassbender et al (2009)
Neurocognitive Theories 2
Executive Dysfunction
• Deficit in executive control (Barkley, 1997)
Delay Aversion
• Individuals have an aversion to waiting (Sonuga-Barke
et al., 1992; 1994)
Dual Deficit
• Inhibition/EF deficit & delay aversion (Sonuga-Barke,
2002, 2004, 2005)
Time Perception Deficit
• Deficit estimating time intervals when reward is offered
(Smith et al., 2002)
Excessive mind wandering
Intra-individual variability
• Fassbender et al (2009)
Executive
Dysfunction
 Executive Dysfunction 1
What is Executive function?
Top-down cognitive processes that facilitate
goal-oriented decision making

• Hot (ventral/medial regions of the pre-

frontal cortex, including anterior cingulate
cortex)
• Behavioural inhibition/ Attention
• Cold (dorsolateral pre-frontal cortex)
• Purposeful, deliberate control processes
- Working memory/ Planning/ Cognitive
flexibility
 Executive Dysfunction 2
So Executive Dysfunction is:

• Weakness in one or more of these areas

• Theories either suggest one primary
deficit with knock-on effects or multiple
primary deficits
• Barkley’s model of behavioural inhibition
(1997) has been particularly prominent
• Primary deficit in development of ‘self-
control’ as a result of biological atypicalities
 Executive Dysfunction 3
Barkley’s model
of behavioural Causal, core deficit
inhibition (1997)

Leads to generalised deficits

Executive Dysfunction 4
Barkley’s model of behavioural
inhibition (1997)
According to this theory:
• Inhibition is a prerequisite for many
other EF skills that underpin motor
control
• This includes working memory, self-
control, internalisation of speech,
emotional regulation, cognitive
flexibility.
• Including reconstitution – referring to
flexible goal planning
Executive
Dysfunction –
Measures 1
There are three common measures of
Executive function:

• Response Inhibition: The stop

signal reaction time task

• Vigilance: Continuous
performance test

• Planning: Tower of Hanoi

ED Measures –
Response Inhibition
Response Inhibition: The stop signal
reaction time task:

• Pps need to press a button each time

they see a cross, and their RT is
measured
• A beep is presented on ~25% of trials
(tells pps to inhibit their response;
stop-signal).
• Intervals between ‘go’ stimulus and
‘stop’ signal varies. And intervals get
longer as the task gets harder
Executive
Dysfunction –
Measures 2
There are three common measures of
Executive function:

• Response Inhibition: The stop

signal reaction time task

• Vigilance: Continuous
performance test

• Planning: Tower of Hanoi

ED Measures -
Vigilance
Vigilance: Measures sustained attention
Continuous performance test – really boring!!!
(e.g., Conners, 1996)

• Sequence of letters for 15 mins

• Press a button when a target sequence occurs
• E.g., when ‘F’ occurs but only when it is preceded by ‘R’

i) Omission errors (missing a target)

ii) Commission errors (responding to ‘F’ when no ‘R’)
Executive
Dysfunction –
Measures 3
There are three common measures of
Executive function:

• Response Inhibition: The stop

signal reaction time task

• Vigilance: Continuous
performance test

• Planning: Tower of Hanoi

ED Measures -
Planning

Planning: Tower of Hanoi

Move a stack of objects from one

position to another in the fewest possible
moves while adhering to a set of rules.
• e.g., ‘the large ring cannot be
placed on the small ring’.
 Executive Dysfunction – Behavioural
Evidence
Meta-Analysis by Willcutt et al (2005):
83 Studies published between 1985-2004
• Group differences were found on all 13
executive function tasks
• Response inhibition (predicted by
Barkeley)
• Vigilance
• Set-shifting
• Planning
• Organisation
• Verbal working memory
• Spatial working memory
Hot EF Skills (Bold & Red text)
Cold EF Skills (Italic & Blue text)
• Effect sizes 0.51-0.57 (medium sized)
• Most consistent group differences for
(ADHD, controls):
• Stop Signal Reaction Time (response
inhibition)
• Omission errors on Continuous
Performance Tests (vigilance)
• Tower of Hanoi (planning)
• Porteus Mazes (planning)
• Note though: fewer than half children
with ADHD show significant
impairment on any specific EF task
(Nigg et al., 2005)
 Menti Pit Stop 4
Which EF measure considers inhibition?
a) Stop Signal Reaction Task
b) Vigilance
c) Tower of Hanoi
Neurobiology of EF: Grey & White
Matter Overview 1

Considering
Executive
Dysfunction in
ADHD

Grey Matter White Matter

 Grey & White Matter Introduction
Gray Matter:
Processes information in the brain. The
structures within the grey matter (e.g.
dendrites, soma) process signals generated in
the sensory organs or other areas of grey
matter and directs sensory stimuli to nerve
cells.

