1. Using ADHD as a model for
understanding neural networks
Dr. Laura Jansons
02/22/2014

2. ADHD
• Diagnosis made by behavior observation:
DSM-V
– 18 symptoms of ADHD, need to meet a
percentage of them to be diagnosed
– Diagnosed using behavioral checklists
– Problem for neuropsychologists:
• DSM-V is not based on NP test data
• DSM-V not based on Neuroanatomy
• DSM-V is based on “lesion” or disease model.

3. – Old: ADHD is dysfunction of frontal lobe
– New: abnormally functioning brain circuitry
– New: Several etiological influences, “common disease-
common variant model”
– New: ADHD is not one thing, there is not one place on
the brain we can map.

4. • Based on what we’ve learned from neuroimaging, we should
be thinking in terms of loops and connections, and not land
marks.
• Those loops recruited in ADHD:
–Cerebro-cortical
–Cortical-basal ganglia
–Cerebo-cerebellar
–Basal ganglia-cerebellar

5. 7 brain networks involved in ADHD
Yeo and colleagues (2011)
• Frontal Parietal network: effortful cognitive tasks, esp. novel.
• Ventral attentional network : directs attn. to salient objects. “What” you are
seeing or “what” an object is used for.
• Dorsal attentional network : Where and How of spatial attn. “Where” is object
located and “how” do I use it.
• Visual Network: interacts with dorsal and ventral route
• Limbic network: anticipation of rewards, monitors errors and conflict resolution.
• Sensory-motor network: motor skills
• Default mode network: What you are imagining at rest.

6. • What this means for neuropsychologists is
that it is no longer appropriate to think of
ADHD as a simple ‘‘frontal-lobe disorder’’
• Need to replace the localizationist view, ADHD
is not just one thing from one place in the
brain with one trajectory.
• This is why there is no NP test available, ADHD
is heterogeneous, the symptoms are
heterogeneous.

7. Functionally mapping ONE symptom of
ADHD using one type of test
• Stevens and colleagues, 2007, provided the first description
of how multiple neural network dynamics are associated with
response inhibition in normal control adolescent and adult
subjects in the performance of a “Go-No-Go” task.

11. • There is not one region in the brain
responsible for inhibiting response.
• There are “loops” of communication that
leads to disinhibition, in fact there are three.
• We are always “idling” and anticipating. When
the light is red, the car is not “off”.
• There is a lot going on when you inhibit a
response.

12. Withholding response
These loops can be mapped on the brain via
fMRI.
The following is the “blue”, “yellow” and “red”
circuit.
Correctly rejected No-Go stimuli involved with
successful response inhibition:

13. 13
Stevens, et al, 2007
Blue: pay attention there’s something unique
going on here, what do I do?
Yellow: transforming senses into actions. Object
recognition, salience/reward value
Red: Executive Control and Working Memory

14. Fig. 1. Brain regions in each component
associated with successful response inhibition.
(A) Fronto-striatal-thalamic indirect pathway
engagement consistent with
modulation of motor function (Blue); (B)
precentral gyri deactivation concurrent with
prefrontal and inferotemporal activation
(Yellow); (C) frontoparietal circuit
activity consistent with higher-order
presentations of No-Go’ response contingencies
(Red). Statistical results are thresholded at a low
of p < .001, corrected for
searching the whole brain.

15. Summary Stevens 2007
• Causal relationships among ensembles of
different brain regions.
• May help understand that there is no one
linear cause for disinhibition, alterations in
specific connections or brain region could
impact psychopathological conditions.

16. Stevens 2009
• Network dynamics supporting correct
responses and errors of commission
• NCs between 11 and 37
• Go/No-Go task

17. Stevens 2009
• The analysis found five distinct functional
networks related to correct hits and errors.

18. Go
XRapidly presented
(1000 ms intervals)
85% Go stimuli
right index finger taps

19. Go
X

20. Go
X

21. No Go
K

22. Correct Button Pushes
A: a motor-execution neural circuit integrated with frontal, parietal, and
striatal regions (Orange),
B: the ‘default mode’ neural network (imagining a task as if you were doing
it)

23. Errors A
A: a motor-
execution neural
circuit showing
absent or decreased
activity in brain
regions engaged for
higher-order control
(things are going on implicitly—without thought)
“whoops”
Car’s going down the road without a driver, disturbance in intention
program, start, stay stop. Connection between working memory and
Impulsivity—environment , stimulus, triggers behavior not thought

24. Errors B
B: a low-probability
stimulus processing
functional circuit that
has a greater response
amplitude to errors

25. Errors C
C: the pregenual
cingulate-temporal
lobe network
possibly reflecting an
affective response to
errors
(bilateral amygdala
activation)

26. • Why are NP task so inadequate?
Behaviorally defined criteria in ADHD
do not easily ‘‘map’’ on to functional
brain networks.
• With the advent of functional
neuroimaging, it was seen conclusively
that these sorting and planning tasks
should not fairly be considered
‘‘frontal’’ tests.

27. • assessment instruments were never designed
to evaluate the networks and interactions in
question.
• CPT’S are not ADHD tests: they measure a
range of impulses and don’t correlate with
one another.
• Current: widely accepted belief of causal
heterogeneity in ADHD. ADHD is not one thing
with one cause.

28. • the challenge to functional neuroimaging is to
find a way to effectively ‘‘diagnose’’ ADHD.

29. • Neuropsychology can establish itself at the
‘‘ground floor’’ in developing methodologies
to explore these different dimensions of
behavior.
• Challenge in the field today seems to need a
way to bring these two worlds together.