White Matter:
Transports the information. Information is
encoded in action potential and propagated
along neurons- WM integrity determines the
speed and fidelity of that information
Neurobiology of EF: Grey & White
Matter Overview 2

Considering
Executive
Dysfunction in
ADHD

Grey Matter White Matter

 ED – Neurobiology, Gray Matter 1
Returning to the EF network:
• We need to add some brain structures so
we will swap this diagram for a slightly
more complex one.

• Still shows the hot and cold regions we

looked at before but includes regions in
subcortical areas that are involved in
fronto-striatal circuits.
 ED – Neurobiology, Gray Matter 2
Grey Matter Structure:
• The fronto-striatal circuit has been
implicated in EF.
• One of the last to mature through
adolescence
• Highest cortical area involved in regulation
of motor action.
• Fronto-striatal circuits are neural
pathways that connect the frontal lobe
regions with the basal ganglia (striatum).
• Mediates motor control, cognitive and
behavioural functions within the brain.
 ED – Neurobiology, Gray Matter 3
Edmond, Joyale & Poissant (2009);
Hoogman et al (2017)

Reviewed a number of studies and found

reduced grey matter volume in the fronto-
striatal circuit.

Particularly in relation to Doperminergic

Innervation involved in the regulation of
executive functioning…… What does this
mean?
 Terminology Check
Dopaminergic
Releasing or involving dopamine as a
neurotransmitter

Innervation:
To stimulate a nerve or organ to
activity

Dopaminergic Innervation:
The releasing of dopamine to
stimulate
 ED – Neurobiology, Gray Matter 4
Edmond, Joyale & Poissant (2009); Hoogman et
al (2017)

In more detail they also found -

• Reduced grey matter volume:
• Total cerebral volume
• Prefrontal cortex
• Dorsal Lateral-Highest cortical area involved in regulation of motor action
• Ventral Lateral- Motor inhibition
• Striatum (Basal Ganglia)
• Highly innervated by dopaminergic neurons
• Goal-directed action
• Dorsal anterior cingulate
• Conflict monitoring
• Amygdala and hippocampus (limbic areas)
• Cerebellum
• Motor control & motor learning
ED – Neurobiology, Gray Matter 5
fMRI Evidence:
Hart et al. (2013) JAMA Psychiatry
Adults with ADHD showed reduce activation
for:
• Inhibition
• right inferior frontal cortex
• Motor area
• Anterior cingulate cortex
• Striato-thalamic areas
• Attention
• Right dorsolateral prefrontal cortex
• Posterior basal ganglia
• Thalamic and parietal regions
ED – Neurobiology, Gray Matter 6
 Neurobiology of EF: Grey & White
Matter Overview 3
Evidence suggest there are
grey matter difference in areas Considering
associated with executive
Executive
function in those with ADHD.
Dysfunction in
ADHD

Grey Matter White Matter

 Reminder:
Gray Matter:
Processes information in the brain. The
structures within the grey matter (e.g.
dendrites, soma) process signals generated in
the sensory organs or other areas of grey
matter and directs sensory stimuli to nerve
cells.

White Matter:
Transports the information. Information is
encoded in action potential and propagated
along neurons- WM integrity determines the
speed and fidelity of that information
Diffusion Spectrum Imaging
(DSI)
We’re going to be looking at some research
evidence which used DSI.
• 3D modelling technique used to visually
represent nerve tracts using data collected by
MRI
• It uses the diffusion of water molecules in
the brain to create this image.
• Water molecule diffusion is not random but
will present different depending on the
different types of tissue it is interacting with.
• When captured, these different diffusion
patterns help create complex images of
multiple fibre distributions and orientations
ED – Neurobiology, White
Matter 1

Children with ADHD show

atypical white-matter tract
structure:
• Chen et al (2016): Atypical
WM tract structures in
fronto-striato-cerebellar,
as well as fronto-posterior
and inter-hemisphere tracts
(see also Silk et al., 2009)
ED – Neurobiology, White Matter 2
Gau et al 2015
Participants: 32 adolescents with ADHD and 32 age-,
sex-, handedness- and IQ-matched TD controls
Method: Diffusion spectrum imaging (DSI) to reconstruct
the fronto-striatal tracts, divided into four functionally
distinct segments:
1. Caudate-dorsolateral
2. Caudate-medial prefrontal
3. Caudate-orbitofrontal
4. Caudate-ventrolateral
Results: ADHD group showed altered white matter
integrity in all four tracts (bilaterally) which was
associated with poor attention, vigilance, inhibition, and
school functioning
ED – Neurobiology, White Matter
Gau et al 2015 Continued…
They further showed:
• EF measures (except WM) and ADHD symptoms
partially mediated the association between fronto-
striatal white matter tract integrity and school
functioning, independent of age and gender

• This was the same in both TD and ADHD groups

• Fronto-striatal integrity – EF – School function –

a continuum?
Executive Dysfunction - Summary

• Executive dysfunction continues to be an

important neuropsychological correlate of
ADHD (Castellanos et al., 2006)
• Well supported with a prefrontal-striatal
model of ADHD, which has been
expanded to also include cerebellar
involvement (Krain & Castellanos, 2006)
• Supported by a number of structural and
functional imaging studies (e.g., Dickstein
et al., 2006; Nakao et al., 2011)
• But is it the whole story?
 Menti Pit Stop 5
Which circuit is important within the Executive Function
Network?
a) Striato-thalamic Circuit
b) Fronto-Striatal Circuit
c) Temporo-Striatal Circuit
d) Parieto-Striatal Circuit
Delay Aversion
 Delay Aversion
Theory – What is it?
Proposes that individuals with ADHD choose immediate-
small rewards to delayed-larger rewards (Sonuga-Barke
et al., 1992; 1994); poor delayed-gratification
• Faster decline in the effectiveness of reinforcement
as delay between stimulus and reward increases
• No difference between ADHD and control when
delays were not associated with rewards
• Suggests that atypical processing is with
rewards/motivationally salient outcomes
• Suggests ADHD is more of an affective disorder
(affects the way you think and feel).
Delay Aversion – The
Reward Network
• Fronto-ventral striatal reward
circuits (in blue)
• Mesolimbic branched terminating
in the nucleus accumbens

The Delay aversion theory suggests

that processing in this network may
differ in those with ADHD to
typically developing/ed individuals.
Delay Aversion – Behavioural Evidence
Sonuga-Barke et al (1992; 1994):
Task:
A child must make a choice between a small reward
associated with a shot delay or a large reward associated
with a long delay
• 1 point in 2 seconds (short delay)
or
• 2 points in 30 seconds (long delay)
Results:
Children with ADHD typically prefer to choose the
reward which will occur sooner despite the fact it is less.
Delay Aversion vs Executive Dysfunction:
One right, one wrong or multiple deficits? 1
Studies have been carried out to examine the extent to which EF
deficits vs delay aversion deficits accounts for the most variance
in ADHD symptoms.

Solanto et al (2001):
Participants: 45 children with ADHD & 29 CA-controls

Method: Stop signal reaction time task to measure

inhibition
Choice-delay task to measure delay aversion
Discriminant function analysis – classify pps into
ADHD or control based on performance
Delay Aversion vs Executive Dysfunction:
One right, one wrong or multiple deficits? 2
Results:
• SSRT classified 68% correctly
• Choice-Delay task classified 71% correctly
• Together classified 87.5% correctly

No correlations between the two measures, suggesting that

the two are independent and account for independent
variance in the ADHD cognitive profile.

Using both tasks led to the best classification rates.

Delay Aversion vs Executive Dysfunction:
One right, one wrong or multiple deficits? 3
This finding was replicated in preschoolers (Sonuga-Bar et
al., 2003) and suggests a multiple deficit approach may
provide the best account of ADHD

EQUIFINALITY
Multiple causal forces converge on parallel
symptom displays

Pennington’s (2006) multiple deficit model

Delay Aversion vs Executive Dysfunction:
One right, one wrong or multiple deficits?
Example of how the multi-deficit
Delay
view can help us understand Aversion
variability even within a
Developmental Disorder

Processing ADH Language

Speed pragmatics
D

Executive
function
deficits
Pennington, 2006
Dual-deficit
model
Characteristics of ADHD – Reminder
Inattention:
• Often fails to pay attention to details & makes
careless mistakes
• Often has difficulty sustaining attention
• Does not seem to listen when spoken to
• Rarely follows through on instructions & fails
to finish work
• Difficulty organising tasks
• Reluctant to engage in tasks that require
sustained effort
• Often loses things needed for a task
• Easily distracted
• Often forgetful in daily activities
Hyperactivity:
• Restless, fidgets with hands or feet, or squirms in
seat
• Often leaves seat in classroom
• Runs about or climbs excessively in situations
where quiet behaviour is expected
• Difficulty planning or engaging in leisure
activities quietly
• Often ‘on the go’ or acts as if ‘driven by a motor’
• Talks excessively
• Blurts out answers before hearing the whole
question
• Has difficulty awaiting turn
• Interrupts of intrudes on others
Dual-Deficit Model 1
Inattention:
Inhibitory/EF deficit (a dysfunction of
dorsolateral prefrontal cortex – a core node in
the striatal and attentional pathways) Most
strongly associated with INATT subtype (Fair
et al., 2012)
Hyperactivity:
Delay aversion (meso-limbic dopamine
branch associated with the reward circuits
(e.g., nucleus accumbens) Prominently
associated with HYP subtype
(Sonuga-Barke, 2002, 2004, 2005)
 Menti Pit Stop 6
Which set of characteristics are proposed to be attributed to the
Reward Network?
a) Hyperactive
b) Hypoactive
c) Attentive
d) Inattentive
Overall
Summary 1
• ADHD is a neurodevelopmental
disorder with a biological basis
• Symptoms of ADHD can be difficult
to accurately detect
• A number of neurocognitive theories
have been proposed to explain
ADHD; a multiple-deficit account is
the favoured approach as different
theories might account for different
‘subtypes’ of ADHD
Overall Summary 2
• Delays to the development of the EF/frontal-
striatal network provides a good, but not
complete account – research into interactions
with other networks is required
• Translational cognitive neuroscience in ADHD
is still very much in its infancy but deserves
further attention.
• This applies neuroscience to translate or
develop it into clinical applications (e.g.,
EEG for diagnosis).
Comorbidity
Watch
Comorbidity Watch 1

ADH
D

Dyslexia ASC

25-45% Co-occurrence
 Comorbidity Watch: ADHD, Dyslexia &
ASC
• Pennington’s Multiple

Biological
Deficit View can again

Environment
help us to see why these
conditions may overlap

• Remember: This view

incorporates the idea of
‘risk factors’ which can
occur at any level
Cognitive
• My examples are for
demonstration purposes
and are not exhaustive. Behavioural
Morton & Frith, 1995; Hulme & Snowling, 2009)
Comorbidity Watch: ADHD and Dyslexia
It might be hard to see how ADHD
and Dyslexia may overlap given

Phonology Dyslexia the risk factors I have covered ….

Presence of ADHD in
population with Reading
Disorder: 18-45% Executive
ADHD
Presence of Reading Disorder Function
in population with ADHD:
18-42%
Comorbidity Watch: ADHD and Dyslexia 1
Phoneme
Awareness
Age 4½

Letter

Age 8
knowledge Reading

Rapid
Automatised
Naming

Thompson et al. (2015) JCPP

Comorbidity Watch: ADHD and Dyslexia 2
Also found that Family Risk
Family Risk
predicts later reading difficulty,
suggesting a strong genetic
Phoneme
component.
Awareness
R2 = .27
Age 4½

Letter Reading
knowledge Age 8

Rapid
Automatised
Naming

Thompson et al. (2015) JCPP

Comorbidity Watch: ADHD and Dyslexia 3
They also found that executive
Family Risk
function significantly predicts
reading performance.
Phoneme
Awareness R2 = .42

Reading Age 8
Age 4½

Letter knowledge

Rapid Automatised
Naming
As we have seen EF is a key
risk factor in ADHD – here is
Executive Function
our common risk factor
Thompson et al. (2015) JCPP
Comorbidity Watch: ADHD and Dyslexia 4
Poor Core Skills
Poor Executive Function

Poor Core Skills

Good Executive Function
Thompson et al. (2015) JCPP
 Comorbidity Watch: ADHD and Dyslexia
5
Pattern of Phonology
phenotypic Verbal
& genetic reasoning
Dyslexia
overlap Working
Memory
Family members of
Processing individuals with
Speed Dyslexia are 2-3 times
ADH more likely to have
D
ADHD and vice-verse.
Inhibition

Willcut et al., (2010)

Comorbidity Watch: ADHD and Dyslexia 6
Working Delay
Memory Aversion

Deficit Dyslexia Processing

Deficit
ADH Executive
Speed
D Functioning

Language
Phonology Pragmatics
Comorbidity Watch: ADHD and ASC 1
Weak
Working Delay Central
Memory Aversion Coherence

Processing ADH Executive

AS ToM
Deficit Dyslexia Deficit
Speed D Functioning
C

Language Language
Phonology Pragmatics Pragmatics
Comorbidity Watch: ADHD and ASC 2
Weak
Working Delay Central
Memory Aversion Coherence

Processing Executive
AS
Deficit Dyslexia Deficit ADHD ToM
Speed Functioning
C

Language
Phonology Pragmatics
Comorbidity Watch: The complexity!
Weak
Working Delay Central
Memory Aversion Coherence

ADH
Deficit Dyslexia
Processing
Deficit
Speed D
Executive
Executive
Functioning
Functioning ASC ToM

Language
Language
Phonology
Phonology Pragmatics
Pragmatics

DL
D

Procedural Language
Deficits grammar
Why view DD as separate?
Why research into each DD is becoming less
isolated and is where the transdiagnostic
approach comes in.
 Why did it start off so separated?
• Everyone needs to start somewhere.

• DD research mainly started within a Medical view, so our

knowledge and understanding has grown within that.

• This has produced deficit-based diagnostic categories which have

then filtered into the bureaucracy of clinical practice, which also
filters back into research.

• However, as we research more in this area as well as linking with

different approaches such as the Social Model view – our
knowledge is growing, and views are changing.

• Particularly when research is showing that control participants

and those with DD are not clearly dichotomous…
 The ‘Transdiagnostic
Approach’ 1
Moreno-De-Luca et al. (2013)
• First introduced in adult psychiatry
• Places symptoms/characteristics at the
forefront
• Neurodevelopmental disorders would be
thought of as different patterns of
symptoms/characteristics reflecting a common
underlying neurodevelopmental continuum –
Ring any bells???
• Rather than being thought of as causally and
pathophysiologically distinct
• Results in a host of disorders referred to as
Developmental Brain Dysfunction.
 Links & Similarities
• ‘A common underlying neurodevelopmental continuum’
is a similar idea to the natural neurological variation put
forward in Singer’s (1998) Neurodiversity view.
• It’s not exactly the same, but it’s interesting how these
ideas and views are converging.

Transdia
Neurodiv gnostic
ersity Approac
h
 The ‘Transdiagnostic
Approach’ 2

This approach applies to both

research and clinical practise and
poses an advantage over
traditional diagnostic systems
which fail to account for the
significant overlap and variability
in clinical presentation of
disorders
 But change is difficult

• Our clinical system has been built and

developed within this modular view of DD
• It’s now full of bureaucratic systems organised
with this in mind, which control access to
resources and money
• Research may be able to move and adapt a
little more easily to new ideas, but it can be
very dependent on the clinical system in terms
of resources, participants, access to grants.
• Change is likely to be difficult and slow, but
the rise in ideas such as neurodiversity may
help this change – if change is the right
thing…
 Support
If you have been affected by any of the topics that have been discussed today
please do seek support if you think this would help you:
• You can contact our Wellbeing Support Officer, Daisy Whitwood:
daisy.whitwood@york.ac.uk

• If you have or think you have a developmental disorder, you can contact
Disabilities Services to find out what support is open to you.

• This link takes you to the student support page on the student wiki – where you
can find links to many support services that can help you, including:
• Mental health and wellbeing support
• Academic and Disabilities support
Any Questions?
I will stick around for a little bit if you have any
questions now.

You can also post any questions you have on the

VLE discussion board.

Link to Wiki page where you

can find information and links
to support services 